WKC Anatomy and Physiology



PART 2: THE HEARTAnatomy of the Heart Location of the HeartThe heart is located in the mediastinum, the central compartment of the thoracic cavity (Figure 20.1).The heart is situated between the lungs in the mediastinum with about two-thirds of its mass to the left of the midline (Figure 20.1).The heart is not centered in the mediastinum; about two-thirds of the heart lies to the left of the midline. The cone-shaped heart has several surfaces:Apex: pointed end of the heart; lies anterior, inferior, and to the left of the midline.Base: broad portion of the heart; lies posterior, superior, and to the right of the apex.Anterior surface: deep to the anterior chest wall.Inferior surface: rests on the diaphragm.Right border: faces the right lung.Left border: faces the left lung.Clinical Connection - because the heart lies between two rigid structures, the vertebral column and the sternum, external compression on the chest can be used to force blood out of the heart and into the circulation.PericardiumThe heart is enclosed and held in place by the pericardium.The pericardium consists of an outer fibrous pericardium and an inner serous pericardium (Figure 20.2a).The fibrous pericardium is composed of dense irregular connective tissue. It:Anchors the heart to the diaphragmProtects the heartPrevent overfilling of the heartThe serous pericardium is composed of two layers of mesothelium.The outer parietal layer is fused to the fibrous pericardium.The inner visceral layer (epicardium) is fused to the surface of the heart.Between the parietal and visceral layers of the serous pericardium is the pericardial cavity, a potential space filled with pericardial fluid that reduces friction between the two membranes.Clinical Connection -Inflammation of the pericardium is known as pericarditis. Associated bleeding into the pericardial cavity compresses the heart (cardiac tamponade) and is potentially lethal.Layers of the Heart WallThe wall of the heart has three layers: epicardium, myocardium, and endocardium (Figure 20.2).The epicardium, or visceral layer of the serous pericardium, is the thin transparent outermost layer of the heart.The myocardium is composed of involuntary cardiac muscle fibers that swirl around the heart in interlacing bundles. The arrangement of the cardiac muscle fibers produces the strong, smooth, and unified pumping action of the heart. The endocardium consists of endothelium and connective tissue. It is continuous with the endothelium lining the large blood vessels attached to the heart and provides a smooth lining for the heart chambers and the valves.Chambers of the HeartThe 4 heart chambers include two superior atria and two inferior ventricles (Figure 20.3).The atria and ventricles are paired, forming two pumps.The right atrium and right ventricle pump blood to the lungs.The left atrium and left ventricle pump blood to the rest of the body.On the surface of the heart are the auricles and sulci.The auricles are small pouches on the anterior surface of each atrium that slightly increase the capacity of each atrium.The sulci are grooves that contain blood vessels and fat and separate the chambers.The deep coronary sulcus encircles most of the heart and separates the atria from the ventricles.The anterior interventricular sulcus separates the ventricles anteriorly.The posterior interventricular sulcus separates the ventricles posteriorly.Right AtriumThe right atrium forms the right border of the heart (Figures 20.3 - 20.5).It receives blood from 3 veins: superior vena cava, inferior vena cava and coronary sinus.Blood passes from the right atrium into the right ventricle through the tricuspid valve (right atrioventricular valve).In the interatrial septum separating the right and left atria is an oval depression, the fossa ovalis, which is the remnant of the foramen ovale.Clinical Connection - Atrial septal defects (ASDs) are due to incomplete closure of the foramen ovale and, while present in 15 – 25% of adults, are of no clinical significance. Large clinically significant ASDs allow oxygenated blood from the lungs to be shunted from the left atrium into the right atrium. Shunting causes enlargement of the right atrium and ventricle, as well as dilation of the pulmonary trunk and arteries.Right ventricleThe right ventricle forms most of the anterior surface of the heart (Figures 20.3 - 20.5).Blood passes from the right ventricle to the pulmonary trunk via the pulmonary semilunar valve.The right and left ventricles are separated from each other by the interventricular septum.Clinical Connection - Ventricular septal defects (VSDs) are the result of incomplete formation of the interventricular septum. VSDs account for 25% of all forms of congenital heart disease. Clinically significant VSDs allow oxygenated blood from the left ventricle to be shunted to the right ventricle, causing enlargement of the right ventricle, pulmonary trunk, and arteries and cardiac failure.Left AtriumThe left atrium forms most of the base of the heart (Figures 20.3 - 20.5).It receives oxygenated blood from the pulmonary veins.Blood passes from the left atrium to the left ventricle through the through the bicuspid valve (mitral valve; left atrioventricular valve).Left ventricleThe left ventricle forms the apex of the heart (Figures 20.3 - 20.5).Blood passes from the left ventricle through the aortic semilunar valve into the aorta.During fetal life the ductus arteriosus shunts blood from the pulmonary trunk into the aorta. At birth it closes and becomes the ligamentum arteriosum.Myocardial Thickness and FunctionThe four chambers’ myocardial thickness varies according to each chamber’s function (Figure 20.4c).Atrial walls are thinner than ventricular walls because the atria deliver “low pressure” blood a short distance to the ventricles.Ventricular walls are thicker than atrial walls because the ventricles pump blood under high pressure for great distances.The walls of the right ventricle are thinner than the left because they pump blood into the lungs, which are nearby and offer very little resistance to blood flow.The walls of the left ventricle are thicker because they pump blood through the body where the resistance to blood flow is greater.Note in Figure 20.4c that the right ventricle is “C”-shaped, while the left ventricle us “O”-shaped.Fibrous Skeleton of the HeartThe fibrous skeleton of the heart consists of four dense connective tissue rings located between the atria and ventricles (Figure 20.5).The functions of the fibrous skeleton are to:Form the foundation for which the heart valves attachServe as insertion points for cardiac musclePrevent overstretching of the valves as blood passes through themAct as an electrical insulator that prevents the direct spread of action potentials from the atria to the ventriclesHeart Valves and Circulation of BloodValves open and close in response to pressure changes as the heart contracts and relaxes.Operation of the Atrioventricular (AV) ValvesAtrioventricular (AV) valves prevent blood flow from the ventricles back into the atria (Figure 20.6).AV valves open when atrial pressure exceeds ventricular pressure.AV valves close when ventricular pressure exceeds atrial pressure.Back flow is prevented by the contraction of papillary muscles tightening the chordae tendinae which prevent the valve cusps from everting.Operation of the Semilunar (SL) ValvesThe semilunar (SL) valves allow ejection of blood from the heart into arteries but prevent back flow of blood into the ventricles (Figure 20.6).SL valves open when ventricular pressure exceeds aortic pressure.SL valves close when aortic pressure exceeds ventricular pressure.Clinical Connection - A Heart Murmur is an abnormal sound consisting of a flow noise heard before, between, or after the lubb-dupp or that may mask the normal sounds entirely. Some murmurs are caused by turbulent blood flow around valves due to abnormal anatomy or increased volume of flow. Not all murmurs are abnormal or symptomatic, but most indicate a valve disorder. Certain infectious diseases, such as rheumatic fever, can damage or destroy heart valves.Systemic and Pulmonary CirculationsThe left side of the heart is the pump for the systemic circulation. It pumps oxygenated blood from the lungs out into the vessels of the body.The right side of the heart is the pump for the pulmonary circulation. It receives deoxygenated blood from the body and sends it to the lungs for oxygenation.Figure 20.7 reviews the route of blood flow through the chambers and valves of the heart and the pulmonary and systemic circulations.Coronary CirculationThe flow of blood through the many vessels that pierce the myocardium of the heart is called the coronary (cardiac) circulation (Figure 20.8a); it delivers oxygenated blood and nutrients to and removes carbon dioxide and wastes from the myocardium.The principal arteries branching from the ascending aorta are the right and left coronary arteries.The principle veins terminating in the right atrium as the coronary sinus are the coronary veins.Coronary ArteriesThe left coronary artery supplies blood mostly to the left heart (Figure 20.8a).Its main branches are:Anterior interventricular branch (left anterior descending artery; LAD) supplies blood to the anterior walls of both ventricles.Circumflex artery supplies blood to the walls of the left ventricle and left atrium.The right coronary artery supplies blood mostly to the right heart (Figure 20.8a).Its main branches are:Atrial branches supply blood to the right atrium.Marginal branch supplies blood to the right ventricle.Posterior interventricular branch (posterior descending coronary artery), supplies the posterior walls of both ventricles.The myocardium contains many anastomoses, which provide alternate routes of blood flow (collateral circuits), which ensures adequate oxygenation of cardiac muscle.Coronary VeinsSuperficial to the coronary arteries are the coronary veins (Figure 20.8b). These veins deliver deoxygenated blood to the right atrium via the coronary sinus. The main vessels that drain into the coronary sinus are:Great cardiac vein in the anterior ventricular sulcus; drains areas of the heart supplied by the left coronary artery (left and right ventricles and left atrium)Middle cardiac vein in the posterior interventricular sulcus; drains areas supplied by the posterior interventricular branch of the right coronary artery (left and right ventricles)Small cardiac vein in the coronary sulcus; drains right atrium and right ventricleAnterior cardiac veins drain the right ventricle and open directly into the right atrium.Clinical Connection - Coronary artery disease (CAD), or coronary heart disease (CHD): a condition in which the heart muscle receives an inadequate amount of blood due to obstruction of its blood supply. It is the leading cause of death in Canada each year. The principal causes of obstruction include atherosclerosis, coronary artery spasm, or a clot in a coronary artery. Risk factors for development of CAD include high blood cholesterol levels, high blood pressure, cigarette smoking, obesity, diabetes, “type A” personality, and sedentary lifestyle. Partial obstruction of blood flow in the coronary arteries may cause myocardial ischemia. Ischemia usually causes hypoxia which may weaken cells without killing them. Angina pectoris is a severe pain that usually, but not always, accompanies myocardial ischemia. A complete obstruction to blood flow may result in myocardial infarction (MI), commonly called a heart attack. Infarction means death of an area of tissue because of an interrupted blood supply. The resulting damage may be so extensive that the individual may die.Clinical Connection - Atherosclerosis: a process in which smooth muscle cells proliferate and fatty substances, especially cholesterol and triglycerides (neutral fats), accumulate in the walls of the medium-sized and large arteries in response to certain stimuli, such as endothelial damage. Treatment options for CAD include drugs and coronary artery bypass grafting.Cardiac Muscle Tissue and the Cardiac Conduction SystemHistology of Cardiac Muscle TissueCompared to skeletal muscle fibers, cardiac muscle fibers are shorter in length, larger in diameter, branched, and have one nucleus (Figure 20.9).Cardiac muscles have the same arrangement of actin and myosin, and the same bands, zones, Z discs, and T tubules as skeletal muscles.They do have less sarcoplasmic reticulum than skeletal muscles and require Ca+2 from extracellular fluid for contraction.They do have more mitochondria than skeletal muscles because they depend on aerobic respiration to make ATP.Like skeletal muscle cells, cardiac muscle cells cannot divide. This explains why injured cardiac muscle tissue damaged cannot regenerate.Cardiac muscles form two separate functional networks in the heart: the atrial and the ventricular networks.Fibers within the networks are connected by intercalated discs, which consist of desmosomes and gap junctions.Desmosomes lock adjacent cell membranes together.Gap junctions allow ions to move from one cell to the next, which permits the spread of action potentials from one cardiac muscle cell to another.Intercalated discs allow the fibers in the network to work together so that each network serves as a functional unit.Autorhythmic Cells: The Conduction SystemCertain cardiac muscle cells are autorhythmic cells because they are self-excitable. They repeatedly and rhythmically generate spontaneous action potentials that then trigger heart contractions.These cells act as a pacemaker to set the rhythm for the entire heart.They form the conduction system, the route for propagating action potentials through the heart muscle.The pathway of cardiac action potentials through the conduction system is as follows (Figure 20.10):Action potentials arise spontaneously in the sinoartrial (SA) node, which is located in the right atrium just below the opening of the superior vena cava.Each SA node action potential spreads throughout both atria via gap junctions in the intercalated discs of atrial cardiac muscle cells.In other words, each action potential causes both atria to contract in unison.Action potentials reach the atrioventricular (AV) node (located in the interatrial septum just in front of the coronary sinus) by traveling through atrial muscle fibers.The velocity of the action potential slows considerably In the AV node because the pacemaker cells have a smaller diameter there.This gives the atria time to completely contract before ventricular contraction begins.The action potential leaves the AV node and enters the atrioventricular bundle (bundle of His), located in the interventricular septum.The AV bundle is the only electrical connection between the atria and the ventricles.The rest of the wall between the atria and ventricles is electrically insulated by the fibrous skeleton.The action potential travels along the AV bundle and enters the right and left bundle branches in the interventricular septum, where it travels towards the apex of the heart.Finally, the action potential is conducted through conduction myofibers (Purkinje fibers), first to the apex of the heart and then to the rest of the muscle fibers in both ventricles.Then, the ventricular muscle cells contract from apex to base, pushing blood upward towards the semilunar valves.In relation to atrial contraction, the ventricles contract 200 msec afterwards. When isolated from other controlling mechanisms, autorhythmic fibers in the SA node initiate action potentials 90-100 times per minute - faster than any other autorhythmic cell in the conduction system of the heart.As a result, action potentials from the SA node stimulate other areas of the conduction system before they are able to generate an action potential of their own.In other words, the SA node sets the pace (the fundamental rhythm) of the heart.Signals from the autonomic nervous system and hormones, such as epinephrine, do modify the timing and strength of each heartbeat, but they do not establish the fundamental rhythm.For example, the parasympathetic nervous system slows SA node pacing to about 75 action potentials per minute. This results in a heart rate of about 75 beats per minute.Clinical Connection - Artificial pacemakers stimulate heart muscle and provide a normal rhythm.Action Potential and Contraction of Contractile CellsAction potentials excite contractile cardiac muscle cells as follows (Figure 20.11):Depolarization.Contractile fibers have a resting membrane potential of –90 mV.When an action potential from neighboring cells brings the contractile cell to threshold, voltage-gated fast Na+ channels open and allow Na+ to flow into the cell, causing rapid depolarization.Within a few milliseconds, fast Na+ channels close and Na+ inflow decreases.Plateau.After rapid depolarization, some voltage gated K+ channels open and the cell begins to repolarize.But, the cell is prevented from repolarizing by the opening of voltage-gated slow Ca2+ channels in the sarcoplasmic reticulum and plasma membrane, which causes Ca2+ levels to rise in the cytoplasm.The influx of Ca2+ into the cytoplasm matches the efflux of K+ from the cell, causing the cardiac muscle cell to remain depolarized for much longer than a skeletal muscle cell (about 250 msec compared to about 1 msec).As in skeletal muscle fibers, depolarization results in contraction of cardiac muscle fibers.The maintained depolarization during the plateau produces the contraction force observed in cardiac muscle fibers.Repolarization.After about 250 msec, voltage-gated slow Ca2+ channels close and more voltage-gated K+ channels open, allowing positive charge (K+) to leave the cell, and causing it to repolarize.The refractory period of a cardiac muscle fiber (the time interval when a second contraction cannot be triggered) is longer than the contraction itself.Thus, tetanus (maintained contraction) cannot occur in cardiac muscle. Since the pumping action of the heart depends on alternating contraction and relaxation, preventing tetanus in cardiac muscle fibers is important. If heart muscle could undergo tetanus, its pumping action would cease, as would blood flow.ATP Production in Cardiac MuscleCardiac muscle relies on aerobic cellular respiration for ATP production (via fatty acid, glucose, and lactic acid metabolism)..Cardiac muscle also produces some ATP from creatine phosphate.Clinical Connection - The presence of creatine kinase (CK) in the blood indicates injury of cardiac muscle usually caused by a myocardial infarction.The ElectrocardiogramImpulse conduction through the heart generates electrical currents that can be detected at the surface of the body. A recording of the electrical changes that accompany each cardiac cycle (heartbeat) is called an electrocardiogram (ECG or EKG).A normal ECG consists of a P wave, QRS complex, and T wave (Figure 20.12 and 20.13).P wave. A small upward wave on the ECG; represents atrial depolarization, which spreads from the SA node to both atria. About 100 msec after the P wave begins, the atria contract.QRS complex. Begins as a downward deflection, continues as a large triangular shaped upward wave, and ends as a downward wave on the ECG. It represents ventricular depolarization. Shortly after the QRS complex begins, the ventricles begin to contract.T wave. Dome-shaped upward wave on the ECG; represents ventricular repolarization. Shortly after the T wave begins, the ventricles relax.Atrial repolarization cannot usually be visualized on the ECG because it is hidden within QRS.P-Q interval - time from the beginning of atrial excitation to the beginning of ventricular excitation.S-T segment - time when the ventricle is fully depolarized, during the plateau phase of the impulse.Clinical Connection - An ECG is an important tool used to diagnose problems in heart function because the size of the waves and lengths of the segments can provide diagnostic clues; for example, an enlarged Q wave or elevated S-T segment may indicate MI.Clinical Connection - A dysrhythmia (arrhythmia) is an abnormality or irregularity in the cardiac rhythm resulting from a disturbance in the conduction system of the heart, due either to faulty production of electrical impulses or to poor conduction of impulses as they pass through the system. There are many causes of dysrhythmia, including congenital defects of the conduction system, degenerative changes, ischemia and myocardial infarction, fluid and electrolyte imbalances, and the effects of drug ingestion. Dysrhythmias are not necessarily pathologic; they can occur in both healthy and diseased hearts. Dysrhythmias exert their harmful effects by interfering with the heart’s ability to pump blood. Examples of arrhythmias include:Heart block is a disorder of atrioventricular conduction. Disease and scarring can damage the conduction pathway between the SA and AV nodes, which can cause the ventricles to contract out of sync with the atria.Atrial flutter is a rapid atrial tachycardia with a rate that ranges from 240-450 beats per minute. Recall that an action potential spreads quickly throughout the atria, causes atrial contraction, and then dissipates. Atrial flutter is often the result of an action potential failing to dissipate and depolarizing the atria again.Fibrillation of the atria or ventricles is the result of chaotic current flow within the heart muscle and results in an irregular heart rate and rhythm. In ventricular fibrillation, the ventricle quivers but does not contract, which results in no cardiac output and no pulse.The Cardiac CycleA cardiac cycle is composed of all the events associated with one heartbeat.Two terms are used when describe events within the cardiac cycle:Systole, which means “contraction”.Diastole, which means “relaxation”.Pressure and Volume Changes during the Cardiac CycleIn a normal cardiac cycle, the two atria are in systole while the two ventricles are in diastole, and vice versa. At 75 beats per minute, each cardiac cycle lasts about 0.8 seconds. The cardiac cycle is divided into three phases:Atrial systoleVentricular SystoleRelaxation PeriodRefer to Figure 20.14 as you study the phases of the cardiac cycle.Atrial SystoleECG Connection: from P wave to Q wave (lasts for about 0.1 seconds)AV valves: openSL valves: closedDescription: Both atria contract simultaneously, causing the atrial pressure to increase.This forces blood through the AV valves and into the ventricles.The ventricles are relaxed and filling with blood (ventricular diastole).The SL valves are closed since the pressure in the ventricles is too low to force them open.At rest, atrial contraction contributes about 30% of the total volume of blood that fills the ventricles.Since the end of atrial systole is also the end of ventricular diastole, the total volume of blood that fills the ventricles at the end of atrial systole is called the end-diastolic volume (EDV; about 130 ml).During exercise, the atria contract with more force and more often, thus their contribution to EDV is greater.Ventricular SystoleVentricular systole lasts about 0.3 seconds and is divided into two periods: isovolumetric ventricular contraction and ventricular ejection.At the same time, the atria are relaxed and filling with blood (atrial diastole).Isovolumetric Contraction PeriodECG Connection: begins with R wave(lasts for about about 0.05 seconds)AV valves: closedSL valves: closedDescription: Both ventricles begin contracting, causing the ventricular pressure to increase.High ventricular pressure (relative to the atria) closes the AV valves (heard as “lubb”).The SL valves remain closed because the pressure in the ventricles is still too low to force them open.Because all heart valves are closed, the volume of the blood in the ventricles remains constant (isovolumetric).Ventricular EjectionECG Connection: from S wave to T wave (lasts for about about 0.25 seconds)AV valves: closedSL valves: openDescription: Both ventricles continue contracting, and ventricular pressure continues to increase.High ventricular pressure forces the SL valves open, and blood is ejected into the pulmonary trunk and the aorta.Like wringing out a wet rag, the ventricles wring the blood out, beginning at the apex and moving upward towards the base. This allows for the maximum volume of blood to be ejected – about 70ml per ventricle.At the end of ventricular systole about 60 ml of blood remains within each ventricle. This volume of blood is called the end-systolic volume (ESV).Stroke volume (SV) is the volume of blood ejected from each ventricle during systole. It is simple to compute if we know EDV and ESV:SV= EDV-ESVAt rest, EDV is about 130 ml and ESV is about 60 mlThus, SV =130 ml – 60 ml.Therefore, SV is about 70 ml.Relaxation PeriodThe duration of the relaxation period is variable; at rest, it lasts about 0.4 seconds. It is divided into two periods: isovolumetric ventricular relaxation and passive ventricular filling.During the relaxation period, both atria and ventricles are in diastole and are filling with blood.Isovolumetric Ventricular RelaxationECG Connection: begins at end of T waveAV valves: closedSL valves: closedDescription: Both ventricles begin to relax , and ventricular pressure begins to decrease to increase.Low ventricular pressure (relative to the pulmonary trunk and aorta) closes the SL valves (heard as “dupp”).The AV valves remain closed because the pressure in the ventricles is still too high to allow them to open.Because all heart valves are closed, no blood flows into the ventricles.Passive Ventricular FillingECG Connection: after T wave to next P waveAV valves: openSL valves: closedDescription: Both ventricles continue to relax , and ventricular pressure continues to decrease.As blood flows into the atria, atrial pressure increases until it exceeds ventricular pressure.This forces the AV valves open, and blood fills the ventricles.Passive ventricular filling is the main way the ventricles are filled, accounting for about 70% of filling. The remaining 30% comes from the next cardiac cycle, which beginning, again, with atrial systole.Some Final Points about the Cardiac CycleAs the body’s metabolic demands increase, the demands on the heart to deliver blood to body tissues increases as well.The heart meets these demands by increasing its rate and force of contraction.During the cardiac cycle (one heart beat), the durations of atrial and ventricular systole remain relatively unchanged regardless of changes in heart rate.Therefore, as heart rate increases, the length of each individual cardiac cycle decreases because the length of each relaxation period decreases.Cardiac OutputBody cells need specific amounts of oxygen each minute to maintain health and life. As they work harder they require greater amounts of oxygen, and thus more blood. Since the body’s need for oxygen varies with the level of activity, the heart’s ability to discharge oxygen-carrying blood must also be variable.Cardiac output (CO) is the volume of blood ejected from the ventricle into the aorta or pulmonary trunk each minute. Cardiac output equals the stroke volume, multiplied by the heart rate (# of beats/minute).CO = SV X HRAt rest CO = 70 ml/beat X 75 beats/minuteAt rest CO = 5.25 L / minuteAt rest, the volume of blood pumped by the heart each minute is approximately equal to total blood volume.During exercise, the volume of blood that the tissues require increases. Thus CO must increase.The body can change cardiac output by regulating either stroke volume or heart rate.Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and the cardiac output at rest. A cardiac reserve of 4 –5 times resting CO is average.This translates into a CO of 21 – 26 L of blood pumped by each ventricle per minute during maximal activity.Elite endurance athletes have a cardiac reserve of 7-8 times resting CO. This translates into a CO of 36 – 42 L of blood pumped by each ventricle per minute during maximal activity.People with severe heart disease may have little or no cardiac reserve. This limits their ability to carry out even the simplest activities associated with daily living.Regulation of Stroke VolumeThree factors regulate stroke volume:Preload, the degree of stretch on the heart before it contracts.Contractility, the forcefulness of contraction of individual ventricular muscle fibers.Afterload, the pressure that must be exceeded before ventricular ejection can occur.Preload: Effect of StretchingA greater preload (stretch) on cardiac muscle prior to contraction increases its force of contraction.Preload can be compared to the stretching of a rubber band; the more the rubber band is stretched, the more forcefully it will snap back.Within limits, the more the heart fills with blood during diastole, the greater the force of contraction during systole. This relationship is called the Frank-Starling Law of the Heart.Preload is proportional to EDV; normally, the greater the EDV, the more forceful the next contraction.Two factors determine preload:Duration of ventricular diastoleAs heart rate increases, the duration of diastole decreasesAs the duration of diastole decreases, filling time decreasesAs filling time decreases, EDV decreasesAs EDV decreases, preload decreasesAs preload decreases, the force of contraction decreasesVenous returnAs venous return increases, blood flow into the ventricles increasesAs more blood flows into the ventricles, EDV increasesAs EDV increases, preload increasesAs preload increases, the force of contraction increasesThis relationship between EDV and preload equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both the systemic and pulmonary circulations.If the left side of the heart pumps a little more blood than the right side, the volume of blood returning to the right ventricle (venous return) increases. The increased EDV causes the right ventricle to contract more forcefully on the next beat, bringing the two sides back into balance.ContractilityMyocardial contractility is the strength of contraction at any given preload.Any chemical that affects contractility is called an inotropic agent.Positive inotropic agents (e.g. epinephrine) increase contractility and SV.Often work by promoting Ca2+ inflowNegative inotropic agents (e.g. acetylcholine) decrease contractility and SV.Often work by inhibiting Ca2+ inflow (e.g. calcium channel blockers).The ANS and endocrine system affect myocardial contractility.The sympathetic nervous system and adrenal medulla of the endocrine system release epinephrine, which increases myocardial contractility.The parasympathetic system releases ACh, which decreases myocardial contractility.AfterloadAfterload is the pressure that the ventricles must overcome to open the SL valves.Anything that impedes blood flow can increase afterload (e.g. hypertension).If afterload increases, the ventricles spend more time in isovolumetric contraction and less time in ventricular ejection.Thus increased afterload decreases stroke volume and causes more blood to remain in the ventricles at the end of systole (increased ESV).Congestive Heart Failure – When Stroke Volume Regulation Breaks DownIn congestive heart failure (CHF), there is a loss of pumping efficiency by the heart.Causes of CHF include coronary artery disease, hypertension, myocardial infarction, and valvular defects.Let’s look at one cause, hypertension:Long-term hypertension increases the afterload, resulting in an increased ESV.Increased ESV gradually leads to increased EDV.Increased EDV increases preload.Initially, preload promotes increased force of contraction (Frank Starling’s Law)As preload increases further, the heart is overstretched and contracts less forcefully (decreased myocardial contractility)CHF is the result of a positive feedback loop: less effective pumping leads to even lower pumping capability.Often, one side of the heart starts to fail before the other.Right heart failure represents failure of the right heart to pump blood into the pulmonary circulation, and ultimately the lungs. Consequently, blood backs up in the systemic circulation, causing peripheral edema.Left heart failure represents failure of the left heart to pump blood into the systemic circulation. Consequently, blood backs up in the pulmonary circulation, causing pulmonary edema.Regulation of Heart RateRegulating heart rate is the body’s principal mechanism of short-term control over cardiac output.Several factors contribute to regulation of heart rate (Figure 20.16).The autonomic nervous system: sympathetic and parasympathetic divisionsChemicals: hormones and ionsOther factors such as age, gender, physical fitness, and body temperature.Autonomic Regulation of Heart RateNervous control of the cardiovascular system stems from the cardiovascular center in the medulla oblongata (Figure 20.16).Proprioceptors, baroreceptors, and chemoreceptors monitor factors that influence the heart rate.Sympathetic impulses increase heart rate and force of contraction.Parasympathetic impulses decrease heart rate but have little effect on contractility.Chemical Regulation of Heart RateThe adrenal medulla releases two hormones that affect heart rate: epinephrine and norepinephrine.Epinephrine and norepinephrine increase heart rate and contractility.Thyroid hormone also increases heart rate and myocardial contractility. One clinical sign of hyperthyroidism is an elevated resting heart rate (tachycardia).Ion concentrations (especially Na+, K+, Ca+2) also affect heart rate.Elevated blood levels of Na+ and K+ decrease heart rate and contractility.Elevated blood levels of Ca2+ increase heart rate and contractility.Other Factors in Heart Rate RegulationOther factors such as age, gender, physical fitness, and temperature affect heart rate:The very young have an elevated resting heart rate that declines with age. Senior citizen often develop an elevated heart rate.Adult females tend to have a slightly higher resting heart rate than adult males.Regular exercise tends to decrease the resting heart rates of both sexes. A physically fit person may exhibit a heart rate below 60 beats per minute (bradycardia).Increased body temperature (e.g. during a high fever or during strenuous exercise; hyperthermia) can raise heart rate. Decreased body temperature (hypothermia) can lower heart rate.For a review of all of the factors that increase cardiac output, see Figure 20.17 ................
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