Cardiovascular disease remains the leading cause of morbidity and mortality in older adults. It often is difficult to separate true age-related changes in the cardiovascular system from disease processes. The aorta and arteries tend to become stiffer and less distensible with age, the heart becomes less responsive to the catecholamines, the maximal exercise heart rate declines, and there is a decreased rate of diastolic relaxation.15
Although approximately 40% of older adults have hypertension, the disorder is not considered a normal age-related process.16 The relationship between blood pressure and risk for cardiovascular disease is continuous, consistent, and independent of other risk factors. It has been shown that the higher the blood pressure, the greater the chance of heart attack, heart failure, stroke, and kidney disease. In persons older than 50 years, systolic blood pressure (SBP) greater than 140 mm Hg is a more important risk factor than a rise in diastolic blood pressure (DBP). The risk for developing cardiovascular disease beginning at 115/75 mm Hg doubles with each increment of 20/10 mmHg. Individuals who are normotensive at age 55 have a 90% lifetime risk for developing hypertension. There is now a push to intervene when individuals are prehypertensive (i.e., SBP of 120 to 139 mm Hg or DBP of 80 to 89 mm Hg) with lifestyle modification strategies to prevent hypertension. There is also a move to treat hypertension aggressively in order to minimize negative outcomes.16 With advancing age, the elevation in blood pressure is generally more pronounced for the SBP than for the DBP, probably as a result of increased aortic stiffness. In the older adult, compensatory cardiovascular mechanisms often are delayed or insufficient, so that a drop in blood pressure due to position change or consumption of a meal is common.17,18 Ortho-static hypotension, or a significant drop in systolic blood pressure on assumption of the upright position, is more common among elderly persons (see Chapter 25). Even in the absence of orthostatic hypotension, older adults respond to postural stress with diminished changes in heart rate and diastolic pressure. This altered response to ortho-static stress is thought to result from changes in autonomic nervous system function, inadequate functioning of the circulatory system, or both.19
Senescent cardiac muscle typically displays a decreased response to β-adrenergic stimulation and circulating catecholamines, and there is increased diastolic stiffness of the ventricles that impedes filling, probably because of a slower rate of diastolic relaxation. Although early diastolic filling decreases by approximately 50% between 20 and 80 years of age, filling volumes are maintained, most likely as a result of an enhanced atrial contraction and its contribution to ventricular filling. The afterload (i.e., opposition to left ventricular ejection) rises steadily with age as the ascending aorta becomes more rigid and the resistance in peripheral arterial vessels increases. Although the overall size of the heart does not increase, the thickness of the left ventricular wall may increase with age, in part responding to the increased afterload that develops because of blood vessel changes.15 The resting heart rate remains unchanged or decreases only slightly with age; however, the maximum heart rate that can be achieved during maximal exercise is decreased.
Despite aging changes and cardiovascular disease, overall cardiovascular function at rest in most healthy elderly persons is considered adequate to meet the body's needs. Cardiac output is essentially maintained in healthy older adults (men more than women) during exercise despite the decreased heart rate response, apparently because of a greater stroke volume resulting from increased end-diastolic volume (i.e., Frank-Starling mechanism) during exercise.17,20
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