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The Cardiovascular System: The Heart Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Anatomy Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.1 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 Pericardium – a double-walled sac around the heart composed of: 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 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Pericardial Layers of the Heart The pericardium: Protects and anchors the heart Prevents overfilling of the heart with blood Allows for the heart to work in a relatively friction-free environment Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Wall Epicardium – visceral layer of the serous pericardium Myocardium – cardiac muscle layer forming the bulk of the heart Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue Endocardium – endothelial layer of the inner myocardial surface Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Four chambers Two atria Separated internally by the interatrial septum Coronary sulcus (atrioventricular groove) encircles the junction of the atria and ventricles Auricles increase atrial volume Two ventricles Separated by the interventricular septum Anterior and posterior interventricular sulci mark the position of the septum externally Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Brachiocephalic trunk Superior vena cava Left common carotid artery Left subclavian artery Aortic arch Right pulmonary artery Ligamentum arteriosum Left pulmonary artery Ascending aorta Pulmonary trunk Right pulmonary veins Right atrium Right coronary artery (in coronary sulcus) Anterior cardiac vein Right ventricle Marginal artery Small cardiac vein Inferior vena cava (b) Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Left pulmonary veins Left atrium Auricle Circumflex artery Left coronary artery (in coronary sulcus) Left ventricle Great cardiac vein Anterior interventricular artery (in anterior interventricular sulcus) Apex Figure 18.4b Atria: The Receiving Chambers Walls are ridged by pectinate muscles Ventricles: The Discharging Chambers Walls are ridged by trabeculae carneae Papillary muscles project into the ventricular cavities Vessel leaving the right ventricle Vessels entering right atrium Superior vena cava Inferior vena cava Coronary sinus Vessels entering left atrium Right and left pulmonary veins Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Pulmonary trunk Vessel leaving the left ventricle Aorta External Heart: Major Vessels of the Heart (Anterior View) Vessels returning blood to the heart include: Superior and inferior venae cavae Right and left pulmonary veins Vessels conveying blood away from the heart: Pulmonary trunk, which splits into right and left pulmonary arteries Ascending aorta (three branches) – brachiocephalic, left common carotid, and subclavian arteries Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries Veins – small cardiac, anterior cardiac, and great cardiac veins Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings External Heart: Major Vessels of the Heart (Posterior View) Vessels returning blood to the heart include: Right and left pulmonary veins Superior and inferior venae cavae Vessels conveying blood away from the heart include: Aorta Right and left pulmonary arteries Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings External Heart: Vessels that Supply/Drain the Heart (Posterior View) Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove) Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Aorta Left pulmonary artery Left pulmonary veins Auricle of left atrium Left atrium Superior vena cava Right pulmonary artery Right pulmonary veins Right atrium Great cardiac vein Inferior vena cava Posterior vein of left ventricle Right coronary artery (in coronary sulcus) Coronary sinus Apex Posterior interventricular artery (in posterior interventricular sulcus) Middle cardiac vein (d) Right ventricle Left ventricle Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.4d Aorta Superior vena cava Right pulmonary artery Pulmonary trunk Right atrium Right pulmonary veins Fossa ovalis Pectinate muscles Tricuspid valve Right ventricle Chordae tendineae Trabeculae carneae Inferior vena cava (e) Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Left pulmonary artery Left atrium Left pulmonary veins Mitral (bicuspid) valve Aortic valve Pulmonary valve Left ventricle Papillary muscle Interventricular septum Myocardium Visceral pericardium Endocardium Figure 18.4e Atria of the Heart Atria are the receiving chambers of the heart Each atrium has a protruding auricle Pectinate muscles mark atrial walls Blood enters right atria from superior and inferior venae cavae and coronary sinus Blood enters left atria from pulmonary veins Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Ventricles of the Heart Ventricles are the discharging chambers of the heart Papillary muscles and trabeculae carneae muscles mark ventricular walls Right ventricle pumps blood into the pulmonary trunk Left ventricle pumps blood into the aorta Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Right and Left Ventricles Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.6 Pathway of Blood Through the Heart and Lungs Right atrium tricuspid valve right ventricle Right ventricle pulmonary semilunar valve pulmonary arteries lungs Lungs pulmonary veins left atrium Left atrium bicuspid valve left ventricle Left ventricle aortic semilunar valve aorta Aorta systemic circulation Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.5 Coronary Circulation: Arterial Supply 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 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Coronary Circulation: Venous Supply Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Homeostatic Imbalances Angina pectoris Thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium Cells are weakened Myocardial infarction (heart attack) Prolonged coronary blockage Areas of cell death are repaired with noncontractile scar tissue Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Valves Heart valves ensure unidirectional blood flow through the heart Atrioventricular (AV) valves lie between the atria and the ventricles AV valves prevent backflow into the atria when ventricles contract Chordae tendineae anchor AV valves to papillary muscles Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Heart Valves Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.8a, b Heart Valves Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.8c, d Atrioventricular Valve Function Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.9 Semilunar Valve Function Review of the Heart Circuit Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.10 Cardiac Intrinsic Conduction Heart Function Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.14a Microscopic Anatomy of Cardiac Muscle Cardiac muscle cells are striated, short, fat, branched, and interconnected Connective tissue matrix (endomysium) connects to the fibrous skeleton T tubules are wide but less numerous; SR is simpler than in skeletal muscle Numerous large mitochondria (25–35% of cell volume) Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Cardiac Muscle Contraction Depolarization of the heart is rhythmic and spontaneous About 1% of cardiac cells have automaticity— (are self-excitable) Gap junctions ensure the heart contracts as a unit Long absolute refractory period (250 ms) Depolarization opens voltage-gated fast Na+ channels in the sarcolemma Reversal of membrane potential from –90 mV to +30 mV Depolarization wave in T tubules causes the SR to release Ca2+ Depolarization wave also opens slow Ca2+ channels in the sarcolemma Ca2+ surge prolongs the depolarization phase (plateau) Ca2+ influx triggers opening of Ca2+-sensitive channels in the SR, which liberates bursts of Ca2+ E-C coupling occurs as Ca2+ binds to troponin and sliding of the filaments begins Duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscle Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings K+ ©channels 1 Depolarization is 2 Tension development (contraction) 3 1 Absolute refractory period Time (ms) Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Tension (g) Membrane potential (mV) Action potential Plateau due to Na+ influx through fast voltage-gated Na+ channels. A positive feedback cycle rapidly opens many Na+ channels, reversing the membrane potential. Channel inactivation ends this phase. 2 Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because few K+ channels are open. 3 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage. Figure 18.12 Heart Physiology: Intrinsic Conduction System A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart Initiate action potentials Have unstable resting potentials called pacemaker potentials Use calcium influx (rather than sodium) for rising phase of the action potential Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Pacemaker and Action Potentials of the Heart Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.13 Cardiac Membrane Potential: Cardiomyocytes Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.12 Superior vena cava Right atrium 1 The sinoatrial (SA) node (pacemaker) generates impulses. Internodal pathway 2 The impulses pause (0.1 s) at the atrioventricular (AV) node. 3 The atrioventricular (AV) bundle connects the atria to the ventricles. 4 The bundle branches conduct the impulses through the interventricular septum. 5 The Purkinje fibers Left atrium Purkinje fibers Interventricular septum depolarize the contractile cells of both ventricles. (a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.14a Heart Physiology: Sequence of Excitation Sinoatrial (SA) node generates impulses about 75 times/minute Atrioventricular (AV) node delays the impulse approximately 0.1 second Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His) AV bundle splits into two pathways in the interventricular septum (bundle branches) Bundle branches carry the impulse toward the apex of the heart Purkinje fibers carry the impulse to the heart apex and ventricular walls Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Homeostatic Imbalances Defects in the intrinsic conduction system may result in 1. Arrhythmias: irregular heart rhythms 2. Uncoordinated atrial and ventricular contractions 3. Fibrillation: rapid, irregular contractions; useless for pumping blood 4. Defective SA node may result in Ectopic focus: abnormal pacemaker takes over 5. If AV node takes over, there will be a junctional rhythm (40–60 bpm) 6. Defective AV node may result in Partial or total heart block Few or no impulses from SA node reach the ventricles Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings The vagus nerve (parasympathetic) decreases heart rate. Dorsal motor nucleus of vagus Cardioinhibitory center Medulla oblongata Cardioacceleratory center Sympathetic trunk ganglion Thoracic spinal cord Sympathetic trunk Sympathetic cardiac nerves increase heart rate and force of contraction. AV node SA node Parasympathetic fibers Sympathetic fibers Interneurons Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.15 Electrocardiography Electrocardiogram (ECG or EKG): a composite of all the action potentials generated by nodal and contractile cells at a given time Three waves 1. P wave: depolarization of SA node 2. QRS complex: ventricular depolarization 3. T wave: ventricular repolarization Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings QRS complex Sinoatrial node Atrial depolarization Ventricular depolarization Ventricular repolarization Atrioventricular node P-Q Interval S-T Segment Q-T Interval Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.16 SA node Depolarization R Repolarization R T P S 1 Atrial depolarization, initiated by the SA node, causes the P wave. R AV node T P Q Q S 4 Ventricular depolarization is complete. R T P T P Q S 2 With atrial depolarization complete, the impulse is delayed at the AV node. R Q S 5 Ventricular repolarization begins at apex, causing the T wave. R T P T P Q S 3 Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Q S 6 Ventricular repolarization is complete. Figure 18.17 Electrocardiography Electrical activity is recorded by electrocardiogram (ECG) P wave corresponds to depolarization of SA node QRS complex corresponds to ventricular depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger QRS complex Cardiac conduction system and its relationship with ECG Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings (a) Normal sinus rhythm. (b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min. (c) Second-degree heart block. (d) Ventricular fibrillation. These chaotic, grossly irregular ECG Some P waves are not conducted deflections are seen in acute through the AV node; hence more heart attack and electrical shock. P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1. Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.18 Heart Sounds Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.19 Heart Sounds Heart sounds (lub-dup) are associated with closing of heart valves First sound occurs as AV valves close and signifies beginning of systole Second sound occurs when SL valves close at the beginning of ventricular diastole Cardiac cycle refers to all events associated with blood flow through the heart Systole – contraction of heart muscle Diastole – relaxation of heart muscle Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle Ventricular filling – mid-to-late diastole Heart blood pressure is low as blood enters atria and flows into ventricles AV valves are open, then atrial systole occurs Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle Ventricular systole Atria relax Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase Ventricular ejection phase opens semilunar valves Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Phases of the Cardiac Cycle Isovolumetric relaxation – early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.20 Cardiac Output (CO) At rest CO (ml/min) = HR (75 beats/min) SV (70 ml/beat) = 5.25 L/min Maximal CO is 4–5 times resting CO in nonathletic people Maximal CO may reach 35 L/min in trained athletes Cardiac reserve: difference between resting and maximal CO Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Stroke Volume SV = EDV – ESV Three main factors affect SV Preload Contractility Afterload Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Stroke Volume Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart) Cardiac muscle exhibits a length-tension relationship At rest, cardiac muscle cells are shorter than optimal length Slow heartbeat and exercise increase venous return Increased venous return distends (stretches) the ventricles and increases contraction force Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Regulation of Stroke Volume Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV Positive inotropic agents increase contractility Increased Ca2+ influx due to sympathetic stimulation Hormones (thyroxine, glucagon, and epinephrine) Negative inotropic agents decrease contractility Acidosis Increased extracellular K+ Calcium channel blockers Afterload: pressure that must be overcome for ventricles to eject blood Hypertension increases afterload, resulting in increased ESV and reduced SV Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Autonomic Nervous System Regulation Sympathetic nervous system is activated by emotional or physical stressors Norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility) Parasympathetic nervous system opposes sympathetic effects Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels The heart at rest exhibits vagal tone (parasympathetic) Atrial (Bainbridge) reflex: a sympathetic reflex initiated by increased venous return Stretch of the atrial walls stimulates the SA node Also stimulates atrial stretch receptors activating sympathetic Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Chemical Regulation of Heart Rate Hormones 1. Epinephrine from adrenal medulla enhances heart rate and contractility Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function 2. Other Factors that Influence Heart Rate Age Gender Exercise Body temperature Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Homeostatic Imbalances Tachycardia: abnormally fast heart rate (>100 bpm) If persistent, may lead to fibrillation Bradycardia: heart rate slower than 60 bpm May result in grossly inadequate blood circulation May be desirable result of endurance training Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Congestive Heart Failure (CHF) Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs Caused by Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM) Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Supplement http://www.youtube.com/watch?v=D3ZDJgFDdk0 http://www.youtube.com/watch?v=H04d3rJCLCE&feature=related http://www.youtube.com/watch?v=aWpuuNopsZI http://www.youtube.com/watch?v=UsTorPkPDXE&feature=channel http://www.youtube.com/watch?v=Lhl897Mz-h8&feature=related http://www.youtube.com/watch?v=rguztY8aqpk&feature=related Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings