An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
Endocarditis
Endocarditis can quietly destroy valves, seed the brain and spine, and produce septic shock or heart failure. The crucial errors are delaying cultures and antibiotics—or treating the infection while missing a mechanical complication requiring urgent surgery.
A 34-year-old man sits forward on the stretcher, shivering beneath a thin blanket while sweat darkens the collar of his shirt. His fingertips are stained with nicotine, and he says the fever has “come and gone” for nearly three weeks; today, walking across the room left him breathless. A new blowing sound fills the left sternal border, but the blood pressure cuff has not yet finished cycling. The question is whether this is a prolonged viral illness—or the beginning of a catastrophe that will travel through his heart and bloodstream.
— What’s your move? Read on.
Before you read
When should antibiotics begin relative to blood cultures?
Which complications demand surgery rather than antibiotics alone?
When to Think of It
Enter endocarditis into the differential with persistent fever plus a new or changing murmur, prosthetic valve, prior endocarditis, injection drug use, indwelling vascular hardware, hemodialysis, congenital heart disease, or recent bacteremia. Also consider it with unexplained embolic stroke, vertebral pain, pulmonary septic emboli, glomerulonephritis, splenic infarct, or culture-negative sepsis.
Sick or Not Sick
Sick vs. not sick: Is there shock, acute pulmonary edema, altered mental status, persistent hypoxemia, or rapidly progressive valve dysfunction? The call that matters most is whether the patient needs immediate resuscitation and emergency cardiothoracic/infectious-disease involvement while cultures are obtained.
The First Fifteen Minutes
Place the patient on a monitor, obtain two large-bore IVs, check glucose, lactate, CBC/CMP, coagulation studies, urinalysis, ECG, and bedside ultrasound for ventricular function, pulmonary edema, and gross valve pathology.
Draw three sets of blood cultures from separate venipuncture sites before antibiotics, if this will not meaningfully delay treatment. In shock, obtain cultures rapidly and treat immediately.
Shock or high suspicion after cultures → vancomycin 20–25 mg/kg IV loading dose, infused according to institutional protocol, because it rapidly covers resistant gram-positive organisms; subsequent dosing requires renal function and pharmacy-guided AUC monitoring. Dose varies by weight, renal function, and local protocol—check Lexicomp, UpToDate, or institutional guidance.
Healthcare-associated infection, prosthetic material, or septic shock → cefepime 2 g IV, because it adds broad gram-negative and antipseudomonal coverage; adjust for renal function. For suspected prosthetic-valve infection, the definitive empiric regimen should be selected with infectious disease and local protocol.
Septic shock with MAP <65 after appropriate crystalloid → norepinephrine 0.05–0.1 mcg/kg/min IV infusion, titrated, because α-adrenergic vasoconstriction restores perfusion pressure while limiting tachyarrhythmia; use a proximal peripheral IV briefly if central access is not yet available.
Sepsis-induced hypoperfusion or hypotension → balanced crystalloid 30 mL/kg IV, reassessing after each bolus for pulmonary edema and ventricular failure; fluid expands preload, but excessive volume worsens acute regurgitant failure.
Acute pulmonary edema with adequate blood pressure → nitroglycerin 0.4 mg SL every 5 minutes for up to 3 doses, because venodilation lowers filling pressures; avoid if hypotensive, right-ventricular infarction is suspected, or recent PDE-5 inhibitor use.
Do not give empiric anticoagulation simply for embolic risk; intracranial hemorrhage, mycotic aneurysm, and septic embolic stroke may make it dangerous.
Definitive Care & Disposition
Admit suspected endocarditis with IV antibiotics, serial cultures, and transthoracic echocardiography; obtain transesophageal echocardiography if TTE is negative or inadequate and suspicion remains high, or with prosthetic valves, intracardiac devices, or persistent bacteremia. Tailor therapy to cultures and susceptibility testing, typically for 4–6 weeks. Urgent surgery is considered for heart failure from valve dysfunction, uncontrolled infection/abscess or prosthetic dehiscence, persistent bacteremia, fungal or highly resistant infection, and selected large mobile vegetations with recurrent emboli. ICU care is appropriate for shock, respiratory failure, acute valve regurgitation, major embolic complications, or invasive monitoring needs.
How This One Kills
The lethal miss is calling the murmur “sepsis-related” while acute valve destruction causes pulmonary edema and cardiogenic shock; more fluid and delayed echocardiography can worsen the patient instead of fixing the obstruction or regurgitation.
The Differential — What Else Looks Like This
Community-acquired pneumonia — focal infiltrate and respiratory symptoms without persistent bacteremia or embolic phenomena; confusing them can delay echocardiography and prolonged therapy.
Systemic lupus erythematosus/nonbacterial thrombotic endocarditis — sterile cultures and autoimmune or malignancy clues; antibiotics alone will not treat the underlying process.
Atrial myxoma — positional symptoms and constitutional illness with an intracardiac mass; mistaking it for vegetation delays surgical evaluation.
Septic thrombophlebitis — bacteremia with a demonstrable infected venous focus but no valve vegetation; treating only as endocarditis can miss necessary source control.
The Second-Day Story
Older adults may have no fever, presenting with delirium, weakness, weight loss, anemia, or new heart failure. Prior antibiotics may sterilize cultures, and prosthetic valves may obscure murmurs while creating perivalvular abscesses or conduction abnormalities. Persistently unexplained inflammation, embolic findings, new AV block, or recurrent bacteremia should keep the diagnosis alive and prompt TEE and infectious-disease consultation.
Back to Our Patient
Back to our 34-year-old man: persistent fever, a new murmur, dyspnea, and likely injection-drug exposure make endocarditis a high-priority diagnosis, while the blood-pressure trend and lung examination determine whether he is sick. Three blood-culture sets are drawn immediately, bedside ultrasound assesses ventricular function and pulmonary edema, and because he is hypotensive with suspected severe infection, empiric vancomycin plus cefepime is started without waiting for results; norepinephrine follows if pressure remains low after cautious crystalloid. Echocardiography is expedited, with TEE if TTE is nondiagnostic, and cardiology, infectious disease, and cardiothoracic surgery are contacted for possible acute valve destruction. He is admitted to the ICU for suspected complicated endocarditis and evolving shock.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 34-year-old man with three weeks of intermittent fever and new exertional dyspnea, now hypotensive and rigoring in the ED. He reports prior injection drug use and has no known immunosuppression or recent respiratory illness; he denies chest pain but has mild pleuritic discomfort. Exam shows a new blowing holosystolic murmur, tachycardia, cool extremities, and bibasilar crackles without focal neurologic deficit. Lactate is elevated, and bedside ultrasound suggests reduced LV function with possible mitral regurgitation. My assessment is suspected complicated infective endocarditis with early septic and possibly cardiogenic shock. We are drawing three blood-culture sets, starting empiric IV vancomycin and cefepime, using cautious crystalloid and norepinephrine as needed, obtaining urgent echocardiography, and admitting him to the ICU with infectious disease and cardiothoracic surgery consultation.”
Study Directive
From memory, list the major risk factors, Duke diagnostic elements, and surgical indications for infective endocarditis.
Practice interpreting three blood-culture collection sites and decide when TTE must be followed by TEE.
Draw a one-page algorithm for fever plus murmur: cultures, empiric coverage, shock treatment, echo, and disposition.
Review local antibiogram-based empiric regimens and verify vancomycin dosing/monitoring in Lexicomp or your institutional protocol.
Li M, Kim JB, Sastry BKS, et al. · Lancet, 2024 · PMID 39067905 · cited 140×
A current, authoritative overview of infective endocarditis covering diagnostic blood-culture and echocardiography strategies, antimicrobial treatment, and recognition of complications requiring urgent surgical consultation.
More in Today's Issue
1 additional topic
2 of 2
What REALLY Works in Cardiac Arrest
Cardiac arrest is won by high-quality, uninterrupted CPR, early defibrillation when indicated, and rapid treatment of reversible causes—not by accumulating...
A 58-year-old woman collapses beside a grocery-store freezer, her shopping bag split open across the floor as a bystander begins compressions. The first monitor image is a coarse, chaotic waveform; her skin is gray, and the bag-valve mask keeps slipping against her face. The team has seconds to decide whether it will deliver a shock, secure an airway, or reach for a drug. The next pause in compressions has not yet been earned.
Before You Read
Which interventions actually improve survival in adult cardiac arrest?
When does an advanced airway help—and when does it harm?
What changes after ROSC, even if the patient still has a pulse?
Why It Matters
Cardiac arrest is won by high-quality, uninterrupted CPR, early defibrillation when indicated, and rapid treatment of reversible causes—not by accumulating procedures. Every unnecessary pause, ineffective ventilation, or delayed shock steals coronary and cerebral perfusion.
When to Think of It
Unresponsiveness, absent normal breathing or agonal gasps, and no definite pulse within 10 seconds define arrest. Immediately identify the rhythm as shockable or nonshockable and search for reversible causes: hypovolemia, hypoxia, hydrogen ion/acidosis, hypo-/hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, pulmonary thrombosis, and coronary thrombosis.
Sick or Not Sick
Sick vs. not sick: Is the rhythm shockable right now, and are compressions effective? The most important call is whether to prioritize immediate defibrillation while minimizing hands-off time; airway sophistication and medications come afterward.
The First Fifteen Minutes
Start high-quality CPR: rate 100–120/min, depth at least 5 cm, full recoil, compressor change every 2 minutes, and interruptions under 10 seconds. Use a manual defibrillator/AED immediately.
VF/pulseless VT → biphasic shock 120–200 J, or the manufacturer-recommended dose; if unknown, use maximum available. Shock interrupts disorganized electrical activity so organized myocardial depolarization can resume.
Resume CPR immediately after every shock; do not pause for a pulse check unless an organized rhythm appears.
After the second shock in persistent VF/pVT → epinephrine 1 mg IV/IO every 3–5 minutes, because α-mediated vasoconstriction raises aortic diastolic pressure and coronary perfusion; do not delay defibrillation to give it.
Persistent VF/pVT after the third shock → amiodarone 300 mg IV/IO bolus, followed by 150 mg IV/IO for recurrent or persistent VF/pVT, because it increases the likelihood of electrical stabilization. Lidocaine is an alternative: 1–1.5 mg/kg IV/IO, then 0.5–0.75 mg/kg.
PEA/asystole → epinephrine 1 mg IV/IO immediately and every 3–5 minutes, because vasoconstriction may improve perfusion while the underlying cause is corrected; defibrillation is not indicated.
Provide bag-mask ventilation with oxygen and an oropharyngeal/nasopharyngeal airway when appropriate; with no advanced airway, use 30:2 compressions-to-breaths. Once an advanced airway is placed, ventilate 1 breath every 6 seconds with continuous compressions, because hyperventilation raises intrathoracic pressure and reduces venous return.
Torsades de pointes or suspected hypomagnesemia → magnesium sulfate 2 g IV/IO, because magnesium suppresses early afterdepolarizations; it is not routine therapy for ordinary VF.
Suspected hyperkalemia or hypocalcemia → calcium chloride 1 g IV/IO (10 mL of 10% solution) or calcium gluconate 3 g IV; calcium stabilizes the cardiac membrane. Verify local protocol and avoid routine calcium in undifferentiated arrest.
Suspected sodium-channel blocker toxicity or severe metabolic acidosis with a protocol-supported indication → sodium bicarbonate 1 mEq/kg IV/IO, because sodium loading and alkalinization can narrow QRS or improve membrane excitability; it is not routine arrest therapy.
Do not use atropine for routine adult PEA/asystole, and do not give routine bicarbonate, calcium, or vasopressin without a specific indication.
Definitive Care & Disposition
After ROSC, confirm airway and waveform capnography, target SpO₂ 90–98%, avoid hyperoxia, obtain ECG, treat hypotension with norepinephrine 0.05–0.1 mcg/kg/min IV infusion or another appropriate vasopressor, and target MAP at least 65 mmHg. Perform urgent coronary angiography for persistent ST-elevation or suspected coronary occlusion with cardiogenic shock/recurrent ventricular arrhythmia; do not delay for routine post-arrest testing. For patients who do not follow commands, initiate protocolized temperature control, commonly maintaining 32–37.5°C, and prevent fever. Admit to an ICU capable of post-arrest neuroprognostication, coronary intervention, ventilatory support, and treatment of the cause.
How This One Kills
The fatal failure is prolonged CPR interruption—often during airway placement, rhythm analysis, or medication administration—when a shockable rhythm could have been terminated with early defibrillation. A technically perfect tube cannot compensate for absent coronary perfusion.
The Atypical Presentation
Arrest may be unwitnessed, occur in a cold environment, or present with a weak agonal respiratory pattern that bystanders mistake for breathing. A low-quality monitor tracing, artifact, or an apparently organized rhythm can conceal VF or pseudo-PEA. Use pulse checks sparingly, assess waveform capnography and ultrasound without delaying compressions, and let the clinical context drive the reversible-cause search rather than waiting for a perfect rhythm label.
Back to Our Patient
Back to our 58-year-old woman: she is unresponsive, apneic except for agonal gasps, pulseless, and the monitor shows VF, so the team recognizes a shockable arrest and immediately delivers a biphasic shock while maintaining excellent compressions. After the second shock, epinephrine 1 mg IV/IO is given without delaying CPR; after the third, persistent VF prompts amiodarone 300 mg IV/IO and another shock. Bag-mask ventilation with capnography continues at 30:2 until an experienced operator places an advanced airway without a prolonged pause, and the team actively checks for coronary thrombosis, hypoxia, toxins, and other reversible causes. ROSC occurs, followed by ECG, oxygen titration, norepinephrine for MAP support if needed, temperature-control planning, and ICU admission for coronary evaluation and post-arrest care.
Patient Presentation to Attending
“This is a 58-year-old woman found unresponsive and pulseless in a grocery store, with bystander CPR already in progress. She had no preceding trauma or witnessed seizure, and the initial monitor showed coarse VF; compressions have been continuous except for brief rhythm checks. We delivered a biphasic shock, resumed CPR, and are following the shockable-arrest algorithm with IV/IO epinephrine after the second shock and amiodarone after persistent VF following the third. Bag-mask ventilation with waveform capnography is in progress, and we are checking glucose and pursuing reversible causes, especially coronary thrombosis, hypoxia, electrolyte abnormality, and toxin exposure. She has now achieved ROSC with an organized rhythm and weak pulse. Our plan is post-arrest airway and oxygen optimization, ECG and emergent coronary assessment if indicated, norepinephrine for hypotension, temperature control if she does not follow commands, and ICU admission.”
Study Directive
Perform a timed mock code: identify arrest, attach defibrillator, shock VF, deliver epinephrine after the second shock, and administer amiodarone after the third with pauses under 10 seconds.
Record your own compression fraction and ventilation rate during simulation; target a compression fraction above 80% and avoid hyperventilation.
Draw the adult cardiac-arrest algorithm and the Hs/Ts from memory, then explain the treatment for each reversible cause.
Practice post-ROSC management: oxygen target, MAP target, ECG/coronary pathway, temperature control, seizure assessment, and ICU disposition.
Review current ACLS guidance and local protocols for defibrillation energy, antiarrhythmic alternatives, calcium, bicarbonate, and pediatric dosing; complete 10 arrest-management questions.
Mechanism Pearl of the Day: Both topics reward fixing the mechanism rather than treating the label: in endocarditis, antibiotics cannot replace valve/source control when infected tissue causes mechanical failure; in cardiac arrest, medications cannot replace coronary perfusion and defibrillation. In each, identify the physiologic bottleneck first—perfusion, oxygenation, rhythm, or source—and intervene without delaying the time-critical step.
Key Medications
Epinephrine: 1 mg IV/IO every 3–5 minutes during adult cardiac arrest.
Amiodarone: 300 mg IV/IO for refractory VF/pVT after defibrillation, then 150 mg once if needed.
Lidocaine alternative: 1–1.5 mg/kg IV/IO, then 0.5–0.75 mg/kg; maximum cumulative dosing varies—check ACLS/institutional protocol.
Magnesium sulfate: 2 g IV/IO for torsades or suspected significant magnesium deficiency; dose and infusion rate vary by context.
Calcium chloride: 1 g IV/IO of 10% solution for hyperkalemia, hypocalcemia, or calcium-channel blocker toxicity; calcium gluconate 3 g IV is an alternative when peripheral extravasation risk matters.
Sodium bicarbonate: 1 mEq/kg IV/IO for selected toxicologic or metabolic indications, not routine arrest.
Norepinephrine after ROSC: start 0.05–0.1 mcg/kg/min IV and titrate to MAP ≥65 mmHg; exact starting dose varies by protocol.
Pediatric cardiac arrest dosing differs substantially: epinephrine 0.01 mg/kg IV/IO of 0.1 mg/mL concentration, maximum 1 mg; use PALS references.
High-Yield Pearls
Defibrillation is time-sensitive; epinephrine and antiarrhythmics are adjuncts, not substitutes for a shock when VF/pVT is present.
A rising ETCO₂ can support ROSC or improved CPR quality, but an isolated number should never replace pulse and rhythm assessment.
Routine calcium, bicarbonate, and atropine do not improve undifferentiated adult arrest; reserve them for specific reversible causes.
The Mimics
Seizure with preserved circulation — palpable pulse and organized arterial waveform; treating it as arrest causes unnecessary compressions and defibrillation.
Pulseless electrical activity from massive pulmonary embolism — sudden arrest with profound RV dilation or risk factors for VTE; missing the cause delays thrombolysis or embolectomy.
Tension pneumothorax — unilateral absent breath sounds, distended neck veins, and sudden deterioration after ventilation; delayed decompression makes CPR ineffective.
Pseudo-PEA — organized electrical activity with subtle cardiac motion but no palpable pulse; confusing it with true asystole can obscure the need for focused ultrasound and cause-directed resuscitation.
Board Question
A 67-year-old man is in witnessed VF arrest. CPR is high quality, and a biphasic shock is delivered. The rhythm remains VF after two minutes of CPR. Which is the next best intervention?
AGive amiodarone 300 mg IV immediately
BGive epinephrine 1 mg IV/IO and resume CPR
CGive sodium bicarbonate 1 mEq/kg IV
DPlace an endotracheal tube before further treatment
Reveal answer
Correct: B
Give epinephrine 1 mg IV/IO and resume CPR. In persistent shockable arrest, epinephrine is given after the second shock while compressions continue; amiodarone follows the third shock if VF/pVT persists. Airway procedures and empiric bicarbonate must not delay defibrillation or CPR.
Post-arrest temperature evidence does not support routine deep hypothermia over controlled normothermia, making active fever prevention the key bedside priority.
Although neurologically favorable survival declines as in-hospital CPR continues, meaningful recovery after prolonged resuscitation occurs, so elapsed time alone should not determine termination.
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
A 32-year-old man presents after a syncopal episode. His father died of a cardiac arrest in his early 40s. What’s the diagnosis, and the first move?
Check your answer
Brugada Syndrome. Type 1 pattern with syncope, documented arrhythmia, or family history of sudden cardiac death warrants admission with cardiology / EP consultation. Treat fever aggressively, avoid sodium channel blockers, and counsel on medication and trigger avoidance. Type 2 / Type 3 patterns alone in an asymptomatic patient warrant outpatient cardiology referral and family screening.
From the July 17 edition
Today, three days ago: Glucagon. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
Hypoglycemia: 1 mg IM/SC/IN. Beta-blocker overdose: 3–10 mg IV bolus, then infusion at effective bolus dose per hour; give antiemetic due vomiting risk. Pheochromocytoma, insulinoma/glucagonoma caution; hypersensitivity.
From the July 10 edition
A 29-year-old diver develops headache, confusion, and unilateral weakness 20 minutes after a rapid ascent. Which is the best next step?
AReassure and observe for spontaneous improvement
BGive 100% oxygen and urgent hyperbaric consultation
CStart high-dose steroids and discharge
DPerform lumbar puncture to exclude meningitis
Reveal answer
Correct · B
Neurologic symptoms after ascent are decompression illness or arterial gas embolism until proven otherwise. High-flow oxygen is the immediate treatment, and hyperbaric recompression is definitive therapy; delay worsens neurologic injury.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
Mike Cadogan and Robert Buttner ECG criteria for left ventricular hypertrophy Review the principal ECG criteria for left ventricular hypertrophy, their historical development, diagnostic performance, limitations and modern use.
Is HFNC as effective as NIV in reducing respiratory rate and improving respiratory distress within 2 hours in ACPE? The post HFNC vs. NIV in Acute Cardiogenic Pulmonary Edema: Go with the Flow? appeared first on REBEL EM - Emergency Medicine Blog .
Podcast Picks
Two for the shift
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Acute hypoxemic respiratory failure is a leading cause of ICU admission worldwide. Oxygen is first-line therapy for patients with acute hypoxemic respiratory failure and can be given via nasal cannula (NC), non-rebreather mask (NRB), high-flow nasal cannula (HFNC), or noninvasive ventilation (NIV). At present, the literature is inconsistent on which mode...
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Critical Care Perspectives in Emergency Medicine
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Host
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UMEM Pearl
Matched to today’s topics
A clinical pearl from the University of Maryland EM group’s Educational Pearls, tied to today’s differential.
For cardiac arrest during interfacility transport, team capability may influence resuscitation success: critical care transport was associated with more than twice the adjusted odds of ROSC versus ALS, while BLS performed worse.
This study by Peters et al. (2026), published in Prehospital Emergency Care, is the first nationwide analysis of cardiac arrest occurring during interfacility transport (IFT) by EMS, finding that critical care transport (CCT) was associated with more than double the odds of ROSC compared to ALS (aOR 2.21, 95% CI 1.42–3.48), while BLS care was associated with significantly worse outcomes.
Critical Care Corner
Matched to today’s topics
A critical-care reference from LITFL’s Critical Care Compendium, tied to today’s differential.
When endocarditis remains likely despite a negative TTE, TOE’s substantially higher sensitivity makes it the decisive next test and can supply a major diagnostic criterion.
TOE superior to TTE (90% vs 50% sensitive); echocardiographic findings are part of the major and minor criteria for diagnosis of infective endocarditis
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Ceftazidime
Third-generation IV cephalosporin (anti-pseudomonal)
1–2 g IV q8h. Febrile neutropenia: 2 g IV q8h. Pediatric: 30–50 mg/kg/dose q8h (max 6 g/day).
Renal Adjustment
Dose-adjust when CrCl < 50 mL/min; HD: dose after dialysis.
Contraindications
Cephalosporin hypersensitivity.
Interactions
Minimal.
Monitoring
Renal function, CBC; watch for neurotoxicity (encephalopathy, myoclonus, seizures) at high levels in renal impairment.
ED Pearl
Strong gram-negative/Pseudomonas coverage but weak against gram-positives — don't use as monotherapy when staph or strep are plausible pathogens.
First-line vasopressor for septic shock; cardiogenic shock; vasodilatory shock from any cause.
What’s your dose? — reveal dosing & cautions
ED Dose
Start 0.05–0.1 mcg/kg/min (≈ 5–8 mcg/min in adult); titrate q2–5 min to MAP ≥ 65 mmHg. Typical max 1–2 mcg/kg/min before adding a second agent.
Renal Adjustment
Titrate to effect; no specific renal dose change.
Contraindications
Profound hypovolemia (treat volume deficit first or simultaneously) and mesenteric/peripheral vascular thrombosis are relative.
Interactions
MAO inhibitors and tricyclic antidepressants (potentiated pressor response); beta-blockers (blunted beta effects, exaggerated alpha).
Monitoring
Arterial line ideal but do not delay starting through a peripheral large-bore IV; check the IV q15min for extravasation, and have phentolamine available.
ED Pearl
You can — and should — start norepi peripherally in septic shock while central access is being obtained. Waiting for a central line is the most common avoidable cause of delayed pressor initiation.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Misc
Biventricular Hypertrophy
Large biphasic QRS complexes across the mid-precordium — the Katz-Wachtel phenomenon — betray hypertrophy of both ventricles when the usual criteria cancel out.
The Tracing
A 6-year-old with a known ventricular septal defect comes in for a febrile illness and gets a screening ECG. The tracing shows enormous QRS voltages, and across the mid-precordial leads V2-5 the complexes are large and biphasic — tall R waves stacked over deep S waves in the same leads. There are voltage criteria that would satisfy LVH, yet there are also persistent deep S waves carried out to V5-6 and peaked P waves in lead II. The forces seem to be pulling in both directions at once, and no single hypertrophy pattern fully explains what you are seeing.
Katz-Wachtel phenomenon: large biphasic QRS complexes (tall R plus deep S) in V2-5
Coexisting LVH criteria (e.g. S in V2 + R in V5 > 35 mm, R in aVL > 11 mm) with added RVH features
RVH signs in the presence of LVH: right atrial enlargement, right axis deviation, deep S waves in V5-6
LVH signs in the presence of RVH: tall R and deep S waves in V2-5, QRS amplitude > 50 mm
Signs of LV strain (ST depression, T-wave inversion in V4-6) may accompany the voltages
Pearls
The ECG has low sensitivity for BVH because opposing left and right ventricular forces cancel each other out, so a normal-looking tracing does not exclude it.
The Katz-Wachtel phenomenon is the classic tell and is most commonly seen in children with congenital heart disease such as a VSD — context and age raise your suspicion.
Look for a second chamber's signature: LVH voltages plus right atrial enlargement or right axis deviation should make you think both ventricles, not just one.
Pitfalls
In children, right axis deviation and T-wave inversion in V1-3 are normal, so do not over-read them as pathologic RVH.
Limb-lead reversal and other artifacts can fake the voltage and P-wave findings — verify lead placement before diagnosing BVH.
Because the two ventricles' forces offset, relying on standard single-chamber criteria will systematically under-call biventricular disease.
At the Bedside
Recognizing BVH — especially the Katz-Wachtel pattern in a child — points toward significant structural or congenital heart disease and should prompt echocardiography and cardiology referral rather than reassurance based on 'just LVH.'
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · Endocarditis
Self-Examination
Test Your Understanding
A 62-year-old man with a prosthetic aortic valve presents with fever and malaise. Three blood-culture sets grow Staphylococcus aureus. TTE is nondiagnostic, and ECG now shows new PR prolongation. Which is the best next diagnostic step?
ARepeat blood cultures in 72 hours before further imaging
BTransesophageal echocardiography
CExercise stress testing
DCoronary CT angiography
Reveal answer
Correct answer · B
Transesophageal echocardiography. Prosthetic material reduces TTE sensitivity, and new conduction delay suggests a perivalvular abscess. TEE is the appropriate urgent study while antibiotics and source-control planning proceed.
Study Pace2 topics today; Issue 6 of 113 — Cardiology (Week 4)Deadline · June 1, 2026