It had previously been held that in elderly adults free of coronary disease, there was no change in cardiac output or pump function despite age-related increases in systolic blood pressure and arterial stiffness [26]. This was thought to be due to adaptations including moderate increase in LV thickness, prolonged contraction times, atrial enlargement, and increased atrial contributions to LV filling [26]. It was further postulated that prolonged contraction during systole maintained the load-bearing capacity of the heart in the face of increased afterload that came with age-related increase in arterial stiffness. Most of these data, however, came from older technology such as M-mode echocardiography and gated blood pool scans. More recently newer technology such as cardiac MRI, 2-D ECHO, 3-D ECHO, and pulsed tissue Doppler echocardiography demonstrates that these previously held theories may not be as accurate as once thought. Indeed contemporary authors have shown that echocardiography is not as efficient as cardiac MRI in distinguishing between concentric remodeling and concentric hypertrophy [27–29].

Newer studies utilizing cardiac MRI demonstrate that left ventricular hypertrophy, once thought to be adaptive, may be suboptimal. Although older myocytes do increase in size, there is overall myocyte depletion (dropout) that is associated with increased collagen deposition and nonenzymatic cross-linking [30–33]. The older ventricle, while increasing in overall mass, does not increase in overall functional mass, as demonstrated by cardiac MRI findings that reveal increasing left ventricular mass to volume ratios and associated declines in LVEDV in relation to left ventricular mass. Additionally, although the EF is preserved, absolute stroke volume is not [7]. Although LVEDV and LVESV both decrease in age, the decrease in LVEDV is proportionally greater than the decrease in LVESV, which leads to an overall age-related decline in stroke volume [7]. The phenomenon of ventricular adaptation and decreased function over time is not unique to the left ventricle. Echocardiography with pulsed tissue Doppler technology demonstrates that right ventricular systolic and diastolic function is similarly affected by an age-related decline [13]. It was previously held that elderly patients could respond to injury nearly as well as their younger counterparts based on lack of change in overall cardiac function at rest [26]. Recent findings of cardiac MRI and newer echocardiographic modalities show this to be false; however, the degree to which this affects the injured elderly patient has yet to be determined.

Gribben and colleagues were among the first to investigate the effect of aging on baroreflex function in a study relating pulse interval to change in systolic blood pressure after phenylephrine injection. There is a linear relationship between pulse interval and change in systolic blood pressure and a distinct decrease in the baroreceptor reflex sensitivity in the elderly. Shimada and colleagues found that an age-related decline in baroreflex sensitivity is independent of systolic blood pressure and systemic noradrenaline levels [34]. Similar findings of decreased baroreceptor reflex sensitivity are found in a study of healthy volunteers examining cardiac response to angiotensin II (ANG II) infusions. The elderly, unlike their younger counterparts, do not exhibit decreases in heart rate when blood pressure is increased via ANG II infusion [35].

Another inevitable consequence of normal aging is a decreased responsiveness to beta-adrenergic stimuli. Age-related decreases in maximal heart rate (HR max) are responsible for decreases in aerobic work capacity [7, 36, 37]. This decline is independent of gender, regular exercise, and other factors [7, 36, 37]. This decrease in chronotropic responsiveness to exercise contributes largely to age-related reduction in maximal cardiac output and is key in determining aerobic exercise capacity [37].

Although otherwise healthy, older adults exhibit decreased chronotropic responsiveness (HRmax) to exercise, the exact mechanism responsible has not been fully elucidated [37]. The elderly have decreased chronotropic and inotropic response to beta-adrenergic stimulation, and this decreased responsiveness to sympathoadrenal stimulation may explain the observed decrease in HRmax [37]. However, historical studies of B-adrenergic responsiveness consist of poorly matched heterogeneous groups and have inconsistent results. Additionally, differences in vagal tone do not seem to contribute at all to differences in HRmax in normoxic conditions. In fact, the elderly exhibit decreasing vagal tone when compared to younger counterparts [38], and incremental decreases in vagal tone accompany increased workloads during exercise. The net sum of these observations would theoretically increase the elderly patient’s HRmax, not reduce it.

Insight into B-adrenergic responsiveness and resultant decreases in HRmax can be drawn from recent work from Christou and Seals. A 2008 study of a cohort of young and elderly men examined the role of reduced intrinsic heart rate (HRint) and decreased B-adrenergic responsiveness in age-associated decreases in HRmax. Maximal heart rate was tested during treadmill exercise to exhaustion. HRint was measured at rest after complete ganglionic blockade, and B-adrenergic responsiveness was likewise tested at rest via exogenously administered isoproterenol after ganglionic blockade. This study reveals that elder men are significantly more likely to have higher serum levels of norepinephrine at rest, lower HRmax, lower HRint, and decreased chronotropic responsiveness. Both decreased HRint and decreased B-adrenergic responsiveness are strongly related to decreased HRmax; however, HRint shows a higher degree of correlation (r = 0.87 vs. r = 0.61). These authors conclude that decreased maximal heart rate observed with aging correlates with reduced B-adrenergic responsiveness but is largely explained by a lower intrinsic heart rate in healthy elderly adults [37].

Decreases in HRint are thought to be clinical manifestations of occult sinoatrial node (SA node) dysfunction, possibly related to age-related myocardial fibrosis and collagen deposition at the SA node [39]. However, SA node dysfunction does not always accompany remodeling and may in fact indicate a molecular change in the pacemaker cells [39, 40]. Recent studies have shown reductions in calcium channel proteins which may lead to decreased sinus node depolarization reserve and thus suppression of action potential formation and propagation [41]. Additionally, connexin [42], a primary gap junction protein, is reduced in aged cells [42]. This reduction is hypothesized to restrict conduction of SA node action potentials within the myocardium.

Although there is very little information regarding the impact of aging on the cardiovascular response to injurious stress, much is known of the cardiovascular response to exercise. Much of our understanding of the cardiovascular response to injury is extrapolated from these data.

The cardiac output response in the elderly during exercise is significantly reduced. However, subsequent studies excluding patients with coronary artery and cardiac disease show no significant age-related change in cardiac output during exercise. Cardiac output modulation is affected by age. Older patients cannot increase cardiac output with increases in heart rate due to decreases in HRint and B-adrenergic responsiveness. The elderly utilize the Frank-Starling mechanism and increase their end-diastolic volume and stroke volume during exercise, thereby increasing cardiac output without substantially increasing heart rate. The elderly do augment their stroke volume during exercise; however, the increase in ejection fraction is less than that observed in younger counterparts secondary to a decreased ability to reduce end-systolic volume. This is similar to what is seen in young patients given exogenous beta-blockade and then stressed with increasing exercise loads. In this scenario, the young similarly increase cardiac output by increasing stroke volume without appreciably increasing heart rate. Interestingly, the elderly have increased plasma levels of epinephrine and norepinephrine during exercise loading. This finding further underscores the elderly patient’s lack of beta-adrenergic responsiveness.

Severe injury often leads to profound states of hypovolemia through blood loss and capillary leak. Critically ill elderly patients are also susceptible to further intravascular depletion from fever (free water loss), poor intake, pharmacologic vasodilation (home medications), and decreased plasma oncotic pressure (poor nutrition). Given the elderly dependence on the Frank-Starling modulation of cardiac output rather than chronotropy, the elderly patient is particularly sensitive to preload reductions secondary to hypovolemia. This is evident in work done by Shannon and colleagues in which elderly patients mount a blood pressure increase and slight HR increase similar to younger patients in tilt test. However, when the same test is performed subsequent to preload reduction with diuretics, elderly patients sustain a symptomatic fall in blood pressure due to an inability to mount a tachycardic response, whereas younger patients exhibit a profound increase in both heart rate and blood pressure [43].

Therefore, based on exercise data, elderly patients are capable of maintaining cardiac output in response to the stress of injury. This is not by heart rate augmentation but rather by effecting stroke volume by increasing end-diastolic volumes and contractility. Research from the early 1980s suggests that elderly patients were unable to mount a cardiac output response to stress. However, subsequent studies of carefully screened healthy elderly patients demonstrate an absence of significant changes in age-related cardiac output variables during exercise in the elderly [6, 62]. Newer technology including cardiac MRI pulsed tissue Doppler echocardiography in 2D and 3D demonstrates that while elderly patients can mount a cardiac output response to stress, this may be much less in magnitude than their younger counterparts due to decreased cardiac reserve [13, 25, 44, 45].

In a study of critically ill trauma patients, Belzberg and colleagues document age-related differences in cardiovascular response to injury [46]. In their 2007 study, they utilized noninvasive primarily transcutaneous devices to collect hemodynamic and oxygen transport variables on 625 consecutive trauma patients at the time of emergency department (ED) admission. Of these, 259 were deemed “high risk” and had pulmonary artery catheters placed for invasive hemodynamic monitoring. Hemodynamic patterns for elderly (>65) and non-elderly (<65) patients were analyzed. Data were stratified by survivors and non-survivors and then further divided by age (elderly vs. non-elderly survivors). Elderly trauma patients had significantly lower CI, HR, arterial oxyhemoglobin saturations (SpO₂), hematocrit (Hct), and oxygen delivery. Interestingly, while elderly survivors have significantly lower values of these parameters than young survivors, elderly and young non-survivors exhibit very similar hemodynamic and oxygen transport values. This study concludes that aggressive resuscitation titrated to hemodynamic and oxygen transport variables may improve outcomes and that the cardiac response to injury seen in elderly patients is much less robust than that of their younger counterparts [46]. It is obvious that elderly patients generate increased cardiac performance in the face of the stress such as surgery and injury; however, the magnitude of this response is attenuated and less robust than that of younger counterparts. It is unknown whether this is due to normal age-related decline in cardiovascular function or to an increased prevalence of cardiovascular disease. Extrapolation from exercise data suggests that it is a combination of both.

Real-time assessment of global cardiovascular function using dense data capture technology and bedside assessment of ventricular-arterial coupling demonstrates the occurrence of myocardial depression in the critically injured and posttraumatic septic shock patient [47]. Prior work by Tacchino and Siegel describes similar phenomena in multiply injured patients [5]. The authors reported a 32 % incidence of myocardial depression, as evidenced by a reduction in cardiac index (CI) and ejection fraction (EF), in patients 65 years and older, and a 21 % incidence in those 13–30 years of age. Furthermore, mortality rate rises to 60 % in the elderly group when myocardial depression occurs.