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In this episode, Sam Ashoo, MD and T.R. Eckler, MD discuss the April 2025 Emergency Medicine Practice article, Sodium Disorders in the Emergency Department: A Review of Hypernatremia and HyponatremiaHypernatremia (High Sodium Levels)Definition: Sodium level greater than 145 mEq/LBreakdown into three categories based on total body water statusHypovolemic HypernatremiaEuvolemic HypernatremiaHypervolemic HypernatremiaCommon causes and conditions associatedHyponatremia (Low Sodium Levels)Definitions: Mild (130-135 mEq/L), Moderate (125-129 mEq/L), Profound (< 125 mEq/L)Breakdown into three categoriesPseudo HyponatremiaHypovolemic HyponatremiaEuvolemic HyponatremiaHypervolemic HyponatremiaCommon causes and conditions associatedTreatment Guidelines and StrategiesEmphasizing slow correction to avoid complications like cerebral edema and osmotic demyelination syndromeSuggested treatment rates for acute and chronic conditionsSpecial ConsiderationsAddressing severe cases and the importance of proper diagnosticsPre-hospital care considerations and scenariosPediatrics and consideration of child abuse in sodium disordersFive Things That Will Change Your PracticeCentral lab sodium values over point-of-care for accuracyRectal temperature checks in endurance athletesLoop diuretics for hypervolemic hyponatremia (e.g., CHF patients)Enteral treatment for hypernatremia, if possibleConsidering COVID-19 as a possible cause for new onset SIADH 

The following question refers to Sections 7.3.3 and 7.3.6 of the 2022 ACC/AHA/HFSA Guideline for the Management of Heart Failure.The question is asked by Palisades Medical Center medicine resident & CardioNerds Academy Fellow Dr. Maryam Barkhordarian, answered first by UTSW AHFT Cardiologist & CardioNerds FIT Ambassador Dr. Natalie Tapaskar, and then by expert faculty Dr. Robert Mentz.Dr. Mentz is associate professor of medicine and section chief for Heart Failure at Duke University, a clinical researcher at the Duke Clinical Research Institute, and editor-in-chief of the Journal of Cardiac Failure. Dr. Mentz has been a mentor for the CardioNerds Clinical Trials Network as lead principal investigator for PARAGLIDE-HF and is a series mentor for this very Decipher the Guidelines Series. For these reasons and many more, he was awarded the Master CardioNerd Award during ACC22.The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. American Heart Association's Scientific Sessions 2024As heard in this episode, the American Heart Association's Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It's a special year you won't want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you're among the first 20 to sign up, you'll receive a free 1-year AHA Professional Membership! Question #39 Ms. Kay Lotsa is a 48-year-old woman with a history of CKD stage 2 (baseline creatinine ~1.2 mg/dL) & type 2 diabetes mellitus. She has recently noticed progressively reduced exercise tolerance, leg swelling, and trouble lying flat. This prompted a hospital admission with a new diagnosis of decompensated heart failure. A transthoracic echocardiogram reveals LVEF of 35%. Ms. Lotsa is diuresed to euvolemia, and she is started on carvedilol 25mg BID, sacubitril/valsartan 49-51mg BID, and empagliflozin 10mg daily, which she tolerates well. Her eGFR is at her baseline of 55 mL/min/1.73 m2 and serum potassium concentration is 3.9 mEq/L. Your team is anticipating she will be discharged home in the next one to two days and wants to start spironolactone. Which of the following is most important regarding her treatment with mineralocorticoid antagonists?ASpironolactone is contraindicated based on her level of renal impairment and should not be startedBSerum potassium levels and kidney function should be assessed within 1-2 weeks of starting spironolactoneCEplerenone confers a higher risk of gynecomastia than does spironolactoneDThe patient will likely not benefit from initiation of spironolactone if her cardiomyopathy is ischemic in origin Answer #39 ExplanationThe correct answer is B – after starting a mineralocorticoid receptor antagonist (MRA), it is important to closely monitor renal function and serum potassium levels.MRA (also known as aldosterone antagonists or anti-mineralocorticoids) show consistent improvements in all-cause mortality, HF hospitalizations, and SCD across a wide range of patients with HFrEF.

Magnesium Sulfate for preeclampisa can be traced back to the work of Horn in 1906! Yet, despite such a long history of use, there are still questions about mag sulfate use that we just don't have good answers for, and that's indicative of the all the continued articles and commentaries on the subject that are still being released. For example, there are still sparse data regarding the ideal dosage of magnesium sulfate for preeclampsia with severe features. Even the therapeutic range of 4–8 mEq/L quoted in the literature is questionable. What to know where that statement comes from? That's in the ACOG PB 222 from 2020! So is the case for mag duration…you know, the 24-hour infusion tradition. The ACOG states in that same PB, “For women requiring cesarean delivery (before onset of labor), the infusion should ideally begin before surgery and continue during surgery, as well as for 24 hours afterwards. For women who deliver vaginally, the infusion should continue for 24 hours after delivery.” But this 24-hour mark, while TOTALLY OK, is more traditional than hard data driven. YES…its true, MOST if not ALL of would give mag for 24 hrs. in cases of eclampsia, and that is SUPER fitting and reasonable since they are the highest to have a recurrent seizure, but what about preeclampsia with severe features, without eclampsia or neurological symptoms. That's where the 24-hour use can get into a greyer zone; can mag be used for less than 24hrs? Can we use diuresis as a clinical marker to stop mag? Two systematic reviews and meta-analyses looking at PP Mag duration were just published in July 2024 and in September 2024. We will summarize these findings- and more- in this episode.

We discuss the approach to diagnosing and managing hypernatremia in the emergency department. Hosts: Abigail Olinde, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hypernatremia.mp3 Download Leave a Comment Tags: Electorlye Show Notes Episode Overview: Introduction to Hypernatremia Definition and basic concepts Clinical presentation and risk factors Diagnosis and management strategies Special considerations and potential complications Definition and Pathophysiology: Hypernatremia is defined as a serum sodium level over 145 mEq/L. It can be acute or chronic, with chronic cases being more common. Symptoms range from nausea and vomiting to altered mental status and coma. Causes of Hypernatremia based on urine studies: Urine Osmolality > 700 mosmol/kg Causes: Extrarenal Water Losses: Dehydration due to sweating, fever, or respiratory losses Unreplaced GI Losses: Vomiting, diarrhea Unreplaced Insensible Losses: Burns, extensive skin diseases Renal Water Losses with Intact AVP Response: Diuretic phase of acute kidney injury Recovery phase of acute tubular necrosis Postobstructive diuresis Urine Osmolality 300-600 mosmol/kg Causes: Osmotic Diuresis: High glucose (diabetes mellitus), mannitol, high urea Partial AVP Deficiency: Incomplete central diabetes insipidus Partial AVP Resistance: Nephrogenic diabetes insipidus Urine Osmolality < 300 mosmol/kg Causes: Complete AVP Deficiency: Central diabetes insipidus

Contributor: Aaron Lessen MD Educational Pearls: The case: A gentleman came in from a nursing home with symptoms concerning for sepsis. He was hypotensive, hypoxic, febrile, and mentally altered. His past medical history included previous strokes which had left him with deficits for which he required a feeding tube. Initial workup included some point of care labs which revealed a sodium of 165 mEq/L (normal range 135-145) Hypernatremia What causes it? Dehydration, from insufficient fluid intake. This might happen in individuals who cannot drink water independently, such as infants, elderly, or disabled people, as was the case for this patient. Other causes of dehydration/hypernatremia include excessive sweating; diabetes insipidus; diuretic use; kidney dysfunction; and severe burns which can lead to fluid loss through the damaged skin. How do you correct it? Need to correct slowly, not more than 10 to 12 meq/L in 24 hours Can do normal saline (0.9%) or half saline (0.45%) and D5, at 150-200 mL per hour. Check the sodium frequently (every 2-3 hours) Will likely need ICU-level monitoring What happens if you correct it too quickly? Cerebral edema Seizures Bonus fact: Correction of hyponatremia too quickly causes osmotic demyelination syndrome (ODS). References Chauhan, K., Pattharanitima, P., Patel, N., Duffy, A., Saha, A., Chaudhary, K., Debnath, N., Van Vleck, T., Chan, L., Nadkarni, G. N., & Coca, S. G. (2019). Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. Clinical journal of the American Society of Nephrology : CJASN, 14(5), 656–663. https://doi.org/10.2215/CJN.10640918 Lindner, G., & Funk, G. C. (2013). Hypernatremia in critically ill patients. Journal of critical care, 28(2), 216.e11–216.e2.16E20. https://doi.org/10.1016/j.jcrc.2012.05.001 Muhsin, S. A., & Mount, D. B. (2016). Diagnosis and treatment of hypernatremia. Best practice & research. Clinical endocrinology & metabolism, 30(2), 189–203. https://doi.org/10.1016/j.beem.2016.02.014 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII

Show notes at pharmacyjoe.com/episode882. In this episode, I'll discuss the change in serum potassium after supplementation. The post 882: Does 10 mEq of Potassium Actually Increase Serum Potassium Levels By 0.1 mEq/L? appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode882. In this episode, I ll discuss the change in serum potassium after supplementation. The post 882: Does 10 mEq of Potassium Actually Increase Serum Potassium Levels By 0.1 mEq/L? appeared first on Pharmacy Joe.

Merhabalar. Bu yazımızda Amerikan Kalp Cemiyeti'nin (AHA) zehirlenmiş hastalarda yaşamı tehdit eden toksisite ve kardiyak arrest yönetimi ile ilgili yayınladığı güncellenmenin​1​ son kısmını paylaşacağız. İlgili güncellemenin; Dr. Emre Kudu tarafından yazılan giriş kısmını içeren 1. Bölümüne buradan Dr. Emir ünal tarafından yazılan 2. Bölümüne buradan Dr. Betül İşcan Er tarafından yazılan 3. Bölümüne buradan ulaşabilirsiniz. Keyifli okumalar dilerim. Sodyum Kanal Blokörleri Giriş Birçok etken madde , sınıf Ia veya Ic antidisritmiklerine benzer özelliklerle kardiyak sodyum kanallarını bloke edebilir. Sodyum kanal blokerleri ile zehirlenme durumları EKG'de QRS uzaması, ventriküler aritmiler, hipotansiyon ve kardiyovasküler kollapsa neden olabilir. Trisiklik antidepresanlar (TCA) sodyum kanallarınıı bloke ettiği bilinen ve en yaygın olarak tanımlanan ajan olmasına rağmen, başka etken maddeler de aşırı doz kullanımlarında hayatı tehdit eden sodyum kanal blokajına neden olabilirler (Tablo 1). Tablo 1: Seçilmiş Sodyum Kanal Blokerleri DifenhidraminLakozamid  TCA'lar‡  KarbamazepinPropafenon  Venlafaksin  Klorokin*Kinin  ZonisamidKokain†Kinidin  Topiramat  FlekainidTiyoridazin  LamotrijinHidroksiklorokin*Taxus spp. (porsuk ağacı)   TCA, trisiklik ve tetrasiklik antidepresanı belirtir.*Klorokin ve hidroksiklorokin toksisitesinin tedavisi bu odaklı güncellemenin kapsamı dışındadır.†Hayatı tehdit eden kokain toksisitesinin yönetimi, bu odaklı güncellemenin 6. Bölümünde tartışılmaktadır.‡Yaygın TCA'lar arasında amitriptilin, amoksapin, klomipramin, desipramin, doksepin, imipramin, maprotilin, nortriptilin, protriptilin ve trimipramin bulunur. Sodyum kanal blokeri zehirlenmesi olan hastalarda karakteristik elektrokardiyogram (EKG) değişiklikleri görülebilmektedir. Bu değişiklikler içerisinde en iyi tanımlananları intraventriküler iletim gecikmesi (QRS aralığı uzaması) ve aVR'de görülen terminal sağ aks sapmasıdır (Şekil 1). Bu bulgular ventriküler aritmilerden önce gelmekte ve aritmi için risk teşkil ettiği düşünülmektedir. Şekil 1. Sodyum kanal blokeri zehirlenmesi olan bir hastada tipik elektrokardiyografik bulgular. Sodyum kanal bloker zehirlenmesine bağlı kardiyopulmoner arrest vakalarının yönetimi ile ilgili yapılmış çalışmalar kısıtlı olup bilgiler vaka raporları üzerinden sağlanmaktadır. En fazla kanıta sahip tedavi, tipik olarak hipertonik solüsyonlarla bolus intravenöz uygulama olarak verilen sodyum bikarbonattır (uygulama dozu yetişkinlerde 1000 mEq/L, çocuklarda 500 mEq/L). Nöbetler için sodyum bikarbonat ve benzodiazepinler, geniş kompleks taşikardi için magnezyum ve hipotansiyon için yüksek doz glukagon dahil olmak üzere diğer tedaviler bir öneride bulunmak için yeterli kanıtla desteklenmemektedir. Hayatı Tehdit Eden Sodyum Kanal Bloker Zehirlenmesi Olan Hastaların Tedavisine Yönelik ÖnerilerCORLOEÖneriler1B-NR1. Trisiklik ve/veya tetrasiklik antidepresan zehirlenmesinden kaynaklanan yaşamı tehdit eden kardiyotoksisiteyi tedavi etmek için sodyum bikarbonat kullanılmasını öneririz.2aC-LD2. Trisiklik veya tetrasiklik antidepresanlar dışındaki sodyum kanal blokerlerinden kaynaklanan zehirlenmenin neden olduğu hayatı tehdit eden kardiyotoksisiteyi tedavi etmek için sodyum bikarbonatın kullanılması mantıklıdır.2aC-LD3. Sodyum kanal bloker zehirlenmesinden kaynaklanan dirençli kardiyojenik şoku tedavi etmek için VA-ECMO gibi ekstrakorporeal yaşam desteğinin kullanılması mantıklıdır.2bC-LD4. Sınıf Ia veya Ic sodyum kanal blokerlerinden kaynaklanan hayatı tehdit eden kardiyotoksisiteyi tedavi etmek için Vaughan-Williams sınıf Ib antidisritmiklerinin (örn. lidokain) kullanılması mantıklı olabilir.2bC-LD5. Diğer tedavi yöntemlerine dirençli, yaşamı tehdit eden sodyum kanal blokeri zehirlenmesinin tedavisinde intravenöz lipid emülsiyonunun kullanılması mantıklı olabilir.COR: Class of recommendation (Tavsiye sınıfı)LOE: Level of evidence (Kanıt düzeyi) Öneriye Özgü Destekleyici Metin 1.

AABP Executive Director Dr. Fred Gingrich is joined by Dr. Geoffrey Smith, a Technical Services Veterinary for Zoetis and member of the AABP ad hoc Cattle Youngstock Committee. If you are interested in joining the Cattle Youngstock Committee, please go to the committee page and click the link to send an email with your request. Include a brief bio statement and your interest in the committee for your nomination to serve on the committee.  Smith discusses the key pathophysiologic changes that occurs in calves with diarrhea which can help veterinarians explain to producers what needs addressed with therapy. Calves with diarrhea lose electrolytes, especially sodium, and have an increased amount of D-lactate leading to acidemia. Most cases of neonatal diarrhea are not due to bacterial pathogens and therefore electrolyte therapy to correct dehydration, hyponatremia and acidosis is warranted more often than antimicrobials. Smith suggests an oral electrolyte solution that contains sodium (90-130 mEq/L), an alkalinizing agent (sodium bicarb, acetate or proprionate 50-60mEq/L), glycine which can help sodium absorption in the intestine, and correct osmolality (avoid products with high osmolality in the 700 or higher mOsm/L range). Smith also suggests evaluating the strong ion difference in the products to determine how well it can correct acidosis in the calf by adding the positive ions and subtracting the negative ions for a goal of 50-60 strong ion difference.  One common question from producers is if electrolytes can be added to milk. Smith cautions that sodium bicarbonate interferes with milk absorption and the osmolality of the final product can increase the risk for abomasitis if total solids are greater than 14-16. Separating electrolyte therapy from milk feeding by at least 2 hours and continuing electrolyte feeding once a day until the diarrhea is resolved. Smith also discusses the indications for IV fluid therapy to rapidly correct acidosis, dehydration and hyponatremia. This can be done with 4 mL/kg of hypertonic saline solution over 2-3 minutes followed by oral electrolyte therapy. If the calf is unable to suckle or stand, rapid correction of acidosis is most important and can be achieved by IV administration of hypertonic sodium bicarbonate (8.4% of 84 g/L) at a rate of 5-10 mL/kg over 5 minutes.  Smith wraps up our conversation by discussing the key points for prevention of calf scours by ensuring a clean environment, proper nutrition, proper vaccination, and an adequate amount of clean, high-quality colostrum immediately after birth. Oral electrolytes can also be fed during the high-risk period for calf diarrhea for a particular farm based on history working with the veterinarian of record. One recommendation is to use the electrolytes that are diluted 1:3 to 1:4 from the treatment dose. AABP members can see previous presentations from Smith on calf diarrhea and fluid therapy by accessing the AABP Online CE portal through the Kansas State Beef Cattle Institute or by downloading the free BCI Mobile Conference App from your device's store. 

We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma) Hosts: Brian Gilberti, MD Jonathan Kobles, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3 Download 2 Comments Tags: Renal Colic Show Notes Introduction Background Physiology: Normal range and the significance of deviations (>5.5 mEq/L) Epidemiology: Prevalence of hyperkalemia in the ER ESRD missed HD → ECG, monitor Causes / Risk Factors Causes Kidney Dysfunction, Medications,  Cellular Destruction,  Endocrine Causes, Pseudohyperkalemia High-Risk Medications: Antibiotics: Bactrim, antifungals Calcineurin inhibitors

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 study​​Nonoliguric 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

In this episode, we review the management of a patient with hypokalemia, including both inpatient and outpatient supplementation with potassium chloride supplements and what dosage forms are available for potassium repletion. Key Concepts Most diets will provide sufficient potassium to avoid hypokalemia. Hypokalemia usually occurs due to drug therapy (such as diuretics) or GI losses from severe vomiting or diarrhea. In patients with chronically low potassium, supplements are dosed to increase dietary intake of potassium by about 20-40 mEq per day. For acute repletion, 10 mEq of potassium should increase serum potassium by about 0.1 mEq/L. Over-the-counter potassium (as potassium gluconate) contains a very small amount of potassium (2.5 mEq). Potassium chloride powders and liquids (like salt substitutes) taste terrible and are poorly tolerated. Most patients will replete potassium via slow-release tablets (Klor-Con or Klor-Con M) or via potassium chloride IV infusions. Most IV fluids do not contain any potassium at all (or very little potassium). Patients receiving these IV fluids who are NPO will eventually become hypokalemic. Certain maintenance fluids do contain potassium – most patients will receive about 40 mEq of potassium per day with these IV fluids.

Contributor: Travis Barlock, MD Educational Pearls: Normal Saline (NS) contains 154 mEq of both Sodium (Na) and Chloride (Cl),  and has a pH of 5.5 Normal Na and Cl in adult humans are about 140 mEq/L and 103 mEq/L. respectively   Excess negative charge resulting from hyperchloremia is managed via bicarbonate excretion leading to loss of base Overall, administration of NS drives metabolic acidosis Lactated Ringers (LR) contains 130 mEq of Na and 109 mEq Cl, and has a pH of 6.5   LR components are closer to physiologic levels thus may generally be a more efficacious fluid choice   NS is still frequently given in scenarios where there is concern for increased intracranial pressure or existing hypochloremic alkalosis from emesis.  ReferencesLi H, Sun SR, Yap JQ, Chen JH, Qian Q. 0.9% saline is neither normal nor physiological. J Zhejiang Univ Sci B. 2016;17(3):181-187. doi:10.1631/jzus.B1500201 ​​Lehr AR, Rached-d'Astous S, Barrowman N, et al. Balanced Versus Unbalanced Fluid in Critically Ill Children: Systematic Review and Meta-Analysis. Pediatr Crit Care Med. 2022;23(3):181-191. doi:10.1097/PCC.0000000000002890 Self WH, Semler MW, Wanderer JP, et al. Saline versus balanced crystalloids for intravenous fluid therapy in the emergency department: study protocol for a cluster-randomized, multiple-crossover trial. Trials. 2017;18(1):178. Published 2017 Apr 13. doi:10.1186/s13063-017-1923-6 Semler MW, Self WH, Wanderer JP, et al. Balanced Crystalloids versus Saline in Critically Ill Adults. N Engl J Med. 2018;378(9):829-839. doi:10.1056/NEJMoa1711584 Summarized by Kirsten Hughes, MS4 | Edited by John Spartz, MD, & Erik Verzemnieks, MD   In an effort to promote diversity, equity, and inclusion in Emergency Medicine, The Emergency Medical Minute is proud to present our 2nd annual Diversity and Inclusion Award. We support increasing the representation of underrepresented groups in medicine and extend this award to individuals applying to emergency medicine residencies during the 2022-2023 cycle. For information on award eligibility and the application process, visit https://emergencymedicalminute.com/edi-award/ Donate to EMM today!

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/LithiumLithonateNursingConsiderations      Generic Name lithium Trade Name Lithizine Indication mania Action alters cation transport and neurotransmitter reuptake Therapeutic Class Mood Stabilizer Pharmacologic Class none Nursing Considerations • do not administer with NSAIDs • monitor drug blood levels frequently • may cause seizures, arrhythmias, fatigue, confusion, nausea, anorexia, hypothyroidism, tremors • Ace Inhibitors may increase serum levels • instruct patient to maintain adequate fluid intake • therapeutic level: 0.5-1.5 mEq/L

In episode 53 of the pharmaceutical calculations podcast, you will learn how to calculate the mEq/L of Na+, Ca2+ and Cl- in a fluid having 0.25M NaCl and 0.075 CaCl2. Key equations and pertinent concepts are also reviewed. This episode was originally broadcast as a video on our YouTube channel: www.youtube.com/pharmaceuticalcalculationseasy Additional Resources for Practice: Pharmaceutical Calculations: 1001 Questions with Answers: https://www.rxcalculations.com/shop/uncategorized/pharmaceutical-calculations-1001-questions-answers/ NAPLEX Question Bank: https://www.rxcalculations.com/shop/uncategorized/gold-membership/ Join Our Social Media Community: Website: http://www.rxcalculations.com Forum: https://forum.rxcalculations.com/ Facebook: https://www.facebook.com/pharmaceuticalcalculations Twitter: https://twitter.com/RxCalculations Instagram: https://www.instagram.com/rxcalculations YouTube: www.youtube.com/pharmaceuticalcalculationseasy About RxCalculations: RxCalculations helps you master pharmaceutical calculations. We make it so you never have to worry about failing an exam or compromising patient safety because of a calculations error. RxCalculations is a leading global educational service platform focused on developing top quality pharmaceutical calculations products to help prospective pharmacists and health care professionals all over the world resolve one of the biggest challenges related to their profession. Our top quality products include affordable courses, personal consults, books, video tutorials, timed quizzes and apps designed to make you an expert in solving any pharmaceutical calculations question. We also have the largest pharmaceutical calculations online question bank which has over 1000 questions covering every important calculations topic as well as step-by-step video solutions. With all these resources at your disposal we have all you need to not only master pharmacy calculations but ace every test as well as passing your board exams.

Contributor: Peter Bakes, MD Educational Pearls: Lithium remains a commonly used medication for treating bipolar disorder Lithium toxicity can be acute, acute-on-chronic, or chronic  Measuring blood lithium level Therapeutic range of lithium is around 1.6-1.8 mEq/L >2 mEq/L is likely to cause significant toxicity >4 mEq/L necessitates lifesaving treatment The lethal dose of lithium is 700 mg/kg Lithium can have delayed absorption resulting in levels increasing during hospitalization Symptoms associated with acute lithium toxicity Gastrointestinal Nausea, vomiting, abdominal pain Neurological Tremor, nystagmus, CNS depression (late finding) Cardiovascular Bradycardia, QT prolongation, EKG changes Treatment for lithium toxicity ABCs Get a good history GI Decontamination: Whole bowel irrigation if patient ingested extended-release tablets Dialysis Most effective treatment for lithium toxicity References Baird-Gunning J, Lea-Henry T, Hoegberg LCG, Gosselin S, Roberts DM. Lithium Poisoning. J Intensive Care Med. 2017;32(4):249-263. Hedya SA, Avula A, Swoboda HD. Lithium Toxicity. In: StatPearls. Treasure Island (FL): StatPearls Publishing. Copyright © 2022, StatPearls Publishing LLC.; 2022. McKnight RF, Adida M, Budge K, Stockton S, Goodwin GM, Geddes JR. Lithium toxicity profile: a systematic review and meta-analysis. Lancet. 2012;379(9817):721-728.   Summarized by Mark O'Brien, MS4 | Edited by John Spartz, MD & Erik Verzemnieks, MD   The Emergency Medical Minute is excited to announce that we are now offering AMA PRA Category 1 credits™ via online course modules. To access these and for more information, visit our website at https://emergencymedicalminute.org/cme-courses/ and create an account.  Donate to EMM today!

The Curious Clinicians unpack why potassium is often repleted to levels >4 mEq/L. Check out the show notes here. Click here to obtain AMA PRA Category 1 Credits™ (0.5 hours), Non-Physician Attendance (0.5 hours), or ABIM MOC Part 2 (0.5 hours). Audio edited by Clair Morgan of Nodderly.com.

Eliminasyon kelime anlamı olarak; eleme, yok etme, ortadan kaldırma, bir maddenin biyoransformasyondan sonra vücut dışına atılmasıdır. Hepimizin bildiği üzere vücudumuz dışarıdan aldığı maddeleri üriner, fekal, pulmoner ve sekresyonlar yolu ile elimine eder. Sınırlı sayıda yöntem ile zehirlenme durumlarında, eliminasyonu artırarak ksenobiyotiklerin vücuttan uzaklaştırılmalarını hızlandırabiliriz. Ancak bu yöntemlerin klinik pratikte kullanımları sınırlıdır ve tüm zehirlenme çeşitlerinde de kullanılmamaktadır (Tablo-1). Korporeal (Vücut içi) yöntemler Ekstrakorporeal (Vücut dışı) yöntemler Üriner alkalinizasyon Hemodiyaliz Tekrarlayan doz aktif kömür Hemoperfüzyon Zorlu diürez Hemofiltrasyon Metal şelasyonu Sürekli Renal Replasman Tedavileri Serebrospinal sıvı replasmanı Plazmaferez, Exchange transfüzyon Reçineler (Prusya mavisi, kolestiramin, kolestipol, kayeksalat) Karaciğer destek araçları Tablo-1. Eliminasyonu artırıcı yöntemler Bu yazımızda klinik pratikte sık uygulanan eliminasyonu artırıcı yöntemleri sizlere sunmayı amaçladık. Üriner Alkalinizasyon Zayıf asit yapıdaki ksenobiyotiklerin eliminasyonunu arttırmak için asidik olan idrar pH'ının (pH:4-5) alkalileştirilmesi esasına dayanan bir yöntemdir. Bu yöntemin en sık uygulandığı ajanlar ise Salisilatlar, Fenobarbital ve Metotreksat'dır.  Bu zayıf asitler, alkali idrar pH'ında iyonize hale gelerek renal tübüllerden reabsorbsiyona uğramadan idrarla atılırlar. Alkalinizasyonda, idrarın hedef  pH'ını 7-8'e çıkarmak için intravenöz sodyum bikarbonat (1-2 mEq/kg hızlı iv bolus ve idame iv infüzyonu) uygulanır. Bu esnada dikkat edilmesi gereken en önemli noktalar; serum pH'nın 7.5'i geçmemesi, serum potasyum seviyesinin 4 mEq/L'nin altına düşmemesidir​1​. Tekrarlayan Doz Aktif Kömür Aktif kömür, dekontaminasyon yöntemi dışında enterohepatik sirkülasyona giren ajanların eliminasyonunu artırmak amacıyla  0.5 g/kg dozunda ve her 6 saate bir, toplam 4 kez olacak şekilde oral yolla veya nazogastrik tüpten uygulanır. Böylece aktif kömür, ilacın veya toksinin enterohepatik dolaşımını engelleyerek sistemik dolaşıma tekrar karışmasını önler ve serum konsantrasyonunu düşürür. Tekrarlayan doz aktif kömür uygulamasının endike olduğu durumlar arasında Karbamazepin, Amitriptilin, Siklosporin, Dapson, Digitoksin, Nadolol, Nortriptilin, Fenobarbitaller, Siklopeptid içeren mantar zehirlenmeleri yer alır. Unutulmaması gereken dekontaminasyon amaçlı aktif kömür uygulamasının kontrendike olduğu her durum tekrarlayan doz aktif kömür uygulaması için de geçerlidir​2,3​. Ekstrakorporeal Yöntemler The Extracorporeal Treatments in Poisoning - EXTRIP çalışma grubu, 30'dan fazla uluslararası derneği temsil eden çeşitli alanlardan uzmanların işbirliğiyle  (tıbbi/klinik toksikoloji, nefroloji, farmakoloji, yoğun bakım, acil tıp) zehirlenmelerde özellikle hemodiyaliz endikasyonları ve diğer ekstrakorporeal tedavi yöntemleri ile ilgili çeşitli önerileri kılavuz şeklinde yayınlamaktadır ve bu önerileri güncellemektedir. Hemodiyaliz Hemodiyaliz keşfedildiğinden bu yana 100 yılı aşkın süredir klinikte kullanılmaktadır ve zehirlenmelerde en sık kullanılan ekstrakorporeal tedavi yöntemidir. Çünkü hemodiyaliz, toksini dolaşımdan uzaklaştırmanın yanısıra asit-baz ve elektrolit bozukluklarının hızlı düzeltilmesi ve böbrek fonksiyonlarının bozuk olduğu durumlarda ultrafiltrasyon ile volüm yükünün azaltılması gibi destek tedavisi amaçlı da kullanılmaktadır. Klasik hemodiyaliz sırasında, kan ve ters akımlı diyalizat, yarı geçirgen bir zar (diyalizör) ile ayrılır. Ksenobiyotikler daha sonra membran boyunca kandan diyalizata konsantrasyon farkı esasına dayanarak difüze olur. Kan, geçici bir diyaliz kateterinin bir lümeninden pompalanır, makineden geçirilir ve ikinci lümenden venöz dolaşıma geri döndürülür. Bir maddenin hemodiyaliz ile kandan uzaklaştırılabilmesi için molekül ağırlığının küçük (

Mit, sözlük anlamı olarak “kuşaktan kuşağa yayılan, toplumun düş gücü etkisiyle zamanla biçim değiştiren, imgesel, alegorik bir anlatımı olan halk öyküsü” demek. Daha genel bir tabirle “söylence”. Her ne kadar günümüz tıp eğitimi kanıta dayalı yapılsa da hali hazırda rutin klinik uygulamamızda, özellikle hayati tehdit eden durumlarda ileriye yönelik değerlendirmenin zorlu doğası nedeniyle, bazı iyi-niyetli fikirlerin, onları destekleyecek çok az kanıt olmasına rağmen nesiller boyu öğretile geldiğini görebiliyoruz. Bu yazıda da acil servislerde sık karşılaştığımız, mortal seyredebilen akut hiperkalemi tedavisinde süregelen bazı mitler ve yanlış kanıları gözden geçireceğiz. 1 Akut hiperkalemi ile karşılaştığımızda yapılacaklar kabaca belli olsa da maalesef klinikler arası yaklaşım farklılıkları mevcuttur ve yönetimi henüz net bir kılavuza bağlanabilmiş değildir. Geleneksel hiperkalemi yönetimi temelde üç bileşen üzerine kurulur; kardiyak depolarizasyonun stabilizasyonu, serum potasyumunun intraselüler alana yönlendirilmesi ve total vücut potasyumunun uzaklaştırılması. Şimdi birlikte geleneksel tedavi yaklaşımının bazı bileşenlerinin doğruluğunu inceleyelim. MİT 1: Kayeksalat güvenlidir ve işe yarar Sodyum polistiren sulfonat (piyasa ismiyle Kayetsalat) hiperkalemi tedavisinde kullanılan katyon değiştirici reçinedir. Oral veya rektal uygulanır ve potasyuma bağlanarak atılımını sağlar. 1958'de beş anürik hastada 5 gün uygulanması sonucu potasyum seviyelerinde minimal düşüş görünmüş ve bu yayınla FDA onayı almıştır. Sonraki 60 yıllık dönemde kayeksalatın etkinliği ile ilgili sadece 4 tane RKÇ yapılmış ve bunlarından yalnızca birinde potasyumda yedinci günde istatistiksel anlamlı bir düşüş gösterilmiştir. Aynı dönemde yapılan yirmiye yakın gözlemsel çalışmanın bazısında ise (süreler farklılık göstermekle birlikte 3 ila 7 günlük kullanım sonrası) potasyum seviyelerinde minimal ( 1 – 1,5 mEq/L) düşüş gözlenmiştir. Cochranedeki derlemelere bakıldığında ise 2005'de yapılmış ilk derleme kayeksalatın ilk 4 saat içerisinde potasyumu düşürmede faydalı olmadığını ve akut hiperkalemi tedavisinde yeri olmadığını vurgulamaktadır. 2020'deki son derlemede ise kronik böbrek yetmezliği olan hastalarda kayeksalatın ayaktan tedavide kullanımıyla ilgili kanıt düzeyinin düşük olduğu belirtilmiş; ancak yazarlar patiromer gibi yeni potasyum bağlayıcıların etkili olabileceğini vurgulamışlardır. Peki işe yaradığı ispatlanamamış kayetsalatın zararı var mı? FDA 2011 yılında paketlerin üzerine kolon nekrozu yapabileceği ile ilgili bir uyarı koydu. Bu risk özellikle sorbitol ile birlikte kullanımlarda artış göstermektedir. Yapılan çalışmalarda kayeksalatın nekroz dışında ülserasyon ve perforasyon gibi çok ciddi birçok gastrointestinal komplikasyon ile ilişkili olduğu ve komplikasyonlara bağlı mortalitenin %20'lere kadar çıkabileceği gösterilmiştir. Ayrıca 15 gr kayeksalat 1500 mg sodyum yükü içerir ki bu durum fazladan volüm yükü ve olası kalp yetmezliği tablosunun kötüleşmesi anlamına gelir. Sonuç olarak Kidney Disease: Improving Global Outcomes (KDIGO) kongresinde kayeksalatın hiperkaleminin acil tedavisinde kullanılması önerilmemiştir. Öneri: Potansiyel zararları ve etkinliğinin olmaması nedeniyle Kayeksalat, akut hiperkalemi yönetiminde rutin olarak kullanılmamalıdır. MİT 2: Hiperkalemide ringer laktat kontraendikedir Dengeli bir kristaloid solüsyon olan ringer laktat içerisinde 4-5 mEq/L potasyum bulundurduğu için, hiperkalemik hastalarda kullanımından çekinilmektedir. Aslında şimdiye kadar yapılan çalışmalarda ringer laktat ve serum fizyolojik karşılaştırıldığında, yoğun bakım hastalarında, günler sonra bile potasyum düzeyleri arasında bir fark gözlenmemiştir. Zaten hiperkalemik bir hastada hastanın ekstrasellüler boşluğundaki potasyum miktarı, dengeli solüsyondaki potasyum miktarından fazla olduğundan, normale-yakın potasyum içeren ringer laktatın, bu hastalarda serum potasyumunu değiştirmesi beklenmez.

Chapter 6 part 2. ReferencesJosh touts the PARADIGM-HF Trial Angiotensin–Neprilysin Inhibition versus Enalapril in Heart Failure | NEJM which found this combination was superior to an ARB alone Joel mentions an early atrial natriuretic peptide trial by Julie Lewis et al. Atrial natriuretic factor in oliguric acute renal failure - American Journal of Kidney Diseases and here's a metanalysis that put this option to bed: Atrial Natriuretic Peptide for Management of Acute Kidney Injury: A Systematic Review and Meta-analysisSnack attack? Check out “Snack induced ANP” Snack-Induced Release of Atrial Natriuretic Factor | NEJMWant more natriuretic peptides than we discussed? Check out this review! Cardiac natriuretic peptides | Nature Reviews Cardiology or this fantastic review: Here's an excellent review of ANP effect on the kidney: ANP-induced signaling cascade and its implications in renal pathophysiologyCerebral salt wasting and elevated brain natriuretic peptide levels after traumatic brain injury: 2 case reportsJoel mentions the study which probed CRIC cohort regarding NSAIDs. Association of Opioids and Nonsteroidal Anti-inflammatory Drugs With Outcomes in CKD: Findings From the CRIC (Chronic Renal Insufficiency Cohort) Study - American Journal of Kidney Diseases and you may like the discussion on NephJC: ​​No Pain for the Kidneys from NSAIDs — NephJCThe KDIGO guidelines can be found here CKD-Mineral and Bone Disorder (CKD-MBD) – KDIGO Regulation and Effects of FGF23 in Chronic Kidney DiseaseElegant work on the calcium sensing receptor by Martin Pollak https://doi.org/10.1016/0092-8674(93)90617-YeClaudin 14, PTH, and calcium absorption in the loop of Henle: Parathyroid hormone controls paracellular Ca 2+transport in the thick ascending limb by regulating the tight-junction protein Claudin14Carboxymaltose induced hypophosphatemia by increasing FGF-23. Randomized trial of intravenous iron-induced hypophosphatemiaCurrent "corrected" calcium concept challenged. | The BMJThe Dialysis Encephalopathy Syndrome — Possible Aluminum Intoxication | NEJMNephMadness covered Aluminum binders in 2016.Roger mentioned the use of ferric citrate as a phosphate binder Ferric Citrate Controls Phosphorus and Delivers Iron in Patients on Dialysis | American Society of NephrologyJoel reminded us of the misadventures in efforts to normalize hemoglobin, first in hemodialysis patients The Effects of Normal as Compared with Low Hematocrit Values in Patients with Cardiac Disease Who Are Receiving Hemodialysis and Epoetin | NEJMLater, in patients with CKD, normalization was also not shown to be better: Correction of Anemia with Epoetin Alfa in Chronic Kidney Disease | NEJM , Normalization of Hemoglobin Level in Patients with Chronic Kidney Disease and Anemia | NEJMA quick shout out for roxadustat and the Nephmadness Anemia region! Roxadustat Treatment for Anemia in Patients Undergoing Long-Term Dialysis | NEJM, #NephMadness 2021: Anemia Region – AJKD BlogIn this review of vasopressin, you can find an excellent discussion of basic stimuli and vasopressin receptors: Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems | Physiological ReviewsX-Linked Nephrogenic diabetes insipidus is very rare and there was theory that all patients originated from the same family and traveled to the US on the Hopewell ship JCI - X-linked nephrogenic diabetes insipidus mutations in North America and the Hopewell hypothesis. This report describes another family from the Netherlands with nephrogenic DI including the finding that the urine osmolarity never exceeds 200 mOsm/kg. Hereditary Nephrogenic Diabetes Insipidus - GeneReviews® (and here's a family with central diabetes insipidus https://academic.oup.com/jcem/article/81/1/192/2649423?login=true )Although we have all learned that thiazides should be used with diabetes insipidus, to induce mild volume depletion, several case reports and animal data have found that acetazolamide might be the best diuretic for the job. Clinicians from Boston Medical Center tried it out in this report: ​​Acetazolamide in Lithium-Induced Nephrogenic Diabetes Insipidus | NEJM based on exciting data in mice! https://jasn.asnjournals.org/content/27/7/2082.shortADH appears to have an effect on potassium excretion. This was investigated by Giebesch who found, with clearance and micropuncture studies in rats plus isolated perfused tubules, ADH increased potassium secretion Influence of ADH on renal potassium handling: A micropuncture and microperfusion study A corollary should be that inhibition of ADH would increase the risk of hyperkalemia but this was not observed in the SALT-1 and SALT-2 trials. 5% of patients developed hyperkalemia in both the tolvaptan group and the placebo group Tolvaptan, a Selective Oral Vasopressin V2-Receptor Antagonist, for Hyponatremia | NEJMV1 vasopressin as a pressor Exogenous Vasopressin-Induced Hyponatremia in Patients With Vasodilatory Shock: Two Case Reports and Literature ReviewWe wondered/debated on our observation that hyponatremia is not reliably seen in patients receiving vasopressin in the ICU. In the VASST trial, Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock, 1 patient in each study arm of nearly 400 patients developed hyponatremia. Note that patients with hyponatremia (

Chapter 6 part 1In this review of vasopressin, you can find an excellent discussion of basic stimuli and vasopressin receptors: Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems | Physiological ReviewsX-Linked Nephrogenic diabetes insipidus is very rare and there was theory that all patients originated from the same family and traveled to the US on the Hopewell ship JCI - X-linked nephrogenic diabetes insipidus mutations in North America and the Hopewell hypothesis. This report describes another family from the Netherlands with nephrogenic DI including the finding that the urine osmolarity never exceeds 200 mOsm/kg. Hereditary Nephrogenic Diabetes Insipidus - GeneReviews® (and here's a family with central diabetes insipidus https://academic.oup.com/jcem/article/81/1/192/2649423?login=true )Although we have all learned that thiazides should be used with diabetes insipidus, to induce mild volume depletion, several case reports and animal data have found that acetazolamide might be the best diuretic for the job. Clinicians from Boston Medical Center tried it out in this report: ​​Acetazolamide in Lithium-Induced Nephrogenic Diabetes Insipidus | NEJM based on exciting data in mice! https://jasn.asnjournals.org/content/27/7/2082.shortADH appears to have an effect on potassium excretion. This was investigated by Giebesch who found, with clearance and micropuncture studies in rats plus isolated perfused tubules, ADH increased potassium secretion Influence of ADH on renal potassium handling: A micropuncture and microperfusion study A corollary should be that inhibition of ADH would increase the risk of hyperkalemia but this was not observed in the SALT-1 and SALT-2 trials. 5% of patients developed hyperkalemia in both the tolvaptan group and the placebo group Tolvaptan, a Selective Oral Vasopressin V2-Receptor Antagonist, for Hyponatremia | NEJMV1 vasopressin as a pressor Exogenous Vasopressin-Induced Hyponatremia in Patients With Vasodilatory Shock: Two Case Reports and Literature ReviewWe wondered/debated on our observation that hyponatremia is not reliably seen in patients receiving vasopressin in the ICU. In the VASST trial, Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock, 1 patient in each study arm of nearly 400 patients developed hyponatremia. Note that patients with hyponatremia (

Kritik Bakım ve Acil Tıp, SF'in içindeki 154 mEq/L klorun ne menem etkileri olduğu konusunda yıllardır ikiye bölünmüş durumda. Önce yıllarca kanayan travma hastasında hızlı sıvı resüsitasyonu için kolloidler mi kristaloidler mi (ayrıca kristoloid ise SF mi Ringer mi) diye tartıştık. Bu konu kristaloidler lehine netleşince aynı hastada ne kadar SF verdikten sonra kan ürünlerinden geçmeli tartışması başladı. 2-3 litre ile başlayıp 1 litrede karar kıldık. Kan gazı değerlendirme ve Stewart metodunun yaygınlaşmasıyla klorün güçlü iyon dengesinin bir bileşeni olarak asit etkisine sahip olduğunun yaygınlıkla bilinmeye başlaması, asidozun da kritik hastadaki zararlarının ispatlanması fiyatları ucuzlayan ve daha yaygın olarak bulunmaya başlayan markalı dengeli solüsyonlarını mantıklı birer opsiyon haline getirdi. "Olm SF başlayalım hastaya" yaklaşımından ziyade desktroz, salin, bikarbonat, serum sale, potasyum kombinleyip özel reçeteler order etmekten keyif alan benim gibi kan gazı meraklıların SF kullanan gençleri "cık cık" diye yermesi de dengeli solüsyonların "yürümesinde" önemli bir faktör oldu. Her tıbbi ilerlemede olduğu gibi önce "rutine" koyup sonra araştırmasını yaptığımız SF mi dengeli solüsyon mu tartışmalarının ilk yayınları gözlemsel çalışmalar olup dengeli solüsyonların kritik hastalarda daha iyi sonlanımlar ile ilişkili olduğunu ortaya koymaktaydı (Yunos et al. 2012​1​, Raghunathan et al. 2014​2​, Zampieri et al. 2016​3​). Ardından RKÇ yapısındaki ünlü SMART ve SALT-ED çalışmaları (Semler et al. 2018 (SMART Çalışması)​4​, Self et al. 2018 (SALT-ED Çalışması)​5​) bu fayda çok kuvvetle olmasa da desteklendi (Sevgili Can Özen'in bu iki çalışmaya dair harika yazısına buradan ulaşabilirsiniz). Ancak SPLIT çalışması​6​ gibi daha büyük RKÇ'ler bu yargıları desteklemedi ve konu ortada kalakaldı. Bu kaygıları gidermek adına daha önceki çalışmaların eksikliklerinin hepsini kapatacak şekilde dizayn edilmeye çalışılmış ve merakla beklenen bu alandaki son çalışma olan BaSICS çalışması​7​ (Balanced Solutions in Intensive Care Study, aslında 2 çalışma) 2 gün önce JAMA'da yayınlandı. Gerçekten bu çalışma amacına ulaşmış mı bir değerlendirmesek olmazdı. O zaman buyrun ayrıntılara... Bu Çalışmanın Cevaplamaya Çalıştığı Klinik Sorular Yetişkin yoğun bakım hastalarında %0.9 salinle karşılaştırıldığında dengeli kristaloid kullanımı 90 günlük tüm nedenlere bağlı mortaliteyi azaltır mı?Resüsitasyon sıvılarının uygulanmasına ihtiyaç duyan yetişkin yoğun bakım hastalarında, sıvı boluslarının hızlı infüzyonuna kıyasla yavaş infüzyon, 90 günlük tüm nedenlere bağlı mortaliteyi azaltır mı? Önceki Bilgilerimiz Yoğun bakım ünitesindeki hemen hemen tüm hastalara intravenöz sıvı verilir.SPLIT ve SMART çalışmaları ile Plasma-Lyte ve %0,9 salin karşılaştırılmıştıHer kolda ortalama 2000 ml uygulanan SPLIT çalışması, 90 günlük AKI'de hiçbir fark göstermedi.Her kolda ortalama 1000 ml uygulanan SMART çalışması, 30 günlük Majör Advers Böbrek Olaylarının (ölüm, yeni RRT veya kalıcı böbrek fonksiyon bozukluğunun bir bileşimi) meydana geldiğini gösterdi.Ağır hastalarda yaygın bir müdahale olan hızlı sıvı bolusları kullanımının, arteriyel elastansın azalması gibi olumsuz kardiyovasküler fizyolojik sonuçlara yol açtığı varsayılmaktadır.FEAST çalışması, hipotansiyonu olan Afrikalı çocuklarda salin veya albümin boluslarının kullanımının 48 saatlik ölüm riskinin artmasına neden olduğunu gösterdi.2000'den fazla YBÜ hastasında sıvı bolus uygulamasını inceleyen FENICE çalışması, uygulama pratiğinin karşılaştırılamayacak kadar değişken olduğunu göstermiştir (hacim, hız, son noktalar açısından) Çalışmanın Tasarımı Faktöriyel 2 x 2 randomize çalışmaÇalışmaya alınan hastalar her bir sıvıya (dengeli solüsyon – Plazma-Lyte ve %0.9 sodyum klorür) ve her uygulama hızına (333 ml/saat ve 999 ml/saat) 1:1:1:1 oranında randomize edilmişRandomizasyon listesi 12 hastadan oluşan rastgele permütasyonlu bloklarla yapılmış Hasta bakımına dahil olanlar sıvı tipine kör...

Merhaba Bu yazımızda gebe hastalarda solunum yetmezliği yönetiminden bahsedeceğiz. Solunum yetmezliği gebelikte nadir karşılaşılan fakat ciddi sonuçlara sebep olabilen acil bir durum. Nadir karşılaştığımız için de yönetimi anlamak biz acilciler için çok önemli. Öncelikle fizyolojik adaptasyon olarak gerçekleşen solunumsal değişikliklere göz atacağız (Tablo 1)​1​. Progesteron etkisiyle dakika ventilasyondaki artış ve parsiyel karbondioksit basıncındaki düşüş sayesinde fetal karbondioksitin maternal dolaşıma transferi sağlanır. Fakat ileri hipokarbi ve maternal alkaloz gelişmesi halinde de uteroplasental vazokonstrüksiyon gelişebileceği ve fetal hipoperfüzyon ve hipoksiye sebep olabileceği unutulmamalıdır. Özellikle mekanik ventilasyon kararı verildiğinde, ventilatör ayarında bu değişiklikleri göz önünde bulundurmak gerekecektir. Fonksiyonel rezidüel kapasite%10-25 azalırDakika ventilasyon%20-40 artarArteriyel parsiyel oksijen basıncıDeğişmezArteriyel parsiyel karbondioksit basıncı28-32 mm Hg düzeyine inerSerum bikarbonat18-21 mEq/L düzeyine inerTablo 1. İleri gebelikte fizyolojik değişiklikler. Her acil servis hastası gibi nefes darlığı şikayeti ile başvuran gebe hastada da bizim için ABC yaklaşımı geçerlidir. Altta yatan sebepten bağımsız olarak önceliğimiz hastanın oksijenizasyonu ve stabilizasyonu olmalıdır. Hipokseminin derecesine göre ek oksijen desteği sağlanır. Hedef SpO2≥95 ve PaO2>70 olmalıdır. Mekanik ventilasyon ihtiyacı mevcutsa, gebe olmayan hastalarda da olduğu gibi, bilinci açık ve havayolu açıklığını koruyabilen hastalarda NIMV uygulanabilir. NIMV uygulanacak gebe hastada özellikle unutulmaması gereken nokta; gebe hastaların gastrik basıncının artması, mide boşalmasının yavaşlaması ve özefagus alt sfinkterinin tonusunun azalması sebebiyle aspirasyon riskinin yüksek olmasıdır. Özellikle NIMV'in de etkisiyle hava ile mide distansiyonunun artması, kusma ve aspirasyon riskini arttıracaktır. Fakat elbette entübasyonun ve bu esnada verilecek sedatiflerin komplikasyonlarından kaçınmak adına uygun hastalarda NIMV tercih edilebilir. NIMV için önerilen başlangıç basınçları IPAP 12-15 cm H2O ve EPAP 5-8 cm H2O'dur ​2​. İnvaziv mekanik ventilasyon ihtiyacı olan gebe hastada solunumsal fizyolojik değişikliklerin yanı sıra entübasyonu zorlaştıran anatomik değişikliklerin varlığı da unutulmamalıdır (Tablo 2)​3​. Başarısız entübasyon, gebe olmayan hastalara göre 8 kat daha olasıdır. Ayrıca başarısız girişimler sırasında hasta daha hızlı desatüre olacaktır. Bu sebeple zor havayoluna hazır olunmalı ve alternatif planlar hazırlanmalıdır. Gebe hastada solunum yetmezliği durumunda sedasyon için kullanılan indüksiyon ajanlarından herhangi birinin üstünlüğü gösterilememiştir. Hastanın hemodinamik durumuna ve altta yatan sebebe göre karar verilebilir. Yine paralizan ajanlardan süksinilkolin ve roküronyumdan biri seçilebilir​4​. Anatomik/Fizyolojik DeğişiklikEtkiUygulamaÜst havayollarında ödem ve hiperemiArtmış mukozal frajiliteÜst havayolu çapında daralmaVokal kordları görmenin zor olabileceğini düşün, ilk denemede başarılı entübasyon için pozisyonu optimize etEntübasyon girişimi ve üst havayolu manipülasyonunu azaltDaha küçük çaplı entübasyon tüpünü hazırlaYüksek yerleşimli diyaframArtmış oksijen tüketimiFonksiyonel rezidüel kapasitede azalmaBibaziller atelektaziDaha kısa güvenli apne süresiPreoksijenizasyon ve nitrojenin uzaklaştırılmasına zaman ayırHızlı desaturasyon riski; paralizan sonrası hızlı entübasyon için hazır ol Daha dik pozisyonda entübasyonu düşünGebe abdomenAortakaval basıEntübasyon öncesi bolus sıvı desteği ile preloadı arttırmayı düşünHastanın düz yatması gerekiyorsa, gebe uterusu yastık/battaniye ile destekleArtmış tidal volum ve dakika ventilasyonFizyolojik kompansesolunumsal alkalozVentilatörü, hastanın entübasyon öncesi dakika ventilasyonu gibi ayarlaAzalmış özefagus alt sfinkter tonusu Artmış intraabdominal basınçArtmış aspirasyon riskiMümkünse ambulamaktan kaçın Daha dik pozisyonda entübasyonu...

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 derlenmiştir​1​. 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,

Episode 19: Bartter and Gitelman  The sun rises over the San Joaquin Valley, California, today is July 10, 2020. In case you did not notice, we did not have an episode last week. We were very busy in our residency. We started a new rotation and a new academic year. We welcomed a new group of PGY1s, along with 3rd-year medical students, and Sub-Is. We also said good bye to our dear graduates: Greg Fernandez, Ronald Gavilan, Yunior Martinez, and Steven Saito. “Spread your wings, it’s time to fly. Make the leap. Own the sky.”(1) Good luck in your careers! Those activities kept us busy, and, as if that wasn’t enough, we saw an increase in incidence of COVID-19 across the nation. In Clinica Sierra Vista, we went from 270 positive cases in May to 700 positive cases in June, we also increased the total tests performed from 1200 in May to 2800 in June. Our positivity rate increased from 21% to 25%. In the county of Kern we have had 5,500 cases and 82 deaths. In California, the total of cases is 260,000 with total deaths of 6,500(2), which may have changed by the time you listen to this episode (numbers were rounded up for easy listening).Also, on a positive note, last weekend we celebrated Independence Day. We hope you had a Happy 4th of July! Especially during these tumultuous times, may America continue to be “the land of the free and the home of the brave.”Welcome to Rio Bravo qWeek, the podcast of the Rio Bravo Family Medicine Residency Program, recorded weekly from Bakersfield, California, the land where growing is happening everywhere.The Rio Bravo Family Medicine Residency Program trains residents and students to prevent illnesses and bring health and hope to our community. Our mission: To Seek, Teach and Serve. Sponsored by Clinica Sierra Vista, Providing compassionate and affordable care to patients throughout Kern and Fresno counties since 1971.“All our dreams can come true, if we have the courage to pursue them.” Walt DisneyWhen you want to reach a goal, dreaming is not enough. At some point, you have to start working to make that dream come true. You may need a little dose of faith, and a big dose of action. What dreams do you have? What kind of doctor do you want to become? Your training in residency is the time to prepare to live that dream. Today we have a resident who is working to reach his goals. Dr Sin is a diligent, trustworthy resident and will participate today for the first time in this podcast. QUESTION NUMBER 1: Who are you?My name is Hasaney and I am a second-year resident at Rio Bravo Family Medicine residency program. I was born and raised in Long Beach, California, to parents who emigrated from Cambodia. I went to Long Beach Polytechnic High School, and continued my studies at UC Irvine majoring in Biological Sciences. I worked in Quality Assurance for a healthcare manufacturing company for a few years, before deciding to pursue a career in Medicine. I enrolled at Ross University School of Medicine in Dominica where I received my medical degree.I’m a pretty simple guy. I love spending time with my girlfriend, my family, and my friends. I love to go camping, especially in Mammoth, California. I love watching and rooting for the Dodgers. QUESTION NUMBER 2: What did you learn this week? I had Nephrology clinic for the first time this past Wednesday and Dr. Moreno gave some little teaching points about different syndromes we may see as family physicians, a couple of them being Bartter Syndrome and Gitelman Syndrome.Bartter SyndromeBartter syndrome is an autosomal recessive disorder associated with metabolic abnormalities: hypokalemia, metabolic alkalosis, hyperreninemia and hyperplasia of the juxtaglomerular apparatus, and hyperaldosteronism; There may also be associated hypomagnesemia. It is a fairly rare disease occurring 1 in 1,000,000, however the similar but milder Gitelman syndrome is more common with a prevalence rate of 1 to 10 in 40,000.In short, Hypokalemia, metabolic alkalosis, and hyperaldosteronism. PathophysiologyThe primary defect in both syndromes is an impairment of the sodium chloride reabsorption in the loop of Henle or distal tubule. The impaired sodium chloride reabsorption leads to volume depletion and activation of the renin-angiotensin-aldosterone system. This increased distal flow of sodium enhances potassium and hydrogen secretion at the secretory sites in the connecting tubules and collecting tubules which leads to hypokalemiaand metabolic alkalosis. Patients generally have a lower blood pressure than the general population in Bartter syndrome but normal blood pressure in Gitelman syndrome. Bartter syndrome mimics chronic ingestion of a loop diuretic, while Gitelman syndrome mimics chronic ingestion of a thiazide diuretic.Presentation and TypesClinical manifestations of Bartter syndrome, besides the metabolic abnormalities we have mentioned, are growth and mental retardation, polyuria and polydipsia. There are four types of Bartter syndrome. Types 1 and 2 are usually severe disorders that cause polyhydramnios during pregnancy and prematurity. They develop hypokalemia, metabolic alkalosis, polyuria and hypocalciuria. Nephrocalcinosis is common and probably contributes to development of kidney dysfunction, sometimes end stage renal disease. Nephrocalcinosis is the deposition of calcium salts in the renal parenchyma. Nephrocalcinosis is related to, but not the same as, kidney stones (nephrolithiasis).Bartter syndrome Type 3 is the classic form, less severe, and presents later in life with the metabolic abnormalities. Late manifestations of Bartter syndrome include proteinuria and a decline in GFR. Bartter syndrome Type 4 causes severe disease, with antenatal presentation and congenital hearing loss.  Gitelman syndromeClinical manifestations of Gitelman are similar to Bartter, except for having normal blood pressure. Patients may develop cramps of arms and legs due to the metabolic abnormalities, as well as fatigue. Hypertension may develop later in life.Both syndromes are usually a diagnosis of exclusion. Patients will present with unexplained hypokalemia, metabolic alkalosis and normal to low blood pressure. Surreptitious vomiting and diuretic use must be ruled out as these could present in a similar way. DiagnosisSurreptitious vomiting is ruled out by measuring urine chloride excretion, with Bartter and Gitelman syndrome showing a urine chloride concentration greater than 25mEq/L, whereas vomiting would show a urine chloride concentration that is less than 25 mEq/L.Suspicion of diuretic use would be ruled out with a urine diuretic screening. Plasma renin and aldosterone levels will be elevated; however, these are not required for diagnosis.TreatmentTreatment requires ad lib NaCl intake with supplements of KCl and if needed magnesium salts. Most patients will require a drug that blocks distal tubule Na-K exchange such as spironolactone. QUESTION NUMBER 3: Why is this knowledge important?As family physicians, we see the full spectrum of Medicine. If we see low blood pressure in a pediatric patient, with the metabolic abnormalities akin to these two syndromes an urgent nephrology referral should be placed. QUESTION NUMBER 4: How did you get that knowledge?Initially, some of it was taught to me by Dr. Moreno. He did not have time to go through most of the details of each syndrome in clinic, so I decided to read a little more about it on Up to Date. Some of the details on Up to Date are very thorough, so I liked to cross reference it with Pocket Pediatrics. QUESTION NUMBER 5: Where did you get that knowledge?The majority of the information were points that I thought were most important from the Up to Date article “Bartter and Gitelman syndromes”.   Speaking Medical: Nephronia by Manpreet Kaur, MS3Nephronia. It may sound like the sister planet of Neptune, but what exactly is it and when would you diagnose a patient with it? Well, on the spectrum of upper UTIs, nephronia would fall at the midpoint between acute pyelonephritis and an intrarenal abscess. It forms when a patient has an acute bacterial infection that results in a renal mass without liquefaction. We usually see this disorder in the pediatric population but there are case reports of this presentation in adults as well. While it sounds rare, it may just be an underdiagnosed disorder. However, with advancements in noninvasive imaging, this diagnosis is being made at an increasing frequency. Acute lobar nephronia (ALN) is similar to acute pyelonephritis (APN). ALN is similar to APN. A few differences are that acute lobar nephronia (ALN) is associated with a longer clinical course, longer fever duration even with treatment, and higher inflammatory markers like CRP and WBC count. A CT is the most sensitive and accurate modality of making the diagnosis but risks of exposure to radiation and possible sedation have to be weighed in small children. Some studies indicate that about 25% of children with ALN can go on to develop renal abscesses and have a higher incidence of renal scarring. Once nephronia has been diagnosed, these patients will require a minimum of 2 weeks of IV antibiotics, followed with 1 week of oral antibiotics. They will show slow improvement with fevers sometimes persisting until the end of the 1st week of treatment.Now you now the medical word of the week: Nephronia. Espanish Por Favor: OrinaOrinaisthat yellowish-colored liquid that comes out of the urethra with a characteristic smell, which in normal circumstances is sterile. Yes, you guessed it, orina is urine in Spanish. Orina can be easily turned into a verb:Orinar. Just like in English, there are several terms to refer to urine (pee, piss, pee-pee), orina can also be called meados(vulgar), orín, pis, pichi, and my favorite: pipí (pronounce pee-pee), normally used with pediatric patients. Now you know the Spanish word of this week: Orina. For your Sanity: A wet noseby Steven SaitoWhat do a puppy and a near-sighted OB doctor have in common? A wet nose.  ConclusionNow we conclude our episode number 19, “Bartter and Gitelman”. Dr Sin briefly shared the highlights of these rare syndromes. Hypokalemia and hypotension may have a long list of differential diagnoses, but keep Bartter and Gitelman on your list. Ms Kaur explained that nephronia is not a planet, but an intermediate state between pyelonephritis and a renal abscess; and we could not leave the word urine out of this renal episode, so we learned the Spanish word orina.This is the end of Rio Bravo qWeek. We say good bye from Bakersfield, a special place in the beautiful Central Valley of California, United States, a land where growing is happening everywhere.If you have any feedback about this podcast, contact us by email RBresidency@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. This podcast was created with educational purposes only. Visit your primary care physician for additional medical advice. Our podcast team for this episode is Hector Arreaza, Hasaney Sin, Manpreet Kaur, and Steven Saito, Audio edition: Suraj Amrutia. See you soon! _____________________References:Ms Moem, http://msmoem.com/2014/poetry-2/spread-your-wings/California Coronovirus Update, https://update.covid19.ca.gov/Emmett M, Ellison DH. Barrter and Gitelman syndromes. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on July 5, 2020)

Martha Sajatovic, MD, conducts a Masterclass lecture on older-age bipolar disorder from the Psychopharmacology Update in Cincinnati. The meeting was sponsored by Global Academy for Medical Education and Current Psychiatry. Dr. Sajatovic is professor of psychiatry and of neurology at Case Western Reserve University in Cleveland. She also directs the Neurological and Behavioral Outcomes Research Center at University Hospitals Cleveland Medical Center. *  *  *  Help us make this podcast better! Please take this short listener survey: https://www.surveymonkey.com/r/podcastsurveyOct2019 *  *  *  Conceptualizing OABD Older–age bipolar disorder (OABD), defined as a person aged 60 years or older with bipolar disorder, makes up one-quarter of bipolar patients. It is a heterogeneous population that includes early- and late-onset disease. Late onset is diagnosed when a person has a manic or hypomanic episode at or after the age of 50 years. Bipolar depression in later life has long been seen as a “special population,” and the treatment has been extrapolated from larger clinical trials of younger patients. Late–onset bipolar disorder usually has attenuated manic episodes and depressive episodes are prolonged and severe. In OABD, the patients are more likely to have multiple morbidities, which makes medication management more complex. People with bipolar disorder lose 1-2 decades of life, compared with the general population. No medications are specifically approved by the Food and Drug Administration for bipolar disorder or bipolar depression in older adults. However, the treatment follows general geriatric psychiatry principles: Start low and go slow.  International guidelines on treating bipolar disorder Starting low means using half or even less of the recommended dose that a clinician would use in mixed-aged populations. Titrate slowly to allow the person time to acclimate to side effects that usually resolve. Bipolar disorder is a chronic disease, so medication adherence is paramount. Adherence can be jeopardized when a person experiences excessive side effects from the beginning of treatment. First-line treatment for bipolar depression in OABD include lurasidone (Latuda) or quetiapine (Seroquel) with low dosing and slow titration. This recommendation is supported by data from a post hoc analysis of the clinical trial data of lurasidone for bipolar depression. Lithium is also recommended and underused. The level should be lower for OABD; an appropriate target for older adults with bipolar disorder is 0.4-0.8 mEq/L, especially in people who are older and frailer. Lamotrigine (Lamictal) also is helpful and fairly well tolerated. Clinicians need to be attentive to a patient’s medical comorbidities and psychosocial support to enhance adherence and improve outcomes. This approach would entail working closely with primary care clinicians and using an integrative approach as the medical comorbidities will influence the success of bipolar treatment.  References Sajatovic M and Chen P. Geriatric bipolar disorder. Psychiatr Clin North Am. 2011 Jun 3;34(2):319-33. Eyler LT et al. Understanding aging in bipolar disorder by integrating archival clinical research datasets. Am J Geriatric Psychiatry. 2019 Oct;27(10):1122-34. Shulman Kl et al. Delphi survey about using lithium in OABD. Bipolar Disord. 2019 Mar;21(2):117-23. Forester BP. Safety and effectiveness of long-term treatment with lurasidone in older adults with bipolar depression: Post hoc analysis of a 6-month, open-label study. Am J Geriatr Psychiatry. 2018 Feb;26(2):150-9. *  *  *  For more MDedge Podcasts, go to mdedge.com/podcasts Email the show: podcasts@mdedge.com Interact with us on Twitter: @MDedgePsych    

Hyperkalemia Intro Potassium is primarily an intracellular ion responsible for maintenance of the resting membrane potential for normal cell conduction. Serum measured potassium is typically between 3.5 and 5.0 mEq/L. Serum K greater than 5.0 mEq/L is generally considered the threshold for hyperkalemia. Potassium is mostly excreted via the kidneys, and the "classic" hyperkalemia patient is one who has missed several dialysis appointments complaining of paralysis or diffuse weakness. Causes of HyperK Most commonly, renal failure.  Transcelluar shift  DKA Acidosis  Other acid-base disturbances Medications  RAAS or ACE inhibitors Effects of HyperK  Most drastically affect cardiac myocytes  Conduction between myocytes is depressed, leading to slower conduction and widened QRS complexes, however, the rate of repolarization is increased.  Leads to ominous “sine wave” pattern on ECG.  Arrythmogenic  May produce classic tall, “peaked” T waves on ECG. Stepwise ECG changes in hyperkalemia: 5.5-6.5 mEq/L - Peaked T Waves 6.5-7.5 mEq/L - P waves amplitude becomes smaller and PR intervals prolong 7.5-8.0 mEq/L - QRS becomes wide ECGs are not always sensitive for hyperkalemia. Patients may have a critical K with no changes on the ECG.  Skeletal muscle tissue is also sensitive to hyperkalemia, and patients may present with weakness or paralysis as a result.  Nondescript symptoms such as muscle cramps, diarrhea, vomiting, nausea, and focal paralysis may also be present - but are also not reliable findings.  Management  Prioritized by a strategy of: Stabilization of cardiac cell membranes  Shifting potassium back into the cells  Eliminating potassium Calcium (Chloride or gluconate) administered to stabilize cell membranes  Stabilizing effect is transient and relatively short lived  Calcium Chloride contains roughly 3 times the amount of elemental calcium as compared to Ca gluconate, but is associated with severe complications if extravasation occurs.  Effects (narrowing of QRS complex, return of more hemodynamic stability) occurs within minutes  Calcium Chloride - generally, 1 gram is administered over 3 minutes. Calcium Gluconate - 1 gram over 2-3 minutes  Repeat either q5min Albuterol / Beta 2 agonists These act on beta 2 receptors to assist in moving potassium back into the intracellular space  Albuterol - 10-20mg (inhalation), with most effect noted in 30 minutes  IV Insulin  Drives K back into the cells (shift) Generally administered with dextrose unless the patient’s BGL is below 250mg/dL 10 units IVP followed by 25G dextrose Incidence of hypoglycemia is high, and this therapy should be administered cautiously Dialysis  Treating reversible cause d/c RASS or ACE inhibiting medicaitions  Volume administration

We have coach, author, five time Kona qualifier, 15 Ironman finisher, podcaster, Debbie Potts with us today. We are going to be discussing two of her books, Life is Not A Race It's a Journey and The Wholeistic Method Manual and Workbook. Today's show is supported by iKOR Labs. iKOR is a clean, natural source of recovery enhancing CBD hemp extract that protects your body from the stresses of training, improves recovery from intense efforts and helps you maintain a positive mental state. The most bio-available CBD product on the market, iKOR is a highly protective anti-oxidant and effective anti-inflammatory. WADA and USADA legal. Used by world class professional athletes. Save 20% by using the code "endurance" at checkout. Go to www.ikorlabs.com for more details. Thanks to last week's guests pro triathlete Meredith Kessler joining us today to talk about a number of topics. We are talking Kona, IMAZ, being an triathlete mom, but the main thing we are talking about today is the Outspoken: Women In Triathlon Summit. If you missed that interview, go back to episode #157 and check it out. Our interview is sponsored by Riplaces. Riplaces are the no tie laces with custom tension for the perfect fit. Pro triathlete proven and endorsed, most durable elastic bungee lace system available and they come in the MHE logo package. The regular price for the custom set is $19.98. For a limited time, through the end of the year Riplaces is going to offer a 25% discount. Just use the code MHE25 to get that 25% discount. Go to https://www.riplaces.com/collections/mile-high-endurance for more information. Debbie Potts has been in the fitness industry for over twenty-five years and a competitive endurance athlete for twenty years. Along her journey, she has accomplished many goals including being nominated as one of the top one hundred best trainers in the U.S. by Men's Journal in 2004 and 2005 as well as participating in fifteen Ironman Triathlons - five of them were the Hawaii World Ironman Championship. Debbie has owned and operated her own fitness studio in Bellevue Washington since 2010 to offer an "all in one" fitness studio - now including The WHOLESTIC Method Nutritional Therapy program to transform the WHOLE person from the inside out. Let's get into the interview now with Debbie Potts.   Our post interview discussion is sponsored by Halo Neuroscience. The Halo Sport from Halo Neuroscience will help you learn the technique and form to get faster. 20 minutes of neural priming with the Halo Headset gives you an hour of neural plasticity to work and lock in the muscle movement that leads to strength, power and endurance. Use code MHE150 to save $150.   Topics: Triathlon Trivia on Adrenal Dysfunction and Fatigue Which of the following are terms is NOT used to refer to problems with the adrenal gland Adrenal dysfunction Adrenal insufficiency Addison's disease Hypoadrenia - Adrenal fatigue is a pseudoscientific diagnosis believed in alternative medicine to be the state when adrenal glands are exhausted and unable to produce adequate quantities of hormones, primarily the glucocorticoid cortisol, due to chronic stress or infections. Hyponatremia - As a result of low sodium, the amount of water in your body rises and causes your cells to swell. ... Your blood sodium level is normal if it’s 135 to 145 milliequivalents per liter (mEq/L)   Which of the following is NOT a common cause of Adrenal fatigue include (from Bulletproof) Poor diet Lack of sleep Working too hard Emotional trauma Physical trauma Lack of exercise Too much exercise Mold exposure   Which of the following is NOT a sign of adrenal dysfunction (from Mayo Clinic) Fatigue Body aches Unexplained weigh loss High blood pressure Low blood pressure Light Headedness Loss of body hair Skin discoloration News 70 Year Old Sets World AG record for Marathon New Years Resolutions Colin O'Brady - 33 years old, 54 days, 930 miles across Antarctica; with Louis Rudd; 400 pound sled; 7000 calories per day Read 12 books 52 weeks of strength training Something epic and new YouTube Video of the Week is sponsored by Rudy Project. Rudy Project has the helmets, glasses and gear to help you ride safe and look great. Use code MHE30 to get 30% off your full price items. YouTube Video of the Week Global Triathlon Network - New Years Resolutions from Pro Triathletes for 2018 Linsey Corbin Lionel Sanders Fredrick Van Lierde Tim Reed Matt Russell   Colin O'Brady - Colin O'Brady defies the 'impossible' with first-ever solo trek across Antarctica   Upcoming Interviews: Scott Fliegelman of Solos Wearables Bob Seebohar on metabolic efficiency and Birota Foods Our show is also supported by 303 Endurance Network, which includes 303Triathlon and 303 Cycling, which covers the endurance culture, news and events on triathlon and cycling. Be sure to subscribe to the 303Radio podcast and follow 303Triathlon's Facebook, Twitter and Instagram. Please support our affiliate brands that support the show and help you get faster! All of these discounts can be found at milehighendurance on the Discounts page. Be sure to follow us on social media to get the show announcement each weekend, plus additional links to show content. We forward information related to our guests and provide teasers for upcoming interviews. We are posting regular videos to the YouTube. Be sure to subscribe to the channel. Facebook @milehighendurance Twitter @milehighpodcast Instagram @tripodcasterrich YouTube Channel @Mile High Endurance We hope you enjoyed today's show. Please rate us on iTunes or your podcast player. Be sure you are subscribed in iTunes so you get the show automatically downloaded on Saturday evening and recommend Mile High Endurance to a friend. Happy New Years, everyone! Stay tuned, train informed, and enjoy the endurance journey!      

Here is a summary of this episode: Geriatric Psychopharmacology Today’s topic is geriatric psychopharmacology. Do one thing at a time. Start low and go slow with medication titration and avoid PRN prescribing. Avoid medications on the Beers list like antihistamines, anticholinergics, and tricyclic antidepressants. In patients with diabetes or those prone to orthostasis, consider ziprasidone or aripiprazole. For glaucoma, consider aripiprazole, risperidone, and quetiapine. For those with Parkinson’s disease, consider low-dose quetiapine or clozapine. The syndrome of inappropriate ADH occurs with SSRI use and is not dose-dependent. Check the serum sodium before the drug is started and at weeks one and two after treatment begins. Lithium is a first line drug for the treatment of acute mania in geriatrics. It is advised to dose it once at night with an immediate acting formulation. Keep serum levels at 0.4 to 0.8 mEq/L.   Download a PDF of this interview here Become a premium member of the Psychopharmacology Institute 

The Free Open Access Medical Education (FOAM)  We cover a post from Dr. Josh Farkas on PULMcrit on lithium toxicity. The key message from the post is: a single serum lithium level doesn't necessitate dialysis, despite a recommendation from the EXTRIP working group  to initiate dialysis in patients with a lithium level > 5 mEq/L [1].  Dr. Farkas advocates for aggressive management in asymptomatic patients with chronic lithium toxicity and patients without impaired renal function. Core Content We review rhabdomyolysis using Rosen's Emergency Medicine (8e)  Chapter 160 and Tintinalli's Emergency Medicine (8e), Chapter 181.   Show notes at FOAMcast.org Thanks for listening! Jeremy Faust & Lauren Westafer

Pediatric airway management is a skill that integrates the three types of knowledge as described by the ancient Greeks: episteme, or theoretical knowledge, techne, or technical knowledge, and phronesis, or practical wisdom, also called prudence. Here we’ll invoke each type of knowledge and understanding as we go beyond the anatomical issues in pediatric airway management – to the advanced decision-making aspect of RSI and the what-to-do-when the rubber-hits-the road. Case 1: Sepsis Laura is a 2-month-old baby girl born at 32 weeks gestational age who today has been “breathing fast” per mother.  On arrival she is in severe respiratory distress with nasal flaring and intercostal retractions.   Her heart rate is 160, RR 50, oxygen saturation is 88% on RA.  She has fine tissue-paper like rales throughout her lung fields.  Despite a trial of a bronchodilator, supplemental oxygen, even nasal CPAP and fluids, she becomes less responsive and her heart rate begins to drop relatively in the 80s to 90s – this is not a sign of improvement, but of impending cardiovascular collapse. She is in respiratory failure from bronchiolitis and likely viral sepsis.  She needs her airway taken over. Is this child stable enough for intubation? We have a few minutes to optimize, to resuscitate before we intubate. Here’s an easy tip: use the sterile flushes in your IV cart and push in 20, 40, or 60 mL/kg NS.  Just keep track of the number of syringes you use – it is the fastest way to get a meaningful bolus in a small child. Alternatively, if you put a 3-way stop-cock in the IV line and attach a 30 mL syringe, you can turn the stop cock, draw up stream from the IV bag into the syringe, turn te stop cock, and push the fluid in the IV. Induction Agent in Sepsis The consensus recommendation for the induction agent of choice for sepsis in children is ketamine. Etomidate is perfectly acceptable, but ketamine is actually a superior drug to etomidate in the rapid sequence intubation of children in septic shock.  It rapidly provides sedation and analgesia, and supports hemodynamic stability by blocking the reuptake of catecholamines. Paralytic Agent in Sepsis The succinylcholine versus rocuronium debate… Succinylcholine and its PROS 82% of RSI in the ED used succinylcholine (According to the National Emergency Airway Registry, in 2005).  We know it, we are comfortable with it. Succinylcholine produces superior intubating conditions when comparing 1 mg/kg succinylcholine versus 0.6 mg/kg rocuronium, succinylcholine is that at 45 seconds. Succinylcholine and its CONs Raises serum potassium in everyone, typically 0.5 to 1 mEq/L.  That is not usually a problem, but for those with preexisting or inducible hyperkalemia, it can precipitate an arrest, as in renal failure, underlying neurologic or myopathic conditions like multiple sclerosis, muscular dystrophy, ALS, or those who had a stroke or a burn more than 72 hours prior. We often have limited information in critical situations. Succinylcholine gives us a false sense of security.  In children, there really is no “safe apnea” period. Succinylcholine’s effect on the nicotinic receptors results in mydriasis, tachycardia, weakness, twitching and hypertension, and fasciculations (Think nicotine overdose: M/T/W/Th/F). Succinylcholine’s effect on muscarinic receptors manifest (as in organophosphate overdose): SLUDGE – salivation, lacrimation, urination, defecation, GI upset or more apropos here: DUMBBELLS – diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation. Second dose of succinylcholine – beware of the muscarinic effects and bradycardia. Co-administer atropine, 0.01 mg/kg, up to 0.5 mg IV. Coda: succinylcholine is not that bad – we would not have had such great success with it during the early years of our specialty if it were such a terrible drug.  The side effects are rare, but they can be deadly.  So, what’s the alternative? Rocuronium and its PROs It has none of the side-effects of succinylcholine Rocuronium and its CONs Argument 1: the duration is too long if there is a difficult airway, since rocuronium can last over an hour. Still need to intubate, and now your patient is potentially worse. Argument 2: succinylcholine produces better intubating conditions at 45 seconds compared to rocuronium. At 0.6 mg/kg, rocuronium is inferior to succinylcholine at all time intervals. At 1.0 mg/kg, rocuronium is still inferior at 45 seconds.  At 1.2 mg/kg rocuronium – the dose now commonly recommended – there was no difference in intubating conditions, per a study by Heier et al. in Anethesia and Analgesia in 2000. Case 2: Multitrauma Joseph is a 3-year-old boy who is excited that there are so many guests at his house for a family party and when it’s starting to wind down and the guests begin to leave, he is unaccounted for. An unsuspecting driver of a mini-van backs over him. He is brought in by paramedics, who are now bagging him. Induction Agent in Trauma Need something that is hemodynamically stable – agents such as midazolam or propofol would cause too many problems. Etomidate is a short-acting imidazole derivative that acts on GABA-A receptors to induce loss of consciousness in 5-15 seconds. It can cause apnea, pain on injection, and myoclonus. Etomidate reduces cerebral blood flow, reduces intracranial pressure, and reduces cerebral oxygen consumption, all while maintaining arterial blood pressure and cerebral perfusion pressure. Ketamine is reasonable as well: there is no contraindication to ketamine except for known hydrocephalus. It is safe in head trauma. It is a good choice for the hypotensive trauma patient.  TBI is not a contraindication. In the case of the critically injured child who is normotensive, ketamine will raise his blood pressure and perhaps foster further bleeding.  The goal is a good general perfusion and a balanced resuscitation, ensuring enough cerebral perfusion without disrupting nascent clots.  On the other side of the spectrum, permissive hypotension is not described in children, as hypotension is a late and dangerous sign of shock. Paralytic Agent in Trauma Are your surgeons in an uproar about a long-acting agent and the pupillary response?  Relax, it’s a myth. Caro et al in Annals in 2011 reported that the majority of patients undergoing RSI preserved their pupillary response.  Succinylcholine actually performed worse than rocuronium. In the rocuronium group, all patients preserved their pupillary response. In the critically ill, we rethink your dosing of both the sedative and the paralytic. In a critically ill child or adult, perfusion suffers and it affects how we administer medications.  The patient’s arm-brain time or vein-to-brain time is less efficient; additionally, as the patient’s hemodynamic status softens, he becomes very sensitive to the effects of sedatives. We need to adjust our dosing for a critically ill patient: Decrease the sedative to avoid falling over the hemodynamic compensation cliff. Increase the paralytic to account for prolonged arm-brain time. Case 3: Cardiac/myocarditis/congenital heart disease Jacob is a 6-year-old-boy with tricuspid atresia s/p Fontan procedure who’s had one week of runny nose, cough, and now 2 days of high fever, vomiting, and difficulty breathing. The Fontan procedure is the last in a series of three palliative procedures in a child with complex cyanotic congenital heart disease with a single-ventricle physiology. The procedure reroutes venous blood to flow passively into the pulmonary arteries, because the right ventricle has been surgically repurposed to be the systemic pump.  The other most common defect with an indication for a Fontan is hypoplastic left heart syndrome. Typical “normal” saturations are 75 and 85% on RA.  Ask the parents or caregiver. Complications of the Fontan procedure include heart failure, superior vena cava syndrome, and hypercoagulable state, and others. A patient with a Fontan can present in cardiogenic shock from heart failure, distributive shock from an increased risk of infection, hypovolemic shock from over-diuresis or insensible fluid loss – or just a functional hypovolemia from the fact that his venous return is all passive – and finally obstructive shock due to a pulmonary thromboembolism. Types of shock mnemonic: this is how people COHDe – Cardiogenic, Obstructive, Hypovolemic, Distributive. Do we give fluids? Children after palliative surgery for cyanotic heart disease are volume-dependent.  Even if there is a component of cardiogenic shock, they need volume to drive their circuit.  Give a test dose of 10 mL/kg NS. Pressors in Pediatric Shock Children compensate their shock state early by increasing their SVR. Epinephrine (adrenaline) is great at increasing the cardiac output (with minimal increase in systemic vascular resistance; tachycardia)  In children the cardiac deleterious effects are not pronounced as in adults.  Later when the child is stabilized, other medication such as milrinone (ionotrope and venodilator) can be used. Epinephrine is also fantastic for cold shock when the patient is clamped down with cold extremities – the most common presentation in pediatric septic shock. Norepinephrine (noradrenaline) is best used when you need to augment systemic vascular resistance, such as in warm shock, where the patient has loss of peripheral vascular tone. Induction Agent in Cardiogenic Shock A blue baby – with a R –> L shunt – needs some pinking up with ketamine A pink baby – with a L –> R shunt – is already doing ok – don’t rock the boat – give a neutral agent like etomidate. Myocarditis or other acquired causes of cardiogenic shock – etomidate. Case 4: Status Epilepticus Jessica is a 10-year-old girl with Lennox-Gastaut syndrome who arrives to your ED in status epilepticus. She had been reasonably controlled on valproic acid, clonazepam, and a ketogenic diet, but yesterday she went to a birthday party, got into some cake, and has had stomach aches – she’s been refusing to take her medications today. On arrival, she is hypoventilating, with HR 130s, BP 140/70, SPO2 92% on face mask. She now becomes apneic. Induction Agent in Status Epilepticus Many choices, but we can use the properties of a given agent to our advantage. She is normo-to-hypertensive and tachycardic. She has been vomiting. A nice choice here would be propofol. Propofol as both a sedative and anti-epileptic agent works primarily on GABA-A and endocannabinoid receptors to provide a brief, but deep hypnotic sedation.  Side effects can include hypotension, which is often transient and resolves without treatment.  Apnea is the most common side-effect. Ketamine would be another good choice here, for its anti-epileptic activity. Paralytic Agent in Status Epilepticus Rocuronium (in general), as there are concerns of a neurologic comorbidity. Housekeeping in RSI What size catheter doe I use?  If you know your ETT size, then it is just a matter of multiplication by 2, 3, 4, or 5. Remember this: 2, 3, 4 – Tube, Tape, Tap The NG/OG/Foley is 2 x the ETT – tube The ETT should be taped at a depth of 3 x the ETT size – tape A chest tube size 4 x the ETT – tap In summary, in these cases of sepsis, multitrauma, cardiogenic shock, and status epilepticus: Resuscitate before you intubate Use the agent’s specific properties and talents to your benefit Adjust the dose in critically ill patients: decrease the sedative, increase the paralytic Have post-intubation care ready: sedation, verification, NG/OG/foley

Introduction Metabolic acidosis during hemorrhagic shock is common and conventionally considered to be due to hyperlactatemia. There is increasing awareness, however, that other nonlactate, unmeasured anions contribute to this type of acidosis. Methods Eleven anesthetized dogs were hemorrhaged to a mean arterial pressure of 45 mm Hg and were kept at this level until a metabolic oxygen debt of 120 mLO(2)/kg body weight had evolved. Blood pH, partial pressure of carbon dioxide, and concentrations of sodium, potassium, magnesium, calcium, chloride, lactate, albumin, and phosphate were measured at baseline, in shock, and during 3 hours post-therapy. Strong ion difference and the amount of weak plasma acid were calculated. To detect the presence of unmeasured anions, anion gap and strong ion gap were determined. Capillary electrophoresis was used to identify potential contributors to unmeasured anions. Results During induction of shock, pH decreased significantly from 7.41 to 7.19. The transient increase in lactate concentration from 1.5 to 5.5 mEq/L during shock was not sufficient to explain the transient increases in anion gap (+ 11.0 mEq/L) and strong ion gap (+ 7.1 mEq/L), suggesting that substantial amounts of unmeasured anions must have been generated. Capillary electrophoresis revealed increases in serum concentration of acetate (2.2 mEq/L), citrate (2.2 mEq/L), alpha-ketoglutarate (35.3 mu Eq/L), fumarate (6.2 mu Eq/L), sulfate (0.1 mEq/L), and urate (55.9 mu Eq/L) after shock induction. Conclusion Large amounts of unmeasured anions were generated after hemorrhage in this highly standardized model of hemorrhagic shock. Capillary electrophoresis suggested that the hitherto unmeasured anions citrate and acetate, but not sulfate, contributed significantly to the changes in strong ion gap associated with induction of shock.