Congestive heart failure case file

Congestive Heart Failure Case File

Eugene C. Toy MD, Donald Briscoe, MD, FA  AFP, Bruce Britton, MD, Joel J. Heidelbaugh, MD, FA  AFP, FACG

Case 27

A 66-year-old woman presents to your office complaining of shortness of breath and bilateral leg edema that have been worsening for 3 months. She emphatically tells you, "I get out of breath when I do housework and I can't even walk to the corner:' She has also noticed difficulty sleeping secondary to a dry cough that wakes her up at night and further exacerbation of her shortness of breath while lying flat. This has forced her to use three pillows for a good night's sleep. She denies any chest pain, wheezing, or febrile illness. She has no past illnesses and takes no medications. She's never smoked and drinks socially. On examination, her blood pressure (BP) is 187 /90 mm Hg, her pulse is 97 beats/min, her respiratory rate is 16 breaths/min, her temperature is 98°F (36.6°C), and her oxygen saturation is 93% on room air by pulse oximetry. She has a pronounced jugular vein. Cardiac examination reveals a pansystolic murmur. Examination of her lung bases produces dullness bilaterally. You find 2+ pitting edema of both ankles. An electrocardiogram (ECG) shows a normal sinus rhythm and a chest x-ray demonstrates mild cardiomegaly with bilateral pleural effusions. You decide she needs further workup, so you call the hospital where you have admitting privileges and arrange for a telemetry bed.

⯈ What is the most likely diagnosis?

⯈ What is the next diagnostic step?

⯈ What is the initial step in therapy?

ANSWER TO CASE 27:

Congestive Heart Failure

Summary: A 66-year-old woman presents to your office with worsening shortness of breath, bilateral leg edema, and three-pillow orthopnea. She is not known to be hypertensive, but her BP is 187/90 mm Hg and her oxygen saturation is 93% on room air. Her examination reveals jugular venous distension (JVD), a cardiac murmur, and decreased breath sounds at both lung bases. On a chest x-ray, you find bilateral pleural effusions and decide to admit her for further workup and management.

• Most likely diagnosis: New-onset congestive heart failure (CHF)
• Next diagnostic step: Serial cardiac enzymes and ECGs; blood work to include a CBC, electrolytes, and renal function; echocardiogram
• Initial therapy: Telemetry monitoring, IV diuretics, and oxygen

ANALYSIS

Objectives

1. Know how to clinically recognize congestive heart failure (CHF).

2. Understand the classification of CHE

3. Understand the mechanism of action of the drugs used in the treatment of acute and chronic CHE

4. Understand the underlying pathophysiology that occurs in CHF and the rationale for treatment options.

5. Be familiar with the outpatient management of CHF and the importance of patient education.

Considerations

This 66-year-old woman presented with CHE Her most immediate problem is oxygenation and volume overload on her weakened heart. The first priority is optimizing oxygen exchange by administering oxygen via nasal cannula, dilating pulmonary vasculature, and decreasing cardiac preload and afterload. Most cases of CHF are caused by either coronary artery disease or hypertension, so it is imperative to evaluate these patients for acute coronary syndrome and coronary arterial disease. The overloading of fluid in the lungs is a common cause of anxiety and distress in patients with acute CHF because of the continuous struggle to oxygenate adequately. This anxiety activates sympathetic pathways and mounts catecholamine induced responses, which produce further worsening of acute heart failure by causing tachycardia and increasing peripheral vascular resistance, leading to greater stress on the heart and worsening of symptoms. These triggers can, in part, be suppressed by the use of an agent such as morphine sulfate, which acts both as an anxiolytic and a vasodilator. Furosemide (Lasix) is the diuretic of choice, not only for its diuretic effect but also for its immediate vasodilatory action on bronchial vasculature. Admitting these patients to the hospital allows for closer maintenance of homeostasis in their fluid balances and evaluation of any underlying condition that may have precipitated the CHF. Other medications, including angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) and β-blockers, help to control heart failure symptoms by decreasing preload and afterload, and reducing cardiac remodeling.

Approach To:

Congestive Heart Failure

DEFINITIONS

CONGESTIVE HEART FAILURE: Impairment of the ventricle's ability to fill with or eject blood which results in inadequate circulation of blood to meet metabolic needs, characterized by dyspnea, fatigue, and fluid retention

FRAMINGHAM HEART STUDY: Large, prospective cohort study of the epidemiologic factors associated with cardiovascular diseases

CLINICAL APPROACH

CHF can be subdivided into systolic or diastolic dysfunction and right- or left sided heart failure, all of which can coexist. Systolic dysfunction exists when there is a dilated ventricle with impaired contractility and possibly concomitant valvular disease. Diastolic dysfunction occurs with normal or intact left ventricular ejection fraction (LVEF) but impaired ventricular relaxation and filling, often associated with left ventricular hypertrophy and stiffness, systemic hypertension, or valvular disease. Left heart failure is a syndrome primarily characterized by pulmonary congestion or edema. Right heart failure is a syndrome usually caused by left heart failure. It is characterized by right ventricular (RV) systolic dysfunction accompanied by RV dilatation and tricuspid regurgitation, which causes tissue congestion, including peripheral edema, ascites, and abdominal organ engorgement.

Etiologies

The most common cause of heart failure in the developed world is coronary artery disease, estimated to account for approximately two-thirds of all cases of CHF. Diabetes also plays a large role, and patients with diabetes are twice as likely to develop CHF as those without. Uncontrolled hypertension and valvular disease have become less common primary culprits but are still significant precipitating factors. The most common valvular cause of heart failure in the developed world is senile degeneration of the aortic valve. In undeveloped countries, valve disease secondary to rheumatic fever is more common. Other important risk factors are smoking, sedentary lifestyle, obesity, and lower socioeconomic status. Table 27-1 describes major categories of heart failure with associated disease processes.

aIndicates disease process that can lead to diastolic CHF as well.

Reproduced, with permission, from Longo DL, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine.

18th ed. New York, NY: McGraw-Hill; 2012. Table 234-1.

Epidemiology

In 2013, the American Heart Association estimated there were 5.1 million Americans with heart failure. The Framingham Heart Study found a prevalence of heart failure in men aged 50 to 59 of 8 per 1000, increasing to 66 per 1000 in men over 80. Similar rate increases based on increasing age were seen in women. African Americans have 25% increase higher rates than whites.

Over 1 million hospital admissions in the United States and at least 20% of admissions for patients over age 65 are due to CHF, making it the most common cause of hospitalization in patients older than 65 years. Poorer prognosis is seen in patients who are male, older, those with more severe symptoms, coronary artery disease and acute coronary syndrome, hypotension, impaired renal function, hyponatremia, and elevated plasma brain natriuretic peptide (BNP). The most common cause of death is worsening heart failure. Sudden cardiac death, often from a ventricular arrhythmia, may account for up to 30% of all deaths.

Evaluation

Patients presenting with symptoms suggestive of heart failure should be evaluated with a history, physical examination, and focused testing. Diagnosis of heart failure is clinical, and there is no single test that can determine its presence or absence.

The symptoms and signs that occur are unique and characteristic of the alterations to the normal physiologic function of the heart. Signs and symptoms of right-sided heart failure stem from increased pressure in the systemic veins, causing hepatic congestion, venous engorgement, and visceral edema. Symptoms include nausea, vomiting, abdominal distention or bloating, diminished appetite, early satiety, and abdominal pain, particularly in the right upper quadrant (due to hepatic congestion and stretching of the liver capsule). Signs of right-sided heart failure are jugular venous distention, peripheral edema, hepatomegaly, right upper quadrant tenderness, hepatojugular reflux, abdominal ascites, and jaundice.

Left-sided heart failure manifests with elevated pressure in the pulmonary veins, resulting in symptoms of dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, wheezing, tachypnea, and cough. The signs of pulmonary congestion are bilateral pulmonary rales, S3 gallop rhythm, Cheyne-Stokes respirations (which are associated with low cardiac output), pleural effusion, and pulmonary edema. Pulmonary edema is often the first manifestation of congestive heart failure, but it can also be caused by a variety of noncardiac conditions.

Dyspnea on exertion is the most sensitive symptom for the diagnosis of CHF, but its specificity is much lower. Orthopnea and paroxysmal nocturnal dyspnea are more specific for CHF, but not as sensitive. Symptoms seen in both right- and left heart failure include weakness, fatigue, nocturia due to increased cardiac preload and decreased renal vasoconstriction in the recumbent position, memory impairment, insomnia, decreased exercise tolerance, headache, stupor, coma, paroxysmal nocturnal dyspnea, and declining functional status. Signs found in both left- and right-heart failure are tachycardia, displaced point of maximal impulse, systolic murmurs (mitral or tricuspid), third heart sound (S3, ventricular filling gallop) associated with volume overload, fourth heart sound (S4, atrial gallop) associated with diastolic dysfunction, pulsus alternans, diminished pulse pressure, cyanosis, oliguria, dependent peripheral edema, and cardiac cachexia.

Testing should be designed to confirm CHF (or lead to an alternate diagnosis), identify a cause, and assess the severity of the disease. These initial tests should include blood tests, radiographic studies, electrocardiography, and echocardiography.

Initial blood tests should generally include a complete blood count (CBC), serum electrolytes, magnesium, calcium, renal function tests, urinalysis, hepatic function tests, cardiac enzymes, and BNP. A high white blood cell count can help to identify the presence of an underlying infection, a common triggering event of CHF. Anemia is another common trigger of CHF. In an anemic patient, the oxygen-carrying ability of the blood is reduced so cardiac output must increase to compensate for this. If the anemia is mild, or if the heart is normal, this compensation may occur without producing symptoms; if the anemia is severe or if there is underlying cardiac abnormality (from previous ischemia, hypertension, valvular abnormality, etc), heart failure may occur. Diabetes and hypo- or hyperthyroidism can also precipitate CHF. Testing for concomitant dyslipidemia is also important.

Electrolyte abnormalities are common in the presence of CHF. Neurohumoral responses to a failing heart result in water and sodium retention and potassium excretion. Hyponatremia is a poor prognostic indicator, signifying activation of the renin-aldosterone-angiotensin system. Medications used by patients with chronic heart disease (diuretics, ACEI, ARB, and aldosterone antagonists) also can lead to electrolyte abnormalities. Some electrolyte abnormalities, specifically hypo- or hyperkalemia, hypomagnesemia, and hypocalcemia, can lead to arrhythmias which could incite heart failure or cause significant morbidity in heart failure patients. Increased venous pressure can lead to passive congestion of the liver, resulting in elevated serum transaminases. Severe CHF can lead to jaundice as a consequence of impaired hepatic function caused by congestion.

Serial measurement of cardiac enzymes is necessary to evaluate for the presence of acute myocardial infarction (MI) as the inciting event. Elevated cardiac enzymes that do not reach levels consistent with acute myocardial infarction are seen in about half of patients with systolic heart failure and indicate elevated left ventricular filling pressure due to volume overload.

One of the neurohumoral responses to the presence of a failing ventricle is release of BNP. BNP and its prohormone (pro-BNP ) can be used to assist in the diagnosis of CHF as a cause of acute dyspnea. Elevated levels of BNP and pro-BNP are sensitive and specific markers for the diagnosis of CHF. In a dyspneic patient, a level of BNP less than 100 pg/mL essentially excludes a diagnosis of heart failure, and BNP higher than 400 pg/mL indicates high likelihood of heart failure. A pro-BNP level greater than 450 pg/mL in younger patients or 900 pg/mL in older patients also suggests CHF. BNP is not recommended as a screening test nor as a method of monitoring progression of CHF, as the level can be increased by advancing age, renal failure, cardiac ischemia, and pulmonary embolism and can be decreased by acute pulmonary edema, acute mitral regurgitation, and mitral stenosis.

ECG findings in CHF are variable, but can help determine the cause of heart failure. An ECG is useful to evaluate for evidence of acute ischemia or arrhythmia as cause of the CHF and can also reveal the presence of ventricular hypertrophy, often seen in chronic hypertension. Left bundle branch block seen in the setting of heart failure indicates higher 1-year all-cause mortality.

Chest x-ray can help to evaluate for other causes of dyspnea, such as pneumonia, chronic obstructive pulmonary disease, pneumothorax, or lung cancer. A chest x-ray showing cardiomegaly, pulmonary venous congestion, interstitial edema, alveolar edema, or pleural effusion increases the likelihood of CHF in a dyspneic patient. A cardiothoracic ratio greater than 50% indicates systolic dysfunction. One of the earliest chest x-ray findings in CHF is cephalization of the pulmonary vasculature (upper lobe pulmonary vein dilation with lower lobe pulmonary vein constriction) which indicates increased preload. As the failure progresses, interstitial pulmonary edema can be seen as perihilar infiltrates, often in a butterfly pattern. Kerley lines, which are spindle-shaped linear opacities in the periphery of the lung bases, appear in later heart failure as well. Pleural effusions can also be found. Effusions are usually bilateral but, if unilateral, are more often seen on the right hemithorax than the left.

Echocardiography is the gold-standard diagnostic modality in the presence of CHF. It can evaluate LVEF, ventricle size, wall thickness, left and right ventricle filling pressures, valve function, and the pericardium, as well as identify regional or global wall motion abnormalities due to ischemic heart disease, and show evidence of cardiomyopathy. It can also find pericardial effusion, tamponade or pericardial constriction. Echocardiography is useful in identifying valvular stenosis or regurgitation, either of which can lead to heart failure. These findings aid in the determination of whether the heart failure is a systolic or diastolic dysfunction, an important distinction in the decision of appropriate treatment.

Some patients may also need cardiac catheterization if coronary artery disease is thought to be a significant contributor to the development of a patient's CHF. Revascularization of coronary lesions causing ischemic heart disease has been shown to improve outcomes in patients with systolic heart failure.

Classification of CHF

CHF severity is characterized by the symptoms a patient has and the degree that the symptoms limit a patient's lifestyle. There are several classification systems in use; two of the most widely used are the New York Heart Association (NYHA) and the American Heart Association (AHA) classifications. Table 27-2 summarizes these systems. The classification of CHF is important in determining the appropriate treatment and prognosis for the patient.

Management of Heart Failure

Prevention is the most important part of managing CHF. The Heart Association classification system helps clinicians identify patients at risk, so that preventive strategies may be implemented early. Aggressive control of hypertension has been shown to reduce incidence of heart failure by up to 50%. Treating patients who have coronary artery disease or who have had a myocardial infarction with ACEI, ARBs, β-blockers, and aldosterone antagonists reduces the risk of progression

to symptomatic heart failure. Treating dyslipidemia with statin therapy can also reduce incidence of heart failure by 20%. 

Controlling other risk factors, such as diabetes mellitus, atherosclerotic vascular disease, and thyroid disease, as well as avoidance of cardiotoxic drugs such as tobacco, alcohol, cocaine, and amphetamines, are important for reducing risk as well.

MANAGING ACUTE CHF

In all cases of acute decompensated CHF, the initial management imperative is the stabilization of the cardiopulmonary system. Supplemental oxygen, initially 100% via non-rebreather face mask, should be administered. If necessary, ventilation can be assisted with continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), or mechanical ventilation. Cardiac and continuous pulse oximetry monitors should be placed and IV access obtained.

The goals of managing an acute exacerbation of CHF are to stabilize hemodynamics, treat reversible underlying conditions contributing to CHF, and to establish an effective regimen for outpatient therapy. About 90% of patients admitted to the hospital with decompensated heart failure are volume overloaded. When volume overload caused by CHF (which frequently causes acute pulmonary edema) is diagnosed, the next step in management is the administration of a loop diuretic. Furosemide is generally the treatment of choice, both for its potent diuretic effect and for its rapid bronchial vasculature vasodilation. Volume overload may also be treated acutely with vasodilators to reduce filling pressures. Nitrates, particularly nitroglycerin when given IV, reduce myocardial oxygen demand by reducing preload and afterload. Nitroglycerin also can rapidly reduce blood pressure and is the treatment of choice in a patient who has CHF and whose blood pressure is elevated. It should be used with caution or avoided in a hypotensive patient.

IV morphine sulfate can be an effective adjunct to therapy. Along with its analgesic

and anxiolytic properties, morphine is a venodilator (primary effect) and

arterial dilator, resulting in a reduction in preload and an increase in cardiac output.

Patients with severely reduced ejection fraction may require short-term use

of inotropic agents such as dobutamine or milrinone to improve cardiac output.

Vasopressors may also be necessary for hypotension, and dopamine is the preferred

agent for CHF patients. Hemodialysis for fluid removal may be required in patients

with concomitant end-stage renal disease.

Most patients who present to the emergency department (ED) with symptomatic

CHF will require admission to a telemetry unit for treatment and monitoring.

To be discharged home directly from the ED, a patient must have had gradual onset

of symptoms, rapid resolution of symptoms with treatment, oxygen saturation of

greater than 90% on room air, and exclusion of an acute coronary syndrome as the

cause of the CHF.

Outpatient Management of Chronic CHF

Patient education is an important aspect of care for all patients with CHF. All patients should be advised about the importance of dietary sodium and fluid restriction. A normal American diet contains 6 to 10 g sodium chloride a day; the American Heart Association, recommends restricting to 1500 mg/d in patients with stage A or B disease because of data correlating the incidence of hypertension and heart failure with sodium intake. Stricter restrictions have been recommended in those with more severe disease, but there is little data to support a specific amount of sodium restriction in patients with stage C or D CHE Fluid restriction can be considered in patients whose fluid retention is difficult to control. Patients should be warned to avoid nonsteroidal anti-inflammatory medications as these can worsen fluid retention, and reduce the efficacy of diuretics and ACEIs. Overweight and obese patients should be counseled on appropriate caloric restrictions and encouraged to exercise to reduce weight. Exercise training such as cardiac rehabilitation in patients with CHF is associated with improved response to pharmacologic vasodilators, reduced hospitalizations, and improvement in well-being and exercise capacity. The importance of strict management of blood pressure and modification of other cardiac risk factors should be emphasized as well. Obstructive sleep apnea and central sleep apnea are common in patients with systolic heart failure, and treatment with positive airway pressure therapies has been associated with improved ejection fraction and survival.

ACEIs or ARBs should be considered first-line therapy in patients with CHF and reduced left ventricular function. ACEIs and ARBs reduce preload, afterload, improve cardiac output without increasing heart rate, and inhibit tissue renin angiotensin systems which improves myocardial relaxation and compliance. The result of this is improvement in symptoms and reduction in mortality and hospitalization. Survival is increased by 20% in patients with systolic CHF and with left ventricular systolic dysfunction after MI even without signs or symptoms of CHE ACEIs or ARBs can also delay the development of symptomatic CHF in asymptomatic patients with a reduced cardiac ejection fraction (AHA stage B or NYHA class I). Better outcomes are seen at higher doses, so patients should be maintained at the highest tolerable dose. ACEIs and ARBs are contraindicated in pregnancy, hypotension, hyperkalemia, and bilateral renal artery stenosis, and should be used with caution in patients with renal insufficiency.

The administration of β-blockers, especially in high doses, in the setting of acute CHF, can worsen symptoms; consequently, they should preferentially be started when patients have minimal evidence of fluid retention and few symptoms, and initial doses should be low and titrated up over several weeks. β-Blockers reduce sympathetic tone and the cardiac muscle remodeling associated with chronic heart failure. In combination with ACEIs, β-blockers improve mortality. Contraindications to β-blocker use include symptomatic bradycardia, atrioventricular block in absence of a pacemaker, hypotension, severe peripheral vascular disease, and severe bronchospasm.

Diuretics should be used to reduce volume overload in both the acute and chronic settings. They are most helpful in symptom management, and should be used with ACEI/ ARBs and P-blockers for long-term reduction in CHF exacerbations. Loop diuretics (furosemide, bumetanide, torsemide, ethacrynic acid) can be used in all stages of CHF and are useful for pulmonary edema and refractory heart failure. These are preferred because they can increase sodium excretion by 20% to 25% and increase free water excretion. Thiazide diuretics (hydrochlorothiazide, chlorthalidone, others) only increase sodium excretion by 5% to 10% and this effect is reduced in renal insufficiency. Their primary role in management of heart failure is in treatment of hypertension. They can also be used in combination with loop diuretics to potentiate diuresis. Diuretic doses can be adjusted based on daily weight measurements by the patient, and patients should be monitored closely for overdiuresis.

The aldosterone antagonists spironolactone and eplerenone reduce mortality in advanced heart failure, as well as improving symptoms and reducing hospitalizations. Elevated aldosterone levels contribute to sodium and water retention, potassium and magnesium loss, myocardial hypertrophy and fibrosis, and endothelial dysfunction. Aldosterone blockade promotes reversal of these effects. It also functions as a potassium-sparing diuretic and should be considered in NYHA class III and IV heart failure. Patients on this medication must be closely monitored for the development of hyperkalemia, which can become profound and lead to arrhythmia. It should be avoided in patients with renal failure.

Calcium channel blockers, in general, increase mortality in systolic CHF and should be avoided. The exception to this is the dihydropyridine calcium channel blocker amlodipine (Norvasc), which does not increase or decrease mortality, and can be very effective in treating hypertension. Nondihydropyridine calcium channel blockers (diltiazem, verapamil) may be useful in heart failure caused by diastolic dysfunction, as they promote increased cardiac output by lowering heart rate, which allows for more ventricular filling time.

The combination of hydralazine with nitrates has been shown to provide increased survival and decreased hospitalizations when used in combination with ACEIs, β-blockers, and spironolactone in patients with systolic heart failure who self-identified as African American. Digoxin is only indicated to reduce hospital stays in patients with uncontrolled heart failure on appropriate medical therapy or for ventricular rate control in patients with known arrhythmias, such as atrial fibrillation. It can improve symptoms, exercise tolerance, and slightly improve ejection fraction and cardiac output, but it has no mortality benefit, and has a very narrow therapeutic window with significant adverse effects in overdose. Symptoms of digoxin toxicity include nausea, vomiting, headache, somnolence, altered color vision, and arrhythmias. Benefits of digoxin therapy are greatest in patients with NYHA class IV disease, cardiomegaly, and ejection fraction less than 25%.

Approximately, one-third of patients with NYHA class III or IV heart failure and reduced ejection fraction have ECG evidence of abnormal ventricular conduction (ie, prolonged QRS duration), which causes ventricular dyssynchrony. This results in reductions in ventricular filling, left ventricular contractility, paradoxical septal wall motion, and worsening of mitral regurgitation. These patients can be helped by promoting synchronous contraction of both the right and left ventricles using a biventricular pacemaker. This process, also known as cardiac resynchronization therapy, has been shown to reduce mortality and hospitalization in patients with symptomatic CHF in spite of maximal medical therapy, as well as improve quality of life, exercise capacity, and LVEF.

Patients with an ejection fraction less than 35%, NYHA class II or III heart failure, and a reasonable life expectancy of at least 1 year are recommended to have an implantable cardioverter-defibrillator (ICD) placed for secondary prevention of sudden cardiac death due to ventricular arrhythmias, especially if the patient has a history of cardiac arrest, ventricular fibrillation, or unstable ventricular tachycardia.

CASE CORRELATION

• See also Case 20 (Chest Pain).

COMPREHENSION QUESTIONS

27.1 A 57-year-old man who has known New York Heart Association class II heart failure presents to clinic after noting to become dyspneic with significant exertion. On physical examination, his BP is 140/86 mm Hg, pulse 86 beats/min, and respiratory rate 20 breaths/min. A 2/6 pansystolic murmur is best heard at the right sternal border. There is no JVD, but 1 + pretibial and pedal edema are noted. He currently takes an ACEI and aspirin. Which one of the following additional medications has been shown to improve longevity in this situation?

A. Warfarin (Coumadin)

B. Digoxin

C. β-Blocker

D. Nondihydropyridine calcium channel blocker

E. Amiodarone (Cordarone)

27.2 A 52-year-old man with a long-standing history of marginally controlled hypertension presents with gradually increasing shortness of breath and reduced exercise tolerance with pain in his calves that causes him to stop walking after one block. His medications include enalapril and metoprolol. His physical examination reveals a blood pressure of 140/90 mm Hg, a respiratory rate of 22 breaths/ min, heart rate of 88 beats/min, bibasilar rales, and trace pitting edema. Posterial tibial and dorsalis pedis pulses are 1+. Which of the following diagnostic tests is most appropriate in the further evaluation of this patient?

A. Cardiac magnetic resonance imaging (MRI)

B. 12-lead ECG

C. Spiral computed tomography (CT) of the chest

D. Two-dimensional echocardiography with Doppler

E. Posteroanterior and lateral chest radiographs

27.3 A 64-year-old man is noted to have congestive heart failure because of coronary artery disease. Over the past 2 days, he has developed progressive dyspnea and orthopnea. On examination, he is found to be in moderate respiratory distress, has JVD, and rales on pulmonary examination. He is diagnosed with pulmonary edema. Which of the following agents is most appropriate at this time?

A. Hydrochlorothiazide

B. Furosemide

c. Carvedilol

D. Spironolactone

E. Digitalis

27.4 A 70-year-old African-American man with New York Heart Association class III heart failure sees you for follow-up. He has shortness of breath with minimal exertion. The patient is adherent to his medication regimen. His current medications include lisinopril 40 mg twice daily, carvedilol 25 mg twice daily, furosemide 80 mg daily, and spironolactone 25 mg daily. His blood pressure is 100/60 mm Hg, and his pulse rate is 70 beats/min and regular. Physical examination findings include a few scattered bibasilar rales, an S3 gallop, and no peripheral edema. An ECG reveals a left bundle branch block and echocardiography reveals an ejection fraction of 25%. Which of the following is the best next step for this patient?

A. Increase the furosemide dosage to 80 mg twice daily.

B. Refer for coronary angiography.

C. Increase the lisinopril dosage to 80 mg twice daily.

D. Increase the carvedilol dosage to 50 mg twice daily.

E. Refer for cardiac resynchronization therapy.

ANSWERS

27.1 C. β-Blockers are recommended to reduce mortality in symptomatic patients with heart failure. Digoxin is only recommended in patients who are already on maximal medical therapy. Nondihydropyridine calcium channel blockers should be used with caution in patients with heart failure because they can cause peripheral vasodilation, decreased heart rate, decreased cardiac contractility, and decreased cardiac conduction. Anticoagulation with warfarin is not indicated, and amiodarone is used for treatment of arrhythmias.

27.2 D. The most useful diagnostic tool for evaluating patients with heart failure is two-dimensional echocardiography with Doppler to assess left ventricular ejection fraction (LVEF), left ventricular size, ventricular compliance, wall thickness, and valve function. It should be performed during the initial evaluation. Chest radiography and 12-lead electrocardiography should be performed in all patients presenting with heart failure, but should not be used as the primary basis for determining which abnormalities are responsible for the heart failure.

27.3 B. Furosemide, a loop diuretic, is a first-line agent in CHF exacerbation with pulmonary edema. The other medications listed may be used in the management of CHF, but are not indicated in an acute exacerbation.

27.4 E. This patient is already receiving maximal medical therapy. Cardiac resynchronization therapy is recommended for patients in sinus rhythm with an EF less than 35%, QRS greater than 120 ms, and those who remain symptomatic (NYHA III-IV) despite optimal medical therapy.

CLINICAL PEARLS

⯈ The initial hour in the management of a patient with either new-onset CHF or an acute exacerbation is crucial to their outcome.

⯈ Simple measures, such as decreasing cardiac preload by sitting the patient up with their legs on the ground and their arms by their side, maintaining an airway and giving oxygen, and giving sublingual nitroglycerin, can alleviate CHF immediately.

REFERENCES

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Francis GS, Tang W, Walsh RA. Pathophysiology of heart failure. In: Fuster V, Walsh RA, Harringron RA. eds. Hurst's the Heart.13th ed. New York, NY: McGraw-Hill; 2011. 

King M, Kingery J, Casey B. Diagnosis and evaluation of heart failure. Am Fam Physician. 2012 Jun 15;85(12):1161-1168. 

King M, Perez 0. Heart failure. In: South-Paul JE, Matheny SC, Lewis EL, eds. Current Diagnosis & Treatment: Family Medicine. 4th ed. New York, NY : McGraw-Hill; 2015. 

Klein L. Heart failure with reduced ejection fraction. In: Crawford MH, ed. Current Diagnosis & Treatment: Cardiology. 4th ed. New York, NY: McGraw-Hill; 2014. 

Mann DL, Chakinala M. Heart failure: pathophysiology and diagnosis. In: Kasper D, Fauci A, Hauser S, et al., eds. Harrison's Principles of Internal Medicine.19th ed. New York, NY: McGraw-Hill; 2015. Available at: http://accessmedicine.mhmedical.com. Accessed May 25, 2015. 

Mehra MR. Heart failure: management. In: Kasper D, Fauci A, Hauser S, et al., eds. Harrison's Principles of Internal Medicine.19th ed. New York, NY : McGraw-Hill; 2015. Available at: http://accessmedicine. mhmedical.com. Accessed May 25, 2015. 

Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/ AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on practice guidelines. Circulation. 2013 Oct 15;128(16):e240.

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