Aging is a process of gradual and spontaneous change that places healthy adults at risk for decline with diminished reserves in most physiologic systems and with an exponentially increasing vulnerability to most diseases and to death. The process of aging is a continuum progressing throughout the individual’s life. Unlike pathologic conditions, the aging process affects all individuals. It is a process that is genetically programmed but modified by environmental influences, so the rate of aging can vary widely among people. At the cellular level, aging can be defined as a progressive deterioration of structure and function that occurs over time [7]. Cellular aging is believed to result from the lifelong accumulation of molecular and cellular damage caused by many mechanisms that are regulated by a complex system of maintenance and repair. The factors that lead to primary aging are poorly understood, however, the interplay between genetics and oxidant damage is believed to play a major role [7, 8].

The changes in cardio-pulmonary, renal, immune and musculoskeletal systems with aging have important implications for the critical care physician and will be briefly reviewed.

Cardiovascular performance impacts on critical illness in the elderly in two ways. First, age is a major risk factor for cardiovascular disease, which accounts for over 40 % of deaths in those aged 65 years and above [9]. Second, the effect of aging on cardiovascular structure and function has implications for hemodynamic support of the elderly. A substantial lack of cardiac reserve is noted by the age of 70. This lack of reserve may not affect the daily functioning of a “well” older individual, but when this same older person experiences physiological stress such as blood loss, hypoxia, sepsis or volume depletion, the lack of reserve becomes apparent through cardiac dysfunction

Aging results in an increase in arterial and myocardial stiffness. Increased arterial stiffness is manifested by an increased systolic arterial pressure, pulse pressure and pulse wave velocity whereas increased myocardial stiffness is manifested by impaired left ventricular diastolic filling [10, 11]. Increased arterial stiffness increases cardiac workload, further aggravating already existing adverse changes in left ventricular structure and function. With aging there is a progressive decrease in the number of myocytes and an increase in myocardial collagen content. Increased cardiovascular stiffness is usually attributed to the development of fibrosis. Ventricular relaxation which is more energy dependent than ventricular contraction, and therefore more oxygen dependant also becomes impaired with aging. Diastolic dysfunction is therefore common in the elderly, particularly in those patients with systemic hypertension [11–14]. Indeed, diastolic dysfunction is responsible for up to 50 % of cases of heart failure in patients over the age of 80 years. These cardiovascular changes result in a decrease in left ventricular ejection fraction with compensatory myocyte hypertrophy; consequently left ventricular mass index increases with aging [11, 13]. Resting cardiac output is maintained despite the increased afterload imposed by the stiffening of the outflow tract. However maximal heart rate, ejection fraction and cardiac output decrease with aging. There is decreased responsiveness to β-adrenergic receptor stimulation and decreased reactivity to baroreceptors and chemoreceptors with aging. Fibrosis and calcification of the fibrous skeleton of the heart, composed of the annular rings and fibrous trigones, together with calcification of the bases of the aortic cusps develops. These changes contribute to the high incidence of sick sinus syndrome, atrial arrhythmias and bundle branch blocks.

In younger persons, cardiac output is increased predominantly by increasing heart rate in response to β-adrenergic stimulation. With aging there is a relative “hyposympathetic state” in which the heart becomes less responsive to sympathetic stimulation, possible secondary to declining receptor function. The aging heart, therefore increases cardiac output predominantly by increasing ventricular filling (preload) and stroke volume rather by an increase in heart rate. Because of the dependence of preload, even minor hypovolemia can result in significant cardiac compromise. The dependence on preload to maintain cardiac output is made even more important by the diastolic dysfunction associated with aging. However, due to decreased ventricular compliance overzealous fluid resuscitation is likely to cause pulmonary edema. These changes dictate scrupulous management of the elderly patient’s volume status. The contribution of left atrial systole to left ventricular filling increases with age [15]. Atrial fibrillation is therefore poorly handed by elderly patients particularly those with marked diastolic dysfunction.

Declining respiratory function in the elderly is the result of changes in both the chest wall and the lung [16, 17]. There is a progressive decrease in chest wall compliance caused by structural changes of kyphosis and vertebral collapse. In the lung there is a loss of elasticity with collapse of the small airways and uneven alveolar ventilation with air trapping. Uneven alveolar ventilation leads to ventilation perfusion mismatch, which in turn causes a decline in arterial oxygen tension of approximately 0.3 mmHg/year from the age of 30 years. There is a progressive decline in respiratory muscle and diaphragmatic strength resulting in a decline in maximal inspiratory and expiratory force by as much as 50 % (see below). The control of ventilation is also affected by aging. Ventilatory response to hypoxia and hypercapnia fall by 50 % and 40 % respectively.

There is a marked decline in renal function with aging. Between the ages of 25 and 85 years, approximately 40 % of the nephrons become sclerotic. The remaining functional units hypertrophy in a compensatory manner. Sclerosis of the glomeruli is accompanied by atrophy of the afferent and efferent arterioles and a decrease in renal tubular cell number. Renal blood flow falls by approximately 50 %. Functionally, there is a decline in glomerular filtration rate of approximately 45 % by age 80 years. Serum creatinine, however, remains unchanged because there is a concomitant decrease in lean body mass and, thus a decrease in creatinine production. Estimates of GFR in the healthy aged can be made from the serum creatinine by using the formula derived by Cockroft and Gault [18]. This formula must be used with caution in critically ill patients as the serum creatine may be altered by factors other than the GFR including numerous medications and increased muscle breakdown due to sepsis, trauma, protein catabolism and immobility.

A progressive decline in the integrity of the immune system occurs with aging [19–22]. The age related changes are most evident in the peripheral T cell pool, which show signs of decreased reactivation to challenge with antigens [21–23]. The age related changes in the immune system, together with the increased burden of chronic disease may explain the increased incidence of infections in the elderly.

Body composition changes dramatically with aging. There is an increase in body fat and a decrease in lean muscle mass by up to 40 % at age 80 years [24]. The rate of loss of lean body mass accelerates after the age of 60 years. The loss of muscle mass or “sarcopenia” in the elderly is strongly associated with impaired mobility, increased risk of falls, lower quality of life and increased morbidity and mortality.

Generally loss of lean body mass is paralleled by changes in diaphragmatic mass; sarcopenia of the elderly is therefore associated with reduced diaphragmatic function. Critical illness is associated with loss of lean body mass. Elderly patients demonstrate greater muscle catabolism during critical illness than their younger counterparts. This is compounded by mechanical ventilation which results in rapid diaphragmatic atrophy. Decreased diaphragmatic mass is strongly implicated in the failure to wean from mechanical ventilation. Consequently, elderly patients are at a greater risk of weaning failure, with ongoing ventilation resulting in further diaphragmatic weakness. This sets up a vicious cycle whereby it may become increasing difficult to wean elderly patients from mechanical ventilation. This may explain the poor outcome of elderly patient’s requiring mechanical ventilation (see below).

Geriatric patients are at high risk of traumatic injuries, particularly those patients with diminished functional status. Falls are the most common mechanism of injury in the elderly population and are responsible for significant morbidity, mortality and medical costs [42–44]. Pedestrian- motor vehicle injuries affect the elderly disproportionately and result in a higher mortality as compared with other age groups. Perdue and colleagues reported that trauma patients older than 65 years were 4.6 times likely to die than younger patients [45]. A number of factors contribute to the increased mortality of elderly patients after traumatic injuries, most notably their limited physiologic reserve together with the presence of comorbid cardio-pulmonary disease. Elderly patients compensate poorly following blood loss due to limited chronotropic and inotropic reserve (hypo-adrenergic state), diastolic dysfunction, and the inability of the kidney to conserve fluid. Many elderly patients are prescribed beta-blockers; these drugs further reduce the ability of the patient to compensate for decreased intravascular volume. In addition, elderly patients are frequently treated with Coumadin and/or anti-platelet drugs which increase the propensity for uncontrolled hemorrhage.

Evidence suggests that many injured elderly patients are under-triaged despite the increased risk of death and complications. One possible cause of under-triage is the late presentation of physical findings indicating hypovolemia. Elderly patients who have severe injuries are best treated in trauma centers where the outcome is reported to be improved [46].

The operative mortality and incidence of postoperative complications are increased in elderly patients undergoing elective surgery [47]. It is not uncommon for elderly patients who appear fit and healthy (physiologic age less than chronologic age) to do poorly following elective surgery (the “knife” is the great equalizer). The decreased physiologic reserve and increased incidence of comorbidities probably accounts for this finding. Liu et al. reported an operative mortality of 4.6 % and a postoperative complication rate of 25 % in a cohort of octogenarians undergoing non-cardiac surgery [48]. Elderly patients have a high incidence of protracted disabilities following major surgery. Lawrence and coworkers reported a high incidence of functional disabilities at 6 months following major abdominal surgery in a cohort of elderly patients [49]. In patients undergoing thoracic surgery dependence for the performance of activities of daily living and impaired cognition were predictors of postoperative complications [50]. Postoperative delirium is common following surgery and is associated with increased length of stay, morbidity and mortality. The operative mortality and rate of postoperative complication are even higher in elderly patients undergoing emergency surgery, being reported in up to 49 % and 68 % of cases respectively [47, 51–53].

Elective surgery must be considered very carefully in the elderly. Most randomized controlled trial comparing surgical to a more conservative approach are performed in patients less than 65 years of age. It is probably not appropriate to extrapolate the results of these trials to the elderly population. Coronary artery bypass surgery is frequently performed in the elderly with no evidence to support the benefit in this population of patients. Rady and Johnson compared the outcome from cardiac surgery in octogenarians compared to younger patients [54]. The octogenarians had a significantly higher incidence of postoperative complications and a significantly higher hospital mortality (13.5 % vs. 1.3 %, p < 0.001) than the cohort of younger patients. Furthermore, significantly more octogenarians were discharge to a subacute/chronic health care facility than their younger counterparts (39.5 % vs. 13 %, p < 0.001). This study demonstrated that only 47 % of the octogenarians (all who were living at home and independent prior to surgery) were discharged to home after surgery and therefore potentially benefited from undergoing coronary revascularization.

Over the last few years, geriatricians have developed an approach to care for the elderly called comprehensive geriatric assessment (CGA). CGA evaluates the comorbid illnesses, mental status, nutritional status, living circumstances, social support systems and polypharmacy [50, 55]. The goal of CGA is to provide information to the surgeon which will allow more accurate risk assessment for surgery. CGA will also allow for a pro-active team-based approach to interventions which will limit complications in those patients who undergo surgery.