Preload (cardiology)

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Heart during ventricular diastole. Heart diasystole.svg
Heart during ventricular diastole.

In cardiac physiology, preload is the amount of sarcomere stretch experienced by cardiac muscle cells, called cardiomyocytes, at the end of ventricular filling during diastole. [1] Preload is directly related to ventricular filling. As the relaxed ventricle fills during diastole, the walls are stretched and the length of sarcomeres increases. Sarcomere length can be approximated by the volume of the ventricle because each shape has a conserved surface-area-to-volume ratio. This is useful clinically because measuring the sarcomere length is destructive to heart tissue. It requires cutting out a piece of cardiac muscle to look at the sarcomeres under a microscope. It is currently not possible to directly measure preload in the beating heart of a living animal. Preload is estimated from end-diastolic ventricular pressure and is measured in millimeters of mercury (mmHg).

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Estimating preload

Though not exactly equivalent to the strict definition of preload, end-diastolic volume is better suited to the clinic. It is relatively straightforward to estimate the volume of a healthy, filled left ventricle by visualizing the 2D cross-section with cardiac ultrasound. [2] This technique is less helpful for estimating right ventricular preload because it is difficult to calculate the volume in an asymmetrical chamber. [2] In cases of rapid heart rate, it can be difficult to capture the moment of maximum fill at the end of diastole, which means the volume may be difficult to measure in children or during tachycardia. [2]

An alternative to estimating the end-diastolic volume of the heart is to measure the end-diastolic pressure. This is possible because pressure and volume are related to one another according to Boyle's law, which can be simplified to

The end diastolic pressure of the right ventricle can measured directly with a Swan-Ganz catheter. For the left ventricle, end diastolic pressure is most commonly estimated by taking the pulmonary wedge pressure, which is approximately equal to the pressure in the left atrium when the lungs are healthy. When the heart is healthy the diastolic pressure in the left atrium and left ventricle are equal. When both the heart and lungs are healthy, pulmonary wedge pressure is equal to left ventricle diastolic pressure and can be used as a surrogate for preload. [3] Pulmonary wedge pressure will overestimate left ventricle pressure in people with mitral valve stenosis, pulmonary hypertension and other heart and lung conditions. [4]

Estimation of preload may also be inaccurate in a chronically dilated ventricles because additional new sarcomeres cause the relaxed ventricle to appear enlarged.

Factors affecting preload

Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood.

Preload is related to the ventricular end-diastolic volume; a higher end-diastolic volume implies a higher preload. However, the relationship is not simple because of the restriction of the term preload to single myocytes. Preload can still be approximated by the inexpensive echocardiographic measurement end diastolic volume or EDV.

Preload increases with exercise (slightly), increasing blood volume (overtransfusion, polycythemia) and neuroendocrine excitement (sympathetic tone).

An arteriovenous fistula can increase preload. [5]

Preload is also affected by two main body "pumps":

See also

Related Research Articles

<span class="mw-page-title-main">Heart</span> Organ found inside most animals

The heart is a muscular organ in most animals. This organ pumps blood through the blood vessels of the circulatory system. The pumped blood carries oxygen and nutrients to the body, while carrying metabolic waste such as carbon dioxide to the lungs. In humans, the heart is approximately the size of a closed fist and is located between the lungs, in the middle compartment of the chest.

Systole Part of the cardiac cycle when a heart chamber contracts

Systole is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood. The term originates, via New Latin, from Ancient Greek συστολή (sustolē), from συστέλλειν, and is similar to the use of the English term to squeeze.

<span class="mw-page-title-main">Ventricle (heart)</span> Chamber of the heart

A ventricle is one of two large chambers toward the bottom of the heart that collect and expel blood towards the peripheral beds within the body and lungs. The blood pumped by a ventricle is supplied by an atrium, an adjacent chamber in the upper heart that is smaller than a ventricle. Interventricular means between the ventricles, while intraventricular means within one ventricle.

In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from the left ventricle per beat. Stroke volume is calculated using measurements of ventricle volumes from an echocardiogram and subtracting the volume of the blood in the ventricle at the end of a beat from the volume of blood just prior to the beat. The term stroke volume can apply to each of the two ventricles of the heart, although it usually refers to the left ventricle. The stroke volumes for each ventricle are generally equal, both being approximately 70 mL in a healthy 70-kg man.

An ejection fraction (EF) is the volumetric fraction of fluid ejected from a chamber with each contraction. It can refer to the cardiac atrium, ventricle, gall bladder, or leg veins, although if unspecified it usually refers to the left ventricle of the heart. EF is widely used as a measure of the pumping efficiency of the heart and is used to classify heart failure types. It is also used as an indicator of the severity of heart failure, although it has recognized limitations.

In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in the right or left ventricle at end of filling in diastole which is the amount of blood in the ventricles just before systole. Because greater EDVs cause greater distention of the ventricle, EDV is often used synonymously with preload, which refers to the length of the sarcomeres in cardiac muscle prior to contraction (systole). An increase in EDV increases the preload on the heart and, through the Frank-Starling mechanism of the heart, increases the amount of blood ejected from the ventricle during systole.

Frank–Starling law

The Frank–Starling law of the heart represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.

Afterload Pressure in the wall of the left ventricle during ejection

Afterload is the pressure that the heart must work against to eject blood during systole. Afterload is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively. Afterload changes to adapt to the continually changing demands on an animal's cardiovascular system. Afterload is proportional to mean systolic blood pressure and is measured in millimeters of mercury.

<span class="mw-page-title-main">Diastole</span> Part of the cardiac cycle

Diastole is the part of the cardiac cycle during which the heart refills with blood after emptying during systole (contraction). Ventricular diastole is the period during which the two ventricles are relaxing from the contortions/wringing of contraction, then dilating and filling; atrial diastole is the period during which the two atria likewise are relaxing under suction, dilating, and filling. The term originates from the Greek word διαστολή (diastolē), meaning "dilation", from διά + στέλλειν.

Mitral stenosis Heart disease with narrowing of valve

Mitral stenosis is a valvular heart disease characterized by the narrowing of the opening of the mitral valve of the heart. It is almost always caused by rheumatic valvular heart disease. Normally, the mitral valve is about 5 cm2 during diastole. Any decrease in area below 2 cm2 causes mitral stenosis. Early diagnosis of mitral stenosis in pregnancy is very important as the heart cannot tolerate increased cardiac output demand as in the case of exercise and pregnancy. Atrial fibrillation is a common complication of resulting left atrial enlargement, which can lead to systemic thromboembolic complications like stroke.

Jugular venous pressure

The jugular venous pressure is the indirectly observed pressure over the venous system via visualization of the internal jugular vein. It can be useful in the differentiation of different forms of heart and lung disease. Classically three upward deflections and two downward deflections have been described.

Atrium (heart) Upper chamber in the heart for blood to enter through

The atrium is one of two upper chambers in the heart that receives blood from the circulatory system. The blood in the atria is pumped into the heart ventricles through the atrioventricular valves.

Cardiac cycle Performance of the human heart

The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole, following a period of robust contraction and pumping of blood, called systole. After emptying, the heart immediately relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems. A normally performing heart must be fully expanded before it can efficiently pump again. Assuming a healthy heart and a typical rate of 70 to 75 beats per minute, each cardiac cycle, or heartbeat, takes about 0.8 seconds to complete the cycle. There are two atrial and two ventricle chambers of the heart; they are paired as the left heart and the right heart—that is, the left atrium with the left ventricle, the right atrium with the right ventricle—and they work in concert to repeat the cardiac cycle continuously,. At the start of the cycle, during ventricular diastole–early, the heart relaxes and expands while receiving blood into both ventricles through both atria; then, near the end of ventricular diastole–late, the two atria begin to contract, and each atrium pumps blood into the ventricle below it. During ventricular systole the ventricles are contracting and vigorously pulsing two separated blood supplies from the heart—one to the lungs and one to all other body organs and systems—while the two atria are relaxed. This precise coordination ensures that blood is efficiently collected and circulated throughout the body.

Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as pulsus paradoxus. Pulsus paradoxus is not related to pulse rate or heart rate, and it is not a paradoxical rise in systolic pressure. The normal variation of blood pressure during breathing/respiration is a decline in blood pressure during inhalation and an increase during exhalation. Pulsus paradoxus is a sign that is indicative of several conditions, including cardiac tamponade, chronic sleep apnea, croup, and obstructive lung disease.

Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.

The E/A ratio is a marker of the function of the left ventricle of the heart. It represents the ratio of peak velocity blood flow from left ventricular relaxation in early diastole to peak velocity flow in late diastole caused by atrial contraction. It is calculated using Doppler echocardiography, an ultrasound-based cardiac imaging modality. Abnormalities in the E/A ratio suggest that the left ventricle, which pumps blood into the systemic circulation, cannot fill with blood properly in the period between contractions. This phenomenon is referred to as diastolic dysfunction and can eventually lead to the symptoms of heart failure.

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

Heart failure with preserved ejection fraction Medical condition

Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; this may be measured by echocardiography or cardiac catheterization. Approximately half of people with heart failure have preserved ejection fraction, while the other half have a reduction in ejection fraction, called heart failure with reduced ejection fraction (HFrEF).

Pathophysiology of heart failure

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

  1. "CV Physiology: Preload". www.cvphysiology.com. Retrieved 2019-10-14.
  2. 1 2 3 Klugman, Darren; Berger, John T (August 2016). "Echocardiography & Focused Cardiac Ultrasound". Pediatric Critical Care Medicine. 17 (8 Suppl 1): S222–S224. doi:10.1097/PCC.0000000000000815. ISSN   1529-7535. PMC   4975424 . PMID   27490603.
  3. "Pulmonary Artery Wedge Pressure • LITFL • CCC Equipment". Life in the Fast Lane • LITFL • Medical Blog. 2019-01-04. Retrieved 2019-10-06.
  4. "CV Physiology | Pulmonary Capillary Wedge Pressure". www.cvphysiology.com. Retrieved 2019-10-06.
  5. "Pulmonary: Heart Failure". Archived from the original on 2009-02-01. Retrieved 2008-12-21.