Definition

Congestive heart failure (CHF) refers to that state in which abnormal circulatory congestion exists as a result of heart failure. The definition of CHF is most readily understood by breaking the condition into its component parts. Congestive, in this sense, is the state of circulatory overload that inhibits the normal physiologic functions of tissue nutrition and elimination of metabolic waste. Heart failure refers to the origin or causative factor of the congestive state. The fundamental definition of heart failure focuses on the functional inability of the heart to pump enough blood to meet the metabolic demands of the body at a given point in time.

History

Symptoms

Dyspnea primarily on exertion but may progress to shortness of breath at rest as heart failure becomes more severe. The worst form of dyspnea is the terrifying air hunger of pulmonary edema. Orthopnea, paroxysmal nocturnal dyspnea, wheezing, nonproductive cough (frequently with exertion and at night), Cheyne Stokes respirations, fatigue and weakness, night sweats, insomnia, diminished daytime urinary frequency and volume, nocturia, weight gain (subtle or sudden), peripheral edema, ascites, constipation, upper abdominal pain, cachexia, anxiety, confusion, and impairment of memory (usually in elderly with severe disease).

General:

The development of symptoms and clinical manifestations is subject to numerous factors including patient’s age, underlying cardiac lesion, extent and rate of cardiac impairment, and precipitating causes. The spectrum of symptoms and signs ranges from the mildest form where symptoms and cardiac impairment are produced only during marked stress to the severe condition where even resting cardiac function cannot sustain life without external circulatory support.

Age: Any.

Onset: Extremely variable. The patient may present describing an indolent course of sporadic, few, and mild symptoms often having no knowledge or recognized history of prior cardiac disease. Conversely, a patient may present with sudden, fulminant, life threatening symptoms, usually with a previous history of cardiac disease but sometimes without, as in the case of sudden myocardial infarction with extensive loss of functional myocardium.

Duration:

Dependent on the state of circulatory congestion. The underlying cardiac diseasenesion may be permanent; however, the patient may avoid manifest CHF through on going treatment or avoidance of precipitating factors (e.g., exertion, infection, medication, compliance, and so forth). This is commonly referred to as a compensated state of heart failure. Heart failure that, by virtue of a sum of signs and symptoms, produces circulatory congestion is often described as decompensated. With progression in severity (or in some cases duration) of the underlying cardiac lesion, a patient may progress to a state of constant circulatory congestion despite avoidance of precipitating factors and be refractory to treatment producing what is sometimes referred to as the state of chronic CHF.

Intensity: Dependent on the degree of circulatory congestion. May be as mild as simple dyspnea on exertion or as severe as florid pulmonary edema with hypotension, acidosis, and impending circulatory collapse.

Aggravating Factors: Increasing severity of underlying cardiac disorder. Development of new cardiac lesion or condition (e.g., arrhythmia, myocardial infarction). Development of disease state affecting other organ systems (e.g., pulmonary emboli, pulmonary or systemic infection, renal failure, prostatic obstruction, liver disease, pregnancy). Development of a metabolic disorder (e.g., thyrotoxicosis). Increased workload (e.g., exertionaUemotional stress, anemia, uncontrolled hypertension, AV fistula). Dietary indiscretion of sodium intake. Increased circulatory volume from intravenous fluid administration, transfusion or drug induced (e.g., corticosteriods, estrogen, and nonsteroidal antiinflammatory drugs (NSAIDs». Most common aggravating factor, however, is lack of compliance with established treatment, diet, medication, or exertional activity .

Alleviating Factors: Recognition of underlying cardiac disease/ disorder and correction of condition if possible. Correction or elimination of external exacerbating factors: physical, environmental, or behavioral. Patients frequently alter their life style, diet, or exertional load (often without conscious intent) to a level that does not produce symptoms.

Associated Factors:

Patients frequently engage in self diagnosis and relate symptoms to other factors or disease entities (e.g., dyspnea and cough secondary to cigarette use, edema secondary to varicose veins). It is not uncommon for a patient to present with a preconceived diagnosis and give a history designed to prove it.

Physical Examination

General: General appearance is affected as the degree and chronicity of heart failure worsens. The patient with mild or early heart failure may appear normal and without distress at rest. Activity such as walking or dressing may produce dyspnea and an increase in pulse rate out of proportion to effort. These patients may be uncomfortable supine and prefer to sit or lie at an elevated angle. Jugular vein distention may be evident. Evidence of chronic, severe disease may be seen with nondependent edema, generalized wasting, and frank cachexia.

Cardiovascular:

The hallmark finding is the S3 gallop sound. Overall, the examination may be variable from patient to patient as one may see, feel, or hear manifestations of the underlying cardiac disorder such as ectopic precordial impulses, murmurs, or dysrhythmias. S4 gallop sound may be heard in combination with the S3 producing a complex referred to as a summation gallop. Many forms of cardiac disorders produce CHF without production of cardiac enlargement, although it is frequently present.

Extremities: Ankle and pretibial edema may be seen.

Gastrointestinal: Tender or non tender hepatomegaly or ascites may be present.

Pulmonary: Moist rales may be heard on auscultation or the chest may be dull to percussion (uni or bilateral). Cheyne Stokes respirations may be present with severe heart failure. Pulmonary edema may present with severe air hunger, anxiousness, fear of impending death.

Skin: Mild diaphoresis, mild jaundice, dusky complexion, extremity pallor and coolness, or peripheral cyanosis may be observed with varying degrees of heart failure.

Pathophysiology

The pathophysiology of CHF focuses on the variables that affect the heart’s ability to pump adequate volumes of blood to meet the metabolic demands of the body. Pathologic entities that compromise this functional ability fall into three categories:

1. Conditions that produce myocardial (muscular) failure such as idiopathic and dilated cardiomyopathy, myocarditis, metabolic! toxic disorders (beriberi, alcohol, thyrotoxicosis), and loss of adequate muscle mass (myocardial infarction, tumor).
2. Conditions that produce mechanical abnormalities such as obstruction of blood from cardiac chambers (stenotic valvular disease, supra or subvalvular obstruction), increased volume and workload (regurgitant valvular disease, cardiac or vascular shunts), pericardial tamponade, restrictive and hypertrophic cardiomyopathy, and ventricular aneurysm.
3. Arrhythmias such as VF and standstill, extreme bradycardia and/or tachycardias, and conduction disturbances.

Diagnostic Studies

Laboratory

Complete blood count: Usually normal but may reflect mild anemia in chronic states. Profound anemia possible as precipitating factor. White blood cell count elevated in infection.

Erythrocyte sedimentation rate: May be very low.

Serum electrolytes: Normal in mild heart failure. In severe states may have hyponatremia of dilutional origin. Frequently with diuretic therapy will have hyponatremia, hypochloremia, and hypokalemia. In latter stages may see hyperkalemia and elevated blood urea nitrogen and creatinine levels due to reduced renal blood flow from severely low cardiac output.

liver function tests: May reflect hepatic congestion with elevated bilirubin, alkaline phosphatase, lactic dehydrogenase, SGOT (aspartate aminotransferase (AST), serum pyruvic transaminase (alanine tachycardia aminotransferase) (SGPT [ALT]).

Thyroid function tests: Usually normal, however, useful in differential diagnosis when coupled with other clinical signs and symptoms. May reflect hyperthyroid (rarely hypothyroid) state.

Arterial blood gasses: Widely variable and dependent on severity of congestion and concomitant pulmonary disease.

Radiology

CXR: Cardiomegaly frequently present but is not a consistent finding. Varying degrees of pulmonary congestion may be present singularly or in combination: redistribution of pulmonary venous flow to upper lobes, Kerley’s B lines, loss of distinct margins of central and peripheral vasculature, hilar fullness (dilatation of central pulmonary veins) and clouding (edema), or diffuse cloudlike haziness of lung fields (alveolar pulmonary edema). Pleural fluid may be present either bilaterally or unilaterally (right side predominates) and may take the form of blunting of costophrenic angles to hydrothorax (free pleural effusion).

Other

ECG: There is no specific ECG abnormality that indicates the presence or absence of CHF. May reflect the changes of the underlying cardiac disorder (e.g., arrhythmia, myocardial infarction).

Lung scan/pulmonary arteriography: Useful when suspicious of pulmonary emboli as an underlying cause or precipitating factor. Positive examination still requires consideration of other causes of heart failure.

Echocardiogram: Variable findings dependent on the underlying cardiac disorder. Useful in evaluating chamber sizes, wall thickness, and motion, valvular integrity, ventricular function/ejection fraction, pericardial thickness, and fluid.

Cardiac catheterization: Variable findings and limited in scope of assessing cardiac function and underlying disorder. Useful in assessing coronary disease, left ventricular function, valvular and subvalvular anatomy, and intracardiac shunts.

Differential Diagnosis

Traumatic

Pneumothorax: May have history of chest injury. Paroxysmal dyspnea not relieved by change in position. Dyspnea rapidly increasing in severity and unremitting. May have displaced trachea, chest tympani, absent breath sounds on affected side, asymmetric respiratory excursions of chest wall. CXR reveals free air in thorax and lung compression.

Infectious

Pneumonia: Febrile, productive cough with purulent sputum. May have pleuritic chest pain. CXR more likely to show consolidation and segmental infiltrate. Laboratory tests may reflect infection with elevated white blood-cell count, positive sputum, and/or blood cultures.

Metabolic

Renal Failure: Not merely prerenal azotemia. Creatinine and blood urea nitrogen levels very high, creatinine clearance very low. Urine may contain many casts and much protein.

Hepatic disease, intrinsic: Hepatitis with very high liver function tests. No evidence of elevated venous pressure. Edema and dyspnea usually absent. No gallop on examination.

Neoplastic: Not applicable.

Vascular

Pulmonary emboli (without production of mechanical heart failure): Chest pain, frequently pleuritic. Dyspnea paroxysmal and may not be relieved by any maneuvers. May have hemoptysis and fever. Frequent evidence of deep venous thrombosis. CXR normal or revealing wedge shaped segmental density(ies).

Acquired

Chronic obstructive pulmonary disease: Dyspnea in COPD more likely to develop gradually and not be relieved by reduction in body fluid volume. Bronchospasm is responsive to bronchodilator therapy. Sputum usually present. Discriminating features may be subtleas COPD and CHF frequently are found concomitantly.

Treatment

Correct underlying cardiac disorder: Surgical repair of valvular lesions, shunts, ventricular aneurysm, congenital malformations. Treat arrhythmia.

Remove precipitating causes: Ensure treatment compliance, correct anemias, control hypertension, restrict sodium intake, reduce or stop, if possible, NSAIDs, corticosteroids, estrogens.

Control circulatory congestion: Reduce cardiac workload: Reduce physical activity and lower emotional/environmental suesses. Control obesity if needed. Institute vasodilator therapy. In late, refractory stage, intraaortic balloon pump.

Improve cardiac contractility: Digitalis the hallmark pharmocologic agent. In severe states, sympathomimetic agents, (e.g., dopamine, dobutarnine), and phosphodiesterase inhibitors, (e.g., amrinone, milrinone). If indicated, pacemaker.

Control/reduce excess Ruid and sodium retention: Low-sodium diet, diuretics. In severe state, may require invasive removal of pleural effusion or ascites. In refractory states, may require dialysis and/or ultra filtration.

Pediatric Considerations

Congenital heart disease is almost always the origin of CHF in the child and the underlying cardiac lesion may have a latent presentation. Early recognition is essential for a favorable prognosis.

The clinical presentation of CHF in infants and children is markedly different from adults. In infants, a history of poor feedings, inability to nurse for extended periods of time, tachypnea and diaphoresis with feedings, poor weight gain, and wheezing or coughing may indicate CHF. Physical examination findings include tachycardia, tachypnea, diaphoresis, nostril flaring, intercostal retractions, dependent peripheral edema, dyspnea on exertion, orthopnea, wheezing rales, gallop rhythm, and hepatomegaly. The presence of cardiomegaly on CXR is perhaps the most consistent finding. The causes of CHF in children are numerous. Causes include defects that result in volume overload or pressure over­load of the heart. Common volume overload defects in infants include patent ductus arteriosis and ventricular septal defects. Pressure overload is most often due to severe pulmonic or aortic stenosis and coarctation of the aorta. Primary management involves pharmacologic treatment with diuretics and digitalis.

Obstetrical Considerations

The routine management of CHF via morphine, oxygen, digitalis, rotating tourniquets, and diuretics is considered safe in the pregnant patient with CHF.

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