Acute Aortic Valve Regurgitation Case File

Acute Aortic Valve Regurgitation Case File

Eugene C. Toy, Md, Michael d . Faulx, Md

Case 6

A 55-year-old man with longstanding hypertension presents to the emergency department with chest pain. He was feeling well this morning but developed sudden, tearing chest discomfort while lifting weights with a friend. He describes the pain as severe and reports discomfort in his back as well. He denies antecedent fevers, shakes, and chills. Vital signs are notable for a heart rate of 140 bpm. blood pressure of 120,/60 mmHg in the left arm supine, respiratory rate of 26 breaths! min. and pulse oximetry of 92% while breathing ambient air. The blood pressure in the right arm is 100/55 mmHg supine. He is afebrile. He appears uncomfortable while lying on the exam table and is clutching the center of his chest. His rhythm is regular. His apical impulse is not displaced, but auscultation reveals a third heart sound and a short diastolic murmur heard best at the left lower sternal border. He exhibits labored breathing. Fine inspiratory rales are heard in both lower lung fields. Abdominal and extremity exams are normal. Laboratory evaluation is normal with the exception of a white blood cell count of 11,000 cells/mm3. The electrocardiogram shows sinus tachycardia and nonspecific ST-Twave abnormalities. The chest radiograph reveals a widened mediastinum and bilateral heterogeneous opacities consistent with pulmonary edema.

c What is the most likely diagnosis?

c What is the best next step in diagnosis?

c What is the best next step in therapy?

Answer to Case 5:

Acute Aortic Valve Regurgitation

Summary: A previous healthy 55-year-old man with longstanding hypertension presents with acute chest and back pain while lifting weights. He seems unwell on arrival with vital signs notable for tachycardia (140 bpm), tachypnea (26 breaths/ min), discrepant blood pressure readings in the upper extremities (120/60 mmHg in the left arm and 100/55 mmHg in the right arm), and mild hypoxemia. Cardiac auscultation reveals a third heart sound and a short diastolic murmur at the left lower sternal border. Fine inspiratory rales are heard in both lower lung fields.

Laboratory evaluation is normal with the exception of a white blood cell count of 11,000 cells/mm3. The electrocardiogram shows sinus tachycardia and nonspecific ST-T wave abnormalities. The chest radiograph reveals a widened mediastinum and bilateral heterogeneous opacities consistent with pulmonary edema.

• Most likely diagnosis: Acute aortic regurgitation caused by acute aortic dissection.
• Next diagnostic step: Echocardiography and computed tomographic angiography.
• Next step in therapy: Hemodynamic stabilization and immediate surgical evaluation.

ANALYSIS

Objectives

1. Understand why acute left-sided valvular regurgitation results in significant hemodynamic compromise.
2. Understand how to recognize acute left-sided valvular regurgitation based on clinical presentation.
3. Understand the diagnostic approach for acute left-sided valvular regurgitation.
4. Understand that hemodynamic stabilization and immediate surgical evaluation are the cornerstones of treatment for acute left-sided valvular regurgitation.

Approach To:

Acute Aortic Valve Regurgitation

DEFINITIONS

VALVULAR REGURGITATION: Backflow of blood through the chambers of the heart due to defective closure of the valves.

AFTERLOAD REDUCTION: Medical and device interventions designed to reduce afterload, defined as left ventricular wall strain during systolic ejection. Afterload increases in acute left-sided valvular regurgitation due to an adaptive increase in systemic vascular resistance, but this increase in afterload is ultimately deleterious because it limits stroke volume and worsens regurgitation. Acute afterload reduction is the key feature of the medical management of acute left-sided valvular regurgitation.

INTRAAORTIC BALLOON PUMP (IABP): A counterpulsation balloon device that provides temporary assistance to a failing left ventricle. The balloon is percutaneously placed via the femoral artery in the descending thoracic aorta, where it is gated to the cardiac cycle, deflating during systole to reduce afterload and inflating during diastole to augment arterial pressure and promote coronary diastolic perfusion.

CLINICAL APPROACH

Etiology

Acute left-sided valvular regurgitation is a clinical entity that requires rapid diagnosis because of its impact on hemodynamics and potential to progress quickly to total cardiovascular collapse. In the normal heart, oxygenated blood returns from the lungs to the left atrium via the pulmonary veins. Blood then flows across the mitral valve into the left ventricle (LV) during diastole before leaving the heart through the aortic valve during systole. Understanding the etiology and mechanism of acute left-sided valvular dysfunction is important for the appropriate management of these conditions.

Acute aortic regurgitation (AR) results from ineffective closure of the valve cusps or a sudden change in the size or integrity of the aortic root. Aortic valve endocarditis, prosthetic valve dysfunction, acute aortic dissection, and chest trauma are leading causes of acute AR. Acute mitral regurgitation (MR) results from abnormalities in any component of the mitral valve apparatus: the anterior and posterior leaflets, the mitral annulus, the chordae tendinae, and the papillary muscles (Figure 6-1). Common triggers for acute mitral regurgitation include endocarditis, papillary muscle ischemia or infarction, rupture of the chordae in the setting of myxomatous valve disease, and chest trauma.

Pathophysiology

Acute left-sided valvular regurgitation produces a sudden decrease in forward stroke volume along with abrupt volume overload of the left side of the heart. Reduction in stroke volume leads to systemic hypoperfusion and cardiogenic shock, whereas a rapid increase in left-sided volumes leads to hypoxemia due to pulmonary congestion. Unlike chronic valvular regurgitation, the left ventricle and atrium do not have time to adapt to this marked volume overload; this is why acute severe regurgitation is so poorly tolerated while patients with chronic severe regurgitation can live with few or no symptoms for many years.

In severe acute AR, sudden high-volume regurgitation into the LV during diastole causes an abrupt drop in systemic perfusion pressure, resulting in adaptive

Figure 6-1. Mitral valve anatomy. The mitral leaflets and chordae are most likely to be affected by endocarditis. The papillary muscles are usually affected by myocardial ischemia or infarction. The mitral annulus is typically not involved in acute mitral regurgitation. (Reprinted with permission, Cleve land Clinic Center for Medical Art & Photography @ 2013. All rights reserved.)

tachycardia and vasoconstriction. The tachycardia, along with high LV diastolic pressure, leads to ineffective LV preloading by shortening diastole and producing premature closure of the mitral valve. The result is a profound drop in stroke volume and cardiac output that is further limited by increased systemic vascular resistance. Additionally, the patient may become hypoxemic as a result of pulmonary edema caused by high LV diastolic pressures, which, in the setting of ineffective mitral valve function, are reflected back into the left atrium and pulmonary veins. Hypoxemia increases tissue-level ischemia and acidosis, which only adds to the problem. Without prompt intervention, this hemodynamic downward spiral can quickly progress to frank cardiogenic shock and death.

In acute MR, sudden high-volume overload of the noncompliant left atrium during systole leads to acute pulmonary edema. Forward ejection of blood by the LV is markedly decreased because with each systolic ejection, a large portion of the stroke volume enters the left atrium. This results in a drop in cardiac output and poor systemic tissue perfusion. As with acute AR, the body adapts by increasing heart rate and systemic vascular resistance (SVR), which may temporarily augment cardiac output. Inevitably the high SVR works to limit cardiac output further and the potentially lethal cycle of increasing hypoxemia, decreasing cardiac output, and tissue-level acidemia can lead to frank cardiogenic shock and death.

CLINICAL PRESENTATION

Patients with acute left-sided regurgitation present with symptoms and signs of poor forward flow such as profound weakness, altered sensorium, dyspnea, and syncope. Many will also present with a marked increase in work of breathing and even frank respiratory failure with tachypnea, distress, and use of accessory muscles to breathe. There may also be symptoms associated with the precipitant of the acute valvular dysfunction. When aortic dissection is the cause of valvular dysfunction, patients classically complain about sudden, tearing chest pain that radiates to the back or abdomen. Fevers, shakes, and chills are usually present in those with aortic or mitral valve endocarditis.

Physical examination of patients with acute left-sided valvular regurgitation is usually notable for signs of hemodynamic compromise such as hypotension, tachycardia, diaphoresis, cool extremities, and pulmonary congestion. In patients with acute MR, the apical impulse is usually nondisplaced but hyperdynamic. Auscultation is notable for a soft S1 and a widely split S2 due to early closure of the aortic valve with decreased afterload. An S3 and a loud S4 can sometimes be heard. The classic, blowing, holosystolic murmur of mitral regurgitation is usually shorter and softer in acute MR, due to high left atrial pressures and subsequent reduction in systolic driving pressures. The murmur can even be inaudible in some patients. Examination of the neck and thorax is usually notable for elevated jugular venous pressure and fine inspiratory rales.

Acute AR differs from its chronic counterpart in that the signs of hyperdynamic circulation are usually absent. Pulse pressure can be normal or minimally widened, and the apical impulse may not be displaced. In patients with aortic dissection, blood pressures in both arms may not be equal. Auscultation of the heart may reveal a soft or absent S1 due to premature closure of the mitral valve. A loud P2 can be heard when pulmonary hypertension is present. An S3 is frequently audible as well. The diastolic murmur of AR is short and soft or may not even be present if the regurgitation is severe.

Diagnostic Approach

Laboratory evaluation of patients with acute left-sided valvular regurgitation may be notable for peripheral leukocytosis in those with endocarditis but is otherwise unrevealing. The electrocardiogram is usually notable for sinus tachycardia and nonspecific ST-T wave abnormalities. Chest radiographs may show pulmonary edema in both acute MR and acute AR. In cases of aortic dissection, a widened mediastinum or enlarged cardiac silhouette may be present.

Echocardiography, both transthoracic and transesophageal, is the mainstay for diagnosis and can often determine both the severity and the cause of valvular dysfunction. Additionally, echocardiography provides insight into LV function and aortic root anatomy. Computed tomographic angiography is helpful when acute aortic dissection is suspected.

Treatment

Patients with acute left-sided valvular regurgitation often require hemodynamic stabilization before surgical correction. Aggressive afterload reduction with potent intravenous agents such as sodium nitroprusside lowers diastolic pressure within the LV and improves forward cardiac output. Intravenous inotropic support may be needed in severe cases to maintain enough forward flow to keep the patient alive before definitive surgical correction can occur. Cardiothoracic surgical consultation should occur immediately, especially when aortic dissection or trauma is the cause of valvular dysfunction. When endocarditis is suspected, blood cultures should be obtained prior to starting antibiotic therapy. In patients with severe MR, placement of an intraaortic balloon pump (IABP) may serve as a temporizing measure while awaiting surgery. IABP placement in patients with severe AR is contraindicated.

CASE CORRELATION

• See also Case 1 (acute coronary syndrome/STEMI) and Case 3 (cardiogenic shock).

COMPREHENSION QUESTIONS

6.1 A 55-year-old hospitalized man develops sudden shortness of breath. He has newly diagnosed coronary artery disease that manifested as an inferior ST elevation myocardial infarction 3 days ago. Coronary angiography at presentation showed a dominant right coronary artery that was occluded in the distal segment. Percutaneous coronary intervention was unsuccessful. He had been doing well over the last few days until now. He denies chest pain. Physical examination is notable for a heart rate of 140 bpm and a blood pressure of 90/60 mmHg. He is extremely uncomfortable. Jugular venous pulsations are biphasic but elevated to approximately 14 cm above the right atrium. He exhibits labored breathing, and fine inspiratory rales are heard in both lower lung fields. The apical impulse is not displaced. Cardiac auscultation reveals a soft S1, an S3, and a new short systolic murmur heard best at the apex. Echocardiography shows severe MR. What is the most likely mechanism responsible for his acute decompensation?

A. Mitral leaflet perforation

B. Recurrent myocardial ischemia

C. Ruptured chordae tendinae

D. Ruptured posteromedial papillary muscle

E. Ruptured anterolateral papillary muscle

6.2 A 25-year-old woman is brought to the emergency department following a motor vehicle accident. She has a heart rate of 120 bpm and a blood pressure of 85/55 mmHg. She is saturating 89% while breathing ambient air. A chest radiograph shows pulmonary edema, and an echocardiogram reveals severe mitral regurgitation. Which of the following would be contraindicated in this patient?

A. Initiation of sodium nitroprusside

B. Initiation of phenylephrine

C. Initiation of dobutamine

D. Placement of an intraaortic balloon pump

E. Immediate surgical evaluation

6.3 A 65-year-old man with a bicuspid aortic valve presents to the emergency department with syncope. He states that he has not been feeling well over the last 2 days. He reports appetite loss, subjective fevers, and chills. Vital signs are notable for a heart rate of 115 bpm and a blood pressure of 95/45 mmHg. He is febrile. Cardiac examination is notable for a short diastolic murmur heard best at the left upper sternal border. Which of the following would be contraindicated in this patient?

A. Initiation of broad-spectrum antibiotics after obtaining blood cultures

B. Initiation of sodium nitroprusside

C. Initiation of inotropes

D. Placement of an intraaortic balloon pump

E. Immediate surgical evaluation

ANSWERS

6.1 D. MR secondary to papillary muscle rupture usually involves the posteromedial papillary muscle because it is supplied only by the posterior descending artery whereas the anterolateral papillary muscle is supplied by both the diagonal branches of the left anterior descending artery and the obtuse marginal branches of the circumflex artery. This patient with a recent, unrevascularized inferior myocardial infarction was at particularly high risk for this early mechanical complication.

6.2 B. Initiation of phenylephrine, a selective α1-adrenergic receptor agonist, would increase afterload and thereby worsen the MR.

6.3 D. This patient likely has infective endocarditis involving his bicuspid aortic valve, resulting in severe AR. Placement of an intra-aortic balloon pump is contraindicated in patients with severe AR.

CLINICAL PEARLS

C Acute left-sided valvular regurgitation presents differently from chronic valvular regurgitation with respect to hemodynamics because there is no time for adaptive atrial or ventricular remodeling.

C Echocardiography is the mainstay for diagnosis and provides information about the severity and mechanism of valvular dysfunction.

C Causes may differ, bur treatment is similar for both acute Mr and acute Ar with afterload reduction. hemodynamic support, adequate ventilation. and emergent cardiac surgery.

References

Carabello BA, Crawford FA. Valvular heart disease. N Engl J Med. 1997;337:32–41. Fauci AS, Braunwald E. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008:1465–1480. 

Griffin BP, Callahan TD, Menon V. Manual of Cardiovascular Medicine. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013:238–295. 

Piérard LA, Lancellotti P. The role of ischemic mitral regurgitation in the pathogenesis of acute pulmonary edema. N Engl J Med. 2004;351:1627–1634. 

Sabatine MS. Pocket Medicine. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:121–123.

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