Cardiac Output
Cardiac output is calculated as the sum of stroke volume and heart rate and expressed in liters per minute. The most typical definition of HR is how many times it beats in a minute. Systolic volume (SV) is the amount of blood expelled during each heartbeat or ventricular contraction. End-diastolic volume, also known as EDV, is the amount of blood that fills the heart at the end of diastole but cannot all be expelled during systole. Several things simultaneously impact heart rate (HR) and SV. Humans typically have a heart rate range of 5–6 L/min while at rest to over 35 L/min while exercising (Kelly et al., 2012). The other main predictor of cardiac output is SV, which is likewise influenced by some variables.
Preload, distensibility, and afterload affect how much blood is expelled during each beat. Preload is the collective term for the causes of passive muscle contractions in the muscles during rest. The volume of blood in the ventricles just before systole, or end-diastolic ventricular volume, determines preload. More significant end-diastolic blood flow volumes boost the heart’s ability to stretch its muscles passively. The Frank-Starling law of the heart, which is a result of this, causes the ventricles to contract more forcefully (Kelly et al., 2012). The strength of myocyte tension, also known as inotropy, is referred to as contractility.
The effect of cardiac output on blood pressure can be explained further using examples. The first instance is when the cardiac output is high, following increased heart contractility and the blood pressure gets elevated. This elevation is due to the direct proportionality between cardiac out and blood pressure. The second instance is in increased dromotrope, meaning the nervous conduction between the sinus node and atrioventricular node is increased.
Increased dromotrope results in raised cardiac output, which heightens blood pressure (Kelly et al., 2012). On the other hand, blood pressure can be reduced by reducing the cardiac out. For example, when the heart rate or stroke volume is reduced through activation of the parasympathetic nervous system, the cardiac output lowers, causing a decline in blood pressure. Additionally, if the rate of nervous conduction between the sinus node and atrioventricular node, which promotes heart contraction is reduced, is reduced, the cardiac output lowers, reducing the overall blood pressure.
Peripheral Vascular Resistance
Peripheral vascular resistance is a circulatory system resistance that affects the heart’s ability to pump blood and regulate blood pressure. SVR rises as a result of vasoconstriction, the tightening of blood vessels. Vasodilation causes blood vessels to widen, which lowers SVR. Pulmonary vascular resistance is the term used to describe resistance found inside the pulmonary vasculature (PVR). Vascular resistance decreases in situations like shock, which results in reduced organ perfusion and organ dysfunction (Kelly et al., 2012). Because metabolites locally mediate peripheral arterial resistance and regionally on a neuro-hormonal level, alterations in many different factors may affect peripheral vascular resistance.
At the level of the arterioles, the central control of the peripheral vascular resistance takes place. Distinct neural and hormonal cues cause the arterioles to dilate and contract. Norepinephrine hormone attaches to the smooth muscle cells of the vascular via binding to an alpha-1 receptor, Gq protein, during an adrenergic response. This leads to a rise in GTP in the cell, which stimulates phospholipase C and produces IP3 (Kelly et al., 2012). The discharge of the calcium that has been held intracellularly as free calcium is signaled by IP3.
Similar to cardiac output, the effect of peripheral resistance can be explained using examples. In the first instance, metabolites such as carbon dioxide accumulate in tissues, especially after strenuous exercises. These metabolites cause arterials to vasodilate to promote their removal from the tissue, thereby reducing blood pressure. Conversely, a lack of metabolites or other vasodilating factors causes the arterial walls to contract, reducing the diameter of the lumen, which increases peripheral resistance and thus raises blood pressure (Kelly et al., 2012). Vasoconstriction increases peripheral resistance while vasodilation reduces it, which in turn raises and lowers blood pressure respectively.
Reference
Kelly A. Y., James A. W., & Peter D. (2012). Anatomy and physiology (1st ed.). OpenStax.