The three factors of contractility, preload, and afterload determine ventricular stroke volume. 1 Coupled with heart rate, stroke volume determines cardiac output. Cardiac contractility is related to the amount of myocardial stretch, known as preload. Clinical measurements of cardiac stretch include the ventricular end-diastolic pressure and volume. Afterload is defined as the ventricular wall tension that develops during systole and reflects the resistance to outward blood flow. It is clinically estimated by the systolic arterial pressure. Many sorts of heart failure are associated with decreased contractility. The Frank-Starling relationships between stroke volume, preload, and contractility in both normal hearts and failing hearts are illustrated in Fig. 49-i1
FIG. 49-1. Left ventricular (LV) performance (Frank-Starling) curves relate preload, measured as LV end-diastolic volume (EDV) or pressure (EDP), to cardiac performance, measured as ventricular stroke volume or cardiac output. On the curve of normal individuals ( middle line), cardiac performance continuously increases as a function of the preload. States of increased contractility (e.g., dobutamine infusion) are characterized by an augmented stroke volume at any level of preload ( top line). Conversely, decreased LV contractility (commonly associated with heart failure) is characterized by a curve that is shifted downward ( bottom line). Point a is an example of a normal individual at rest. Point b represents the same individual after developing systolic dysfunction and heart failure (e.g., after a large myocardial infarction): stroke volume has fallen, and the decreased LV emptying results in elevation of the EDV. Because point b is on the ascending portion of the curve, the increased EDV serves a compensatory role because it results in an increase in subsequent stroke volume, albeit much less so than if operating on the normal curve. Further augmentation of LV filling (e.g., increased circulating volume) in the heart failure patient is represented by point c, which resides on the relatively flat part of the curve: stroke volume is only slightly augmented, but the markedly increased EDP results in pulmonary congestion.
Heart failure can be further classified into three categories related to physiology and functional anatomy: high versus low cardiac output, right versus left heart failure, and systolic versus diastolic dysfunction. 1,2.,Z,8,9,,i0,,l and 12
Heart failure can produce either low or high cardiac output states. 1 Whereas low-output failure is due to an inherent problem in myocardial contraction, high-output failure is due to an inability of functionally intact myocardium to keep up with excess functional demands. The causes of high-output failure are relatively few and include anemia, thyrotoxicosis, large arteriovenous shunts, beriberi, and Paget disease of the bone.
In congestive heart failure, excess fluid accumulates behind the affected chamber of the heart. In patients with left ventricular dysfunction due to either mechanical overload or infarction, excess fluid develops in the lungs. This resulting pulmonary edema, or congestion, is the cardinal manifestation of left-sided heart failure. In patients where the right ventricle is compromised (pulmonary embolus, right ventricular infarction), jugular venous distention and other signs of right-sided heart failure occur. Long-standing heart failure, however, usually results in compromise of both ventricles. 11
Systolic heart failure is characterized by an impairment of myocardial contraction, and diastolic failure by an impairment in myocardial relaxation. Systolic failure can occur from excessive afterload (systemic hypertension) or from damaged myocytes (infarction).11 Diastolic failure can be seen in both acute and chronic heart failure. Inhibited early diastolic relaxation as seen in myocardial ischemia is due to altered energy availability. 10 Chronic processes such as hypertrophic cardiomyopathy increase ventricular stiffness and inhibit relaxation. Many etiologies, such as transient myocardial ischemia, can result in either systolic or diastolic failure.
Once heart failure has developed, several neurohormonal compensatory mechanisms occur.12 Alterations in adrenergic tone redistribute blood flow to the brain and myocardium, reducing blood flow to the skin, kidneys, gastrointestinal tract, and skeletal muscle. The reduction in blood flow to the kidneys results in increased stimulation of the renin-angiotensin-aldosterone axis and secretion of antidiuretic hormone. The end result of these processes is enhanced sodium and water retention by the kidneys, which leads to fluid overload and the clinical manifestations of CHF. Additionally, the increased adrenergic tone leads to arteriolar vasoconstriction, a significant raise in afterload, and finally, to increased cardiac work.
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