Cardiac output

Introduction Cardiac output (CO) is the mechanism by which blood circulates throughout the body, particularly to the brain and other vital organs. It is the amount of blood pumped by the heart every minute. Modulating both the heart rate (HR) and the stroke volume (SV) alters both the cardiac output and the body's demand for oxygen, such as when exercising. Because every tissue in the body depends on the heart pumping blood for nourishment, any cardiovascular dysfunction has the potential to result in significant morbidity and mortality. As a result, the regulation of cardiac output is subject to a complex mechanism that involves the autonomic nervous system, endocrine, and paracrine signaling pathways. Heart disease is the leading cause of death in the United States and affects nearly 30 million people each year. There are a number of ways to determine the degree of functional impairment, which informs diagnosis, prognosis, and treatment. A clinician should be familiar with the fundamentals of cardiac function because they will encounter heart disease in their work.

For the delivery of nutrients and the removal of waste products, cellularly active metabolizing tissue requires a constant supply of blood. Biochemical processes can proceed at their optimal speeds when the blood supply to the tissue is synchronized with oxygen consumption. When there isn't enough blood flowing, vital reactions slow down or stop completely. More specifically, cells undergo a switch to anaerobic metabolic pathways as a result of subprime perfusion, which results in the production of lactic acid and other bioactive compounds. Reduced pH in the cell, enzyme denaturation, and altered membrane potentials are all effects of toxic metabolite accumulation. If they are not corrected, these changes have negative effects on cells, tissues, organs, and eventually the entire planet.

Organ Systems Involved Both the circulatory system—arteries and veins—and the heart are involved in cardiac output. CO is the sum of the stroke volume (SV) and the heart rate (HR), which is the volume of blood ejected with each beat. Thus, CO can be changed directly by the heart. However, the volume of blood that is able to leave the heart (SV) is directly affected by arterial compliance, vasoconstriction, and arterial pressure (afterload), which in turn affects CO. Last but not least, CO is dependent on the volume of blood entering the heart from the veins, or venous return VR, due to the closed-loop nature of the circulatory system. The central venous pressure, which is influenced by venoconstriction, also affects the venous return. It is important to keep in mind that the capacitance vessels store approximately 60% of the blood and can alter the volume of blood returned to the heart.

Function The heart pumps a precise amount of blood in response to the world's metabolic requirements. Changes in total body oxygen requirements are directly correlated with changes in cardiac output from baseline. In order to ensure sufficient tissue perfusion, cardiac output will rise during physiologic stress. This idea is shown by Fick's principle, which can be used to calculate cardiac output based on the exchange of oxygen through a capillary bed. Forming an equation: CO = VO2/(a – v O2 difference), where a-V O2 is the difference in oxygen content between arterial and venous blood and VO2 is the oxygen used by tissue. Another way to measure CO is represented by this Fick's principle.

The thermodilution method, which uses the change in blood temperature between a catheter port and a thermistor, is another way to measure CO function. The proximal (injection) port of a thermodilution catheter is typically located in the right atrium or superior or inferior vena cava, while the thermistor is typically located in the pulmonary arteries.

Mean arterial pressure (MAP) and total peripheral resistance (TPR), also known as systemic vascular resistance, alter CO dynamically. CO = MAP/TPR can be used to represent this.

Mechanism Heart rate (HR) and stroke volume (SV) are combined to produce cardiac output, which is measured in liters per minute. The most common definition of HR is the number of heart beats per minute. The volume of blood released during each heartbeat or ventricular contraction is known as SV. The end-diastolic volume, or EDV, of the blood that fills the heart at the end of diastole cannot all be ejected from the heart during systole. Thus, the end-systolic volume (ESV) is the heart's remaining volume at systole's end. As a result, the EDV-ESV ratio determines whether the stroke volume matches the end-diastolic volume. Multiple factors simultaneously affect HR and VS. At rest, human cardiac output typically ranges from 5-6 L/min to more than 35 L/min for elite athletes during exercise.

 

The sinoatrial node, which naturally depolarizes 60 to 100 times per minute, sends signals that are used to calculate HR. Several factors also have an impact on SV, which is the other major factor that affects cardiac output. The preload, contractility, and afterload all have an impact on the amount of blood ejected each beat. All of the factors that contribute to passive muscle tension in the muscles at rest are represented by preload.

The amount of blood in the ventricles immediately prior to systole, or the end-diastolic ventricular volume, is inversely proportional to preload. The passive stretching of the heart muscles increases when end-diastolic blood volumes return to the heart. The Frank-Starling law of the heart is the result of this, which causes the ventricles to contract with greater force.

 The force of myocyte contraction, also known as inotropy, is referred to as contractility. The heart is able to pump more blood out of the body as the force of contraction increases, resulting in a larger stroke volume. Afterload is the final factor that determines stroke volume. All of the factors that affect total tension during isotonic contraction are represented by afterload.

 As a result, the amount of systemic resistance that the ventricles must overcome in order to eject blood into the vasculature can be related to afterload. Contrary to preload and contractility, afterload is inversely correlated with stroke volume and is proportional to systemic blood pressures.

 Increasing sympathetic tone, increasing catecholamine secretion, and increasing thyroid hormone circulation are all signaling strategies that have the potential to boost cardiac output. Chronotropy (timing), dromotropy (conduction speed), and lusitropy (myocardial relaxation rate) are positive effects of these mechanisms that boost HR. By increasing venous return through receptor-mediated vasoconstriction, these influences also increase preload. The Frank-Starling mechanism and direct catecholamine stimulation both have an impact on contractility. When there is less need for oxygen, the parasympathetic tone gets stronger, which has the opposite effect on HR and SV.