Sunday, April 4, 2021

Acute Right Ventricular Failure Complicating Myocardial Infarction Case File

Posted By: Medical Group - 4/04/2021 Post Author : Medical Group Post Date : Sunday, April 4, 2021 Post Time : 4/04/2021
Acute Right Ventricular Failure Complicating Myocardial Infarction Case File
Eugene C. Toy, Md, Michael d . Faulx, Md

Case 20
A 57-year-old man is seen in the emergency room for chest heaviness. Last week, while sitting on his couch. he noted an episode of chest discomfort that spontaneously resolved after 10 minutes. He assumed that it was indigestion. However, this morning he had an episode of severe recurrent chest discomfort that did not resolve and was associated with diaphoresis and nausea. The patient has a history of type 2 diabetes mellitus, hypertension, hyperlipidemia, and obstructive sleep apnea. His medications are aspirin, metformin, candesartan, and rosuvastatin. Vital signs were normal in the ambulance, so he was treated with chewable aspirin 325 mg and one sublingual nitroglycerin. This partially relieved his pain but caused him dizziness and lightheadedness. On examination in the emergency room he appears diaphoretic. Temperature is 98.4°C, heart rate 105 bpm, blood pressure 85/57 mmHg, respirations 18 breaths/min, and O2 saturation 94% on room air. Cardiac auscultation reveals a regular tachycardia without murmurs, rubs, or gal lops. The lungs are clear to auscultation bilaterally. The abdomen is soft without distension or tenderness. The extremities are cool with thready pulses and no edema. Neurological exam is normal. Jugular venous distension is hot seen. An ECG is shown in Figure 20-1.
  • What is the most likely diagnosis?
  • What is the best next diagnostic step?
  • What is the best next step in acute management?
Acute Right Ventricular Failure Complicating Myocardial Infarction

Figure 20-1. ECG of the main subject of this case.


Answer to Case 20: 
Acute Right Ventricular Failure Complicating Myocardial Infarction

Summary: A 57-year-old man with type 2 diabetes, hypertension, hyperlipidemia, and obstructive sleep apnea presented with severe chest pain. He has several risk factors for coronary artery disease, and his symptoms are typical of crescendo angina. He was treated with aspirin and nitroglycerin in the ambulance, which caused him to become hypotensive. His ECG reveals ST elevations in the inferior leads.
  • Most likely diagnosis: Right ventricular infarction.
  • Next step in acute management: Intravenous fluids to raise preload.
  • Next diagnostic step: Cardiac catheterization.
ANALYSIS

Objectives
  1. Recognize the signs and symptoms of right-heart failure.
  2. Know the most common etiologies of right-heart failure.
  3. Understand the management of right-heart failure on the basis of the given etiology.
Considerations
This 57-year-old man with coronary artery disease risk factors presented to the emergency room with chest pain. The first priority should be assessment of his vital signs and electrocardiogram. Vital signs were normal in the ambulance; however, sublingual nitroglycerin led to hypotension. This should immediately suggest right ventricular involvement of a myocardial infarction to the care provider. An acutely failing right ventricle depends on preload to maintain cardiac output. Dropping the preload via nitrates will lead to hypotension. Electrocardiography was appropriately done next and showed inferior ST elevations. A right-sided ECG can also be performed to look for RV involvement, which shows up as ST elevations in lead V4R.

Approach To:
Right Ventricular Failure

DEFINITIONS

RIGHT VENTRICULAR (RV) FAILURE: The inability of the right ventricle to provide adequate blood flow through the pulmonary circulation at normal central venous filling pressures.

ANASARCA: Extreme generalized edema.

COR PULMONALE: Right ventricular enlargement and dysfunction secondary to increased pulmonary artery resistance or pressure.

EBSTEIN ANOMALY: A congenital malformation in which the septal and posterior leaflets of the tricuspid valve are displaced toward the apex, leading to atrialization of the right ventricle and tricuspid regurgitation

CLINICAL APPROACH

Etiologies
The right heart is often forgotten in typical discussions of heart failure. The RV is thinner-walled, more difficult to visualize on echocardiography, and functions to pump blood to only one organ. However, dysfunction of the right ventricle can lead to severe morbidity and mortality.

The right ventricle can fail from a variety of primary and secondary causes (Table 20-1). Primary right ventricular dysfunction can result from RV myocardial infarction, myocarditis, or cardiomyopathy. However, the most common causes are secondary ones, where the RV is a bystander to left ventricular, valvular, or pulmonary vascular dysfunction (cor pulmonale). This secondary involvement of the right ventricle portends a worse prognosis.

Specifially noteworthy here is tricuspid regurgitation, which is most commonly a functional problem. In other words, the right ventricle is secondarily volume overloaded, leading to dilatation of the ventricle, and tricuspid annulus, which causes regurgitation. The severity of this regurgitation often varies with the patient’s volume status. Primary tricuspid regurgitation is typically caused by endocarditis, valvulopathy (carcinoid heart disease), or genetic abnormality such as Ebstein anomaly.

Pathophysiology
The right ventricle has the same cardiac output as the left ventricle at about 25% the stroke work given the low resistance in the pulmonary circulation. Thus, the RV myocardium is more thin-walled than the LV. The blood supply to the right ventricular free wall arises from RV branches off the right coronary artery, while the septum is supplied by the septal perforators off the left anterior descending artery

causes of right ventricular failure

and the posterior descending artery. Given the subsystemic pressures of the RV, its coronary supply is filled during both systole and diastole.

It is also important to recognize that left ventricular preload is dependent on the function of the right ventricle. A failed right ventricle requires an adequate blood volume to maintain blood pressure and cardiac output. This is why the treatment for hypotension in the setting of a right ventricular infarction is to first administer intravenous fluids to maintain preload.

Clinical Presentation
A failed right ventricle leads to fluid backup into the periphery and venous congestion of the abdominal organs. Patients complain of peripheral edema, abdominal distension, and fullness. Hepatic congestion can lead to liver failure, ascites, and coagulopathy. Renal vascular congestion can lead to acute kidney injury. This condition can be misdiagnosed as other conditions that cause anasarca, such as primary liver failure or nephrotic syndrome. The lack of lung symptoms and pulmonary edema on chest x-ray often confuse clinicians into prematurely ruling out heart failure. However, as most right-heart failure is caused by left-sided heart failure or pulmonary hypertension, patients will often have some pulmonary complaints.

On physical exam, vital signs may be abnormal in states of low cardiac output. There may be a low blood pressure or a compensatory increase in heart rate. Weight gain over time should be evaluated. Head and neck exam will show elevated jugular venous pressure (JVP). This is calculated by positioning the patient at a 45° angle and measuring the jugular venous pulsation. JVP above 8 cm of water above the right atrium is considered elevated. Kussmaul’s sign appears when neck veins rise paradoxically during inspiration. This is due to right-heart failure or pericardial tamponade. Another way of approximating central venous pressure is to view the superficial veins in the patient’s arm. The arm is raised until the veins disappear, and this distance in centimeters above the heart will estimate the central venous pressure. One can also elicit the hepatojugular reflux and look for a sustained elevation in JVP, which signifies elevated right-sided filling pressures.

On cardiac exam it is important to listen for murmurs, especially right-sided murmurs, which increase with inspiration. A loud P2 signifying pulmonary hypertension and a right-sided S3 of RV failure may also be heard. Abdominal exam may reveal hepatomegaly, ascites, or distended abdominal wall veins. A pulsatile liver is a sign of severe tricuspid regurgitation. The peripheral exam often reveals edema. It is important to remember to look for edema in the sacral region, especially in patients who are bedbound. There may also be bruising from coagulopathy.

Electrocardiography may show an acute inferior infarct, or Q waves in the inferior leads signifying an old inferior myocardial infarction. Right-axis deviation, a right bundle branch block, or tall R waves (larger than the corresponding S wave) in lead V1 are all possible signs of right ventricular disease. Chest radiography will show an enlarged right atrial or ventricle (Figure 20-2), while pulmonary findings will vary with the etiology. Laboratory abnormalities may be found, including hyponatremia, elevated BUN, and creatinine and transaminitis due to hepatic congestion. Elevated cardiac biomarkers or brain natriuretic peptide may be found in chronic heart failure or may be a sign of an acute ischemic event.

Enlarged right atrium

Figure 20-2. Enlarged right atrium, right ventricle, and bilateral pulmonary arteries in a patient with primary pulmonary hypertension.

Echocardiography should be used to assess for left and right ventricular function and valvular disease. It can also be used to estimate pulmonary and right atrial pressures.

The presence of right ventricular failure portends a poorer prognosis for most patients with cardiovascular disease. Right ventricular systolic dysfunction detected by echocardiography is associated with a nearly twofold increase in mortality in patients with chronic left ventricular systolic heart failure. Significant right ventricular failure also affects the management of patients with advanced heart failure. Mechanical therapies such as left ventricular assist devices (LVADs) may not provide adequate hemodynamic support in patients with failing right ventricles; such patients may require implantation of a biventricular support device or a total artificial heart instead. Evidence of acute right ventricular strain detected by echocardiography or ECG is also associated with increased mortality in patients presenting with acute pulmonary thromboembolism (PE). The presence of right ventricular strain in the setting of PE, even in the face of hemodynamic stability, is a criterion for the use of intravenous fibrinolytic therapy.

Treatment
Treatment of right ventricular failure centers around treating the underlying etiology of the dysfunction. Symptoms of RV failure due to volume overload states of left ventricular failure are remedied by proper diuresis and treatment of the LV failure. If the cause is pulmonary arterial hypertension, targeted therapies such as epoprostenol infusions appear to improve right ventricular function. Other pressure
overload states such as pulmonary embolism should be treated with anticoagulation with the consideration of thrombolytic therapy in cases of hemodynamic compromise. Severe valvular heart disease typically needs to be corrected surgically.

Functional tricuspid regurgitation should be treated with diuresis, while symptomatic primary tricuspid regurgitation should be surgically corrected. Undergoing operative treatment for tricuspid regurgitation prior to the onset of advanced heart failure symptoms is associated with a decreased postoperative mortality.

Right ventricular failure from myocardial infarction typically also involves the left ventricular myocardium, and coronary artery disease management and neurohormonal blockade with renin-angiotensin-aldosterone system inhibition and beta-blockers is the treatment of choice. Unfortunately, it is unknown whether this therapy is beneficial in isolated RV failure due to other causes. In acute cases of cardiogenic shock due to RV failure, inotropic agents such as dobutamine can be used. Hypoxemia (which causes pulmonary arterial vasoconstriction) should be corrected, and pure alpha agonists should be avoided because of the increase in pulmonary vascular resistance.

CASE CORRELATION
  • See also Case 16 (acute heart failure), Case 17 (advanced heart failure), Case 18 (cardiomyopathies), and Case 19 (chronic heart failure).

COMPREHENSION QUESTIONS

20.1 A 66-year-old man presented to the emergency room with acute-onset severe 10/10 chest pain. He was found to have ST elevations in leads II, III, and aVF. His blood pressure is 101/64 mmHg. He was given 325 mg of chewable aspirin. What is your next step in management?
A. Sublingual nitroglycerin
B. Intravenous morphine
C. Right-sided ECG
D. Echocardiogram
E. Cardiac enzymes

20.2 A 42-year-old woman with a history of human immunodeficiency virus (HIV) and active drug use presents to the clinic with 3 weeks of low-grade fevers. She also notes leg swelling and abdominal fullness. On exam, her jugular venous pressure is elevated and she has 2+ edema to her midthighs bilaterally. She has clear lungs and a heart murmur. What do you expect her murmur to sound like?
A. Holosystolic murmur at the left lower sternal border that increases with inspiration
B. Crescendo-decrescendo murmur heard best at the right upper sternal border
C. Blowing diastolic mumur heard best at the right upper sternal border while sitting forward
D. Holosystolic murmur at the apex that radiates to the axilla and increases with expiration

20.3 A 72-year-old man with a history of mitral valve prolapse, moderate mitral regurgitation, and a remote history of smoking presents with worsening lower extremity edema. Echocardiography shows the aforementioned findings as well as a dilated left atrium and moderate right ventricular dysfunction. His ejection fraction is 60%. What is the cause of his right ventricular dysfunction?
A. Right ventricular myocardial infarction
B. Primary pulmonary hypertension
C. Mitral regurgitation
D. COPD
E. Left ventricular systolic heart failure


ANSWERS

20.1 C. A patient with ST elevations in the inferior leads should have a right-sided ECG done to look for RV infarction (diagnosed with ST elevations in lead V4R). Acute right ventricular failure, as seen in an RV infarction, requires preload to maintain blood pressure. Giving nitroglycerin prior to this may drop his blood pressure even more. After an ECG, a heart catheterization should be facilitated before obtaining an echocardiogram or cardiac enzymes.

20.2 A. The patient is a drug user with fever, signs of right-sided heart failure, clear lungs, and a new heart murmur. All of these factors point to right-sided valvular infective endocarditis. This most commonly affects the tricuspid valve and causes tricuspid regurgitation, which results in a holosystolic murmur best heard at the left lower or sternal border. This murmur classically increases with inspiration.

20.3 C. The most likely cause of this patient’s right ventricular failure is due to volume overload from mitral regurgitation. A normal left ventricular ejection fraction coupled with a dilated left atrium signals left ventricular diastolic dysfunction or significant mitral valve disease.


CLINICAL PEARLS
  • The most common cause of right ventricular failure is left-sided heart failure.
  • Right-sided heart failure should be considered in patients presenting with anasarca or cryptogenic cirrhosis.
  • The typical heart failure regimen of ACE inhibitors, ARBs. aldosterone receptor blockers, beta-blockers, and hydralazine-nitrate combinations has not been shown to work in isolated right ventricular heart failure.
  • Identifying the etiology of right-heart failure is essential in providing targeted therapy.
  • Functional tricuspid regurgitation is often a sign of right ventricular volume overload and is treated with diuresis, while severe primary tricuspid regurgitation requires surgical management.
References

Aksoy O, Tuzcu EM. Complications of myocardial infarction. In: Griffin BP, Kapadia SR, Rimmerman CM, eds. The Cleveland Clinic Cardiology Board Review. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013. 

Jacob M, Tang WHW. Pathophysiology of congestive heart failure. In: Griffin BP, Kapadia SR, Rimmerman CM, eds. The Cleveland Clinic Cardiology Board Review. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013. 

Rogers JH, Bolling SF. The tricuspid valve. Perspective and evolving management of tricuspid regurgitation. Circulation. 2009;119:2718–2725. 

Voelkel NF, Quaife RA, Leinwand LA, et al. Right ventricular function and failure: report of a National Heart, Lung, and Blood Institute Working Group on Cellular and Molecular Mechanisms of Right Heart Failure. Circulation. 2006;114(17):1883–1891.

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