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Chapter 15: The Cardiovascular System 1 Myocardial Thickness and Function The thickness of the myocardium of the four chambers varies according to the function of each chamber. The atria walls are thin because they deliver blood to the ventricles. The ventricle walls are thicker because they pump blood greater distances The right ventricle walls are thinner than the left because they pump blood into the lungs, which are nearby and offer very little resistance to blood flow. The left ventricle walls are thicker because they pump blood through the body where the resistance to blood flow is greater. 2 Locating the Heart Posterior to sternum medial to lungs Anterior to vertebral column Base lies beneath 2nd rib Apex at 5th intercostal space Lies upon diaphragm Coverings of the Heart 4 Layers of the Heart Wall 5 Layers of the Heart Wall 6 Heart Chambers • Right Atrium • receives blood from • inferior vena cava • superior vena cava • coronary sinus • Right Ventricle • receives blood from right atrium • Left Atrium • receives blood from pulmonary veins • Left Ventricle • receives blood from left atrium 7 EXTERNAL HEART Anterior View 8 EXTERNAL HEART Posterior View 9 Right Atrium • Receives blood from 3 sources – superior vena cava, inferior vena cava and coronary sinus • Interatrial septum partitions the atria • Fossa ovalis is a remnant of the fetal foramen ovale • Tricuspid valve – Blood flows through into right ventricle – has three cusps composed of dense CT covered by endocardium 10 Right Ventricle • Forms most of anterior surface of heart • Papillary muscles are cone shaped trabeculae carneae (raised bundles of cardiac muscle) • Chordae TENDINAE: cords between valve cusps and papillary muscles • Interventricular septum: partitions ventricles • Pulmonary semilunar valve: blood flows into pulmonary trunk 11 Left Atrium • • • • Forms most of the base of the heart Receives blood from lungs- 4 Pulmonary VEINS (2 right + 2 left) Red blood in a vein? Weird! Bicuspid valve: blood passes through into left ventricle – has two cusps – to remember names of this valve, try the pneumonic LAMB • Left Atrioventricular, Mitral, or Bicuspid valve 12 Left Ventricle • Forms the apex of heart • Chordae tendineae anchor bicuspid valve to PAPILLARY muscles (also has trabeculae carneae like right ventricle) • Aortic semilunar valve: – blood passes through valve into the ascending aorta – just above valve are the openings to the coronary arteries 13 Heart Valves 14 Atrioventricular Valves Open • A-V valves open and allow blood to flow from atria into ventricles when ventricular pressure is lower than atrial pressure – occurs when ventricles are relaxed, chordae tendineae are slack and papillary muscles are relaxed 15 Atrioventricular Valves Close • A-V valves close preventing backflow of blood into atria – occurs when ventricles contract, pushing valve cusps closed, chordae tendinae are pulled taut and papillary muscles contract to pull cords and prevent cusps from everting 16 Semilunar Valves • SL valves open with ventricular contraction – allow blood to flow into pulmonary trunk and aorta • SL valves close with ventricular relaxation – prevents blood from returning to ventricles, blood fills 17 valve cusps, tightly closing the SL valves Valve Function Review Atria contract, blood fills ventricles through A-V valves Ventricles contract, blood pumped into aorta and pulmonary trunk through SL valves 18 Fibrous Skeleton of Heart Dense CT rings surround the valves of the heart, fuse and merge with the interventricular septum Support structure for heart valves Insertion point for cardiac muscle bundles Electrical insulator between atria and ventricles prevents direct propagation of AP’s to ventricles 19 Path of Blood Through the Heart 20 Blood Supply to the Heart Muscle 21 Heart Contraction Atrial Systole/Ventricular Diastole Atrial Diastole/Ventricular Systole https://www.youtube.com/watch?v=waOSUpEHPQs 22 Cardiac Cycle • Atrial Systole/Ventricular Diastole • blood flows passively into ventricles • remaining 30% of blood pushed into ventricles • A-V valves open/semilunar valves close • ventricles relaxed • ventricular pressure increases 23 Cardiac Cycle Ventricular Systole/Atrial diastole • A-V valves close • chordae tendinae prevent cusps of valves from bulging too far into atria • atria relaxed • blood flows into atria • ventricular pressure increases and opens semilunar valves • blood flows into pulmonary trunk and aorta 24 Heart Sounds Lubb • first heart sound • occurs during ventricular systole • A-V valves closing Dupp • second heart sound • occurs during ventricular diastole • pulmonary and aortic semilunar valves closing Murmur – abnormal heart sound 25 Heart Sounds 26 Cardiac Muscle Fibers Cardiac muscle fibers form a functional syncytium • group of cells that function as a unit • atrial syncytium • ventricular syncytium 27 Cardiac Conduction System 28 Cardiac Conduction System 29 Muscle Bundles of the Myocardium • Cardiac muscle fibers swirl diagonally around the heart in interlacing bundles 30 Electrocardiogram • recording of electrical changes that occur in the myocardium • used to assess heart’s ability to conduct impulses P wave – atrial depolarization QRS wave – ventricular depolarization T wave – ventricular repolarization 31 Electrocardiogram • Impulse 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). • The ECG helps to determine if the conduction pathway is abnormal, if the heart is enlarged, and if certain regions are damaged. • Figure 20.12 shows a typical ECG. 32 Electrocardiogram---ECG or EKG • EKG – Action potentials of all active cells can be detected and recorded • P wave – atrial depolarization • P to Q interval – conduction time from atrial to ventricular excitation • QRS complex – ventricular depolarization • T wave 33 – ventricular repolarization 34 ECG • In a typical Lead II record, three clearly visible waves accompany each heartbeat It consists of:. • P wave (atrial depolarization - spread of impulse from SA node over atria) • QRS complex (ventricular depolarization - spread of impulse through ventricles) • T wave (ventricular repolarization). • Correlation of ECG waves with atrial and ventricular systole (Figure 20.13) 35 ECG • As atrial fibers depolarize, the P wave appears. • After the P wave begins, the atria contract (atrial systole). Action potential slows at the AV node giving the atria time to contract. • The action potential moves rapidly through the bundle branches, Purkinje fibers, and the ventricular myocardium producing the QRS complex. • Ventricular contraction after the QRS complex and continues through the ST segment. • Repolarization of the ventricles produces the T wave. • Both atria and ventricles repolarize and the P wave appears. 36 Regulation of Cardiac Cycle Additional Factors that Influence HR • physical exercise • body temperature • concentration of various ions • potassium • calcium • parasympathetic impulses decrease heart action • sympathetic impulses increase heart action • cardiac center regulates autonomic impulses to the heart 37 CARDIAC OUTPUT • Cardiac output (CO) is the volume of blood ejected from the left ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each minute. – Cardiac output equals the stroke volume, the volume of blood ejected by the ventricle with each contraction, multiplied by the heart rate, the number of beats per minute. – CO = SV X HR • Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and the cardiac output at rest. 38 Cardiac Output • CO = SV x HR – at 70ml stroke volume & 75 beat/min----5 and 1/4 liters/min – entire blood supply passes through circulatory system every minute • Cardiac reserve is maximum output/output at rest – average is 4-5x while athlete’s is 7-8x 39 Influences on Stroke Volume • Preload (affect of stretching) – Frank-Starling Law of Heart – more muscle is stretched, greater force of contraction – more blood more force of contraction results • Contractility – autonomic nerves, hormones, Ca+2 or K+ levels • Afterload – amount of pressure created by the blood in the way – high blood pressure creates high afterload 40 Stroke Volume and Heart Rate 41 Preload: Effect of Stretching • 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. – Preload is proportional to EDV. – EDV is determined by length of ventricular diastole and venous return. • 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. 42 Contractility • Myocardial contractility, the strength of contraction at any given preload, is affected by positive and negative inotropic agents. – Positive inotropic agents increase contractility – Negative inotropic agents decrease contractility. • For a constant preload, the stroke volume increases when positive inotropic agents are present and decreases when negative inotropic agents are present. 43 Afterload • The pressure that must be overcome before a semilunar valve can open is the afterload. • In congestive heart failure, blood begins to remain in the ventricles increasing the preload and ultimately causing an overstretching of the heart and less forceful contraction – Left ventricular failure results in pulmonary edema – Right ventricular failure results in peripheral edema. 44 Chemical regulation of heart rate • Heart rate affected by hormones (epinephrine, norepinephrine, thyroid hormones). • Cations (Na+, K+, Ca+2) also affect heart rate. • Other factors such as age, gender, physical fitness, and temperature also affect heart rate. 45 Arteries and Arterioles Artery • thick strong wall • endothelial lining • middle layer of smooth muscle and elastic tissue • outer layer of connective tissue • carries blood under relatively high pressure Arterioles • thinner wall than artery • endothelial lining • some smooth muscle tissue • small amount of connective tissue • helps control blood flow into a capillary 46 Walls of Artery and Vein 47 Arteriole • smallest arterioles only have a few smooth muscle fibers • capillaries lack muscle fibers 48 Capillaries • smallest diameter blood vessels • extensions of inner lining of arterioles • walls are endothelium only • semipermeable • sinusoids – leaky capillaries 49 Exchange in the Capillaries • • • water and other substances leave capillaries because of net outward pressure at the capillaries’ arteriolar ends water enters capillaries’ venular ends because of a net inward pressure substances move in and out along the length of the capillaries according to their respective concentration gradients 50 Venules and Veins • Venule • thinner wall than arteriole • less smooth muscle and elastic tissue than arteriole • Vein • thinner wall than artery • three layers to wall but middle layer is poorly developed • some have flaplike valves • carries blood under relatively low pressure • serves as blood reservoir 51 Venous Valves 52 Characteristics of Blood Vessels 53 Blood Volumes in Vessels 54 Arterial Blood Pressure Blood Pressure – force the blood exerts against the inner walls of the blood vessels Arterial Blood Pressure • rises when ventricles contract • falls when ventricles relax • systolic pressure – maximum pressure • diastolic pressure – minimum pressure 55 Factors That Influence Arterial Blood Pressure 56 Control of Blood Pressure If blood pressure rises, baroreceptors initiate the cardioinhibitory reflex, which lowers the blood pressure 57 Control of Blood Pressure Dilating arterioles helps regulate blood pressure 58 Venous Blood Flow • not a direct result of heart action • dependent on • skeletal muscle contraction • breathing • venoconstriction 59 Blood Flow Through Alveoli • cells of alveolar wall are tightly joined together • the high osmotic pressure of the interstitial fluid draws water out of them 60 Life-Span Changes • • cholesterol deposition in blood vessels • heart enlargement • death of cardiac muscle cells • increase in fibrous connective tissue of the heart • increase in adipose tissue of the heart • increase in blood pressure • decrease in resting heart rate 61 Clinical Problems • 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 62 CAD • Coronary artery disease (CAD), or coronary heart disease (CHD), is 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 the United States 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. 63 CAD • Atherosclerosis is 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 (Figure 20.18). • Diagnosis of CAD includes such procedures as cardiac catherization and cardiac angiography. • Treatment options for CAD include drugs and coronary artery bypass grafting (Figure 20.19). 64 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 male gender high blood levels of fibrinogen left ventricular hypertrophy 65 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 • low-density lipoproteins (LDLs) • high-density lipoproteins (HDLs) • very low-density lipoproteins (VLDLs) – HDLs remove excess cholesterol from circulation – LDLs are associated with the formation of fatty plaques – VLDLs contribute to increased fatty plaque formation • There are two sources of cholesterol in the body: – in foods we ingest & formed by liver 66 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 10190 mg/dl. • Among the therapies used to reduce blood cholesterol level are exercise, diet, and drugs. 67 Coronary Artery Disease • Heart muscle receiving insufficient blood supply – narrowing of vessels--atherosclerosis, artery spasm or clot – atherosclerosis-smooth muscle & fatty deposits in walls of arteries • Treatment – drugs, bypass graft, angioplasty, stent 68 By-pass Graft 69 Percutaneous Transluminal Coronary Angioplasty Stent 70