Heart Failure



Essentials of Diagnosis






  • Left ventricular failure.
  • Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, fatigue, and peripheral edema.
  • Third or fourth heart sound, increased jugular venous pressure, hepatojugular reflux, displaced cardiac apex, rales, wheezing, murmur, or peripheral edema.
  • Any electrocardiographic (ECG) abnormality, radiographic evidence of pulmonary venous congestion, cardiomegaly, or pleural effusion; elevated B-type natriuretic peptide; echocardiographic evidence of left ventricular dysfunction.
  • Right ventricular failure: increased jugular venous pressure, hepatomegaly, peripheral edema.






General Considerations



Increased survivorship after acute myocardial infarction (MI) and improved treatment of hypertension, valvular heart disease, and coronary artery disease (CAD) have led to a significant increase in the prevalence of heart failure in the United States. Overall prevalence of any congestive heart failure (CHF) diagnosis is estimated at 2.6% (2.7% in men; 1.7% in women). In addition, 10% of the population may have isolated moderate to severe diastolic dysfunction, with age greater than 65 years and female gender being consistent predictors of preserved left ventricular systolic function. Diastolic dysfunction is rarely associated with acute MI. Based on this apparent bias, the possibility of biological changes associated with increasing age and female gender have been proposed as underlying reasons for the increased likelihood of diastolic heart failure in these populations.



The prevalence of any type of heart failure increases with age. Asymptomatic left ventricular systolic dysfunction (LVSD) has been found to be as prevalent as symptomatic LVSD: 1.4% and 1.5%, respectively. Moderate or severe isolated diastolic dysfunction appears to be as common as systolic dysfunction, and systolic dysfunction appears to increase with the severity of diastolic dysfunction.






Pathogenesis



As defined by the American Heart Association (AHA) and the American College of Cardiology (ACC), heart failure is “a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.”



Heart failure results from a complex interplay of compensatory mechanisms used by the body to adjust for decreased cardiac output in response to stresses placed on the myocardium (Table 20-1). These compensatory mechanisms are rooted in the activation of the sodium-retaining renin-angiotensin-aldosterone and sympathetic nervous systems (neurohormonal adaptations). The purpose is to maintain blood pressure and tissue perfusion. However, these compensatory mechanisms, which increase afterload, lead to myocardial deterioration and worsening myocardial contractility. The heart then enters into a vicious cycle of increasing release of neurohormones (norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines) that further increases afterload, allowing the heart to spiral into failure in a progressive fashion through cardiac remodeling. These neurohormones act both in an indirect and in a directly toxic fashion to affect hemodynamic stressors and myocardial cell performance and phenotype.




Table 20-1. Possible Causes of Heart Failure. 






Causes of Cardiac Failure



With the advent of improved hypertension treatment, earlier identification of valvular heart disease, and improved survival following MI, CAD and diabetes mellitus are now the leading causes of heart failure in the United States. It is estimated that 66% of patients having systolic heart failure have coronary heart disease as the underlying etiology. CAD is a substantial predictor of developing clinically evident heart failure or symptomatic versus asymptomatic LVSD. CHF has also been found to be twofold higher in all diabetic patients. Diabetes mellitus is one of the most significant factors for developing heart failure in women. Even in women with increased hyperglycemia but no diagnosis of diabetes mellitus, the risk of heart failure is increased compared with normoglycemic women. Evidence points to a diabetic cardiomyopathy independent of CAD that is more prominent in diabetic women. This raises the question of the direct effect of diabetes on the myocardium and endothelium. This association could also be related to the overt effect of diabetes on progression of CAD. It is also unknown whether treatment of long-standing diabetes mellitus decreases the risk of developing heart failure.



Poorly controlled hypertension and valvular heart disease remain major precipitants of heart failure. Often-overlooked risk factors in the development of heart failure are smoking, physical inactivity or obesity, and lower socioeconomic status. Tobacco is estimated to cause approximately 17% of CHF cases in the United States. The effect of cigarettes may be direct or indirect in relation to promoting CAD risk. Lower socioeconomic status may limit access to higher quality health care, resulting in decreased adherence to treatment of modifiable risk factors such as hypertension, diabetes mellitus, and CAD.





Aurigemma GP et al: Predictive value of systolic and diastolic function for incident congestive heart failure in the elderly: the Cardiovascular Health Study. J Am Coll Cardiol 2001;37:1042.  [PubMed: 11263606]


Bibbins-Domingo K et al: Predictors of heart failure among women with coronary disease. Circulation 2004:110:1424.  [PubMed: 15353499]


Gheorghiade M, Bonow RO: Chronic heart failure in the United States: a manifestation of coronary heart disease. Circulation. 1998;97:282-289 [Review].  [PubMed: 9462531]


He J et al: Risk factors for congestive heart failure in US men and women: NHANES I epidemiologic follow-up study. Arch Intern Med 2001;161:996.  [PubMed: 11295963]


Masoudi FA et al: Gender, age, and heart failure with preserved left ventricular systolic function. J Am Coll Cardiol 2003;41:217-223.  [PubMed: 12535812]


Rogers VL et al: Trends in heart failure incidence and survival in a community-based population. JAMA 2004;292:344.  [PubMed: 15265849]


Stratton IM et al: Association of glycaemia with macrovascular and microvascular complications type 2 diabetes (UKPDS 35): Prospective observational study. BMJ 2000;321:405.  [PubMed: 10938048]






Classification & Prevention



The American College of Cardiology (ACC)/American Heart Association (AHA) classification of heart failure emphasizes the progressive nature of the syndrome. This classification replaced the New York Heart Association (NYHA) classification with four stages that help define appropriate therapy at each level. The new classification recognizes that there are risk factors and structural prerequisites for the development of heart failure and that therapeutic interventions initiated early in the disease process can reduce morbidity and mortality and delay the onset of clinically evident disease (Table 20-2).




Table 20-2. Progression of Heart Failure and Recommended Evidence-Based Therapies. 



Patients in ACC/AHA stages A and B do not have clinical heart failure but are at risk for developing heart failure. Stage A includes those at risk but not manifesting structural heart disease. Early identification and aggressive treatment of modifiable risk factors remain the best prevention for heart failure. Lifestyle modification, pharmacologic therapy, and counseling can improve or correct conditions such as CAD, hypertension, diabetes mellitus, hyperlipidemia, obesity, tobacco abuse, and alcohol or illicit substance abuse. Stage B represents persons who are asymptomatic but have structural heart disease or impaired left ventricular function. Stage C comprises the bulk of persons with heart failure who have past or current symptoms and associated underlying structural heart disease. Stage D includes refractory patients with heart failure who may need advanced and specialized treatment strategies.



The NYHA classification gauges the severity of symptoms for patients with stage C and D heart failure. This is a subjective assessment that can change frequently, secondary to treatment response.






Clinical Findings



A high index of suspicion is necessary to diagnose the syndrome of heart failure early in its clinical presentation, because it is frequently manifested by nonspecific signs and symptoms. Patients are often elderly with comorbidity, symptoms may be mild, and routine clinical assessment lacks specificity. A prompt diagnosis allows for early treatment with therapies proven to delay the progression of heart failure and improve quality of life.



Evaluation is directed at confirming the presence of heart failure, determining cause, identifying comorbid illness, establishing severity, and guiding response to therapy. Heart failure is a clinical diagnosis for which no single examination or test can establish the presence or absence with 100% certainty.





Hunt SA et al: 2009 focused update incorporated into ACC/AHA 2005 guidelines for a report of the American College of Cardiology Foundation/; American Heart Association Task Force on Practice Guidelines. Developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009;119:e391-479. Also available at .



Symptoms and Signs



The primary manifestations of symptomatic heart failure are dyspnea and fatigue, with dyspnea being the most common. Limited exercise tolerance and fluid retention may eventually lead to pulmonary congestion and peripheral edema. Neither of these symptoms necessarily dominates the clinical picture at the same time. Dyspnea, whether at rest or with exertion, is present in nearly all patients with heart failure and indicates left ventricular dysfunction. Its absence makes heart failure highly unlikely. The absence of dyspnea on exertion essentially rules out the presence of heart failure due to left ventricular dysfunction in a predominantly symptomatic population with a reported 100% sensitivity.



Other symptoms that are helpful in diagnosing heart failure include orthopnea, paroxysmal nocturnal dyspnea (PND), and peripheral edema. PND has the highest specificity of any symptom for heart failure. Likewise, if PND, orthopnea, or edema is not present, the likelihood of heart failure decreases. Nonspecific symptoms include chronic nonproductive cough, wheezing, and nocturia. Patients with right ventricular failure may present with right upper quadrant pain secondary to hepatic congestion and peripheral edema.



No single clinical symptom has been shown to be both sensitive and specific. A substantial portion of the population has asymptomatic left ventricular dysfunction and the history alone is insufficient to make the diagnosis of heart failure. However, a detailed history and review of symptoms remain the best approach in identifying the cause of heart failure and assessing response to therapy.



Physical Examination



The clinical examination can provide important information concerning the degree to which cardiac output is reduced and the degree of volume overload and ventricular enlargement. It can also provide clues to non-cardiac causes of dyspnea. The presence of a third heart sound, S3 (ventricular filling gallop), increases the likelihood of heart failure with the most specificity of any physical examination finding. An S3 or a fourth heart sound, S4 (atrial gallop), are specific for increased left ventricular end-diastolic pressure and decreased left ventricular ejection fraction. The presence of an S3 has been found to be superior to S4 in identifying patients with abnormal left ventricular function. Gallop rhythm (S3 and S4) and displacement of cardiac apex have also been found to be specific predictors of left ventricular dysfunction.



The presence of jugular venous distention, pulmonary rales, pitting peripheral edema, and hepatojugular reflux also helps to make the diagnosis, and the absence of the first three of these findings is useful for lowering the likelihood of heart failure. Cardiac murmurs may be an indication of primary valvular disease. Asymmetric rales or rhonchi on the pulmonary examination may indicate primary pulmonary pathology such as pneumonia or chronic obstructive pulmonary disease (COPD). Examination of the thyroid can exclude thyromegaly or goiter—causes of abnormal thyroid function that can precipitate heart failure. Dullness to percussion or auscultation of the lungs could indicate pleural effusion. Hepatomegaly can indicate passive hepatic congestion. The absence of any of these findings alone does little to help rule out heart failure.



The patient’s appearance and vital signs may be affected by heart failure. Acute increases in body weight are indicative of fluid overload versus changes in body mass. Early in the disease of heart failure, blood pressure may be elevated or normotensive; and as the disease progresses, the blood pressure usually becomes low.



Laboratory Findings



Objective tests can aid in confirmation of heart failure by assessing the differential diagnosis by excluding other possible causes for the signs and symptoms or clearly defining the heart failure.



A complete blood count is necessary to rule out anemia as a cause of high-output failure. Electrolyte (including magnesium and calcium) analysis may reveal deficiencies, commonplace with treatment, which can make the patient prone to arrhythmias. Hyponatremia is a poor prognostic sign indicating significant activation of the renin-aldosterone-angiotensin system. Abnormalities on liver tests can indicate hepatic congestion. Thyroid function tests can detect hyper- or hypothyroidism. Fasting lipid profile, fasting glucose, and hemoglobin A1c level can reveal comorbid conditions that may need to be better controlled. Iron studies can detect iron deficiency or overload. If the patient is malnourished or an alcoholic and presents with high-output failure, thiamine testing is indicated to rule out deficiency related to beriberi. Further testing to determine etiologic factors of heart failure must be based on historical findings.



B-Type Natriuretic Peptide


Specific laboratory testing includes evaluation of B-type natriuretic peptide (BNP) levels. BNP is a cardiac neurohormone secreted from the ventricles and, to some extent, the atrial myocardium in response to volume and pressure overload. Circulating BNP levels are increased in patients with heart failure and have rapid turnover, indicating that BNP responds in proportion to the size of the exacerbation and in turn increases and decreases with each individual exacerbation. Although no BNP threshold indicates the presence or absence of heart failure with 100% certainty, the BNP level is the most accurate predictor of heart failure and, in conjunction with the history and physical examination, helps differentiate between pulmonary and cardiac causes of dyspnea (Table 20-3). Factors to take into consideration when interpreting BNP levels: they are lower in men than women, they are inversely related to body weight, and they increase with age.




Table 20-3. Factors Influencing B-Type Natriuretic Peptide (BNP) Levels. 



The likelihood of heart failure increases with BNP levels greater than 100 pg/mL, as follows:




  • Less than 100 pg/mL: Negative predictive value high excluding the diagnosis of heart failure; consider alternate diagnoses.
  • 100-400 pg/mL: Increased likelihood of heart failure; history, physical examination, and other tests are required to improve the probability of the diagnosis.
  • Greater than 400 pg/mL: Diagnosis of heart failure is highly likely.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jun 5, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Heart Failure

Full access? Get Clinical Tree

Get Clinical Tree app for offline access