Arterial Pressure Is Determined by the Cardiac Output and the Total Peripheral Resistance
Three examples illustrate the application of the concept that the mean aortic blood pressure is determined by cardiac output and TPR. First, in the most common form of human essential hypertension, the cardiac output is normal.
The blood pressure is elevated because of excessively constricted systemic arterioles, which increases TPR above normal. What remains unclear about human essential hypertension is why the arterioles are constricted and why the body does not compensate for the elevated TPR by lowering the cardiac output below normal (which would keep the arterial pressure close to normal). High blood pressure is a serious health problem in human medicine, because patients with uncontrolled hypertension often develop cardiac hypertrophy, and they are at high risk for cardiac arrhythmias, myocardial infarction, renal failure, and stroke. Naturally occurring hypertension is rare in veterinary species, although several techniques have been developed to induce hypertension in laboratory animals for research purposes.Severe hemorrhage or dehydration is another condition in which the arterial pressure becomes abnormal, and it provides several distinct contrasts to chronic hypertension. For example, hemorrhage and dehydration arc often encountered in veterinary medicine. Also, the arterial pressure is reduced in these conditions, not elevated. T he cause of the decreased pressure is a decreased cardiac output. Hemorrhage or dehydration characteristically reduces the cardiac preload, which reduces the stroke volume and cardiac output. TPR is actually increased above normal because the body constricts the arterioles in the kidneys, splanchnic circulation, and resting skeletal muscle. Vasoconstriction in these organs minimizes the fall in arterial pressure and diverts the available cardiac output to the “more critical” organs, which include the brain, heart, and any exercising skeletal muscle.
The response to vigorous exercise provides a third application of the concept that the mean aortic blood pressure is determined by the cardiac output and TPR. As in hemorrhage, exercise causes the cardiac output and TPR to change in opposite directions. In exercise, however, the cardiac output is elevated, and TPR is decreased. TPR decreases because the arterioles in the working skeletal muscle dilate, which increases the skeletal muscle blood flow. During vigorous exercise, TPR decreases to about one fourth of its resting value. The cardiac output increases about fourfold. The result is that the aortic pressure is negligibly changed. Figure 22-6 depicts the cardiovascular adjustments to vigorous exercise.