Andersons pediatric cardiology 1736

Basic Concepts in Chronic Heart Failure Although, for centuries, heart failure was considered to be the result of a severe and irreversible injury to the heart leading to an irremediable abnormality of the ventricle's systolic function, it is now recognized that the syndrome of heart failure reflects a more complex, dynamic, and progressive process that can no longer be defined in simple hemodynamic terms and that affects not only on the heart itself but also a myriad of extracardiac physiologic processes The current framework considers heart failure―whether due to ischemia, infection, altered cardiac load, or tachycardia―to be a condition in which a primary insult to the heart results in a cascade of secondary responses affecting the heart as well as related organs.5,6 It appears that irrespective of the precise nature of the primary insult, for the most part the secondary responses and clinical evolution share common features, so that the progression of heart failure represents an ordered, predictable, coordinated cascade of events Although this may initially be reversible, it can, in the absence of treatment, result in terminal heart failure and ultimately death.6 These secondary responses to cardiac injury may, at least in the initial phase, be adaptive and designed to preserve the flow of blood to the vital organs.6 Thus, in response to a regional injury of the myocardium, global function is maintained by invoking a number of compensatory mechanisms The regional function of the uninjured myocardium increases and the ventricle hypertrophies as growth factors within the myocyte accelerate the synthesis of protein and growth of the myocyte As described later, a reduction in perfusion pressure within the kidneys is detected by receptors in the renal arterioles, activating the complex reninangiotensin-aldosterone system to cause constriction of the efferent arterioles so that the glomerular filtration pressure is maintained along with a balance of salt and water Increased activation of the neuroendocrine system, manifest by the systemic release of neurohormones such as noradrenaline and adrenaline, maintains cardiac output through chronotropic and inotropic activity With time, these mechanisms become maladaptive as the patient progresses into a phase of decompensated heart failure.5 The increase in left ventricular mass together with dilation of the ventricle augments mural stress within the myocardium and its consumption of oxygen, potentially worsening the myocardial injury Chronic activation of the renin-angiotensin system results in edema, the elevation of pulmonary arterial pressure, and increased afterload Sympathetic activation increases the risk of arrhythmia and sudden death Although these changes may be reversed by successful treatment, it has been suggested that such treatment must be initiated before the patient reaches the socalled terminal threshold, after which recovery of left ventricular function is not possible (Fig 65.1).7 FIG 65.1 Responses to myocardial injury Injury results in adaptive responses within the heart and related systems As the condition progresses, these adaptive responses become counterproductive (maladaptive), leading to progression of the disease and increasing symptoms Treatment may reverse these maladaptive changes until a terminal threshold is reached, after which recovery of left ventricular function is not possible and irreversible heart failure ensues (Modified from Delgado RM 3rd, Willerson JT Pathophysiology of heart failure: a look at the future Tex Heart Inst J 1999;26:28–33.) Function of the Normal and the Failing Heart The ability to accurately describe the function of the heart, its metabolic demands and its interactions with the vasculature, is of paramount importance in analyzing the mechanisms of circulatory failure and the effects of interventions in patients with myocardial disease In clinical practice our assessment of cardiac function is usually limited to the indirect estimation of ventricular systolic and end-diastolic pressure, ejection fraction, and, in some echocardiography laboratories, the assessment of mural stress However, a complete evaluation of cardiac function would extend further, ideally to include an indicator of ventricular systolic and diastolic performance that is relatively independent of load, an assessment of the myocardial consumption of oxygen, and an examination of the relationship between ventricular performance and cardiac load Since Suga presented his analysis of the instantaneous pressure-volume relationship8 and subsequently developed the concept of time-varying elastance,9 there has been heightened interest in the use of the pressure-volume relationship in assessing ventricular performance This has been especially true in recent years with the introduction of the conductance catheter technique,10 which allows high-fidelity online measurements of ventricular pressure and volume at fast acquisition speeds The classic work of Wiggers,11 which describes changes in left ventricular pressure and volume during the cardiac cycle, has provided the foundations for our current understanding of ventricular function In Wiggers’ schema, the cardiac cycle begins with the onset of depolarization on the electrocardiogram, which is soon followed by an increase in pressure within the ventricle When left ventricular pressure exceeds left atrial pressure, the mitral valve closes The aortic valve remains closed while aortic pressure still exceeds left ventricular pressure, and ventricular volume therefore remains constant; so-called isovolumic contraction exists When left ventricular pressure exceeds aortic diastolic pressure, the aortic valve opens and the ventricle begins to eject Consequently the volume of the left ventricle falls (Fig 65.2)