In response to a falling cardiac output, neuroendocrine activation leads to vasoconstriction and, in the longer term, salt and water retention. Vasoconstriction is mediated via sympathetic and renin-angiotensin pathways, redistributing blood flow away from cutaneous, splanchnic, and muscular beds to more 'vital' organs such as brain and heart. Venous tone also increases, enhancing venous return. While vasoconstriction is an appropriate response to hemorrhage and hypovolemia, it is often deleterious in heart failure as myocardial work and function are adversely affected. The body initially attempts to compensate by raising circulating levels of atrial natriuretic peptide and adrenomedullin which enhance natriuresis and vasodilatation. However, over time, salt and water retention will predominate. This is primarily mediated by increased secretion of aldosterone and, to a lesser extent, antidiuretic hormone.

The negative consequences of these compensatory mechanisms include (i) a progressive decrease in renal blood flow and the potential development of renal dysfunction, (ii) pulmonary and systemic interstitial edema which may worsen oxygenation and symptoms, and (iii) a further fall in ventricular compliance and an increase in cardiac work, placing greater strain upon an already damaged heart.

Thus increased ventricular stiffness will result from pathophysiological processes occurring either as a direct consequence of heart failure or secondary to the body's compensatory mechanisms. Ischemia, ventricular hypertrophy, excessive afterload or preload, or an inadequate preload with compensatory vasoconstriction will all contribute further, as will misguided treatment regimens such as excessive diuresis. For the same end-diastolic pressure, a less compliant ventricle on a flatter ventricular function curve will generate a much lower stroke volume (Fig...^). This underlines the potentially catastrophic consequences of afterload increases, the therapeutic importance of optimizing compliance, and the problems inherent in an over-reliance on pressure measurements (central venous pressure, pulmonary artery wedge pressure) to the exclusion of volume or flow. It further illustrates how a vicious downward spiral is actually facilitated by the body's attempts at correction.

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