Cardiac output measures how effectively the heart functions as a pump, representing the total volume of blood ejected into the circulatory system each minute. This continuous flow is essential for delivering oxygen and nutrients to cells and tissues, and for removing metabolic waste products.
The Core Components of Cardiac Output
Cardiac output (CO) is determined by two main physiological measures: heart rate (HR) and stroke volume (SV). Heart rate is the number of times the heart beats per minute. Stroke volume is the amount of blood pumped out of one ventricle with each beat.
These two components are directly related through the formula: Cardiac Output = Heart Rate × Stroke Volume (CO = HR × SV). For instance, a typical resting cardiac output is around 5 liters per minute, resulting from a heart rate of 70 beats per minute and a stroke volume of 70 milliliters per beat. Any change in either heart rate or stroke volume directly alters cardiac output.
Factors Determining Heart Rate
Heart rate is primarily influenced by the autonomic nervous system. The sympathetic nervous system, associated with “fight or flight” responses, increases heart rate by releasing norepinephrine, quickening the sinoatrial node. Conversely, the parasympathetic nervous system, promoting “rest and digest” functions, decreases heart rate through acetylcholine release. These opposing influences allow for precise adjustments to the heart’s rhythm.
Hormonal influences also regulate heart rate. Epinephrine, released from the adrenal glands, mimics sympathetic stimulation, leading to an increased heart rate. Thyroid hormones can also impact heart rate by influencing the heart’s sensitivity to sympathetic signals.
Beyond nervous and hormonal controls, intrinsic factors affect heart rate. Body temperature, for example, can cause heart rate to rise with fever or intense exercise. Age also influences resting heart rate, which tends to be higher in infants and gradually declines. Physical fitness levels significantly impact heart rate; trained athletes often have lower resting rates due to improved heart efficiency.
Factors Determining Stroke Volume
Stroke volume, the amount of blood ejected by the heart with each beat, is influenced by three primary factors: preload, afterload, and contractility. These factors determine how much blood the heart effectively pumps to the body.
Preload refers to the stretch of heart muscle cells at the end of diastole, just before contraction. It is the volume of blood filling the ventricles. Factors increasing blood return to the heart, such as increased central venous pressure or overall blood volume, will increase preload. According to the Frank-Starling law, increased preload generally leads to a stronger contraction and greater stroke volume, as muscle fibers are stretched to an optimal length for contraction.
Afterload is the resistance the heart must overcome to eject blood into the arteries. This resistance is primarily determined by systemic vascular resistance and arterial blood pressure. When afterload is high, such as in high blood pressure, the heart works harder to push blood out, which can decrease stroke volume. Conversely, lower afterload makes it easier for the heart to eject blood, leading to increased stroke volume.
Contractility is the intrinsic ability of the heart muscle to contract and pump blood, independent of changes in preload or afterload. This force is largely influenced by the availability of calcium ions within heart muscle cells. Signals from the nervous system and certain hormones can increase contractility, leading to a more forceful ejection of blood and a greater stroke volume. For example, increased sympathetic stimulation also enhances contractility.
How the Body Regulates Cardiac Output
The body regulates cardiac output to meet varying physiological demands. These regulatory systems dynamically adjust both heart rate and stroke volume. During physical activity, for instance, the body requires more oxygen, leading to a substantial increase in cardiac output.
Baroreceptors, specialized stretch receptors in major arteries like the aorta and carotid arteries, constantly monitor blood pressure. If blood pressure drops, these receptors signal the brain, activating the sympathetic nervous system to increase heart rate and contractility, raising cardiac output. If blood pressure rises, the parasympathetic nervous system is stimulated to lower heart rate.
Chemoreceptors, found in the aorta and carotid arteries, detect changes in blood oxygen, carbon dioxide, and pH levels. A decrease in oxygen or an increase in carbon dioxide triggers responses that increase heart rate and breathing, aiming to improve oxygen delivery and carbon dioxide removal. The central nervous system integrates these sensory inputs, coordinating responses to maintain stable cardiac output.
Hormonal regulation also contributes to cardiac output control by influencing blood volume and vascular tone, indirectly affecting preload and afterload. The renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone (ADH) are important. RAAS increases blood volume and causes vasoconstriction, increasing preload and afterload. ADH promotes water reabsorption in the kidneys, increasing blood volume and preload. These controls allow the cardiovascular system to adapt to conditions from rest to intense exercise, maintaining adequate blood flow.