Chapter 20 - The Heart PDF

The Cardiovascular System The Heart Some of the information, figures, graphs, tables and images in the notes are obtained from the Seeley’s Anatomy & Physiology 13th Edition, published by McGraw Hill and used only for the purpose...

The Cardiovascular System The Heart Some of the information, figures, graphs, tables and images in the notes are obtained from the Seeley’s Anatomy & Physiology 13th Edition, published by McGraw Hill and used only for the purpose of classroom education. Introduction The heart is a cone-shaped organ, about the size of the clenched fist of its owner, which pumps blood through the blood vessels. The heart is located in the center of chest cavity in an area known as mediastinum. The heart is slanted diagonally, with about two-thirds of its bulk to the left of the chest’s midline. The surfaces of the heart are called the anterior (next to the sternum and ribs), inferior (against diaphragm), left side (next to the left lung), and posterior (base). The pointed end of the blunt cone is called the apex, which extends forward, downward, and to the left (between the 5th and 6th ribs midclavicular line). The uppermost part of the heart is called base, which extends upward, backward, and to the right (below the 2nd rib). The base is in fixed position because of its attachments to the great vessels, but the apex is able to move. When the ventricles contract, they change shape just enough so that the apex moves forward and strikes the left chest wall near the 5th intercostal space, which normal is felt from the outside as a heartbeat. Structure and Function of the Heart The heart is surrounded and protected by pericardium or pericardial sac. It composed of main parts: Fibrous pericardium – is fibrous connective tissue around the heart which prevents overstretching of the heart, and provides attachment of the heart to the mediastinum. Serous pericardium – is delicate inner tissue, which consists of two part: Parietal layer – lines inner part of fibrous pericardium. Visceral layer – lines the outer surface of the heart or epicardium. The serous pericardium surrounds the pericardial cavity, which contains a small amount of serous pericardial fluid. The pericardial fluid reduces friction between the membranes as the heart moves. Anatomy & Physiology II – The Heart 1  The wall of the heart is made up of three layers Epicardium – is the outer thin layer of the wall, and composed of delicate connective tissue. Myocardium – is the middle thick layer of cardiac muscle, which gives the heart its special pumping ability. Endocardium – is the innermost thin layer of connective tissue, that covers the inside cavities of the heart, and all of the associated valves and muscles. Chambers & Valves of the Heart The heart is a hallow organ composed of four chambers or cavities. Atria – are the two superior cavities of heart. Each atrium has a wrinkled appendage called auricle on its anterior surface, which increases the atrium capacity. Ventricles – are the two inferior cavities of heart. Dividing the heart vertically down the middle into a right and left heart is a wall of muscle called septum. Interatrial septum separates the two atria. Interventricular septum separates the two ventricles. On the surface of the heart are some depressions called sulci that are helpful in locating specific features of the ventricles and atria, as well as coronary vessels. Coronary sulcus – encircling the heart, indicates the border between the atria and ventricles. Embedded in a fat with the coronary sulcus are the right and left coronary arteries. Anterior interventricular sulcus – marks the location of the interventricular septum, the anterior part of the septum, separating the ventricles. Embedded within the sulcus are the anterior interventricular vein and great cardiac vein. Posterior interventricular sulcus – marks the location between the two ventricles on the posterior aspect of the heart. Embedded within the sulcus are the posterior interventricular descending artery and the middle cardiac vein. Anatomy & Physiology II – The Heart 2  Right atrium Right atrium receives blood from the systemic circulation via two veins, the superior and inferior vena cava. The internal surface of the auricle and the adjacent anterior atrial wall contain a number of muscular ridges called pectinate muscles. On the interatrial septum wall of the right atrium is an oval depression called fossa ovalis, where the fetal foramen ovale used to be before it closed at birth. Blood passes from right atrium to right ventricle by way of right atrioventricular valve of tricuspid valve. Tricuspid valve consists of three leaflets or cusps. Right ventricle Right ventricle contains a series of ridges called trabeculae carneae, which are formed by bundles of cardiac muscle fibers. The leaflets of tricuspid valve are connected to tendon-like cords called chordae tendineae, and in turn are connected to cone-shaped trabeculae carneae called papillary muscles. Blood leaves the right ventricle through pulmonary valve into the pulmonary trunk and divides into right and left pulmonary arteries. Left atrium The internal wall of left atrium is smooth and pectinate muscles are confined in left auricle only. Left atrium receives blood from lings through pulmonary veins and delivers it to left ventricle through bicuspid or mitral valve. Left ventricle Left ventricle forms the apex of the heart and contains the same structures as right ventricle The left ventricle is much thicker to accommodate the higher pressure required to pump blood a greater distance against resistance. Blood leaves the left ventricle through aortic valve and enters the ascending aorta and from there some of blood enters coronary arteries which carry blood to the heart, and the rest into the arch of aorta and descending aorta, finally the rest of the body. During fetal life a temporary vessel known as ductus arteriosus shunts blood from the pulmonary trunk into the aorta. At birth the ductus arteriosus closes and becomes the ligamentum arteriosum. Anatomy & Physiology II – The Heart 3  Myocardial thickness and function The atria walls are thin because they deliver blood to the ventricles. The wall of the left ventricle is thicker, because it must be strong enough to supply blood to all parts of the body, whereas the right ventricle is thinner than left because it supplies only the lungs. The fibrous skeleton of the heart forms the place for which the heart valves attach, serve as point of insertion for cardiac muscle bundles, prevents overstretching of the valves as blood passes through them, and acts as an electrical insulator that prevents direct spread of action potentials from the atria to the ventricles. Valves of the heart The heart valves direct the flow of blood through the heart in the proper direction. Valves open and close in response to pressure change as the heart contracts and relaxes. There are four valves within the heart. Right and left atrioventricular valves (tricuspid and mitral valves) When blood flowing from the atrium to the ventricle, the valve cusps open against the ventricular wall. When the ventricle contracts, the cusps are brought together by the increasing ventricular pressure, and the atrioventricular opening is closed. At the same time papillary muscle contract, putting tension on the chordae tendineae. The chordae tendineae pull on the cusps, preventing them from being forced upward into the atria. Otherwise, blood would flow backward from the ventricle into the atrium. Semilunar valves – prevent blood in the pulmonary artery and aorta from flowing back into the ventricles. The right semilunar valve is in the opening between the right ventricle and the pulmonary artery, and is called pulmonary semilunar valve. It allows oxygen- poor blood to enter the pulmonary artery on its way to lungs. The left semilunar valve is the aortic semilunar valve, which allows freshly oxygenated blood to enter the aorta from the left ventricle. Anatomy & Physiology II – The Heart 4  Route of Blood Flow Through the Heart 1. Deoxygenated blood enters the relaxed right atrium from the systemic circulation through the superior and inferior venae cavae and from the heart wall through the coronary sinus. 2. Most of the blood in the right atrium then passes into the relaxed right ventricle. The right atrium then contracts, pushing the remaining blood in the atrium into the right ventricle to complete right ventricular filling. 3. Contraction of the right ventricle pushes blood against the tricuspid valve, forcing it closed. Closing of the tricuspid valve prevents blood from moving back into the right atrium. Blood also pushes against the pulmonary semilunar valve, forcing it open. Blood then flows into the pulmonary trunk. 4. The pulmonary trunk branches to form the pulmonary arteries, which carry blood to the lungs, where CO2 is released and O2 is picked up. 5. Blood returning from the lungs enters the left atrium through the four pulmonary veins. 6. Most of the blood passes from the left atrium, through the bicuspid valve, into the relaxed left ventricle. Contraction of the left atrium completes left ventricular filling. 7. Contraction of the left ventricle pushes blood against the bicuspid valve, closing it and preventing blood from moving back into the left atrium. Blood is also pushed against the aortic semilunar valve, opening it and allowing blood to enter the aorta. 8. Blood flowing through the aorta is distributed to all parts of the body, except to the parts of the lungs supplied by the pulmonary blood vessels. Anatomy & Physiology II – The Heart 5  Systemic, Pulmonary, and Coronary Blood Circulation Systemic circulation involves the left side of the heart. It pumps the oxygenated blood from the lungs into the aorta and from there to the general systemic circulation. Pulmonary circulation involves the right side of the heart, in which it receives deoxygenated blood from the body through superior and inferior vena cava. Coronary circulation involves the heart vessels. The heart receives its blood supply from arterial branches that arise from the aorta. It delivers oxygenated blood and nutrients to and removes carbon dioxide and wastes from the myocardium. The two main coronary arteries are: Right coronary artery – exits from the aorta, supplies small branches to the right atrium and divides into: Posterior interventricular branch which supplies the walls of the two ventricles. Right marginal branch which supplies the myocardium of the right ventricle. Left coronary artery – passes inferior to left auricle and divides: Anterior interventricular branch / left anterior descending artery (LAD) – supplies blood to both ventricles. Circumflex branch – supplies left ventricle and left atrium. Coronary veins – most of the cardiac veins drain into the coronary sinus, a large vein located in the coronary sulcus on the posterior surface of the heart, and then into right atrium. The main coronary sinuses are: Great cardiac vein – located in the anterior interventricular sulcus and drains the anterior aspect of the left and right ventricles and left atrium. Middle (posterior) cardiac vein – located in the posterior interventricular sulcus and drains the posterior aspect of both ventricles. Small cardiac vein – drains right atrium and ventricle Posterior vein of the left ventricle - drains lateral wall of the left ventricle Oblique vein of the left atrium (vein of Marshall) – drains the posterior wall of the left atrium directly into coronary sinus Left marginal vein – drains lateral wall of the left ventricle Anterior cardiac veins – are three or four small vessels which collect blood from the front of the right ventricle and open into the right atrium Anatomy & Physiology II – The Heart 6  Cardiac Muscle Tissue Cardiac muscle cells (cardiomyocytes) are striated like skeletal muscle cells but with very different structural and functional activities. Cardiac muscle cells function as a single unit in response to physiological stimulation, rather than as a group of separate units as skeletal muscle does. Cardiomyocytes are relatively short, thick and branched cells. Through these branches, each cardiac cell contacts several others, so collectively they form a network throughout each pair of heart chambers. A cardiomyocyte usually has only one centrally located nucleus which often surrounded by glycogen. The sarcoplasmic reticulum is less developed than skeletal muscles. During excitation of the cell, they admit supplemental calcium ions from the extracellular fluid to activate muscle contraction. Mitochondria are larger and more numerous than skeletal muscle. The transverse tubules are wider but less abundant than those of skeletal muscles. Cardiac muscle cells are connected end-to-end by intercalated discs, in a complex step like structures with three distinctive features Interdigitating folds - the plasma membrane at the end of the cell is folded with interlock with adjoining cells and increase the surface area of intercellular contact. Mechanical junctions - cells are joined tightly with two types of junctions. Fascia adherence is a broad band which the action of thin myofilaments is anchored to the plasma membrane and each cell is linked o the next via transmembrane proteins. Desmosomes are patches of mechanical linkage between cells that prevent the contracting cardiomyocytes from pulling apart. Electrical junctions – they contain gap junction, which allow action potentials to be conducted from one cardiomyocyte to its neighboring cell. This allows the entire myocardium of the atria or the ventricles to contact as a single, coordinated unit which is essential for the effective pumping of a heart chambers. Physiological cardiomegaly vs. pathological cardiomegaly Anatomy & Physiology II – The Heart 7  Metabolism of Cardiac Muscle Cardiac muscle depends on aerobic respiration to make ATP. Cardiac muscle is more vulnerable to oxygen deficiency that it is to lack of any specific fuel. Because it makes little use of anaerobic fermentation or oxygen debt mechanism, it is not prone to fatigue. Cardiac muscle is rich in myoglobin (oxygen source), glycogen (stored energy) and large mitochondria. Cardiac Conduction System An important feature of cardiac muscle cells is self-excitability or autorhythmic action of the cells. They repeatedly generate spontaneous action potentials that produce heart contraction. These cells have two main functions: These cells act as a pacemaker by setting the rhythm of electrical excitation for the entire heart. They form the conduction system, which is a route for propagation of action potential through the heart muscle. The route is as follow: The electrical stimulation that starts the heartbeat and controls its rhythm originates in the superior wall of the right atrium, in a mass of specialized cardiac muscle tissue called sinoatrial node (SA node). The pacemaker activity causes the SA node to depolarize spontaneously at regular interval (70 to 80 times per minute). The SA node contacts adjacent atrial muscle cells, and causes them to be depolarized by conduction through the gap junctions of the intercalated discs. These atrial cells later cause their neighboring cells to start action potential. A wave of electrical activity spreads throughout the right atrium and then left atrium and causing the contraction of both atria, and blood is forced down into the ventricles. The wave of electrical activity reaches the atrioventricular node (AV node), which is located in the septum between the two atria. There is a delay at this junction to allow time for the atria to force blood into the ventricles. Cardiac muscle of the atrial wall contracts in response to the action potentials conducted through the atrial wall. Anatomy & Physiology II – The Heart 8  When the heart beats under resting conditions, approximately 0.04 second is required for action potentials to travel from the SA node to the AV node. Action potentials are propagated slowly through the AV node, compared with the remainder of the conducting system. The slow rate of action potential conduction in the AV node is due, in part, to the smaller-diameter muscle cells and fewer gap junctions in their intercalated disks. Like the other specialized conducting cells in the heart, they have fewer myofibrils than most cardiac muscle cells. As a consequence, a delay of 0.11 second occurs from the time action potentials reach the AV node until they pass to the AV bundle. The delay of action potentials at the AV node allows for completion of the atrial contraction before ventricular contraction begins. When the heart beats under resting conditions, approximately 0.04 second is required for action potentials to travel from the SA node to the AV node. Action potentials are propagated slowly through the AV node, compared with the remainder of the conducting system. The slow rate of action potential conduction in the AV node is due, in part, to the smaller-diameter muscle cells and fewer gap junctions in their intercalated disks. Like the other specialized conducting cells in the heart, they have fewer myofibrils than most cardiac muscle cells. As a consequence, a delay of 0.11 second occurs from the time action potentials reach the AV node until they pass to the AV bundle. The delay of action potentials at the AV node allows for completion of the atrial contraction before ventricular contraction begins. After action potentials pass from the AV node to the highly specialized conducting bundles, the velocity of conduction increases dramatically. The action potentials pass through the left and right bundle branches and through the individual Purkinje fibers that penetrate the myocardium of the ventricles. Because of the arrangement of the conducting system in the ventricles, the first part of the ventricular myocardium that is stimulated is the inner wall of the ventricles near the apex. Thus, ventricular contraction begins at the apex and progresses throughout the ventricles toward the base of the heart. The spiral arrangement of muscle layers in the wall of the heart results in a wringing action. During the process, the distance between the apex and the base of the heart decreases and blood is forced upward from the apex toward the great vessels at the base of the heart. Anatomy & Physiology II – The Heart 9  Autorhythmic Fibers Conduction System Pacemaker physiology Unlike skeletal muscles and neurons, SA node does not have a stable resting membrane potential. Their membrane potential starts at about -60 mV and moves upward, showing gradual depolarization called the pacemaker potential. This results primarily from a slow inflow of sodium without outflow of potassium. When pacemaker potential reaches a threshold of -40mV, voltage gated calcium channels open and calcium flows in from the extracellular fluid which produces depolarizing phase of action potential that peaks slightly above 0 mV. The, potassium channels open and potassium leaves the cell that makes the cytosol increasingly negative and creates a repolarizing phase of action potential. When repolarization is complete, the potassium channels close and pacemaker potential starts over, producing the next heartbeat. When SA node fires, it excites the other components in the conducting system, thus SA node is a pacemaker. Nerve impulses from autonomic nervous system and hormones (epinephrine) modify the timing and strength of each heartbeat, but they do not establish the fundamental rhythm. At rest, the release of acetylcholine from parasympathetic division of ANS slows SA node to about 0.8 second or 75 beats per minute. Although most cardiac muscle cells respond to action potentials produced by the SA node, some cells in the heart’s conducting system can also generate spontaneous action potentials. Example: an ectopic focus is any part of the heart other than the SA node that generate a heartbeat. If the SA node does not function properly, the part of the heart that can produce action potential at the next highest frequency is the AV node, which produces a heartbeat of 40-60 bpm. If there is blockage in the pathway between the SA node and other parts of the heart, then action potentials do not pass through the AV node. An ectopic focus can develop in an AV bundle, resulting in a heat rate of only 30 bpm. Also, injury to the heart muscles cells, inflammation, lack of adequate blood flow, and alteration in blood levels of potassium and calcium can change cardiac muscle membrane potential. Calcium channels blocker. Epinephrine and norepinephrine. Anatomy & Physiology II – The Heart 10  Action Potential & Contraction of Contractile Fibers Unlike action potentials in skeletal muscles (less than 2 ms), action potential in cardiac muscles last longer (200-500 ms), and the membrane channels are somewhat different. The longer action potentials in cardiac muscle can be divided into five phases. 1) Depolarization phase results from a large increase in the inward movement of sodium ions through voltage-gated fast Na+ channels, which causes the membrane potential to reverse from its resting potential of –90 mV to a potential of about +20 mV. The voltage change occurring during depolarization affects other ion channels in the plasma membrane. Several types of voltage-gated K+ channels exist, each of which opens and closes at different membrane potential, causing changes in membrane permeability to potassium. At rest, the movement of potassium establishes the resting membrane potential in cardiac muscle cells. Depolarization causes these voltage-gated potassium channels to close, thereby decreasing membrane permeability to potassium. Depolarization also causes voltage-gated calcium channels to begin to open. Compared with sodium channels, the calcium channels open and close slowly. 2) Early repolarization phase occurs when the voltage-gated sodium channels and some voltage- gated calcium channels close, and small number of voltage-gated potassium channels open. Sodium ions movement into the cell slows, and some potassium moves out of the cell. At this point, repolarization begins, but in cardiac muscle cells, early repolarization is slow due to the influx of calcium, resulting in a plateau phase. 3) Plateau phase is the period of maintained depolarization due to opening of voltage-gated slow calcium channels. This movement prevents the membrane potential from returning to its normal electrical potential of –90 mV. Plateau falls slightly because of some potassium (K+) leakage, but most potassium channels remain closed until end of plateau. 4) Repolarization phase occurs when potassium ion channels open, and calcium ion channel close, so that potassium ions move out of the cell, causing the inside of the cell to become more negative as the positive potassium ions move out. The increasing negative inside the cell returns the membrane to its normal –90 mV. 5) Refractory period - is the time interval during which a second contraction cannot be triggered. The refractory period of a cardiac muscle fiber lasts longer than the contraction. This long refractory period prevents tetanus (sustained contraction), which would stop the pumping action of the heart. Anatomy & Physiology II – The Heart 11  Electrocardiogram The rhythm of the heart, and the passage of electrical current generated, can be measured with an instrument called the electrocardiograph. The recording is called electrocardiogram (EKG or ECG). The electrocardiograph has electrodes, which when placed at certain points on the body that can detect electrical activity in the heart. The electrodes do not detect individual action potentials; rather, they detect a summation of all the action potentials transmitted by the cardiac muscle cells through the heart at a given time. Does not directly measure the mechanical events in the heart, and neither the force of contraction nor the blood pressure. For any chamber in the heart, the cardiac cycle can be divided into two phases. Systole refers to contraction of atria and ventricles Diastole refers to relaxation of atria and ventricles. Different electrical impulses during the cardiac cycle are recorded in an EKG as distinct deflection waves. P wave – it is caused by the electrical voltage generated by the passage of the impulse from SA node, through the muscle fibers of the atria and reaching the AV node. It represents atrial depolarization. Atrial systole – as both atria contract, action potential slows at AV node due to presence of smaller fibers. This produces a delay which allows ample time for atria to contract, and adds to ventricle volume before ventricles relaxation QRS complex – represents ventricular depolarization, in which action potential propagate along bundle branches, Purkinje fibers and the entire ventricular myocardium. Atrial diastole – or relaxation of the atria. The ventricles remain contracted, and the atria begin refilling with blood from the large veins. Ventricular systole – begins after the QRS and causes the contraction of ventricles, which allow ejection of blood toward the semilunar valves. T wave – represents ventricular repolarization, which occurs in the apex of heart. Ventricular diastole – begins after T wave and allows relaxation of ventricular contractile fibers. Anatomy & Physiology II – The Heart 12  Analysis of an EKG also involves measuring the time spans between wave, which are called intervals and segment P-Q interval – represents the conduction time from the beginning of atrial excitation to the beginning of ventricular excitation S-T segment – represents the time when the ventricular contractile fibers are depolarized during the plateau phase of action potential Q-T interval – represents the time from the beginning of ventricular depolarization to the end of ventricular repolarization. Basic Information Revealed By ECG Heart rate Heart rhythm Conduction efficiency Conduction velocity Mechanical performance of heart Plasma electrolyte imbalance Possible effect of drugs ECG useful in diagnosing Myocardial ischemia Ventricular hypertrophy Arrhythmia Cardiac Cycle The period between the start of one heartbeat and the beginning of the next represents a single cardiac cycle. The cardiac cycle therefore includes alternate periods of contraction and relaxation. The heart functions as a pump by contracting its chambers in order to generate the pressure that forces blood through the heart, into the blood vessels throughout the body, and back to the heart. The events that occur during a single cardiac cycle can be shown by measuring the pressures and pressure differences in the chambers of the heart and by measuring blood volume. The pressure and volume events of the cardiac can be divided into five steps. Atrial systole – the contraction force of the atria completes the emptying of blood (25 mL) out of the atria into the ventricles (105 mL). AV valves are open during this phase; the ventricles are relaxed (diastole) and filling with blood (130 mL). This blood volume is called the end-diastolic volume (EDV). It lasts about 0.1 second. Anatomy & Physiology II – The Heart 13  Isovolumetric contraction – during the brief period of isovolumetric contraction, which is (0.05 seconds) between the start of ventricular systole and the opening of the semilunar (SL) valves, ventricular volume remains constant (isovolumic). All four valves are closed (isovolumic), as the pressure increases rapidly within the ventricles, but no muscle shortening at this time (isometric). Ventricular ejection - the pressure in the ventricles continues to rise quickly, and when it exceeds that in the atria, the AV valves are forced to close. This closing of the AV valves produces the first heart sound. Pressure continues to rise, and when it exceeds that in the aorta, the SL valves open. Left ventricle pressure increase (120 mmHg) above the aortic pressure (80 mmHg). Causing opening of aortic valve. Pressure of right ventricle increase (25-30 mmHg) above the pulmonary valve (20 mmHg) and causing opening of the valve. Each ventricle ejects about 70 mL of blood into aorta and pulmonary trunk. The remaining volume of blood in the ventricles (60 mL) is called end-systolic volume (ESV) Stroke volume, the volume ejected per beat from each ventricle, equals end-diastolic volume minus end-systolic volume. Isovolumetric relaxation – ventricular diastole (relaxation) decreases the pressure of myocardium, which leads to decrease in pulmonic and aortic blood flow. Blood from the aorta and pulmonary trunk briefly flows backward through the semilunar valves. The backward flow, however; quickly fills the cusps and closes semilunar valves. Closure of aortic valve produces the dicrotic wave (incisura) which represents blood that has rebounded against the aortic valve.in this phase semilunar valves are closed, the AV valves have not yet opened, and the ventricle are therefore taking in no blood. Ventricular filling – because the ventricles are relaxing during ventricular diastole, their volume increase greatly. As a result, their pressure decrease below the atrial pressure, which allows opening of AV valves and beginning of ventricular filling. In a resting person, atrial systole lasts about 0.4 second; ventricular systole, 0.3 second; and the period when all four chambers are in diastole, 0.4 second. Total duration of cardiac cycle is therefore 0.8 second in a heart beating at 75 bpm. Volume change during cardiac cycle End-systolic volume left from the previous heartbeat 60 mL Passively added to the ventricle during atrial diastole + 30 mL Added by atrial systole + 40 mL Total: End-diastolic volume 130 mL Stroke volume ejected by ventricular systole - 70 mL Leaves: End-systolic volume 60 mL Each ventricle pumps out as much blood as it receives during diastole – 70 mL. Both ventricles eject the same amount of blood even though pressure in the right ventricle is only one-fifth the pressure in the left. Blood pressure in the pulmonary trunk is relatively low, so the right ventricle does not need to generate very much pressure to overcome it. Equal output by both ventricles is important to homeostasis. If the right ventricle pumps more blood into the lungs than the left ventricle can handle on return, blood accumulates in the lungs, causing pulmonary hypertension, and edam which leads to fluids in lungs and respiratory distress. Anatomy & Physiology II – The Heart 14  If the left ventricle pumps more blood than the right ventricle, blood accumulates in the systemic circulation, causing hypertension and systemic edema. Systemic edema is marked by liver enlargement, ascites, distension of jugular vein, selling of ankles, feet and fingers. Fluid accumulation in either circuit due to insufficiency of ventricular pumping is called congestive heart failure. Causes of CHF are myocardial infarction, chronic hypertension, valvular defects and congenital heart defects. Heart Sounds Detectable heart (valve) sounds are produced with each heartbeat. These sounds represent the auscultatory events of the cardiac cycle. There are four heart sounds associated with cardiac cycle, but only the first and second sounds (lubb and dupp) can be heard easily with a stethoscope. The first heart sound (S1) – occurs when the ventricles have been filled and AV valves are closed. The mitral valve closure is best heard in the apex of the heart at 5th intercostal space at the left midclavicular line, and the tricuspid valve closure is best heard at 5th intracostal space approximately underneath of sternum. It is described as a “lubb” sound. It is loud and longer than second sound. The second heart sound (S2) – is high pitch and lasts for only a short time. It is described as “dubb” sound. It is produced by closing of SL valves at the beginning of the ventricular diastole. Aortic semilunar valve sound is best heard at 2nd intercostal space to the right of the sternum, and pulmonic semilunar valve closure is best heard over the 2nd intercostal spec to the left of sternum. The third heart sound (S3) – a low- pitched sound produced during ventricular filling. It is best heard in the tricuspid area. The fourth heart sound (S4) – is caused by blood rushing into ventricles during atrial systole. It is best heard in the mitral area. Cardiac Output Cardiac output (CO) is the amount of blood pumped by either ventricle (not both) in one minute. It is expressed in liters per minutes. The quantity of blood ejected with each ventricular contraction (volume per beat) is called the stroke volume (SV). Anatomy & Physiology II – The Heart 15  The SV is the difference between the volume of the left ventricle at the end of diastole (filling) and its volume at the end of systole (empting). SV = End-Diastolic Volume – End-Systolic Volume Cardiac Output = Stroke Volume x Heart Rate CO = SV x HR Heart at rest pumps about 70 mL of blood with every beat. At average rate of 75 beats per minutes, the heart pumps more than 5.25 L a minutes, 315 L an hour, 7560 L a day, and 2,759,000 L a year. This number fluctuates as the HR increases during exercise. Cardiac reserve is the difference between the actual volume of blood pumped and the volume of blood pumped under stressful conditions. It measures the potential blood-pumping ability of the heart, while cardiac output measures the actual work done. Regulation of the Heart To maintain homeostasis, the amount blood pumped by the heart must vary dramatically, depending on the level of activity and the oxygen and nutrient needs of the body tissue. There are two types of regulatory mechanisms that control the cardiac output. Intrinsic regulation results from the heart’s normal functional characteristics and does not depend on either neural or hormonal regulation. Extrinsic regulation involves neural and hormonal control. Intrinsic regulation of the heart Three factors regulate stroke volume. These factors ensure that the left and right ventricles pump equal volumes of blood Preload – the degree of stretch in the heart before it contracts. According to the Frank-Starling law of the heart, a greater preload (stretch) on cardiac muscle fibers just before they contract increases their force of contraction during systole. So the preload is proportional to the volume of blood that fills the ventricles at the end of diastole end-diastolic volume (EDV). Normally, the greater the EDV, the more forceful the next contraction. The Frank-Starling law of the heart equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both the systemic and pulmonary circulations. Contractility – the forcefulness of contraction of individual ventricular muscle fibers at any given preload. Myocardial contractility is affected by positive and negative inotropic agents Positive inotropic agents promote calcium inflow, which strengthen the contraction. Example: stimulation of sympathetic division of ANS, hormones such as epinephrine and norepinephrine, and digitalis. Negative inotropic agents such as inhibition of sympathetic division of ANS, anoxia and acidosis, and increase potassium level have negative effects. Afterload – the pressure that must be exceeded, for ejection of blood to occur from the ventricles. Extrinsic regulation of the heart We know that cardiac output depends on both heart rate and stroke volume. So changes in heart rate are crucial in the short-term control of cardiac output and blood pressure. Increase in cardiac output during exercise to supply oxygen and nutrients Nervous system controls of the cardiovascular system originate in the cardiovascular center in the medulla oblongata. The effects of the ANS on the heart are strictly regulatory, speeding up or slowing down the heart rate, and are not essential for the heart to beat. Anatomy & Physiology II – The Heart 16  The sympathetic postganglionic fibers are adrenergic and release norepinephrine, which binds to beta-adrenergic fibers in the heart. This activates cyclic AMP which activates an enzyme that opens a calcium channel in the plasma membrane. The calcium inflow increases depolarization of SA node and contraction of the cardiocytes, so it speeds up the heart rate (tachycardia). Adrenergic stimulation can increase heart rate to as high as 230 bpm. This is limit set by the refractory period of the SA node, which prevents it from firing any faster. Cardiac output peaks at heart rate of 160 to 180 bpm. At rates any higher than this, the ventricles have too little time to fill between beats. At resting heart rate of 65 bpm, ventricular diastole last about 0.62 second, but at 200 bpm, it last 0.14 second. Thus, at excessive high heart rates, diastole is too brief to allow complete filling of the ventricles, therefore reduced stroke volume and cardiac output. The parasympathetic vagus nerves, by contrast, have cholinergic, inhibitory effects on the SA and AV nodes (bradycardia) Acetylcholine binds to muscarinic receptors and opens potassium gates in the nodal cells. As potassium exits the cells, they become hyperpolarized and fire less frequently, so the heart slows down. If all sympathetic and parasympathetic stimulation of the heart is blocked, or if the cardiac nerves are severed, the heart beats at a rate of about 100 bpm which is the natural firing rate of the SA node free of autonomic nervous system influence. With intact functional innervation, however; the resting heart rate is held down to about 70 to 80 bpm by vagal tone, a steady background firing rate of the vagus nerves. Extensive vagal stimulation can reduced the heart rate to as low as 20bpm or even stop the heart briefly. Heart rate under the influence of cardiac centers in the medulla. These centers can receive input from many other sources and integrate it into a decision as to whether the heart rate should beat faster or slower. Sensory and emotional stimuli can act on the cardiac centers by way of the cerebral cortex, limbic system and hypothalamus, therefore; heart rate can climb even as you anticipate running or exercising. It is also influenced by emotions such as love and anger. The medulla also receives input from receptors in the following tissues. Proprioceptors that are monitoring the position of limbs and muscles send an input which stimulates the quick rise in heart rate that occurs at the onset of physical activity. Chemoreceptors monitor chemical changes in the blood such as oxygen and carbon dioxide. Baroreceptors, which monitor stretching, caused by blood pressure in the major arteries and veins. Heart rate is also affected by hormones (epinephrine, norepinephrine, thyroid hormones), ions (sodium, potassium, and calcium), and other factors such as age, gender, physical fitness and temperature Anatomy & Physiology II – The Heart 17  Baroreceptor and Chemoreceptor Reflexes 1. Changes in blood pressure stimulate baroreceptors, which then communicate with control centers in the medulla oblongata. 2. Sensory neurons, which are primarily found in the glossopharyngeal (cranial nerve IX) and vagus (cranial nerve X) nerves, carry action potentials from the baroreceptors to an area in the medulla oblongata called the cardioregulatory center, where sensory action potentials are integrated.3 3. There are two parts to the cardioregulatory center: (1) the cardioacceleratory center increases heart rate, and (2) the cardioinhibitory center decreases heart rate. 4. Action potentials then travel from the cardioregulatory center to the heart through both the sympathetic and the parasympathetic divisions of the autonomic nervous system. 5. The cardioregulatory center influences the secretion of epinephrine and some norepinephrine from the adrenal medulla via sympathetic nerves. Epinephrine and norepinephrine increase heart rate and stroke volume. Heart Disorders Coronary Artery Disease is a constriction of the coronary arteries Arteriosclerosis is a general term for all types of arterial changes. It is best applied to degenerative changes in the small arteries and arterioles, commonly occurring in individuals over age of 50 and those with diabetes. Atherosclerosis is differentiated by the presence of plaques consisting of lipids, cells, fibrin and cell debris, often with attached thrombi, which form inside the walls of the large arteries. Angina pectoris – (chest pain) occurs when there is a deficit of oxygen to the heart muscle. Myocardial infarction – (heart attack) occurs when a coronary artery is totally obstructed, leading to prolonged ischemia and cell death, or infarct. Of the heart wall. Arrhythmia – (cardiac dysrhythmia) deviation from normal cardiac rate or rhythm may results from damage to the heart’s conduction system or systemic causes such as electrolyte abnormalities, fever, Anatomy & Physiology II – The Heart 18  hypoxia, stress, infection or drug toxicity. It also can be due to inflammation and scar tissue associated with rheumatic fever or myocardial infarction. Congestive heart failure – occurs when the heart is unable to pump sufficient blood to meet the metabolic needs of the body. CHF may results from a problem in the heart, such as infarction or a valve defect; it may arise from increased demands on the heat, such as those imposed by hypertension or lung disease, or it may involve a combination of factors. Depending on the cause, one side of the heart usually fails first, followed by the other side. Example: an infarction in the left ventricle or essential hypertension affects the left ventricle first, whereas pulmonary valve stenosis or pulmonary disease affects the right ventricle first. Congenital heart defects are structural defects in the heart that develop during the first 8 weeks of embryonic life. Septal defect is an opening in the septum that separates the interior of the heart into left and right side. Atrial septal defect vs ventricular septal defect. Coarctation of the aorta is a congenital condition in which a segment of the aorta is too narrow, and thus the flow of oxygenated blood to the body is reduced. Left ventricle is forced to pump harder, and high blood pressure develops. Valvular defect – malformations most commonly affect the aortic and pulmonary valves. Valve problems may be due to stenosis or narrowing of a valve, which restricts the forward flow or blood, or valvular incompetence which is a failure of a valve to close completely, allowing blood to regurgitate or lead backward. Valvular prolapse is a common occurrence. Teratology of Fallot is the most common cyanotic congenital heart condition which is a combination of four abnormalities. The infants are sometimes called “blue babies”. The four defects are: Pulmonary valve stenosis Ventricular septal defect Dextroposition of the aorta Right ventricular hypertrophy Anatomy & Physiology II – The Heart 19