Sunday, April 4, 2021

Chronic Heart Failure Case File

Posted By: Medical Group - 4/04/2021 Post Author : Medical Group Post Date : Sunday, April 4, 2021 Post Time : 4/04/2021
Chronic Heart Failure Case File
Eugene C. Toy, Md, Michael d . Faulx, Md

Case 19
A 72-year-old man is seen in your clinic for dyspnea on exertion. Over the past week, he has noticed worsening shortness of breath with moderate amounts of housework and when walking to his car. He has also noticed difficulty falling asleep, so he has been sleeping in his recliner chair. Two weeks ago, his children were in town and they ate out frequently at fast-food restaurants. The patient has a history of hypertension, hyperlipidemia, and a myocardial infarction 3 years prior. His medications are aspirin, lisinopril, and atorvastatin. On examination, he appears tachypneic but not in respiratory distress. His temperature is 98.9°F, heart rate 94 bpm, blood pressure 134/74 mmHg, respirations 24 per minute, and 02 saturation 93% on room air. Cardiac auscultation reveals a regular rate and rhythm without murmurs or rubs. A low-pitched gallop is heart after the second heart sound. There are wet crackles at the bases of both lungs bilaterally. The abdomen is soft without organomegaly. The extremities are well perfused, and there is 1+ bilateral pedal and presacral edema. Jugular venous distension is 12 cm. ECG shows sinus rhythm with Q waves in V1-V4. Results of a complete blood count and chemistry panel are unremarkable.
  • What is the most likely diagnosis?
  • What is the best next diagnostic step?
  • What is the best next step in therapy?

Answer to Case 19:
Chronic Heart Failure

Summary: A 72-year-old man with a history of hypertension, hyperlipidemia, and an old myocardial infarction presented with worsening dyspnea on exertion. His exercise tolerance has worsened after a week of eating high-sodium foods. He is mildly tachypneic on exam with borderline low oxygen saturation. He has an S3 gallop, crackles, lower extremity edema, and elevated neck veins on exam. An ECG reveals Q waves in the anteroseptal leads signifying an old myocardial infarction.
  • Most likely diagnosis: Acute heart failure exacerbation.
  • Next diagnostic step: Echocardiography.
  • Next step in therapy: Loop diuretics.


  1. Recognize the signs and symptoms of heart failure.
  2. Know the diagnostic approach and common etiologies of systolic heart failure.
  3. Understand the medical and device management for chronic systolic heart failure.
This 72-year-old man presented to clinic with worsening dyspnea on exertion and physical exam findings of volume overload (wet profile) and heart failure. The first priority in the office should be to assess his vital signs and tissue perfusion. Signs of low tissue perfusion (cold profile) are hypotension, cold extremities, altered mental status, elevated creatinine, abnormal liver transaminases, and an elevated lactate. Patients with abnormal tissue perfusion should be triaged to a higher level of care. Our patient did not show signs of low tissue perfusion and falls into the “warm and wet” category. Further categorization of heart failure into systolic or diastolic is an important step and can be accomplished by echocardiography. Equally important is determining the etiology of the heart failure. For our patient, systolic heart failure and ischemic cardiomyopathy are the most likely scenarios given his old anterior myocardial infarction. Treatment centers around relieving acute congestion, starting evidence-based medical therapy, and educating patients on diet and lifestyle changes needed to prevent further exacerbations and improve mortality.

Approach To:
Chronic Heart Failure


HEART FAILURE: A clinical syndrome characterized by shortness of breath or fatigue as a result of underlying structural or functional heart disease.

CARDIOMYOPATHY: Disease or dysfunction of the myocardium. Cardiomyopathies are commonly categorized as ischemic or nonischemic. Further classifications are based on ventricular structure or etiology (dilated, hypertrophic, restrictive, Takotsubo, alcoholic, etc).

ORTHOPNEA: Shortness of breath in a recombinant position.

PAROXYSMAL NOCTURNAL DYSPNEA: Respiratory distress that awakens the patient from sleep.

Heart failure defines a persistent and growing segment of the US healthcare system,
with an estimated prevalence of over 6 million people. It is associated with high
morbidity, mortality, and cost to the healthcare system. In addition, heart failure is
the most common reason for hospital readmission in both the medical and surgical

Heart failure can be broken down into systolic, or heart failure with reduced ejection fraction (HFrEF); and diastolic, or heart failure with preserved ejection fraction (HFpEF). The former is defined as a clinical presentation consistent with heart failure along with an ejection fraction of <45%. The cause of this decreased ejection fraction may be variable. Common etiologies are seen in Table 19-1. Diastolic dysfunction results from impaired ventricular relaxation or distensibility. The most common cause of HFpEF is chronic systemic hypertension leading to left ventricular hypertrophy. Other etiologies include myocardial ischemia, other forms of hypertrophic cardiomyopathy or left ventricular outflow obstruction, and restrictive cardiomyopathies.

etiologies of systolic heart failure

The body adapts to the failing heart through both short- and long-term responses. Initially, cardiac output is preserved through activation of the sympathetic nervous system and the Frank Starling mechanism. The renin-angiotensin-aldosterone system is activated, leading to vasoconstriction, facilitation of norepinephrine and aldosterone release, and vascular and cardiac myocyte growth and hypertrophy. Natriuretic peptides are released in response to increased myocardial wall tension, which promotes salt and water excretion.

Over time these adaptive responses lead to deleterious effects in the patient with heart failure. Overstimulation of β-adrenergic receptors leads to their downregulation, which decreases reserve in response to inotropic stimulation and may precipitate arrhythmias. Angiotensin and aldosterone in high levels are cardiotoxic, altering the size and shape of the heart and leading to renal vasoconstriction. This decreases renal blood flow, mimicking a prerenal state that ultimately triggers salt and water retention. The left ventricular remodeling caused by these neurohormonal changes in chronic heart failure leads to a dilated, often stiffened and less efficient myocardium (Figure 19-1).

Clinical Presentation
The master clinician and teacher W. Proctor Harvey described the “five-finger” approach to assessing cardiovascular diagnoses. In descending order of clinical

systolic heart failure

Figure 19-1. deleterious pathways involved in chronic systolic heart failure. (Reproduced, with permission, from Fuster V, Walsh RA, Harrington RA. Hurst’s The Heart. 13th ed, 2010. Figure 26-2.)

NYHA heart failure classification

usefulness, the approach consists of a careful history, physical examination, electrocardiogram, chest radiography, and sensible laboratory testing.

Patients with chronic systolic heart failure classically present with shortness of breath and peripheral edema. The first symptoms of volume overload may be orthopnea and paroxysmal nocturnal dyspnea (PND). Orthopnea may be quantified by the number of pillows needed behind the patient’s head in order to sleep comfortably. Dyspnea on exertion can be elucidated by asking how far a patient can walk before stopping to catch breath. Other symptoms of heart failure include fatigue, cough, abdominal swelling, nausea, early satiety, and chest pain. When questioning patients, be sure to ask them about possible triggers for a worsening in heart failure symptoms such as dietary indiscretion, medication noncompliance, recent medication changes, blood pressure, chest pain, and palpitations. The patient’s symptoms can be categorized into New York Heart Association (NYHA) classes, which aids in clinical assessment and management options (Table 19-2).

On physical exam, it is important to initially focus on the vital signs. An increased heart rate may represent an arrhythmia or a compensatory increase due to decreased blood pressure and cardiac output. Weight gain should also be noted. The key to examining a patient with heart failure is the assessment of that patient’s volume status and tissue perfusion. Volume status is assessed by assessment of jugular venous pulsation, hepatojugular reflux, ascites, and peripheral and presacral edema. Cardiac examination may reveal a displaced point of maximal impulse, with murmurs indicating valvular heart disease or an S3 or S4. Crackles or pleural effusions may be discovered on pulmonary examination. Palpation of pulses may reveal a pulsus alternans in patients with moderate to severe systolic dysfunction.

Electrocardiography is variably abnormal in patients with systolic heart failure. The ECG is essential for ruling out brady- or tachyarrhythmia as a precipitating factor. There may be evidence of an old myocardial infarction, particularly if the etiology of the heart failure is ischemic. An ischemic ECG may suggest acute coronary syndrome or myocarditis. Low QRS voltage in the presence of ventricular hypertrophy by echocardiography may suggest amyloidosis or another infiltrative cardiomyopathy.

Chest radiography is helpful in assessing cardiomegaly as well as atrial enlargement. Increased hilar markings may be a sign of pulmonary venous congestion or pulmonary hypertension. Parenchymal infiltrates and Kerley B lines suggest pulmonary edema, although over time these x-ray findings can become less apparent.

Laboratory abnormalities may include hyponatremia, elevated BUN, and creatinine and transaminitis due to hepatic congestion. Elevated cardiac biomarkers may be found in chronic systolic heart failure or may be a sign of an acute ischemic event. Brain natriuretic peptide is often elevated.

Additionally, it is extremely important to have a recent assessment of cardiac function and ejection fraction in the form of an echocardiogram on all patients with a suspected exacerbation of heart failure. Echocardiography will allow one to define valvular abnormalities, diastolic dysfunction, pulmonary hypertension, and even volume status in the form of estimated right and left atrial pressure measurements.

There is a multipronged approach to treating chronic systolic heart failure that focuses on managing symptoms and combating neurohormonal disarray. Nonmedical management includes device therapy, patient education, and the use of coordinated outpatient care to optimize medical therapy and avoid exacerbations. It is important to note that this discussion pertains to systolic heart failure. There are currently no evidence-based therapies that affect mortality in diastolic heart failure (HFpEF).

The relief of congestion is accomplished using loop diuretics. Furosemide is the most common loop diuretic used, although newer agents such as bumetanide and torsemide provide increased gastrointestinal bioavailability. ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) accomplish reduction of preload and afterload while decreasing circulating levels of the cardiotoxic hormones angiotensin and aldosterone. Combination drug therapy using nitrates as a venodilator and hydralazine as an arterial vasodilator accomplishes a reduction in preload and afterload and has been shown to decrease mortality when added to standard heart failure therapy (particularly in African Americans). Beta-blockers, once considered contraindicated in heart failure because of their negative inotropic effects, are now the cornerstone of management because of their beneficial neurohormonal effects and their ability to reverse left ventricular remodeling. Proper dosing of an appropriate beta-blocker (carvedilol, metoprolol succinate, and bisoprolol) can actually
improve left ventricular ejection fraction in some patients. Low doses should be initially prescribed with gradual uptitration over several weeks. The aldosterone receptor antagonists spironolactone (for classes III and IV patients) and eplerenone (for class II patients) have also been shown to reduce heart failure mortality. Digoxin has positive inotropic effects that led to its initial use in heart failure. Unlike the aforementioned medications, digoxin does not have a mortality benefit in heart failure, but it has been shown to decrease heart failure readmissions.

Device therapy in the form of an implantable cardioverter defibrillator (ICD) to prevent sudden cardiac death should be considered in patients with an ejection fraction of <35% and an anticipated life expectancy of >1 year. Cardiac resynchronization therapy in the form of a biventricular pacemaker defibrillator (BiVICD) can be offered to patients with a left bundle branch block on ECG and a QRS length of >120 ms.

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


19.1 A 65-year-old man with heart failure has pillow orthopnea and shortness of breath while walking around his house. He is comfortable only at rest. 
What NYHA heart failure class symptoms does he have?
A. Class I
B. Class II
C. Class III
D. Class IV

19.2 A 45-year-old man presents with dyspnea on exertion and four-pillow orthopnea. JVP is elevated, and you hear an S3 on exam. ECG is normal sinus rhythm without Q waves, ST, or T wave changes. Echocardiography shows global left ventricular hypokinesis and an EF of 30% with no valvular abnormalities. 

What is the next best step in diagnosis or management?
A. Order a chest CT for a coronary calcium score
B. Assess for coronary artery disease with a stress test or cardiac catheterization
C. Implant a biventricular implantable cardioverter defibrillator (for CRT)
D. Order a multigated acquisition (MUGA) scan to better assess cardiac function

19.3 A 56-year-old white man with a history of a large anterior wall myocardial infarction and an EF of 20% presents to your clinic. He notes shortness of breath after climbing two flights of stairs and after walking four or five blocks but denies PND or orthopnea. He takes aspirin, atorvastatin, metoprolol, and lisinopril. Which of the following is the best step in managing his heart failure?
A. Begin hydralazine and isosorbide dinitrate
B. Begin digoxin
C. Begin eplerenone
D. Hospitalization for intravenous dobutamine infusion
E. Referral for consideration of a left ventricular assist device

19.4 A 75-year-old man with chronic systolic heart failure presents to your clinic with class III symptoms. His most recent echo showed an EF of 25%. He takes losartan, metoprolol, aspirin, and spironolactone. Which of the following interventions will decrease his mortality?
A. Digoxin
B. Low-salt diet and fluid restriction to 1.5 L/day
C. Implantable cardioverter defibrillator
D. Cardiac rehabilitation


19.1 C. The patient is having class III heart failure symptoms with minimal amounts of exertion.

19.2 B. An ischemic evaluation is essential in a patient presenting with recentonset heart failure since the most common cause of cardiomyopathy in the United States is ischemic heart disease.

19.3 C. Eplerenone is indicated in patients with heart failure and class II symptoms, and is the most reasonable choice provided.

19.4 C. While digoxin, dietary recommendations, and cardiac rehab can improve symptoms and decrease readmission in heart failure, only an ICD has been shown to decrease mortality.

  • Heart failure is a clinical syndrome that affects over 6 million Americans and is the leading cause of hospital readmission after both medical and surgical discharges.
  • The most important part of the physical exam is an assessment of volume status and tissue perfusion.
  • ACE inhibitors or ARBs and beta-blockers are the cornerstones of heart failure management. Aldosterone receptor blockers and hydralazine-nitrate combinations can be added in select patients.
  • Identifying the etiology of heart failure is essential in providing targeted therapy.
  • Remember to check the ECG for a left bundle branch block and a QRS duration of >120 ms to assess candidacy for implantation of a BiV-ICd.

Grant A, Hanna M. Medical treatment of heart failure. 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. 

Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360(14):1418–1428. 

Nohria A, Lewis E, Stevenson LW. Medical management of advanced heart failure. JAMA. 2002;287(5):628-640.


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