EM@3AM: Mitral Regurgitation

Author: Vivek Medepalli, MD (EM Resident Physician, UTSW / Parkland Memorial Hospital) // Reviewed by: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX), Colin Danko, MD (EM Attending Physician, UTSW / Parkland Memorial Hospital) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.


A 63-year-old male presents to the ED complaining of sudden onset shortness of breath for the past 2 hours. He has a history of CAD, HTN, and T2DM He states that he has been compliant with his medications. BP 97/68, HR 108, RR 21, 92% RA. Physical exam is notable for a holosystolic murmur most prominent over the apex and radiating to the axilla, mild bibasilar rales, JVD, and 2+ lower extremity pitting edema.

What is the most likely cause of this patient’s symptoms, and what are the next steps in management?


Answer: Mitral Regurgitation

 

Epidemiology:

  • Primary mitral regurgitation secondary to valvular disease occurs in 1.5-3% of the population [1,2]
    • Most commonly due to mitral valve prolapse in developed countries and rheumatic heart disease in developing countries [3]
  • Prevalence of mitral regurgitation during cardiac catheterization in the setting of acute MI is 9-13% [4]
    • Moderate-to-severe regurgitation in 3-4% of acute MI patients
  • Mitral regurgitation seen in 38% of patients with dilated cardiomyopathy
  • More common in males

 

Etiology:

  • Primary Mitral Regurgitation [3,5]
    • Degenerative mitral valve disease (ex. Mitral valve prolapse)
    • Rheumatic heart disease
    • Endocarditis
    • Trauma
    • Congenital malformations
    • Drug-related valvular disease (ex. Cabergoline, bromocriptine)
  • Secondary Mitral Regurgitation [3,5]
    • Coronary artery disease
    • Acute myocardial infarction (ruptured papillary muscle)
    • Dilated cardiomyopathy
    • Hypertrophic cardiomyopathy

 

Pathophysiology:

  • Acute Mitral Regurgitation: Commonly seen with acute MI, chordae tendinae rupture, endocarditis, and trauma[2,5]
    • Regurgitant flow through diseased mitral valve leads to systolic backflow into the left atrium
    • Subsequent backflow into the pulmonary circulation leads to pulmonary edema and sudden-onset shortness of breath
    • Pulmonary hypertension leads to backflow into venous circuit, resulting in JVD, hepatomegaly, peripheral edema
    • Decreased filling of left ventricle leads to decreased forward flow, resulting in hypotension and cardiogenic shock
  • Chronic Mitral Regurgitation: [2,5]
    • Changes occur more slowly, leading to eccentric hypertrophy and dilation of the left atrium
    • Chronic left atrial dilation can lead to atrial fibrillation

 

Clinical Features:

  • Acute Mitral Regurgitation: [6]
    • Sudden-onset pulmonary edema and hypotension
    • Cardiogenic shock
    • Physical exam will show pulmonary rales, peripheral edema, JVD, hepatomegaly, S3, hyperdynamic cardiac apex
      • Classic murmur described as holosystolic, most prominent over the cardiac apex, and radiating to the axilla
        • Only present in 50% of cases; however, absence of murmur does not exclude acute mitral regurgitation [2,7]
  •  Chronic Mitral Regurgitation
    • Majority of patients have mild regurgitation at baseline, which is often asymptomatic or associated with mild dyspnea [7]
    • Some patients with mild symptoms at rest can have profound acute regurgitation with exercise, resulting in acute pulmonary edema [3,8]

 

Evaluation:

  • Transthoracic Echocardiogram:
    • Recommended to evaluate the presence, etiology, severity, and further hemodynamic consequences of the regurgitation [3,10]
      • Often shows an elevated ejection fraction (>60%) due to forward flow into the systemic circulationcombined with backflow into the left atrium [10]
      • Since regurgitant lesions tend to overestimate LV function, the absence of hyperdynamic function is concerning for impaired function
    • Color doppler shows backward flow into the left atrium
    • Consider transesophageal echocardiogram in patients with inconclusive transthoracic echocardiogram

  • Chest X-Ray
    • May show cardiomegaly, enlarged left atrium, or pulmonary edema in symptomatic patients [2, 6]

  • EKG
    • Will not show changes strictly due to mitral regurgitation acutely, but may reveal underlying cardiac ischemic event as source of symptoms
    • May reveal left atrial enlargement (biphasic P waves) or left ventricular hypertrophy in the setting of chronic mitral regurgitation [6]
  • Supplemental laboratory evaluation: tailor to patient’s clinical presentation
    • Troponins if ACS is suspected
    • Blood cultures if the patient has clinical signs of endocarditis
    • Pro-BNP is often elevated and nonspecific

 

Treatment:

  • Severe acute mitral regurgitation typically requires emergent surgical valve repair or replacement [6]
  • Volume overload and hypertension worsen regurgitation
  • Patients are afterload sensitive; the goal blood pressure is the lowest value that provides organ perfusion
  • Volume overload but perfusing
    • Decreasing afterload reduces regurgitant flow and increases cardiac output
      • Utilize dihydropyridine calcium channel blockers such as nicardipine or clevipidine; nitroglycerin may also be used
    • Preload reduction assists with gas exchange and cardiac function
      • Utilize nitroglycerin infusion with titration
      • Noninvasive positive pressure ventilation (NIPPV) and diuretics may be used
    • Target slightly higher heart rates, as slow heart rates increase regurgitant flow
  • Volume overload but poor perfusion
    • Provide inotropic support while maintaining mean arterial pressure
      • Start epinephrine infusion, or use dobutamine (be ready with norepinephrine)
      • Milrinone can be used in the ICU
    • Preload reduction
      • Use NIPPV
    • HR control; avoid bradycardia and severe tachycardia
      • If significantly tachycardic, use amiodarone or even IV digoxin
  •  Emergent consultation recommended to interventional cardiology and cardiothoracic surgery
    • Mechanical circulatory support may be used as a bridge to surgery
  • In the setting of ACS, prompt revascularization therapy is indicated
    • May be sufficient to reverse acute mitral regurgitation not caused by chordae tendinae or papillary muscle rupture [6]
  • If patient has clinical signs of endocarditis, start broad spectrum antibiotic therapy

 

Consultation:

  • Cardiology/Interventional Cardiology
  • Cardiothoracic Surgery

 

Disposition:

  • Mild-to-moderate symptomatic mitral regurgitation with hemodynamic stability can be admitted to floor/ward with telemetry capabilities [6]
  • Severe mitral regurgitation may require ICU admission and/or emergent surgical repair

 

Summary and Pearls:

  • The most common cause of primary mitral regurgitation is prior structural valve disease (ex. Mitral valve prolapse) and secondary mitral regurgitation is ischemic heart disease
  • Acute mitral regurgitation presents with sudden onset dyspnea, JVD, peripheral edema
  • The diagnostic modality of choice is transthoracic echocardiogram (TTE); EKG and laboratory markers can provide supplementary information to reveal etiology
  • Mild to moderate mitral regurgitation can be managed with symptomatic medical therapy, while severe valve disease requires ICU admission and possible emergent surgical valve repair or replacement

References

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