Cardiovascular Considerations in the Older Patient

Original Editor - Wendy Walker

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Age-Related Structural Changes[edit | edit source]


Structural changes with aging involve the myocardium, the cardiac conduction system, and the endocardium. There is a progressive degeneration of the cardiac structures with aging, including a loss of elasticity, fibrotic changes in the valves of the heart, and infiltration with amyloid. The age-associated structural characteristics that have the greatest impact involve the contractility of the heart's left ventricular wall. The pumping capacity of the heart is reduced with age due to a variety of changes affecting the structure and function of the heart muscle.
For decades, it was thought that the heart undergoes atrophy with advancing age, but evidence suggests that an age-related increase in the left ventricular posterior wall thickness of approximately 25% has been found between the second and the seventh decade. An increase in heart mass with aging, for the most part, is due to an increase in the average myocyte size, whereas the number of myocardial cells declines.[1]

Valves[edit | edit source]

An age-related increase in valvular circumference has been reported in all four cardiac valves (aortic semilunar valve, semilunar valve, bicuspid valve, tricuspid valve), with the greatest changes occurring in the aortic valve (the valve between the left ventricle and the aorta). This photograph shows a case of aortic stenosis:

PP Aortic stenosis.jpg

Calcific deposits frequently are present [2] on one or more aortic valve cusps. These changes do not usually cause significant dysfunction, although in some older adults, severe aortic valvular stenosis and mitral valvular insufficiency are related to degenerative changes with age. Clinical heart murmurs are detected more frequently.

Myocardial Subcellular Changes[edit | edit source]

The nucleus, containing DNA, becomes larger and may show invagination of its membrane.The mitochondria show alterations in size, shape, cristal pattern, and matrix density, which reduce their functional surface.The cytoplasm is marked by fatty infiltration or degeneration, vacuole formation, and a progressive accumulation of pigments such as lipofuscin. The combined age-related changes in the subcellular compartments of the cells result in decreased cellular activities such as altered homeostasis, protein synthesis, and degradation rates.[3]

Cardiac Muscle Compliance[edit | edit source]

Again, the decline in left ventricular compliance provides an increased workload on the atria, resulting in hypertrophy of the atria.[4]

Age-Related Changes in the Blood Vessels[edit | edit source]

The decrease of elasticity of the arterial vessels with aging may result in chronic or residual increases in vessel diameter and vessel wall rigidity, which impair the function of the vessel. Factors that contribute to the increased wall thickening and stiffening
in aging include increased collagen, reduced elastin, and calcification.
One important set of changes involves the aorta, the wall of the aorta becomes less flexible, or shows an increase in wall stiffness, so that the blood leaving the left ventricle of the heart is faced by more resistance and cannot travel as far into the arteries[5]. Age-associated changes also occur in the more peripheral vessels the walls of the arteries throughout the body become thicker so that they, too, are less flexible and stiffer. The walls of veins may become thicker with age because of an increase in connective tissue and calcium deposits. The valves also tend to become stiff and incompetent. Varicose veins develop. Because of low blood pressure in veins, these changes probably are not significant for cardiovascular function. They may be of concern because of the possibility of phlebitis and thrombus formation.


Age-Related Changes in the Electrical Conduction System of the Heart[edit | edit source]

First, cardiac conduction is affected by the decrease in the number of pacemaker cells in the sinoatrial node with age. Beginning by age 60 there is a pronounced "falling out:' or decrease, in the number of pacemaker cells in the sinoatrial node, and by age 75 less than 10% of the cell number found in the young adult remains. With advancing age, there is an increase in elastic and collagenous tissue in all parts of the conduction system. Fat accumulates around the sinoatrial node, sometimes producing a partial or complete separation of the node from the atrial musculature. The conduction time from the bundle of His to the ventricle is not altered. There is a leftward shift of the QRS axis with advancing age, perhaps reflecting a variable degree of fibrosis in the anterior fascicle of the left bundle branch as well as mild left ventricular hypertrophy. The S-T segment becomes flattened, and the amplitude of the T wave diminishes.


Change in Cardiac Output, Stroke Volume, Blood Pressure[edit | edit source]

Cardiac output
Cardiac output at rest is unaffected by age. Maximum cardiac output and aerobic capacity are reduced with age.
Stroke volume
Stroke volume is changed little by aging; at rest in healthy individuals, there may even be a slight increase.
Blood pressure
Blood pressure is a measure of cardiovascular efficiency. Although blood pressure is characteristically heightened among older adults,53.54 there is evidence suggesting that there are no effects of aging on this index of cardiovascular[8]

Changes in Heart Rate[edit | edit source]

As we age, one of the most notable changes in the cardiac system is the decline in maximal heart rate.

  • One of the common means of establishing a guideline for change in maximal heart rate is the following formula[9]:
220 - age = max heart rate
Therefore whereas a young adult of 20 can be expected to have a maximal heart rate of 200 bpm (beats per minute), in a 70 year old this will be only 150 bpm, in an 80 year old 140bpm and in a 90 year old 130 bpm.

Causes of Changes in Heart Rate[edit | edit source]

The reduction in maximal heart rate is thought to be due to changes in the autonomic nervous system[10][11], along with age-related decrease in the number of cells in the sinoatrial node.

Consequences of Reduction in Maximum Heart Rate[edit | edit source]

  • Smaller aerobic workload possible - ie. reduction in the extent of cardiac exertion that can be tolerated for a period of time
  • Slower aerobic performance - eg. 90-year-olds completing the New York City marathon typically do so in 7-8 hours

Changes in Vascular Tissues[edit | edit source]

Stiffer Vascular Tissues[edit | edit source]

Changes in connective tissue as we age include:

  • increased crosslinking of collagen
  • loss of elastin
  • thickening of the basement membrane in the capillary walls[12]

These result in the heart and blood vessels being stiffer and less compliant[13], and this, in turn, leads to increased blood pressure[14][15]; it is noticeable that the majority of patients who 70 years of age or older are likely to be taking antihypertensive medication.

The thickening of the basement membrane of the capillary walls means that the delivery of oxygen and nutrients is slower than in younger people, although there is some evidence to suggest that this effect is modifiable with high levels of exercise[16].

Reduction in Contractitility of Vascular Walls[edit | edit source]

This contributes to the slowing of heart rate, lower VO2max and results in a reduction in the aerobic workload possible.

Challenges for physiotherapy management[edit | edit source]

Despite the fact that maximum heart rate and aerobic capacity are reduced, exercise in healthy older adults has been demonstrated in many studies to be effective in improving cardiac function and increasing aerobic capacity[17][18][19].

The further reading section of the page on Physical Activity and Older Adults  has links to some useful resources.

References[edit | edit source]

  1. geriatric physical therapy Dale L. Avers, PT, MSEd Vice President of Academic Affairs Rocky Mountain University of Health Professions Los Angeles, California
  2. Section of Cardiovascular Pathology, Department of Pathology, Indiana University School of Medicine, Indianapolis, Indiana, USA
  3. geriatric physical therapy Dale L. Avers, PT, MSEd Vice President of Academic Affairs Rocky Mountain University of Health Professions Los Angeles, California
  4. geriatric physical therapy Dale L. Avers, PT, MSEd Vice President of Academic Affairs Rocky Mountain University of Health Professions Los Angeles, California
  5. Clinical Hypertension and Vascular Diseases: Hypertension in the Elderly Edited by: L. M. Prisant © Humana Press Inc., Totowa, NJ
  6. (Accessed September 11, 2017)
  7. (Accessed September 11, 2017)
  8. geriatric physical therapy Dale L. Avers, PT, MSEd Vice President of Academic Affairs Rocky Mountain University of Health Professions Los Angeles, California
  9. Ehrman JK, Gordon PM, Visich PS, Keteyian SJ: Clinical exercise physiology, Champaign, IL, 2009, Human Kinetics
  10. Heckman GA, McKelvie RS: Cardiovascular aging and exercise in healthy older adults. Clin J Sport Med 18:479-485, 2008
  11. Brown SP, Miller WC, Eason JM: Exercise physiology: basis of human movement and disease, Baltimore, MD, 2006, Lippincott Williams & Wilkins
  12. Vaitkevicius PV, Fleg JL, Engel JH, et al: Effects of age and aerobic capacity on arterial stiffness in healthy adults. Circulation 88(4 Pt 1):1456–1462, 1993
  13. Franzoni F, Galetta F, Morizzo C, et al: Effects of age and physical fitness on microcirculatory function. Clin Sci (Lond) 106(3):329–335, 2004
  14. Kasch FW, Boyer JL, Van Camp S, et al: Cardiovascular changes with age and exercise. A 28–year longitudinal study. Scand J Med Sci Sports 5(3):147–151, 1995
  15. Ferreira I, Twisk JW, Stehouwer CD, et al: Longitudinal changes in VO2max: associations with carotid IMT and arterial stiffness. Med Sci Sports Exerc 35(10):1670–1678, 200
  16. Schroeder TE, Hawkins SA, Hyslop D, et al: Longitudinal change in coronary heart disease risk factors in older runners. Age Ageing 36(1):57–62, 2007
  17. Leicht AS, Allen GD, Hoey AJ: Influence of age and moderate-intensity exercise training on heart rate variability in young and mature adults. Can J Appl Physiol 28(3):446–461, 2003
  18. Ogawa T, Spina RJ, Martin WH 3rd, et al: Effects of aging, sex, and physical training on cardiovascular responses to exercise. Circulation 86(2):494–503, 1992
  19. Kohrt WM, Malley MT, Coggan AR, et al: Effects of gender, age, and fitness level on response of VO2max to training in 60–71 yr olds. J Appl Physiol 71(5):2004–2011, 1991