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The Cardiovascular System

The Cardiovascular System


The Structure of the Heart

The size and position of the heart – Despite its heavy workload, the heart is not a large organ. It is about the size of the person’s clenched fist and weighs 10 to 12 ounces. It is hollow and roughly conical in shape, with the narrow end pointed downward, to the left, and slightly forward. Its location in the chest cavity is just to the left of the midline, behind the sternum and between the second and sixth left ribs.

The heart wall – The wall of the heart consists of three layers: the pericardium, a fibrous sac surrounding the heart whose inner lining is a thin, transparent membrane covering the outside of the heart muscle; the endocardium, the delicate innermost lining of the heart; and, the myocardium, the thick muscular layer that separates the two linings. The myocardium is a specialized type of muscle that is unique to the heart and responsible for its contraction.

The chambers of the heart – The heart has four cavities or chambers. Two of these are thin-walled receiving chambers, the left and right atria (singular, atrium), and two thick-walled pumping chambers, the ventricles. Actually, the heart consists of two parallel pumps that work simultaneously. The right-sided pump receives deoxygenated blood from the veins and pumps it to the lungs where it is re-supplied with oxygen. The left-sided pump receives the reoxygenated blood from the lungs and pumps it through the arteries to the rest of the body.

The valves of the heart – The heart contains four valves. There is a valve between the right atrium and right ventricle, the tricuspid valve, and one between the left atrium and the left ventricle, the mitral valve. These valves are open when the ventricles are filling and receiving blood from the atria, but close when the ventricles contract and are so structured that they prevent back-flow or regurgitation of blood from the ventricle into the atrium. The right ventricle pumps blood into the pulmonary artery on its way to the lungs. There is a valve, the pulmonic valve, at the outflow area of the right ventricle. It opens when the ventricle contracts, but closes during diastole, thus preventing regurgitation of blood from the pulmonary artery back into the right ventricle. A similar valve, the aortic valve, is present at the outflow area of the left ventricle. It is open when the left ventricle contracts sending blood into the aorta, but closes during diastole so that blood cannot regurgitate from the aorta back into the left ventricle. The contraction of the ventricles and the closure of the valves contribute to the sounds of the heart, often described as lubb, the contraction or first sound, and dupp, the second cardiac sound.

The flow of blood through the heart – Blood enters the right atrium from the veins and passes through the tricuspid valve into the right ventricle. The right ventricle contracts, expelling blood through the pulmonic valve into the pulmonary artery on its way to the lungs. As the right ventricle contracts, the tricuspid valve closes, preventing regurgitation of blood into the right atrium. Following right ventricular contraction, the pulmonic valve closes to prevent regurgitation of blood back into the right ventricle. Reoxygenated blood returns from the lungs by way of the pulmonic veins and enters the left atrium. Blood flows through the open mitral valve into the left ventricle. After the left ventricle fills, it contracts sending blood through the aortic valve into the aorta and the rest of the body. As the left ventricle contracts, the mitral valve closes to prevent regurgitation into the left atrium. After left ventricular contraction, the aortic valve closes to prevent regurgitation of blood from the aorta back into the left ventricle.

The systemic circulation – After returning from the pulmonary circulation, the oxygenated blood begins its systemic circulation. Systemic (peripheral) circulation is that part of circulation in which blood is transported to all body tissues and returned to the heart. It begins when oxygenated blood leaves the left ventricle. When the ventricles relax, oxygenated blood flows from the left atrium through the mitral valve into the left ventricle. When the ventricles subsequently contract, this blood is pumped with considerable force through the aortic valve into the major artery of the body, the aorta.

As the aorta descends, it branches into several smaller arteries. Some of these arteries, such as the carotid arteries, carry blood to the head and neck. Other arteries, such as the subclavian arteries and the femoral arteries, carry blood to the upper and lower extremities, respectively.

From these arteries, blood enters the arterioles and then the capillaries, where oxygen is exchanged for carbon dioxide and nutrients for metabolic wastes. The deoxygenated blood that has been used by the body then travels back to the heart by way of the venules and veins. It finally empties into two principal veins: the superior vena cava, which carries blood from the upper portion of the body; and the inferior vena cava, which carries blood from the lower portion of the body. Blood from both the superior and inferior vena cavae enters the right atrium, where systemic circulation ends. With the next heart relaxation, the blood again flows from the right atrium through the tricuspid valve into the right ventricle, and the cycle of pulmonary circulation to systemic circulation is repeated.

The following diagram summarizes the flow of blood through the body, tracing it from the peripheral venous system into the heart, through the pulmonary circulation, back to the heart, to the systemic circulation, and back again to the heart.

The circulation of the heart (coronary circulation) – The heart also has its own important blood supply, the coronary circulation. The two main coronary arteries, the left and the right coronary arteries, branch from the aorta as it leaves the heart. The left coronary artery then divides into the circumflex artery and the left descending artery. These three arteries are the principal coronary arteries and they, in turn, give rise to numerous branches guaranteeing the heart a rich supply of blood and oxygen.

The major coronary arteries lie on the surface of the heart. From them, smaller arteries pass into the myocardium, ultimately forming arterioles and capillaries and comprising the collateral circulation. When needed, coronary arterioles have the ability to increase the size and number of collateral vessels. This forms a valuable increase in the blood supply in the event of an occlusion of a coronary artery.

A decrease in the oxygen supply to the heart as a result of narrowing or complete obstruction of a coronary artery results in angina pectoris if the obstruction is incomplete and transient. When a portion of the myocardium is deprived of blood permanently, that portion of the myocardium sustains myocardial infarction due to death of that portion of the myocardial muscle.

The nervous system of the heart – Although the heart has the remarkable property of automaticity and is capable of contracting on its own, it is supplied with two sets of nerves to augment its work. There are sympathetic nerves that stimulate the heart causing it to beat faster and with greater strength, and parasympathetic nerves that calm the heart and slow its rate. These nervous systems carry impulses from the brain and elsewhere in the body that help the body respond and adjust to internal and external factors. Both systems respond to a variety of drugs that may be used in the treatment of various cardiac disorders and hypertension.

The Cardiac Cycle

The cardiac cycle is defined as the series of events that occur during a single heartbeat. It consists of two phases: systole and diastole. Systole refers to a period of contraction by the heart muscle, whereas diastole refers to a period of relaxation by the heart muscle. The heart does not undergo the cardiac cycle as one unit. Rather, the atria and ventricles act as separate units, entering systole and diastole at different times. However, both atria and both ventricles act simultaneously.

The duration of these events during a typical cardiac cycle is approximately 0.8 seconds. Because the series of contractions and relaxations of the different chambers of the heart occur cyclically, there is no real “beginning” or “ending” of the cardiac cycle. However, for the purpose of discussion, we will artificially label atrial systole, or atrial contraction, as the “beginning” of the cycle.

Atrial Contraction: Just prior to atrial contraction, both the atria and ventricles are relaxed. The pulmonic and aortic valves connecting the ventricles to the major arteries are closed. However, the atrioventricular valves that connect the atria to the ventricles are open. During this period of relaxation, blood flows continually from the veins into the atria, filling these chambers. Some of this blood passes through the open atrioventricular valves to the ventricles. When the atria contract, they force the remaining blood contained in them to flow into the ventricles. By the end of atrial contraction, the ventricles contain a full supply of blood, while the atria contain virtually none.

Ventricular Systole:Ventricular systole occurs only a fraction of a second after atrial contraction. As the ventricles begin to contract, the pressure within them quickly exceeds that within the atria, forcing the atrioventricular valves to close. This action prevents a backward flow of blood (regurgitation) from being forced into the atria from the ventricles. As ventricular contraction continues, the pressure within the ventricles reaches a point where it exceeds that in the aorta and the pulmonary arteries. At this point, the aortic and pulmonic valves open, and the blood from the ventricles is ejected through these valves into the aorta and pulmonary artery, respectively.

At about the same time that the ventricles enter systole, the atria begin to relax. During this period, blood flows into the left atrium from the pulmonary veins and into the right atrium from the superior and inferior vena cavae. However, this blood remains in the atria during ventricular systole, since the high pressure in the ventricles during its contraction forces the atrioventricular valves to remain closed.

Ventricular Diastole: When ventricular diastole begins, the ventricles start to relax and the pressure within the ventricles decreases. Once the ventricular pressure becomes lower than the pressure in the aorta and the pulmonary artery, the pulmonic and aortic valves close, preventing regurgitation of blood into the ventricles. As the ventricles fully relax, the ventricular pressure becomes lower than the pressure in the atria. This allows the atrioventricular (mitral and tricuspid) valves to open.

Because the ventricles are now in diastole and the atrioventricular valves are open, some of the blood that has been flowing into the atria flows through the open valves into the ventricles. The ventricles reach about 80% of their capacity before the atria begin to contract and the cardiac cycle is repeated.

Regulation of the Cardiac Cycle: In order for the heart to effectively complete each cardiac cycle, cardiac muscle cells must contract more or less simultaneously. The coordination of cardiac muscle contractions is made possible by two factors. First, the cells in cardiac muscle are tightly interwoven, so that muscle contraction spreads rapidly throughout the heart. Second, the heart contains specialized cardiac muscle cells that are organized into a conducting system, spreading muscle contraction impulses throughout the heart at regular intervals.

The heart has the unique ability to beat (contract) on its own. Although in real life it is assisted in this function by nerves and hormones in the blood, it still functions even when removed from these influences. This is best illustrated by the donor organ in heart transplantations.

The mechanism by which the heart generates and transmits the signal to contract is quite complex. Actually, a minute electrical current of about 2 millivolts is generated and passes down from its origin through the conducting system of the heart, causing muscular contraction of each chamber as it passes through it. The impulse or action potential normally arises in a specialized group of cells located in the wall of the right atrium called the sinoatrial (SA) node. Normally, an electrical difference (potential difference) exists between the inside and outside of all cells, which is due to the differences in electrical charges inside the cell from those outside the cell. The impulse is initiated by passage of electrical charges across the membrane (covering) of the cell, causing a change in the potential difference and creating an action potential.

Leaving the SA node, the impulse passes through both atria causing them to contract thus helping blood pass into their respective ventricles. On its way to the ventricles, the action potential next encounters the atrioventricular (AV) node, another group of specialized cells. From there the impulse passes down an anatomical pathway called the Bundle of His which branches out and spreads throughout both ventricles (Purkinje fibers), resulting in contraction of the ventricles.

The Hemodynamics of the Cardiac Cycle: Vital Signs

Left ventricular systole produces a surge of blood through the blood vessels that gives rise to two important vital signs. Vital signs are readily available indices used to monitor the general state of health of an individual and include pulse, blood pressure, body temperature, and rate of respirations. In hospitalized patients, these are the measurements the physician or nurse records on the patient’s chart and which provide an indication of the patient’s general condition. Of the vital signs, two, pulse and blood pressure, are generated by left ventricular systole.

Pulse: The pulse is a direct result of the surge of blood produced by left ventricular systole. It is a ready means of recognizing the rate of the heart and its regularity. The strength of the pulse is also of importance; a weak, thready pulse may be an indication of a serious problem. The pulse can be taken at any point where a large artery runs close to the skin. Common sites for this are the temple, neck, armpit, groin and foot. For convenience, the pulse is usually “taken” at the wrist at the base of the thumb, where the large radial artery to the hand is close to the skin. In case of doubt, the pulse can be verified by listening to the heart with a stethoscope, a procedure referred to as auscultation.

Blood pressure: The blood pressure is the second of the vital signs that is related to the heart. It is a measurement of the outward pressure exerted on arterial walls by the blood and consists of two components; the systolic (SBP) and the diastolic blood pressure (DSP). The systolic blood pressure is the pressure generated by left ventricular systole. The diastolic pressure is the residual pressure in the arterial system during the diastolic phase of ventricular relaxation and refilling. It is important to remember that there is always a supply of blood in the vascular system, both during systole and diastole. Blood pressure is measured by various types of sphygmomanometers which register the pressure in terms of the height of a column of mercury expressed in millimeters – mm/Hg (mercury is a liquid element 13 times heavier than water and provides an easy and useful means of measurement). The blood pressure is expressed as the ratio of systolic to diastolic pressures (systolic/diastolic).

Normally, the systolic pressure is 140 millimeters of mercury (mm/Hg) or less and the diastolic is 90 mm/Hg or less. Hypertension (high blood pressure) exists when either the systolic or diastolic readings are above 140 and 90 respectively. There are no set standards for hypotension (low blood pressure) since it is relative to the patient’s known normal blood pressure. Thus a systolic blood pressure of 120 mm/Hg, considered normal under usual conditions, might represent hypotension in an individual who had a systolic blood pressure of 180 mm/Hg. Generally speaking, however, a systolic blood pressure of 100 mm/Hg or below suggests hypotension. The diagnosis is usually made in the presence of other confirmatory signs and symptoms.

According to guidelines set by the JNC (Joint National Committee) on Detection, Evaluation, and Treatment of High Blood Pressure, blood pressure under 140/90 mmHg is considered normal. Systolic readings between 130-139 mmHg and diastolic readings from 85-89 mmHg are high normal, while blood pressure under 120/80 mmHg is optimal.

Arterial blood pressure is determined by two primary factors: the total amount or volume of blood pumped by the heart (cardiac output) and the resistance arterioles present to blood flow (total peripheral resistance). In turn, each of these primary factors is influenced by a number of secondary factors.

Cardiac output (CO) is the volume of blood that is pumped each minute from the left ventricle to the tissues. If all other variables remain equal, increased cardiac output leads to increased arterial blood pressure. Resistance to blood flow is determined by the diameter of every arteriole in the body and is called Total Peripheral Resistance (TPR) or systemic vascular resistance. TPR is controlled by arterioles because their diameters, under control of the autonomic nervous system, can vary according to the body’s needs.

If expressed mathematically, the relationship between CO, TPR, and arterial blood pressure can be represented with the following equation:


According to this equation, a change in cardiac output or peripheral resistance will result in a proportional change in arterial blood pressure (i.e., if CO or TPR increase, BP will also increase). Numerous factors influence cardiac output and peripheral resistance.

Cardiac Output: Cardiac output can be calculated by multiplying the heart rate by the stroke volume. Heart rate (HR) is the number of ventricular contractions per minute, regulated by the autonomic nervous system. The normal range for heart rate is 60-100 contractions per minute. Stroke volume (SV) is the volume of blood ejected by the left ventricle each time it contracts. It is determined by calculating the difference between the volume of the ventricle at the end of systole and the end of diastole. Stroke volume is influenced largely by venous return, the volume of blood returned to the heart by the veins. The normal range for left ventricular stroke volume is 60-130 mL per contraction.

HR x SV = CO

(It is important not to confuse stroke volume with the term ejection fraction. The ejection fraction is the ratio of the stroke volume to the volume of the left ventricle at the end of diastole. In other words, the ejection fraction is the percentage of the end diastolic volume. That is the volume of blood present in the ventricle at the end of diastole that is actually forced out of the left ventricle into the aorta during contraction. Typically, ejection fraction averages around 67%.)

Since changes in stroke volume or heart rate can alter cardiac output, these variables can also affect arterial blood pressure. For example, an increase in heart rate, with no compensating decrease in other parameters, will increase cardiac output and thus increase overall blood pressure. Similarly, if stroke volume increases, but heart rate does not drop accordingly, overall blood pressure will rise.

Peripheral Resistance: Peripheral resistance can be changed by both chronic and temporary factors. Chronic changes in arteriolar diameter, such as the narrowing caused by atherosclerosis, can produce a constant change in resistance to blood flow. Temporary changes may occur from either vasodilation (relaxation of smooth muscle in the arteriolar walls, which causes the vessel diameter to increase and resistance to blood flow to drop) or vasoconstriction (contraction of smooth muscle in the arteriolar walls, which causes the vessel diameter to decrease and resistance to rise). If peripheral resistance increases or decreases while cardiac output remains unchanged, overall blood pressure will rise or fall accordingly.

The relationship between heart rate and cardiac work is fairly simple. If the heart beats more quickly (during exercise, for example), it performs more work. However, the ways in which cardiac wall tension and myocardial contractility affect cardiac work are somewhat more complex.

Cardiac Wall Tension: Cardiac wall tension is the force cardiac muscle fibers exert to contain the blood and to contract against it. As blood enters the heart, it exerts an outward pressure on the cardiac walls. To prevent the heart from expanding like a balloon filling with air, the heart fibers are able to resist excessive stretching and thus exert the pressure necessary to contain the blood. When the heart contracts to pump the blood, the cardiac walls must exert even greater pressure to expel the blood into the circulation. Increasing the wall tension increases the total effort that must be exerted by the heart muscle and it must work harder to contract.

Two factors play a significant role in determining cardiac wall tension. These factors are:

1. preload 2. afterload

Preload and Cardiac Wall Tension

Preload refers to the pressure exerted by the blood against the ventricular wall the instant prior to contraction. Preload is synonymous with venous return to the heart, and this is often monitored as left ventricular end diastolic pressure (LVEDP). Any change in the body that increases the return of blood to the heart will increase the preload.

Increases in preload increase myocardial work. To understand this relationship, imagine two bicycle tires, with one containing more air than the other. If you try to compress each tire with your hand, you must squeeze harder on the tire with the higher air pressure to push the wall inward. In a similar way, the heart must work harder to “push” its walls inward during contraction if the preload has been increased.

Two factors can increase preload: increased blood/fluid volumes and constriction of blood vessels. Increases of blood/fluid volume means that more fluid is available in the cardiovascular system to enter the heart prior to each contraction. Constriction of blood vessels affects preload by reducing the area in the vascular system through which blood can flow. Vasoconstriction decreases the capacity of the veins and venules to hold blood. This reduces the amount of blood that is allowed to pool in the veins, thus forcing more blood back into the heart. Vasoconstriction is primarily controlled by activation of the sympathetic nervous system, which stimulates vasoconstriction through the action of norepinephrine.

Afterload and Cardiac Wall Tension

Afterload is the pressure that the ventricles must work against to pump blood into the aorta and pulmonary artery. It varies with arteriolar resistance to the flow of blood (peripheral resistance). An increase in afterload increases cardiac work by forcing the ventricles to pump against a higher pressure in the arteries.

If afterload remains increased for a long period of time, the heart must work harder to pump the blood through the arterial system. To compensate for this, the muscles of the heart increase in size (hypertrophy). Eventually, this compensatory mechanism fails and the heart is no longer capable of pumping blood against the elevated arterial pressure and its pump action begins to fail. This condition is known as congestive heart failure (CHF), and requires therapy.

Myocardial contractility and cardiac work

Myocardial contractility is the strength or forcefulness of contraction of individual cardiac muscle fibers. Depending on its health, the heart may contract vigorously or weakly. A strong contraction allows expulsion of a greater volume of blood. Thus, if a heart’s contractions are strong, it has to pump fewer times (i.e., it does less work) than it would if its contractions were weakened by disease.

Myocardial contractility can be augmented by sympathetic nervous stimulation. This is mediated by the actions of epinephrine (adrenaline) and norepinephrine on muscle fibers. In periods of stress, fright, or other conditions that initiate sympathetic activity, myocardial contractility and the work performed by the heart increase. Certain drugs, called inotropic agents, have the capability of increasing the force of myocardial contraction and are valuable therapeutic agents.

The Frank-Starling Principle and Myocardial Contractility

One further concept important to understanding cardiac function is the Frank-Starling Principle. The Frank-Starling Principle states that the output of the heart increases in proportion to the amount of stretch in the cardiac muscle fibers. In other words, if the heart is forced to stretch to accommodate higher volumes of blood, myocardial contractility will increase. Thus, the amount of blood pumped out of the heart per beat will increase if the amount of stretch of the ventricle increases.

Increased preload can cause cardiac muscle fibers to stretch. An increased volume of blood returning to the heart can fill the heart’s chambers to the point where muscle fibers have to stretch more than normal to expel the blood. As the Frank-Starling Principle states, the increased stretch provides increased force for contraction. However, if the myocardium is stretched too far or too frequently, it can lose the ability to return to its original contracted state. If the heart muscle is stretched excessively, it can eventually lose its ability to contract with its normal force.

The Vascular System

The vascular system is divided into three components. The arterial system is responsible for the delivery of blood and oxygen to every cell, tissue and organ in the body. The arteries carry blood away from the heart. Veins comprise the venous system that is responsible for returning deoxygenated (deprived of oxygen) blood from the tissues and organs back to the heart. The capillary system links the two systems together and is responsible for the exchange of oxygen for carbon dioxide at the cellular level.

The vascular system is not a passive system of pipes, but actually plays a critical role in supplementing the action of the heart in the distribution of blood. Its status also plays a major role in the determination of the blood pressure.

The arterial system: aorta, the largest blood vessel in the body. The aortic valve is situated at the entrance to the aorta. During left ventricular systole, the valve opens, allowing the free flow of blood into the aorta. During diastole, the relaxation and refilling stage of the cardiac cycle, the aortic valve snaps shut, preventing regurgitation of blood from the aorta back into the left ventricle. Anatomically, the aortic valve consists of three cusps (posterior, right, and left) that come together during diastole to completely occlude the valve and prevent regurgitation. Because the edge of each cusp is in the shape of a half moon, the valve is sometimes called the semilunar valve.

Within the cavities formed by the right and left aortic cusps are the origins of the left and right coronary arteries. These are the arteries which branch to form the coronary circulation of the heart muscle and provide oxygenated blood to the heart muscle. Shortly after leaving the heart, the aorta arches to the left and sends large branches to the neck and head and to the upper extremities. The large arteries supplying the neck, head and brain with blood are called the carotid arteries. Their strong pulsations can be felt in the neck on both sides of the larynx. The aorta then descends down the back of the body in front of the spine, supplying branches to the chest and to the organs in the abdomen. In the pelvis, the aorta splits into two large branches, each supplying one of the legs with blood.

As the arteries approach their goals, they get increasingly smaller and are called arterioles. Finally, they attain a thread-like diameter and are called capillaries.

If one examines the wall of an artery under the microscope, three layers are apparent. The intima is the innermost layer of the artery and is composed of endothelium, the delicate inner lining of the blood vessel. It is the endothelium that becomes involved with atherosclerosis, commonly referred to as hardening of the arteries. The middle layer of the arterial wall, the media has a layer of elastic tissue which is capable of decreasing and increasing the caliber of the blood vessel and thus controlling the flow of blood through it. The media of the large arteries also have a layer of . The arterial elastic and muscular tissues play important roles in supplementing the heart in the propulsion of blood through the vascular system. The nervous system and circulating hormones also play important roles in this action. The outer arterial wall layer, the adventitia, is composed of protective fibrous tissue.

Vasoconstriction is the term applied to constriction of a blood vessel. Vasoconstrictor substances are formed within the body, especially in the kidneys and adrenal glands. They play an important role in the control of blood pressure. Vasoconstriction causes an increase in blood pressure by increasing the resistance against which the heart has to work. The administration of vasoconstrictors is helpful in raising blood pressure and in the control of bleeding.

Vasodilatation is the term applied to dilatation of the blood vessels. This also occurs within the body under certain circumstances, causing a fall in blood pressure. Vasodilatation plays a role in the development of circulatory shock. Vasodilators are important therapeutic agents in the treatment of hypertension.

Both vasoconstriction and vasodilatation are under the control of ner-vous and hormonal influences over which we have little or no voluntary control.

The venous system: The venous system is responsible for the return of blood from the tissues and organs of the body to the heart. The blood carried by the venous system has been depleted of oxygen in exchange for carbon dioxide (CO2). The transport of the blood from the heart to the lungs for replenishment of oxygen is considered by some as part of the venous system.

For the most part, arteries and veins travel and branch out through the body side-by-side, similar to the opposite sides of a highway with the traffic (or blood) flowing in opposite directions. In many instances, arteries and veins share the some name. All venous channels from the head and chest lead into the superior vena cava. Blood from below the chest drains into the inferior vena cava. Both of these large veins empty into the right atrium from which their contents are passed into the right ventricle. Right ventricular systole then pumps the blood to the lungs by way of the pulmonary arteries.

There are striking anatomical and physiological differences between arteries and veins. Whereas arteries are strong, muscular and elastic, veins are more delicate in structure and to a significant degree, lack the elasticity and muscular power of the arteries. They have a limited capability for vasoconstriction, but have a prominent capacity for vasodilatation. Arterial blood flow is much faster than venous blood flow because it reflects the power of the left ventricular contraction as well as the artery’s own capability for contraction. Arterial bleeding is pulsatile, again reflecting the contraction of the left ventricle, whereas venous bleeding is slower and steady in character. In some of the major arteries, blood moves at a rate of over a foot a second, whereas the flow rate in veins is about 4 inches per second. Contraction of the muscles surrounding a vein assists in promoting venous blood flow. This mechanism is sometimes referred to as the venous pump. The venous pressure varies throughout the body, depending on the position of the individual and the site of measurement. It averages 50 to 100 mm of water, much lower than the pressure of 120 mm of mercury seen in arteries during systole. Arterial blood is much brighter and redder than venous blood because of its oxygen content.

To prevent the reversal of the flow of venous blood, veins have valves that prevent this from happening. For example, standing in the upright position for a prolonged period would be expected to increase the pressure in the veins of the leg and promote backflow of blood. The venous valves prevent this. Unfortunately, the valves are prone to damage and this may result in edema (swelling), and the presence of permanently dilated veins (varicose veins).

The veins have a greater capacity to widen or dilate than do arteries. Because of this, the volume of blood in our venous system is 2 to 2 1/2 times that in the arterial system. This pool of blood acts as an important reservoir that becomes available if the circumstances require more blood. When the venous circulation makes more blood available, there is a resultant important increase in cardiac output. Thus, the venous circulation, once thought to play a rather passive role in the circulation and serve only as a passageway for the flow of blood, is now recognized as playing an important, active role in the circulation.

The capillary system: It is the function of the capillaries, the thread-like blood vessels that link the arterial with the venous system, to exchange fluid, oxygen, carbon dioxide, nutrients, electrolytes, hormones, and other substances between the blood and the interstitial space, the space outside the capillaries and separating the cells. In the lungs, the capillary system exchanges oxygen and carbon dioxide with the alveoli, the tiny air spaces of the lungs.

Every cell must be in close proximity to a capillary in order to survive. In addition, the capillary walls are very thin, consisting of a single layer of cells, in order to allow the passage of small molecular-sized substances through its wall. There are tiny pores or clefts in the capillary wall which allow passage of molecules from the interior to the exterior of the capillary wall and vice versa. In addition, substances can be transported through the wall with the help of small bubbles, called vesicles, which carry the substance to be transferred within them.

By far, the most important means by which substances are transferred from the plasma, the liquid portion of the blood, and the interstitial fluid surrounding the cells is the process of diffusion. Diffusion allows the passage of substances through the capillary wall without the necessity of pores, clefts or vesicles. Diffusion occurs from an area of high concentration to an area of low concentration. The method of transportation that is used depends on many complex factors including the size of the particle, pressure and concentration differences between the interior and exterior of the capillary, and the solubility of the substance in water and lipids (fats).

The body’s most essential task is the continuous transport of oxygen from the blood to the tissues and the return of oxygen to the blood in exchange for carbon dioxide (CO2). This is the exchange process that occurs in the pulmonary capillary circulation. In the lung, the capillary system takes up oxygen from the alveoli (air sacs) and releases carbon dioxide to be exhaled.

The blood has special carriers for the oxygen it delivers to the tissues; they are the red blood cells, tiny concave discs. Red blood cells are so small that about 75 billion of them would fit into a one-inch cube. Red cells get their color from hemoglobin, a protein that contains iron and is capable of carrying, releasing, and retrieving oxygen.

In the tissues, oxygen leaves the blood for the interstitial fluid by the process of diffusion. The concentration or partial pressure of oxygen in the interstitial fluid is low because it has been used by the cells. On the other hand, the content of oxygen in the capillary is high. Thus, by the process of diffusion, oxygen passes from the area of high concentration to the area of low concentration. Simultaneously, by the same process, carbon dioxide, a waste product of the cells is picked up by the blood and carried by way of the venous circulation to the right atrium and right ventricle and sent to the lungs. The exchange of carbon dioxide for oxygen occurs between the pulmonary capillary system and the alveolus, that tiny air sac in the lungs, which has received oxygen from inhaled air. The process again is one of diffusion across the delicate membrane that separates the pulmonary capillary from the alveolus.

These processes of gas exchange are continuous and essential for survival. Impairment of the process by any mechanism (tissue, lung, or blood) leads to serious consequences. The body does not tolerate continuous low concentrations of oxygen and high concentrations of carbon dioxide for a prolonged period of time.

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