contribute to changes in electrical conduction through the heart and to changes in heart rate that occur with aging. Even in healthy individuals, the maximal heart rate decreases 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 (Paneni et al., 2017), 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. Calculating Maximal Heart Rate Maximal heart rate (HR max ) can be estimated in older adults using the following Gelish formula (Liguori & American College of Sports Medicine, 2020): 207 – (0.7 × age) This newer formula for HR max has replaced the older formula (220 – age) as a better predictor of maximal heart rate in older adults. Specialized regression equations for calculating HR max may be superior to the equation of 220 – age because this equation can under- or overestimate measured HR max , as found by Tanaka et al. They proposed a similar formula (208 – [0.7 × age]) after conducting an extremely large meta- analysis of formulae (2001). Older adults, as a result of both conduction and sympathetic changes, not only have a lower HR max , 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 (Paneni et al., 2017). 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, this 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 and lead to further systemic changes. How to measure resting heart rate and blood pressure A comprehensive physical assessment includes the measurement of resting heart rate and blood pressure. No special preparatory measures are usually needed to measure heart rate or blood pressure, but doing the following can ensure the most accurate measurement (Mayo Clinic, 2022): ● Have the client sit upright and relax in a chair for 5 minutes before the test. ● Ensure that the client does not smoke, exercise, or use caffeine 30 minutes before the test. Such activities can increase blood pressure and heart rate. ● Have clients wear a short-sleeved shirt so that the blood pressure cuff can be more easily placed on the arm. ● Be aware of medications that client may take that may affect blood pressure. Heart rate can be measured through several means, including pulse palpation or stethoscope auscultation on the wrist (radial artery), the neck (jugular artery), or the ankle (brachial artery) (Mayo Clinic, 2022). A heart rate monitor can also be used. A blood pressure test measures the pressure in the arteries as the blood pumps. It is ideal to have the client sit upright in a chair with both feet on the floor. For blood pressure of the arm the arm should rest comfortably at heart level. Wrap the blood pressure cuff around the top part of the arm, with the bottom of the cuff just above the elbow. Ensure that the blood pressure cuff fits, that it is not too large or too small. If using an automated cuff, follow the written directions. If taking a manual measurement of blood pressure, place the stethoscope over the brachial artery to listen to blood flow. Using the small hand pump, inflate the cuff pressure until you can no longer hear the arterial blood flow through the brachial artery. Open the valve on the hand pump slowly, deflate the handcuff until you hear a heartbeat, note the systolic pressure reading, continue to deflate until you no longer hear the arterial flow, and note the diastolic pressure. Blood pressure cuffs can also be used for wrist (radial) and ankle (brachial) pressure assessment, which are described on the Mayo Clinic website (2022).
from larger differences between systolic and diastolic pressure, indicates the 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). Cardiac output 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 four to six 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 older adult’s heart is unable to keep pace with a young adult’s heart, and large differences are seen between young and old individuals’ ability to perform vigorous exercise. Heart failure with preserved ejection fraction (HFpEF) is common in older adults, especially women, with the risk skyrocketing with age (Paneni et al., 2017). Maximal cardiac output, or the maximal amount of blood the heart can pump in one minute, decreases with age by as much as 25%. Maximal oxygen uptake, VO 2max , decreases by 50% between the ages of 20 and 80 (Strait & Lakatta, 2012). VO 2max is a measure of an individual's cardiovascular fitness, and decreased rates indicate lower physical fitness. While even master athletes experience declines in VO 2max with age, inactivity can accelerate the loss, and sedentary individuals may experience decreases in VO 2max by as much as 10% per decade after age 25 (Strait & Lakatta, 2012). Cardiovascular system changes are numerous and take place throughout the entire body. While it is clear that we do not fully understand the age- related changes that occur in the cardiovascular system, we do know that exercise intervention can delay and even reverse some of these changes (Booth et al., 2011; Booth & Zwetsloot, 2010). Pulse There is a connection between heart rate and pulse, but they are not the same. Your heart rate is how fast your heart is beating, and your pulse is how you can feel your heart rate. Vagal tone declines markedly with age (Tanaka et al., 2001). Basal (resting) cardiac vagal modulation (or ‘tone’) of the R–R interval (the time between two successive R waves on the QRS interval of an electrocardiogram) is how it can be interpreted on a heart monitor. Regular aerobic exercise modulates selective age-associated impairments of the autonomic nervous system’s physiological function. Tonic vagal modulation of the cardiac period (R–R interval) decreases with age and in more sedentary adults (50% more) than in those who habitually exercise (Tanaka et al., 2001). Those who regularly walk more than 8,000 steps a day are significantly less likely to die from cardiovascular disease than those that take 4,000 steps a day (Saint-Maurice et al., 2020). Heart rate Aging also leads to a progressive infiltration of fat into the heart muscle as well as an increase in 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 (SA) node, which sometimes creates a partial or complete separation of the node from the surrounding heart tissue and eventually changes the heart’s electrical conduction. This fatty and connective tissue may also contribute to the increased thickness of the left ventricle that is seen with aging. In addition to the fatty infiltrations’ influence on the heart’s electrical conduction, there is a pronounced decrease in the number of pacemaker cells with aging. By age 70, fewer than 10% of the pacemaker cells typically seen in younger adults remain (Strait & Lakatta, 2012). The fatty and connective tissue infiltration and the decrease in the number of pacemaker cells
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