Podcasts about hco3

Nursing Mnemonics Show by NRSNG (Memory Tricks for Nursing School)

Play Episode Listen Later Sep 18, 2023 91:40

ReferencesJC mentioned that the diagnostic accuracy of 24 hour urine collection increases with more collections! Metabolic evaluation of patients with recurrent idiopathic calcium nephrolithiasisWe didn't refer to a particular study on sodium intake and the 24 hour urine but this meta-analysis Comparison of 24‐hour urine and 24‐hour diet recall for estimating dietary sodium intake in populations: A systematic review and meta‐analysis - PMC 24‐hour diet recall underestimated population mean sodium intake.Anna looking up ace i and urinary sodium Effects of ACE inhibition on proximal tubule sodium transport | American Journal of Physiology-Renal PhysiologyThe original FENa paper by Espinel: The FeNa Test: Use in the Differential Diagnosis of Acute Renal Failure | JAMA | JAMA NetworkSchreir's replication and expansion of Espinel's data: Urinary diagnostic indices in acute renal failure: a prospective studyHere's a report from our own JC on the Diagnostic Utility of Serial Microscopic Examination of the Urinary Sediment in Acute Kidney Injury | American Society of NephrologyJC shared his journey regarding FENa and refers to his recent paper Concomitant Identification of Muddy Brown Granular Casts and Low Fractional Excretion of Urinary Sodium in AKIAnd Melanie's accompanying editorial Mind the Cast: FENa versus Microscopy in AKI : Kidney360 (with a great image from Samir Parikh)JC referenced this study from Schrier on FENa with a larger series: Urinary diagnostic indices in acute renal failure: a prospective studyNonoliguric Acute Renal Failure Associated with a Low Fractional Excretion of Sodium | Annals of Internal MedicineUrine sodium concentration to predict fluid responsiveness in oliguric ICU patients: a prospective multicenter observational study | Critical Care | Full TextA classic favorite: Acute renal success. The unexpected logic of oliguria in acute renal failure Marathon runners had granular casts in their urine without renal failure. Kidney Injury and Repair Biomarkers in Marathon RunnersCute piece from Rick Sterns on urine electrolytes! Managing electrolyte disorders: order a basic urine metabolic panelThe Urine Anion Gap: Common Misconceptions | American Society of NephrologyThe urine anion gap in context CJASNExcellent review from Halperin on urine chemistries (including some consideration of the TTKG): Use of Urine Electrolytes and Urine Osmolality in the Clinical Diagnosis of Fluid, Electrolytes, and Acid-Base Disorders - Kidney International ReportsRenal tubular acidosis (RTA): Recognize The Ammonium defect and pHorget the urine pH | SpringerLinkOutlineChapter 13- New part: Part 3, Physiologic approach to acid-base and electrolyte disorders - Do you remember the previous two parts? - Renal physiology - Regulation of water and electrolyte balance- Chapter 13: Meaning and application of urine chemistries - Measurement of urinary electrolyte concentrations, osmolality and pH helps diagnose some conditions - There are no fixed normal values - Kidney varies rate of excretion to match intake and endogenous production - Example: urine Na of 125/day can be normal if patient euvolemic on a normal diet, and wildly inappropriate in a patient who is volume depleted. - Urine chemistries are: - Useful - Simple - Widely available - Usually a random sample is adequate - 24-hour samples give additional context - Gives example of urinary potassium, with extra renal loss of K, urine K should be < 25, but if the patient has concurrent volume deficiency and urine output is only 500 mL, then urine K concentration can appropriately be as high as 40 mEq/L - Table 13-1 - Seems incomplete, see my notes on page 406 - What is Gravity ARF?- Sodium Excretion - Kidney varies Na to maintain effective circulating volume (I'd say volume homeostasis) - Urine Na affected by RAAS and ANP - Na concentration can be used to determine volume status - Urine Na < 20 is hypovolemia - Says it is especially helpful in determining the etiology of hyponatremia - Calls out SIADH and volume depletion - Used 40 mEq/L for SIADH - Also useful in AKI - Where differential is pre-renal vs ATN - In addition to urine Na (and FENa) look at urine osmolality - Again uses 40 mEq/l - Mentions FENa and urine osmolality - Urine Na can estimate dietary sodium intake - Suggests doing this during treatment of hypertension to assure dietary compliance - 24 hour urine Na is accurate with diuretics as long as the dose is stable and the drugs are chronic - Diuretics increase Na resorption in other segments of the tubule that are not affected by the diuretic - Points to increased AT2 induced proximal Na resorption and aldosterone induced DCT resoprtion - In HTN shoot for less than 100 mEq/Day - Urine Na useful in stones - Urine uric acid and urine Ca can cause stones and their handling is dependent on sodium - Low sodium diet can mask elevated excretion of these stone forming metabolites - 24-hour Na > 75 and should be enough sodium to avoid this pitfall - Pitfalls - Low urine sodium in bilateral renal artery stenosis or acute GN - High urine sodium with diuretics, aldo deficiency, advanced CKD - Altered water handling can also disrupt this - DI with 10 liters of urine and urine sodium excretion of 100 mEq is 10 mEq/L but in this case there is no volume deficiency - Opposite also important, a lot of water resorption can mask volume deficiency by jacking up the urine sodium - Advises you to use the FENa - THE FENA - < 1% dry - >2-3% ATN - It will fail with chronic effective volume depletion - Heart failure, cirrhosis, and burns - Suggests that tubular function will be preserved in those situations - Also with contrast, rhabdo, pigment nephropathy - Limitations - Dependent on the amount of Na filtered - Goes through the math of a normal person with GFR of 125/min and Na of 150 has filtered sodium of 27,000/day so if they eat 125-250 mEq their FENa will be 600-800 - Urine osm < plasma osm in face of hypernatremia indicates renal water loss due to lack of or resistance to ADH - In ATN urine OSM < 400 - In pre-renal disease it could be over 500 - Specific but not sensitive due to people with CKD who are unable to concentrate urine- Specific gravity - Plasma is 8-10% igher than plasma so specific gravity is 1.008 to 1.010 - Every 30-35 mOsm/L raises urine Osm of 0.001 - so 1.010 is 300-350 mOsm/L H2O - Glucose raises urine specific gravity more than osmolality - Same with contrast - Carbenicillin- pH - Normally varies with systemic acid-base status - PH should fall before 5.3 (usually below 5.0) with systemic metabolic acidosis - Above 5.3 in adults and 5.6 in children indicate RTA - PH goal 6.0-6.5 - Separate individual RTAs through FR of HCO3 at various serum HCO3 levels - Also can monitor urine pH to look for success in treating metabolic alkalosis - Look for pH > 7 - In treatment of uric acid stone disease - Want to shift eq: H + urate – uric acid to the left because urate is more soluble - PH goal 6.0-6.5

Arterial Blood Gases Nursing Mnemonic (ROME)

Play Episode Listen Later Aug 29, 2023 2:10

Download for FREE today - special Mnemonics Cheatsheet - so you can be SURE that you have that Must Know information down: bit.ly/nursing-memory Outline ROME R-Respiratory O-Opposite M-Metabolic E-Equal Description First look at the pH: if it is low it is acidosis, high indicates alkalosis. Second use the ROME mnemonic to determine if you have respiratory vs. metabolic. For Metabolic look at HCO3. For Respiratory, look at pCO2. Metabolic Acidosis – pH Low, HCO3 Low. Metabolic Alkalosis – pH High, HCO3 High. Respiratory Acidosis – pH Low, pCO2 High. Respiratory Alkalosis – pH High, pCO2 Low.

blood rome nursing must know gases mnemonics arterial pco2 hco3

Podcast 864: Arterial Blood Gas (ABG) vs Venous Blood Gas (VBG)

Emergency Medical Minute

Play Episode Listen Later Aug 14, 2023 2:33

Contributor: Aaron Lessen MD Educational Pearls: What is measured in an ABG/VBG? Blood values for oxygen tension (pO2), carbon dioxide tension (pCO2), acidity (pH), oxyhemoglobin saturation, and bicarbonate (HCO3) in either arterial or venous blood Other tests can measure methemoglobin, carboxyhemoglobin, hemoglobin levels, base excess, and lactate What are they used for? Identification of ventilation/acid-base disturbances. For example: if a patient is in septic shock, oxyhemoglobin saturation can be used to guide resuscitation efforts (early goal- directed therapy) What's the difference between an ABG and VBG? One of the main differences is how the blood samples are collected. Venous blood gas is normally collected from existing venous access such as a central venous catheter. Arterial blood gases must be drawn from an artery, such as the radial artery. Arterial blood draws can be difficult, painful, and contraindicated in many situations. ABGs have traditionally provided more accurate measurements for assessing oxygenation, ventilation, and acid-base status. However, several studies have found that VBGs can still be used to accurately assess pH, pCO2, HCO3, lactate, sodium, potassium, chloride, ionized calcium, blood urea nitrogen, base excess, and arterial/alveolar oxygen ratio. This is supported by a recent study in 2023 in the International Journal of Emergency Medicine which specifically studied patients with hypotension and use of VBGs for resuscitation guidance. Are there other non-invasive methods that can be used to fill in the gaps to avoid ordering an ABG? Oxygenation can be measured by pulse oximetry Arterial carbon dioxide tension can be estimated by end-tidal carbon dioxide (PetCO2) Mixed venous blood gases are another alternative for patients who already have a pulmonary artery catheter References Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M; Early Goal-Directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001 Nov 8;345(19):1368-77. doi: 10.1056/NEJMoa010307. PMID: 11794169. Prasad H, Vempalli N, Agrawal N, Ajun UN, Salam A, Subhra Datta S, Singhal A, Ranjan N, Shabeeba Sherin PP, Sundareshan G. Correlation and agreement between arterial and venous blood gas analysis in patients with hypotension-an emergency department-based cross-sectional study. Int J Emerg Med. 2023 Mar 10;16(1):18. doi: 10.1186/s12245-023-00486-0. PMID: 36899297; PMCID: PMC9999648. Summarized by Jeffrey Olson, MS2 | Edited by Jorge Chalit, OMSII

blood identification emergency medicine international journal correlation pmid abg arterial new england journal of medicine venous summarized oxygenation abgs vbg po2 pco2 hco3

Treatment with furosemide indirectly increases inhibitory transmission in the developing hippocampus

PaperPlayer biorxiv neuroscience

Play Episode Listen Later Jul 12, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.11.548438v1?rss=1 Authors: Peerboom, C. N. E., Wijne, T. B., Wierenga, C. J. Abstract: During the first two postnatal weeks intraneuronal chloride concentrations in rodents gradually decrease, causing a shift from depolarizing to hyperpolarizing {gamma}-aminobutyric acid (GABA) responses. GABAergic depolarization in the immature brain is crucial for the formation and maturation of excitatory synapses, but when GABAergic signaling becomes inhibitory it no longer promotes synapse formation. Here we examined the role of chloride transporters in developing postnatal hippocampal neurons using furosemide, an inhibitor of the chloride importer NKCC1 and chloride exporter KCC2 with reported anticonvulsant effects. We treated organotypic hippocampal cultures made from 6 to 7-day old mice with 200 M furosemide from DIV1 to DIV8. Using perforated patch clamp recordings we observed that the GABA reversal potential was depolarized after acute furosemide application, but after a week of furosemide treatment the GABA reversal potential but was more hyperpolarized compared to control. Expression levels of the chloride cotransporters were unaffected after one week furosemide treatment. This suggests that furosemide inhibited KCC2 acutely, while prolonged treatment resulted in (additional) inhibition of NKCC1, but we cannot exclude changes in HCO3-. We assessed the effects of accelerating the GABA shift by furosemide treatment on inhibitory synapses onto CA1 pyramidal cells. Directly after cessation of furosemide treatment at DIV9, inhibitory synapses were not affected. However at DIV21, two weeks after ending the treatment, we found that the frequency of inhibitory currents was increased, and VGAT puncta density in stratum Radiatum was increased. In addition, cell capacitance of CA1 pyramidal neurons was reduced in furosemide-treated slices at DIV21 in an activity-dependent manner. Our results suggest that furosemide indirectly promotes inhibitory transmission, but the underlying mechanism remains unresolved. The furosemide-induced increase in inhibitory transmission might constitute an additional mechanism via which furosemide reduces seizure susceptibility in the epileptic brain. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

developing llc treatments copy expression increases transmission directly gaba hippocampus indirectly biorxiv inhibitory gabaergic furosemide wierenga ca1 hco3

306. Decompensated Right Ventricular Failure in Pulmonary Arterial Hypertension with Dr. Mardi Gomberg-Maitland and Dr. Rachel Damico

Cardionerds

Play Episode Listen Later Jun 8, 2023 60:13

The CardioNerds and Pulm PEEPs have joined forces to co-produce this important episode, delving into the management of decompensated right ventricular failure in pulmonary arterial hypertension. Joining us for this informative discussion are Pulm PEEPs co-founders, Dr. David Furfaro and Dr. Kristina Montemayor, along with Dr. Leonid Mirson (Internal Medicine Resident at Johns Hopkins Osler Medical Residency and Associate Editor of Pulm PEEPs), Dr. Bavya Varma (Internal Medicine Resident at Johns Hopkins, rising Cardiology Fellow at NYU, and CardioNerds Academy graduate), Dr. Mardi Gomberg-Maitland (Medical Director of the Pulmonary Hypertension Program at George Washington Hospital), and Dr. Rachel Damico (Pulmonologist and Associate Professor of Medicine at Johns Hopkins Hospital). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. CardioNerds Heart Success Series PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Decompensated Right Ventricular Failure in Pulmonary Arterial Hypertension A 21-year-old woman with a past medical history notable for congenital heart disease (primum ASD and sinus venosus with multiple surgeries) complicated by severe PAH on home oxygen, sildenafil, ambrisentan, and subcutaneous treprostinil is presenting with palpitations, chest pain, and syncope. She presented as a transfer from an outside ED where she arrived in an unknown tachyarrhythmia and had undergone DCCV due to tachycardia into the 200s and hypotension. On arrival at our hospital, she denied SOB but did endorse nausea, leg swelling, and poor medication adherence. Her initial vitals were notable for a BP of 80/50, HR 110, RR 25, and saturating 91% on 5L O2. On exam, she was uncomfortable appearing but mentating well. She had cool extremities with 1-2+ LE edema. Her JVP was 15cm H2O. She has an RV Heave and 2/6 systolic murmur. Her lungs were clear bilaterally. Her labs were notable for Cr 2.0, an anion gap metabolic acidosis (HCO3 = 11), elevated lactate (4.1), elevated troponin to 14, and a pro-BNP of ~5000. Her CBC was unremarkable. Her EKG demonstrated 2:1 atrial flutter at a rate of 130. Diagnosing RV failure in patients with PH: RV dysfunction and RV failure are two separate entities. RV dysfunction can be measured on echocardiography, but RV failure can be thought of as a clinical syndrome where there is evidence of RV dysfunction and elevated right sided filling pressures. RV failure is a spectrum and can present with a range of manifestations from evidence of R sided volume overload and markers of organ dysfunction, all the way to frank cardiogenic shock. Most patients with RV failure are not in overt shock. One of the first signs of impending shock in patients with RV failure is the development of new or worsening hypoxemia. Patients with decompensated RV failure approaching shock often do not present with symptoms classic for LV low flow state. Instead, hypoxia 2/2 VQ mismatching may be the first sign and they can be otherwise well appearing. Particularly because patients with PH tend to be younger, they can often appear compensated until they rapidly decompensate. Causes of decompensation for patients with RV dysfunction and PH: Iatrogenesis (inadvertent cessation of pulmonary vasodilators by providers, surgery if providers are not familiar with risks of anesthesia), non-adherence to pulmonary vasodilators (either due to affordability issues or other reasons), infections, arrhythmias (particularly atrial arrhythmias), and progression of underlying disease. Patients with atrial arrhythmias (atrial flutter or atrial fibrillation) and pulmonary hypertension do not tolerate the loss of...

failure medicine patients discovery associate professor nyu rv paths bp johns hopkins rr associate editor asd mardi lv sob circulation h2o maitland bnp johns hopkins hospital pah ventricular vq pulmonary arterial hypertension hco3 pulmonary hypertension program cardionerds

Chapter Eleven, part 2: Regulation of Acid-Base Balance

Play Episode Listen Later May 20, 2023 90:48

ReferencesWe considered the complexity of the machinery to excrete ammonium in the context of research on dietary protein and how high protein intake may increase glomerular pressure and contribute to progressive renal disease (many refer to this as the “Brenner hypothesis”). Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal diseaseA trial that studied low protein and progression of CKD The Effects of Dietary Protein Restriction and Blood-Pressure Control on the Progression of Chronic Renal Disease(and famously provided data for the MDRD eGFR equation A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study GroupWe wondered about dietary recommendations in CKD. of note, this is best done in the DKD guidelines from KDIGO Executive summary of the 2020 KDIGO Diabetes Management in CKD Guideline: evidence-based advances in monitoring and treatment.Joel mentioned this study on red meat and risk of ESKD. Red Meat Intake and Risk of ESRDWe referenced the notion of a plant-based diet. This is an excellent review by Deborah Clegg and Kathleen Hill Gallant. Plant-Based Diets in CKD : Clinical Journal of the American Society of NephrologyHere's the review that Josh mentioned on how the kidney appears to sense pH Molecular mechanisms of acid-base sensing by the kidneyRemarkably, Dr. Dale Dubin put a prize in his ECG book Free Car Prize Hidden in Textbook Read the fine print: Student wins T-birdA review of the role of the kidney in DKA: Diabetic ketoacidosis: Role of the kidney in the acid-base homeostasis re-evaluatedJosh mentioned the effects of infusing large amounts of bicarbonate The effect of prolonged administration of large doses of sodium bicarbonate in man and this study on the respiratory response to a bicarbonate infusion: The Acute Effects In Man Of A Rapid Intravenous Infusion Of Hypertonic Sodium Bicarbonate Solution. Ii. Changes In Respiration And Output Of Carbon DioxideThis is the study of acute respiratory alkalosis in dogs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC293311/?page=1And this is the study of medical students who went to the High Alpine Research Station on the Jungfraujoch in the Swiss Alps https://www.nejm.org/doi/full/10.1056/nejm199105163242003Self explanatory! A group favorite! It Is Chloride Depletion Alkalosis, Not Contraction AlkalosisEffects of chloride and extracellular fluid volume on bicarbonate reabsorption along the nephron in metabolic alkalosis in the rat. Reassessment of the classical hypothesis of the pathogenesis of metabolic alkalosisA review of pendrin's role in volume homeostasis: The role of pendrin in blood pressure regulation | American Journal of Physiology-Renal PhysiologyInfusion of bicarbonate may lead to a decrease in respiratory stimulation but the shift of bicarbonate to the CSF may lag. Check out this review Neural Control of Breathing and CO2 Homeostasis and this classic paper Spinal-Fluid pH and Neurologic Symptoms in Systemic Acidosis.OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

Alkolik Ketoasidoz

Play Episode Listen Later May 15, 2023 7:29

Alkolik ketoasidoz (AKA), genellikle aşırı alkol kullanım öyküsü olan, yetersiz beslenen hastalarda ortaya çıkan bir sendromdur.1Karın ağrısı, mide bulantısı ve kusma sonrası aktif alkol alımı durmuştur. Bu hastalar alkole ara verdikleri dönemden 1-3 gün sonra hastaneye başvururlar. Bu dönemde alınan kan etanol seviyeleri normalin altında çıkabilir.2Normalde vücudun açlığa verdiği yanıt, glikoz üretmek için hepatik glikojen depolarını kullanmaktır. Kalori ihtiyacını karbonhidrat yerine alkol ile karşılayan hastalarda, yetersiz beslenen, yağ asitlerini ve proteinleri parçalayarak hem beyin hem de kalp tarafından kullanılacak keton cisimleri üretilir. Ek olarak, kusma ve mide bulantısı, gastrointestinal sistemden yeterli çözünen maddelerin alınımını da engeller. Alkol yoksunluğuna bağlı gelişen anksiyetik hal de yemek yememe isteğini tetikleyen durumlar arasında yer alır. Patofizyoloji3,4 Hasta oral alımı yetersiz olduğu hem de alkolün diüretik etkisi nedeniyle dehidratedir. Yukarıda da bahsettiğimiz düşük glikojen depoları bittikten sonra metabolizma protein ve yağ yıkımına kayar. Bununla birlikte oral alımın az olması, insülin seviyelerinin düşmesine, kortizol, glukagon ve epinefrin gibi diğer düzenleyici hormonları yükselterek lipolizde belirgin bir artışa neden olur. İnsülin eksikliği ayrıca hormona duyarlı lipaz aktivitesini de attırarak, etanolün asetaldehit ve asetil-CoA'ya dönüşümünü de arttırır. Her asetaldehit asetil-Coa dönüşümde NAD+, NADH'ye dönüşür. (şekil-1) Şekil-1: Alkolik ketoasidoz patofizyolojisi NAD+/NADH oranının NADH'ye doğru kayması; Glikoneogenezi baskılayarak hipoglisemiye neden olabilir Piruvat'ın laktata dönüşümünü kolaylaştırır.* Lipid metabolizmasını daha da arttıracak kısır döngüye neden olur. Asetoasetik asit/beta-hidroksibütirik asit oranını beta-hidroksibütirik aside doğru kaydırır. * Piruvat'ın laktata dönüşümü klinik olarak önemli değildir. Alkolik ketoasidozlu bir hastada laktik asidozun yüksek bulunması halinde, hipovolemi, kalp yetmezliği veya sepsis gibi doku perfüzyon bozukluğuna neden olan klinik durumlar ekarte edilmelidir. Ayırıcı tanıda artmış anyon açıklı metabolik asidozun diğer nedenleri de araştırılmalıdır. Klinik5 Alkolik ketoasidoz, genellikle aşırı alkol kullanım öyküsü olan, yetersiz beslenen ve son zamanlarda aşırı içki içme öyküsü ile başvururlar Bulantı, kusma, karın ağrısı, en sık görülen semptomlar arasındadır Kusma veya diyare gibi gastrointestinal kayıplar, ketoasit anyonlarıyla (çoğunlukla beta-hidroksibutirat) sodyum ve potasyumun idrar çıkışını azaltması, etanole bağlı gelişebilecek pankreatite sekonder üçüncü boşluğa geçebilecek sıvı hastada volümün azalmasına, bu duruma sekonder taşikardi ve hipertansiyon görülebilir. Olası metabolik asidozu kompanse etmek için solunum hızında artış (takipneik olabilir, kussmaul solunumu) görülebilir. Diyabetik ketoasidoz hastaları ile karşılaştırıldığında alkolik ketoasidoz hastalarının bilinçleri daha açık ve berraktır. Kanda etanol seviyesi düşük olabilir. Glikoz konsantrasyonu düşük veya normal olabilir. Hasta düzgün beslenemediği için hipokalemi, hipomagnezemi, hipopotasemi gibi elektrolit bozuklukları görülebilir. Kan gazında pH düşük veya normal olabilir. HCO3 seviyesi de normalden düşük çıkabilir. HatırlatmaAKA hastalarını Wernicke Ensefalopatisi açısından değerlendirmeyi unutmayın. Karakteristik triad: ensefalopati, ataksi ve oftalmopleji olarak bilinir. Daha detaylı bilgi için sitemizde Dr. Merve Yazla'nın yazmış olduğu Wernicke Ensefalopatisi yazısını okuyabilirsiniz. Tanı Tanı için net bir kriter yok. AKA tanısı klinik olarak konur. Laboratuvar değerlerine bakarken, diğer metabolik asidoz ve ketoasidoz nedenlerinin laboratuvar bulguları dikkate alınmalıdır.AKA hastalarında sık rastlanan laboratuar bulguları: Kombine asit-baz bozuklukları görülebilir6 Anyon açığı artmış(AAA) metabolik asidoz + solunumsal alkaloz (en sık) alt...

hasta aka aaa bu ay nad klinik kar ek olas daha lipids coa kanda nadh bununla alkol yukar kalori laboratuvar hco3

Updates: CWI,PRP, HCO3, stretching/Dr. Izzy Smith of FEMMI

The TriDoc Podcast

Play Episode Listen Later Mar 24, 2023 58:35

In this episode:Science is not static and as new papers come out it is worthwhile revisiting previous topics to see if any of my previous conclusions should be updated. On this episode I look at newer research on topics previously covered in several different episodes to see if I should revise what I concluded at that time. Specifically, cold water immersion, platelet rich plasma injections, bicarbonate supplementation and stretching. Plus, endocrinologist Dr. Izzy Smith joins me to talk about FEMMI a women's coaching and educational organization in Australia and New Zealand that helps women and the men that work with them better understand the female reproductive cycle and how it may impact individual training and racing.Segments:[08:55]- Science updates[29:28]- Izzy Smith Links@doctorizzyksmith on Instagram FEMMI

australia science new zealand stretching izzy segments hco3

20. Acute nierinsufficiëntie en CVVH(D) - met Dr. Marc Vervloet

Intensief de Podcast

Play Episode Listen Later Feb 23, 2023 53:30

In deze aflevering (nummer 20 al weer!) is Professor Marc Vervloet (Internist-Nefroloog) te gast in de podcast. We bespreken alles omtrent (Acute) Nierinsufficiëntie en de behandelingen daarvan, waaronder CVVH(D).Marc vertelt met enorm veel enthousiasme over zijn passie en deelt op goed begrijpbare wijze deze ingewikkelde concepten.We bespreken onder andere de volgende onderwerpen:Wat is nierinsufficiëntie, en wat zijn op de IC frequente oorzaken hiervan?Waarom zijn de nieren zo gevoelig voor schade in vergelijking met andere organen?Is kreatinine en/of ureum een slechte maat voor acute nierinsufficiëntie?Moeten we vocht of juist furosemide geven aan oligure patiënten?Is furosemide schadelijk voor de nieren of helpt het juist?Waarom krijgen patiënten met AKI een metabole acidose?Moeten we ze in dat geval HCO3 infunderen?Wat is de geschiedenis van dialyse?Welke vormen van nierfunctievervangende therapie zijn er?Hoe werkt citraat, en wat is citraataccumulatie?Wanneer kan een patiënt weer zonder CVVH?Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU):EMCrit: Acute Kidney InjuryBedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

waarom welke acute ic wanneer sodium moeten volg aki hco3

Chapter Eleven, part 1: Regulation of Acid-Base Balance

Play Episode Listen Later Feb 12, 2023 97:04

ReferencesWe considered the effect of a high protein diet and potential metabolic acidosis on kidney function. This review is of interest by Donald Wesson, a champion for addressing this issue and limiting animal protein: Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney DiseaseHostetter explored the effect of a high protein diet in the remnant kidney model with 1 ¾ nephrectomy. Rats with reduced dietary acid load (by bicarbonate supplementation) had less tubular damage. Chronic effects of dietary protein in the rat with intact and reduced renal massWesson explored treatment of metabolic acidosis in humans with stage 3 CKD in this study. Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rateIn addition to the effect of metabolic acidosis from a diet high in animal protein, this diet also leads to hyperfiltration. This was demonstrated in normal subjects; ingesting a protein diet had a significantly higher creatinine clearance than a comparable group of normal subjects ingesting a vegetarian diet. Renal functional reserve in humans: Effect of protein intake on glomerular filtration rate.This finding has been implicated in Brenner's theory regarding hyperfiltration: The hyperfiltration theory: a paradigm shift in nephrologyOne of multiple publications from Dr. Nimrat Goraya whom Joel mentioned in the voice over: Dietary Protein as Kidney Protection: Quality or Quantity?We wondered about the time course in buffering a high protein meal (and its subsequent acid load on ventilation) and Amy found this report:Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of Anesthesiologists Roger mentioned that the need for acetate to balance the acid from amino acids in parenteral nutrition was identified in pediatrics perhaps because infants may have reduced ability to generate acid. Randomised controlled trial of acetate in preterm neonates receiving parenteral nutrition - PMCHe also recommended an excellent review on the complications of parenteral nutrition by Knochel https://www.kidney-international.org/action/showPdf?pii=S0085-2538%2815%2933384-6 which explained that when the infused amino acids disproportionately include cationic amino acids, metabolism led to H+ production. This is typically mitigated by preparing a solution that is balanced by acetate. Amy mentioned this study that explored the effect of protein intake on ventilation: Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of AnesthesiologistsAnna and Amy reminisced about a Skeleton Key Group Case from the renal fellow network Skeleton Key Group: Electrolyte Case #7JC wondered about isolated defects in the proximal tubule and an example is found here: Mutations in SLC4A4 cause permanent isolated proximal renal tubular acidosis with ocular abnormalitiesAnna's Voiceover re: Gastric neobladder → metabolic alkalosis and yes, dysuria. The physiology of gastrocystoplasty: once a stomach, always a stomach but not as common as you might think Gastrocystoplasty: long-term complications in 22 patientsSjögren's syndrome has been associated with acquired distal RTA and in some cases, an absence of the H+ ATPase, presumably from autoantibodies to this transporter. Here's a case report: Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosisCan't get enough disequilibrium pH? Check this out- Spontaneous luminal disequilibrium pH in S3 proximal tubules. Role in ammonia and bicarbonate transport.Acetazolamide secretion was studied in this report Concentration-dependent tubular secretion of acetazolamide and its inhibition by salicylic acid in the isolated perfused rat kidney. | Drug Metabolism & DispositionIn this excellent review, David Goldfarb tackles the challenging case of a A Woman with Recurrent Calcium Phosphate Kidney Stones (spoiler alert, many of these patients have incomplete distal RTA and this problem is hard to treat). Molecular mechanisms of renal ammonia transport excellent review from David Winer and Lee Hamm. OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

Acil Serviste ARDS Hastasının Mekanik Ventilasyonu

Nursing Mnemonics Show by NRSNG (Memory Tricks for Nursing School)

Play Episode Listen Later Jan 30, 2023 15:03

Her iki yatağa bir hemşirenin baktığı ve kontrollü hasta yatışı sağlanan yoğun bakımlara göre acil serviste mekanik ventilasyonda hasta izlemi önemli bir sorundur. Bugün birçok üçüncü basamak acil serviste kritik bakım alanları olmakla beraber, engellenemez hasta sirkülasyonu nedeniyle, hastanın yoğun bakım ünitesine hızlı nakli en uygun çözümdür. Buna karşılık günümüzde yoğun bakım gereksinimi olan çok sayıda hasta yoğun bakımların dışında takip edilmek zorunda kalınmaktadır. ABD'de yoğun bakıma yatırılan hasta sayısı %48.8 artmış bildirilmektedir.1 ABD'de her yıl 200 binden fazla hastaya acil serviste mekanik ventilasyon uygulanmaktadır ve üçte biri 5 saatten uzun süre acil serviste kalmaktadır. Üstelik mortaliteleri yoğun bakıma yatırılan diğer hastalara göre belirgin olarak daha yüksektir (%24'e %9.3). 2 Ülkemizde de acil servislerimizde her geçen gün daha fazla sayıda mekanik ventile hastayı acil serviste beklenenden uzun süre takip etmek zorunda kalıyoruz. Belki de bu nedenle daha fazla sayıda hekim konuya ilgi gösteriyor. Sitemizde invaziv mekanik ventilasyon konusunda çok sayıda yazı yazıldı. Uzun süredir kurslarda acil hekimleri için konuyu basitleştirmeye çalışsam da burada bu konuda az sayıda yazı yazmıştım. Bu nedenle bu yazıda ARDS(Acute Respiratory Distress Syndrome Akut Solunum Sıkıntısı Sendromu) hastasının acil serviste mekanik ventilasyonu konusunda yazmak istedim. Olgu AS'e nefes darlığı şikayeti ile getirilen 71 yaşında erkek hastanın son 3 gün içerisinde artan öksürük, balgam ve nefes darlığı şikayetleri mevcut. AS'e getirildiğinde GD kötü, nonkoopere olan hastanın ilk değerlendirilmesinde KB: 160/90 mmHg, KH: 128/dk, SS: 32/dk, Oksijen satürasyonu: %75 olarak saptanıyor. Fizik muayene akciğerde bilateral ralleri olan hastaya CPAP başlanıyor (CPAP: 8cmH2O ve %60 oksijenle). Arteriyel kan gazında pH:7.447, PaCO2: 46.1mmHg, PaO2: 43.2mmHg, HCO3: 29.8 mmol/L, Laktat: 1.4 mmol/L saptanıyor. İzlemde genel durumunda düzelme olmayan hasta RSI ile entübe ediliyor. Entübasyon sonrasında çekilen toraks BT'si aşağıda görülen hastanın mekanik ventilasyonunda nelere dikkat edelim? Öncelikle hastanın durumunun hızlı anlaşılması oksijen uygulamalarının yönteminde ilk adım olmalı. Bunun için yönettiğimiz bu hastada ARDS olduğunu anlamamız gerekiyor. ARDS tanısı için Berlin kriterlerini kullanıyoruz, bunu hatırlayalım; Son bir hafta içerisinde yeni ya da kötüleşen olunum etmezliği (Kalp yetmezliği veya Hipervolemiye bağlı değil !) Akciğer görüntülemesinde füzyon, kollapsların veya modülle açıklanamayan bilateral opasiteler Son olarak oksijenizasyon durumu PaO2/FiO2 oranı değerlendirilir. Hafif: 200-300 mmHg (PEEP veya CPAP ≥5 cm H₂O) Orta: 100-200 mmHg (PEEP ≥5 cm H₂O) Ciddi: ≤ 100 mmHg (PEEP ≥5 cm H₂O) Berlin kriterleri, PaO2/FiO2 oranının en az 5 cmH2O'luk pozitif ekspirasyon sonu basınç (PEEP) seviyesinde ölçülmesi gerektiğini belirtiyor. Yani en azından noninvaziv ventilasyon almayan bir hastada değerlendirme mümkün gözükmüyor. Bu hastalarda tanı izlemde konur. Bir çalışmada bilateral infiltrasyonları olan ve standart oksijen altında PaO2/FiO2≤300 mmHg olan hemen hemen tüm hastaların noninvaziv ventilasyon altında ilk 24 saat içinde ARDS kriterlerini karşıladığı ve ölüm oranlarının Berlin tanımlarında bildirilene benzer olduğu bildirildi.3 Bu nedenle, ARDS kriterlerine sahip spontan soluyan hastalar pozitif basınçlı ventilasyon olmadan erken tanımlanabilir. Tabi sadece bu kriterler yeterli olmayacak. Hastanın risk faktörlerini ( pnömoni, travma, sepsis, pankreatit vs); sorgulamalıyız. Hiçbir risk faktörü yoksa hidrostatik ödemi dışlamak için objektif değerlendirmeye (örn. ekokardiyografi) ihtiyaç vardır.4 NOT: Akut hipoksemik solunum yetmezliğinde hastada KOAH ve/veya hipoventilasyon düşünülüyorsa noninvaziv ventilasyon(NİV) veya yüksek akışlı nazal oksijen (YANO)tedavisi öncelikli düşünülür. Bunun dışındaki hastalarda entübasyon ihtiyacı yoksa yine NİV düşü...

berlin ent bu ss bug nv yano bt peep kb bir kh abd gd cpap rsi uzun yani ards bunun tabi buna belki akci kalp mmhg acil fizik laktat hafif koah hco3 paco2

Arterial Blood Gases (Rome)

Play Episode Listen Later Oct 14, 2022 2:04

First look at the pH: if it is low it is acidosis, high indicates alkalosis. Second use the ROME mnemonic to determine if you have respiratory vs. metabolic. For Metabolic look at HCO3. For Respiratory, look at pCO2. Metabolic Acidosis – pH Low, HCO3 Low. Metabolic Alkalosis – pH High, HCO3 High. Respiratory Acidosis – pH Low, pCO2 High. Respiratory Alkalosis – pH High, pCO2 Low.

blood rome gases arterial pco2 hco3

BAZ AÇIĞI: Ne ola ki?

Play Episode Listen Later Jul 18, 2022 7:41

Baz açığı (baz eksesi) ilk kez 1960 yılında Siggaard-Andersen tarafından; respiratuar durumdan bağımsız olarak metabolik asidoz/alkoloz varlığının değerlendirilebilmesi ve varsa ciddiyetinin tanımlanabilmesi amacıyla ortaya konmuştur. Aslında önceleri metabolik değişimleri değerlendirmek amaçlı ilk kullanılan parametre aktüel HCO3 (HCO3a) seviyesi olmuştur (plazma örneğinde ölçülen HCO3 değeri). Ancak HCO3 parsiyel CO2 basıncına oldukça bağımlı bir değişken olduğundan, respiratuar değişikliklerin etkisini nötralize etmek amaçlı standart HCO3 (HCO3st) tanımlanmıştır. Standart HCO3 değeri PCO2 40 mmHg olduğunda olması gereken HCO3 konsantrasyonudur. Dolayısıyla: HCO3a = HCO3st ise hastada solunumsal dengenin korunduğu düşünülür. HCO3a > HCO3st ise SOLUNUMSAL ASİDOZ vardır. HCO3a < HCO3st ise SOLUNUMSAL ALKOLAZ vardır. HCO3st değerlendirmeyi bir tık daha doğru hale getirmiş olsa da halen nonkarbonik asitlerin (albümin başta olmak üzere, sülfat, fosfat gibi) zayıf tampon etkisi hesaba dahil edilmemektedir. Yani örneğin HCO3 seviyesi 24 mmol/L olan kana 10 mmol/L lik güçlü asit eklendiğinde HCO3st beklendiği gibi 14mmol/L (24-10) yerine 16 mmol/L olarak ölçülür çünkü eklenen asitin 2 mmol/L lik kısmı non-karbonik tamponlar ile nötrlenmiştir. Bu problemi çözmek için ise Singer ve Hastings buffer base (BB) (tampon bazı) nı tanımlamışlardır. BB tüm tampon anyonların toplamına eşittir. BB= HCO3- + A- Ancak her ne kadar teorikte BB CO2 bağımsız bir değer olsa da, pratikte non-karbonik tampon konsantrasyonlarındaki farklılıklara bağlı BB değerinin değişkenlik gösterdiği bulunmuştur. Bunun üzerine Siggaard- Andersan aktüel BB ile normal BB (NBB) arasındaki farkı alarak Baz açığını tanımlamıştır. NBB deneysel olarak elde edilen PH 7.40 ve PCO2 40 mmHg iken olması gereken BB değeridir. Bu durumda baz açığı (BE) PCO2 40 mmHg kabul edildiğinde kan örneğinin PH sını 7.40 yapmak için eklenmesi gereken kuvvetli asit veya baz değeridir. Normal değeri -2 +2 arasındadır. Teorikte metabolik bozukluğu değerlendirmede kullanılır ve < -2 olması metabolik asidozu, > +2 olması metabolik alkolozu gösterir.1 BE = ∆ BB = BB – NBB Klinik kullanımda direkt ölçümü zor olacağından belli formüller ile hesaplanır; bunlardan en sık kullanılanı: BE = (HCO3- - 24.8) + ᵝ . (PH -7.40) dır. ᵝ değeri hemoglobin konsantrasyonuna dayalı bir formülle hesaplanabileceği gibi sabit olarak 16.2 mmol/L olarak da kabul edilebilir. Klinik uygulamada bu kısmın tampon etkisinin non-karbonik asitleri yansıttığı ve baz açığı üzerinde düşük bir etkisinin olduğu unutulmamalıdır. Baz açığı tüm kan için ifade edilebilir. Bu durumda BE(B) olarak ifade edilir ve intersisyel aralık ile kanın etkileşimi hesaplamada dikkate alınmaz. Standart baz açığı (SBE) ise ekstaselüler boşluğu hesaba katarak ulaşılan bir değerdir ve bu durumda hesaplamada kullanılan ᵝ değeri belirlenirken hemoglobin konsantrasyonu 1/3 ile çarpılır. Ancak zaten formülde bu kısmın etki değeri düşük olduğundan ciddi anemi veya polisitemi durumlarında bile klinik açıdan anlamlı bir fark oluşması beklenmez. Baz açığının dezavantajları neler? Baz açığı, her ne kadar metabolik bozuklukların değerlendirilmesinde faydalı bir parametre olsa da bazı dezavantajları mevcuttur. Bunlardan ilki altta yatan patolojik mekanizma hakkında bize bilgi vermez. Kompozit bir belirteç olduğundan son değer laktat, ketoasitler, albümin gibi birçok farklı değere bağlıdır. Örneğin hastada hem hiperkloremi (güçlü anyonlarda artış), hem de hipoalbuminemi (negatif yükte azalma) bir arada olabilir. Böyle bir durumda baz açığı 0 bulunabilir. Baz açığı değerlendirilmesiyle ilgili bazı klinik tablo örnekleri aşağıda verilmiştir. Ama daha iyi bir yorum yeteneği için kan gazı analizini ve Steward metodunu sindirmeniz gerekir ( ki bunun için Melis'in yazısına bakmanızı öneririm https://acilci.net/steward-metodu-ile-asit-baz-ve-kan-gazi-degerlendirmesi-kantitatif-teori/) . Durum A: Normal durum

normal singer co2 ama bu bb steward hastings klinik asl baz yani bunun ancak melis standart nbb dolay mmhg sbe bunlardan pco2 hco3

Approach to Acid Base Disorders

Play Episode Listen Later Jul 3, 2022 24:36

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode: In today's episode, we discuss about a 12-year-old male with lethargy after ingestion. Here's the case presented by Rahul: A 12-year-old male is found unresponsive at home. He was previously well and has no relevant past medical history. The mother states that he was recently in an argument with his sister and thought he was going into his room to “have some space.” The mother noticed the patient was in his room for about 1 hour. After coming into the room she noticed him drooling, minimally responsive, and cold to the touch. The patient was noted to be moaning in pain pointing to his abdomen and breathing fast. Dark red vomitus was surrounding the patient. The mother called 911 as she was concerned about his neurological state. With 911 on the way, the mother noticed a set of empty vitamins next to the patient. She noted that these were the iron pills the patient's sister was on for anemia. EMS arrives for acute stabilization, and the patient is brought to the ED. En route, serum glucose was normal. The patient presents to the ED with hypothermia, tachycardia, tachypnea, and hypertension. His GCS is 8, he has poor peripheral perfusion and a diffusely tender abdomen. He continues to have hematemesis and is intubated for airway protection along with declining neurological status. After resuscitation, he presents to the Pediatric ICU. Upon intubation, an arterial blood gas is drawn. His pH is 7.22/34/110/-6 — serum HCO3 is 16, and his AG is elevated. To summarize key elements from this case, this patient has: Lethargy and unresponsiveness after acute ingestion. His hematemesis is most likely related to his acute ingestion. And finally, he has an anion gap metabolic acidosis, as evidenced by his low pH and low HCO3. All of these salient factors bring up the concern for acute iron ingestion! In today's episode, we will not only go through acute management pearls for iron poisoning, but also go back to the fundamentals, and cover ACID BASE disorders. We will break this episode down into giving a broad overview of acid base, build a stepwise approach, and apply our knowledge with integrated cases. We will use a physiologic approach to cover this topic! Pradip, can you give us a quick overview of some general principles when it comes to tackling this high-yield critical care topic? Absolutely, internal acid base homeostasis is paramount for maintaining life. Moreover, we know that accurate and timely interpretation of an acid–base disorder can be lifesaving. When we conceptualize acid base today, we will focus on pH, HCO3, and CO2. As we go into each disorder keep in mind to always correlate your interpretation of blood gasses to the clinical status of the patient. Going back to basic chemistry, can you comment on the relationship between CO2 and HCO3? Yes, now this is a throwback. However, we have to review the Henderson–Hasselbalch equation. The equation has constants & logs involved, however in general this equation shows that the pH is determined by the ratio of the serum bicarbonate (HCO3) concentration and the PCO2, not by the value of either one alone. In general, an acid–base disorder is called “respiratory” when it is caused by a primary abnormality in respiratory function (i.e., a change in the PaCO2) and “metabolic” when the primary change is attributed to a variation in the bicarbonate concentration. Now that we have some fundamentals down, let's move into definitions. Can you define acidemia and alkalemia and comment on how...

children healthcare current hospitals dark disorders co2 ems lethargy picu acid base his ph podcast dedicated pediatric icu pco2 hco3 cleveland clinic children paco2 henderson hasselbalch

1. Bloedgas Interpretatie

Intensief de Podcast

Play Episode Listen Later Jun 1, 2022 35:57

In deze aflevering bespreken we de interpretatie van een bloedgas.- Waarom is de normale pH eigenlijk 7,4?- Waarom partiële compensatie niet bestaat.- Wanneer gebruik je de anion gap?- Wat is de functie van het base excess?- Kan je een veneus bloedgas net zo interpreteren als een arterieel bloedgas?- Wat is de Winters Formule?- Hoezo worden patiënten acidotisch van NaCl 0,9%?Buffer vergelijking:CO2 + H2O H2CO3 HCO3- + H+Bloedgas oefenen:Casus 1:Septische patiënt van de verpleegafdeling, flink gevuld aldaar.pH 7,30pCO2 26mmHg/3,5kPaHCO3 12,7 mmol/lCasus 2:Patiënt met gastro-enteritis en frequent braken.pH 7,56pCO2 37,5 mmHg/5,0kPaHCO3 31 mmol/lCasus 3:Hartpatiënt met forse benauwdheid en crepitaties en mogelijk NSTEMIpH 7,16pCO2 56mmHg/7,5kPaHCO3 19,5 mmol/lCasus 4:Patiënt in weantraject 1h na aanpassen PS naar CPAP.pH 7,48pCO2 29mmHg/3,8kPaHCO3 22 mmol/lCompensatie berekenen?We nemen als normaal waarden een pCO2 van 40mmHg en een HCO3 van 24 mmol/lVerwacht HCO3:Acute respiratoire acidose: Elke 10mmHg (1,3 kPa) stijging van het pCO2 stijgt het HCO3 met 1mmol/lChronische respiratoire acidose: Elke 10mmHg stijging van het pCO2 stijgt het HCO3 met 3,5mmol/lAcute respiratoire alkalose: Elke 10mmHg daling van het pCO2 daalt het HCO3 met 2mmol/l, voor chronisch 5mmol/lAcute respiratoire alkalose: Elke 10mmHg daling van het pCO2 daalt het HCO3 met 5mmol/lVerwacht pCO2Metabole acidose: 1,5 x (HCO3) + 8 (+-2mmHg range) (in mmHg of /7,5 in kPa) Metabole alkalose: 0,7 x (HCO3) + 21 (+-2mmHg range) (in mmHg of /7,5 in kPa)pCO2 | pH | Metabool of respiratoirHoog | Hoog | MetaboolNormaal | Hoog | MetaboolLaag | Hoog | RespiratoirHoog | Laag | RespiratoirNormaal | Laag | MetaboolLaag | Laag | MetaboolBronnen:Interpretation of arterial blood gasBase excess and standard base excessArterial blood gas interpretationBedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

ps waarom wanneer buffer pati volg cpap hoezo nacl mmhg kpa casus pco2 hco3

Providing Kidney Support in the PICU

Play Episode Listen Later May 29, 2022 43:10

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. I am Pradip Kamat. I am Rahul Damania, a current 3rd year pediatric critical care fellow. I am Kate Phelps- a second year pediatric critical care medicine. We come to you from Children's Healthcare of Atlanta Emory University School of Medicine. We are delighted to be joined by guest expert Dr Stephanie Jernigan Assistant Professor of Pediatric-Pediatric nephrology, Medical Director of the Pediatric Dialysis Program at Children's Healthcare of Atlanta. She is the Chief of Medicine and Campus Medical Director at Children's Healthcare of Atlanta, Egleston Campus. Her research interests include chronic kidney disease, and dialysis. She is on twitter @stephaniejern13 I will turn it over to Rahul to start with our patient case... A 3 year old previously healthy male presents with periorbital edema. Patient was initially seen by a pediatrician who prescribed anti-histamines for allergy. After no improvement in the eye swelling after a two week anti-histamine course, the patient was given a short course of steroids, which also did not improve his periorbital edema. The patient progressed to having abdominal distention and was prescribed miralax for constipation. Grandparents subsequently noticed worsening edema in his face, eyes, and feet. The patient subsequently had low urine output, low appetite and lack of energy patient was subsequently brought to an ED and labs were obtained. Grandparents denied any illness prior to presentation, fever, congestion, sore throat, cough, nausea, vomiting, gross hematuria, or diarrhea. In ED patient was noted to be hypertensive (Average systolic 135-highest 159mm HG), tachycardic (HR 130s-140s), breathing ~20-30 times per minute on RA with SpO2 92%. Admission weight was recorded at 16.5Kg. Physical exam showed periorbital edema, edema of ankles, there was mild abdominal distention (no tenderness and no hepatosplenomegaly), heart and lung exams were normal. There were no rashes on extremities. Labs at the time of transfer to the PICU: WBC 10 (62% neutrophils, 26% lymphocytes) Hgb 7.2, Hct 21, Platelets 276. BMP: Na 142/K 8.4/Cl 102/HCO3 19/BUN 173/creatinine 5.8. Serum phosphorus was 10.5, Total Ca 6.4 (ionized Ca= 3.4), Mag 2.0, albumin 2.6, AST/ALT were normal. An urine analysis showed: 1015, ph 7.5, urine protein 300 and rest negative. Chest radiograph revealed small bilateral pleural effusions. After initial stabilization of his hyperkalemia-patient was admitted to the PICU. PTH intact 295 (range 8.5-22pg/mL). Respiratory viral panel including for SARS-COV-2 was negative. C3 and C4 were normal. A nephrotic syndrome/FSGS genetic panel was sent. A renal US showed: bilateral echogenic kidneys and ascites (small volume). Pradip: Dr Phelps what are the salient features of the above case presented? Kate Phelps: This patient has a subacute illness characterized by edema, anemia, and proteinuria. His labs show that he has severe acute kidney injury with significantly elevated BUN and Creatinine, hyperkalemia, hyperphosphatemia, and hypocalemia. Rahul: Dr Jernigan welcome to PICU Doc on Call Podcast. Thanks Kate, Rahul and Pradip for inviting me to your podcast. This is a such a great way to provide education and it is my pleasure to come today to speak about one of my favorite topics, pediatric dialysis. I have no financial disclosures or conflicts of interest and am ready to get started. Rahul: Dr Jernigan as you get that call from the ED and then subsequently from the PCCM docs, as a nephrologists whats going on in your mind ? When I get the call from the outside hospital my first job is to make sure the patient is safe and stable for transfer to a tertiary care center. This includes concern about airway, breathing and level of alertness. From a renal standpoint, I am worried about elevated blood pressure, electrolyte abnormalities, in this case primarily the hyperkalemia, and fluid...

Your Daily Meds - 19 November, 2021

Your Daily Meds

Play Episode Listen Later Nov 18, 2021 4:10

Good morning and welcome to your Friday dose of Your Daily Meds.Bonus Review: How is H+ produced in the stomach and secreted into the gastric lumen?Answer: So CO2 reacts with water under the influence of carbonic anhydrase. This produces the H+, which is then actively transported into the gastric lumen by H+K+-ATPase. The HCO3- in the reaction passes across the basolateral membrane in exchange for Cl- via an antiport.Question:With regard to episodes of delirium, which of the following is not a feature of extrinsic and environmental management?Well-lit room or patient cubicleRemove seeing glasses to reduce risk of injuryRoom or patient cubicle near nursing stationFamily member present Frequent orientation with calendars and clocksHave a think.Scroll for the chat.Quick Investigation:Consider the following ECG:What is the correct rate, rhythm, axis and interpretation, respectively?Ventricular rate 40/min; atrial fibrillation; left axis deviation; rapid ventricular responseVentricular rate 60/min; atrial flutter; normal axis; 3:1 blockVentricular rate 40/min; sinus rhythm; normal axis; complete heart blockVentricular rate 40/min; sinus rhythm; normal axis; left bundle branch blockVentricular rate 60/min; atrial fibrillation; right axis deviation; ischaemic changesHave a think.Do some counting.More scroll for more chat.The Environment:The principles of extrinsic or environmental management of delirium include:Quiet, well-lit rooms or cubicles, near windows to orient to time of dayOptimise hearing and visionRoom or cubicle near nursing station for closer observation and increased cares if agitatedFamily members present for reassurance and re-orientationFrequent orientation with clocks, calendars and remindersSo removing the patients’ seeing glasses is least likely to be an effective method of environmental, non-pharmacological management of delirium.It would probably just make them more crazy…Squiggly Lines:This ECG shows sinus rhythm with complete heart block and ventricular escape rhythm.So sinus rhythm because the sinus node is ticking away regularly giving P waves at a rate of approximately 90/min. But complete heart block because there seems to be no relationship between this sinus rhythm and the ventricular rhythm. So the ventricles will tick along at their own rate (the escape rhythm - which is slower than that of the atrial pacemakers).Note: there are three characteristics of complete heart block. These are A-V dissociation, atrial rate > ventricular rate, and a regular ventricular rate.The ventricular rate is approximately 40/min with sinus rhythm - yep. The QRS complexes are wide with left bundle branch block (LBBB) morphology - wide because the depolarisation is coming from the slow lumbering ventricles, not the snappy quick atria. The axis is normal. And there is a prolonged QT at 600ms.So this person probably looked quite sick…Bonus: What humoral factors stimulate parietal cell gastric acid production?Answer in Monday’s dose.Closing:Thank you for taking your Meds and we will see you Monday for your MANE dose. As always, please contact us with any questions, concerns, tips or suggestions. Have a great day!Luke.Remember, you are free to rip these questions and answers and use them for your own flashcards, study and question banks. Just credit us where credit is due. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit yourdailymeds.substack.com

quiet scroll frequent mane meds qt ventricular qrs closing thanks hco3 lbbb

29: Macrophage Activation Syndrome

Play Episode Listen Later Sep 19, 2021 23:30

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode of 17-year old with h/o of SLE and now acute liver failure. Here's the case presented by Rahul: A 17-year old teenage female year old presents to the PICU with acute liver failure. Important past h/o includes a diagnosis of SLE on therapy with prednisone, mycophenolate (cellcept), and plaquenil. 4 days prior to this admission, patient presented to an OSH with RUQ pain, vomiting (non bloody & no bilious), fever & malaise. Initially due to concern for "lupus Flare" patient was given steroids at the OSH. At the OSH notable initial labs included a mild transaminitis and an INR of 1.5. She suddenly at the OSH developed fluid refractory hypotension and was started on a pressor. Due to continued worsening of her transaminitis well as a rising INR on her repeat labs she was referred to our tertiary PICU for further management. Pertinent history also includes a negative urine pregnancy test. No recreational drug use, and only as needed use of Tylenol. She now is in the PICU. She generally appears tired and ill. She is tachypneic on 4 LPM of nasal canulla and her oxygen saturation is 98%. She has a non-focal lung exam. Her cardiac exam is notable for tachycardia, and pertinently no gallop, rub or murmur. Her abdominal exam is non-focal except for mild discomfort on palpation of the RUQ with a palpable liver edge. Her extremities are cool with 3-4 capillary refill time. She is able to answer questions but intermittently doses off. No rash is noted. To summarize key elements from this case, this patient has: H/o of lupus and is on immunosuppressive medications New onset fever/malaise This sounds like a LUPUS flare as she has a clinical picture of generalized inflammation. Rahul: Lets pause right here and take a look at key history and physical exam components in a patient who has a chronic auto-immune condition: Fever, malaise and feeling tired all signs of constitutional symptoms. She has abdominal pain and vomiting that could again be related to systemic inflammation but also an intra-hepatic lesion. Are there some red-flag symptoms or physical exam components which you could highlight? This patient has signs of shock! Tachycardia with delayed cap refill and cool extremities Tachypnea & hepatomegaly which could indicate increased central venous pressures. Initially her outside presentation of fluid refractory shock is of utmost concern! Fluid refractory shock with multi organ presentation involving liver, kidney and the blood/coagulation systems All of these elements bring up a concern for some acute life threatening process such as sepsis, or even immune dys-regulation due to her h/o of Lupus To continue with our case, the patients labs were consistent with:Acute liver dysfunction (Elevated AST and ALT in the thousands, Total bilirubin 1.6, GGT 56) although the total bilirubin is not elevated to a degree I would expect. AKI (creatinine 2.18) An uptrending Coagulopathy with elevated PT and INR: PT 120 and a peak INR of 16 Thrombocytopenia: Platelets < 50K She had a peak lactate 9.2 and concurrent Metabolic acidemia: serum HCO3 7, and pH 7.18. A Pertinent negative: Normal serum ammonia

28: Teenager with SLE, Hypotension, and Liver Dysfunction

Play Episode Listen Later Sep 5, 2021 23:30

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode of 17-year old with h/o of SLE and now acute liver failure. Here's the case presented by Rahul: A 17-year old teenage female year old presents to the PICU with acute liver failure. Important past h/o includes a diagnosis of SLE on therapy with prednisone, mycophenolate (cellcept), and plaquenil. 4 days prior to this admission, patient presented to an OSH with RUQ pain, vomiting (non bloody & no bilious), fever & malaise. Initially due to concern for "lupus Flare" patient was given steroids at the OSH. At the OSH notable initial labs included a mild transaminitis and an INR of 1.5. She suddenly at the OSH developed fluid refractory hypotension and was started on a pressor. Due to continued worsening of her transaminitis well as a rising INR on her repeat labs she was referred to our tertiary PICU for further management. Pertinent history also includes a negative urine pregnancy test. No recreational drug use, and only as needed use of Tylenol. She now is in the PICU. She generally appears tired and ill. She is tachypneic on 4 LPM of nasal canulla and her oxygen saturation is 98%. She has a non-focal lung exam. Her cardiac exam is notable for tachycardia, and pertinently no gallop, rub or murmur. Her abdominal exam is non-focal except for mild discomfort on palpation of the RUQ with a palpable liver edge. Her extremities are cool with 3-4 capillary refill time. She is able to answer questions but intermittently doses off. No rash is noted. To summarize key elements from this case, this patient has: H/o of lupus and is on immunosuppressive medications New onset fever/malaise This sounds like a LUPUS flare as she has a clinical picture of generalized inflammation. Rahul: Lets pause right here and take a look at key history and physical exam components in a patient who has a chronic auto-immune condition: Fever, malaise and feeling tired all signs of constitutional symptoms. She has abdominal pain and vomiting that could again be related to systemic inflammation but also an intro-hepatic lesion. Are there some red-flag symptoms or physical exam components which you could highlight? This patient has signs of shock! Tachycardia with delayed cap refill and cool extremities Tachypnea & hepatomegaly which could indicate increased central venous pressures. Initially her outside presentation of fluid refractory shock is of utmost concern! Fluid refractory shock with multi organ presentation involving liver, kidney and the blood/coagulation systems All of these elements bring up a concern for some acute life threatening process such as sepsis, or even immune dys-regulation due to her h/o of Lupu To continue with our case, the patients labs were consistent with: Acute liver dysfunction (Elevated AST and ALT in the thousands, Total bilirubin 1.6, GGT 56) although the total bilirubin is not elevated to a degree I would expect. AKI (creatinine 2.18) An uptrending Coagulopathy with elevated PT and INR: PT 120 and a peak INR of 16 Thrombocytopenia: Platelets < 50K She had a peak lactate 9.2 and concurrent Metabolic acidemia: serum HCO3 7, and pH 7.18. A Pertinent negative: Normal serum ammonia

Hemodiyaliz Acilleri

Play Episode Listen Later Jun 28, 2021 17:51

Hemodiyaliz (HD) ilk kez 1945'de Alman Hekim Willem Kolff tarafından Akut Böbrek Hasarına (ABH) bağlı üremi gelişen bir hastada uygulanmış ve başarılı sonuçlar elde edilmiştir. Sonrasında kullanımı yaygınlaşmış, 60'ların başında maddi yükünden dolayı sadece seçilmiş şanslı bir azınlığa uygulanan tedavi, günümüzde ABD'de yılda 50 milyondan fazla kez uygulanır olmuştur. Acil servislerde sık karşılaştığımız bu hasta grubunda, hemodiyalize bağlı gelişebilecek komplikasyonları tanımak ve yönetebilmek acil hekimleri için oldukça önemlidir. Bu yazıda vaka örnekleri üzerinden hemodiyaliz komplikasyonları derlenmiştir1. İyi okumalar…. Diyalizör reaksiyonları ve diğer alerjik reaksiyonlar Vaka 1 HT, DM ve evre 5 KBH olan 68 yaşında kadın hastada diüretiklere rağmen sıvı yüklenmesi devam ettiğinden hemodiyalize başlanmıştır. İlk diyaliz tedavisinin 10. dakikasında hastada kaşıntı, dispne ve göğüs ağrısı gelişmiştir; ayrıca duyulabilir bir wheezing de vardır. Hastanın tansiyonu 86/50 mmHg olarak ölçülmüştür (diyaliz öncesi kan basıncı 145/90 mmHg). Hastada diyalizör reaksiyonundan şüphelenilmiştir. Bu hastanın yönetiminde uygun yaklaşım aşağıdakilerden hangisidir? A. Diyalize devam et ve IV antibiyotik uygula B. Diyalize devam et ve nebülizatör ile inhaler albuterol uygula C. Diyalize devam et ve IV steroid ve antihistaminik uygula D. Diyalizi durdur ve ekstrakorporeal dolaşımdaki kanı hastaya geri ver E. Diyalizi durdur ve ekstrakorporeal dolaşımdaki kanı hastaya geri verme Diyalizör reaksiyonları iki tiptir. Tip A genellikle erken tedavi döneminde, diyalizin 20-30. dakikalarında gelişir. Hastada kaşıntı, ürtiker, larinks ödemi, bronkospasm, dispne, göğüs ağrısı, kusma, hipoksi, hipotansiyon ve hatta kardiyak arrest gelişebilir. Bu durumda yapılması gereken diyalizi hemen durdurmak ve ekstrakorporeal dolaşımdaki kanı hastaya geri vermemektir. Ayrıca rutin anaflaksi tedavisi uygulanır. Tip B reaksiyonlar tedavinin daha geç döneminde ortaya çıkar ve daha hafif seyreder. Göğüs ağrısı, bulantı, kusma olabilir. Semptomlar hafifse diyalize devam edilebilir ancak farklı bir diyalizöre geçmek bu hastalarda uygun olacaktır. Diyalizör reaksiyonları, diyalizörün yapısındaki membrana veya bu membranın sterilizasyonunda kullanılan maddelere karşı gelişen bir hipersensitivite reaksiyonudur. Eskiden sık görülen bu komplikasyon, günümüzde biyouyumlu diyalizörlerin kullanılmasıyla oldukça azalmıştır. Hipersensitivite reaksiyonları membran ve sterilizatör dışında; heparin, demir ve eritropoez-uyarıcı-ajan gibi ilaçlara karşı da gelişebilir. Cevap 1 E. Diyalizi durdur ve ekstrakorporeal dolaşımdaki kanı hastaya geri verme Diyaliz Disekilibriyum Sendromu Vaka 2 75 yaşında bilinen HT, DM, KBH ve iskemik stroke öyküsü olan erkek hastada bulantı, iştah kaybı ve hiperkalemi nedeniyle hemodiyalize başlanıyor. Hastanın diyaliz öncesi kan tablosunda kreatinin 10,1 mg/dl, serum üre nitrojen 170 mg/dl, Na 128 mEq/L, K 7,2 mEq/L, HCO3 12 mEq/L ve glukoz 101 mg/dl. Hastaya 2 saat, kan akımı 400 ml/dk, diyalizat akımı 800 ml/dk, standart sodyum diyalizat kullanılarak, 2 Lt ultrafiltrasyon hedefi yönergesi ile diyaliz yapılıyor. Düşük etkili diyalizör kullanılıyor. Diyaliz sırasında bir problem yaşamayan hasta tedavi sonunda yeni başlayan bir baş ağrısı tarifliyor. Kan basıncı 145/96 mmHg olan hastanın diyaliz boyunca tansiyon değerinin stabil olduğu öğreniliyor. Hemen ardından nöbet geçiren hastada diyaliz durduruluyor. Hastada diyaliz disequlibrium sendromu riskini azaltmak için, diyaliz yönergesi nasıl değiştirilebilir? A. Ultrafiltrasyon hedefi azaltılmalıdır B. Diyalizattaki sodyum konsantrasyonu azaltılmalıdır C. Kan akımı azaltılmalıdır D. Tedavi süresi uzatılmalıdır Diyaliz disekilibriyum sendromu (DDS), HD sırasında veya hemen sonrasında gelişen nörolojik semptom ve bulgularla karakterize bir durumdur. İlk kez 1960'larda tanımlanan klinik tabloda hastada baş ağrısı, bulantı, kusma, konfüzyon,

dm iv lt bu abh abd dds ayr ht sonras hemen kbh mmhg acil eskiden tedavi hco3 meq l

19: Acute Salicylate Toxicity

Play Episode Listen Later Jun 27, 2021 18:12

Today's episode focuses on salicylate toxicity, specifically in the case of a teenager with abdominal pain and emesis. Join us in this discussion of symptoms, patient history, diagnosis, management, and treatment. Show Highlights: Our case: A 15-year-old female is admitted to the PICU for intentionally ingesting a large amount of aspirin tablets. She had epigastric abdominal pain with some non-biliary, non-bloody emesis when she presented to the outside emergency department twelve hours post-ingestion. She denies any neurological symptoms, including tinnitus but appears anxious and tachypneic. In the emergency department, her salicylate level was 45 mg/dL after her ingestion of about 250 aspirin tablets of 325 mg each. The patient is previously healthy, denies the use of illicit drugs and alcohol, is not sexually active, and has no allergies. To summarize the key elements of this case and patient history, she has ingested potentially toxic amounts of aspirin and has suicidal ideation but has no tinnitus or other neurological symptoms. Physical examination results show stable vital signs except for a temp of 38.8C; she has persistent tachypnea and mild epigastric tenderness but no rashes or previous cutting scars. Patient labs were consistent with a 12-hour salicylate level of 45 mg/dL, liver function, Bun/Creatinine, and coagulation profile are all normal. Her anion gap is slightly elevated, urine pH is 6, specific gravity is normal, and urine pregnancy test is negative. Based on patient history, physical exam, and labs, it appears that the patient has GI symptoms of early salicylate toxicity. Ingesting potentially toxic amounts of aspirin brings concern for life-threatening injuries to organs and possible loss of life. Let's quiz ourselves with a short multiple-choice question: A teenager with a previous history of suicidal attempt now presents with confusion, increased respiratory rate, fever, and diaphoresis. Her physical exam including the pupillary exam is normal. Her labs are remarkable for a pH of 7.45, CO2 of 19, HCO3 of 11, serum anion gap of 20meQ/L, serum K of 2.9, and serum glucose of 180 mg/dL. There are weakly positive ketones in the urine. The next step in management of this patient is: A) NaHCO3 infusion B) Insulin infusion C) Oral activated charcoal D) Hemodialysis dialysis The correct answer to this question is A) Sodium bicarbonate infusion. Insulin therapy is not the answer because serum glucose is low, and a patient with a pH>7.25 is unlikely to have DKA. While activated charcoal can be used, especially followed by sorbitol given with the first dose, we need to be cautious about its use with an altered mental status as in the patient above. Since we do not have a salicylate level at this stage, offering hemodialysis should not be the first step, although it can be considered later given the neurological symptoms. Remember: Any patient with a previous history of suicidal ideation who presents with confusion, fever, and diaphoresis with the above labs is suggestive of mixed respiratory alkalosis with high anion gap metabolic acidosis is highly suggestive of aspirin poisoning. Always examine the pupils in any case of poisoning, as that may point one towards a possible toxidrome. Let's highlight how basic science correlates with ASA poisoning: Remember the mechanism of action. Aspirin is a cyclo-oxygenase inhibitor which blocks prostaglandin production and has an antithrombotic effect by inhibiting platelet generation of thromboxane A2. Salicylates are weak acids which interfere with the Krebs cycle and specifically uncouple oxidative phosphorylation. This leads to acidosis, heat production, and hypoglycemia. Although not common, neuromuscular irritability manifested as paratonia (inability to relax muscles) and extreme muscle rigidity can develop, further contributing to hyperthermia and increasing the risk of rhabdomyolysis. Salicylates induce...

patients co2 gi toxicity dl insulin krebs acute a2 sodium aspirin picu dka ingesting 8c salicylate hco3 salicylates

Chapter Three: The Proximal Tubule

Dr. Baliga's Internal Medicine Podcasts

Play Episode Listen Later May 10, 2021 81:38

Chapter Three: How the proximal tubule is like Elizabeth Warren and other truths my friends from Boston taught me References for Chapter 3: Faisy C, Meziani F, PLanquette B et al. Effect of Acetazolamide vs. Placebo on Duration of Invasive Mechanical Ventilation among patients with chronic obstructive pulmonary disease: a randomized clinical trial. JAMA 2016 https://pubmed.ncbi.nlm.nih.gov/26836730/This randomized controlled double blinded multi-center study of acetazolamide to shorten the duration of mechanical ventilation (known as DIABLO) there was no statistically significant difference (though it may have been underpowered to do so).Salazar H, Swanson J, Mozo K, White AC, Cabda MM Acute Mountain sickness impact among travelers to Cusco, Peru J Travel Med 2012 https://pubmed.ncbi.nlm.nih.gov/22776382/ Investigators found that altitude sickness is common and alters travel plans for 1 in 5 travelers but was prescribed infrequently.Buzas GM and Supuran CT. Journal of enzyme inhibition and medicinal chemistry 2015 https://www.tandfonline.com/doi/full/10.3109/14756366.2015.1051042This review describes the use of acetazolamide to treat peptic ulcers and how it was later learned that H. pylori have carbonic anhydrase NORDIC idiopathic intracranial Hypertension Study Writing Committee. The effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: the idiopathic intracranial hypertension treatment trial. JAMA 2014 https://pubmed.ncbi.nlm.nih.gov/24756514/In this multi-centered trial, acetazolamide and low sodium weight reduction diet improved mild visual loss more than diet alone. Mullens W et al. Rationale and design of the ADVOR (acetazolamide in decompensated heart failure with volume overload trial) Eur J Heart Failure 2018 https://pubmed.ncbi.nlm.nih.gov/30238574/This reference explains the rationale for this ongoing trial.Gordon CE, Vantzelfde S and Francis JM. Acetazolamide in Lithium-induced nephrogenic diabetes insipidus NEJM 2016 https://www.nejm.org/doi/full/10.1056/NEJMc1609483A case report of efficacy of acetazolamide in a patient with severe polyuria.Zehnder D et al. Expression of 25-hydroxyvitamin D-1alpha hydroxylase in the human kidney. JASN 1999 This report explores the activity in the enzyme in nephron segments and suggests that the distal nephron may play an important part in the formation of 1,25 vitamin D https://jasn.asnjournals.org/content/10/12/2465Outline: Chapter 3 - This is chapter three, kind of the first real chapter of the book- Proximal Tubule- Reabsorbs 55-60% of the filtrate - Active sodium resorption - 65% of the sodium - 55% of the chloride - 90% of HCO3 - 100% glucose and amino acids - Passive water resorption - Water resorption is isosmotic - Secretion of - Hydrogen - Organic anions - Organic cations - Anatomy - S1, S2, S3 can be differentiated by peptidases - S1 more sodium resorption and hydrogen secretion, high capacity - S2 more organic ion secretion - Cell model - Basolateral membrane - Na-K-ATPase powers all the resorption - Luminal membrane - 100 liters a day crosses the proximal tubule cells - Microvilli to increase surface area - Microvilli has brush border which has carrier proteins as well as carbonic anhydrase - Water permeable, so sodium resorption leads to water resorption - Aquaporin-1 (sounds like this transporter is unique to the proximal tubule and RBC) - HCO3 is reabsorbed early, along with Na, resulting in increased chloride concentration which passively reabsorbed via paracellular route. - Tight junction has only one strand (on freeze fracture) as opposed to 8 in distal nephron - The Na-K-ATPase - Lower activity than in the LOH and distal nephron - Maintained intracellular Na at effective concentration of 30 mmol/L - Interior of the cell is negative due to 3 sodium out and 2 K in, then K leaks back out. - 3 Na out for 2 K in - An ATP sensitive K outflow channel on the basolateral membrane - Increased ATP slows potassium eflux - The idea is if Na-K slows, ATP will accumulate and this will slow K leaving, because there is less potassium entering. - K channel is ATP sensitive, ATP antagonizes K leak. - Highly favorable ELECTROCHEMICAL gradient for sodium to flow into the cell through the luminal membrane - Must be via a channel or carrier - Cotransporters - Amino acids - Phosphate - Glucose - Called secondary active transport - Countertransporters - Only example is H excretion - Basolateral membrane - Na-3HCO3 transporter - Powered by the negative charge in the cell- Chloride resorption - Formate chloride exchanger - Formate combines with hydrogen in the lumen, becomes neutral formic acid, and is reabsorbed where the higher pH causes it to dissociate and recycle again. - Dependent on continued H+ secretion - Chloride moves across basolateral membrane thanks to Cl and KCl transporters, taking advantage of negative intracellular charge- Passive mechanisms of proximal tubule transport - Accounts for one third of fluid resorption - Mechanism - Early proximal tubule resorts most of the bicarb and less of the chloride - Tubular fluid gets a high chloride concentration - Chloride flows through the tight junction down its concentration gradient - Sodium and water follow passively behind - Water moves osmotically into intercellular space from tubular fluid even though the osmolalities are equal since chloride is an ineffective osmole, so tonicity is not the same. ****** - Argues that bicarb is primarily important solute for passive resorbtion - Acetazolamide blocks Na and chloride resorption - Similar thing happens with metabolic acidosis where less bicarb is available to drive passive resorbtion of Na and Cl - Summary - Other than Na-K-ATPase Na-H antiporter main determinant of proximal Na and water resorption - 1. Direct bicarb resorption - Preferential bicarb resorbtion proximally drives passive chloride resorption - Drives active the formate exchanger for chloride resorption- Neurohormonal influence - AT2 drives a lot of Na resorption, primarily in S1 segment - Does not have a net effect on H-CO3 movement - Dopamine antagonizes sodium resorption - Blocks both Na-K-ATPase and - Na H antiporter- Capillary uptake - Starlings. Again - Low hydraulic pressure due to glomerular arteriole - High plasma on oncotic pressure from loss of the filtrate - The two together promote resorption - There maybe movement from interstitial back into tubular fluid (back diffusion) conflicting data- Glomerular tubular balance - The fractional tubular reabsorption remains constant despite changes in GFR (tubular load) - It is essential the GFR is matched by resorption - The rise in capillary osmotic pressure with increased GFR via increased filtration fraction is one mechanism of GT balance - Glomerular tubular balance os one of three mechanisms that prevents fluid delivery from exceeding the resorptive capacity of the tubules - GT balance - TG feedback - Autoregulation - GT balance can be altered if patients are volume overloaded or depleted - Closes this section with a story of a kid born without a brush border - Primacy of sodium in proximal tubule activity - Discusses bicarb resorbtion - There is no Tm for Bicarb as long as volume overload is prevented, in rats can rise over 60! - If you give NaHCO3 you get volume overload and the Tm I about 60 - Glucose - S1 and S2 have high capacity, low affinity glucose resorption - S3 has high affinity 2 Na fo every glucose - Tm glucose is 375 mg/min - For a GFR of 125t that comes out to 300mg/dL - 125 ml/min * 3mg/ml (300 mg/dL) = 375 mg/min - Functionally this is 200 mg/dL due to splay - Urea - Only 50-60 of filtered urea is excreted - Calcium Loop and distal tubule - Phosphate - 3Na-Phosphate high affinity transporters late in proximal tubule - three types of Na-Phos transporters, type 2 are the most important - regulated by PTH and plasma phosphate - PTH suppresses Phos resorption -Metabolic acidosis also reduces phosphate resorption (good to have phosphate in the tubule to soak up H+ - Decreased tubular pH converts HPO42- to H2PO4- which has lower affinity for phosphate binding site - Mg Loop and distal tubule - Uric AcidWhy do I love acetazolamide?- I love the proximal tubule- Many uses- Often forgottenMOA- Inhibit carbonic anhydraseMain effects- Renal: less bicarb reabsorption (ie less H secretion) à more distal Na/bicarb delivery à hypokalemic metabolic acidosis- Brain: reduce CSF production, reduce ICP/IOP, aqueous humor- Pulm: COPDNotes- Tolerance develops in 2-3 days- Sulfonamide derivative- Highly protein bound, eliminated by kidneys Source: Buzas and upuran, JEIMC, 2016S Data:1968 - High altitudeHigh altitude usually results in respiratory alkalosisAcetazolamide – lessens symptoms of altitude sickness (insomnia, headache) which occur because of periodic breathing/apnea1979- NEJM study took 9 mountaineers asleep at 5360 meters à improvement in sleep, improved SaO2 from 72 to 78.7 mmHg, reduce periodic breathing, increased alveolar ventilation (pCO2 change from 37 mmHg to 30.8mm Hg)1950s - Seizures/migrainesCAI reduces pH (more H intracellularly), K movement extracellularly à hyperpolarization and increase in seizure thresholdWeak CAI (Topamax, zonisamide) but not though to be important mechanism of antiseizure effect (topamax enhances inhibitory effect of GABA, block voltage dependent Na and Ca channels)Pulmonary/COPDThought to help with the metabolic alkalosis and as a respiratory stimulant to increase RR, TV, reduce ventilator timeIn 2001 Cochrane review – no difference in clinical outcomes, but did reduce pH and bicarb minimallyDIABLO study (RCT) on ventilated COPD patients – no difference in median duration of mechanical ventilation despite correction of metabolic alkalosisHigh altitude erythropoiesis (Monge disease)First described in 1925 via Dr. Carlos Monge Medrano (Peruvian doctor), seen in people living > 2500-3000 meters (more common in South America than other high altitude areas)Usually chronic altitude sickness with HgB > 21 g/dL + chronic hypoxemia, pHTNAcetazolamide – reduces polycythemia because induces a met acidosis à increases ventilation and arterial PPO2 and SaO2 à blunts erythropoiesis and reduces HCT and improves pulmonary vascular resistanceGI ulcersWhen H2 and PPI available, less useHistory: 1932 – observed alkaline tide, presumed existence of gastric CA (demonstrated in 1939)Acetazolamide was used to inhibit acid secretion in 1960s, ulcer symptoms, with reversible metabolic acidosis, BUT lots of SE (electrolyte losses, used Na/K/Mg salts to help, renal colic, headache, fatigue, etc)Later found H. Pylori encodes for two different CasHelps to acclimatize to acidic environmentBasically, the Ca changes CO2 into H+ and HCO3They also have a urease which produces NH3The NH3 binds with H+, leaving an alkaline environment for them to live inInhibition of CA with acetazolamide is lethal for pathogen in vitro1940sFound there was CA in pancreasThought acetazolamide to reduce volume of secretions from NGT (output from exocrine pancreas) Source: Human Anatomy at Colby Blog Diuretic resistanceIf develop hyperchloremic metabolic alkalosis, short course of acetazolamide + spironolactone (b/c need distal Na blockage) à can helpMay help with urine alkalization (ie uric acid stone) but increases risk of calcium phosphate stonesADVOR trial acetazolamide in HF exacerbation in Belgiumuse may help to prevent new episode, lower total diuretic doseCSF reduction (pseudotumor cerebri)Reduces CSF by as much as 48% when > 99.5% of CA in choroid plexus is inhibitedNORDIC trial (acetazolamide v. placebo) – improvement in visual symptoms especially if advanced papilledema, and reduced opening pressure)Side note also used off label to help with increased ICP and CSF leaks, as alternative to VP shunts, repeat LPs, etc Source: Eftekari et al, Fluid Barriers CNS, 2019.

30. Johnny Carmona, Técnicas educativas.

Hablemos con orgullo

Play Episode Listen Later Jan 15, 2021 55:09

Estrenamos temporada, Y sí, el maravilloso johnny Carmona fue nuestro padrino. Hablamos de mil cosas, pero entre lo mas destacado esta que hablaremos sobre su papel en la educación y lo que la pedagogía significa para él. No te pierdas este inicio de temporada con nuevas secciones y canciones espectaculares. #HCO3 #hablemosconorgullotj #iberotj #lgbt #radiouniversitaria #ibero

estrenamos carmona educativas hco3

DKA--diabetic ketoacidosis

WeR4Peds

Play Episode Listen Later Nov 30, 2020 11:52

What criteria do we use for an insulin infusion? pH < 7.3 and/or serum bicarb (HCO3) < 15.

diabetic ketoacidosis hco3

Arterial Blood Gases (ABGs) Crash Course

Nurse Dose

Play Episode Listen Later Oct 8, 2020 10:03

This week's episode is a short crash course into ABG interpretation. This is only meant to get your feet wet with the concept of arterial blood gas interpretation. Respiratory Acidosis: decreased pH, increased PaCO2Respiratory Alkalosis: increased pH, decreased PaCO2Metabolic Acidosis: decreased pH, decreased HCO3Metabolic Alkalosis: increased pH, increased HCO3

blood crash course gases abg arterial abgs hco3

Acid-Base Disorders: 'emia' vs 'osis" & Anion Gap

Play Episode Listen Later Oct 5, 2020 21:39

Dr RR Baliga's Internal Medicine "Got Knowledge Doc" Podcasts for Physicians. Not Medical Advice or opinion

board medicine internal disorders physicians certification residency acid base acidosis anion pco2 hco3

ACID-BASE BALANCE (FOP & TAS)

Dr Waqar Ali Khokhar

Play Episode Listen Later Sep 28, 2020 25:37

Interpretation of pH, CO2 and HCO3 in theory exam.

balance co2 interpretation acid base hco3

Episódio 53: Caso Clínico - Acidose Metabólica ft. Joanne Alves

Ta de Clinicagem

Play Episode Listen Later Aug 20, 2020 43:40

No episódio de hoje, Pedro traz um caso clínico de acidose metabólica. João, Fred e a convidada especial Joanne Alves discutem sobre causas de acidose metabólica e as etapas durante sua investigação. Gostou do episódio? Quer deixa uma crítica ou sugestão? Entra em contato com a gente no instagram @tadeclinicagem ou pelo email tadeclinicagem@gmail.com MINUTAGEM ep 53 Caso clínico - Acidose metabólica (0:37) Apresentação da convidada Dr. Joanne Alves (2:45) Caso clínico (5:04) Abordagem inicial (8:58) Antibioticoterapia (10:36) Quais exames solicitar (12:16) continuação do caso: conduta e exames laboratoriais (18:20) Discussão Gasometria Arterial (25:27) Discussão Anion Gap (28:05) Diagnósticos Diferenciais (32:15) Cálculo do Delta - delta (35:54) Cálculo do caso clínico (38:45) Seguimento do caso (40:20) Desafio da semana anterior (41:11) Desafio da semana (42:00) Salves FÓRMULAS: 1. Compensação respiratória (Winter): pCO2(esperado) = 1,5(HCO3) + 8 (podendo variar ±2) 2. Anion Gap (AG): AG = Na - (HCO3+Cl) - correção para albumina: AG(corrigido) = AG + 0,25(albumina normal - albumina mediada) - usar albumina em g/L 3. Delta/delta = (AG - 12)/ (24 - HCO3) REFERÊNCIAS: Rastegar, Asghar. "Use of the ΔAG/ΔHCO3− ratio in the diagnosis of mixed acid-base disorders." Journal of the American Society of Nephrology 18.9 (2007): 2429-2431. Emmett, Michael, and Biff F. Palmer. "The delta anion gap/delta HCO3 ratio in patients with a high anion gap metabolic acidosis." (2018). Berend, Kenrick, Aiko PJ de Vries, and Rijk OB Gans. "Physiological approach to assessment of acid–base disturbances." New England Journal of Medicine 371.15 (2014): 1434-1445. SEIFTER, Julian L. Integration of acid–base and electrolyte disorders. New England Journal of Medicine, v. 371, n. 19, p. 1821-1831, 2014. JUNG, Boris et al. Diagnosis and management of metabolic acidosis: guidelines from a French expert panel. Annals of intensive care, v. 9, n. 1, p. 92, 2019.

COVID-19 Files: Ep. 3

Gut Check Project

Play Episode Listen Later Apr 4, 2020 64:17

All right, gut check fans and everybody at KBMD health. Thank you all for joining us again for a third installment of the COVID file. Dr. Brown and I are here to talk a little bit about the physiology and kind of how people actually get sick. And Dr. Brown actually asked me to do a little role reversal. So can you want to explain a little bit what's going on here?Yeah, so this is COVID files number three, and we got a lot of feedback when Dr. Ackerman and I did 2.5 we're all we did is talk about the gastrointestinal stuff. Then everybody else is in the news is talking about respiration, pulmonary stuff. And so we got a lot of questions about that. And I just happen to see that like, a world renowned infectious disease doctor, Dr. Peter Hotez was on Joe Rogan. And Joe was asking all these lung questions in detail, so I realized that you know, you're an expert in this your training is a crna. This is right in your wheelhouse. So I thought that we could just do some of that. Even on some of these other shows, they're interviewing virality and they're interviewing epidemiologists and they go really, really into the science. What we know that calm is contagious. And we know that the more information you have that can actually calm you down. And that's what we're trying to do in this show. We're trying to get people through this crisis. But I do believe that if you understand the physiology, then it makes sense why some people can get really sick and it makes sense why some people get better. And so you being an expert in this is just perfect. And we're getting questions like this like from a Mike Logzen from Texas. Interesting. We have one of those working for us also. Yeah I know, names like that. Just keep popping up there's Mike Logzen one, Mike Logzen two I wonder if there's a Mike Logzen three.I know, so Mr. Mike Logzen and asked what are your thoughts on why younger people and healthcare workers are getting hit hard as this disease goes on? That's a great question. And in fact very relevant. Newsweek just did an online publication that I received this morning, where it said the over 100 healthcare workers have died from COVID-19 So this is this is an important question. So really what we're going to do with you today is talk about the pulmonary physiology and what happens and when people say, oh, this can affect you, and you get this rapid progression that can be very frightening and different things like that. But just understanding what's going on, I think is the real important thing. So, I just want you to take it away. I'll interrupt. I'm hopefully not too much, because I have a tendency to do that. And if I am just gonna wait I got a slide on that. We'll get to that. SoA couple a couple of quick apologies that we learned in technology since we are all practicing social distancing and Dr. Brown or Ken is, is addressing his patients over in the Plano area I'm trying to help out over here in the in the Denton area. We actually are not together obviously, it's while we're recording like this, so I had to make some really bad drawing slides. Ken, you're gonna love these they are they're really, really artistic. And as I share them with you gonna pull our faces down from the screen. So bear with us, it's not normal. But we'll try to take some breaks in there, we've learned we can't put them all up at the same time at least we're not smart enough to do that. And Ken if I go too deep, if you feel like I'm losing votes just going back, hang with us though. The goal here is to show you how the disease itself is probably going to affect your lungs. And then to get to a point of showing you how we think we can work through it. I'm going to show you the tough parts, but at the same time, what it is that we're hoping to do to really get people through it. So that'sReally even if this is not relevant to you, I I do know where we're going to go with this. And right now, the mayor of New York City is thinking about bringing in a doctor draft where basically they're going to pull doctors out of retirement, they're going to ask doctors in different specialties to try and help out with these pulmonary issues. So you can even forward this to your doctor if you have family or friends that are in the healthcare field. This is something you could forward to them. Because if I happen to get called in, I want to be informed on how to treat people with their pulmonary situation, not just their gastrointestinal. So this this could also be very relevant for healthcare workers, our frontline people.I agree, I agree. And I'm hoping that we can make some make some light of not necessarily light but bring some information that gives some people some comfort. So you'll see here my very first drawing right off the bat did not load the way I wanted it to. So that's a little bit of humor there. And that's about as good as these drawings are going to get. So I'm sorry, these are loans. That little green arrow is pointing up to a diaphragm, just a quick refresher, as a diaphragm contracts, it pulls down on the lungs, giving a negative pressure or pulling air into the lungs. And that's important when you're healthy. You're pulling air in, you're not necessarily having it pushed in some but what you need to recognize is that the lungs are made up of five different lobes the left lobe has two the right lobe has three and every single one of those lobes has tons, literally over 300 million alveoli per lung. So you a 70 kilogram average adult has around 600 million alveoli and that gives you tremendous surface area for oxygen and co2 exchange. That's what keeps us alive and that's what the oxygen keeps us alive in the co2, of course, is our waste gas that our body is pushing out. And if you were to spread it out flat, that equals to roughly a little bit larger than a tennis court, so Ken.Wow, and so the analogy I always thought about this is a tree the main bronchus is the trunk, then you get split, and then it keeps going into smaller branches where the leaves could kind of represent the gas exchange or the alveoli. Do you visualize it like that?Yeah, tree is exactly what they call it. It's a tracheobronchial tree and it runs all the way out. There's actually I believe, 23 generationss of tubes getting smaller and smaller and smaller until we get out to the alveolus itself. So alveoli is all of them. Alveolus is a singular one, don't hold me to it, I often interchange them myself while talking about them. So one particular alveolus. I've just drawn an arrow, it's in the lungs, it's everywhere. But I'm making an arrow and a draw here, because this is what we're really going to get started with on how it all functional I'm sorry, here's the heart. We'll we'll talk about this a little bit later in positioning but know that the heart lies anterior towards the front of your body a little bit, and a little bit over to the left. So but that's where the heart is located as it receives blood pushes it to the lungs receives the blood again and then pushes it out to your body. So let's look at that alveolus. The alveolus right here, you'll see inside the circle, that's actually the external air that we've just breathed in. So that's where our fresh air oxygen, oxygen rich air will come to, and it will be taken up by the capillary. The capillary is the blood supply that's bringing up the gas that needs to pick up oxygen and let go of excessive co2 carbon dioxide, that's the waste gas.So that's the exchange, the oxygen goes in carbon dioxide goes into the little alveoli, then we breathe that out.That's exactly right. And you'll notice, even though my drawings are poor, you'll notice you'll see the capillary here in a moment is going to start to kind of pull away in distance and that just makes it harder for that gas exchange. Inside the alveolus there are two specific cells that we have in there pneumocytes. So site means cells, pneumocyte one offer gas exchange pneumocyte two are there for surfactant, they make surfactant. Now, granted, the there are more pneumocyte twos than there are pneumocyte ones, but the pneumocyte ones actually take up far more real estate for gas exchange but the pneumocyte twos make that very important surfactant which allows the alveoli to expand without collapsing. And that becomes a problem for us as we as we move along. What we've returned to you here in this particular drawing, I've only drawn a pneumocyte two because that's where the infection occurs with the current virus that we're addressing the coronavirus.We'll just say Remember, a lot of people were talking about the ACE two receptor, this is what they're talking about on the news, the these type two pneumocytes have a lot of these h2 receptors. So that's the target. That's correct. I didn't throw that on there. But that's, that's a definite point. H2 receptors are located right there on that type two pneumocyte. The little blue dot at the top is going to represent a Coronavirus. And it's going to attach to this type two pneumocyte. So next what happens we're just going to be reminded here that surfactant is important. It breaks the surface tension. Without it, the alveolus will collapse. Very important. I'm going to remind you a few times about that. So now, the little blue dots inside of the type two pneumocytes represent the replication or basically the the increasing number of viruses that have just now been transcripted. They're they're multiplying, and now it's infected the cell.So just to go back to our very first COVID episode, the virus gets into the cell hijacks, it gets the cell to produce more of the virus. That's why they're growing inside the cell itself.They definitely are. And then this is not what the cell is programmed to do. So unfortunately, the cell is going to rupture and die, and the virus is going to escape to the alveolus. Now I'm going to stop real quick and remind everyone. Remember, I said that there are type two pneumocytes actually out number the type one. So the problem is it's not just one type two pneumocyte in this particular alveolus is is infected, probably most, if not all of them in this alveolus certain thing. And so this is happening all over this alveolus. Well, not only is new virus going to escape. These little red dots I just added in there represent inflammatory mediators, and they carry a message. They are searching for help. And not only that we now have a ruptured and dying and dead cell. So you'll notice I've drawn in here, Ken, what would be inside an alveolus like this? What are these things called? You remember?Yeah, I believe you're going to talk about macrophages now.Yeah, macrophages. Exactly. They are the janitors of the immune system. And he's there to just generally clean up regular debris and cellular debris and then take it in and then basically, it usually gets ushered out or absorbed by left, etc. But what we have now is a crisis situation because it's not just happening at this time to new massage. It's happening probably to most of them. They all begin to be picked up these inflammatory mediators are picked up by the macrophage itself, and that's going to activate it. It now knows it needs to release some messengers of its own to call for help. And right here is the beginning of something they've been talking a lot about in the news, especially for young people. And that's the cytokine storm. Because these interleukin one, interleukin six, and tumor necrotic, factor alpha are all cytokines. And they are going to be released and picked up by the blood supply the capillary right down here, and they are going to have some immediate local action. And as this is happening, remember I said there are up to 600 million alveoli throughout the throughout your lungs is this begins to happen in this section. Imagine all of the interleukin one, six and TNF alpha that will be picked up by the blood supply and now begin to spread throughout the body. So you can see now they've made their way into the capillary bed, and a few things are going to happen right off the bat. Once they first enter the capillary bed. The capillary itself is going to dilate. That's going to lower the blood pressure, but it's going to increase the blood flow. This happens with injury all over the body we we have an injury, you have swelling, it's very, very normal because you're bringing in other things to help repair. But when this happens over and over again kind of an uncontrollable situation like we're going to talk about, that's why we know that we need to manage this particular situation. The permeability of the capillary itself is going to increase that's going to allow for some fluid to escape the capillary bed, and then begin to infiltrate the alveolus itself. So fluid, also known as blood plasma escapes to the interstitial space, which is the space between the capillary and tissues, and then also goes into the alveolus. So, the permeability or now we've got a leaky capillary bed. Permeability is not necessarily something that is in response to it it is because the capillary basal dilation is stretching it too much, are you aware of how the leaky capillary happens?In a, in a really microbiology term, I think what happens is that those cytokine, if I'm recalling correctly, the cytokine mediators activate endothelial cells, which are the cells inside of the capillary. It actually caused them individually to constrict which makes holes. So if you can think of two large men and suddenly they become skinny men without moving their feet, there's now space between them. Does that make sense?Yes.That's kind of that's kind of how I remember it anyway. But that allows the blood plasma which is normally contained in the capillary bed to then escape go into the interstitial space migrates into the alveolus. And this is not what we want. I'm going to reiterate that surfactant is important. It breaks the surface tension of liquid. Without it, the alveolus will collapse. Well, we just had those type two pneumocytes that were producing surfactant. But now they are beginning to be damaged and not produced surfactant at all. And when they were producing it, they were producing the correct ratio, which meant that for the fluid that was there, remember, when we breathe in it's 100% humidity in the alveoli. Once we don't have surfactant, now we don't have enough in the ratio to help keep it open. So losing cells that produce surfactant, and then we dilute the existing surfactant that is going to increase our surface tension. And the potential of collapse of the alveolus is inevitable.So the surfactant the way I've always kind of thought about it when you don't have surfactant, the alveolus they will stick to each other they cannot slide and open up and so it becomes a very in the dumbed down terms like it like a stuck balloon that's that can't expand.That's correct. Now written consolidation up here, it may be a little premature at this point. But we will return to it. This is the method of how consolidation occurs. Like I said, forgive me for my drawings, I just did these and snapped them and loaded in the computer. I knew, I knew I couldn't draw and talk at the same time very well. But regardless, you'll see that fluid's beginning to build up. Little red dots in there represent cellular debris. Also, some virus is still trapped in there. Some proteins which are broken ours are still stuck in there. But remember, I warned you earlier, the capillary beds beginning to pull away, right, the interstitial space is also continuing to fill up along with the alveolus. That pressure outside the alveolus and in the water on the inside of the fluid on the inside, will basically make this alveolus you have the potential to collapse it will not expand nor contract with each breath. It basically just kind of floats as a membrane would between two liquids. I've also drawn oxygen up here at the top and co2 still in the capillary bed. The sheer distance for the diffusion is going to render This alveolus is incapable of gas exchange. That's that...So in this picture, just to clarify the oxygen that you breathe in hits this fluid, because the alveoli is filling up, and it's not getting to the other side where it needs to go.That's correct. It cannot just really won't diffuse that even though macroscopically may look like a short distance. It's it's still far too far for efficient gas exchange for oxygen and co2. So remember, this is what it should look like the oxygen will come in you right next to the alveolus to the capillary co2 goes, goes out O2 comes in. No big deal. That's just not what's happening right now. The next step that happens and takes us to full consolidation is going to be the summoning of these neutrophils another part of our immune system, they normally would come in, and in a healthy IV alveolus would more or less be able to target viruses and other pathogens that could be found within the lung. But in this particular situation, especially with the amount of fluids taken on, they actually become a little bit indiscriminate. And they use two agents primarily: the reactive oxygenation species and various proteases. And instead of a targeted attack, with the dilution here, inside the alveolus it actually just becomes kind of a, a wide away, wide array spray of attack. And not only do they grab ahold of some of the proteins that don't belong there and some of the cellular debris that needs to go. They'll also end up attacking indiscriminately against healthy lung tissue, healthy pneumocyte ones and pneumocyte twos. So when people talk about a bacterial pneumonia, this is the beginning of having a super infection in addition to the damage that the virus has already caused.It is it is and again, Brown and I are not telling you any of this stuff so that you become panicked. But really it's the opposite. knowing what's happening may help you understand number one, what it is that your health care provider needs to do to keep you and your family safe if you happen to find yourself in this situation. And number two, I think here in a moment, as we wrap up some of this, this discussion, you'll see maybe some things you could do at home to outrun some of this.Yeah. So what we're doing, what you're doing is you're setting the stage work that you if you understand the physiology and the pathophysiology, then you can start doing some modifications to try and improve. And that's where we're headed here.Definitely. And again, this is called consolidation at this point. This just basically establishes it's just a word that says that this side has been consolidated, it's not functioning, air will not be exchanged here, we will not have oxygen pick up nor co2 blown out by this alveolus. Now you kind of have to picture not just this alveolus but the entire portion of the affected lung is now experiencing a portion of consolidation. So let's talk about what's happened so far. We've lost type one and type two pneumocytes: one is how we breathe or the gas exchange two makes the surfactant to keep the alveoli open. Our gas exchange, of course is going down. Our surface area, our tennis court size of surface area for us to pick up oxygen is being decreased. And our diffusion distance at the alveolar level is increasing, even for those that haven't been consolidated, right. So we have a decrease in gas exchange. You'll see this little abbreviation I've debated on whether or not to put it up there, they'll PaO2. That simply just represents the pressure of oxygen in the artery. Big P means pressure little a means artery. O2. So that's just a cool shorthand that medical workers use to identify the partial pressure of the oxygen in a particular location. Inevitably, it just means that we have low oxygen and that gives us a word called hypoxemia.Low oxygen.Yeah, low oxygen. Can you just on that note right there because we use pulse oximeters all the time, and even get them at Walgreens, can you explain the difference between the number on the pulse oximeter and the PaO2?That's a, that's a great thing. So on a pulse oximeter that really is only reading the percentage of the red blood cells that are fully saturated. So there are actually four binding sites on a normal red blood cell for an oxygen molecule to bind on to an iron molecule. If all four of the sites are occupied before the red blood cell has delivered it to a tissue, and it will be counted as one that's saturated. So if you have 98% saturation, that means 98% of your red blood cells have all four sites occupied before they deposit one. This is a little bit different. This is actually the carrying capacity of, of the red blood cells and how much of the oxygen is actually present to make a difference. So SPO2 talks about how well the red blood cells are actually picking up the oxygen to take it somewhere. But let's talk a little bit about this. Ken you said that your son went to play in in I believe was in Mexico?Yeah it was Mexico, very high altitude. He was there for four weeks, I think. Yeah, very high altitude. So essentially it was high altitude training in several tournaments.We can use that kind of an example, when he was up there, do you think for one second that his oxygen saturation was ever at risk? Probably not. No. He was saturating them just fine. But what he didn't have was a high enough oxygen pressure. So his body sensed that sensed the decrease in oxygen pressure and begin to produce more mature red blood cells to become more of the bus carriers to pick up more oxygen and take it out. So we probably remained at 99% saturation the entire time, but he actually just needed more oxygen molecules themselves to sustain it because there's just less atmospheric pressure at 7,000 feet.Yeah, and that's what we had to come to that conclusion because when it came back, we he got to work up by his pediatrician. And we were all a little bit alarmed to see that his hemoglobin and hematocrit had jumped way up. And it was in response to being in high altitude. So it was the body's adaption to it.Well, that's I completely agree with that. And that's actually you guys, that's actually a normal thing to have happen. You have a higher red blood cell count at a higher altitude.So now you're going to talk about the thing that's, that's the hard part, which is the work of breathing goes up.It definitely definitely work of breathing goes up fighting this tougher distance of diffusion losing a portion of your lung capacity to move gas is going to increase the work of breathing and then throughout this theme Ken, you're going to see the word work pop up because it works in the complete opposite direction of what's happening in the lungs for someone to more or less recover on their own. So cough is going to set in if it hasn't already, that's going to increase the work of breathing. And don't forget these viruses are pretty smart. That's actually going to help spread the virus. So that's a, that's no good either. Work by the body requires more oxygen again, that's why I'm going to highlight that and just kind of think about that for a moment. If I'm decreasing my availability to get oxygen, but the work and the demand is going up. I've got an intersection of a problem here. And if not recognized soon enough, it could just get worse. So let's talk about why the why hurting your lung and recovering from an injury is probably more important than just hurting your ankle now. This is Mike Logzen's number three. This is his ankle.Yeah, he sent us a picture. He said you can use my ankle as an example. Thank you. Yes. So Mike number three thank you for sending in this photo. And Mike is into jujitsu and he showed me after one of his injuries that he has that ankle twisted, and he said ouch. But the good thing about hurting your ankle, okay? You do get edema just like what we're having up here, the fluid buildup in the lungs, you could get edema have a swollen ankle. But the good thing is I don't have to breathe through my ankle, there is no mouth there, I'm not going to have to draw any air at my ankles, so I can just lay up and rest. The problem with having adema or fluid buildup in the lungs is we're compromising our ability to simply recover. And so that's why it's such an urgent situation. And I didn't I don't think we mentioned this before we moved on here Ken. What we're describing here is a acute respiratory distress syndrome. And so that's ARDS. You may hear people in the news reference, acute respiratory distress syndrome or ARDS. This is kind of more or less getting to the point where we're spiraling a little out of control as far as the lungs are specifically. So let's look systemically or all over the body. Remember interleukin one and interleukin six. Well...Those were the the initial inflammatory mediators set off when the virus attacked the type two pneumocyte, then the response of that is to release these inflammatory mediators.That's correct. And they were picked up by the capillary beds. And now remember, they're not just working locally. If we have a large portion of the lungs, releasing these same mediators, they're going to eventually make their way to the central nervous system or the brain and spinal cord. They're going to trigger the hypothalamus, which will then release prostaglandins, that raises your body temperature. And guess what, that's what we end up turning into a fever. And unfortunately, fever is just going to be more work. It requires more metabolic work for your body. So we are still yet increasing the demand for oxygen. We as we referenced earlier, PaO2 remembers just a simple shorthand for the pressure of Oxygen or the number of oxygen molecules in the artery. It's low. So this is hypoxemia. Now the trigger that Lucas had whenever he ended up producing red blood cells was they his chemo receptors, noticed that they were a little bit low on oxygen carrier, so they produced more red blood cells. The chemo receptors here are going to try that. But in the interim, they're also going to trigger the sympathetic nervous system. And when they do that, that's going to set off anxiety, getting people a little bit worked up, but it's also going to be don't forget the sympathetic nervous system is your fight or flight response is going to increase your heart rate, it's going to increase your respiratory rate. That is just more work. The demand for this oxygen just keeps going up.And all of that just on that last slide there, Eric, remember that the heart rate is that that's compensatory, because it says we're not getting enough oxygen. So if I pump faster, we'll at least get more oxygen around if I breathe in, quickly I'm hoping to bring in more oxygen in the heart tries to pump it fast. And that just becomes a bit of a slippery slope. And that's where you're going to get into right now.You're right. And think of healthy lung at this point. If we were simply just had healthy lung at just this point and these are the triggers that high heart rate and a high respiratory rate would basically put everything at ease because hypoxemia would be solved. That's not what we're dealing with at the moment. So this is obviously a progressive disease, we have this increase in cytokines, interleukin one, six, TNF alpha, you can have what they call SIRS for short or systemic inflammatory response syndrome. Then this is kind of interchangeably been used with cytokine storm, but essentially, this is what's happening. These cytokines are triggering all levels and manners of other problems throughout the body. And what we have because of the dilation everywhere, is we have a decrease in peripheral vascular resistance, that's just the resistance that we have at the edges of our of our water, right, we have an increase in permeable capillaries that Dr. Brown described earlier just means that they become more porous. That's where we're leaking that blood plasma, the fluid when we leave that fluid that decreases our blood volume. And we have this systemic all over the body vasodilation, so all of the vessels have lost this resistance. And it's because all of the vessels are trying to get more of the blood flow, that basically we're running out of that amount of blood.When I did Critical Care Medicine, the way to think of that when the body's when the body's trying to compensate by trying to get more blood to everything. If you open up the arteries, or if they vasodilate, and you can keep up with it. Then you get more blood flow where it needs to go. But if you can't keep up with it, imagine a hose. You know the hose that has a little nozzle on it. You can run water and that the smaller the hose, the higher the pressure it goes through. If you keep putting on bigger hoses, then it just comes out as like a little trickle. And that's what's going on and that's what creates this hypotension or severely low blood pressure.Now it's a it's an excellent visual. Yeah, it's a high pressure with a garden hose. Same amount of water through fire hose. Not so much pressure.Exactly. Yeah.So just like Dr. Brown just described, we now are hypotensive. We don't have that pressure everywhere. So now we're systematically hypotensive. That comes with its own consequences. It's going to retrigger the SNS as if we didn't need more agitation.SNS-sympathetic system: fight or flight.Thank you for batting clean-up there. Sympathetic nervous system, there poor profusion of organs. This is where things begin to really kind of spiral out of control if we didn't get there soon enough. Okay. So we we have the lungs that's that's a set of organs right? But we've got brain, heart, liver, kidney, also very, very important. If we have poor perfusion we risk getting multi system organ failure or msof. So kidneys liver and heart. Here's here's the the reason why I'm highlighting these is these are the ones and almost in this order which will begin to throw off markers that we can we can sample for with laboratory with laboratory work and see the status of a patient. As kidneys begin to lose perfusion, they will increase our blood, our blood, blood urea nitrogen will begin to increase as well as the creatinine and it's simply because the pressure is not great enough for to be cleared by the kidneys. And the problem is is those are toxic at high levels. We don't we don't need those circulating like that. The liver itself will begin to sustain some acute damage because it's not being perfused and the wastes aren't being carried away. So we have an increase in AST increase ALT and an increase in bilirubin We also may end up detecting later as we progress an increase in C reactive protein. More interleukin six, just in case we didn't have enough of that circulating around your, your liver guy here is going through us and interleukin six as well as possibly some fibrinogen. And then if we get to this point and the heart begins to not be able to perfuse, the myocardium or the heart muscle, the heart could begin to throw off some chaperonin or CKMB markers, very similar to what we would test for for somebody who's had a heart attack. Or they may also, unfortunately be at the point that could suffer uh...Looking at this looking at multi system organ failure. When I was a resident or when I was a medical student, you'd show up and you have to do rounds. And so you'd have your patient the attending would show up. You'd go 24 hours, what's gone on the last 24 hours you tell them you're like okay, well we've got blood pressure has consistently been dropping, we either try and keep it up or we keep an eye on it. BUN has gone up creatinines gone up. We've got a slight bump in the liver test. So far troponin is normal. And that's almost how you would say it because you're like, we're heading there. We have to stop it before. Because once that heart once you start having a heart attack, that's your last. That's that's the thing that's going to really give up, so...No joke. There's there's a, and let's reiterate, before we get to this point, this is why we want you to know what's happening. We don't want to get to this point. We're going to reiterate what we want to steer away from.This is why whenever they talk about the healthcare resources, why it's so important, because one thing that I want to get out there right now, because we're learning data about COVID19. And now it looks like we're getting close to 30%. I've seen some studies when you're looking at the data of young people getting it not dying, but needing hospital facilities to stop them from going into multi-organ failure. So it is no longer just very old and sick people, they just have, they already walk in before all this starts happening with some other underlying problem. We believe that's why they go into multi-organ failure quickly. So this is relevant for everybody, that this is why we need to make sure that we continue to practice social distancing so that we do not overwhelm the health care system 100%.That's, that's what we're trying to work against, for certain. So let's look at this patient right quick. We've had a decrease in oxygen. Remember, our lungs are damaged. And I've kind of just made a summation of the workload, these are the demands, we've increased the work on the work of breathing, the fever, the heart rate, respiratory rate, the anxiety, not to mention, the organs are starved for it. We've got hypotension everywhere. We're in a little bit of trouble here. So come in, whenever, certainly when it's appropriate, and you have the right signs and symptoms which we've addressed in in the COVID files one and two and two and a half. But what will happen if you end up getting managed in this particular situation, first, they're going to try to find out how much fluids that can give you to resuscitate some of that blood volume. And it's not just as easy just giving you what's missing because remember, we have permeable capillaries, giving too much of fluids. This is a delicate balancing act, giving too much of the fluids could actually exacerbate or make the problem worse with some of the interstitial fluid bonds. So we'll be using some medicines as well. Some medicines that will help what we call pressors to bring your pressure up some diuretics to help pull off some of the excessive fluid. So there's there's a significant balance there, butIt just shows why people like you get subspecialty training and ICU doctors and pulmonologists that anybody that works in a critical care unit. That's why it's so important. They're really good at this and there's an art to it, and it requires definite increase learning not just this is what's a little bit scary. If they ask a gastroenterologist like me to come in and say, hey, look, we're losing people, we need your help in the ICU. One of the reasons why we're doing this is because as a health care worker, I feel like I need to refresh myself on things that I've not done in a long time. That's a really good point, because a lot of what you do is a long term solution as you take care of the patient and a lot of what I do both in anesthesia and then whenever we were doing critical care is, it's very acute. It's very short term. Most of the medicines we use are, I mean, they're they're instant, they're in and they're gone, right? So it's very much like that. So what happens after this is fluids and medicines aren't going to do it. Well we need to ventilate, which is how we breathe, duh. But if you can't do it on your own, we're going to look at mechanical ventilation. That essentially means that we're going to have to insert an endotracheal tube to control the airway now. Ken at a later time or if we have enough time today, we can talk about some of the alternatives between just breathing room air to this but for this particular episode not to get too far, let's just go straight to ventilation if that's okay.Absolutely, yeah. Okay. Because that's that that's what everybody's been hearing on the news also is just we're gonna run out of ventilators.Well, yeah. Very, very good point. So some of the other stop gaps in between the cpap, the bipap and in high flow in the tents over the head. Those are all great if they work. I mean, goodness gracious, high flow nasal cannulas absolutely but there's there's peculiarities with each one of them. The critical part here is we just don't have enough ventilators if anybody gets pushed to this area. So we're going to have to connect that endotracheal tube to the ventilator. And you're gonna love this drawing. I mean, anybody would obviously recognize this anywhere that's that's definitely a ventilator, or a flux capacitor.Yeah, I was gonna say it looks more like a flux capacitor than a ventilator but...The blue represents the endotracheal tube that goes down through the trachea there, but I want to call your attention to one small thing, that little bitty red circle represents a balloon. We...after we put a tube into someone's trachea, we actually inflate this little balloon, and it secures the tube in place. And it gives a true closed circuit meaning air is not breathed around it, we can now control the ventilation. And in this particular case, with such a contagious virus, we can prevent the spread of the virus from coming out of the lungs and through the mouth of nose because it's closed.That was the that was the big argument in the very beginning. Is this just droplets or can this be aerosolized and in the beginning, it felt that possibly if you don't have a closed circuit, then you're allowing somebody to aerosolize it in a room. And now we're putting healthcare workers in a room with higher amounts of virus and so the likelihood of getting infected without proper protective equipment. I think that's why health care workers are our frontline people and they're putting themselves they're heroes because people taking care of these patients especially in the beginning, that's why so many Chinese doctors died when they didn't realize what they were dealing with.Yeah, it's it's a pretty hairy topic all around and the intermediary steps to getting someone from, you know, being able to walk around to the event, where do you stop and is there enough...is there enough PPE for the others outside of this little bitty ballooned cuff to handle that? Some things that we're going to do with and I don't want to get too deep here, but some things that someone would do when they when they put somebody on a ventilator is they would have to look at small measurements, one called tidal volume, that's just the amount of air that you're breathing in and out with each breath. If the if, for instance, the average 70 kilogram person takes in around 500 to 550 milliliters or cc's of air, which with each breath and blows it out at rest,So that that's just your normal breathing. So everybody that's listening to this, their breathing normal, that is your tidal volume. That's what you normally do.Correct. And the amount of times that you breathe in a minute is just a respiration rate. At rest, relatively healthy people, adults about 12 to 14 times a minute. So you can see something here though the bottom two minute volume and PEEP, those are those are our calculations and and therapies that are specific to a ventilator and minute volume is simply the respiration rate times the tidal volume. So if somebody breathes in and out 500 cc's, and they do it 12 times a minute, their minute volume would be six, six liters. Does that make sense?It does. And I think the key here is the PEEP because this now the physiology that you taught in the beginning, pathophysiology. This is where the PEEP becomes really interesting.Yeah. So let's, I'm so glad you said that. So everybody remember PEEP, we're going to address it. This is what the vent can do for us, and that we can't do with without it, okay. So just just looking at what we would do with someone who happens to be sick and dealing with an ARDS situation acute respiratory distress syndrome, we've lost some of the lung availability, so we can't put in the same volumes as normal. So we're gonna have to turn it down. But we want to maintain a relatively close minute volume. So we're going to increase the respiration rate to make that equation somewhat balance out. Now, that's just to get us started. Granted, we will be able to check what we call arterial blood gases and make certain that we're doing it the right way. And we can check our therapy but at the same time to get someone set up. These are some of the calculations that we would make, but what we're going to do is begin to apply PEEP, okay, and I'm going to break that down here in just a moment. But first, you may wonder why am I seeing people on TV or why do I see someone that I know who's being treated for ARDS or specifically COVID ARDS in this prone position. Prone means face down spine to the sky laying on their abdomen or stomach, and getting respiratory therapy. If you recall, I drew the heart earlier in one of the earlier slides, and I showed that the heart is located a little anterior, so towards the front, and a little bit over to the left. But essentially, when you lay on your back, that gravity is still pulling down on the heart, you're you're kind of occluding a good portion of the lungs that lay along the back part of your body. Does that make sense?It does and I think that this is something that we need to get through because this may be early intervention. We're seeing a little bit more of this, and here's why.Yeah, so that's exactly right. And something you can actually do at home, even if you're not feeling great. Recruitment I've written on here, increasing recruitment, recruitment just simply means I can make use of these alveoli all those allow the alveoli everywhere else. If I can use them, I'm recruiting them to be a part, right. So if the heart is more anterior and I'm getting more exposure to more lung tissue that's still healthy, I'm increasing my recruit. So we're going to have to monitor for status after we get onto a ventilator. Like I said before, we're going to look at arterial blood gases. These are just figures that we look at. I'm going to show you the numbers but you don't have to memorize them of course.You make it seem like it's a test.I know, I know, I want everybody to write in email. If you can recall this you can recall this slide. Normal pH which is how we measure our acidity or bass or alkalinity is 735 to 745. CO2 is 35 to 45. That's that's what we breathe out. HCO3 is bicarbonate. Okay, that's what our kidneys are doing to help give us balance. But remember, they're not being perfused so they're not really making it like they need to in our PaO2 we've referenced it several times, but that's the pressure of oxygen in the arteries. It's normally for a healthy person. 80 to 100. Well, this is what it looks like when we run the first ABG, we're going to be acidic, because we're not getting rid of waste gas, and we're not producing enough bicarb. Okay. And so our oxygen is really what we're going to have to get control of first. And then we're going to work towards a better acid base balance as we as we treat the patient.So for non healthcare workers. This is an arterial blood gas. This is a measure when somebody is in the ICU. And these numbers tell a story, depending on what's happening, they say if you're getting slightly better, slightly worse. And by the time what's really cool, as I'm looking at all of this, usually there's involvement of multiple specialties, helping out which is why one ICU person can occupy possibly a critical care doctor, possibly infectious disease, possibly a nephrologist-a kidney doctor, and they all look at these numbers and make decisions and tweaks on the patient. This is just shows how complex a patient in the ICU really is.Without question. Positive end-expiratory pressure. This is our PEEP. This is PEEP. So we drew attention to the few slides back. And if I've done a little bit better job of putting them in the correct order, we would've hopped straight to this. A healthy person when we bring them into, to the OR, and we end up having to use intubation or something like that. Super healthy, you may not have to give PEEP at all. Generally, people end up having, you know, two, three, and all the way up to five. A healthy person can have up to five centimeters of water of pressure and just represents pressure, but just look at the five. And what that does is that holds open the alveolus after you've expired gas. Now this is kind of important in that when we breathe and you're healthy, remember at the very beginning so your diaphragm pulls down, you're pulling air in your chest wall, is expanding out. It's literally pulling an external force outward to create a negative pressure to pull air in. Well, that doesn't happen with a ventilator, we're having to force air in. So we use people and healthy people, just so that we can keep recruitment up of healthy alveoli already. Well remember, right now we're not only fighting the fact that we're pushing air in, we're actually fighting the fact that we've got fluid trying to leak into our healthy alveoli. And if we lose an alveolus to consolidation, it's 99% chance that we are not going to reareate or re-recruit that alveolus we end up just losing it. So somebody who is already in ARDS, we're going to start start at 10 to 12 centimeters of water pressure for P and that's a healthy dose of P and does a few things for us for certain it keeps the alveolus open. It allows us not to give too long of a period of time of high flow oxygen which is 100% oxygen and that's a whole that's a whole 'nother issue. But it really will allow us to save good good parts of the lung. And I should say here Ken, there are possibilities of applying PEEP, where you're not necessarily intubated somebody with a cpap or bipap mask on this solely secure. You can still experience PEEP in that particular situation or even I think some high flow nasal cannulas are credited with some some portions of PEEP.So yeah, so just the whole PEEP thing was always confusing to me when I was studying it, but the way the way that you're describing it, we know that when these alveoli start to go through that whole process that you talked about in the beginning, capillaries start dilating. Well, these, it starts to put pressure on the alveoli. And by the PEEP, you can actually force that alveoli to try and maintain at least some gas exchange so that the leakiness and the fluid creeping in doesn't win. It doesn't completely close off the alveoli.100%. It's this, the PEEP is...you're exactly right. The peak is literally there, not only to keep the alveolus open, but in this particular situation on an ARDS patient, we've increased it because we need that extra help to help keep that fluid at bay in the capillary bed. We're not we've already lost the part of the lung right now during this disease state that we can't re recruit while it has fluid in it and is going through its consolidation phase. We need to maintain what we still have. So I wrote right here, increase area recruitment, maybe. It's a really, really, really slight, maybe. We're doing that but by proning and turning down. We're doing that by oh, and Ken you've seen these beds before, there are beds that actually are are specific for ARDS patients where you lay them in prone, but they actually turn them from side to side and move them around. And that's literally to increase and maintain the area of recruitment,And those are very high level high specialty beds, specifically only for this type of patient. And there's if we are, we have few ventilators, we got even fewer of those real specialty beds.That's exactly what I was thinking. But we our main job here with PEEP, our main job here with the ventilation is to preserve the area of recruitment. And of course with the PEEP like as I mentioned earlier, we want to decrease the need for 100% O2. Some people have even even to ask why. Why would you want to do that? The here's the danger of the fine line here working through mechanical ventilation. Yeah, so to higher pressure. So we want to be able to dial in and give someone enough of the air that they need to ventilate. We've lost part of the lungs, so that's going to increase the pressure if we don't dial back the volumes etc, etc. Just remember, if we are apply too much pressure, we can actually spread ARDS because we're causing damage to healthy tissue. If we give 100% oxygen for too, for too long, we can actually spread ARDS because it leaves reactive oxygenation species, which is exactly what the neutrophils were using to destroy what remained of the virus and unfortunately, healthy tissue. I know this is not ventilators are not like the way I treat a microwave which is just on high every time and just turn it on and let it roll. Ventilators...it's such a it's such a nuanced art. And, you know, and nobody's discussing that on the news where they're like, you know, we're going to run out of vents Well, we're also going to run out of people like you that know how to run these vents. So, you know, and I, this was not to scare anybody, this is not to get too sciency. You and I talked about this. I feel that here on gut check project COVID files, we see that there are going to be some doctors. And when I was watching the Joe Rogan show, they were they were talking about how doctors are stepping up, they're switching and trying to help out in this area. And I know that there are probably some doctors like me that are like, okay, I want to help out. There's going to be or if we get recruited to get in there, then I better do a refresher course. And all I have are a bunch of, you know, really old textbooks that will take a long time to get through. This is just the beginning of something so that they can at least go talk to a family member maybe so that maybe other people will go oh, I understand why my grandpa's on a ventilator now, not necessarily to COVID. This is just what happens. So I really appreciate you taking the time to do that. I think this is the opportunity to teach a lot more people about this kind of thing. And hopefully this will spread with some healthcare workers. So it will make them feel more comfortable.And when I told you that was a a because you only asked me a couple days ago if I could, if I would consider, you know, kind of throwing these together and, and I threw something by you. I said what, what would you think if somebody kind of had an idea on something they could implement that actually would be positioning, but not necessarily related to ventilation? And then you threw out the idea of what how did you say if you feel like you're getting sick, and you're not feeling well get ahead of the curve, lay down down on your stomach...why you kind of talk about...Well, it was just one of those things. So an ER doc did an observation. And he he published something where he showed that he actually published it on Twitter, of a patient on there in the prone position on their phone, kind of said when she was on her back, she was struggling. So when when she rolled over, she could breathe easier. I think one of the problems is when we feel real sick, and we're just laying in the same position the whole time by rolling around and at least laying on your stomach for a bit...then you could switch to your side and back to your stomach. This is the same thing you're talking about this could actually help recruit. And in the early stages might be able to buy a little time. And maybe ER doctors watching this would understand, okay, if somebody comes in, put them on their belly, then we can do some of these other things like high flow nasal cannula, or this this particular guy was looking at it and he was trying to give a whole flow gram of what he's been doing, and preventing people from going on ventilators. So it's a it's a really cool concept. And by understanding the pathophysiology that you explained...now that makes sense, why that could be a way to help people out.It's interesting that you say in that in those terms, too. And what it is he's doing with the flow gram because it reminds me back when I first started helping manage some, some ARDS patients. We were told that it's just not common to have to get into this. It's not commonplace to have to always do ARDS patients. It's usually your larger hospitals that really kind of encounter those right? Yeah.So being reminded of that, I will say that the one takeaway I had from well over a decade ago is whenever somebody is in ARDS, they can't be proned fast enough. They they cannot be proned fast enough, nobody will say that's too early, you know, actually getting ahead of the curve. Recognizing that you're having a loss of gas exchange real estate built, get some for yourself lay down on your stomach begin to breathe. It doesn't matter if you look a little funny. So what saves your life. But if you began to feel sick or have shortness of breath while you're waiting for someone to go and seek help for you, get yourself in that position so I mean, ER, home, waiting to get a ride,, whatever it takes.Because well, yeah, I mean, so if this actually pans out, this may make a big difference, especially if what what he discovered. So we have a lot more cpap machines available and bipap machines, which are just the same thing that many people have obstructive sleep apnea. If what he's suggesting is that he's seen people he'll put prone put them on a bipap or a cpap machine, increase the PEEP. Basically that's what they're doing is increasing the PEEP, put them on a prone position and saving them from going on a vent. There's a lot of people with cpap machines next to their bed including this guy right here talking. I've got apnea, and I wear a little nasal pillow. I know I'm not alone because Chang Raun did a social media post about how people if you have sleep apnea, then you're going to be at risk for developing something, also. So make sure you wear your CPAP machine if it's dusty in the closet.Yeah, that article. I found that really interesting how, how well he described being able to do some of the intermediary steps to cpaps the high flow nasal cannula. I don't disagree with the thing that he's saying the and he even addresses it in there. If you could just simply answer the question of the danger of the aerosolization of the disease versus preventing someone from having to get some mechanical ventilation, but the one thing he uses that several people still do is the rocks equation know the threat. But essentially you're taking some status measurements to see...okay, are we beyond any of these intermediary steps, do we need to move to a ventilation? But I think I think that his piece is...it preserves equipment, it still requires people that don't feel well, they feel like that they're beginning to lose their breath to go seek help now.Yeah, that's, that's, that's the key people are like, well, when should I go in? And, you know, the ERs are trying to say, well, if you've got a mild fever and see if you can ride it out if you can do this, but the second any shortness of breath starts happening, I think you got to get in and get some of this equipment on you to prevent you from going into ARDS. It's almost like you have an obligation to get there before because it's becoming a slippery slope, then.Hey, you know, Mike wrote that question over to you and I and he was asking specifically about the healthcare worker, and younger people, you and I kind of have similar takes on what we think and maybe maybe slightly different. Did you have an idea on what you thought could possibly total theory but just could possibly be lending itself to younger people or healthcare workers? Yeah, I mean, my my view on the healthcare worker is just repeated exposure and repeated exposure and repeated exposure. You took a little different take on it on the workload. So tell, go ahead and tell me your take on that one.I mean, I number one, I completely agree with repeated exposure. I think that somebody who's healthy and they're a healthcare worker, they probably can fend off a couple of small assaults, right. But if it's continuing to attack other healthy pneumocytes, kind of what we laid out today that you're going to initiate a cytokine storm, unfortunately for somebody else who had they just small, you know, had a small encounter probably wouldn't even notice that they have been contaminated. But yes, the workload, ultimately, that's, that's the sign of failure for really any organ system is their workload, and there's just not enough supply whatever that supply happens to be for any one of our organs. So when the lungs just simply cannot produce and share enough oxygen for the rest of the body, but the rest of the body is churning and it's programmed responses to basically kind of amp up. It's a tough scenario to work out on one's own without some medical intervention for sure.Mm hmm. And that's it. So that's a really good point that maybe the healthcare workers themselves number one, repeated exposure, but number two, are still yeah, they're still running around still, you know, busting their butt and, you know, maybe subtle changes in that tidal volume like you're talking about is really what what starts the downhill, slippery slope. So, but it's so you know, the whole point is to educate on this and hopefully, if a healthcare worker gets something out of it, that's why we're doing this one. Normally, I think you and I try to be a little bit more lighthearted and jokey but I asked you as a favor to me to refresh my memory. So thank you very much for doing that. I've I'm dusting the cobwebs off, but I think that...If you have any specific questions and if I can answer them, shoot, I don't mind answering questions about vents or any of that kind of stuff. So any questions about any of the episodes you know, you can always email us at kbmdhealth.com go to contact us and let us know or gutcheckproject.com same thing. Well, probably...You know what, I mean I think that's thing once we get on Instagram, I have a I would like if anybody is a healthcare worker, a respiratory tech or an ICU doctor and ICU nurse and we got something wrong let us know because...Oh, yeah. This is this is not you know. My specialty is a gastroenterologist so this is a learning curve for me on this one, but yeah, I think we did. We're right at about right at about 55 minutes or so. So we try to keep this around an hour we you know, and see what we can do and you covered a lot of material in an hour, so that's awesome. That is absolutely awesome.Hey, man, my dry erase board is worn out.Yeah. Oh, Yeah, because you would have to erase...oh, you only had one.Man it was it was it was draw, take a picture and then wipe it away. Yeah and unfortunately I didn't have I didn't have Gauge or Mac available to help me kind of sketch those out because those are really really rough Picassos I just threw together.Yeah and you know what it looks like your drawing skills were just starting to improve if you would have done a little bit started looking like real lungs. If only you knew how long it took me just to print the words I used.Well, that's awesome. All right, well, I'm gonna call this our COVID-19 file number three in the books. Share it with somebody if you think that they could benefit from this information. So great job, Eric. We'll see y'all next time. Thank you.Take care.

01.07 Pediatric DKA, the Right Way

Coffee Break HEMS Podcast

Play Episode Listen Later Mar 23, 2020 32:20

Hey everyone, today we'll be discussing the proper way to both treat and transport a pediatric DKA patient. We'll go over the treatments and why they matter, and talk about the dangers of inappropriate management in pediatrics with a diagnosis of DKA. Some visual info for you is below: Sample IV fluid maintenance schedule for pediatrics • 20kg = (1500ml + 20ml/kg) / day Labs for Case 1: • pH 7.11, PCO2 17, HCO3 9, BE -19, Lactate 2.7 • Na 132, K 5.2, Cl 95, CO2 8, glucose 540 • Urine: positive for glucose and ketones And don't forget! If you like this podcast, please give us a 5-Star rating, it helps us to be found by others! You can always reach me at: kisercpr@gmail.com #HEMS #criticalcare #flightparamedic #flightnurse #coffeebreakhems #FOAMed

co2 right way pediatric urine dka lactate hems foamed pco2 hco3

064 – Can you die from vomiting in pregnancy – hyperemesis gravidarum more than just morning sickness

Obsgynaecritcare

Play Episode Listen Later Dec 30, 2019 27:44

(*Hypothetical Case) A woman is brought into your emergency dept by her husband at 14 weeks gestation. He tells you that she has been "really sick" for almost two months now. He states that they have seen their GP multiple times and have "tried almost everything". This is the second time they are presenting to your ED - they came 2 weeks ago where he recounts she was given some IV fluids and antiemetics before going home - but they were reluctant to come back because a member of staff was quite dismissive to them last time apparently she told them that if she ate ginger and sipped water she should be fine and "it all stops at 15 weeks anyway so not to worry it will be over soon". This time he tells you that she has practically eaten nothing in the last 4 weeks and she is now having trouble getting out of bed, because of almost 4 weeks of continuous vomiting. He thinks she has probably lost at least 8-10kg since becoming pregnant. He is "super-worried" and "she is just not herself anymore - please do something". She appears listless, drowsy and distracted when you try to question her directly, and she tells you she is thirsty, nauseated and has had enough - she even asks you as you take some bloods and place an iv whether it is permissible to get a termination for untreatable nausea. Bloods: pH 7.58 HCO3 28, PCO2 56, Na 126, K2.3, Gluc 8, LFTs normal Urinary Ketones +++, no glucose How would you approach the management of this woman? Join Graeme and I as we discuss this under appreciated & poorly understood yet potentially catastrophic condition...... USEFUL TREATMENT GUIDELINE https://www.rcog.org.uk/globalassets/documents/guidelines/green-top-guidelines/gtg69-hyperemesis.pdf LINKS Profound Hypokalaemia Resulting in Maternal Cardiac Arrest: A Catastrophic Complication of Hyperemesis Gravidarum? Wernicke's encephalopathy in hyperemesis gravidarum: A systematic review. http://www.hyperemesis.org/ Pregnancy sickness can kill – why are doctors so uninformed about it? Why are Women Still Dying from Nausea and Vomiting of Pregnancy? http://theconversation.com/when-nausea-from-pregnancy-is-life-threatening-46709

pregnancy iv gp k2 nausea vomiting morning sickness hyperemesis gravidarum gluc pco2 hco3

A History of Seep Science and Multibeam for Exploration Today

Beneath the Subsurface

Play Episode Listen Later Aug 6, 2019 71:47

In this episode of Beneath the Subsurface we turn back time with Daniel Orange, our ONE Partner for multibeam technology and seafloor mapping - and incredible storyteller - and Duncan Bate, our Director of Project Development in the Gulf of Mexico and Geosciences. Dan takes Duncan and Erica on an expansive journey through time to meet a special variety of archea that dwell in the impossible oases surrounding sea bottom vents. We also explore the relatively recent discoveries in geoscience leading to seafloor mapping and how seep hunting offshore can enrich the exploration process today. TABLE OF CONTENTS00:00 - Intro03:35 - What is a seep?09:06 - The impossible oasis11:45 - Chemotrophic life24:15 - Finding seeps26:51 - The invention of multibeam technology30:11 - Seep hunting with multibeam32:48 - Seismic vs. multibeam34:43 - Acquiring multibeam surveys44:32 - The importance of navigation46:20 - Water column anomalies49:12 - Seeps sampling and exploration56:23 - Multibeam targets59:12 - Multibeam strategy1:03:11 - Reservoir content1:06:44 - A piece of the puzzle1:10:21 - ConclusionEXPLORE MORE FROM THE EPISODELearn more about TGS in the Gulf of MexicoOtos MultibeamEPISODE TRANSCRIPTErica Conedera:00:00:12Hello and welcome to Beneath the Subsurface a podcast that explores the intersection of Geoscience and technology. From the Software Development Department here at TGS. I'm your host, Erica Conedera. For our fourth episode, we'll welcome a very special guest speaker who offers a uniquely broad perspective on the topic of sea floor mapping. We'll learn about the technology of multibeam surveys, why underwater oil seeps are the basis of life as we know it and how the answer to the age old question of which came first, the chicken or the egg is the Sun. I'm here today with Duncan Bate, our director of projects for the US and Gulf of Mexico. Do you want to go ahead and introduce yourself Duncan?Duncan Bate:00:00:56Sure, yeah, thanks. I basically look after the development of all new projects for TGS in the, in the Gulf of Mexico. I'm here today because a few years ago we worked on a multi beam seep hunting project in the Gulf of Mexico. So I can share some of my experiences and - having worked on that project.Erica:00:01:15Awesome. And then we have our special guest star, Dan Orange. He is a geologist and geophysicist with Oro Negro exploration. Hi Dan.Dan Orange:00:01:24Good morning.Erica:00:01:25Would you like to introduce yourself briefly for us?Dan:00:01:28Sure. Let's see, I grew up in New England, Texas, so I went to junior high school, just a few miles from where we're recording this. But I did go to MIT where I got my bachelor's and master's degree in geology, then went out to UC Santa Cruz to do my PhD and my PhD had field work both onshore and offshore and involved seeps. So we'll come back to that. And also theoretical work as well. I had a short gig at Stanford and taught at Cal State Monterey Bay and spent five years at the Monterey Bay Aquarium Research Institute. Again, pursuing seeps. I left MBARI and started working with the oil patch in 1997 and it was early days in the oil industry pushing off the shelf and heading toward deep water and seeps were both a bug and a feature. So we started applying seep science to the oil industry and have been doing that for oh, now 21-22 years.Dan:00:02:32The entire time that I was at Embargin, and working with the oil patch. And in fact, ongoing, I do research for the US Navy through the Office of Naval Research. It started out involving seeps and canyon formation and it's evolved into multibeam seafloor mapping and acoustics. And that continues. So in the oil patch I was with AOA geophysics, we formed a company AGO to commercialize controlled source EM sold that to Schlumberger. And then we formed an oil company, Black Gold Energy, that would use seeps as a way to, go into oil exploration. And we sold that to NYKO, since leaving Black Gold with Oro Negro. We've been teaming with TGS since 2014 so now going on five years mapping the sea floor, I think we just passed one and a quarter million square kilometers, mapping with TGS as we mapped the sea floor and sample seeps, pretty much around the world for exploration.Erica:00:03:35Awesome. So let's begin our discussion today with what is a seep, if you can elucidate that for us.Dan:00:03:41So a seep is just what it sounds like. It's, it's a place on the earth's surface where something leaks out from beneath. And in our case it's oil and gas. Now seeps have been around since the dawn of humanity. The seeps are referenced in the Bible and in multiple locations seeps were used by the ancient Phoenicians to do repairs on ships they use as medicines and such. And in oil exploration seeps have been used to figure out where to look for oil since the beginning of the oil age. In fact that, you know, there seeps in, in Pennsylvania near Titusville where colonel Drake drilled his first well, where Exxon, had a group of, of people that they call the rover boys that went around the world after World War II looking for places on the Earth's surface that had big structures and oil seeps.Dan:00:04:39Because when you have a seep at the sea floor with or on the Earth's surface with oil and gas, you know that you had organic matter that's been cooked the right amount and it's formed hydrocarbons and it's migrating and all those things are important to findings, you know, economic quantities of oil and gas. So seeps have been used on land since the beginning of oil and gas exploration. But it wasn't until the 1990s that seeps began to affect how we explore offshore. So that's seeps go back to since the dawn of humanity, they were used in oil exploration from the earliest days, the 1870's and 80's onward. But they've been used offshore now since the mid 1990s. So that's, that's kind of, that seeps in context.Duncan:00:05:31But it's actually the, I, the way I like to think about it, it's the bit missing from the, "What is Geology 101" that every, everyone in the oil and gas industry has to know. They always show a source rock and a migration to a trap and a seal. But that actually misses part of the story. Almost every basin in the world has leakage from that trap, either, either directly from the source rock or from the trap. It either fills to the spill point or it just misses the trap. Those hydrocarbons typically make their way to the surface at some point-Dan:00:06:04at some point and somewhere. The trick is finding them.Duncan:00:06:08Yeah, that's the seep. And thus what we're interested in finding.Erica:00:06:12As Jed Clampett from the Beverly hillbillies discovered.Erica:00:06:15Exactly.Dan:00:06:15I was going to include that!Erica:00:06:19Yes.Dan:00:06:19Jed was out hunting for some food and up from the ground came a bubbling crude. That's it.Erica:00:06:27Oil that is.Dan:00:06:29Black gold.Erica:00:06:29Texas tea.Dan:00:06:30That's right. So that's that seep science. So today what we're going to do is we're going to talk about seep communities offshore because what I hope to be able to, you know, kind of convince you of is if oil and gas leak out of the sea floor, a seep community can form. Okay. Then we're going to talk about this thing called multibeam, which is a technique for mapping the sea floor because where you get a seep community, it affects the acoustic properties of the sea floor. And if we change the acoustic properties of sea floor or the shape of the sea floor with this mapping tool, we can identify a potential seep community and then we can go sample that.Dan:00:07:14And if we can sample it, we can analyze the geochemistry and the geochemistry will tell us whether or not we had oil or gas or both. And we can use it in all sorts of other ways. But that's where we're going to go to today. So that's kind of, that's kind of a map of our discussion today. Okay. So as Duncan said, most of the world, he Duncan talked about how in- if we have, an oil basin or gas basin with charge, there's going to be some leakage somewhere. And so the trick is to find that, okay. And so, we could, we could look at any basin in the world and we can look at where wells have been drilled and we can, we can look at where seeps leak out of the surface naturally. And there's a correlation, like for example, LA is a prolific hydrocarbon basin. Okay. And it has Labrea tar pits, one of the most charismatic seeps on earth cause you got saber tooth tigers bubbling outDuncan:00:08:18It's literally a tourist attraction.Dan:00:08:20Right there on Wilshire Boulevard. Okay. And it's a hundred meters long by 50 meters wide. So a hundred yards long, 50 yards wide. And it, that is an oil seep on, on the earth surface in LA okay.Duncan:00:08:32Now, it's important to mention that they're not all as big as that.Dan:00:08:34No, no. Sometimes they're smaller. It could just literally be a patch of oil staining in the sand.Erica:00:08:41Really, that's little.Duncan:00:08:41Oh yeah. I mean, or just an area where there's a cliff face with something draining out of it or it, you know, it could be really, really small, which is easy to find onshore. You know, you send the rover boys out there like you mentioned, and you know, geologists working on the ground, they're going to find these things eventually. But the challenge, which we've been working on with, with the guys from One for the last few years, and now is finding these things offshore.Dan:00:09:06So let's, let's turn the clock back to 1977. Alvin, a submarine, a submersible with three people in it went down on a Mid-ocean Ridge near the Galapagos Islands. And what they found, they were geologists going down to map where the oceanic crust is created. But what they found was this crazy community, this incredible, oasis of life with tube worms and these giant columns with what looked like black smoke spewing into the, into the ocean. And so what they found are what we now call black smokers or hot vents, and what was so shocking is the bottom of the ocean is it's a desert. There's no light, there's very little oxygen, there's not a lot of primary food energy. So what was this incredible, oasis of life doing thousands of meters down on, near the Galapagos Island? Well, it turns out that the base of the food chain for those hot vents are sulfide rich fluids, which come spewing out of the earth and they fuel a chemically based, community that thrives there and is an oasis as there because there's so much energy concentrated in those hot sulfide rich fluids that it can support these chemically based life forms.Dan:00:10:34So that's 1977 in 1985 in the same summer, chemically based life forms, but based on ambient temperature, water, not hot water were found in the Gulf of Mexico and off the coast of Oregon that same summer, 1985 in the Gulf of Mexico, the base of the food chain, what was fueling this chemical energy was hydrocarbons, oil and gas, and off the coast of Oregon, what was fueling it was hydrogen sulfide. So this is 1985, the year I graduated college. And so I started graduate school in 1986 and part of my research was working with the group that was trying to figure out the plumbing that was bringing these chemically rich fluids up to the earth's surface that were feeding this brand new community of life. You know, what we now call cold seeps. So, we, you know, depending on what you had for breakfast today, you know, eggs or pancakes or had your coffee, all the energy that we've got coursing through our veins right now is based upon photosynthesis.Dan:00:11:45We're either eating plants that got their energy from sunlight or we're eating eggs that came from chickens that eat the plants that can, where the came from, sunlight. Everything in our world up here is based upon photosynthesis. So, but the seep communities, the hot vents and the black smokers and the cold seeps, the base of the food pyramid is chemical energy. So they're called chemosynthetic communities or chemoautotrophic because the bacteria get their trophic energy, the energy that they need to live from chemicals. And so the bacteria utilize the chemicals and organisms have evolved to host these bacteria inside their bodies. And the bacteria metabolize the chemical energy to produce the enzymes that these larger organisms need to live. So these larger organisms can include clams, tube worms, the actual bacteria themselves. But, so the kind of how does this work is- let's get, because if we understand how seeps work and we know that seeps can be based upon oil and gas seepage, then you'll understand why we're using these seeps to go out and impact, oil and gas exploration.Dan:00:13:09So the- at the bottom of the ocean, we have a little bit of oxygen, but as we go down into the sediments, below the surface, we, we consume all that oxygen and we get to what's called the redox boundary to where we go from sulfate above it to hydrogen sulfide below it. And so below this redox boundary, we can have methane, we can have oil, but above that redox boundary, the methane will oxidize and the oil will be biodegraded and eaten by critters and whatnot. Now, living at that boundary, are bacteria who metabolize these compounds, and that's where they get the energy they need to live. These bac- Okay, now kind of turned the clock even farther back before the earth had an oxygen atmosphere, the only way that organisms got energy to live was from chemicals. Okay? So before we had algae and we created this oxygen atmosphere that we breathe billions of years ago, the organisms that lived on earth were chemosynthetic.Dan:00:14:13So these bacteria survive today and they live everywhere where we cross this redox boundary. Okay? So there they're actually archaea, which are some of the most primitive forms of bacteria, and I'm not a biologist, so I can't tell you how many billions of years ago they formed, but they're ancient and they're living down there.Erica:00:14:33So they haven't changed since then. They're basically the same?Dan:00:14:36Nope.Erica:00:14:36Wow.Dan:00:14:36They figured out a way to get energy to survive. It works.Erica:00:14:40Why change it?Dan:00:14:41If you're an Archea, right? So they're living down there at that redox boundary. Now, if we have seepage-seepage, is the flow of liquids. You actually lift that redox boundary. And if you have enough seepage, you can lift that boundary right to the sediment water interface. If you step in a pond and you smell that, sulfide, that rotten egg smell, your foot has gone through the redox boundary.Dan:00:15:08Okay? And you've disturbed some archaea down there and they'll get nudged aside. They'll go find someplace else. Okay? So with seepage, we lift the redox boundary to the sediment water interface and, and the bacteria are there and they're ready to utilize the reduced fluids as their source of energy. And so you can see them, we have pictures. You can do an internet search and say, you know, bacteria chemosynthetic bacteria and images and look at and look at photos of them. They it, they look like, okay, when you put the Guacamole in the back of the fridge and you forget it for three weeks and you open it up, that's what they look like. It's that fuzzy. It's this fuzzy mat of bacteria. And those are the bacteria. They're out there. They're metabolizing these fluids. Okay. Now in the process of metabolizing these fluids, they produce the bacteria, produce enzymes like ATP.Dan:00:16:01And I wish my partner John Decker, was here because he would correct me. I think it's adinase triphosphate and it's an enzyme that your body produces and sends out to basically transmit chemical energy. Okay. Now at some point in geologic time, and I'll, I'll actually put a number on this in a second. The larger fauna like clams and tube worms, evolve to take advantage of the fact that the bacteria are producing energy. And so they then evolve to use the bacteria within themselves to create the energy that they need to live. Okay? So, what happens is these seep fauna produce larva, the larva go into, you know, kind of a dormant stage and they're flowing around the ocean. And if they sense a seep, okay. They settle down and they start to grow and as, and then they, they, they, the bacteria become part of them.Dan:00:16:56They're the, the clams. You open a clam in the bacteria live in the gills. Okay. And so they'd grow and, and so these clams and tube worms start to grow and they form a community. Okay. So that a clam, what a clam does these clams, they stick their foot into the, into the sediment and they absorb the reduced fluids into their circulation system. They bring that, that circulating fluid to their gills where the bacteria then metabolize these reduced fluids and send the enzymes out to the tissues of the clam so it can grow. So this clam does not filter feed like every other clam on the planet. The tube worms that host these bacteria in them don't filter feed. So the base of the food chain is chemosynthetic. But the megafauna themselves, don't get their energy directly from methane or hydrogen sulfide. They get their energy from the bacteria, which in the bacteria, you know, the bacteria happy, they'll live anywhere.Dan:00:17:59But sitting here in a clam, they get the reduced fluids they need to live and they grow. Now it's what's cool for us as, as seep hunters is different species have evolved to kind of reflect different types of fluids. So if you know a little bit about seep biology, when you pick up like a batheum Modiolus mussel, you go, Huh? There could be oil here. Okay. Because that particular mussel is found in association with, with oil seeps. Okay. So that we won't go too far down that path, but there are different organisms. The important thing is that these communities, form again an oasis of life, a high concentration of life where we have a seep. Now, the oldest seep community that I'm aware of is Devonian. So that's between 420 and 360 million years. It's found in the high atlas mountains of Morocco.Dan:00:18:58And that seep community, a fossil seep community includes the same types of clams in tube worms that we find today. Okay. But they're also found with authigenic carbonate. Okay. Which is like limestone. And so, and that limestone in cases, this fossil seep community and has preserved it for hundreds of millions of years. So where does limestone come from? So remember we've got methane, CH4 in our, in some of our seep fluids. Well, if that's oxidized by bacteria, cause they're going to get energy from the methane they produced bicarbonate, which is HCO3 as a negative charge on it. And that bicarbonate, if it sees calcium, they like each other. And so they'll form calcium carbonate, limestone. And since sea water is everywhere saturated with calcium, if we have a natural gas seep, the bacteria will oxidize in natural gas and the bicarbonate will grab the calcium to form this cement.Dan:00:20:04Now deep enough in the ocean, it actually is acidic enough that that cement will start to dissolve. So we just have this, we have a factory of of bacteria. It might be dissolving some places, but most of the places we look, the carbonate doesn't dissolve. So we've got clams, tube worms, we've got the limestone authigenic carbonate, and if the pressure and temperature are in the right field, that methane can also form this really cool substance called gas hydrate and gas hydrate is a clathrate the, it's a combination of water and methane where the water forms an ice-like cage and the methane sits in that cage. And so you can light this on fire in your hand and the gas will burn. Nice yellow flame will go up from your hand and the cage will melt. The ice melts. So you get cold water on your hand with flames going up. It, it's cool stuff.Erica:00:21:03Did you bring one of these to show us today?Dan:00:21:06The pressure and temperature in this room are not, methane's not an equilibrium. You need hot, you need high pressure, moderately high pressure and you need very low temperatures. So, if we had-Duncan:00:21:20Neither are common in Houston, (Laughter)Dan:00:21:22No, and we wouldn't be terribly comfortable if that was what it was like here in this room. But the, the important thing for us now as we think about seep science and, and seep hunting is that this, this limestone cement, the authigenic carbonate, the gas hydrate, the shells of a clam, okay. Are All harder. Okay? Harder, I will knock on the table. They're harder than mud. So the sea floor, most of the most of the world's ocean is gray-green mud and ooze from all sorts of sediment and diatoms and plankton raining down onto the ocean floor. So most of the world's oceans is kind of just muddy sandy some places, but sediment, it's where you get these seep communities that now we've, we've formed a spot that some that's harder and rougher than the area around it. And that's our target when we, deploy technologies to go out and, and look at seeps.Dan:00:22:26So, so hot smokers, hot vents were discovered in 1977. Cold seeps were discovered in 1985 and were found to be associated, in the Gulf of Mexico with oil and gas seepage. That's 1985. Those were discovered with human beings in a sub in submersibles. Later, we deployed robotic submersibles to go look at seeps, ROV's and even later we developed tools to go sample seeps without needing to have eyes on the bottom and we'll come and talk and we'll come back and talk about that later.Dan:00:22:57But for kind of recap, a seep is a place where something is leaking out of the earth surface. When we talk about seeps, we're talking about offshore seepage of oil and gas that supports this profusion of chemically-based life forms as well as these precipitants, the authigenic carbonate limestone and gas hydrate. And the important thing is they change the acoustic properties of the sea floor.Duncan:00:23:28Yeah. Then the key thing is that you've gone from having, seeps onshore, which are relatively easy to walk up to and see, but hard to find, to seeps offshore, which are impossible to walk up to or very difficult. You need a submersible to do it. But because of this, chemosynthetic communities that build up around it and our knowledge of that and now gives us something to look for geophysically. So we can apply some geophysics, which we'll get on to talk about next in terms of the multibeam, to actually hunt for these things in a very cost effective way and a very fast manner. So we can cover, as Dan said, right at the start, hundreds of thousands of square kilometers, even over a million now, in a cost effective, timely manner and identify these seeps from the sea surface.Dan:00:24:15Now fishermen, know where seeps are because all of this limestone provides places for fish to leave their larva where they might live, they call them refugia. It's a, it's a place where, you know, lots of little fish and where you have lots of little fish, you have lots of big fish. And since we're also increasing this primary productivity, you get, you get profusions of fish around seep communities. So we've found authigenic carbonate in the front yards of fishermen in areas where that we've gone to study seeps. And if you chip a little bit off it, you can go and analyze it in the lab or if you can get somebody who fishes for a living to tell you their spots. And that involves convincing them that you're not going to steal their spots and you're not gonna tell everybody where their spots are. But if you go into a frontier area, if you can get somebody who fishes for a living to talk to you, you might have some ideas of where to go look for them.Dan:00:25:14So it kind of, one other point that I wanted to make here about seeps is, remember I talked about how seep organism creates kind of a larva, which is dormant and it's kind of flowing through the world's ocean, looking for a seep community, doing some back of the envelope calculations. If, if a larva can survive for about a month. Okay. And you have a one knot current that larva can move about 1300 kilometers in a month, which is about the length of the island of Java. And it might be about the length of the state of California. So if you think now, so if you think about that, then all you need is a seep community somewhere to be sending out larva. Most of which of course never gonna survive. And then if we get a seep somewhere else, the odds are that there's going to be a larva bouncing along the sea floor that is going to see that and start growing.Dan:00:26:08So for us as explorationists as the, the important thing is if there's a seep, there's a pretty good chance that, that a seep community will start to form, if the seepage lasts long enough, it will form a community depending, you know, might be large, might be medium size, but it changes the acoustic properties of the sea floor. Okay, so that, remember we're going to talk about seeps what they, what, what's a seep and that is how it's related to hydrocarbon seepage out of the or natural gas oil, you know, reduced fluids. What we were going to talk about, and now we're going to talk about how offshore we use this technology called multibeam to go and find them. Okay.Dan:00:26:51So back in, back in the Cold War, the air force came up with a tool to map the former Soviet Union called synthetic aperture radar. And when the navy saw the air forces maps, they said, we want a map of the sea floor. And at the time, you know, if you remember your World War II movies, the submarine sends out a Ping, somebody listening on, their, on their headphones and and the ping comes back and the amount of time that it took for the ping to go out and the ping come back is how deep the water is. If you know the speed of sound in water. But that's, that's just one point directly beneath you, that's not good enough to get a detailed map of the sea floor. So, driven by these cold war needs, the navy contracted a company called general instruments to develop a tool to map the sea floor and they develop what's called SASS, the sonar array sounding system, which we now call multibeam.Dan:00:27:49In the 1960s, it was unveiled to the world during a set of, submersible dives to the mid Ocean Ridge, I believe in 1975 as part of the famous project. And the geoscientist looked at that map and it was a contour map of the mid ocean region. They said, holy smokes, what's that? Where'd that come from? And the navy said, well, we kind of developed a new technology and it was first commercialized in 1977 the same year hot smokers were discovered on the world's oceans. And it has been continuously developed since then. And in about the 1990s, it got resolute enough for, for us to take this, this kind of seeps, seep hunting science and take it offshore. So until then, 1980s, we were deploying submersibles. We were going down and looking at them. We had very crude maps. We had some side scan shows, a little bit about, the acoustic properties of the sea floor.Dan:00:28:46But it wasn't until the mid 1990s that we realized that with these tools, these sea floor mapping tools that had acoustic, analyzing techniques that we could identify areas that were harder and rougher and had a different shape, that allowed us to start, instead of just driving around and, and, we're finding one by, by luck or chance actually saying, Huh, there's a, there's an interesting acoustic signature over there. Let's go take a look at it. And deploying submersibles and ROVs and realizing that yes, we had tools that could, be used to, to map the sea floor and identify seeps and driven by their own interests. The Navy, the US navy was very interested in these and, was, was a early, early funder of seep science and they've continued with it as well as academic institutions around the world that got very interested in seep communities.Dan:00:29:45And in fact, NASA, NASA is really interested in seep communities because they're chemically based life forms in what are basically extreme environments. And so if NASA wants to figure out what life is going to look like on a different planet, or a different moon on it, or surrounding a different planet that doesn't have an oxygen atmosphere, here's a, a laboratory on earth that, that they can use. So NASA has been funding seep science as well.Dan:00:30:11So multibeam what is it and how does it apply to, to, to hunting seeps. So multibeam, which is this technology that was developed by and funded by the navy in the 1960s and commercialized in the 70s uses two acoustic arrays of transducers. one array is mounted parallel to the length of a ship. And when you fire off all those transducers, it sends out a ping. And the longer the array is, the narrower that beam is. That's how antennas work. So that that long array sends out a ping, which is narrow along track and a shape, kind of like a saucer. So if you can imagine two dinner plates put together, that's what this, ping of energy looks like. And that's what we call the transmit beam. So then if you listen to the sea floor with an array that's perpendicular to the transmitter ray, we are now listening to an area that's, that's narrow across track. Okay. And it's long elongate a long track. So we've got this narrow transmit beam in one direction that's, that's now perpendicular to the ship. And we've got a narrow receive beam that's parallel to the ship and where those two intersect is what we call a beam. And so with, with lots of different, transducers mounted, perpendicular to the ship, we can listen from all the way out to the port about 65 degrees down below the ship and all the way over to starboard, again, about 65 degrees. And we have lots of beams.Dan:00:31:51So right now the system that we're using, on our project has 455 beams across track. So every time we send out a ping, we ensonify the sea floor on, on these 455 beams. And as we go along, we send out another ping and another ping. And we're basically, we're painting the sea floor. It's, it's like mowing the lawn with a big lawn mower or using a Zamboni to drive around an ice rink. You can just think of it as as a ship goes along. We are ensonifying and listening to a wide patch of sea floor and we typically map, about a five kilometer, about a three mile, a wide swath, and we send out a ping every six or 10 seconds. Depends how, you know, depends on the water depth. And so we're able to map 1000 or 2000 square kilometers a day with this technique. This multibeam technique.Duncan:00:32:48Since a lot of our podcast listeners might be familiar with seismic is that's probably the biggest percentage of the, the geophysical industry. This is not too different. It's an acoustic based technique. I guess the main difference is are we live working in a different, frequency bandwidth. And also that we have both the receiver and the transmitter both mounted on the same boat. So we're not dealing with a streamer out the back of a boat. we have transmitter and receiver are both whole mounted. But after that it's all pretty similar to seismic. We go backwards and forwards, either in 2D lines or in a, in a 3D grid and we build up a picture. Now because of the frequencies we're working with, we don't penetrate very deep into the sea floor. but as, as we mentioned, we're interested in seeing those seep communities on the sea floor. So that's why we this, this is the perfect technology for, for that application.Erica:00:33:40Oh, can you talk a little bit about the post-processing that's involved with multibeam?Dan:00:33:44Well, let me- Erica, Great question. Let me, come back to that later cause I want to pay, I want to pick up on what Duncan talked about in and add one very important wrinkle. So first of all, absolutely correct, the frequencies are different. In seismic, we're down in the hertz to tens of Hertz and in Multibeam we're in the tens of kilohertz and in very shallow water, maybe even over higher than a hundred kilohertz. In seismic, we have air guns that send that radiate out energy. And we, we designed the arrays so that we get most of the energy in the direction that we're looking with multi beam. We have a narrow, remember it's one degree wide in here. If you got kids, see if anybody still has a protractor anymore, grab a protractor and look at how wide one degree is. It's very narrow.Duncan:00:34:39There's probably an iPhone app for that. (Laughter) see what one used to look like.Dan:00:34:43But with, with seismic, the air guns sends out energy and we listened to the reflected energy out on the streamer back behind the ship or on a node somewhere else. It's reflected energy. With multibeam, the energy goes out and it interacts with the sea floor and the shallow subsurface. Most of it gets reflected away and we don't, we don't, hear that it, but some of it actually comes back in the same direction that the sound went out and we call that backscatter. So backscatter energy comes back to you and it's that backscatter that, can increase when we have hard and rough material either on the sea floor or buried below the sea floor. So the way that we process it is since we know the time of length, the time of path on how long it took to get out, hit the sea floor and come back, or you can correct for path lengths, energy radiates outward and spherical patterns. So we correct for spherical spreading. we know the angle that it hit the sea floor, so we correct for angle of ensonification. And then the next and most important things are where was the ship, when the pulse went out? And where is the ship when the pulse comes back, including what's the orientation of the ship? So we need to know the location, the position of the ship in X, Y, and Z to centimeters. And we need to know the orientation of the ship to tenths of a degree or better on both the transmit and the receive. But the key thing is, if we know that path length in the spherical spreading and we correct for all of that and we get a response that's much greater than we expected, we get higher backscatter energy and it's, it's those clams and tube worms authigenic carbonate gas hydrate that can increase the hardness and the roughness of the sea floor that kicked back the backscatter energy.Dan:00:36:46Okay. Now what happens if the oil and gas, or the reduced fluids if they shut off? Well, I'm sorry to say for the clams and the tube worms that they will eventually die. The bacteria will still live at that redox boundary as it settles back below the sediment. And then when we pile some sediment on top of that dead seep community, it's still there. The shells are there, the carbonate's still there. So with the, with multibeam that the frequencies, we use 12 and 30 kilohertz penetrate between two, three 10 meters or so into the sediment. So if you shut off the seepage and bury that seep community, they're still there. And if we can sample that below that redox boundary at that location, chances are we're going to get a oil or gas in, in our sample. And in fact, we encounter live seep communities very, very, very, very rarely, you know, kind of one in a thousand.Dan:00:37:50But, we, we encounter seep fauna down in our sample cores, which we'll talk about later, much more frequently. And, and we, we find hydrocarbons, we are very successful at finding hydrocarbons. And the key thing is we're using seep science to go look in, in basins or extend outward from basins in areas where there may be no known oil or gas production. And that's why the seeps are useful. So multibeam unlike a seismic, we got to collect the data, then we got it and you to do all sorts of processing and it takes a while to, to crank the computers and whatnot. Multibeam we can, we can look at it as it comes in and we can see the backscatter strength. We can see what the swath that it's mapping every ping, every six seconds. And it takes about, it takes less than a day to process a days worth of multibeam.Dan:00:38:47So when our ships are out there working every morning, when we get the daily report from the ship, we see another thousand or 2000 square kilometers of data that were mapped just the previous day. So it's for, those who can't wait, it's really satisfying. But for those of us who are trying to accelerate projects, it's great because when the data come off the ship, they're already processed. We can start picking targets and we can be out there, you know, in weeks sampling. So that's so multibeam it's, it's bathymetry, it's backscatter, but we're also imaging the water column. So if there's, a gas plume, coming out of the sea floor, naturally we can see that gas plume and, so that we can see the water column. We can see the sea floor or the bathymetry, and the backscatter. Erica, you asked, you know, about the processing and I talked about how we have to know the position and the orientation, of the ship, that means that we have to survey in using a laser theodolight.Dan:00:39:54We have to survey in every component of the system on the ship to, you know, fractions of a millimeter. And we drive the surveyors nuts because we are, we are more demanding than the, the BMW plant in South Carolina. And they point that out to us every time. Yes, we're more demanding. But if they have a problem with, with a robot in the BMW plant, they can go out and survey it again, once we put this ship in the water, I can't go survey the array that's now welded to the bottom of the ship. It's there. And so that's why we make them do three replicate surveys and do loop ties and convince us that we've got incredibly accurate and precise system. So that's when we survey the ship. We use, well we go back and we go and we check their math and we make sure all the numbers are entered into the system correctly.Dan:00:40:46We, measure the water column every day so that we have the best velocity data that we use to correct the, that position. We measure the salinity in the water column because it affects how energy is absorbed. It's called the absorption coefficient. We measure the acoustic properties of the ship. So we understand maybe we need to turn off the starboard side pump in order to get better multibeam data. And we evaluate every component of the ship. Something. Sometimes they'll have, you know, the, the waste unit was, was mounted onto the, onto the deck of the ship and nobody thought about putting a rubber bushing between that unit and the hall to isolate the sound. And it just so happens it's at 12 kilohertz. So it swamps your acoustic energy or degrades our data quality because it's all about data quality so that we can find these small, interesting high backscatter targets. We polish the hull. We send divers down every eight weeks or 12 weeks or 16 weeks because you get biofouling you get, you get these barnacles growing in a barnacle in between your acoustic array in the sea floor is going to affect the data. So we send divers down to go scrape the hull and scraped the prop.Duncan:00:42:05So it's probably worth mentioning that this is the same type of multibeam or multibeam data is the same data that is used in other parts of the oil and gas industry as well. So I mean, any pipeline that's ever been laid in the last few decades has had a multibeam survey before it. Any bit of marine infrastructure that an oil and gas company wants to put in the Gulf of Mexico. Certainly you have to have a multibeam survey ahead of time. what's different here is that we're, we're trying to cover big areas and we're trying to get a very specific resolution. So maybe it's worth talking a bit about that. Dan what we're actually trying to achieve in terms of the resolution to actually find seeps.Dan:00:42:42You got it. So we, we can, we can control the resolution because we can control how wide a swath we go and how fast we go. So, if you're really interested in, if you want to do a site survey and you want to get incredibly detailed data of a three kilometer by three kilometer square, you could deploy an autonomous underwater vehicle or an ROV and get very, very, very resolute, like smaller than half a meter of bin size. for what we do, where our goal is exploration, the trade off is between, do I want more resolute data or do I want more data and it that that is a tradeoff and it's something that we struggle with. And we think that the sweet spot is mapping that five kilometers swath and three miles wide, swath at about oh eight to 10 knots. So let's say about 16 kilometers an hour.Dan:00:43:40That gets us a thousand to 2000 square kilometers a day. And by acquiring data in that manner, we get a 15 meter bathymetric bin independent of water depth and our backscatter since we subsample that bathymetric bin for the backscatter, we can get a five meter backscatter pixel. So now if I have four, if I have four adjacent pixels, you know, shaped like a square, that's a 10 meter by 10 meter spot on the sea floor, it's slightly larger than this room. We could, you could see that now you might need a couple of more to be larger than that. So to have a target actually stand out, and that's about how accurate our sampling is with the core barrel. So, the long answer to your question is about a 15 meter bathymetric bin and a five meter backscatter pixel is what we're currently doing for our exploration work.Dan:00:44:32Now we pay attention to what's going on in the navigation and the positioning world because it affects our data quality. So the higher the quality of, of our navigation, the higher the quality of our data on the sea floor. So about a decade ago, the world's airlines asked if they could fly their airplanes closer together and the FAA responded and said, not unless you improve GPS and so sponsored by the world's airlines. They set up ground stations all in, in the, in the most heavily traveled parts of the world that improve the GPS signal by having an independent orbital corrections. What that means is for us working off shore, we take advantage of it. It's called wide area augmentation. And, using this system, which is now it's a, it's add on for a GPS receiver, we're able to get six centimeter accuracy of a ship that's out there in the ocean that surveying.Dan:00:45:27So that's six centimeters. What's that? About two and a half inches. And for those of us who grew up with low ran and very, you know, where you were lucky if you knew where you were to within, you know, a quarter of a mile. it's, it's just astonishing to me that this box can produce data of that quality, but that flows through to the quality of the data that we get on our surveys, which flows through to our ability to find targets. So I think, I told you about sub sampling, the bathymetry for backscatter and I've told, I told you about the water column and we've talked about the resolution. I think we've, we've pretty much hit what multibeam is. It's, it's a real time near real time acquisition, high frequency narrow beam. We image the sea floor and the shallow subsurface. Okay and we use that to find anomalous backscatter targets.Duncan:00:46:20Well, let's talk about the water column a little bit more done because I know we've published some pictures and images from our surveys. Showing the water column anomalies. The backscatter data, in the water column itself can actually help us find seeps. The right mixture of oil and gas coming out of this, an active seep and migrating up through the water column can actually be picked up on these multibeam data also. So that's, a real direct hit that you've got to see and that it's actually still producing oil today,Dan:00:46:53Right, so when, when gas and oil leak out of the sea floor, the gas bubble begins to expand as it comes up, just like a would in a, in a carbonated beverage because there's less pressure. So that gap, that bubble is expanding. If there's oil present, the oil coats the outside of the bubble and actually protects it from dissolving into the water column. And so the presence of gas with a little bit of oil leaking out of the sea floor creates these bubbles that, are big enough to see with these 12 and 30 kilohertz systems. And so when we see a plume coming out of the sea floor, that's natural, a seepage of gas, possibly with a little bit of oil and it provides a great target for us to go and hit. Now those seeps are flowing into the water column and the water column has currents and the currents aren't the same from one day to the next and one week to the next.Dan:00:47:47So if we image a seep a couple of different times, one day it will be flowing in one direction and the next time we see it flowing in a different direction. The area in common between the two is pointing us toward the origin point on the sea floor. And that's what we're going to target. And if you, if you hunt around, look for NOAA studies of, of the US Gulf of Mexico, over Mississippi Canyon near where the deep water horizon, went down because there are, the, NOAA has published, images of the gas seeps in that area where there are natural oil and gas seeps leaking, leaking other, the sea floor. And these natural seeps occur all over the world. Okay? And they're bringing oil and gas into the water column. But remember, nature has basically provided, the cleanup tool, which is the bacteria. So where oil and gas settle onto the sea floor, there are bacteria that will consume it. You don't want a lot of it in one place, cause then then you've got, you know, a real environmental disaster. But natural oil and gas seepage goes hand in hand with natural seep consuming organisms that metabolize these fluids. So a multi beam seeps backscatter okay. That I think we've, we've talked about what the target looks like. Let's talk about how we go in and sample it.Duncan:00:49:12Yeah, no, I think that's the real key thing. Particularly here in the Gulf of Mexico. I mean we talked at the start about how I'm using seeps can tell you whether a basin has hydrocarbons in it or not. Clearly we're decades past the point of knowing whether there's oil and gas in the Gulf of Mexico. So even in the deep water gulf of Mexico, especially here in the US side, we know that there's oil and gas, so that information is long gone. We don't, we don't need an update on that anymore. What we need to know is information about the type of oil, the age of the oil, the deep positional environment that the oil is deposited in. And if we can actually get a sample from these seeps, then that's the sort of information that modern geochemistry can start to pull out for us.Dan:00:49:57we've sat in the same meetings where the, the potential client companies have said, why are you, why are you gonna map the deepest part of the Gulf of Mexico? There's no oil out there. And lo and behold, we found anomalous backscatter targets on a diapirs, which are areas, mounds out in the deepest parts of the Gulf of Mexico. And lo and behold, if you, if you look at the data, know that that statement was incorrect. There is oil and gas out there in other parts of the world. We've had companies say, oh, this part's all oil and this part's gas. Well, how do you know that? Well, because we've drilled for oil out here and we don't think there's any oil. Once you get out there and you don't know, you don't know what you don't know until you go map it and sample it and then you come back, you put the data on their desk and they go, huh, hey, we were wrong man. I guess there's oil out there. And, and in other parts of the world where you know, we've done all our exploration close to land or in shallow water, we go out into the deepest part and nobody's ever drilled a well out there. So, you use the seep science to go to basically fill that in.Dan:00:51:09So in order to make money exploring for oil, you had to have organic matter. Originally it had to be, it had to be buried and cooked. Okay. So you needed temperature and pressure. You need time takes time to do that, then it needs to migrate. Okay. With the exception of unconventionals, we're not gonna talk about unconventional today with the exception of unconventionals, the hydrocarbons have to migrate, so they're concentrated so that you can go drill them and recover them. And they need to be in a reservoir.Dan:00:51:41And it has to be sealed. And so when we find a seep and all of that goes into what we talk about in oil exploration as the risk equation, like what's the probability of success? If you don't know whether you have a migration, you have maximum uncertainty and that flows through into your, into your risk. Well, if we find a seep, remember we've proven that there was organic matter. We've proven that it was buried and cooked for the right amount of time to create oil and gas and that it's migrated. We can't tell you anything about reservoir or seal or timing, but we can, we can materially impact the risk equation by finding a seep. Okay. So right before you drill a well, wouldn't you like to know whether or not there's oil or gas in the neighborhood? Cause a well can be a can be $100 million risk.Dan:00:52:34Okay. Usually you wouldn't, wouldn't you like to know? So remember when we started looking at seeps, 1977 for the hot vents 85 for the cold vents, we used human beings in a submersible. Later we shifted to using robotic submersibles where a human being sit on a ship in a control room, operate the ROV with joysticks, and you watch the videos come through. Well, those are great, but they're really expensive and you can't look at much sea floor on any given day because you're limited to how fast you can move across the sea floor and how much you can look at. So if we surveyed 2000 square kilometers in a day, we want to be able to evaluate that in less than 20 years. We want to be able to evaluate that in, you know, in a similar length of time, a day or two. So what we've done is we've shifted toward using what we, what's called a piston core, which, which is a six meter long, 20 foot long tube with about a thousand kilos on a 2,000 pounds.Dan:00:53:37And we lower it through the sea floor, operating it with a winch from a ship. And by putting a navigation beacon on that core, we can track it through the water column in real time. And if we have this high backscatter target on the sea floor, we can lower it to the water column. Once we're about fit and we're within 50 meters, 150 feet of the sea floor, we can see whether we're on target and then we let it go. When the pist- when the, it has a trigger weight on it, you can look this up, how to, how do piston cores work, that the core, lets go and it free falls that last little bit and it penetrates the sea floor. You haul it back to the surface. Now if it had gas hydrate in it, if it has oil in it, if it has gas in it, you can see it right away. when you pull the clear liner out of the core, and there it is, you know, whether or not you've got success, for most cores, there's no visual evidence of hydrocarbons that we sample that core tube, three different samples. One of them, we take a sample into what we call a gas can and seal that. And then we put a couple of hockey puck size chunks of sediment into Ziploc bags and everything goes into the freezer. And you ship that back, from the next port call. And about a month later you get a spreadsheet in your email, that says, oh, guess what you found methane, ethane, propane, butane, and Pentane. And look at this, you've got enough fluorescents that this is a guaranteed oil hit. So, again, you think about the time we map a couple thousand square kilometers a day.Dan:00:55:18We mapped for a month, we'll look the data for a month. We go out and core for a couple of weeks and a month later the Geochemistry starts flowing in. So real quick, multibeam as we've, as we've discussed as a way to get a detailed map of the sea floor, both the shape of it and the hardest roughness, acoustic properties. So any company laying a fiber optic cable across the world's oceans is acquiring multibeam data. Any, municipality that's worried about how deep their ports are and whether there's enough space for the ships to come in, is acquiring multibeam data. The corps of engineers who pays companies to dredge sand in the Mississippi River has to have a before and after multibeam a map, when MH370 went down and needed to be hunted for before they deployed the real high resolution tools. They needed a map of the sea floor and that was a part of the ocean that has never been mapped in detail before.Dan:00:56:23So most of the world's oceans have net have never been mapped in the detail that we're mapping them. We're using the tool to go hunt seeps. But there are all sorts of other uses of, of that multi beam technology. So, what are we looking for when we, when we, when we're looking for seeps, you know, what have, where have people found oil and gas leaking out of the sea floor? What does it look like? Or what are the targets? Well, if the gas burps out of the sea floor, it creates a pockmark. And those are targets, in many parts of the world, the Apennines of Italy, Azerbaijan, there are what we call mud volcanoes, where over pressured mud from deep down in the earth is kind of spewing out gently, slowly and continuously at the earth's surface. And lo and behold, it's bringing up oil and gas along with it. So mud volcanoes are known, oil and gas seeps onshore. Of course we're going to use them, offshore. Any place where we have a fault, you can create fracture permeability that might let oil and gas up. Faults can also seal, but a fault would be a good target, an anticline, a big fold that has a, can have seeps coming out of the crest of, it's similar to the seeps that were discovered early in late 18 hundreds. And in, in the USA, we can have areas where we have oil and gas leaking out of the sea floor, but it's not enough to change the shape of the sea floor. So we get high backscatter but no relief. Those, those are targets. So when we go out and we sample potential seep targets, we don't focus on only one type of target because that might only tell you one thing.Dan:00:58:04So we spread our, our targets around on different target types and we'll spread our targets around an area. Even if we, if we have more targets in one area than another area, we will spread our targets all the way around. Because the one thing that we've learned in decades of seep hunting is we're not as smart as we think we are. Nature always throws a curve ball. And you should, you should not think that you knew, know everything before you go into an area to analyze it because you might, you probably will find something that's, that startles you. And you know, as someone who's been looking at seeps since 1986, I continue to find things that we've never seen before. like our recent projects in the Gulf of Mexico, we found two target types that we've never seen before. The nearest analog on earth, on the surface is called a Pingo, which is when ice forms these really weird mountains up in the Arctic. And the one thing I can guarantee you that's not on the bottom of the world's ocean is an ice mound similar to what's forming the Arctic. But, but it had that shape. So we went and analyzed it and lo and behold, it told us something about the hydrocarbon system.Dan:00:59:12So those are all different types of target types so that the core comes back, we send it to the lab, we get first the very, what call the screening geochemistry, which is a light gases, methane through Pentane. We look at how fluorescent it is, cause that'll tell you whether or not you, you have a chance of of having a big oil hit. And we also look at what's called the chromatogram, which is a gas chromatography. And that tells us between about C15 and C36 C being the carbon length. So the, all your alkanes. And by looking at a Chromatogram, a trained professional will look that and say, oh, that's biodegraded oil. Or, oh, that's really fresh oil cause really fresh oil. All the, alkane peaks get smaller as they get bigger. So it has a very, very distinctive shape. Or they can look at it and they can tell you, you can, you can figure out the depositional environment. You can figure out whether the organic matter came from a lake, lacustrine, or maybe it's marine algal. We can say something about the age of it because flowering plants didn't evolve on earth till about the end of the age of dinosaurs. So at the end of the cretaceous, we got flowering plants. And so flowering plants create a molecule called oleanane. And so if there's no oleanane in the oil, that oil is older than cretaceous. So now we're telling something about a depositional environment.Dan:01:00:39We're saying something about the age, we can say the, the geochemist can say something about the maturity of the oil by looking at the geochemistry data. So all of this information, is now expanding what we know about what's in the subsurface and everything we know about seepage is that it is episodic in time. And it is distributed on earth's surface, not in kind of a random scattered, fashion. You get seepage above above a mud mud volcano, but for the surrounding hundred square kilometers around this mud volcano, we don't find any seep targets. Okay. So, our philosophy is that in order to find, in order to analyze the seats, we have to go find where we've got the highest probability of seepage and leakage. And that's where we target. So if you went out and just dropped a random grid over an area, you have a very, very low chance of hitting a concentrated site of seepage. And so, our hit rate, our success rate is, is high because we're using these biological and chemical indicators of seepage to help us guide where we sample. We have very precisely located sampling instruments this core with this acoustic beacon on it. And so we have, we have a very, very high success rates. And when we get hydrocarbons, we get enough hydrocarbons that we can do all of this advanced geochemistry on it.Duncan:01:02:13That's a good point Dan, even with- even without just doing a random grid of coring, piston coring has been done in the the US Gulf of Mexico for a long time now. And using seismic information, to target it. So like you say, looking for the faults and the anticlines and those type of features and very shallow anomalies on the seismic data. Even even guiding it with that information, typically a, a 5% hit rate might be expected. So you take two or 300 cores you know, you're going to get maybe 5%-10% hit rate, where you can actually look at the oils, and the geochemistry from the samples that you get. Using the multibeam, we were more like a 50 to 60% hit rate. And that's even with like Dan said, we're targeting some features where we know we're not going to find oil. so we could probably do even better than that if we, if we really focused in on finding oil. But obviously we're trying to assemble all the different types of seeps.Dan:01:03:11One of the things that we're asked and that we've heard from managers since we started working in the oil industry is what is this sea floor seep tell me about what's in my reservoir. And there's only, there have been very few, what we, what we call the holy grail studies published where a company has published the geochemistry at the reservoir level and the geochemistry on a seep that they can tie to that reservoir in the Gulf of Mexico. We collected dozens of seeps that can be tied to the same basin where there is known production. So in that Gulf of Mexico Dataset, a company that purchased that data and who had access to the reservoir oils could finally have a sufficient number of correlations that they could answer that question. What is the sea floor seep? Tell me about the reservoir. Because once you're comfortable in the Gulf of Mexico, that that seep is really telling you what's down in your reservoir.Dan:01:04:08Now you go into other parts of the world where you don't know what's in the reservoir before you drill and you find a good, a fresh seep with fresh oil right at the sea floor. Now you're confident that when you go down into the reservoir that you're going to find something, something similar. So let me talk a little bit about other things that you can do with these cores. And I'll start by kind of looking at these mud volcanoes. So this mud volcano, it had over pressured mud at depth. It came up to the surface of the earth and as it came up, it grabbed wall rock on its way up. So by analyzing a mud volcano, if we then go look at, say the microfossils, in all the class in a mud volcano, we can tell you about the age of the rocks that mud volcano came through without ever drilling a well.Dan:01:04:54So you can look at, at the, at the vitrinite reflectance, you can look at the maturity of the, of these wall rocks that are brought to you on the surface. You can look at heavy minerals. And when we go out and we do field geology, you know, you remember you're a geologist has a rock pick they and they go, the geologist goes up to the cliff and, and she or he chips a rock out and they take it back to lab and take a look at it. And that's how they tell something about what's in the outcrop. Well, it's hard to do field geology on the bottom of the ocean using a multibeam map and - acoustically guided core. We can now go and do field work on the, on the ocean floor and expand our knowledge of what's going on in a field area.Duncan:01:05:42So maybe it's worth talking a bit Dan about how we're jointly using these technologies or this group of technologies, at TGS, to put together projects. So the, I think generally the approach has been to look at, basin wide study areas. So we're not just carving off little blocks and doing, one of these, one of these projects over, over a particular block. We'll take on the whole Gulf of Mexico. So we, we broke it up into two. We looked at the Mexico side and the US side. But in total, I think it was nearly a million square kilometers that we covered and, about 1500 cores that I think we took, so we were putting these packages together in different basins all over the world, whether they're in mature basins like the Gulf of Mexico or frontier areas like places we're working in West Africa at the moment. But I think we're, we're looking to put more and more of these projects together. I think the technology applies to lots of different parts of the world. Both this side of the Atlantic and the eastern side of the Atlantic as well.Dan:01:06:44So since 2014, five years, we've mapped, we as in One and TGS have mapped, I believe over 1,250,000 square kilometers. We've acquired over 2000 cores. Oh. We also measure heat flow. We can use - is how the earth is shedding heat. And it's concentrated in some areas in, and you want to know heat flow if you're looking for oil, cause you got to know how much your organic matter has been cooked. So we've, we've collected thousands of cores, at dramatic success rates and we've used them. We've used these projects in areas of known hydrocarbon production, like the shallow water Gulf of Mexico, but we've, we've extended out into areas of completely unknown hydrocarbon production, the deep water Gulf of Mexico, the east coast of Mexico over in the Caribbean. We're looking at northwest Africa, Senegal, The Gambia, Guinea-Bissau, and the area, that's a jointly operated AGC. And we're looking at other frontier areas where we can apply this to this technology in concert with traditional tools, multichannel, seismic, gravity and magnetics to help, our clients get a better feel for the hydrocarbon prospectivity. You've got to have the seismic cause you've got to see what the subsurface looks like. But the, the multibeam which leads to seep targets, which leads ultimately to the geochemistry is what then affects the risk going forward into a basin.Duncan:01:08:20That's a good point, Dan. We don't see this as a technology that replaces seismic or gravity or magnetics or anything else, but it's another piece in the puzzle. And it's a very complimentary piece as well.Dan:01:08:31It is. And any areas you could argue that probably the best places to go look are where, your colleagues and other companies have said, oh, there's no oil there. Well, how do you know? Well, we don't think there's oil because we don't think there was a organic matter or we don't think that it was cooked enough. Well, you don't know until you go there and you find, so if you found one seep in that field area that had live oil and gas in it, you would know that that premise was incorrect. And now you have a competitive edge, you have knowledge that others don't and that can, that can affect your exploration, strategy in your portfolio. we haven't talked about cost. Multi beam is arguably one of the least expensive tools per square kilometer in the geophysical toolkit. Just because we don't need chase boats. We're not towing the streamer, we're going 10 knots. We're covering a couple of thousand square kilometers a day. So it's, it's, it's a tool that's useful in frontier exploration. It is complimentary to seismic, and it's a tool that, that you can use to guide where you want to spend money and how much money if you, if we survey a huge area and let's say half of it has no evidence of oil and gas and half of it has excellent hydrocarbon seeps, both oil and gas. I would argue that as a company you might want to spend less money on the first and more money on the second. You migh

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