Cardiovascular system changes Age is a major risk factor for cardiovascular disease. More than 50% of all heart failure patients are over the age of 70, and 90% of all deaths that occur due to heart failure occur in those who are over the age of 70 (Strait & Lakatta, 2012). As individuals age, the heart and arteries undergo major changes, resulting in a markedly different cardiovascular system for older adults compared to that of younger individuals (Strait & Lakatta, 2012). In the past 50 years, researchers have determined that progressive alterations in the cardiovascular system occur as part of the normal aging process even in the absence of any major cardiac disease or dysfunction, although inactivity and disease may accelerate these changes (Booth et al., 2011). While our understanding of why these changes occur is still evolving, current theory holds that many of the changes may be due to a lifetime of cellular stress on the cardiovascular system. A lifetime of wear and tear eventually results in permanent changes to the cells, and this in turn leads to changes in the cardiovascular system’s structure and function (Chester & Rudolph, 2011; Kelly, 2011). The structural changes that occur in the cardiovascular system can be found both at a microscopic cellular level and at a macroscopic whole body level. With advancing age the heart’s cells, also known as cardiomyocytes, decrease in number (North & Sinclair, 2012). This decrease takes place even in apparently healthy hearts without any sign of cardiac disease, though inactivity and disease may increase the loss of cardiomyocytes (North & Sinclair, 2012). As one ages, the cardiomyocytes become increasingly susceptible to stress and injury, eventually leading to their death and a decreased total number of cardiomyocytes (North & Sinclair, 2012). Partially due to the decrease in cardiomyocyte numbers, the remaining cardiomyocytes increase in size by up to 40% (North & Sinclair, 2012). The hypertrophy of the cardiomyocytes is thought to be an attempt to compensate, at least in part, for the decreased number of cells (North & Sinclair, 2012). Unfortunately, this enlargement, while it may temporarily compensate, ultimately leads to an enlargement of the heart, a thickening of the left ventricle, and a compromised ability of the enlarged cardiomyocytes to pump blood efficiently (North & Sinclair, 2012). The increase in thickness of the left ventricle muscle may serve as a temporary compensation for the decreased efficiency of the enlarged cardiomyocytes but ultimately leads to a harsh cycle of increasing oxygen demands for the enlarged cardiomyocytes, leading to further increases in the thickness of the left ventricle and increased oxygen demand. Aging also leads to a progressive infiltration of fat into the heart muscle as well as an increase in the collagen and connective tissue found in the extracellular space around the heart cells (Chester & Rudolph, 2011). The fatty accumulation in the heart can be found in particular around the sinoatrial node, sometimes creating a partial or a complete separation of the node from the surrounding heart tissue and eventually creating changes in the heart’s electrical conduction. This fatty and connective tissue may also contribute to the increase in thickness in the left ventricle seen with aging. In addition to the fatty infiltrations’ influence on the heart’s electrical conduction, there is also a pronounced decrease in the number of pacemaker cells with aging. By the age of 70, fewer than 10% of the pacemaker cells typically seen in younger adults remain (Strait & Lakatta, 2012). The fatty and connective tissue infiltration, as well as the decrease in the number of pacemaker cells, contribute to changes in both the electrical conduction through the heart and changes in heart rate that occur with aging. Even in healthy individuals, decreases in maximal heart rate occur with aging. Numerous changes occur that alter the autonomic signaling of the heart in older adults, contributing to the alterations and decreases in maximal heart rate seen with aging. A decrease in the sensitivity of sympathetic receptors in the body also occurs (Hotta & Uchida, 2010), and the combination of changes in the electrical conduction of the heart and changes to the autonomic response ultimately leads to a decrease in maximal heart rate. Maximal heart rate can be
estimated in older adults using the following formula (Tanaka, Monahan, & Seals, 2001): 208 – (.7 x age) This newer formula has replaced the older formula of 220 – age as a better predictor of maximal heart rate in older adults. Tanaka and colleagues (2001) found that the formula of 220 – age frequently underestimated the maximum heart rate of older adults. Older adults, as a result of both conduction and sympathetic changes, not only have a lower maximal heart rate, but they also have a decreased ability to alter (increase or decrease) their heart rate as functional demands dictate, resulting in a decrease in heart rate variability (North & Sinclair, 2012). This leads to a decreased ability to respond to any additional demands placed on the body, and in extreme circumstances, such as after surgery or during illness, may lead to an inability to meet the body’s demands for oxygen, resulting in death (Struthers et al., 2008). Numerous cardiovascular changes occur outside of the heart, which lead to further systemic changes within the heart. As age increases, so does the thickness and stiffness of the arterial walls. A decrease in the ability of endothelial cells to proliferate and migrate after injury may contribute to these changes in the arteries (North & Sinclair, 2012). As arteries become increasingly thick and stiff, they are less able to adapt to changes of blood flow within the artery. In a young and healthy individual, as increased blood is pumped through the arteries, the arteries are able to expand to maintain a relative amount of pressure in the arterial system. However, as aging occurs, the arteries are no longer able to expand and adapt to changes in blood flow. As the arteries are less able to adapt to both increases and decreases in blood flow, older adults are more likely to experience increased blood pressure and orthostatic hypotension or decreases in blood pressure when moving to a standing position. A decrease of more than 20 mm Hg in systolic pressure or 10 mm Hg in diastolic pressure is diagnostic of orthostatic hypotension. More than 30% of patients in outpatient clinics and 50% of nursing home patients complain of orthostatic hypotension, making this a common problem among older adults (Chester & Rudolph, 2011). Perhaps even more troubling than orthostatic hypotension is the systemic rise in blood pressure also related to the decreased compliance of the arteries. An increase in blood pressure increases the pressure against which the heart must pump, which results in additional left ventricular hypertrophy (North & Sinclair, 2012). Many older adults experience an increase in systolic blood pressure with aging that may be partially attributed to increased stiffness of the arteries (Chester & Rudolph, 2011; North & Sinclair, 2012). However, while systolic blood pressure increases, after the age of 50, diastolic blood pressure typically decreases (Strait & Lakatta, 2012). This leads to progressively larger differences between systolic and diastolic blood pressure. The difference between systolic blood pressure and diastolic blood pressure, known as the pressure product, is an important indicator of arterial health in older adults. An increase in the pressure product, resulting from larger differences between systolic and diastolic pressure, indicates a decreased ability of the arteries to adapt to changes in blood flow. A pressure product of greater than 60 mm Hg is indicative of less compliant, thicker arterial walls and has been associated with an increased risk of cardiovascular disease, stroke, and heart attack in older adults (Strait & Lakatta, 2012). Aging also leads to numerous functional changes that take place within the cardiovascular system. Many of these functional changes result from the previously mentioned structural changes that take place in the heart and arteries. In a body at rest, the cardiac output, measured as the amount of blood pumped through the heart each minute, averages 4 to 6 liters – regardless of age – in the absence of disease. However, with vigorous activity the older adult’s heart is no match for that of a young adult. With exercise or extreme stress the
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