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What's the reason for isovolumic contraction and isovolumic relaxation?

What's the reason for isovolumic contraction and isovolumic relaxation?


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During cardiac cycle, there are two periods in which the heart volume doesn't change, but there is a change in tension/pressure. It takes about 0.25-0.35 second to achieve this change.

I searched in Google and Wikipedia, but could not find the reason, so I decided to ask this question.


To put it in very simple words the reason for isovolumetric contaction and relaxation is to make the necessary pressure changes that is necessary to allow blood to flow into or flow out of the ventricles.

The basic formula you need to remember to understand this is:-

  • Fluids flow from high pressure area to low pressure area along the pressure gradient (Eg: Injecting a drug into blood stream - as the pressure in the syringe is higher than the pressure in blood vessel, the drug flows into the blood vessel)
  • Pressure is inversely proportional to volume (when temperature is constant) - this is Boyle's law. In a container with a fixed amount of fluid an increase in the volume of container will cause a proportionate amount of fall in the pressure in the container and vice-versa

Isovolumetric contraction:

The end-diastolic pressure in the aorta is in the range of approximately 90-100 mm of Hg. For blood to flow from left ventricle to aorta, the pressure in the left ventricle should exceed the pressure in the aorta.

As long as the pressure in the left ventricle is lesser than the pressure in the left atrium, the blood flows from Left Atrium to Left Ventricle. When Left Ventricle starts contracting the pressure in the LV rapidly overcomes the pressure in left atrium leading to closure of the mitral valve.

Now the pressure in the LV is greater than the pressure in the LA. So no blood flows in. At the same time the pressure in the LV is not sufficient to overcome the pressure in the aorta. So the semilunar valve remains closed. The ventricle continues contracting causing a time period in which there is increase in pressure without volume change as both inlet and outlet are closed. This period is called period of isovolumic contraction.

The isovolumic contraction ends when the pressure in the left ventricle becomes higher than the pressure in the aorta, which will cause the semilunar valves to open and blood to flow from left ventricle to aorta.

Isovolumic Relaxation:

The reverse happens in isovolumic relaxation.

As the blood volume in the ventricle decreases and the left ventricle starts relaxing the pressure in the left ventricle falls. When the pressure gets below that of the aorta, the semilunar valve closes. But the pressure in the ventricle is still higher than the pressure in the left atrium. So the mitral valve remains closed. So here too both the inlet and outlet are closed but as the ventricle is relaxing the pressure keeps falling. So till the pressure in the left ventricle falls below that of the left atrium, there is a time period volume is constant and the pressure keeps falling - this is called Isovolumic Relaxation.

This period is followed by opening of the mitral valve (as the pressure in the LV falls below that of the LA) and blood flows into the ventricle.

Take a look at the phonocardiogram linked in Majid's answer. It will help you understand what I explained.

Hope this explains your question


You might have heard that a fluid is incompressible. That means that even if you push very very hard it will be impossible to contract a 1 L bottle to a half liter bottle. If you imagine somebody squeezing your hand, you will feel a big increase in pressure, but your hand will practically not decrease in volume. It is the same that happens for the blood.


Wiggers diagram

A Wiggers diagram, named after its developer, Carl Wiggers, is a standard diagram that is used in teaching cardiac physiology. [1] In the Wiggers diagram, the X-axis is used to plot time, while the Y-axis contains all of the following on a single grid: [ citation needed ]

The Wiggers diagram clearly illustrates the coordinated variation of these values as the heart beats, assisting one in understanding the entire cardiac cycle. [ citation needed ]


What's the reason for isovolumic contraction and isovolumic relaxation? - Biology

The atrioventricular (AV) valves close at the beginning of this phase.

Electrically, ventricular systole is defined as the interval between the QRS complex and the end of the T wave (the Q-T interval).

Mechanically, the isovolumic phase of ventricular systole is defined as the interval between the closing of the AV valves and the opening of the semilunar valves (aortic and pulmonary valves).

Pressures & Volume:

The AV valves close when the pressure in the ventricles (red) exceeds the pressure in the atria (yellow). As the ventricles contract isovolumetrically -- their volume does not change (white) -- the pressure inside increases, approaching the pressure in the aorta and pulmonary arteries (green).

The electrical impulse propagates from the AV node through the His bundle and Purkinje system to allow the ventricles to contract from the apex of the heart towards the base.


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Systole is the period when the heart chambers contract that causes the ejection of blood into the aorta and pulmonary trunk.

Diastole is the part of the cardiac cycle during which the heart refills blood after it is emptied during the systolic phase.

The major symptoms of diastolic dysfunction include:

The human heart is a muscular organ that is about the size of a fist. It pumps blood through a set of connections between arteries and veins, known as the cardiovascular system. It involves systemic and pulmonary circulation.

“Cardiac cycle refers to the sequence of events that take place when the heart beats.”

The cardiac cycle attributes to a comprehensive heartbeat from its production to the commencement of the next beat. It comprises diastole, the systole, and the intervening pause. The occurrence of a cardiac cycle is illustrated by a heart rate, which is naturally indicated as beats per minute. A healthy human heart beats 72 times per minute which states that there are 72 cardiac cycles per minute. The cardiac cycle involves a complete contraction and relaxation of both the atria and ventricles and the cycle last approximately 0.8 seconds. Also Refer: Structure & Functions of Human Heart

The diagram below represents the different phases of the cardiac cycle. The atrial systole, ventricular diastole, ventricular systole and ventricular diastole are clearly mentioned in the cardiac cycle diagram given below.

The human heart consists of four chambers, comprising left and right halves. Two upper chambers include left and right atria lower two chambers include right and left ventricles. The key function of the right ventricle is to pump deoxygenated blood through the pulmonary arteries and pulmonary trunk to the lungs. While the left ventricle is responsible for pumping newly oxygenated blood to the body through the aorta.

Following are the different phases that occur in a cardiac cycle: Atrial Diastole : In this stage, chambers of the heart are calmed. That is when the aortic valve and pulmonary artery closes and atrioventricular valves open, thus causing chambers of the heart to relax. Atrial Systole : At this phase, blood cells flow from atrium to ventricle and at this period, atrium contracts. Isovolumic Contraction : At this stage, ventricles begin to contract. The atrioventricular valves, valve, and pulmonary artery valves close, but there won’t be any transformation in volume. Ventricular Ejection : Here ventricles contract and emptying. Pulmonary artery and aortic valve close. Isovolumic Relaxation : In this phase, no blood enters the ventricles and consequently, pressure decreases, ventricles stop contracting and begin to relax. Now due to the pressure in the aorta – pulmonary artery and aortic valve close. Ventricular Filling Stage: In this stage, blood flows from atria into the ventricles. It is altogether known as one stage (first and second stage). After that, they are three phases that involve the flow of blood to the pulmonary artery from ventricles. Also Read: Cardiac Output

In a normal person, a heartbeat is 72 beats/minute. So, the duration of one cardiac cycle can be calculated as: 1/72 beats/minute=.0139 minutes/beat At a heartbeat 72 beats/minute, duration of each cardiac cycle will be 0.8 seconds. Duration of different stages of the cardiac cycle is given below:

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C) Ventricular Diastole

Ventricular diastole, represented by the T wave on the EKG, follows the repolarization of the ventricles. During the early phase of ventricular relaxation, the pressures inside begin to fall to less than that in the pulmonary trunk and aorta, and thus allows blood to flow back to the heart. There is the closure of the semilunar valves to prevent the backflow of blood into the heart. As a result, there is no change in the volume of blood in the ventricles, and this is the isovolumic ventricular relaxation phase.

In the late phase of ventricular diastole, the blood pressure continues to fall due to ventricular muscle relaxation and falls below that of the atria. Blood, therefore, flows from the atria into the ventricles pushing open the atrioventricular valves. Blood continues to flow from the major veins to the atria and into the ventricles. As a result, there is the completion of the cardiac cycle.


Cardiac Function

The primary function of the heart is to produce the driving force that propels blood through the vessels of the circulatory system. Along with the lungs, the heart works to distribute oxygenated blood and nutrients to tissues and organs of the body. Complex regulatory mechanisms function to match the cardiac output with the metabolic needs of the tissues. Cardiac dysfunction can lead to abnormal function or death of cells in tissues throughout the body. Cardiovascular disease is the leading cause of mortality in the United States, and a significant proportion of the population suffers from physical limitations associated with impaired cardiac function. Familiarity with cardiac anatomy and physiology is requisite to understanding cardiac diseases and therapy.

Cardiovascular Anatomy

Heart

The heart is located in the mediastinum, suspended between the lungs, behind the sternum, and in front of the vertebral column, thoracic aorta, and esophagus (Figure 17-1). 1 When viewed from the front, the heart appears to be rotated to the left, so that the right atrium and right ventricle are most anterior. The base of the heart protrudes somewhat into the right side of the chest and is relatively fixed in place by its attachments to the great vessels. The apex of the heart lies primarily in the left side of the chest and is directed forward toward the anterior chest wall. With each heartbeat, a characteristic thrust, or point of maximal impulse (PMI), is generated and can be palpated where the apex strikes against the chest. The PMI is normally located on the left side of the chest where the fifth intercostal space and midclavicular line intersect. Variations in heart size and position within the chest may be related to age, body size, shape, weight, or pathologic conditions of the heart and other nearby structures.

Functionally important cardiac tissues include connective tissues, which form the fibrous skeleton and valves cardiac muscle, which produces the contractile force and epithelial tissue, which lines the cardiac chambers and covers the outer surfaces of the heart. The fibrous skeleton includes an extensive network of matrix that supports cardiac cells and four rings that provide a firm scaffold for attachment of the cardiac valves. Four cardiac valves control the direction of blood flow through the heart (Figure 17-2). The mitral valve (bicuspid) directs blood flow from the left atrium to the left ventricle, whereas the tricuspid valve directs blood from the right atrium to the right ventricle. The edges of these atrioventricular (AV) valves are attached to rings formed by the fibrous skeleton. Valve leaflets are tethered to papillary muscles of the ventricular chambers by connective tissues called chordae tendineae. Papillary muscles attach to ventricular walls and help prevent the valve leaflets from bending backward into the atria during ventricular contraction (Figure 17-3). The AV valves open passively during diastole when the pressure of blood in the atria exceeds that in the ventricles. Ventricular contraction reverses the pressure gradient and causes AV valves to snap shut, preventing blood from flowing backward into the atria.

Two semilunar valves are located in the ventricular outflow tracts. The pulmonic valve lies between the right ventricle and pulmonary artery, and the aortic valve lies between the left ventricle and aorta. Compared to the AV valves, the semilunar valves are thicker and are not supported by fibrous cords. They open and close passively according to pressure gradients, just as the AV valves do. When intraventricular pressures exceed pulmonary and aortic pressures, the semilunar valves remain open and then close when ventricular pressures fall below aortic and pulmonary artery pressures.

The cardiac muscle layer (myocardium) produces the contractile force that pushes blood through the circulatory system. Heart muscle is organized into four separate chambers of varying muscular wall thickness, reflecting the degree of pressure each chamber must generate to pump blood. Atria serve primarily as conduits and have a thinner layer of muscle than the ventricles. The left ventricular muscle is two to three times thicker than that of the right ventricle because higher pressures are required to eject blood into the systemic circulation than into the pulmonic system. Normal chamber pressures are shown in Table 17-1. Alterations in chamber pressures may reflect pathologic cardiovascular changes such as valvular disorders, blood volume abnormalities, and heart failure (see Chapters 18 and 19).

























LOCATION PRESSURE (mm Hg) ∗
Right atrium 0-8
Right ventricle 15-28/0-8
Pulmonary artery 15-28/4-12
Left atrium 4-12
Left ventricle 100-120/4-12
Aorta 100-120/60-80

Cardiac chambers and valves are lined by a layer of squamous epithelial cells called the endocardium. The endocardial layer provides a smooth surface that prevents clotting and minimizes trauma to red blood cells. The endocardium is continuous with the endothelium of the vascular system. Outer surfaces of the heart are also covered by a layer of epithelial cells called the epicardium, which is part of a protective covering called the pericardium. The pericardium is composed of two layers that envelop the heart like a sac (Figure 17-4). The inner layer (visceral pericardium or epicardium) is attached directly to the heart’s outer surface, whereas an outer layer (parietal pericardium) forms a sac around the heart. The parietal pericardium is composed of an epithelial layer and a tough fibrous layer.

Visceral and parietal pericardial layers are separated by a thin, fluid-filled space (pericardial space) that usually contains 10 to 30 ml of serous fluid. This fluid lubricates pericardial surfaces and reduces friction while the layers slide against one another during cardiac contraction. Accumulations of fluid in the pericardial space or inflammation of the pericardial sac can restrict cardiac filling and impair cardiac output.

Circulatory System

The circulatory systems of the lungs and body can be viewed as two separate but interdependent systems (Figure 17-5). The left-sided heart chambers produce the force to propel blood through the vessels of the systemic (body) circulation. The left atrium receives oxygenated blood from the lungs by way of the pulmonary veins and delivers it to the left ventricle. This oxygenated blood is pumped by the left ventricle into the aorta, which supplies the arteries of the systemic circulation. Venous blood is collected from capillary networks of the body and returned to the right atrium by way of the vena cavae. Blood from the head returns to the right atrium through the superior vena cava blood from the body returns via the inferior vena cava. There are no valves between the vena cavae and the right atrium, and the atrial pressure waves that are generated during the cardiac cycle cause characteristic visible pulsations in the jugular veins. An increased right atrial pressure may be observed as distention within the jugular veins.

The right side of the heart receives deoxygenated blood from the systemic circulation and pumps it through the lungs by way of the pulmonary artery. The pulmonary artery divides into left and right branches, which subdivide to supply blood to pulmonary capillary beds. Exchange of respiratory gases occurs at the pulmonary capillaries so that blood delivered to the left atrium by the pulmonary veins is well oxygenated.

Blood flow through the left and right heart chambers is connected in series such that the output of one becomes the input of the other. Thus, the functions of the right and left sides of the heart are interdependent. Failure of one side of the heart to pump efficiently soon leads to dysfunction of the other side.

Characteristic changes in the anatomy and physiologic functioning of the heart and circulatory systems occur with aging (see Geriatric Considerations: Changes in the Heart). In general, these changes result in a decreased cardiac reserve and a greater predisposition to cardiac muscle ischemia.

Cardiac Cycle

Each heartbeat is composed of a period of ventricular contraction (systole) followed by a period of relaxation (diastole). The interval from one heartbeat to the next is called a cardiac cycle and includes ventricular, atrial, and aortic (or pulmonic) events. Each of these events is associated with characteristic pressure changes within the cardiac chambers. 2 Pressure changes result in valvular opening and closing and unidirectional movement of blood through the heart. The various events of the cardiac cycle are illustrated as a function of time in Figure 17-6. Another method of graphing ventricular function is the pressure-volume loop (Figure 17-7). Pressure-volume loops are useful for assessing the relationships between pressure and volume at various points in the cardiac cycle to evaluate left ventricular function. Abnormalities in these waveforms may occur with diseases of the cardiac valves, changes in blood volume, or changes in pumping capacity of the heart (see Chapter 18). These waveforms are commonly monitored with specialized cardiac catheters in patients with cardiac or hemodynamic disorders.

The cardiac cycle can be described sequentially, beginning with ventricular filling. During diastole the ventricles are relaxed and blood flows in from the atria through open AV valves. Initially, ventricular filling occurs passively because of a pressure gradient between the atria and ventricles. Toward the end of ventricular diastole, the atria contract, squeezing more blood through the AV valves into the ventricles. The “atrial kick” provided by atrial contraction is particularly important during fast heart rates, when the time for ventricular filling is shortened the atrial contraction helps to load the ventricle quickly to prevent a reduction in stroke volume. Ventricular events include isovolumic contraction, ejection, and isovolumic relaxation. Each of these cycle events is further described in the following sections.

Isovolumic Contraction

Immediately following atrial systole the ventricles begin to contract, causing intraventricular pressure to rise and the AV valves to close. AV valve closure produces a sound that can be heard at the chest wall and is termed S 1 . Ventricular pressure rises rapidly during isovolumic contraction because all four cardiac valves are closed, and the volume of blood within the ventricular chamber is forcefully compressed by the powerful ventricular myocardium (see Figure 17-6, red tracing ). Volume remains constant during this phase. The rate of rise in pressure is an indication of the contractile state of the heart. The greater the change in pressure per unit time (d P /d t ), the higher the contractile state. Sympathetic nervous system activation increases d P /d t whereas conditions such as heart failure are characterized by a slower rate of pressure development. The term inotropy is commonly used interchangeably with contractility and is reflected by the velocity and degree of cardiac muscle shortening during systole.

Ventricular Ejection

Ventricular contraction results in a rapid rise in ventricular pressure. As ventricular pressure exceeds aortic pressure (or pulmonic), the valve is forced open and a period of rapid ejection of blood from the ventricle follows. The rapid ejection phase is followed by a period of reduced ejection as aortic (or pulmonic) pressure rises and ventricular pressures and volumes fall. The amount of blood ejected with each contraction of the ventricle is called the stroke volume (SV). The volume of blood in the ventricle before ejection is the end-diastolic volume (EDV) and the amount of blood that remains in the ventricle after ejection is the end-systolic volume (ESV). Thus, stroke volume equals EDV minus ESV. An important and commonly used index of pumping effectiveness is the ejection fraction (EF), which is calculated by dividing SV by EDV. A normal EF is

With aging, there is a decrease in the number of myocytes, but normally the heart size does not change appreciably. With the loss of overall cardiac muscle tissue, a corresponding expansion occurs in myocardial collagen and fat. The left ventricular muscle wall becomes thicker, with a resulting increase in oxygen demand. The endocardium becomes fibrotic and sclerosed. Cross-linking of the collagen tissue within the heart muscle increases myocardial stiffening, which causes decreased compliance. The decrease in compliance produces a decline in cardiac contractility, which reduces the heart’s pumping ability. The rate of ventricular relaxation decreases.

Fibrotic changes in cardiac valves result from a combination of hemodynamic stress and generalized thickening. There is also a decrease in coronary artery blood flow to the myocardium, which affects myocardial oxygen and nutrient supply. The myocardial cells increase in size, with increased lipofuscin pigment and lipid deposition.

Within the specialized electrical conduction tissue, there is loss of myocytes and fibrosis of conduction pathways, especially in the sinoatrial (SA) node, AV node, and bundle of His. There is a decreased number of pacemaker cells in the SA node, resulting in less responsiveness of that node to adrenergic stimulation. Myocardial cell irritability increases. On the ECG, the P wave may be notched or slurred. The PR interval is longer, and the QRS amplitude decreases. The axis may shift left as a result of left ventricular muscle thickening (hypertrophy). The T wave may be notched, and the amplitude may decrease.

The changes previously noted affect cardiac function. The resting heart rate in the elderly is unchanged. During stress or exercise, the aging heart is unable to respond quickly with an elevated rate, and the maximal heart rate elevation is reduced. Once the heart rate is elevated, it takes a much longer time for the heart rate to return to the resting level. The cardiac stroke volume and cardiac output generally decrease with age. Oxygen consumption in the myocardium is reduced, resulting in less efficient function when stressed and an overall decreased cardiac reserve.

60% to 80% patients with systolic heart failure often have an EF of less than 40%.

Isovolumic Relaxation

The isovolumic relaxation phase begins with semilunar valve closure in response to falling ventricular pressures and ends when the AV valves open to allow ventricular filling. Ventricular blood volume remains constant during this period because all four cardiac valves remain closed. Closure of the semilunar valves causes the second heart sound, S 2 . Opening of the AV valves signals the beginning of rapid ventricular filling and the start of another cardiac cycle. The rate of ventricular relaxation is indicated by the drop in ventricular pressure per unit time and is called the −d P /d t . The rate and degree of ventricular relaxation is called lusitropy and is an energy-requiring process that reflects the efficiency of calcium removal from the cytoplasm. Rapid relaxation is necessary to allow the ventricle to fill quickly and at a low pressure before the next systole. Impaired relaxation (lusitropic dysfunction) is a common finding in patients with heart failure and contributes to the symptoms of congestion (see Chapter 19). Because relaxation of the ventricle is an energy-requiring process, it may become impaired when blood flow and oxygen delivery to the heart are inadequate.

Atrial Events

Atrial pressure waves have three characteristic curves: a , c , and v (see Figure 17-6, green tracing ). The a wave corresponds to atrial contraction, which immediately precedes AV valve closure. The c wave occurs early in ventricular systole and is thought to represent bulging of AV valves into the atrial chambers. The v waves have a gradual incline, which represents filling of the atrium as blood returns from the circulation. The v wave drops rapidly as atrial pressure is relieved by AV valve opening. A large v wave is often associated with inadequate closure of the AV valve, resulting in regurgitation of ventricular blood back into the atrium during ventricular systole. The mean right atrial pressure, also called the central venous pressure (CVP), is commonly measured as an indicator of the blood volume in the heart, which is dependent in part on the amount of blood being returned from the systemic circulation.

Aortic and Pulmonary Artery Events

Aortic and pulmonary artery pressures rise and fall in relation to the cardiac cycle. Arterial pressures fall to their lowest value just before semilunar valve opening. This lowest pressure is called diastolic blood pressure . Arterial pressure reaches its maximum during ventricular ejection and is called systolic blood pressure . A characteristic notch ( dicrotic notch ) in the arterial pressure curve may be seen as the semilunar valves close (see Figure 17-6, blue tracing ).

The difference in aortic pressure between systole and diastole is partly dependent on the aorta’s elastic characteristics. During systole, the aorta stretches to accommodate blood ejected by the ventricle. The stretched aorta has “stored” or potential energy that is released during diastole to maintain driving pressure and to keep blood flowing continuously through the circulation. Aortic stiffening, as occurs with aging or arteriosclerosis, may result in higher systolic and lower diastolic blood pressures attributable to loss of aortic elastic properties. 3 When aortic or pulmonic pressures are chronically elevated, the ventricles must generate more pressure to open the semilunar valves and eject the stroke volume. Over time this extra effort required to increase the pressure can damage the heart muscle and lead to hypertrophy or failure.

Coronary Circulation

Anatomy of the Coronary Vessels

The blood supply to heart muscle is provided by the coronary arteries (Figure 17-8). Right and left coronary artery openings are located in the sinuses of Valsalva, in the aortic root, just beyond the aortic valve. 2 The right coronary artery originates near the aortic valve’s anterior cusp and passes diagonally toward the right ventricle in the AV groove. In approximately 50% of the population, the right coronary artery gives rise to a posterior descending vessel that supplies blood to the heart’s posterior aspect. In 20% of the population, the left coronary artery is dominant in supplying blood to the ventricles, and in 30% of the population the right and left coronary arteries deliver about the same amount of blood and neither is dominant. 3 The left main coronary artery arises near the aortic posterior cusp and travels a short distance anteriorly before dividing into the left anterior descending and circumflex branches. The anterior descending branch supplies septal, anterior, and apical areas of the left ventricle, whereas the circumflex artery supplies the lateral and posterior left ventricle. The three major coronary arteries give rise to a number of smaller branches that penetrate the myocardium and branch into small arterioles and capillaries. Regular exercise and stable atherosclerotic plaques in the coronary arteries are thought to stimulate the development of more extensive collateral circulation in the heart. Collateral vessels may help limit infarct size in patients suffering acute coronary occlusions (see Chapter 18). Areas supplied by divisions of the coronary arteries are listed in Table 17-2. Most of the heart’s capillary beds drain into the coronary veins, which then empty into the right atrium through the coronary sinus (Figure 17-9).
















ARTERY AREA SUPPLIED
Right coronary Right atrium (55% of persons)
Right ventricle
Intraventricular septum
Sinus node (55% of persons)
Atrioventricular node
Bundle of His
Left anterior descending Right atrium (45% of persons)
Right ventricle (minor)
Left ventricle (anterior, apex)
Anterior papillary muscles
Right and left bundle branches
Intraventricular septum
Left circumflex Left atrium
Left ventricle (posterior, anterior)
Sinus node (45% of persons)

Regulation of Coronary Blood Flow

Blood flow through coronary vessels is determined by the same physical principles that govern flow through other vessels of the body, namely, driving pressure and vascular resistance to flow. 3 According to Ohm’s law, an increase in driving pressure (P) increases blood flow (Q) , whereas an increase in resistance (R) reduces blood flow: Q = P / R (see Chapter 15). Driving pressure through the coronary arteries is determined by aortic blood pressure and right atrial pressure. This relationship can be expressed in the following equation:

Coronary driving pressure ( P ) = ABP − RAP

where ABP is aortic blood pressure and RAP is right atrial pressure. Thus, an increase in aortic pressure enhances coronary blood flow, whereas an increase in right atrial pressure opposes coronary flow.

Coronary vascular resistance (R) has two major determinants: (1) coronary artery diameter and (2) the varying degrees of external compression attributable to myocardial contraction and relaxation. Coronary artery diameter is continuously adjusted to maintain blood flow at a level adequate for myocardial demands. Autoregulation is the term used to describe the intrinsic ability of the arteries to adjust blood flow according to tissue needs. Vessel dilation (vasodilation) occurs in response to increased tissue metabolism or reduced driving pressure, whereas decreased metabolic activity or increased driving pressure results in a decreased vessel diameter (vasoconstriction) .

The mechanism of autoregulation can be explained by the metabolic hypothesis, which proposes that increased metabolism, reduced oxygen concentration, or decreased blood flow results in a buildup of vasodilatory chemicals in the vessel. Smooth muscle encircling the vessel relaxes in response to the presence of the chemicals, increasing vessel diameter. Several vasodilating substances have been proposed, including potassium ions, hydrogen ions, carbon dioxide, nitric oxide, prostaglandins, and adenosine. The endothelial cells that line vessels are known to secrete a variety of relaxing and constricting factors, which may contribute to autoregulation. 4 Vasodilatory substances are washed away as blood flow increases in response to increased vessel diameter. A declining level of vasodilatory chemicals results in vasoconstriction. Thus, vessel diameter is continuously adjusted according to concentrations of vasodilatory chemicals, which are directly related to the tissue’s metabolic activity.

One mechanism for autoregulation of coronary blood flow involves an ATP-sensitive potassium channel in vascular smooth muscle. 5 When ATP levels rise in response to increased coronary flow, the channel closes, making it easier to depolarize the cell and contract vascular smooth muscle. Contraction of vascular smooth muscle reduces the diameter of the coronary arteries and reduces blood flow. The opposite also occurs: a reduction in ATP level, due to low flow or increased metabolism, opens the K + channels. Potassium then leaks out of the vascular smooth muscle and short-circuits the depolarizing influences. This inhibits vascular contraction, leading to vasodilation and increased coronary blood flow. Adenosine also contributes to regulation of the ATP-sensitive K + channels, causing vasodilation when adenosine levels are elevated.

Nitric oxide (NO) produced by endothelial cells lining the coronary arteries is an important regulator of coronary blood flow. NO is a diffusible gas produced by the enzyme inducible nitric oxide synthase in response to numerous stimuli including hypoxemia and platelet factors. NO is a potent vasodilator, and inhibition of its production is associated with reduced coronary blood flow. Many known risk factors for coronary heart disease have been shown to impair nitric oxide–dependent vasodilation of coronary arteries. 5

Vessel diameter also is regulated by the autonomic nervous system. The coronary arteries are primarily innervated by sympathetic nerves, but they also receive a small amount of parasympathetic innervation. The sympathetic neurotransmitter norepinephrine (NE) binds to both α 1 and β 2 receptors in coronary arteries α 1 stimulation results in vasoconstriction, whereas β 2 stimulation dilates. Under normal conditions the vasodilator response predominates, but in pathologic states, excessive α 1 -mediated constriction can occur. The increased metabolic activity associated with sympathetic nervous system stimulation generally causes autoregulatory vasodilation and overrides the direct effect of norepinephrine on the vessels. Parasympathetic activity contributes to vasodilation by promoting the production of nitric oxide by coronary endothelial cells.

In addition to vessel diameter, coronary resistance is affected by myocardial contraction. During systole, cardiac muscle compression creates a marked rise in coronary resistance that reduces coronary blood flow (perfusion). Blood flow to the left ventricle is greatly decreased during systole because of the pressures generated by the thick muscular layer. Blood vessels that penetrate the myocardium to supply the innermost endocardial areas are more compressed during contraction than are outer epicardial vessels. Even though coronary artery driving pressure is greatest during ventricular systole, little blood flow reaches the left ventricle because of the high external pressure applied to the coronary vessels as the myocardium contracts. Therefore, most myocardial blood flow occurs during the diastolic interval between ventricular contractions. The time the heart spends in diastole is directly related to heart rate. Faster heart rates reduce diastolic time and decrease coronary artery blood flow.


Coronary Veins

Coronary veins drain the heart and generally parallel the large surface arteries (see Figure (PageIndex<1>)). The great cardiac vein can be seen initially on the surface of the heart following the interventricular sulcus, but it eventually flows along the coronary sulcus into the coronary sinus on the posterior surface. The great cardiac vein initially parallels the anterior interventricular artery and drains the areas supplied by this vessel. It receives several major branches, including the posterior cardiac vein, the middle cardiac vein, and the small cardiac vein. The posterior cardiac vein parallels and drains the areas supplied by the marginal artery branch of the circumflex artery. The middle cardiac vein parallels and drains the areas supplied by the posterior interventricular artery. The small cardiac vein parallels the right coronary artery and drains the blood from the posterior surfaces of the right atrium and ventricle. The coronary sinus is a large, thin-walled vein on the posterior surface of the heart lying within the atrioventricular sulcus and emptying directly into the right atrium. The anterior cardiac veins parallel the small cardiac arteries and drain the anterior surface of the right ventricle. Unlike these other cardiac veins, it bypasses the coronary sinus and drains directly into the right atrium.


Aortic Pressure Curve

When the left ventricle contracts, the ventricular pres-sure increases rapidly until the aortic valve opens. Then, after the valve opens, the pressure in the ventri-cle rises much less rapidly, as shown in Figure 9–5, because blood immediately flows out of the ventricle into the aorta and then into the systemic distribution arteries.

The entry of blood into the arteries causes the walls of these arteries to stretch and the pressure to increase to about 120 mm Hg.

Next, at the end of systole, after the left ventricle stops ejecting blood and the aortic valve closes, the elastic walls of the arteries maintain a high pressure in the arteries, even during diastole.

A so-called incisura occurs in the aortic pressure curve when the aortic valve closes. This is caused by a short period of backward flow of blood immediately before closure of the valve, followed by sudden cessa-tion of the backflow.

After the aortic valve has closed, the pressure in the aorta decreases slowly throughout diastole because the blood stored in the distended elastic arteries flows continually through the peripheral vessels back to the veins. Before the ventricle contracts again, the aortic pressure usually has fallen to about 80 mm Hg (dias-tolic pressure), which is two thirds the maximal pres-sure of 120 mm Hg (systolic pressure) that occurs in the aorta during ventricular contraction.

The pressure curves in the right ventricle and pul-monary artery are similar to those in the aorta, exceptthat the pressures are only about one sixth as great.


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Aortic Pressure Curve

When the left ventricle contracts, the ventricular pressure increases rapidly until the aortic valve opens. Then, after the valve opens, the pressure in the ventricle rises much less rapidly, as shown in Figure 9-5, because blood immediately flows out of the ventricle into the aorta and then into the systemic distribution arteries.

The entry of blood into the arteries causes the walls of these arteries to stretch and the pressure to increase to about 120 mm Hg.

Next, at the end of systole, after the left ventricle stops ejecting blood and the aortic valve closes, the elastic walls of the arteries maintain a high pressure in the arteries, even during diastole.

A so-called incisura occurs in the aortic pressure curve when the aortic valve closes. This is caused by a short period of backward flow of blood immediately before closure of the valve, followed by sudden cessation of the backflow.

After the aortic valve has closed, the pressure in the aorta decreases slowly throughout diastole because the blood stored in the distended elastic arteries flows continually through the peripheral vessels back to the veins. Before the ventricle contracts again, the aortic pressure usually has fallen to about 80 mm Hg (dias-tolic pressure), which is two thirds the maximal pressure of 120 mm Hg (systolic pressure) that occurs in the aorta during ventricular contraction.

The pressure curves in the right ventricle and pulmonary artery are similar to those in the aorta, except that the pressures are only about one sixth as great, as discussed in Chapter 14.

Relationship of the Heart Sounds to Heart Pumping

When listening to the heart with a stethoscope, one does not hear the opening of the valves because this is a relatively slow process that normally makes no noise. However, when the valves close, the vanes of the valves and the surrounding fluids vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest.

When the ventricles contract, one first hears a sound caused by closure of the A-V valves.The vibration is low in pitch and relatively long-lasting and is known as the first heart sound. When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap because these valves close rapidly, and the surroundings vibrate for a short period. This sound is called the second heart sound. The precise causes of the heart sounds are discussed more fully in Chapter 23, in relation to listening to the sounds with the stethoscope.

Work Output of the Heart

The stroke work output of the heart is the amount of energy that the heart converts to work during each heartbeat while pumping blood into the arteries. Minute work output is the total amount of energy converted to work in 1 minute this is equal to the stroke work output times the heart rate per minute.

Work output of the heart is in two forms. First, by far the major proportion is used to move the blood from the low-pressure veins to the high-pressure arteries. This is called volume-pressure work or external work. Second, a minor proportion of the energy is used to accelerate the blood to its velocity of ejection through the aortic and pulmonary valves. This is the kinetic energy of blood flow component of the work output.

Right ventricular external work output is normally about one sixth the work output of the left ventricle because of the sixfold difference in systolic pressures that the two ventricles pump. The additional work output of each ventricle required to create kinetic energy of blood flow is proportional to the mass of blood ejected times the square of velocity of ejection.

Ordinarily, the work output of the left ventricle required to create kinetic energy of blood flow is only about 1 per cent of the total work output of the ventricle and therefore is ignored in the calculation of the total stroke work output. But in certain abnormal conditions, such as aortic stenosis, in which blood flows with great velocity through the stenosed valve, more than 50 per cent of the total work output may be required to create kinetic energy of blood flow.

Graphical Analysis of Ventricular Pumping

Figure 9-7 shows a diagram that is especially useful in explaining the pumping mechanics of the left ventricle. The most important components of the diagram are the two curves labeled "diastolic pressure" and "systolic pressure." These curves are volume-pressure curves.

The diastolic pressure curve is determined by filling the heart with progressively greater volumes of blood and then measuring the diastolic pressure immediately before ventricular contraction occurs, which is the end-diastolic pressure of the ventricle.

The systolic pressure curve is determined by recording the systolic pressure achieved during ventricular contraction at each volume of filling.

Period of filling Left ventricular volume (ml)

Relationship between left ventricular volume and intraventricular pressure during diastole and systole. Also shown by the heavy red lines is the "volume-pressure diagram," demonstrating changes in intraventricular volume and pressure during the normal cardiac cycle. EW, net external work.

Until the volume of the noncontracting ventricle rises above about 150 milliliters, the "diastolic" pressure does not increase greatly. Therefore, up to this volume, blood can flow easily into the ventricle from the atrium. Above 150 milliliters, the ventricular diastolic pressure increases rapidly, partly because of fibrous tissue in the heart that will stretch no more and partly because the pericardium that surrounds the heart becomes filled nearly to its limit.

During ventricular contraction, the "systolic" pressure increases even at low ventricular volumes and reaches a maximum at a ventricular volume of 150 to 170 milliliters. Then, as the volume increases still further, the systolic pressure actually decreases under some conditions, as demonstrated by the falling systolic pressure curve in Figure 9-7, because at these great volumes, the actin and myosin filaments of the cardiac muscle fibers are pulled apart far enough that the strength of each cardiac fiber contraction becomes less than optimal.

Note especially in the figure that the maximum systolic pressure for the normal left ventricle is between 250 and 300 mm Hg, but this varies widely with each person's heart strength and degree of heart stimulation by cardiac nerves. For the normal right ventricle, the maximum systolic pressure is between 60 and 80 mm Hg.

"Volume-Pressure Diagram" During the Cardiac Cycle Cardiac Work Output. The red lines in Figure 9-7 form a loop called the volume-pressure diagram of the cardiac cycle for normal function of the left ventricle. It is divided into four phases.

Phase I: Period of filling. This phase in the volume-pressure diagram begins at a ventricular volume of about 45 milliliters and a diastolic pressure near 0 mm Hg. Forty-five milliliters is the amount of blood that remains in the ventricle after the previous heartbeat and is called the end-systolic volume. As venous blood flows into the ventricle from the left atrium, the ventricular volume normally increases to about 115 milliliters, called the end-diastolic volume, an increase of 70 milliliters. Therefore, the volume-pressure diagram during phase I extends along the line labeled "I," with the volume increasing to 115 milliliters and the diastolic pressure rising to about 5 mm Hg. Phase II: Period of isovolumic contraction. During isovolumic contraction, the volume of the ventricle does not change because all valves are closed. However, the pressure inside the ventricle increases to equal the pressure in the aorta, at a pressure value of about 80 mm Hg, as depicted by the arrow end of the line labeled "II." Phase III: Period of ejection. During ejection, the systolic pressure rises even higher because of still more contraction of the ventricle. At the same time, the volume of the ventricle decreases because the aortic valve has now opened and blood flows out of the ventricle into the aorta. Therefore, the curve labeled "III" traces the changes in volume and systolic pressure during this period of ejection. Phase IV: Period of isovolumic relaxation. At the end of the period of ejection, the aortic valve closes, and the ventricular pressure falls back to the diastolic pressure level. The line labeled "IV" traces this decrease in intraventricular pressure without any change in volume. Thus, the ventricle returns to its starting point, with about 45 milliliters of blood left in the ventricle and at an atrial pressure near 0 mm Hg.

Readers well trained in the basic principles of physics should recognize that the area subtended by this functional volume-pressure diagram (the tan shaded area, labeled EW) represents the net external work output of the ventricle during its contraction cycle. In experimental studies of cardiac contraction, this diagram is used for calculating cardiac work output.

When the heart pumps large quantities of blood, the area of the work diagram becomes much larger. That is, it extends far to the right because the ventricle fills with more blood during diastole, it rises much higher because the ventricle contracts with greater pressure, and it usually extends farther to the left because the ventricle contracts to a smaller volume—especially if the ventricle is stimulated to increased activity by the sympathetic nervous system.

Concepts of Preload and Afterload. In assessing the contractile properties of muscle, it is important to specify the degree of tension on the muscle when it begins to contract, which is called the preload, and to specify the load against which the muscle exerts its contractile force, which is called the afterload.

For cardiac contraction, the preload is usually considered to be the end-diastolic pressure when the ventricle has become filled.

The afterload of the ventricle is the pressure in the artery leading from the ventricle. In Figure 9-7, this corresponds to the systolic pressure described by the phase III curve of the volume-pressure diagram. (Sometimes the afterload is loosely considered to be the resistance in the circulation rather than the pressure.)

The importance of the concepts of preload and after-load is that in many abnormal functional states of the heart or circulation, the pressure during filling of the ventricle (the preload), the arterial pressure against which the ventricle must contract (the afterload), or both are severely altered from normal.

Chemical Energy Required for Cardiac Contraction: Oxygen Utilization by the Heart

Heart muscle, like skeletal muscle, uses chemical energy to provide the work of contraction. This energy is derived mainly from oxidative metabolism of fatty acids and, to a lesser extent, of other nutrients, especially lactate and glucose. Therefore, the rate of oxygen consumption by the heart is an excellent measure of the chemical energy liberated while the heart performs its work. The different chemical reactions that liberate this energy are discussed in Chapters 67 and 68.

Efficiency of Cardiac Contraction. During heart muscle contraction, most of the expended chemical energy is converted into heat and a much smaller portion into work output. The ratio of work output to total chemical energy expenditure is called the efficiency of cardiac contraction, or simply efficiency of the heart. Maximum efficiency of the normal heart is between 20 and 25 per cent. In heart failure, this can decrease to as low as 5 to 10 per cent.