The aged cardiovascular risk patient.
It is mostly acknowledged that 'normal' or 'healthy' ageing of the cardiovascular system is distinct from the increasing incidence and severity of cardiovascular disease with advancing age (e.g. hypertension, ischaemic heart disease and congestive heart failure). It is also recognized that chronological and biological age may differ considerably. Nevertheless, even in the absence of overt coexisting disease, advanced age is always accompanied by a general decline in organ function, and specifically by alterations in structure and function of the heart and vasculature that will ultimately affect cardiovascular performance. Actual biological age is thus the net result of the interaction between age-related and concomitant disease-associated changes in organ function. As cardiovascular performance at a given moment is the net result of interactions between heart rate, intrinsic contractility, diastolic and systolic function, ventricular afterload and coronary perfusion, it is important to be aware of the age-related changes in each of these variables, independent of disease, as they determine cardiac performance at rest and its response to stress in the elderly. The most relevant age-related changes in cardiovascular performance for perioperative management are the stiffened myocardium and vasculature, blunted beta-adrenoceptor responsiveness and impaired autonomic reflex control of heart rate. These changes are of little clinical relevance at rest, but may have considerable consequences during superimposed cardiovascular stress. Such stress can take the form of increased flow demand (as in exercise or postoperatively), demand for acute autonomic reflex control (as in change of posture) or severe disease (as during myocardial ischaemia, tachyarrhythmias or uncontrolled hypertension). It may interfere with diastolic relaxation (i.e. ventricular filling), systolic contraction (i.e. ventricular emptying) and vasomotor control (i.e. arterial pressure homeostasis). Three factors contribute most of the increased perioperative risk related to advanced age. First, physiological ageing is accompanied by a progressive decline in resting organ function. Consequently, the reserve capacity to compensate for impaired organ function, drug metabolism and added physiological demands is increasingly impaired. Functional disability will occur more quickly and take longer to be cured. Second, ageing is associated with progressive manifestation of chronic disease which further limits baseline function and accelerates loss of functional reserve in the affected organ. Some of the age-related decline in organ function (e.g. impaired pulmonary gas exchange, diminished renal capacity to conserve and eliminate water and salt, or disturbed thermoregulation) will increase cardiovascular risk. The unpredictable interaction between age-related and disease-associated changes in organ functions, and the altered neurohumoral response to various forms of stress in the elderly may result in a rather atypical clinical presentation of a disease. This may, in turn, delay the correct diagnosis and appropriate treatment and, ultimately, worsen outcome. Third, related to the increased intake of medications and altered pharmacokinetics and pharmacodynamics, the incidence of untoward reactions to medications, anaesthetic agents, and medical and surgical interventions increases with advancing age. On the basis of various clinical studies and observations, it must be concluded that advanced age is an independent predictor of adverse perioperative cardiac outcome. It is to be expected that the aged cardiovascular risk patient carries an even higher perioperative cardiac risk than the younger cardiovascular risk patient. Although knowledge of the physiology of ageing should help reduce age-related complications, successful prophylaxis is hindered by the heterogeneity of age-related changes, unpredictable physiological and pharmacological interactions and diagnostic difficultie
Priebe
H J
HJ
Department of Anaesthesia, University Hospital, Freiburg, Germany.
D000367:Age Factors; D000368:Aged; D000375:Aging / Q000502:physiology; D000758:Anesthesia / Q000379:methods*; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D002320:Cardiovascular Physiological Phenomena; D017079:Exercise Tolerance; D006801:Humans; D018570:Risk Assessment; D012307:Risk Factors