Cardiovascular System

The cardiac manifestations of aging are a direct result of complex biophysical, biochemical, molecular, ionic, and structural changes that occur at the level of the myocyte. There is a global reduction in the number of cardiac myocytes with aging (Vuyk 2003). Additional changes in the structural components [extracellular matrix (i.e., collagen)] result in a natural degree of "stiffening" of the myocardium and the vasculature.

The stiffened myocardium and vasculature become gradually less compliant to changes in fluid volume. This means that at similar filling volumes, the cardiovascular system operates at a higher pressure (mean arterial pressure, MAP). Increases in the MAP consequently cause a steady increase in left ventricular afterload, resulting in decreased stroke volume. Compensatory changes in the left ventricle (concentric hypertrophy) attempt to restore stroke volume (SV) at the expense of further reductions in myocardial compliance. This results in increased diastolic dysfunction and reduced left ventricular end diastolic volume (EDV). Preload is therefore reduced, causing further reductions in stroke volume and cardiac output. Though CO appears to be maintained in well-conditioned healthy elderly individuals, compensatory responses of CO to "stress" can be decreased (Mangoni and Jackson 2004, Morgan 2007).

In addition to changes at the cardiac myocyte level there are accompanying changes in the autonomic nervous system. There is an overall dampening of autonomic and baroreceptor activity with aging (Vuyk 2003, Mangoni and Jackson 2004, Prough 2005). This results in a decreased resting heart rate (HR). In addition, there is a decreased ability to increase cardiac output by changes in HR. As compared to younger patients, increases in CO are facilitated by increasing EDV, as opposed to increasing HR. This results in an increased reliance on atrial filling for maintenance of CO. As a result, dysrhythmias in the elderly can significantly affect their hemodynamic integrity. Overall, the hemodynamic response to physiological stress is diminished with aging.

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