Cardiac Output

Introduction

Cardiac output is the amount of blood pumped through the circulatory system by the heart in one minute. Cardiac output can be determined by the stroke volume and heart rate. The stroke volume is referred to as the amount of blood pumped out by the left ventricle of the heart during a single contraction.

The cardiac output of a healthy adult is 4.7 litres (5 quarts) per minute. A variety of factors have a direct impact on cardiac output. The degree of an individual’s metabolism, whether at rest or exercising, their age, and size are all considerable factors. Let us discuss cardiac output in detail.

Cardiac output definition 

The cardiac output definition states that it is the amount of blood pumped into the aorta by the heart per minute and it can be matched by the body’s complete metabolic need that a healthy person requires. As a result, a complicated mechanism combining the autonomic nervous system, endocrine and paracrine signalling pathways regulates cardiac output.        

As the heart pumps blood to nourish every tissue in the body, any cardiovascular malfunction can cause considerable morbidity and mortality. Every year, almost 30 million Americans are affected by heart disease, which is the leading cause of mortality in the country. A variety of methods can be used to determine the degree of functional impairment, which can help with diagnosis, prognosis and treatment.

Involved organ systems

Cardiac output (CO) is influenced by the heart and the circulatory system, including veins and arteries. CO is calculated by multiplying the heart rate (HR) by the stroke volume (SV), which is the amount of blood expelled by the heart with each beat. As a result, the heart has direct control over CO. However, arterial compliance, vasoconstriction, and arterial pressure (afterload) all have a direct impact on the amount of blood that may leave the heart (SV), and hence on CO. 

Finally, CO is determined by the volume of blood entering the heart from the veins, or venous return (VR), because the circulatory system is closed. Venous return is also influenced by central venous pressure, which is affected by vasoconstriction. It is important to remember that the capacitance vessels hold around 60% of the blood and can affect the volume of blood returning to the heart.

Function

The amount of blood pumped by the heart is proportional to global metabolic requirements. Compared to baseline, cardiac output changes are proportional to changes in total body oxygen requirements. 

The cardiac output will rise during periods of physiologic stress to provide appropriate tissue perfusion. This idea is illustrated by Fick’s concept, which may be used to compute cardiac output via oxygen exchange through a capillary bed.

Mechanism

The heart rate (HR) and stroke volume (SV) is cardiac output, measured in litres per minute. The number of heartbeats in one minute is the most popular definition of HR. The volume of blood evacuated during ventricular contraction, or each cardiac stroke, is called SV. 

During systole, not all of the blood that fills the heart at the conclusion of diastole (end-diastolic volume or EDV) can be evacuated. As a result, the end-systolic volume remains in the heart after systole has ended (ESV). Therefore, the stroke volume is equal to the EDV- ESV, not the end-diastolic volume. Several factors influence HR and VS at the same time. Cardiac output in humans ranges from 5-6 L/min at rest to more than 35 L/min during exercise in elite athletes.

Measurement of cardiac output

The product of stroke volume and heart rate is called the cardiac output. Changes in one or both of these parameters can impact cardiac output (unless the disease affects both in opposite directions and to equal degrees). Depending on the patient, lower heart rates might either increase or impair cardiac output. 

Due to the higher filling during diastole, patients with rigid, noncompliant ventricles or tachyarrhythmias may benefit from a lower heart rate. A patient with severe atrioventricular node disease, on the other hand, can have a lower cardiac output due to a low (ventricular) heart rate. 

Heart rate and stroke volume have a complicated relationship. Moderate increases in heart rate can enhance stroke volume due to the “staircase effect,” whereas higher heart rates can limit stroke volume due to diastolic filling impairment.

In clinical patients, cardiac output can be measured using a variety of techniques, but it is rarely measured in veterinary medicine. The concept of cardiac output should be at the forefront of one’s monitoring and therapeutic concerns; after all, it’s all about maintaining adequate cardiovascular function. 

Poor cardiac output is suspected when preload parameters (CVP or PVP, pulmonary artery occlusion pressure, jugular vein distention, postcaval distention on chest radiograph, and large end-diastolic diameter on cardiac ultrasound image) are elevated and forward flow parameters (pulse quality, arterial blood pressure, signs of vasoconstriction, urine output, and physical and laboratory measures of tissue perfusion) are abnormal. Even when arterial blood pressure is normal, cardiac output is a flow metric that might be below.

Monitoring of patients

Clinical, hematologic, cardiac, radiological, and hemodynamic factors must be closely monitored in cardiac patients. Body temperature, respiration rate and depth (in hospital and at home), breath sounds, heart rate, heart rhythm, mucous membrane colour and refill time, pulse strength, attitude, and noninvasively detected arterial blood pressure should all be tabulated and established as a trend. 

The clinician can get helpful information on fluid dynamics and the requirement for fluid treatment by measuring simple variables like water and food intake, estimated urine output, body weight, and diuretic dosage on a regular basis. In resting dogs, home respiratory rates of 35 to 40 correspond well with radiographic indications of pulmonary edema. 

Fluid, diuretic, and cardiac therapy can be monitored by measuring serum creatinine, Blood urea nitrogen (BUN), salt, and potassium values on a regular basis. Physical and radiological indicators of fluid accumulation in hospitalised patients may signal the need to lower fluid volume, increase the diuretic dosage, or seek further treatments.

In patients with heart failure, the effect of fluid therapy on central venous pressure (CVP) and pulmonary venous pressure(PVP) is a critical concern, and it can influence the rate of fluid administration. Inadequate venous pressure lowers cardiac output, while excessive pressure increases edema development. Although an ideal venous pressure is required to maintain cardiac output in heart failure, pulmonary venous pressure greater than 20 mm Hg and CVP larger than 10 to 12 cm H2O have been linked to edema formation.

Conclusion

Cardiac output can be raised through a variety of signalling mechanisms, including sympathetic tone enhancement, catecholamine production, and thyroid hormone circulation. These processes raise HR by having a beneficial influence on chronotropic (timing), dromotropy (conduction speed), and lusitropy (conduction speed) (myocardial relaxation rate). 

Preload is also raised by receptor-mediated vasoconstriction, which increases venous return. Additionally, the Frank-Starling mechanism and direct catecholamine stimulation enhance contractility. When the parasympathetic tone is raised in response to lower oxygen demand, the opposite effects on HR and SV occur.