Heart failure is the pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of metabolizing tissue and/or can only do so at the cost of an abnormally elevated diastolic volume/pressure. Heart failure is often, but not always, caused by impaired myocardial contractility, in which case the more accurate term is myocardial failure. The cause may be a primary abnormality of the heart muscle, as in cardiomyopathy, viral myocarditis, or excessive programmed cell death (apoptosis). It may also be coronary atherosclerosis, which interferes with contractility by causing ischemia and infarction. Valvular and/or congenital heart disease can be responsible too: the long-standing excessive hemodynamic burden imposed by the valvular abnormality or cardiac malformation eventually damages the heart muscle.
In other cases of heart failure, however, the clinical syndrome is similar except that there are no detectable abnormalities of myocardial function. In some such patients, the normal heart is suddenly presented with a mechanical load that exceeds its capacity, such as an acute hypertensive crisis, rupture of an aortic valve cusp, or massive pulmonary embolism. Heart failure in the presence of normal myocardial function also occurs in chronic conditions in which ventricular filling is impaired by a mechanical abnormality such as tricuspid and/or mitral stenosis, constrictive pericarditis without myocardial involvement, endocardial fibrosis, and some forms of hypertrophic cardiomyopathy. In many patients, particularly those with valvular or congenital heart disease, impaired myocardial function is combined with hemodynamic overload.
In evaluating patients with heart failure, it is important to identify not only the underlying, but also the precipitating cause. The cardiac abnormality produced by a congenital or acquired lesion such as aortic valve stenosis may exist for many years and cause no clinical disability. Frequently, however, the first clinical manifestations of heart failure are precipitated by an acute disturbance that places an additional load on an already chronically overburdened myocardium. In such cases, compensatory reserve is minimal, and the new load simply precipitates cardiac dysfunction. It is crucial to be able to identify such causes the most frequent of which are itemized below since appropriate intervention can be lifesaving.
Pulmonary vascular congestion due to left ventricular failure is a risk factor for pulmonary infection. The resulting fever, tachycardia, hypoxemia, and increased metabolic demand place a further burden on the overloaded, but compensated, myocardium in chronic heart disease.
In anemia, only an increase in cardiac output can meet the oxygen needs of metabolizing tissue. This is well within the compensatory reserve of a normal heart, but not that of a diseased, overloaded, and already largely compensated organ. Acute-on-chron-ic failure ensues, with inadequate oxygen delivery to the periphery.
Thyrotoxicosis and pregnancy
Thyrotoxicosis and pregnancy are other examples of high-output states. Hyperthyroidism may present as emergent or exacerbated heart failure in a patient with previously compensated heart disease. Similarly, heart failure not infrequently presents during pregnancy in women with rheumatic valvular disease, in whom compensation may be restored after delivery.
Arrhythmia is a frequent precipitating cause of heart failure, for a variety of reasons:
Tachyarrhythmia shortens the ventricular filling time and in the presence of ischemic heart disease may also cause ischemic myocardial dysfunction.
The dissociation between atrial and ventricular contraction characteristic of many brady- and tachyarrhythmias causes loss of the atrial booster pump mechanism, thereby raising atrial pressures.
Cardiac performance may be further impaired by the loss of normally synchronized ventricular contraction typical of any arrhythmia associated with abnormal intraventricular conduction.
Marked bradycardia associated with complete atrioventricular block or other severe bradyarrhythmia reduces cardiac output unless there is a reciprocal rise in stroke volume; this compensatory response cannot occur with serious myocardial dysfunction, even in the absence of heart failure.
Rheumatic, viral, and other forms of myocarditis
Acute rheumatic fever and a variety of other inflammatory or infectious processes affecting the myocardium can precipitate heart failure in patients with or without preexisting heart disease.
The additional valvular damage, anemia, fever, and myocarditis characteristic of infective endocarditis can, singly or in concert, precipitate heart failure.
Physical, dietary, fluid, environmental, and emotional excess
The abrupt augmentation of sodium intake in a large meal, noncompliance with heart failure medication, blood transfusion, physical overexertion, excessive environmental heat or humidity, and emotional crises can all destabilize previously compensated disease.
Rapid elevation of blood pressure, as in renal hypertension or discontinuation of antihypertensive medication, may result in cardiac decompensation.
In patients with chronic, but compensated, ischemic heart disease, reinfarction even if asymptomatic may further impair ventricular function and precipitate heart failure.
Physically inactive patients with low cardiac output are at increased risk of developing thrombi in the leg veins or pelvis. Pulmonary emboli cause a further elevation of pulmonary blood pressure, which in turn may produce or intensify ventricular failure. In the presence of pulmonary vascular congestion, such emboli also may cause pulmonary infarction.
Every patient with emergent or exacerbated heart failure should be systematically screened for these precipitating causes. If duly recognized, the precipitating cause can usually be treated more effectively than the underlying cause. The prognosis in such patients is clearly better than in those in whom the underlying disease has progressed to the point of producing heart failure without a precipitating cause. Screening can usually avoid invasive investigations such as angiography if guided by the following epidemiological data:
The Framingham study found hypertension in 70% of cases, and coronary artery disease in 59% of men and 48% of women; diabetes mellitus and electrocardiographic left ventricular hypertrophy were also associated with an increased risk of heart failure.
The Eastern Finland study found noninvasive evidence of coronary artery disease in 61% and hypertension in 55%.
Multivariate regression analysis in the study of men born in 1913 in Gothenburg, Sweden identified hypertension and smoking as the major independent risk factors.
The population-based study by Cowie et al illustrated the difficulty of establishing a precise etiology from noninvasive investigations. In one third of cases, the etiology remained undetermined: a predominantly elderly population is unlikely to be systematically investigated in detail for underlying coronary artery disease by coronary arteriography; the medical background, including hypertension, may be poorly documented; and simple noninvasive investigations such as echocardiography often fail to identify an etiological diagnosis. In the remaining two thirds, the single most common cause was coronary artery disease, followed by hypertension, valve disease, atrial fibrillation or flutter, cor pulmonale, alcohol, and hypertrophic and restrictive cardiomyopathy.
The conventional criteria for diagnosing coronary artery disease in an individual patient include documented myocardial infarction, a history of angina supported by evidence of reversible myocardial ischemia, and evidence of coronary disease on arteriography. In the absence of coronary arteriography, the above criteria will almost certainly underestimate the true prevalence.
In the UK, the Bromley Heart Failure Study quantified the extent of this underestimation by determining the prevalence and clinical relevance of coronary artery disease and hibernating myocardium in incident cases of heart failure, using coronary arteriography and myocardial perfusion imaging. Coronary artery disease was the cause of 52% of incident heart failure in the general population under 75 years, while myocardial perfusion scans detected significant hibernating myocardium in 37%. Noninvasive assessment thus seriously underestimates the prevalence of coronary disease and fails to identify those patients who may benefit from revascularization.
As expected, the etiology of heart failure reflects the heart disease developing in a particular community. Yet the above findings relating to the British, Finnish, and Swedish populations are not dissimilar from those in the US: the National Health And Nutrition Examination Survey (NHANES) I epidemiological follow-up study confirmed that most cases of heart failure are attributable to coronary artery disease.
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