# Heart rate and stroke volume relationship in chemical equations

### Cardiac output - Wikipedia

The amount of blood circulated throughout your body is based on two measurable components -- stroke volume and heart rate. The amount of each that your. Or use this formula triangle to help: Formula triangle of cardiac output, stroke volume and heart rate. Cover up what you want to find with your finger and write. Define cardiac output and explain how heart rate and stroke volume effect it; Describe the It can be represented mathematically by the following equation: . NE binds to the beta-1 receptors and opens chemical- or ligand-gated sodium and.

Stroke Volume Stroke volume is defined as the amount of blood pumped in one beat. Generally, stoke volume is an estimated measurement. Actual measurements are performed on heart patients by measuring arterial pressure. Estimated average stroke volume amounts range between 50 to 70ml at rest to to ml during cardio training. Elite athletes have estimated stroke volumes between 90 to ml at rest to to ml during cardio training. Cardiac Output Cardiac output is defined as the total amount of blood circulated throughout your body in one minute.

Cardiac output is measured by multiplying heart rate by stroke volume. Healthy individuals with higher cardiovascular fitness levels have lower heart rates, allowing a longer time for the heart to fill with blood. HR gradually decreases until young adulthood and then gradually increases again with age.

Maximum HRs are normally in the range of — bpm, although there are some extreme cases in which they may reach higher levels.

As one ages, the ability to generate maximum rates decreases. So a year-old individual would be expected to hit a maximum rate of approximatelyand a year-old person would achieve a HR of Bradycardia is the condition in which resting rate drops below 60 bpm, and tachycardia is the condition in which the resting rate is above bpm.

Trained athletes typically have very low HRs. If the patient is not exhibiting other symptoms, such as weakness, fatigue, dizziness, fainting, chest discomfort, palpitations, or respiratory distress, bradycardia is not considered clinically significant.

However, if any of these symptoms are present, they may indicate that the heart is not providing sufficient oxygenated blood to the tissues.

The term relative bradycardia may be used with a patient who has a HR in the normal range but is still suffering from these symptoms. Most patients remain asymptomatic as long as the HR remains above 50 bpm. Bradycardia may be caused by either intrinsic factors or causes external to the heart. While the condition may be inherited, typically it is acquired in older individuals. Intrinsic causes include abnormalities in either the SA or AV node.

### Cardiac Equations

If the condition is serious, a pacemaker may be required. Other causes include ischemia to the heart muscle or diseases of the heart vessels or valves. External causes include metabolic disorders, pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest.

Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen. Tachycardia is not normal in a resting patient but may be detected in pregnant women or individuals experiencing extreme stress.

In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the endocrine or autonomic nervous system. In some cases, tachycardia may involve only the atria. Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpations, chest pain, or fainting syncope.

While tachycardia is defined as a HR above bpm, there is considerable variation among people. Further, the normal resting HRs of children are often above bpm, but this is not considered to be tachycardia Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation.

Elevated rates in an exercising or resting patient are normal and expected. Resting rate should always be taken after recovery from exercise.

Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery. During exercise, the rate of blood returning to the heart increases. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood.

Even though there is less filling time, SV will initially remain high.

### Cardiovascular physiology – Knowledge for medical students and physicians

However, as HR continues to increase, SV gradually decreases due to decreased filling time. CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV.

Consider this phenomenon in a healthy young individual. Initially, as HR increases from resting to approximately bpm, CO will rise. As HR increases from to bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV. So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between and bpm, so CO is maintained.

It is also important to note that the coronary circulation nourishes the heart during diastole so as the HR increases the ability of the coronary circulation to nourish the myocardium decreases. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age. Cardiovascular Centers Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata Figure The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X.

Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart.

## Resting Cardiac Output

The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia the cervical ganglia plus superior thoracic ganglia T1—T4 to both the SA and AV nodes to increase heart rate, plus additional fibers to the atrial and ventricular myocardium to increase force of contraction see section on Contractility.

The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. In both skeletal and cardiac muscles, vasodilation is mediated by local metabolic factors, and in the skin, it is achieved mainly by a decrease in the firing of sympathetic neurons supplying skin vessels.

Cardiac Output and Stroke Volume Equations

Simultaneously with vasodilation in these three regions, a vasoconstriction occurs in the kidneys and gastrointestinal organs, due to an increase in activity of sympathetic neurons supplying them.

Distribution of the systemic cardiac output at rest and during strenuous exercise Vasodilation of arterioles in the skeletal and heart muscles and skin causes a decrease in total peripheral resistance to blood flow.

## Cellular respiration and transport

This decrease is partially offset by vasoconstriction of arterioles in other organs. But the vasodilation in muscle arterioles is not compensated, and the net result is a marked decrease in total peripheral resistance to blood flow. During exercise, the cardiac output increases more than the total resistance decreases, so the mean arterial pressure usually increases by a small amount. Pulse pressure, in contrast, markedly increases because of an increase in both stroke volume and the speed at which the stroke volume is ejected.

The cardiac output increase is due to a large increase in heart rate and a small increase in stroke volume. The heart rate increases because of a decrease in parasympathetic activity of SA node combined with increased sympathetic activity.