CONTENTS

• Introduction
• Physiology
• Epidemiology
• Clinical findings
• Echocardiographic diagnosis
• Management
  • Esmolol
• Podcast
• Questions & discussion
• Pitfalls
• Supplemental Media

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introduction

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• Dynamic left ventricular outflow tract obstruction (LVOTO) creates a confusing hemodynamic picture. If unrecognized, LVOTO will fail to respond to standard hemodynamic therapies. Indeed, LVOTO will often respond to various interventions in the opposite fashion than might be expected for most patients (e.g., inotropes will make the cardiac function worse!).
• Clinically significant LVOTO is often defined on the basis of echocardiography that demonstrates a pressure gradient across the LV outflow tract of >30 mm Hg.📖 However, merely the identification of qualitative LVOTO (without precise definition of a pressure gradient) may have important therapeutic implications regarding hemodynamic management of shocked patients.

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physiology

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• LVOTO is caused by fast-flowing blood through the LV outflow tract which pulls the mitral valve anteriorly (towards the LV outflow tract) due to a Venturi effect. This is known as systolic anterior motion (SAM) of the mitral valve.
• Anterior motion of the mitral valve has two consequences:
  • (#1) The mitral valve causes an obstruction of the LV outflow tract, which impairs systolic ejection of blood into the aorta. This tends to reduce cardiac output, potentially causing cardiogenic shock.
  • (#2) The mitral valve is opened during systole, causing mitral regurgitation. This increases pressure in the left atrium, causing congestion and potentially cardiogenic pulmonary edema.

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epidemiology

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substrates

• Dynamic LVOTO may be generated by various combinations of the following factors:
• Anatomic substrates
  • Small cavity size of the base of the heart, due to hypertrophy of the left ventricle (especially the septum). This narrows the LV outflow tract (increasing blood velocity) and pushes the mitral valve and LV outflow tract closer together – both factors which facilitate LVOTO.
  • Mitral valve with floppy leaflets.
• Physiologic substrates
  • Many patients may have latent LVOTO, wherein LVOTO is provoked only by a combination of specific physiologic conditions. Factors which promote LVOTO include any that cause the left ventricle to be hyperkinetic and underfilled (thereby increasing the velocity of blood ejected through the LV outflow tract and reducing the end-systolic chamber dimensions). Such factors include:
  • Exogenous inotropes.
  • High endogenous sympathetic tone.
  • Tachycardia.
  • Reduced preload.
  • Reduced afterload.

clinical situations where LVOTO occurs

• Distributive shock with volume depletion
  • LVOTO may occur in ~2% patients with sepsis (due to a combination of vasodilation and high inotropic tone).(32488425)
• Hypertrophic obstructive cardiomyopathy (HOCM)
  • This is the classic textbook scenario where LVOTO occurs.
  • One third of patients with HOCM have LVOTO at baseline. However, most patients with HOCM have inducible LVOTO during maneuvers that change loading conditions.
• Hypertensive cardiomyopathy
  • Chronic hypertension may cause hypertrophy of the septum.
  • LVOTO is particularly common in elderly patients with a “sigmoid septum,” which is more prominent hypertrophy of the basal septum (image below).
• Takotsubo cardiomyopathy
  • LVOTO can occur in the classic pattern of takotsubo cardiomyopathy with apical hypokinesis and hypercontractility of the base of the heart. Apical hypokinesis causes septal angulation which, combined with basal hyperkinesis, causes LVOTO.
• Left anterior descending artery (LAD) ischemia with apical hypokinesis
  • This has similar functional and anatomic consequences compared to takotsubo cardiomyopathy (hypokinetic apex plus hypercontractile base). Treatment includes revascularization and beta-blockade (with avoidance of nitrates).(33841598)
• Cor pulmonale
  • Dilation of the RV may cause compression of the LV, which reduces chamber size and promotes LVOTO.
  • Note that in this scenario, the treatment should usually focus on management of the right ventricular failure (rather than the LVOTO). 📖

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clinical findings

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• Hypotension and/or cardiogenic shock may occur (which may even progress to cardiac arrest).(30122151)
• Cardiogenic pulmonary edema may occur.
• A new systolic murmur might be noted.
• Inotropes will exacerbate (rather than alleviate) the cardiogenic shock.
  • Inotropes increase the ejection speed of blood through the LV outflow tract, which will worsen the anterior mitral motion.
  • 💡 This may present clinically as “vasopressor refractory shock.”
• Diuresis will exacerbate (rather than alleviate) the pulmonary edema.
  • Diuresis reduces the diastolic volume of the left ventricle. This moves the mitral valve closer to the LV outflow tract, worsening obstruction.
  • 💡 This may present clinically as “diuretic refractory cardiogenic pulmonary edema.”

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echocardiographic diagnosis

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2-dimensional echo findings

• (1) The first feature to recognize may be a ventricle susceptible to LVOTO; for example, one of the following:
  • Left ventricular hypertrophy with small chamber size.
  • Takotsubo pattern (apical dilation with basal hyperkinesis).
• (2) Mitral regurgitation is generally present, typically hugging the posterolateral left atrium.
• (3) Systolic anterior motion of the mitral valve:
  • During systole, the mitral valve leaflets are tugged towards the septum.
• (4) One clue may be a hyperkinetic left ventricle with near obliteration of the left ventricular cavity during systole (i.e., a pathologically elevated ejection fraction).

Doppler echo findings

• The hallmark of dynamic LVOTO is a high-velocity, late-peaking continuous-wave Doppler signal on examination through the LV outflow tract (described as “dagger-shaped”).
  • The late-peaking nature may help differentiate this from aortic stenosis, which increases velocity with a more symmetric appearance.
• The maximal pressure gradient can be calculated based on the modified Bernoulli equation (pressure = 4 x velocity squared).
  • LVOT gradient >30 mm Hg (2.7 m/s) is considered pathologically elevated.(28072930)
  • LVOT gradient >50 mm Hg (3.5 m/s) is severely elevated.

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management

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interventions to discontinue

• Inotropes.
• Afterload-reducing medications (e.g., nitrates).
• Intra-aortic balloon pump (which reduces afterload).

fluid administration

• For patients who are hypovolemic, fluid resuscitation will improve preload and ventricular filling.

pure vasoconstrictors (phenylephrine, vasopressin)

• These are the vasopressors of choice for LVOTO.
  • Phenylephrine is often more convenient, since it has a shorter half-life, allowing it to be more titratable.
• Vasoconstriction reduces LVOTO via many mechanisms:
  • (a) Increases afterload.
  • (b) Increases preload (due to venoconstriction, which increases venous return).
  • (c) Vasoconstriction can cause a mild reflexive bradycardia, which improves ventricular filling and increases ventricular volume.
• In many patients, LVOTO may be induced by systemic vasodilation (e.g., sepsis, anesthetic agents). Phenylephrine is a rational approach to reversing this physiology.
• Norepinephrine primarily functions as a vasoconstrictor, so it shouldn't be a strong inducer of LVOTO. However, case reports do describe norepinephrine causing LVOTO – so this agent isn't optimal in patients with LVOTO.(31796448)

beta-blockers

• Beta-blockers may decrease LVOTO, thereby improving cardiac output and blood pressure.
• In hemodynamically unstable patients, it may be safest to use an esmolol infusion with gradual uptitration and careful monitoring of hemodynamic effects.
  • If beta-blockade causes hemodynamic deterioration, the diagnosis of LVOTO may be reconsidered.
  • If beta-blockade causes hemodynamic improvement, this may eventually be transitioned to a longer-acting agent.
  • Further discussion of esmolol below.

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esmolol

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advantages & general comments 💊

• Very short-acting beta blocker, allowing it to be used as a titratable agent.

drawbacks & contraindications

• Contraindications
  • Bradycardia.
  • Heart block or sick sinus syndrome.
  • Cardiogenic pulmonary edema.
  • Asthma exacerbation.
  • Acute cocaine/sympathomimetic intoxication.

onset & duration

• Onset in 1-2 minutes.(30165588)
• Lasts 10-30 minutes.(30165588)

dose

• Loading dose = 0.5 mg/kg.
• Start infusion at 50 mcg/kg/min.
• For inadequate effect, re-load (with 0.5 mg/kg) and increase infusion by 50 mcg/kg/min. Up-titrate as needed to a max dose of 200 mcg/kg/min.

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podcast

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

• The main pitfall is simply not considering or looking for LVOTO. Failure to diagnose LVOTO is extremely problematic, because standard hemodynamic interventions will be harmful in these patients (e.g. inotropes).

Guide to emoji hyperlinks

• = Link to online calculator.
• = Link to Medscape monograph about a drug.
• = Link to IBCC section about a drug.
• = Link to IBCC section covering that topic.
• = Link to FOAMed site with related information.
• 📄 = Link to open-access journal article.
• = Link to supplemental media.

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supplemental media

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