A 27-year-old man collapses midway through a basketball game, waking with sweat on his upper lip and the metallic taste of blood from a bitten tongue. His teammates say he had complained of “heart pounding” but had not mentioned chest pain. In the ED, his blood pressure is 82/54 mm Hg, pulse 138/min, and a harsh systolic sound intensifies when he stands. The next move has not yet been made.
— What’s your move? Read on.
Before you read
- What bedside maneuver distinguishes dynamic outflow obstruction from fixed stenosis?
- Which therapy restores forward flow without increasing contractility?
When to Think of It
Think HOCM with exertional syncope, sudden cardiac arrest, palpitations, family history of sudden death, a systolic murmur that increases with standing or Valsalva, and ECG evidence of LV hypertrophy, deep narrow Q waves, or repolarization abnormalities. Echocardiography shows asymmetric septal hypertrophy, systolic anterior motion of the mitral valve, and a dynamic LVOT gradient.
Sick or Not Sick
Sick versus not sick hinges on hemodynamic compromise or malignant ventricular arrhythmia. Hypotension, pulmonary edema, ischemia, altered mental status, or sustained VT requires resuscitation and monitored critical care; stable patients still require urgent cardiology assessment because exertional syncope may be an aborted sudden-death event.
The First Fifteen Minutes
- Hypotension with suspected LVOTO and adequate oxygenation → phenylephrine 100–200 mcg IV bolus, repeat as needed, then 0.2–1 mcg/kg/min IV infusion, because pure α-agonism raises afterload without increasing contractility or heart rate.
- Tachycardia with persistent obstruction and blood pressure supported → esmolol 500 mcg/kg IV loading dose over 1 minute, then 50–300 mcg/kg/min IV infusion, because slowing diastolic filling and reducing contractility decrease the gradient. Avoid or reduce the bolus in severe shock; check an institutional reference for titration.
- Likely preload depletion without pulmonary edema → 250–500 mL isotonic crystalloid IV bolus, reassessing after each bolus, because increased ventricular filling can reduce cavity obliteration. Avoid indiscriminate large-volume loading if pulmonary congestion is present.
- Pulmonary edema with hypertension rather than shock → furosemide 40–80 mg IV, because reducing congestion may improve oxygenation; use cautiously since excessive preload reduction can worsen LVOTO.
- Sustained unstable VT or VF → immediate synchronized cardioversion for VT with a pulse, typically 100–200 J biphasic, or defibrillation for VF/pulseless VT at 200 J biphasic, because electrical instability—not the obstruction alone—is the immediate threat.
Definitive Care & Disposition
Obtain urgent echocardiography, serial ECG/troponin testing, electrolytes, and family history. Admit unstable patients to the ICU; even a stable patient with exertional syncope, sustained arrhythmia, significant gradient, or suspected HCM-related collapse needs monitored cardiology admission. Definitive management includes beta-blockade or nondihydropyridine calcium-channel blockade for symptoms, septal reduction therapy for refractory obstruction, ICD assessment for sudden-death risk, exercise counseling, and family screening. Avoid dehydration and unnecessary vasodilators or positive inotropes.
How This One Kills
Treating hypotension with dobutamine, epinephrine, nitrates, or aggressive diuresis can increase contractility or reduce afterload/preload, intensify systolic anterior motion, and convert a partially obstructed ventricle into catastrophic low-output shock.
The Differential — What Else Looks Like This
- Aortic stenosis — fixed murmur and limited valve opening on echocardiography; confusing it may lead to the wrong preload/afterload strategy.
- Massive pulmonary embolism — RV dilation, hypoxemia, and a pulmonary-pressure pattern rather than asymmetric septal hypertrophy; missing it delays reperfusion.
- Acute coronary syndrome — ischemic symptoms, regional wall-motion abnormality, and dynamic troponin rise; attributing everything to HCM can miss an occluded coronary artery.
- Vasovagal syncope — prodrome and rapid recovery without exertional arrhythmia or structural obstruction; mislabeling exertional syncope may miss sudden-death risk.
The Second-Day Story
Older adults may present with exertional dyspnea, falls, chest discomfort, or “heart failure with preserved EF” rather than syncope or a dramatic murmur. Tachycardia, anemia, sepsis, or dehydration can unmask obstruction in someone without a known diagnosis. Look for a small, hyperdynamic LV, septal hypertrophy, systolic anterior motion, and a late-peaking Doppler gradient rather than relying on the bedside murmur alone.
Back to Our Patient
Back to the 27-year-old basketball player: exertional collapse, hypotension, tachycardia, and a murmur that increases with standing make dynamic LVOTO with an unstable ventricular rhythm the leading concern. He is placed on a monitor and defibrillator pads, receives a cautious crystalloid bolus, and persistent hypotension is supported with phenylephrine while tachycardia is addressed with carefully titrated esmolol once pressure improves. Echocardiography shows asymmetric septal hypertrophy with systolic anterior motion and a dynamic LVOT gradient; cardiology identifies the rhythm as sustained monomorphic VT and performs synchronized cardioversion. He is admitted to the cardiac ICU for arrhythmia evaluation and ICD-risk assessment.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 27-year-old previously healthy man who collapsed during basketball with palpitations and brief loss of consciousness, now hypotensive at 82/54 and tachycardic at 138. He has no fever, pleuritic pain, or preceding viral symptoms, but his teammates report exertional palpitations and his father died suddenly at 42. He is cool and diaphoretic, with a harsh late-peaking systolic murmur that increases with standing, and no clear pulmonary edema. ECG shows wide-complex tachycardia, and bedside echo shows asymmetric septal hypertrophy with systolic anterior motion. My leading diagnosis is HOCM with dynamic LVOTO and sustained VT; I’m applying pads, supporting pressure with phenylephrine, giving cautious fluid, and will cardiovert immediately if unstable while arranging ICU cardiology care.”
Study Directive
- Draw the HOCM pressure-volume problem from memory: reduced preload, reduced afterload, and increased contractility all worsen LVOTO.
- Review one echocardiographic clip showing systolic anterior motion and identify the LVOT gradient.
- Practice a 30-second shock plan using phenylephrine, cautious fluid, and esmolol.
- Memorize the exertional-syncope and sudden-death-risk features that prompt ICD evaluation.
Recent Literature
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Review or guideline Hypertrophic obstructive cardiomyopathy
A comprehensive clinical reference emphasizing that acute obstructive physiology is worsened by reduced preload or afterload and excessive contractility, supporting cautious fluids, beta-blockade, and pure vasoconstrictors when hypotension