Heart
The heart increases in size during aging as a result of concentric ventricular hypertrophy. This occurs in response to the increase in left ventricular afterload. This increase in afterload occurs as the result of fibrosis and endothelial damage, which increase arterial stiffness and reduce the capacity for nitric oxide–induced vasodilation. Hypertrophy of cardiac myocytes occurs and accounts for a 30% increase in left ventricular wall thickness. Meanwhile, the number of cardiac myocytes is decreased due to necrosis and apoptosis. Despite these changes, resting systolic function tends to be well preserved in healthy individuals. However, the heart rate response to severe exercise is diminished. As a result, increases in cardiac output in response to severe exertion are attenuated by approximately 20% to 30%.
Cardiac dysfunction in aging is largely related to impaired diastolic left ventricle function with increased prevalence of diastolic heart failure.7 There is an age-related increase in cardiac connective tissue that, when combined with ventricular hypertrophy, increases wall stiffness and reduces diastolic compliance. Ventricular filling in the elderly is especially dependent on active diastolic relaxation. In this process, calcium is removed from troponin C binding sites, triggering the dissociation of actin and myosin, thus facilitating isometric relaxation. Active diastolic relaxation uses approximately 15% of the energy consumed during the cardiac cycle. This process is significantly impaired in the elderly and exacerbates the adverse effects of ventricular hypertrophy on diastolic filling. As such, the elderly heart is markedly dependent on the atrial “kick” for adequate ventricular preload. It is estimated that atrial contraction contributes approximately 30% of ventricular filling in the elderly versus 10% in younger individuals. Because of the importance of atrial contraction, and because filling is delayed by reduced ventricular compliance, ventricular filling is typically not complete until very late in diastole. Tachycardia and shortened diastolic intervals are associated with marked decreases in ventricular preload in the elderly. Atrial fibrillation is a common rhythm in the elderly. Loss of the atrial kick is particularly poorly tolerated by elderly patients because of decreased capacitance of the left ventricle from the previously noted changes. Perioperative events that reduce venous return, such as hypovolemia, positive pressure ventilation, and increased venous capacitance, may be accompanied by significant decreases in cardiac output. Conversely, excessive perioperative increases in blood volume or decreases in contractility can precipitate congestive cardiac failure. Diastolic dysfunction is now recognized as a major contributor to cardiovascular disease in the elderly population and is exacerbated by several coexisting diseases8,9 (Table 46-1).
It is difficult to distinguish systolic dysfunction from diastolic dysfunction during routine clinical evaluation. Furthermore, routine preoperative echocardiographic indices of function such as left ventricular ejection fraction will fail to identify diastolic dysfunction. However, diastolic filling can be evaluated by comparing Doppler echocardiographic measurements of mitral valve inflow velocities during the early and late (atrial contraction) phases of diastole. Dyspnea in the elderly may indicate congestive cardiac failure and/or pulmonary disease.
Large Vessels
Structural changes in the large vessels are an important element of the aging process and contribute significantly to the age-related changes in the heart described earlier.10 The large vessels become elongated, tortuous, and dilated in the elderly. Their intima and media are thickened, causing these vessels to be less distensible. The normal cushioning function of the large vessels is impaired; causing accelerated and enhanced pulse wave propagation. In the elderly, the pulse wave is reflected back from the peripheral circulation and augments systolic pressure. In young adults, the reflected pulse wave generally has lower amplitude and its return from the peripheral circulation is delayed such that diastolic rather than systolic pressure is augmented. As a result, diastolic pressure tends to be lower in the elderly than in younger individuals. Thus, in the elderly, both systolic pressure and pulse pressure are increased and left ventricular afterload is elevated. All of the aforementioned age-related vascular structural changes are accelerated in the presence of hypertension or atherosclerosis.
Endothelial Function
The vascular endothelium is an important regulator of vasomotor response, coagulation, fibrinolysis, immunomodulation, and vascular growth and proliferation. Endothelial dysfunction is an important element in the early pathogenesis of atherosclerosis, diabetes mellitus, and systemic hypertension.11 Aging is associated with altered endothelial structure and function, even in the absence of disease. Reactive oxygen species, such as superoxide anions, have been implicated in age-related endothelial dysfunction. Endothelial dysfunction is accelerated by smoking, diabetes, hypertension, and hyperlipidemia. In the elderly, endothelial nitric oxide release is decreased in all vascular beds, including the coronary circulation.12 Furthermore, the vasodilator response to nitric oxide of the adjacent vascular smooth muscle is also reduced. Vasodilator responses to β2 agonists and vasoconstrictor responses to α-adrenergic stimulation are similarly attenuated in the elderly. Thus, age-related endothelial dysfunction can be characterized as a decrease in the ability of the endothelium to dilate or contract blood vessels in response to physiologic and pharmacologic stimuli.
Conduction System
There are several important age-related structural and functional changes in the cardiac conduction system.5 The sinoatrial node undergoes a progressive change over time such that the proportion of pacemaker cells decreases from 50% in late childhood to less than 10% at 75 years. The sinoatrial node, atrioventricular node, and conduction bundles also become infiltrated with fibrous and fatty tissue. These changes are responsible for the increased incidence of first- and second-degree heart block, sick sinus syndrome, and atrial fibrillation in the elderly. The development of atrial fibrillation is also facilitated by left atrial enlargement, which typically accompanies aging in otherwise healthy individuals. Otherwise, healthy elderly men also experience an age-related increase in the prevalence, frequency, and complexity of ventricular ectopy.
Autonomic and Integrated Cardiovascular Responses
Aging is associated with increased norepinephrine entry into the circulation and deficient catecholamine reuptake at nerve endings. Therefore, elevated circulating concentrations of norepinephrine are usual, generating chronically increased adrenergic receptor occupancy. However, the cardiovascular response to increased adrenergic stimulation is attenuated by downregulation of postreceptor signaling and reduced contractile response of the myocardium. The number of the β-adrenergic receptors is reduced in the elderly myocardium.7 The decreased chronotropic and inotropic response of elderly patients to β-adrenergic drugs also has a contribution from downstream changes in the mechanism by which binding at the receptor is coupled to cyclic adenosine monophosphate. The response to exogenously administered β agonists, such as isoproterenol, is similarly attenuated. Receptor downregulation is responsible for the age-related decline in maximum heart rate during exercise. Indeed, receptor downregulation in the elderly makes their cardiovascular function similar to that of a younger individual who has received β-adrenergic antagonists.
Orthostatic hypotension is common in the elderly and is associated with syncope, falls, and cognitive decline. Impaired baroreceptor reflexes and attenuated peripheral vasoconstriction are partially responsible. Hypovolemia and salt depletion also contribute and are the result of iatrogenic diuretic administration or increased atrial natriuretic peptide release. Orthostatic hypotension is more common in patients who are hypertensive at baseline. It is difficult to separate the effects of aging per se from those of age-related chronic increases in systolic pressure. Straining against a closed glottis (Valsalva maneuver) typically produces a decrease in venous return and cardiac output. The normal baroreceptor response to this maneuver includes an increase in heart rate and peripheral vascular tone and restoration of blood pressure. However, this response is markedly attenuated in the elderly. Age-related impairment of baroreceptor responses makes hypotension more likely after the initiation of positive pressure ventilation, particularly in the presence of hypovolemia. Similarly, neuraxial local anesthetic–induced sympathetic blockade is more likely to be accompanied by hypotension in the presence of an impaired baroreceptor response. In the Irish Longitudinal Aging Study, antidepressants and β blockers were associated with orthostatic hypotension, and hypnotics and sedatives worsened preexisting orthostatic intolerance.13 Antihypertensive drugs that did not act through β-adrenergic blockade were not associated with orthostatic hypotension. These findings should be considered in the mobilization of elderly patients who may have received these drugs in the perioperative period.
Anesthetic and Ischemic Preconditioning in the Aging Heart
It is now recognized that, under certain circumstances, exposure to volatile anesthetics (anesthetic preconditioning) or several brief periods of ischemia (ischemic preconditioning) may enhance tolerance to subsequent ischemia, enhance cardiac function, and reduce infarction size.14 Because the incidence of atherosclerosis and coronary artery disease is age-related, the elderly would seem be most likely to benefit from a preconditioning strategy. However, both anesthetic and ischemic preconditioning may be markedly attenuated in the elderly, potentially explaining the difficulty of translating promising preclinical results to treatment.15,16 Furthermore, potent volatile drugs may induce significant cardiovascular depression in this age group. Therefore, the use of preconditioning strategies in this age group is uncertain.
Aging and the Respiratory System
The respiratory system undergoes a multifactorial decline in functional reserve with aging (Tables 46-2 and 46-3).17 Under normal circumstances, this decrease in respiratory function is not associated with significant limitation of daily activity. However, decreased respiratory reserve may be unmasked by illness, surgery, anesthesia, and other perioperative events. Common respiratory diseases and the effects of smoking and environmental pollution frequently exacerbate the decline in respiratory function with aging. The anticipation and amelioration of their effects is critically important to anesthetic management in the elderly, as postoperative respiratory complications result in 40% of perioperative deaths in patient older than 65 years.18
Respiratory System Mechanics and Architecture
The chest wall becomes less compliant with aging, presumably related to changes in the thoracic skeleton and a decline in costovertebral joint mobility. These changes produce a restrictive functional impairment. The noncompliant thoracic cage makes intercostal muscle activity less efficient. Therefore, the diaphragm and abdominal muscles assume a greater role in tidal breathing. However, diaphragmatic function declines with age, predisposing the elderly to respiratory fatigue when required to significantly increase minute ventilation. Although the diaphragm does not appear to undergo significant atrophy or change in muscle fiber type with aging, it does occupy a flatter position and therefore has a less favorable mechanical advantage. These changes predispose the elderly to respiratory insufficiency in the setting of high regional anesthesia.
Aging is associated with a loss of lung elasticity that is responsible for a decrease in lung recoil, thus making the lung more distensible. Changes in surfactant function may also contribute to age-related changes in lung compliance. The net result of these changes in the elastic properties of the lung and chest wall is an increase in intrapleural pressure that significantly impacts on respiratory function. Intrapleural pressure is a critical determinant of small airway caliber. Increased intrapleural pressures increase the tendency for small airway collapse to occur, thus causing gas trapping and/or expiratory airflow limitation.
Lung Volumes and Capacities
Vital Capacity
Vital capacity (VC) is the volume generated when a maximal inspiration is followed by a maximal expiration. There is a progressive loss of VC with aging that results from increased chest wall stiffness, decreased lung elastic recoil, and decreased respiratory muscle strength.
Residual Volume
The residual volume is the volume remaining in the lungs after a maximal expiration. In young individuals, the residual volume is determined primarily by ability of the expiratory muscles to overcome the elastic recoil properties of the lung and chest wall. However, in the elderly, dynamic airway closure also limits expiration. Therefore, aging is associated with a progressive increase in residual volume of up to 10% per decade (Fig. 46-2).19
Total Lung Capacity
Total lung capacity is the sum of the residual volume and the VC. Thus, the combined effect of the decline in VC and increase in residual volume is that the total lung capacity remains relatively constant with aging.
Functional Residual Capacity
The functional residual capacity (FRC) is the volume remaining in the lungs at the end of a normal expiration. The FRC is the volume at which the elastic recoil forces of the lung and chest wall are at equilibrium. The opposing recoil forces of the lung and chest wall generate the subatmospheric intrapleural pressure. Aging is associated with a progressive increase in FRC that occurs as a result of the decreased elastic recoil force of the lungs. However, the increase in FRC is less than would be predicted from the change in lung elastic recoil alone. This is because the increased stiffness of the chest wall counteracts the increase in lung volume.
Closing Capacity
Airway closure may occur in small airways (<1 mm) whose caliber is determined by their transmural pressure. Airway closure typically occurs in dependent areas of the lung where the surrounding intrapleural pressure is likely to be greater. In young adults, airway closure occurs only at low lung volumes (approximately 10% of VC). Thus, airway closure is unlikely during normal tidal breathing. However, as intrapleural pressure increases with age, airway closure occurs at progressively greater lung volumes. Indeed, in the elderly, airway closure occurs at approximately 40% of the VC reflecting lung volumes that exceed FRC. Although the FRC increases by up to 3% per decade, closing capacity increases at a greater rate. Thus, gas exchange impairment due to shunting in regions of airway closure is typical in the elderly during normal tidal breathing. The supine position is associated with a decrease in FRC when compared to the standing position. In this regard, the supine position makes airway closure during normal tidal breathing more likely. Indeed, airway closure may occur during tidal breathing as early as the mid-40s in the supine position.
Expiratory Flow
There is a progressive decline in forced exhaled volume in 1 second (FEV1) and forced vital capacity (FVC) with age that is independent of smoking or environmental exposure. Age-related loss of lung elastic recoil predisposes to dynamic airway collapse during forced expiratory maneuvers. Expiratory muscle strength also declines with age.
Diffusing Capacity and Alveolar-to-Arterial Oxygen Gradient
Gas exchange efficiency declines with aging as a result of increasing intrapulmonary shunting and decreasing lung diffusing capacity. The result is a linear decline in resting supine PaO2 between early adulthood and 65 years of age (Fig. 46-3).20 Small airway closure causes ventilation to perfusion (V/Q) mismatch and shunting. Cardiac output is often decreased in the elderly to the extent that mixed venous oxygen tension is decreased. Thus, even modest amounts of shunting may produce a significant decrease in PaO2 because of the contribution of desaturated venous blood. The diameter of the alveolar ducts is increased and their respective alveoli are wider and shallower. These architectural changes significantly reduce alveolar surface area. As a result, diffusing capacity for carbon monoxide may decline by up to 50% between early adulthood and 80 years of age.
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