Cardiovascular effects of obesity and hypertension.
Although often coexisting in the same patient, obesity and essential hypertension exert disparate cardiovascular effects. An excess of adipose tissue augments cardiac output, stroke volume, and left ventricular filling pressure, expands intravascular volume, and lowers total peripheral resistance. In contrast, essential hypertension in a non-obese patient is associated with a contracted intravascular volume, high total peripheral resistance, and normal cardiac output, but increased left ventricular stroke work due to high afterload. Left ventricular adaptation will consist of eccentric hypertrophy in the obese (irrespective of arterial pressure) and concentric hypertrophy in the non-obese hypertension patient. The combination of obesity and hypertension burdens the heart with high preload and high afterload, thereby greatly enhancing the risk of congestive heart failure. Peripheral resistance and intravascular volume may be normal in mildly hypertension obese patients because of the mutually antagonising effects of the increase in arterial pressure and the increase in body weight. The fall in arterial pressure associated with weight loss seems to be caused by a decrease in adrenergic activity which leads to a fall in cardiac output without change in vascular resistance. Obesity hypertension may be the result of an inappropriately raised cardiac output in the presence of a relatively restricted arterial capacity due to the low vascularity of adipose tissue. In morbid obesity increased blood viscosity may contribute to the raised arterial pressure.
D001794:Blood Pressure; D001835:Body Weight; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000209:etiology; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D008954:Models, Biological; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D012084:Renin-Angiotensin System; D012119:Respiration