Heart Failure - Case Study

Case Scenario:
A 42-year-old white man is seen in the ER with a chief complaint of shortness of breath that has lasted for 1 week. He reports having had a viral syndrome approximately 3 weeks before admission. Subsequently, he noted the development of lower extremity edema, a 15-lb weight gain, dyspnea on
exertion, and orthopnea. Currently he complains of dyspnea at rest.
Physical examination reveals an irregularly irregular heart rate of 130 per minute. His blood pressure is 90/60 mm Hg, and his respiratory rate is 22 per minute.
Examination of the jugular venous pressure demonstrates a mean pressure of 12 to 14 cm of water with a prominent V wave.
Lung examination reveals bibasilar dullness with rales extending one fourth of the way up from the basal lung fields bilaterally.
Cardiac examination findings are significant for a diffuse point of maximal impulse, which is displaced to the anterior axillary line. The S1 and S2 are of variable intensity, and a prominent S3 gallop over the displaced cardiac apex is appreciated. There is a grade 2/6 holosystolic murmur that is heard best at the cardiac apex, with prominent radiation to the axilla and no change w ith respiration. On examination of the abdomen, an enlarged, tender liver is found.
The extremities are cool and exhibit 2+ pitting edema.
The ECG show s atrial fibrillation with nonspecific ST-T–w ave changes, a left bundle branch block (LBBB) and occasional ventricular premature beats.
Arterial blood gas measurements performed with the patient on 4 L of oxygen per minute by nasal cannula reveal a pH of 7.46, a PO2 of 52 mm Hg, a PCO2 of 32 mm Hg, and a bicarbonate (HCO3) concentration of 26 mmol/L.

Answer the following questions:
1. Does this patient have left, right, or biventricular failure?
2. An S3 is heard, but no S4. Why?
3. What chest radiographic findings would you expect to see in this patient?
4. What neurohormonal mechanisms are likely to be activated in this patient?
5. What diagnostic tests should be performed?
6. What treatment options would likely be beneficial in this patient?
7. Is it possible that the ventricular function w ill improve with medical therapy?

Answers:


1. Does this patient have left, right, or biventricular failure?
This patient has findings indicating both right and left ventricular failure (biventricular failure).
The cool extremities, tachycardia, and narrow pulse pressure suggest poor forward cardiac output and could reflect either right or left ventricular failure. A left ventricular S3 gallop and pulmonary rales are signs of left ventricular failure. The bibasilar dullness suggests the presence of bilateral pleural effusions, which may be seen in the setting of either right or left ventricular dysfunction. The apical murmur most likely represents mitral regurgitation because it is loudest at the apex, it radiates to the axilla, and it does not change with respiration.
We do not know from the history whether the patient had a preexisting valvular disorder. Secondary mitral or tricuspid regurgitation occurs commonly in patients with ventricular enlargement and
dysfunction due to distortion of the supporting structures of the atrioventricular valves. Tricuspid regurgitation causes a large V w ave in the jugular venous pulse.
There are many signs of right ventricular failure in this patient. Elevated central venous pressure is apparent from the patient's jugular venous distention. Kussmaul's sign is the lack of a fall in the jugular venous pressure with inspiration and is due to the right ventricle's inability to handle the
augmented venous return. It may be encountered in patients with right ventricular failure or constrictive pericardial disease. The patient's enlarged liver is the result of hepatic congestion stemming from increased back pressure on the hepatic vein. The pitting edema in the lower extremities is caused by elevated hydrostatic pressure in the venous system, resulting in
extravasation of fluid into the interstitial space of the ankles, where the forces of gravity are the greatest.

2. An S3 is heard, but no S4. Why?
An S3 is a low -frequency sound heard 0.13 to 0.16 second after S2. An S3 occurs at the end of the rapid phase of ventricular filling and is most likely due to the vibration of the chordae tendineae or the left ventricular wall with rapid filling, and may arise from the right or left ventricle. A left ventricular S3 is best heard with the bell of the stethoscope at the cardiac apex. A right
ventricular S3 is also best heard with the bell, but is most audible at the lower left sternal border or over the epigastrium.
An S3 is a normal finding in children or young adults, but in middle-aged or older patients it is usually a sign of volume overload most often due to HF, as it is in this patient.
An S4 is a presystolic atrial sound (gallop) that is heard w hen the ventricle is poorly compliant. Given the patient's volume overload, it is likely that both ventricles are poorly compliant. How ever, the patient is in atrial fibrillation, and therefore there are no effective atrial systoles to give rise to an S4 (rarely, an S4 may be heard even in atrial fibrillation because of the high left atrial pressure and increased flow in late diastole).

3. What chest radiographic findings would you expect to see in this patient?
The likely findings on a chest radiography stem from the effects of volume overload and elevated pulmonary venous pressure.
Cardiomegaly, which is defined as a cardiac-to-thoracic diameter ratio exceeding 0.5, is present in most cases in which there is depressed left ventricular systolic function.
Cephalization of the pulmonary blood flow occurs and is evidenced by the enlarged pulmonary vessels in the superior portion of the pulmonary tree.
The haziness of the central vasculature is a result of the increased hydrostatic pressure and subsequent transudation of fluid into the tissue surrounding the vessels.
Kerley B lines are horizontal, thin, sharp lines that extend inward from the periphery of the lungs. They represent edema formation within the lungs and hypertrophy of the interlobular septa.
Pleural effusions may be found in the setting of right or left ventricular failure. When pulmonary congestion is severe and alveolar edema is present, a “butterfly” or “bat-wing” infiltrate may be seen centered over the main pulmonary artery.

4. What neurohormonal mechanisms are likely to be activated in this patient?
The two neurohormonal mechanisms most likely to be activated in this patient are the renin–angiotensin–aldosterone system and the adrenergic nervous system. The serum norepinephrine level has been shown to correlate inversely with the EF and patient survival in those with chronic HF. Cardiac adrenergic activation occurs even earlier than systemic adrenergic activation. Other hormones that may be activated include vasopressin, endothelin, and multiple cytokines such as tumor necrosis factor α and interleukin 1.

5. What diagnostic tests should be performed?
Initially a complete blood count, and thyroid stimulating hormone (TSH), electrolyte, renal and hepatic function tests should be obtained to determine if there are electrolyte abnormalities that need to be corrected, if there is significant underlying renal or hepatic disease, and to determine if anemia or thyroid abnormalities may have exacerbated the heart failure.
An ECG should be performed to determine if there has been an MI or if arrhythmias are present.
A chest x-ray will confirm the HF and detect significant underlying pulmonary problems.
An echocardiogram will evaluate ventricular size and function, the presence of valve abnormalities, and may often suggest the underlying etiology of the ventricular dysfunction. For example, if the anterior wall is akinetic and scarred, a previous MI can be inferred. When the left
ventricle is large and has global dysfunction, it may be difficult to determine if there is underlying CAD.
When the patient has stabilized an exercise, echocardiogram or nuclear study may reveal reversible ischemia.
Coronary angiography may be necessary to exclude significant CAD if noninvasive studies do not clearly exclude ischemia. If there is no significant coronary disease and no significant valve disease, the diagnosis is likely idiopathic cardiomyopathy. The type of cardiomyopathy can generally be categorized by echocardiogram as dilated, hypertrophic, or restrictive with dilated cardiomyopathy being the most common. A series of tests, depending on the type of cardiomyopathy, should be carried out to exclude specific etiologies.

6. What treatment options would likely be beneficial in this patient?
The general goals for the medical treatment of HF are as follows:
a. Identify and treat the underlying condition.
b. Eliminate any precipitating factors.
c. Treat the symptoms.
d. Improve survival.
The first step is to identify the underlying cause of HF. This may be hypertension, CAD, cardiomyopathy, valvular heart disease, or many other causes. Treatment includes medical treatment for hypertension, coronary angiography and coronary angioplasty or coronary bypass surgery for
coronary disease, and valve replacement or repair for valve disease. In patients with HF, it is important to eliminate precipitating factors (e.g., dietary or medication noncompliance, arrhythmias, anemia). Excess alcohol use may cause a cardiomyopathy, but excess alcohol may also exacerbate
HF of any cause.
Symptomatic improvement is usually achieved by relieving the excess salt and water retention with diuretics and by improving preload and afterload with vasodilators—particularly the ACE inhibitors. Loop diuretics such as furosemide, torsemide, or bumetanide are most often used because they are
more effective than thiazide diuretics when renal perfusion is decreased. Care must be taken to avoid overdiuresis and to replace potassium and magnesium because hypokalemia and/or hypomagnesemia may promote ventricular arrhythmias.
The combination of ACE inhibitors and β-adrenergic antagonists (β-blockers) is the cornerstone of therapy for patients with HF due to systolic dysfunction. Many ACE inhibitors are now available (captopril, enalapril, lisinopril, quinapril, ramipril, benazepril, trandolapril, fosinopril, moexipril), and there does not appear to be a clear therapeutic advantage to the use of one over another. How ever, the target dose of an ACE inhibitor is best determined from the individual agents that have been studied in patients with HF. By decreasing the conversion of angiotensin I to angiotensin II, these drugs reduce preload and afterload, improve symptoms, and prolong survival in patients w ith systolic dysfunction. Cough is the most common side effect of ACE inhibitors, but cough is also a common symptom of HF. Care should be taken to exclude HF as a cause of the cough before these drugs
are discontinued. Hypotension, renal insufficiency, and hyperkalemia are less frequent but serious side effects of the ACE inhibitors. In general, these occur in patients with severe HF and/or preexisting renal insufficiency. In patients with severe HF or intrinsic renal insufficiency, the ACE inhibitors should be started in very low doses, and the blood pressure and serum
potassium and creatinine levels must be monitored carefully.
β-Adrenergic blockers have also been shown to improve survival in patients with systolic dysfunction and HF. Although the benefit on symptoms is less clear than with ACE inhibitors, β-blockers produce a larger improvement in remodeling, EF, and survival. Because β-blockers reduce heart rate and
initially decrease contractility, introduction of treatment or up-titration may result in worsening of symptoms. These drugs must therefore be started in low doses and up-titrated slowly, and patients must be monitored carefully.
Patients with decompensated HF usually should not be given β-blockers. Several β-blockers (carvedilol, metoprolol, and bisoprolol) have been shown to reduce mortality in patients w ith HF. It is not yet clear if there are advantages of one over another.
There are several possible additions to medical therapy in patients with chronic HF due to systolic dysfunction, who remain symptomatic after maximum tolerable doses of ACE inhibitors and β-blockers. The addition of aldosterone antagonists reduces mortality in patients w ith severe chronic HF and in those  ho have experienced HF follow ing an MI. ARBs such as losartan, candesartan, irbesartan, and valsartan block the angiotensin II receptor directly. They appear to have beneficial effects in reducing cardiovascular mortality and hospitalization for HF w hen added to ACE inhibitors and β-blockers. Adding both aldosterone antagonists and ARBs to ACE inhibitors is probably not reasonable for most patients because of the increased risk of hyperkalemia.
The combination of hydralazine and isosorbide dinitrate reduces mortality and hospitalizations and improves quality of life in African Americans with severe chronic HF due to systolic dysfunction. The benefits are less clear in non–African Americans.
Another option is the use of digoxin, which results in an improvement in symptoms and a reduction in hospital admissions but no reduction in mortality.
Sodium restriction is an essential part of any program designed to treat patients with HF. Patients should avoid excess salt and water, weigh themselves daily, avoid NSAIDs, and report any increase in symptoms or weight gain promptly to their physicians.

7. Is it possible that ventricular function will improve with medical therapy?
This patient has an EF of 20%. ACE inhibitors help prevent further deterioration in EF. β-Blockers, if up-titrated to recommended doses, are likely to improve this individual's EF by 7% to 10%. The full improvement may not be seen for up to 6 months.

Your patient improved after diuresis and administering ACE inhibitors and β-blockers. Six months later his EF has increased from 20% to 29%. He is on digoxin with therapeutic levels and an aldosterone antagonist w ith normal serum creatinine and potassium. He has no resting dyspnea or edema, but does have dyspnea with simple tasks.