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). The cardiac output is simply the amount of blood pumped by the heart per minute . Necessarily, the cardiac output is the product of the heart rate, which is the. Pulse pressure: Difference between diastolic blood pressure (DP) Mean arterial pressure (MAP) = 1⁄3 systolic blood pressure + ⅔ diastolic blood pressure = (SP + 2 x DP) / 3 .. Length-tension relationship: larger volumes of blood in the .. thousands of USMLE-formatted multiple choice questions in the.
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. 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.
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. 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. During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately bpm.
At the nodes sympathetic stimulation causes the release of the neurotransmitter norepinephrine NE at the neuromuscular junction of the cardiac nerves. NE binds to the beta-1 receptors and opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions.
NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR. Some cardiac medications for example, beta blockers work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension. Overprescription of these drugs may lead to bradycardia and even stoppage of the heart.
Cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in the medulla oblongata of the brain. They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus parasympathetic nerves that slow cardiac activity. Draw in and label the SA and AV nodes, add labels to the cardioaccelerator and cardioinhibitory centers.
Suggest this figure comes after the first paragraph. Parasympathetic stimulation originates from the cardioinhibitory region with impulses traveling via the vagus nerve cranial nerve X. Parasympathetic stimulation releases the neurotransmitter acetylcholine ACh at the neuromuscular junction.
ACh slows HR by opening chemical- or ligand-gated potassium ion channels to slow the rate of spontaneous depolarization and increase the time before the next spontaneous depolarization occurs. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR.
This is similar to an individual driving a car with one foot on the brake pedal.
Cardiovascular physiology – Knowledge for medical students and physicians
In the case of the heart, decreasing parasympathetic stimulation decreases the release of ACh, which allows HR to increase up to approximately bpm. Any increases beyond this rate would require sympathetic stimulation. The wave of depolarization in a normal sinus rhythm shows a stable resting HR. Following parasympathetic stimulation, HR slows. Following sympathetic stimulation, HR increases. Input to the Cardiovascular Centers The cardiovascular center receive input from the limbic system as well as a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus.
Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors. Collectively, these inputs normally enable the cardiovascular centers to regulate heart function precisely, a process known as cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. Any such increase in physical activity would logically warrant increased blood flow.
Regulation of the Stroke Volume Sympathetic Effect Autonomic nerves not only innervate the SA node, but also are found elsewhere in the heart. This tends to be significant mainly at the greatest levels of exercise. For example, the ventricle of a 70 kg person at rest might hold about ml of blood at the end of diastole.
As noted above, a typical stroke volume is about 70 ml. This is the fraction of the blood in the ventricle that is ejected during systole. 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.
Cardiac Physiology | Anatomy & Physiology
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?
Regulation of Cardiac Output
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.
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.