18 Cardiovascular System - The Heart


The cardiovascular system consists of the blood, the blood vessels, and the heart. The blood has already been discussed. The current discussion will concentrate on the heart and its physiology. It must be remembered that the heart and the blood vessels simply move the blood to the various regions of the body. The bulk of the functions that we associate with the cardiovascular system are really functions of the blood per se.


A. Function - The heart pumps blood. It provides the pressure which is responsible for moving the blood through the vessels and filtering the blood across the smallest vessels (capillaries) to provide the tissue fluid which bathes the cells.


B. Anatomy of the heart - The heart is a dual pump. It consists of two sides, the left and the right, which pump blood into two distinct circulatory pathways, the systemic and the pulmonary respectively.


1. Size and shape - The heart is cone shaped. The pointed end of the cone is known as the apex while the broad portion is termed the base. The heart is about the size of a clenched fist.


2. Location - The heart lies in a space between the lung which is termed the mediastinum. The base of the heart lies behind the sternum and the apex projects downward and towards the left.


3. Pericardium - This is a double layered membrane that surrounds the heart. There are two layers.


a. Parietal layer - This is a tough, fibrous membrane that forms the outer layer.


b. Visceral layer - This is the inner layer. It is a delicate serous layer which closely adheres to the heart muscle. It forms the outer layer of the heart which is known as the epicardium.


c. Pericardial cavity - This is the space between the two membranes. It is filled with pericardial fluid (10 to 20 ml) which reduces the friction between the two membranes when the heart moves during the beating cycle.


4. Structure - The heart is a hollow muscular organ which consists of four chambers. Each chamber has two openings, one for blood entrance and one for blood exit. Large blood vessels open into the chambers and exit the heart from its base.


a. Left and right atria - These are the upper two chambers. The right atrium receives blood from the vena cava veins and the left atrium receives blood from the pulmonary veins. Each atrium empties into the lower chambers, the ventricles.


b. Left and right ventricles - These are the lower chambers that pump blood into the two circuits. The right ventricle pumps blood out the pulmonary artery to the lungs (pulmonary circuit)while the left ventricle pumps blood out the aorta to the rest of the body (systemic circuit).


c. Wall structure - The wall of the heart is built in three layers which are as follows.


(1) Endocardium - This is the lining of the heart and consists of a single layer of squamous epithelium. It is continuous with the endothelium that lines the remainder of the circulatory system. Folding of this endothelium and the connective tissue which supports it are what form the valves of the heart.


(2) Myocardium - This is the muscle layer and it is the thickets of the three layers. The myocardial layer is very thin in the atria but much thicker in the ventricles. The right ventricle has three layers of muscle in its wall while the thicker left ventricle has four layers. In both ventricles the inner surface of the muscle is folded to form the cone shaped papillary muscles which function in heart valve movements.


(3) Epicardium - This is the thin serous membrane that adheres to the surface of the myocardium. It is the visceral pericardial membrane.



d. Valves - The flow of blood through the heart is regulate by four valves.


(1) Atrioventricular valves - These regulate the blood flow from the atria to the ventricles. There is a valve in each side of the heart.


(a) Tricuspid - This is a three flap valve located between the right atrium and the right ventricle.


(b) Bicuspid (mitral) - This valve is made up of two flaps and it separates the left atrium from the left ventricle.


The atrioventricular valves prevent the back flow of blood into the atria during ventricular contraction. They accomplish this in the following manner.


(a) When blood is flowing into the atria and into the ventricles the pressure of the incoming blood forces the valves open.


(b) When the ventricles begin to contract the pressure causes the valves to swing shunt.


(c) The valves are prevented from opening into the atria by connective tissue strands called chordae tendineae which are attached to the valve flaps and the papillary muscles.

(2) Semilunar valves - These separate the arteries from the ventricles.


(a) Pulmonic semilunar - This valve separates the right ventricle from the pulmonary artery.


(b) Aortic semilunar - This valves separates the left ventricle from the aorta.


The semilunar valves prevent the back flow of blood from the arteries into the ventricles during ventricular relaxation. Each valve has three pockets or cusps which flatten out when blood leaves the ventricles. When blood begins to flow back toward the ventricles the pockets balloon outward and come together to form a seal.


5. Path of blood through the heart - Beginning with the vena cava, a drop of blood would pass through the following structures on its path through the heart.


vena cava - right atrium - tricuspid valve - right ventricle -

pulmonic semilunar valve - pulmonary artery - lungs -

pulmonary veins - left atrium - bicuspid valve - left

ventricle - aortic semilunar valve - aorta


6. Coronary circulation - Cardiac muscle is one of the most metabolically active tissues and requires a constant supply of blood for nourishment. This blood is supplied through the following vessels.


a. The aorta gives rise to a right and left coronary artery just past the semilunar valve.


b. The right coronary artery gives off branches that supply the right atrium and ventricle and a major branch called the posterior interventricular artery which supplies the posterior surface of both ventricles.


c. The left coronary artery divides to form the anterior interventricular artery which supplies the anterior surface of both ventricles, and the circumflex artery which supplies the posterior of both the left atrium and ventricle.


d. After passing through an extensive capillary network the blood is drained from the myocardium by the cardiac veins. The cardiac veins join to form a large vessel, the coronary sinus, which drains into the right atrium, along with the anterior cardiac vein.


Blockage of the coronary arteries leads to a condition known as heart attack.


C. Physiology of the heart - Although the heart is composed of several tissues it is predominantly cardiac muscle. The physiology of the heart is really the physiology of cardiac muscle.


1. Cellular organization - Cardiac muscle is made up of branching, striated cells which are separated from one another by intercalated disks. These disks have two types of membrane junctions: desmosomes which fasten the cells together and gap junctions which permit movement of action potentials from cell to cell. This free movement of action potentials from cell to cell yields two important properties for the heart.


a. Functional syncytium - A syncytium is a multinucleated mass of protoplasm which is not divided into cells by membranes. The heart is divided into cells, but because the gap junctions provide no barrier to the action potential it moves over the entire mass of the cardiac muscle as if it were a single large cell.


b. All or none response - Because the action potential moves across every cell, the heart contracts with a maximum force during any contraction cycle.

2. Action potential in cardiac muscle - The resting membrane potential of cardiac muscle is -90 mv, similar to that of skeletal muscle. The action potential on a cardiac muscle cell lasts from 250 - 300 msec, thirty times as long as one on skeletal muscle. There are three major aspects to this action potential.


a. Rapid depolarization - This is the same as in skeletal muscle, at threshold, voltage regulated sodium gates open allowing sodium to pass through fast channels. These channels are so named because they open quickly and remain open only a few milliseconds.


b. Plateau - This represents an extended period of depolarization that is characteristic of cardiac muscle. It is due opening of voltage-regulated calcium channels. These are termed slow channels because they open slowly and remain open for an extended period (175 msec). These channels open in response to the depolarization brought about by the fast sodium channels. It is the influx of positively charged calcium from the extracellular fluid that maintains the depolarized condition. Another function of this calcium is to trigger the release of more calcium from the sarcoplasmic reticulum. The combination of the SR calcium (80%) and extracellular calcium (20%) initiate the contraction process. The extended period of the action potential provides for a persistence of contraction (200 msec) that is needed to eject blood from the heart.


c. Repolarization - As the slow calcium channels begin to close, slow potassium channels begin to open. This permits the outward movement of positive potassium and a resultant rapid repolarization which restores the resting potential.



3. Absolute refractory period - The absolute refractory period (time when a cardiac muscle cell cannot by stimulated again) is very long (250 msec) when compared to that of skeletal muscle (5 msec).


a. It is longer than the contraction period of the cardiac muscle and it is therefore impossible to drive the heart muscle into a tetanus contraction. This of course means that there will always be a relaxation period during which the heart can fill up.


b. The reason for its length is the plateau period of the action potential.


4. Origin and conduction of the heart beat


a. Inherent excitability - Cardiac muscle will spontaneously depolarize. This is because of specialized cells which make up the nodal system of the heart. These represent about 1% of the heart cells. These cells have lost their ability to contract and have an unstable resting potential known as a prepotential which constantly drifts toward threshold. This "drifting" is brought about by a slow inward leaking of sodium coupled with a reduced outward leaking of potassium. Once threshold is reached in a nodal cell, fast calcium channels open and calcium floods inward causing depolarization. The first cell to depolarize will spread the depolarization wave to the next cell via the gap junction connection and therefore will serve as the pacemaker.


b. Origin - In the normal heart a special group of cells located in the wall of the right atrium and known as the sinoatrial (SA) node always depolarize first and therefore function as the pacemaker. This is where the heart beat originates.


c. Conduction - The depolarization wave spreads out from the SA node to the myocardium of the atria. Just above the ventricles, in the interatrial septum, lies a second node known as the atrioventricular (AV) node. The depolarization wave from the atria activates this node which then passes the depolarization wave through a special conducting system for the ventricles. The path is as follows.


SA node - Atrial myocardium - AV node - Bundle of His -


Left and Right bundles - Purkinje fibers - Ventricular



d. All elements of the conducting system are made up of modified cardiac muscle cells which have lost their ability to contract (nodal cells). They specialize in conducting the action potentials rapidly to all sections of the heart.


e. Loss of the SA node will result in the AV node taking over as the pacemaker. The heart rate will drop from a normal rate of 70 BPM to about 60 BPM. If this node is also lost the bundle of His takes over and the heart rate drops to 50 BPM. If the entire conduction system is lost then the ventricles will establish their own pacemaker region and the heart rate will be about 35 BPM. This will not sustain life.


5. ECG - Electrocardiogram - This is a measure of the electrical activity of the heart. Each cardiac cycle shows a complex wave form designated by the letters P, Q, R, S, and T.


a. P wave - This represents the depolarization of the atria.


b. QRS wave - This represents the depolarization of the ventricles.


c. T wave - This represents the repolarization of the ventricles.


d. P-R interval - The time it takes from the P wave to the R portion of the QRS wave. It is normally about 0.16 seconds. If it is over 0.2 seconds then something is wrong.


e. QRS interval - This is the amount of time it takes for the depolarization wave to spread over the ventricles. The normal length of time is 0.08 seconds. If is over 0.1 seconds then something is wrong.


f. The following are some of the kinds of information that can be obtained from an ECG.


(1) Heart rate

(2) Rhythmicity

(3) Conducting system efficiency

(4) Presence of ischemia

(5) Presence and location of scar tissue

(6) Relative position of the heart in the chest


6. Cardiac cycle - These are the events that occur during a complete heart beat.


a. Phases - There are two major phases to the cardiac cycle, systole (contraction) and diastole (relaxation). During systole blood is being expelled from the heart and during diastole the heart is filling up. The details of the cycle are as follows.


(1) At about mid diastole the pressure in the atria is greater than in the ventricles so the AV valves open. Blood rushes into the atria and ventricles. Nearly 75% of the total volume of blood flows into the ventricles by gravity. The remaining 25% is due to contraction of the atria.


(2) Atrial systole begins and the last of the remaining blood is forced into the ventricles. The ventricles are still in diastole.


(3) Ventricular systole now begins. As soon as the ventricles begin to contract the pressure inside of them exceeds that of the atria and consequently the AV valves close. The semilunar valves are not yet open and consequently the pressure in the closed and contracting ventricles increases dramatically in a short period of time. This is known as the isovolumetric contraction period.


(4) As soon as the pressure in the ventricles exceeds that of the pulmonary artery and the aorta, the semilunar valves open and blood is injected into the two arteries. This is the ventricular ejection period.


(5) Blood being forced into the arteries causes the pressure inside of them to rise. Simultaneously, the loss of blood by the ventricles results in a pressure decline within them. Eventually the pressure in both arteries exceeds that of the ventricles. Blood now flows back towards the ventricles which forces the semilunar valves closed. The ventricles are now in diastole again. The isovolumetric relaxation period is the period of time when all valves are closed during diastole.


(6) The ventricles continue to relax and eventually the intraventricular pressure is less than the intratrial pressure and the AV valves again open. The cycle is now complete. It is important to recognize that throughout the cycle, the opening and the closing of the valves is due to pressure differences.


b. Heart sounds - A stethoscope detects two heart sounds during the cardiac cycle - "lub-dub."


(1) The first sound ("lub") is due to the closing of the AV valves. As soon as the valves close, back flowing blood bounces off of them causing the sound.


(2) The second sound ("dub") is due to the closing of the semilunar valves. The mechanism that produces the sound is the same as for the AV valves.


7. Cardiac output


a. Definition - This the amount of blood pumped by one ventricle per minute. It is equal to the heart rate times the stroke volume (volume of blood expelled per beat).


(1) C.O. = HR X SV


(2) An average value for a resting heart would be


70 BPM X 70 ml = 4900 ml or about 5 liters per minute.


(3) Cardiac reserve - This is the difference between the cardiac output at rest and the maximum cardiac output. Under stress, cardiac output may reach 30 liters per minute. In this case the cardiac reserve would be about 25 liters.


b. Regulation - Tissues must have a constant supply of oxygen. It is the oxygen demand of the tissues which is the ultimate regulating factor for cardiac output. As the tissue oxygen demand increases, blood flow, and therefore cardiac output, must increase. Mechanisms for altering cardiac output involve altering heart rate, stroke volume, or both.


(1) Regulation of heart rate - The alteration of heart rate is the most important factor in regulating cardiac output. Normal resting heart rate can range from the 40 to 100 BPM with 70 being about average. Heart rate can be altered by nervous and hormonal mechanisms. Factors that increase HR are said to be positively chronotropic while those that decrease it are negatively chronotropic.


(a) Nervous control - This is the most immediate and important mechanism for altering heart rate. It utilizes cardiac reflex centers located in the medulla and both divisions of the ANS.


/1/ Cardiac control centers - These are located in the medulla. There are two centers, the cardiac accelerator center which speeds up the heart and the cardiac inhibitor center which slows down heart rate.


/2/ Efferent pathways - The cardiac accelerator center exercises control through the sympathetic division of the ANS. Fibers from the cardiac nerves terminate in the heart and release norepinephrine which speeds up the heart rate. The cardiac inhibitor center works through the parasympathetic division of the ANS. Fibers from the vagus nerve release acetylcholine on the heart muscle slowing it down.


/3/ Afferent pathways - The cardiac control centers receive a wide variety of inputs from receptors located in various parts of the body and other parts of the brain. Therefore many different changes that occur in the other parts of the body as well as in the nervous system can alter heart rate.


(b) Hormonal control - Epinephrine and norepinephrine which are released into the blood by the adrenal medulla gland will increase pacemaker cell activity. Epinephrine appears to be about three times as effective at increasing heart rate as is norepinephrine.


(2) Control of stroke volume - Stroke volume is equal to end diastolic volume (EDV) or the amount of blood in the ventricle at the end of diastole, minus the end systolic volume (ESV) or the amount of blood left in the ventricles following systole.




For example, if EDV is 120 ml and ESV is 50 ml then SV will be equal to 70 ml. Stroke volume may be altered by altering EDV, ESV, or both. There are three major factors that regulate stroke volume, preload, contractility, and afterload.

(a) Altering EDV (preload) This is brought about by altering venous return. Venous return is the amount of blood returning to the heart per unit of time. If venous increases then the EDV will increase and so will stroke volume. The mechanism is as follows.


/1/ Increasing EDV stretches the cardiac muscle fibers.


/a/ As cardiac muscle fibers are stretched during the relaxed state, the force of contraction will increase. This is the concept of initial length or load versus tension that was described for skeletal muscle.


/b/ The amount of stretching (preload) is directly proportional to the EDV. The more blood that returns during diastole, the greater will be the stretch, and the greater will be the force of contraction. This means that stroke volume increases with increasing preload.

/c/ Starling's law of the heart - The relationship between preload and stroke volume is formalized in Starling's law. This law simply states that within limits the heart will pump all of the blood which it receives: output equals input.


\1\ Increased EDV will stretch the muscle fibers. This will cause them to contract with greater force thereby forcing out all of the blood received.


\2\ This means that the heart automatically adjusts its contractility and therefore automatically adjusts stroke volume depending upon venous return.


\3\ The major physiological significance of Starling's law is that it insures that the outputs of the left and right ventricles are equal. If the right ventricle should pump one more ml of blood that the left ventricle during one cycle then the left ventricle will stretch to accept that ml and during the next contraction cycle increase its force of contraction to expel that extra ml therefore keeping both side of the heart in balance. If the two sides get out of balance heart failure will eventually result.


(b) Altering ESV, Contractility and afterload.


/1/ Contractility - This is the amount of force produced during a contraction independent of the preload. Under most circumstances, contractility is the most important factor in altering ESV and therefore stroke volume. Factors which increase contractility are said to be positively inotropic and those which decrease it or said to be negatively inotropic. Positive inotropic factors include


/a/ Sympathetic stimulation - Intense stimulation by the sympathetic nerves can increase the force of contraction about 100% above normal.


/b/ Hormones - Epinephrine and norepinephrine from the adrenal medulla increase force of contraction. Likewise the hormone glucagon from the pancreas and the thyroid hormones also have positive inotropic effects.


Negative inotropic factors include decrease sympathetic activity, increased parasympathetic activity, elevated potassium levels and elevated hydrogen ion (decreased pH).


/2/ Afterload - This represents the amount of force the ventricle must develop to force open the semilunar valves. Increased arterial pressure will increase afterload and ESV by decreasing the amount of time that the semilunar valves will be open. Therefore, high blood pressure will decrease cardiac output. This means that the heart must work harder in order to assure adequate blood flow.


(c) Summary of stroke volume regulation


/1/ Stroke volume may be increased by increasing EDV(preload). This is usually accomplished by increasing venous return.


/2/ Stroke volume may be increased by decreasing ESV. This is accomplished by increasing increasing contractility of the myocardium, and decreasing afterload.


/3/ Increased contractility is the most important factor in increasing stroke volume.


E. Pathologies of the heart


1. Heart attack (coronary occlusion, myocardial infarction) - All three of these terms mean approximately the same thing. A coronary artery has been blocked (occlusion) thereby blocking blood flow to a section of the heart. This section may become damaged and die (MI). If the damaged area is not too large or in a key area it may heal by replacement of the dead myocardium with scar tissue.


a. Fibrillation - This is a condition which frequently follows a heart attack and if it is not correct will result in death. During fibrillation the beating of the ventricles loses all synchrony. Different parts of the ventricles begin to contract at different rates and no blood is pumped.


b. Defibrillation - This s a reversal of fibrillation that can sometimes be brought about by passing a powerful electric current through the heart. The current completely depolarizes the heart and hopefully it will begin a new cycle in a normal manner.


2. Congestive heart failure - This occurs when the pump begins to fail. The heart is no longer pumping all of the blood which it receives and as a result blood begins to pool in the blood vessels. Usually one side of the heart fails before the other.


a. If the left side fails then blood backs up in the pulmonary circulation resulting in fluid accumulation in the lungs (pulmonary edema). This results in difficulty in breathing and eventual suffocation if the fluid is not eliminated.


b. If the right side fails first then there is backup in the systemic circuit which results in peripheral edema. This is usually most noticeable in swelling of the ankles and feet.


Causes include heart attacks, artery disease, and high blood pressure.


3. Angina pectoris - This is a pain felt in the chest and left arm and is due to a partial blockage of one or more coronary arteries. Under resting conditions sufficient blood may flow to the myocardium but when increased cardiac output is needed the flow becomes inadequate and the heart becomes ischemic which causes the pain. Mild to moderate cases may be treated with drugs, diet, and exercise. Severe cases are often treated by bypass surgery.


4. Risk factors for heart disease - The preceding conditions are all part of a general syndrome known as heart disease. Most heart disease of the type discussed is due to coronary artery disease, specifically to the accumulation of blockages termed plaque, a condition known as atherosclerosis. Atherosclerosis will be discussed in the next section. Heart disease is the number one killer of people in the U.S. each year. Of the 1.5 million who suffer heart attacks each year, fully one third will die before reaching a hospital! The major risk factors for developing heart disease are high blood cholesterol, high blood pressure, smoking, obesity, lack of exercise, diabetes mellitus, genetics, and male gender.


5. Heart blocks - These involve malfunctions in the conducting system.


a.  Partial blocks - The depolarization wave is delayed at the (

AV node so that the atria may beat two, three, or even four times before a signal gets to the ventricles. These are termed 2 to l, 3 to l, or 4 to l blocks.


b. Complete block - Here no impulses get through to the ventricles. The atria beat at one rate and the ventricles establish their own pacemaker and beat at a different, unrelated rate.


6. Premature beat (preventricular contraction or PVC) - This occurs when an extra beat of the ventricles occurs out of synchrony. It is due to the development of an ectopic focus, an area which becomes so irritable that it initiates a beat of its own. Following a premature beat there is usually a compensatory pause while the ventricle is refractory. Caffeine stimulates PVCs.


7. Heart murmur - This is a squishy sound that can be heard during the normal heart sounds. It is due to a heart valve that does not close completely and permits some back flow of blood. Mild murmurs usually pose no problem, but severe valvular deficiency may require the installation of an artificial valve.