# Heart rate and cardiac output relationship questions

Cardiac output is the total volume of blood pumped by the heart per minute. It is the product of blood pumped by each heartbeat (stroke Volume)and the number of beats (heart rate). Undo. Related Questions (More Answers Below). Related Questions (More Answers Below). What are the differences Views · What is the relation between cardiac output and blood pressure? 2, Views. Calculate cardiac output, given stroke volume and heart rate. Explain the relationship between changes in HR and changes in filling time and EDV. . EF = SV/EDV x %, fill in the following table and answer the questions below it.

Clinically, this is observed as angina. Function The amount of blood pumped by the heart is closely matched to global metabolic needs. HR is most commonly defined as the number of times the heart beats in one minute. SV is the amount of blood ejected during ventricular contraction. Each component is the composite of a variety of factors that can be modulated based on need.

Values of cardiac output in humans are dependent on body size and activity level. HR is determined by the speed of signal propagation through the electrical conducting system. Signals begin in the sinoatrial node which fires at an intrinsic rate of 60 to times each minute following unique alterations in ion conductance across the cell membrane. Chronotropy describes the rate of spontaneous discharge and can be altered by a variety of influences. Once at threshold, an action potential AP is generated and is conducted through the atria to the atrioventricular AV node.

Propagation of the signal through the AV node is relatively slow and represents another locus of control, termed dromotropy. From here, the AP is passed to the bundle of His and then the right and left bundle branches. Next, the signal reaches the Purkinje fibers and eventually arrives at the ventricular myocytes, producing a contraction. Lastly, the pathway returns to its resting state before the next impulse arrives.

The final relaxation and repolarization of electrical conducting cells and myocytes are called lusitropy. SV, the other major determinant of cardiac output, can also be manipulated when required.

The amount of blood ejected each beat depends on preload, contractility, and afterload. Preload is synonymous with end-diastolic ventricular volume, or the amount of blood in the ventricles immediately before systole.

Higher preload volumes mean the ventricles must eject more blood. Contractility describes the force of myocyte contraction, also referred to as inotropy.

As the force of contraction increases so does the stroke volume. The final determinant of stroke volume is afterload. Afterload is the amount of systemic resistance the ventricles must overcome to eject blood into the vasculature. Afterload is proportionate to systemic blood pressures and is inversely related to stroke volume, unlike preload and contractility.

Cardiac output can be increased by a variety of signaling methods including enhancement of sympathetic tone, catecholamine secretion, and circulation of thyroid hormone. These mechanisms increase HR by exerting positive effects at chronotropic, dromotropic, and lusitropic control points.

These influences also increase preload through receptor-mediated vasoconstriction. Additionally, contractility is improved through the Frank-Starling mechanism and also by direct catecholamine stimulation. The opposite effects on HR and SV occur when the parasympathetic tone is strengthened in response to decreased oxygen requirements. Pathophysiology Impairment of cardiac function can arise through a variety of pathophysiologic mechanisms.

Common etiologies include hypertension, coronary disease, congenital problems, myocardial ischemia and infarction, congestive heart failure, shock, arrhythmias, genetic diseases, structural abnormalities, pericardial effusions, emboli, tamponade, and many others. It may take decades for a chronic problem like hypertension or coronary atherosclerosis to cause noticeable symptoms.

Clinical Significance Diseases of the heart are the number one cause of death in the United States, killing more thanpeople annually and accounting for one out of every four American deaths.

Cardiac deterioration occurs in both acute and chronic fashion. Major modifiable risk factors attributed to the development of chronic cardiac pathology include body weight, tobacco use, serum glucose and lipid levels, and blood pressure.

Secondary prevention of chronic disease focuses on correcting deviations from these goals.

Tools include aids for smoking cessation, hypoglycemic agents, antihypertensives, lipid-altering therapies, weight loss, and dietary modification. Once the decline in cardiac function becomes evident, assessment by echocardiogram is warranted. Interventions for each diagnosis is variable and complex, but the goal for each is to preserve function, minimize symptoms, and prevent disease progression. Acute failure of the heart to perfuse tissue is called shock.

Three primary categories exist based on origin: Cardiogenic shock denotes the heart as the reason for poor blood supply. Most often, it arises secondary to an underlying chronic disease.

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Norepinephrine, by increasing the force of contraction, would tend to increase the ejection fraction and thus the stroke volume. Afterload The aortic pressure influences the stroke volume for a straightforward reason.

If the aortic pressure increases, this pressure reduces the volume of blood that flows into the aorta during systole. The aortic pressure is called afterload because it is the "load" experienced by the ventricle after it begins contracting. A drug might reduce the afterload, for example, by dilating arterioles. This allows blood to flow from the arteries more easily, thereby preventing the arterial pressure from increasing as blood is injected into it by the ventricle.

Frank-Starling Mechanism However, the factor we will be most concerned with is the Frank-Starling mechanism. Unfortunately, it is also the one most difficult to get your mind around. The Frank-Starling mechanism leads to changes in the stroke volume as a result of changes in the end-diastolic volume.

The end-diastolic volume is the volume of a ventricle at the very end of filling and just before systole begins. This can change because the ventricles are flexible and under different circumstances, the amount of blood flowing in during diastole varies.

If less blood flows into the ventricle as it fills, the end-diastolic volume goes down. If more blood flows in, the end-diastolic volume goes up. The Frank-Starling effect is due to the fact that heart muscle fibers respond to stretch by contracting more forcefully. This is not a passive, elastic effect, but rather due to an increased expenditure of ATP energy. We are not going to try to explain the cellular basis of this effect. It is not as straightforward as you might think.

Thus, if the end-diastolic volume increases, the muscle fibers are lengthened and the ventricle contracts more forcefully, ejecting a greater stroke volume.

The figure to the right shows this Frank-Starling effect. What factor alters the filling during diastole? For the right ventricle, this is the pressure in the right atrium, because this is the pressure that is experienced by the right ventricle as it fills. Since there is no valve at the entrance to the right atrium, the pressure in the right atrium is necessarily the same as the pressure in the veins at the entrance to the right atrium.

This pressure in the large veins at the entrance to the right atrium is called the central venous pressure.

### Physiology, Cardiac Output - StatPearls - NCBI Bookshelf

In other words, the central venous pressure is the same at the right atrial pressure, and this is the pressure that determines the filling of the right ventricle and thus its end-diastolic volume. The central venous pressure always is only a few mm Hg, but nonetheless it does change enough to significantly affect the stroke volume.

In particular, posture changes this pressure and that is the factor with which we are here most concerned. The Effect of Posture on Stroke Volume Recall how voluminous and thin-walled the superior and inferior vena cava are.

You probably were able to put two fingers into the superior vena cava of the pig heart. When a person is lying down, the large veins in the chest are plump with blood. And because these veins are stretched, the pressure in them is higher than when they contain less blood. Consequently, when lying down, the central venous pressure is relatively high, the end-diastolic volume is relatively high and thus the stroke volume is comparatively high.

But this changes when we stand. The pressure in the large veins in the legs increases greatly. For example, one meter below the heart, the effect of gravity adds about 74 mm Hg of pressure. This causes the distensible, voluminous veins to expand, and blood pools in the leg veins. This reduces the blood in the central veins, and the central venous pressure drops. Because these central veins are very compliant structures, pressure cannot increase again in them until blood flows back into the thorax.

The Effect of Muscle Contraction on Stroke Volume Lying down, of course, is one factor that would increase the amount of blood in the veins in the thorax and thus the central venous pressure.