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An Uncommon Cause of Shortness of Breath in the Emergency department: Acute Mitral Regurgitation

Acute mitral regurgitation is a rare cause of cardiogenic shock and is most commonly caused by papillary muscle rupture. This differs from chronic mitral regurgitation in that there are no compensatory physiologic adaptations and the patient will suffer from left heart failure in an accelerated pattern. In order for this patient to be stabilized, a thorough understanding of cardiac physiology is key. Recalling the Starling Curve, one can intuit that by reducing afterload and increasing preload cardiac function can improve. Enter vasodilator therapy. Many of these patients will improve on a nitroglycerin drip especially if hypertensive. Just as in acute congestive heart failure exacerbations…

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 Acute Mitral Regurgitation in the Emergency Department

Patients with acute MR can present with a range of symptoms including acute respiratory failure from pulmonary edema and/or cardiogenic shock. Acute MR also shares similar clinical features to other cardiopulmonary conditions, and often is initially diagnosed generally as decompensated heart failure without recognizing the underlying valvular etiology. History and physical exam findings can be subtle, with approximately 50% of patients with moderate to severe acute MR having no audible cardiac murmur.

 Acute Mitral Regurgitation: The Dreaded Masquerader

Unilateral pulmonary edema in patients with hypoxemic respiratory failure is usually secondary to infectious etiology. However, cardiogenic unilateral pulmonary edema is a rare yet important entity that is often misdiagnosed initially, leading to significant delays in treatment. Cardiogenic unilateral pulmonary edema is often secondary to acute mitral regurgitation (MR), a life-threatening hemodynamic abnormality that requires urgent medical attention and usually surgical intervention.

Articles of Interest

Acute Mitral Regurgitation- An Easy-to-Miss but Critical-to-Diagnose Condition

There are two basic mechanisms for acute mitral regurgitation (AMR)- ruptured chordae tendinae or papillary muscle rupture1 . Ruptured chordae tendinae can result from mitral valve prolapse (myxomatous disease)2 , infective endocarditis, trauma, rheumatic valvular disease, or spontaneous rupture. Rupture of the papillary muscle can be due to trauma, acute myocardial infarction, or papillary muscle displacement from myocardial ischemia/infarction.

Acute Valve Disasters - Critical Aortic & Mitral Regurgitation

Suspect acute structural heart disease with pulmonary edema and a normal size cardiac silhouette on CXR. Pulmonary edema may be symmetric or asymmetric. An asymmetric regurgitant jet with flow directed into one pulmonary vein can preferentially lead to asymmetrical pulmonary edema easily confused for PNA.

Acute Valvular Emergencies

Things to look for in the history to help you decipher out this scary presentation include → MI 2-7 days ago (papillary muscle rupture), Endocarditis, takosubo cardiomyopathy, or blunt chest trauma (papillary muscle or chordae tendineae rupture from elevated Ventricular pressures during the event, which is rare). (McDonald et al.) These patient’s will likely need operative repair, so get your thoracic surgeons on board soon. In the meantime, you can help them symptomatically, give BIPAP or Nitrates for fluid overload, Dobutamine for shock, etc. Acute Mitral regurgitation (unlike it’s chronic compatriot) is a medical and surgical emergency. Up until now their left atrium has not had to compensate for the back-flow of so much blood, so it isn’t all dilated and stretchy as you may see in the chronic version. Because of this blood just backs up further and further into the lungs. Furthermore, as nature likes to follow the path of least resistance- these patients are losing a lot of their cardiac output; much of the stroke volume is lost back through the mitral valve. As their cardiac output tries to make up for their loss of stroke volume, heart rate will likely increase. With the back-flow, these patients are going to present in florid heart failure with acute onset dyspnea and fluid overload. And they may possibly already be in shock.

Acute Valvular Emergencies: Pearls and Pitfalls

Like acute AR, acute MR frequently leads to overt cardiogenic shock. One key historical difference is that these patients typically present 2-7 days after acute MI.13 Patients with acute MR present with sudden onset of dyspnea from rapidly amassing pulmonary edema, as well as tachycardia.

Approach to Acute Mitral Regurgitation in the ED

Acute MR contrasts chronic MR because the left side of the heart has not had sufficient time to compensate by increasing left atrial compliance and left ventricular stroke volume. Acutely, this results in decreased cardiac output and increased pulmonary capillary wedge pressure. The diagnosis is one that is extremely important to make within the emergency department as surgical intervention is necessary, but often gets overlooked – especially in patients presenting in only mild shock.

Diagnosis and Management of Severe Mitral Regurgitation Made Easy!

The clinical presentation of MR is variable. Development of signs and symptoms depends on multiple factors including mechanism and etiology, course of the disease (rate of progression), “severity” of MR, the hemodynamic impact of MR, and presence of other coexisting cardiac diseases.

EM@3AM: Mitral Regurgitation

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

Mitral regurgitation in the critically ill: the devil is in the detail

Mitral regurgitation (MR) is common in the critically unwell and encompasses a heterogenous group of conditions with diverging therapeutic strategies. MR may present acutely with haemodynamic instability or more insidiously with failure to wean from mechanical ventilation. Critical illness is associated with marked physiological stress and haemodynamic changes that dynamically influence the severity and implication of MR.