CD DR. CHINTAN DAVE CLINICAL EP 23

@drchintandave

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The content provides valuable, actionable medical information in a clear, concise, and visually engaging format, addressing a complex topic with a logical progression of information.

Summary

This slideshow presents a case challenge about a patient with bradycardia and a wide complex rhythm, ultimately diagnosed as hyperkalemic pseudo-VT. It details the physiology behind the condition, the key treatment principle of administering calcium, and common mistakes to avoid.

Structure

1Case presentation: bradycardia and wide complex rhythm
2Diagnosis: Hyperkalemic pseudo-VT
3Key principle: Calcium before anything else
4Physiology: The gap that makes a cell fire
5Treatment sequence and common errors
6Take-home message: Measure potassium before shocking

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Starting to systematically answers to my older case challenges. So make sure you are following along! Four things that didn’t fit on the slides but change what you do at the bedside: 1. Stop waiting on the central lab. A VBG or i-STAT returns a whole-blood K⁺ in 60–90 seconds; the send-out takes much longer. In a dialysis patient with a wide complex, that gap is the entire case. Know that whole-blood K⁺ runs slightly lower than serum (no clot-related platelet release), so a POC value of 7 is not reassurance — it’s an underestimate. 2. Pseudohyperkalemia is real and it is not a reason to pause. Hemolysis, tourniquet fist-clenching, extreme leukocytosis or thrombocytosis all falsely elevate the number. But when the story fits and the ECG fits, treat first and redraw simultaneously. Nobody has ever been harmed by 3g of calcium gluconate they didn’t strictly need. The reverse is not true. 3. Hypertonic saline is the forgotten rescue. In refractory hyperkalemic conduction failure — QRS still wide after repeated calcium — 3% NaCl improves conduction by increasing the driving force for the sodium current, independent of the potassium level. Highest yield if the patient is also hyponatremic. Underused, and it works. 4. If a dialysis patient arrests, give calcium empirically. Don’t wait for a potassium. Undifferentiated arrest + ESRD = hyperkalemia until proven otherwise. And extend your resuscitation — hyperkalemic arrests have documented neurologically intact survival after prolonged CPR once the potassium comes down. This is one of the arrests worth being stubborn about, and one of the few where ECMO/ECPR has a genuinely reversible target. #criticalcare #internalmedicine #icu #meded #doctor

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CD DR. CHINTAN DAVE CLINICAL EP 23 BEDSIDE PHYSIOLOGY CASE CHALLENGE - 58M, MISSED DIALYSIS Do you shock it? He arrived bradycardic at 30 bpm and the ER started dopamine. Then he went into a wide complex rhythm at 140pm. He is talking to you. HR 30 -> 140 QRS 168 ms BP 124/70 K+ 8.1 @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE BEFORE YOU NAME IT This rhythm has a history ARRIVAL Bradycardic at 30 bpm NOW Regular, wide, 140-160pm INTERVENTION Dopamine started CLINICAL Patient mentating throughout CURRENT RHYTHM Last dialysis five days ago. K+ 8.1, HCO3 16, creatinine 9.8. He is awake and answering questions. CD DR. CHINTAN DAVE ANSWER Hyperkalemic pseudo-VT A conduction failure amplified by a chronotrope — not ventricular tachycardia. 01 It began as bradycardia at 30 bpm; VT does not announce itself slow 02 No P waves, capture/fusion beats, and no AV dissociation to find 03 Dopamine on board 04 The QRS is melted, not blocked 05 K+ 8.1, five days without dialysis @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE KEY PRINCIPLE Calcium, before anything else The endpoint is the QRS on the monitor, not a repeat potassium. 3g 1g q5 Calcium gluconate 10%, 30 mL over 2-3 min A peripheral line is fine. This is the default agent. Calcium chloride 10%, 10 mL over 5 min Three times the elemental calcium — central access. Repeat every five minutes until the QRS narrows Onset 1-3 min. One dose lasts 30-60 minutes. Do not defibrillate. Do not pace. No amiodarone, procainamide or adenosine. Digoxin is not a reason to withhold calcium. @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE THE PHYSIOLOGY The gap that makes a cell fire REST -90 REST -65 THRESHOLD -70 Normal gradient: 140 mEq/L inside the cell, 4 outside. At K+ 8.1 the gradient flattens. Sodium channels sit inactivated and phase 0 slows. The gap that makes the cell excitable has closed. Calcium does not lower the potassium. It raises threshold away from rest — the gap reopens and the QRS narrows. @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE WHAT THAT DOES TO CONDUCTION Think twice before shocking Conduction velocity is biphasic. Below ~8 mmol/L cells reach threshold sooner and conduct faster, above it, inactivated Na+ channels slow conduction to failure. Premature beats fail first. Na+ channels recover from inactivation slowly, so an extrasystole blocks locally — the reentry substrate. The atrium goes silent before the sinus node. Nodal phase 0 is calcium-driven, so sinus impulses still arrive — without a P wave. Escape pacemakers are suppressed too. Shock this heart and nothing takes over. @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE WHAT THE ECG IS WORTH A normal ECG never rules it out 5.5-6.5 6.5-7.5 7.0-8.0 > 8.0 TERMINAL Peaked, narrow-based T waves PR prolongs, then P waves vanish QRS widens, bizarre axis, sinoventricular Sine wave — the QRS merges into the T Ventricular fibrillation, asystole Those thresholds are unreliable. Physicians reading ECGs from dialysis patients detected hyperkalemia with a sensitivity of 0.19-0.29 when the potassium was 6.5 or above. Chronic dialysis patients adapt and can look ordinary at 7. @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE THE SYNDROME NEXT DOOR BRASH is a loop, not a checklist B BRADY- CARDIA R RENAL FAILURE A AV NODE BLOCK S SHOCK H HYPER- KALEMIA Hyperkalemia and an AV nodal blocker suppress the node synergistically. Each component looks too mild to explain the picture - K+ 6.0 should not cause a rate of 35, and neither should therapeutic metoprolol. Together they do. Treat the loop, not the labs: calcium, perfusion, shift, dialysis. Isoproterenol or epinephrine over atropine — the block is nodal, not vagal. Pacing often fails to capture. This patient has R and H only — no AV nodal blocker, no shock. Not BRASH. Ask anyway: metoprolol, diltiazem, digoxin, ACEI, spironolactone, TMP-SMX, or NSAIDs ingestion? @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE HYPERKALEMIA TREATMENT The whole sequence 01 Calcium first. Repeat every five minutes until the QRS narrows. 02 Call nephrology now. Mobilising dialysis could take up to 30-45 mins; a dose of calcium lasts 30-60. 03 Stop the dopamine. 04 Insulin 0.1 U/kg with dextrose, can also give flat 10 units. Check glucose out to four hours. 05 Albuterol 10-20 mg nebulised, eight times the usual dose. Additive with insulin, never monotherapy. 06 Hemodialysis — the only definitive step. Low-potassium bath. Will correct very quickly! Skip loop diuretics if anuric, and bicarbonate without acidosis. Never run calcium through a bicarbonate line — it precipitates. @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE HOW TEAMS GET THIS WRONG Four ways to lose this patient The bradycardia was read as a rate problem, so it was treated with a rate drug. Dopamine did not restore conduction. It drove a diseased substrate faster and shortened the runway. Shock it and you get asystole. You cannot reset a myocardium with no available sodium channels. Insulin and albuterol relocate potassium; they do not remove it. Expect rebound at 4-6 hours. Recheck at 1, 2 and 4 hours on telemetry. Never sign this patient out as resolved after one run. @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE EVIDENCE Where this comes from 01 Farkas JD, Long B, Koyfman A, Menson K. BRASH syndrome. Journal of Emergency Medicine. 2020. 02 Palmer BF, Carrero JJ, Clegg DJ, et al. Clinical management of hyperkalemia. Mayo Clinic Proceedings. 2021. 03 Can physicians detect hyperkalemia based on the electrocardiogram? American Journal of Emergency Medicine. 2019. 04 Moussavi K, Garcia J, Tellez-Corrales E, Fitter S. Reduced alternative insulin dosing in hyperkalemia. Pharmacotherapy. 2021. 05 Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity. Journal of Emergency Medicine. 2011. 06 Weiss JN, et al. Electrophysiology of hypokalemia and hyperkalemia. Circulation: Arrhythmia and Electrophysiology. 2017. @DRCHINTANDAVE SWIPE → CD DR. CHINTAN DAVE TAKE-HOME Before you shock, measure the potassium. Hyperkalemia decouples how a patient looks from how close he is to arrest. SAVE THIS SHARE WITH YOUR TEAM FOLLOW @DRCHINTANDAVE BEDSIDE PHYSIOLOGY EP 23 EDUCATIONAL ONLY, NOT MEDICAL ADVICE @DRCHINTANDAVE