emDOCs Podcast – Episode 119: Left Ventricular Outflow Tract Obstruction

Today on the emDOCs cast with Rachel Bridwell, MD, and Brit Long, MD (@long_brit), we cover left ventricular outflow tract obstruction, or LVOTO.

Episode 119: Left Ventricular Outflow Tract Obstruction

 

Underlying Principles

  • LVOTO occurs secondary to the systolic anterior motion (SAM) of the mitral valve (MV)
    • Blood velocity increases due to narrowed LV outflow, forcing outflow tract and mitral valve in closer proximity1
      • Venturi effect causes the mitral valve to lift anteriorly towards increased velocity of blood flow2
        • Causes physical obstruction of outflow3
      • SAM of the MV additionally generates mitral regurgitation, increasing left atrial pressures and in turn, resulting in cardiogenic pulmonary edema3

 

Contributing Factors

  • Physiologic:
    • Dormant LVOTO—subset of patients have an amount of outflow tract obstruction without effect until pathophysiologically provoked4
      • g. hyperdynamic contractility, reduced preload and/or afterload, inotropes, tachycardia4
    • Anatomic
      • Floppy mitral valve1
      • Decreased left ventricular volume, especially secondary to septal hypertrophy5

 

Phenotypes of presentation

  • Apical hypokinesis in the setting of Left Anterior Descending coronary artery occlusion4,5
  • Volume depletion with distributive shock4
    • Present in up to 2% of septic patients6
  • Takotsubo cardiomyopathy7,8
  • Hypertensive cardiomyopathy9
  • Hypertrophic obstructive cardiomyopathy5
  • Cor pulmonale10

 

Clinical Presentation

  • These patients are critically ill.
  • Vital signs:
    • Hypotensive and tachycardic, despite escalating vasopressor and inotropic requirements11
    • Hypoxia and respiratory distress – due to pulmonary edema
    • Cardiac arrest12
  • Cardiogenic pulmonary edema13
    • Refractory or exacerbated by diuresis13
  • Cardiogenic shock13
    • Refractory or exacerbated by inotropes and any vasopressor with beta activity13
  • May appreciate new end systolic murmur on auscultation11

 

Evaluation

  • Chest Radiograph
    • Non-specific but may show pulmonary edema
  • ECG
    • Non-specific – Tachycardia
    • Evaluate for anterior ST elevation myocardial infarction (STEMI)
    • If associated with HCM:
      • High voltages, “dagger-like” Q waves
    • Echocardiography4,11,14
      • Assess LV size4,11,14
        • Hypertrophy especially at septum with resulting obstruction and decreased LV size:

          Courtesy of POCUS Atlas: https://www.thepocusatlas.com/pediatrics-1/3gcr6yneuyx87qxkx71bgsnkywqmi1
      •  Apical hypokinesis with basal hyperkinesis causing functional obstruction
        • Look for a hyperdynamic LV with a very small ventricular cavity during systole
      • SAM
      • Poor LV filling and outflow obstruction in sepsis on vasopressors and inotropes with LVOTO:

        Courtesy of Pocus Atlas: https://www.thepocusatlas.com/valvulopathy/left-ventricular-outflow-tract-obstruction
      •  Mitral regurgitation (may be secondary to SAM)

        Courtesy of POCUS Atlas: https://www.thepocusatlas.com/valvulopathy/voxh2mkf0tal26fvdya3qgmq0go7ey
      • Doppler4,14
        • High-velocity, late-peaking continuous-wave Doppler through LV with classic dagger shape4
        • Maximal LVOT pressure gradient:
          • > 30 mm Hg (2.7 m/s)—problematic and elevated
          • > 50 mm Hg (4.5 m/s)—severely elevated
    •  Labs
      • May acquire ECG, complete blood count, comprehensive metabolic panel, troponin, beta natriuretic peptide
        • May demonstrate evidence of heart failure, acute renal failure, shock liver, or other evidence of end organ damage, though does not change management

 

Treatment:

  • Medications/interventions to stop/avoid:
    • Inotropes4,15
    • Afterload reduction4,15
    • Intra-aortic balloon pump (in discussion with cardiology)
  • Administer judicious fluids to increase preload
  • Pure vasoconstriction without beta agonism
    • Phenylephrine—convenient and short half-life15
      • Directly treats vasoplegia associated with sepsis6
    • Vasopressin6
    • Please avoid norepinephrine and epinephrine due to beta agonism16
  • Beta blockade: decreases LVOTO with increased filling time and mitigates hyperdynamic LV17
    • Esmolol — for careful titration and short half-life17

 

Disposition:

  • Admit to ICU
  • Formal echocardiography
    • Quantification of LVOT pressure gradient

 

Pearls:

  • Similar to LVOTO will have the opposite expected physiologic result in response to medications given.
    • Suspect in patients with shock refractory or worsened by vasopressors and inotropes
      • Additionally, consider in cardiogenic shock worsening by diuresis
    • Systolic anterior mitral valve motion both impairs left ventricular outflow and causes mitral regurgitation.
    • Occurs secondary to a various of anatomic and pathophysiologic conditions including:
    •         Distributive shock with volume depletion
      • Cor pulmonale
      • Hypertrophic obstructive cardiomyopathy
      • Hypertensive cardiomyopathy
      • LAD occlusion with apical hypokinesis
      • Takotsubo cardiomyopathy
    • To correct the outflow obstruction, increase the size and filling time of the left ventricle:
      • Stop inotropes and diuretics
      • Judicious volume resuscitation
      • Increase the systemic vascular resistance with phenylephrine and/or vasopressin
      • Rate control with beta blockade using esmolol
    • Admit these patients to the ICU

 

Further Reading:

 

References:

  1. Slama M, Tribouilloy C, Maizel J. Left ventricular outflow tract obstruction in ICU patients. Curr Opin Crit Care. 2016;22(3):260-266. doi:10.1097/MCC.0000000000000304
  2. Alrammah H, Ghazal S. Significant left ventricular outflow tract obstruction secondary to systolic anterior motion in a patient without hypertrophic cardiomyopathy: An echocardiographic study. J Saudi Hear Assoc. 2018;30(4):336. doi:10.1016/J.JSHA.2018.07.001
  3. Sherrid M V., Chu CK, Delia E, Mograder A, Dwyer EM. An echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. J Am Coll Cardiol. 1993;22(3):816-825. doi:10.1016/0735-1097(93)90196-8
  4. Evan JS, Huang SJ, McLean AS, Nalos M. Left ventricular outflow tract obstruction-be prepared! Anaesth Intensive Care. 2017;45(1):12-20. doi:10.1177/0310057X1704500103
  5. Louie EK, Edwards LC. Hypertrophic cardiomyopathy. Prog Cardiovasc Dis. 1994;36(4):275-308. doi:10.1016/S0033-0620(05)80036-2
  6. Balik M, Novotny A, Suk D, et al. Vasopressin in Patients with Septic Shock and Dynamic Left Ventricular Outflow Tract Obstruction. Cardiovasc drugs Ther. 2020;34(5):685-688. doi:10.1007/S10557-020-06998-8
  7. Shah BN, Curzen NP. Reversible systolic anterior motion of the mitral valve and left ventricular outflow tract obstruction in association with Takotsubo syndrome. Echocardiography. 2011;28(8):921-924. doi:10.1111/J.1540-8175.2011.01446.X
  8. Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: A systematic review. Int J Cardiol. 2008;124(3):283-292. doi:10.1016/J.IJCARD.2007.07.002
  9. Meuwese CL, Boulaksil M, van Dijk J, Polad J, Meijburg HW. Transient left ventricular outflow tract obstruction with systolic anterior motion of the mitral valve: A stunning cause. Echocardiography. 2017;34(7):1089-1091. doi:10.1111/ECHO.13553
  10. Kim S, Kim SJ, Kim J, Yoon P, Park J, Moon J. Dynamic obstruction induced by systolic anterior motion of the mitral valve in a volume-depleted left ventricle: an unexpected cause of acute heart failure in a patient with chronic obstructive pulmonary disease. J Thorac Dis. 2015;7(9):E365-E369. doi:10.3978/J.ISSN.2072-1439.2015.09.22
  11. Pérez C, Diaz-Caicedo D, Almanza Hernández DF, Moreno-Araque L, Yepes AF, Carrizosa Gonzalez JA. Critical Care Ultrasound in Shock: A Comprehensive Review of Ultrasound Protocol for Hemodynamic Assessment in the Intensive Care Unit. J Clin Med. 2024;13(18):5344. doi:10.3390/JCM13185344
  12. Yamagishi T, Tanabe T, Fujita H, et al. Conventional cardiopulmonary resuscitation-induced refractory cardiac arrest due to latent left ventricular outflow tract obstruction due to a sigmoid septum: a case report. J Med Case Rep. 2018;12(1). doi:10.1186/S13256-018-1767-Z
  13. Madias JE. Left ventricular outflow tract obstruction/hypertrophic cardiomyopathy/takotsubo syndrome: A new hypothesis of takotsubo syndrome pathophysiology. Curr Probl Cardiol. 2024;49(8). doi:10.1016/J.CPCARDIOL.2024.102668
  14. Geske JB, Sorajja P, Ommen SR, Nishimura RA. Left ventricular outflow tract gradient variability in hypertrophic cardiomyopathy. Clin Cardiol. 2009;32(7):397-402. doi:10.1002/CLC.20594
  15. MOZELL D, SHAH N, CASTILLON JJR, GONUGUNTLA VT, AWERBUCH E. EPINEPHRINE-INUDCED SHOCK: LEFT VENTRICULAR OUTFLOW TRACT OBSTRUCTION ON VASOPRESSORS. Chest. 2024;166(4):A3026-A3027. doi:10.1016/J.CHEST.2024.06.1821
  16. Mampuya WM, Dumont J, Lamontagne F. Norepinephrine-associated left ventricular outflow tract obstruction and systolic anterior movement. BMJ Case Rep. 2019;12(12). doi:10.1136/BCR-2018-225879
  17. Dawood S, Hill A, Al Rawi O. Esmolol for acute pulmonary embolism with left ventricular outflow tract obstruction. Anaesth Reports. 2021;9(1):e12099. doi:10.1002/ANR3.12099

 

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