Our understanding of hemodynamics depends on measuring the blood flow at different points in the circulatory system (Figure 2). A basic approach to understanding hemodynamics is by “feeling the pulse.” This gives simple information regarding the strength of the circulation and blood flow via the systolic stroke and the heart rate—both important components of the circulation which may be altered in disease. The blood pressure, which is the pressure exerted by circulating blood upon the walls of blood vessels, is one of the principal vital signs, and it can be simply measured using a plethysmograph or cuff connected to a pressure sensor (mercury or aneroid manometer). Blood pressure determines flow rate within blood vessels. Blood pressure is the most common clinical measure of circulation and provides a peak systolic pressure and a diastolic pressure.
Pressure and Flow
During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastolic) pressure. The blood pressure in the circulation is principally due to the pumping action of the heart. Differences in average blood pressure are responsible for blood flow from one location to another in the circulation. The rate of average blood flow depends on the resistance to flow presented by the blood vessels. The average blood pressure decreases as the circulating blood moves away from the heart through the arteries and capillaries due to viscous losses of energy. The average blood pressure drops during circulation, although most of this drop occurs as the blood travels through the small arteries and arterioles. The pulsatile nature of blood flow also creates a pulse wave that is propagated down the arterial tree. At arterial bifurcations or divisions, reflected waves rebound to return to semilunar valves and the origin of the aorta. These return waves create the dicrotic notch displayed in the aortic pressure curve during the cardiac cycle, as these reflected waves push on the aortic semilunar valve. This rebounding wave can increase overall blood pressure. Gravity affects blood pressure via hydrostatic forces (i.e. during standing). Valves in veins, breathing, and an induced pumping force from contraction of skeletal muscles also influences blood pressure.
The heart and the vascular beds are a dynamic and connected part of the circulatory system and combine to effect efficient transportation of the blood. Circulation is influenced by the resistance of the vascular bed against which the heart is pumping. For the right heart this is the pulmonary vascular bed, creating pulmonary vascular resistance (PVR), while for the systemic circulation this is the systemic vascular bed, creating systemic vascular resistance (SVR). The vessels actively change diameter under the influence of physiology or therapy. Vasoconstrictors decrease vessel diameter and increase resistance, while vasodilators increase vessel diameter and decrease resistance. Put simply, increasing resistance (narrowing the vessel) decreases cardiac output (CO), and decreased resistance (widening the vessel) increases CO. Total peripheral resistance (TPR) is the sum of the resistance of all peripheral vasculature in the systemic circulation. Changes in pressure that occur in the aorta and large arteries are minimal. About 70 percent of pressure reductions in the vasculature occur in small arteries and arterioles. Thus, small arteries and arterioles are the main regulators of TPR. The significance of smooth muscles (Figure 1) in the control TPR is major. While contracting and relaxing, the smooth muscles that line the walls of vessels alter the radius therefore influencing flow of blood through them.
Blood viscosity, vessel length, and radius influence resistance. Increases in oxygen-carrying capacity by increased red blood cell number augments viscosity hence the benefit is offset by the increased resistance to flow. The danger of this phenomena is evident in athletes who transfuse excess RBCs, negatively effecting viscosity with fatal repercussions. The correct balance between enough red blood cells for oxygen carriage must be balanced against the negative effect of excess RBCs on the resistance to blood flow. Length of vessels does not change significantly, so it does not determine the resistance. Vessel radius is major factor in determining the changes in TPR. However, small changes in radius cause large changes in resistance because resistance is proportaional to r4.