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HLTAP401A The Heart The Heart Martini Chapter 20 Heart Anatomy Approximately the size of your fist Location Superior surface of diaphragm Left of the midline Anterior to the vertebral column, posterior to the sternum 3 Position in Thorax Base: Where the Great Vessels enter and exit Apex: points inferiorly, anteriorly and to the left 4 Position in Thorax Base Normal chest X-Ray Apex 5 Position of Heart Hint: Nipples are at the 4th intercostal space Apex at 5th intercostal space during ventricular systole (contraction) Point of Maximum Impulse: PMI is the apex on surface anatomy 6 Pericardium Pericardium: a double-walled sac around the heart A superficial fibrous pericardium A deep two-layer serous pericardium The parietal layer lines the internal surface of the fibrous pericardium The visceral layer or epicardium lines the surface of the heart They are separated by the fluid-filled pericardial cavity 7 Pericardial Layers of the Heart Outer balloon wall: superficial fibrous pericardium, the inside is lined by the parietal layer of the serous pericardium Air: The Pericardial cavity which contains the pericardial fluid Inner balloon wall is the visceral layer of the serous pericardium Figure 18.2 8 Pericardium: 3 Layers Visceral Pericardium touches the heart (aka: epicardium) Parietal Pericardium Pericardial Fluid is between the two layers Parietal Pericardium Parietal Pericardium: Lines the internal surface of the outer layer of fibrous dense connective tissue 9 Pericardium Visceral Pericardium: Appears as a shiny surface Parietal Pericardium: Inside the sack around the heart 10 Layers of the Heart Myocardium: Heart muscle is thickest in the left ventricle because this area of the heart needs to generate the most force. (Think about where blood in this chamber is going) Endocardium: simple squamous epithelium lines the chambers of the heart 11 Medical Examples Pericarditis: Inflammation of the pericardium Pericardial Tampanade: Compression of the heart caused by blood or fluid accumulation in the space between the heart and the fibrous pericardium 12 Cardiac tamponade radiographics.rsna.org/.../g07nv13g04x.jpeg www.beliefnet.com 13 Heart Wall – 3 layers Epicardium: Visceral layer of the serous pericardium on the outside Exposed layer of simple squamous epithelium underlain by loose connective tissue Myocardium: Cardiac muscle layer Contains blood vessels and nerves Fibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissue that provides the origins and insertions for the cardiac muscle cells 14 Heart Wall Endocardium: Endothelial layer of the inner myocardial surface (the chambers) Simple squamous epithelium Is continuous with the endothelial lining of the blood vessels 15 Heart Wall 16 Great Vessels of the Heart Vessels returning blood to the heart include: Superior and inferior venae cavae Right and left pulmonary veins Vessels conveying blood away from the heart include: Pulmonary trunk, which splits into right and left pulmonary arteries Ascending aorta, which curves into the aortic arch that has three vessels branching from it – brachiocephalic, left common carotid, and subclavian arteries 17 Great Vessels of the Heart Superior Vena Cava Right Pulmonary Artery Pulmonary Artery Trunk Aortic Arch Ascending Aorta Left Pulmonary Artery Inferior Vena Cava 18 Ascending Aorta Coronary Artery The coronary arteries are the only vessels that branch off the Ascending Aorta 19 Aortic Arch Right Common Carotid Artery Left Common Carotid Artery Right Subclavian Artery Brachiocephalic Trunk Left Subclavian Artery Aortic Arch Right Pulmonary Artery Left Pulmonary A. 20 Right Common Carotid Artery Left Common Carotid Artery (2) Right Subclavian Artery Brachiocephalic Trunk (1) 1 2 3 Aortic Arch Left Subclavian Artery (3) 21 Chambers of the Heart: External Left Atrium Right Atrium Right Ventricle Left Ventricle 22 Outer Surface Landmarks Left Ventricle Superior & Inferior Vena Cava enter the Right Atrium Right Ventricle connects with the pulmonary trunk Left Ventricle connects with the Aorta, it fits behind the pulmonary trunk 23 Heart Chambers 24 Double Pump The basic job of the heart is to pump blood. Blood is actually pumped through 2 separate circuits. Pulmonary circuit: Runs between the heart and the gas exchange surfaces of the lungs. Right ventricle-pulmonary arteries-pulmonary capillaries-pulmonary veins-left atrium Systemic Circuit: Runs between the heart and the tissues of the rest of the body. Left ventricle-aorta-arteries-capillaries-veinsvena cava or coronary sinus-right ventricle. 25 26 Atria of the Heart Atria are the receiving chambers of the heart They are superior and mostly posterior to the ventricles Each atrium has a protruding auricle which slightly increases its volume Blood enters right atria from superior and inferior venae cavae and coronary sinus Blood enters left atria from pulmonary veins 27 Atria of the Heart The right atrium receives deoxygenated blood from the systemic circuit and passes it into the right ventricle, which discharges it into the pulmonary circuit. The left atrium receives oxygenated blood from the pulmonary circuit and passes it into the left ventricle, which discharges it into the systemic circuit. 28 Atria of the Heart Atria have thin, flaccid walls corresponding to their light workload. Serve as receptacles for the blood returning from the systemic and pulmonary circuits. Most of this blood flows into the ventricles due to gravity. The right and left atrium are separated by the interatrial septum. 29 Ventricles of the Heart Ventricles are the discharging chambers of the heart Papillary muscles and trabeculae carneae (create the waffle pattern) muscles mark ventricular walls Right ventricle pumps blood into the pulmonary trunk Left ventricle pumps blood into the aorta 30 Ventricles of the Heart Interventricular septum: Separates the left and right ventricles. The left ventricle is 2-4x as thick as the right ventricle LV has a greater workload (The LV and RV pump EQUAL amounts of blood, but the LV has to pump it against greater resistance) 31 Consist of 2-3 flaps of connective tissue covered by endothelium Valves 32 Right Side of Heart Tricuspid: Between Right Atrium and Right Ventricle Pulmonic Semilunar: Between Right Ventricle and Pulmonary Trunk Valves Left Side of Heart Mitral: Between Left Atrium and Left Ventricle Aortic Valve: Between Left Ventricle and Aorta Chordae Tendineae are only on the Tricuspid and Mitral Valves (valves between atrium and ventricle) 33 AV Heart Valves Heart valves ensure one-way blood flow through the heart Atrioventricular (AV) valves lie between the atria and the ventricles Right: Tricuspid Valve Left: Mitral Valve AV valves prevent backflow into the atria when ventricles contract 34 AV Heart Valves Chordae tendineae anchor AV valves to papillary muscles Made of strings of collagen Prevent valve flaps from flipping upward into the atria 35 Tricuspid Valve: Between RA & RV The leaflets are thin and delicate, and have thin chordae tendineae that attach the leaflet margins to the papillary muscles of the ventricular wall below. 36 AV Valves: Tricuspid & Mitral When the ventricles contract they are pressed closed from the ventricular side. 37 AV Valves: Tricuspid & Mitral When the heart is relaxed the flaps hang open. 38 AV Valves Figure 18.8c, 39 d Semilunar Heart Valves Aortic semilunar valve lies between the left ventricle and the aorta Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk Semilunar valves prevent backflow of blood into the ventricles 40 Semilunar Heart Valves When the ventricle contracts blood is pushed against the AV valve and blood is expelled through the SL valve into the artery 41 Semilunar Heart Valves When the ventricle relaxes blood pressure is higher in the vessels, which closes the valve. 42 Pathway of Blood Through the Heart and Lungs Superior & Inferior Vena Cava - Right atrium tricuspid valve right ventricle pulmonary semi lunar valve pulmonary trunk pulmonary arteries lungs Lungs pulmonary veins left atrium mitral valve left ventricle aortic semilunar valve aorta systemic circulation 43 44 45 Pathway of Blood Through the Heart and Lungs Figure4618.5 Blood Flow Through the Heart 1. Right Atrium Blood arrives at the heart from the body (systemic circuit) Blood from the systemic circuit is high in carbon dioxide and low in oxygen and will arrive in the right atrium from 3 vessels. Superior vena cava: Drains head, torso, and upper arms. Inferior vena cava: Drains abdomen, pelvis, and legs. Coronary sinus: Drains the coronary circulation. 47 Blood Flow Through the Heart 2. Right Ventricle From the right atrium, blood passes the tricuspid valve and enters the right ventricle Blood leaves from the right ventricle and enters the pulmonary trunk to begin the pulmonary circuit. 48 Blood Flow Through the Heart 3. Pulmonary Circuit The pulmonary trunk splits into the right and left pulmonary arteries. Arteries branch into capillaries in the lungs The capillary beds are the place where O2 and CO2 are exchanged. Capillaries lead to the pulmonary veins (the blood is now oxygen rich) Pulmonary veins lead back to the heart with oxygenated blood 49 50 Blood Flow Through the Heart 4. Left Atrium Blood arrives at the left atrium from the 4 pulmonary veins: right superior, right inferior, left superior, and left inferior pulmonary veins Left Atrium Posterior View 51 Blood Flow Through the Heart 4. Left Ventricle From the left atrium, blood passes the mitral valve and enters the left ventricle Blood leaves the left ventricle and enters the aorta to begin the systemic circuit. 52 Blood Flow Through the Heart 4. Systemic Circuit The aorta branches into arteries Arteries lead into capillaries Capillaries in the body exchange O2 and CO2 Oxygen poor blood then enters veins Veins converge into the inferior and superior vena cava 53 54 Coronary Circulation Coronary circulation is the functional blood supply to the heart muscle itself Collateral routes ensure blood delivery to heart even if major vessels are occluded These are the vessels that get blocked during a heart attack 55 Coronary Circulation: Arterial Supply Posterior descending Left anterior descending (LAD) artery (PDA) 56 Coronary Circulation: Venous Return •20% drains directly into right ventricle •80% returns to right atrium 57 Figure 18.7b Coronary Blood Flow When the heart relaxes high pressure of blood in aorta pushes blood into coronary vessels Reduced during ventricular contraction Increased during ventricular relaxation Blood flows into coronary arteries during ventricular diastole 58 Coronary Artery Disease (CAD) Heart muscle receiving insufficient blood supply Narrowing of vessels: atherosclerosis, artery spasm or clot Atherosclerosis: smooth muscle proliferation & fatty deposits in walls of arteries Treatment Drugs, bypass graft, angioplasty, stent 59 Clinical Problems: CAD MI: Myocardial infarction Death of area of heart muscle from lack of O2 Replaced with scar tissue Results depend on size & location of damage Blood clot Use clot dissolving drugs streptokinase or t-PA & heparin Balloon angioplasty Angina pectoris: heart pain from ischemia of cardiac muscle 60 Coronary Artery Bypass Graft (CABG) 61 Angioplasty Thread a catheter through the arteries (like a maze) – usually the femoral artery Once in position, blow up the balloon to push open the blockage 62 Stent in an Artery Same situation as angioplasty, but you put in this stent to keep it open. 63 Cardiac Physiology Major concepts: 1. 2. 3. 4. 5. Contraction physiology Electrical system Cardiac cycle Cardiac output Health issues Microscopic Anatomy of Heart Muscle Cardiac muscle is striated, short, fat, branched, and interconnected The connective tissue endomysium acts as both tendon and insertion Intercalated discs anchor cardiac cells together and allow free passage of ions Heart muscle behaves as a functional syncytium 65 Functional Syncytium The thousands of cardiac muscle cells behave as if they were one giant cell. All Cells are connected electrically and mechanically. This allows the heart to beat in an organized fashion Scar tissue from a heart attack interrupts the functional syncytium and causes fibrillation (we will examine this issue more later) 66 Microscopic Anatomy of Heart Muscle 67 Figure 18.11 Cardiac Muscle Histology Branching cells Once central nucleus Intercalated disc: contains many gap junctions connecting the adjacent cell cytoplasm, creates a functional syncytium 68 Cardiac Muscle Metabolism Aerobic respiration Minimal anaerobic respiration Rich in myoglobin and glycogen Large mitochondria Organic fuels: fatty acids, glucose, ketones Fatigue resistant 69 Physiology of Contraction Compare to skeletal muscle 70 Physiology of Contraction: Depolarization Myocytes have stable resting potential of -90 mV Depolarization (very brief) Stimulus opens voltage regulated Na+ gates, (Na+ rushes in) membrane depolarizes rapidly Excitation spreads through gap junctions Fast Na+ channels open for rapid depolarization Action potential peaks at +30 mV Na+ gates close quickly Ca+2 rushes into cytoplasm from SR and extracellular fluid and binds to troponin to allow for actin-myosin cross-bridge formation & tension development 71 Physiology of Contraction: Plateau Phase & Repolarization Plateau phase Period of maintained depolarization 250 msec (only 1msec in neuron) Slow Ca+2 channels open, let Ca+2 enter from outside cell and from storage in sarcoplasmic reticulum Repolarization Ca+2 channels close and K+ channels open Rapid K+ out returns to resting potential of -90mv 72 Physiology of Contraction Refractory period (from plateau to beginning of repolarization Very long so heart can fill Absolute refractory period continues until relaxation has started (200 msec)(relative refractory is another 50 msec) Tetanus (continuous contraction) and wave summation cannot happen • Why is this a good thing??? Skeletal muscle refractory period 0.4 to 1 msec • Ends before peak tension develops so tetanus can occur 73 Action Potential in Cardiac Muscle Absolute refractory period Changes in cell membrane permeability. 74 Terminology An inotrope is an agent which increases or decreases the force or energy of muscular contractions. A Chronotropic effects are those that change the heart rate 75 Medical Example: Calcium Channel Blockers Keep in mind, there are many different types of CCB, they can work on arterial smooth muscle, cardiac contractile cells or the electrical system The negative inotropic (decrease force of contraction) effect is due to reduced inward movement of Ca++ during the action potential plateau phase Good for patients with HTN We will see later how contractility effects cardiac output 76 Cardiac Physiology Cardiac Electrical System Cardiac Myocytes 99% are the contractile cardiac muscle cells. Generate the force that pumps blood through the systemic and pulmonary circuits. 1% are the autorhythmic cells of the heart Lack the elaborate sarcomeres and other contractile machinery 78 Autorhythmic Cells Autorhythmic cells have the ability to spontaneously depolarize to threshold and generate action potentials These cells set the rhythm of the heart without any input from any external organs, tissues, or signals. (Keep in mind, the ANS does modify the rate and strength of contraction, this is just the baseline rhythm) 79 Spontaneous Depolarization These cells are characterized as having no true resting potential because they generate regular, spontaneous action potentials. Depolarizes because Ca2+ leaks in without help from neural stimulation Contrast to voltage gated Na+ channels in muscle and neurons that must be activated SA node depolarizes 100 times per minute AV node depolarizes 40-60 times per minute All other pacemaker cells: 20-35 times per minute 80 Autorhythmic Cells Sinoatrial Node (SA node) - Adjacent to the SVC opening in the right atrium. Atrioventricular Node (AV node) - Near the right AV valve at the bottom of the interatrial septum. Atrioventricular Bundle (AV bundle or Bundle of His) - Inferior interatrial septum. Left & Right Bundle Branches Interventricular septum. Purkinje Fibers - Distributed throughout the right and left ventricle. 81 82 Sinoatrial Node (SA Node) Pacemaker of the heart because they have the fastest rate of depolarization Depolarization begins in the SA node travels throughout the atria to all the contractile cells as well as to the cells in the AV node. The atrial contractile cells will respond to the depolarization by contracting. 83 84 The purple corresponds to the path of the electrical impulse and the wave of contraction 85 At this point the atria are contracting and the electrical impulse is traveling through the interventricular septum 86 Atrioventricular Node (AV node) At the AV node, the impulse is delayed momentarily to allow the atria to complete their contraction before the ventricles begin to contract. This delay is due to the smaller diameter of the fibers Takes about 50 msec From the AV node, the impulse travels to the AV bundle. 87 AV Bundle The AV bundle is the only electrical connection between the atria and the ventricles. The position ensures that the electrical signal goes down the septum before going to the myocardium This causes the ventricles begin contracting at the septum then the bottom (the apex) rather than the top. 88 AV Bundle Bundle Branches 89 Bundle Branches & Purkinje Fibers The impulse travels on to the left and right bundle branches and then onward to the purkinje fibers The Purkinje fibers direct the wave of depolarization through the myocardium so it can start contracting Depolarization travels to the ventricular contractile cells via the gap junctions in the intercalated discs. The ventricular contractile cells respond by contracting. 90 91 Summary – conduction system 1. 2. 3. 4. Sino-atrial node Atrio-ventricular node AV bundle (Bundle of His) Perkinje fibres. Atrial contract Ventricle contract 92 Medical Example: Calcium Channel Blockers (Again) Negative chronotropic effects (slow rate) are also seen with some of the Ca++ channel blockers Decrease the rate of recovery of the slow channel in AV conduction system and SA node, and therefore act directly to depress SA node pacemaker activity and slow conduction These ones are good for patients with HTN and arrhythmias ? Why would you choose this type of drug over a BBlocker to slow the rate? 93 Extrinsic Influences on Heart Rate The autonomic nervous system provides a large influence on the activity of the heart. Sympathetic nervous system increases both the rate and the force of heartbeat The cardio-acceleratory center of the medulla is the source of the sympathetic output to the heart. Sympathetic nerve fibers project to the SA node, AV node, and the bulk of the myocardium 94 Extrinsic Influences on Heart Rate Parasympathetic nervous system decreases heart rate but has little effect on the force of contraction. The cardio-inhibitory center of the medulla is the source of the parasympathetic output to the heart the vagus nerve (CN X) to the SA and AV nodes. Dominant during rest Endocrine system plays a role as various hormones (e.g., epinephrine, thyroid hormone) can exert an effect on the heart's rhythm. 95 96 Conduction Problems Arrhythmia: An irregular heart rhythm. Fibrillation: A condition of rapid and out-of-phase contractions. In ventricular fibrillation, the depolarization and contraction of the ventricular muscle cells is not coordinated. Without a coordinated contraction as a unit, the ventricles cannot generate enough force to propel blood through the arterial system. This is the one they shock you for! 97 Cardiac Physiology Cardiac Cycle The Cardiac Cycle Cardiac cycle: Everything that occurs between the start of one heartbeat and the beginning of the next. For any one chamber in the heart, the cardiac cycle can be divided into 2 phases: Systole = contraction. Diastole = relaxation. Blood will only flow from point A to point B if the pressure at point A is greater than at point B. 99 The Cardiac Cycle The cardiac cycle can be broken down into 4 phases: Ventricular Filling Isovolumetric Contraction Ventricular Ejection Isovolumetric Relaxation. 100 1. Ventricular Filling AV valves are open Tricuspid and mitral (inflow from atria to ventricles) Semilunar valves are closed Aortic and pulmonary (outflow from ventricles) Atrial pressure exceeds ventricular pressure Both the atria and the ventricles are in diastole About 70% of the blood enters the ventricle passively 101 1. Ventricular Filling Towards the end of ventricular filling, the SA node will depolarize. The resulting atrial depolarization will cause atrial systole. The contraction of the atria completes the filling of the ventricles (final 30%). The final ventricular volume (achieved just prior to the beginning of ventricular systole) is known as the end diastolic volume (EDV) and is typically about 130mL. 102 2. Isovolumetric Contraction The atria repolarize and remain in diastole for the rest of the cardiac cycle. Meanwhile, the ventricles depolarize and begin to contract. Blood surges upward and the AV valves are forced shut This causes the first of the 2 heart sounds (S1) that can be auscultated with a stethoscope (phonetically it's given as LUB). 103 2. Isovolumetric Contraction After the AV valves are closed, the heart continues to contract as it tries to generate enough pressure to open the semilunar valves. During this time, the ventricular pressure is rising (because the ventricles are contracting) but the ventricular volume is not changing. Thus this period is known as isovolumetric contraction. 104 3. Ventricular Ejection Ejection of blood begins when ventricular pressure exceeds arterial pressure About 120mmHg in the left ventricle and 25mmHg in the right ventricle. Blood spurts out of each ventricle rapidly at first and then more slowly. It's important to note that the ventricles do NOT expel all their blood. The amount ejected (typically about 70mL) is known as the stroke volume. The blood remaining in the ventricles is known as the end systolic volume. ESV is typically about 60mL. 105 Stroke Volume Stroke Volume= End Diastolic Volume - End Systolic Volume The stroke volume of the left ventricle must equal the stroke volume of the right ventricle. 106 Right sided failure Left sided failure 107 4. Isovolumetric Relaxation The ventricles now repolarize and enter diastole. The ventricles begin to relax. Pretty quickly, the pressure in the aorta and pulmonary trunk exceeds ventricular pressure and the semilunar valves shut (this causes the 2nd heart sound (S2) the DUP). 108 4. Isovolumetric Relaxation However, it takes a lot longer for ventricular pressure to drop below atrial pressure. Remember, the blood will only flow from a higher pressure area to a lower pressure area Before this happens, the ventricles are relaxing and pressure is dropping, but the volume is not changing - thus we have isovolumetric relaxation. When ventricular pressure does drop below atrial pressure, the AV valves open and ventricular filling begins anew 109 110 111 Cardiac Cycle Summary Atrial contraction begins Atria ejects remaining 30% of blood into ventricles (S4) Atrial systole ends, AV valves close (S1) Isovolumetric ventricular contraction Ventricular ejection occurs Semilunar valves close (S2) Isovolumetric relaxation occurs AV valves open, rapid ventricular filling (70%) (passive: this is atrial diastole) (S3) Repeat …. (keep in mind, there is a constant flow of blood into the atria) 112 Cardiac Physiology Cardiac Output Cardiac Output Cardiac Output is the volume of blood ejected by each ventricle in one minute Stroke Volume(mL/beat) x Heart Rate(beats/minute) = Cardiac Output(mL/minute) Cardiac output varies with the body's state of activity. For example, cardiac output increases during exercise. 114 Example Suppose Bob's heart rate was 1 beat per second. His EDV was 140mL and his ESV was 60mL. What was his cardiac output? Heart Rate = (1 beat/second) x (60 seconds/minute) = 60 beats/minute SV = EDV - ESV = 140 mL/beat - 60 mL/beat = 80mL/beat CO = SV x HR = 80ml/beat x 60 beats/minute = 4800 mL/minute 115 Cardiac output will vary directly with both heart rate and stroke volume 116 Factors Affecting Stroke Volume Stroke volume is primarily governed by 3 factors: Preload: The amount of tension in the ventricular myocardium just prior to contraction Contractility: The contraction force at any given preload Afterload: The blood pressure just outside the semilunar valves (in the aorta and pulmonary trunk). 117 Preload Amount of tension in ventricular myocardium before it contracts ↑ preload causes ↑ contraction strength exercise ↑ venous return, stretches myocardium (↑ preload) , myocytes generate more tension during contraction, ↑ CO matches ↑ venous return Frank-Starling law of heart: Stroke volume is proportional to EDV The more the heart fills during diastole, the greater the force of contraction during systole (within limits) 118 Contractility Contraction force for a given preload Tension caused by factors that adjust myocyte’s responsiveness to stimulation Factors that ↑ contractility are positive inotropic agents NE, hypercalcemia, catecholamines, glucagon, digitalis Factors that ↓ contractility are negative inotropic agents Hyperkalemia (K+), hypocalcemia, hypoxia, hypercapnia 119 Afterload Pressure in arteries above semilunar valves opposes opening of valves Basically, this is the pressure in the aorta or pulmonary arteries that the heart needs to work against ↑ Afterload ↓ SV any impedance in arterial circulation ↑ afterload Continuous ↑ in afterload (lung disease, atherosclerosis, etc.) causes hypertrophy of myocardium, may lead it to weaken and fail 120 Cardiac Physiology Health Issues Valvular Pathologies Murmur: Abnormal heart sound due to turbulent blood flow. Not always pathologic Prolapse: Malfunction where one or more valve flaps bulge backward. (valves are leaky) Blood goes back from where it came (backflow) because the door is left open Example Mitral valve prolapse: blood goes back to the left atrium and can congest the lungs 122 Valvular Pathologies Stenosis: Narrowing of the opening of a valve often caused by the stiffening of valve cusps due to scar tissue formation. Greater force is needed to push blood through Mitral valve stenosis can cause ↑ left atrial pressure, which leads to ↑ pulmonary venous pressure → pulmonary edema Aortic stenosis, get left ventricular hypertrophy and/or pulmonary edema 123 Medical Example Lowering arterial resistance (blood pressure) will decrease cardiac afterload Some calcium channel blockers: Decreased intracellular Ca++ in arterial smooth muscle results in relaxation (vasodilatation) Little or no effect on venous beds (no effect on cardiac preload Alpha blockers: decrease sympathetic vasoconstriction in arteries Other blood pressure lowering agents also decrease afterload 124 Exercise and Cardiac Output Effect of proprioceptors HR ↑ at beginning of exercise due to signals from joints, muscles Effect of venous return Muscular activity ↑ venous return causes ↑ SV ↑ HR and ↑ SV cause ↑CO Effect of ventricular hypertrophy Caused by sustained program of exercise ↑ SV allows heart to beat more slowly at rest, 40-60bpm ↑ cardiac reserve, can tolerate more exertion 125 Risk Factors for Heart Disease Risk factors in heart disease: High blood cholesterol level High blood pressure Cigarette smoking Obesity & lack of regular exercise. Other factors include: Diabetes mellitus Genetic predisposition High blood levels of fibrinogen Left ventricular hypertrophy 126 Plasma Lipids and Heart Disease Risk factor for developing heart disease is high blood cholesterol level. Promotes growth of fatty plaques Most lipids are transported as lipoproteins HDLs (high-density lipoproteins) remove excess cholesterol from circulation LDLs (low-density lipoproteins) are associated with the formation of fatty plaques VLDLs (very low-density lipoproteins) contribute to increased fatty plaque formation There are two sources of cholesterol in the body: in foods we ingest & formed by liver 127 Desirable Levels of Blood Cholesterol for Adults TC (total cholesterol) under 200 mg/dl LDL under 130 mg/dl HDL over 40 mg/dl Normally, triglycerides are in the range of 10-190 mg/dl. Among the therapies used to reduce blood cholesterol level are exercise, diet, and drugs. 128 In these patients you want a positive inotrope Congestive Heart Failure When the pumping efficiency, i.e., the cardiac output, is so low that the blood circulation is inadequate to meet tissue needs Causes: coronary artery disease, high BP, MI, valve disorders, congenital defects Left side heart failure Less effective pump so more blood remains in ventricle (right side pumps more blood) Blood backs up into lungs as pulmonary edema Right side failure Fluid builds up in tissues as peripheral edema 129 The End