The Heart 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 Heart Anatomy Coverings of the Heart: Anatomy 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 Coverings of the Heart: Physiology 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 Pericardial Layers of the Heart 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 Cardiac Muscle Bundles External Heart: Major Vessels of the Heart (Anterior View) Vessels returning blood to the heart include: Superior and inferior vena cava 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 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) 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 External Heart: Arteries that Supply the Heart 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 External Heart: Arteries that Supply the Heart Right coronary artery (in atrioventricular groove) Supplies Right atrium Portions of both ventricles SA and AV nodes Branches Marginal artery Posterior interventricular artery External Heart: Arteries that Supply the Heart Left coronary artery Supply Left atrium Portions of both ventricles Branches Circumflex Anterior interventricular Arterial Coronary Circulation External Heart: Veins that Drain the Heart Veins that empty in the coronary sinus Great cardiac vein Posterior cardiac vein Middle cardiac vein Small cardiac vein Vein that empty into the right atrium Anterior cardiac vein Venous Coronary Circulation External Heart: Major Vessels of the Heart (Posterior View) Vessels returning blood to the heart include: Right and left pulmonary veins Superior and inferior vena cava Vessels conveying blood away from the heart include: Aorta Right and left pulmonary arteries 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 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) 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 Atria of the Heart Atria are the receiving chambers of the heart Each atrium has a protruding auricle Pectinate muscles mark atrial walls In the left atrium only in the wall of the auricle Blood enters right atria from superior and inferior venae cavae and coronary sinus Blood enters left atria from pulmonary veins 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 Right and Left Ventricles 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 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 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 Heart Valves Heart Valves Atrioventricular Valve Function Semilunar Valve Function 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 Microscopic Anatomy of Heart Muscle Heart is resistant to fatigue Many mitochondria Z discs, I band, A band, Fewer and wider T tubules Simpler sarcoplasmic reticulum No triads Microscopic Anatomy of Cardiac Muscle Cardiac Muscle Contraction Heart muscle: Is stimulated by nerves and is self-excitable (automaticity) Contracts as a unit or does not contract at all Has a long absolute refractory period that prevents tetany Cardiac muscle contraction is similar to skeletal muscle contraction Heart Physiology: Intrinsic Conduction System Autorhythmic cells: Initiate action potentials Have unstable resting potentials called pacemaker potentials Use calcium influx (rather than sodium) for rising phase of the action potential The intrinsic conducting system Hyperpolarization leads to: Loss of K Opening of Na channels Membrane becomes less and less negative Threshold is reached Ca channels opens Influx of Ca causes the rising phase of the action potential Pacemaker and Action Potentials Mechanisms of contraction 1) Rapid depolarization Threshold Opening of the voltage-regulated Na channels Fast channels Massive influx of Na Mechanisms of contraction 2) Plateau Transmembrane potential approaches +30mV Na channels close and remain inactivated Na is actively pumped out of the cell Voltage-regulated Ca channels opens (slow channels) Ca enters the cytoplasma It stimulates more Ca release from the SR Mechanisms of contraction This influx of Ca balances out the efflux of Na Transmembrane potential is kept near 0mV plateau Mechanisms of contraction 3) Repolarization Slow Ca channels start to close Ca is reabsorbed by the SR or pumped out of the cell Slow K channels begin to open Efflux of K causes the repolarization Mechanisms of contraction Heart Physiology: Sequence of Excitation Sinoatrial (SA) node generates impulses about 75 times/minute Atrioventricular (AV) node delays the impulse It generates impulses about 40-60 times/min Smaller diameter of the fibers Fewer gap junctions Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His) Bundle of His is the only electrical connection between atria and ventricle Heart Physiology: Sequence of Excitation 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 Depolarize spontaneously at the rate of 20-40 beats/min They supply the papillary muscles Contract before the rest of the ventricles Cardiac Intrinsic Conduction Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins SA node Impulse delayed at AV node AV node Impulse passes to heart apex; ventricular excitation begins Bundle branches Ventricular excitation complete Purkinje fibers Extrinsic Innervation of the Heart Heart is stimulated by the sympathetic cardioacceleratory center Heart is inhibited by the parasympathetic cardioinhibitory center 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 Electrocardiography Electrocardiography PR interval Atrial depolarization and contraction QT interval Ventricular depolarization, contraction and repolarization PR segment Atrial contraction ST segment Ventricular contraction ECG Tracings Heart Sounds Heart Sounds Heart sounds (lub-dup) are associated with closing of heart valves First sound (S1)occurs as AV valves close and signifies beginning of systole Second sound (S2) occurs as SL valves close at the beginning of ventricular diastole Cardiac Cycle Cardiac cycle refers to all events associated with blood flow through the heart Systole – contraction of heart muscle Diastole – relaxation of heart muscle 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 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 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. This backflow causes the valve to close and creates a slight pressure rebound Phases of the Cardiac Cycle Cardiodynamics End-diastolic volume (EDV) Maximum amount of blood held in the ventricles during diastole End-systolic volume (ESV) Amount of blood that remains in the ventricles after the contraction and closing of the semilunar valves 59 Cardiodynamics Venous return- amount of blood returning to the heart or blood flow during filling time Heart rate – number of heart beats in a minute Filling time- duration of ventricular diastole Stroke volume (SV) – amount of blood ejected from the ventricles with each beat SV = EDV – ESV 60 Cardiodynamics Cardiac output (CO) – the amount of blood pumped by each ventricle in one minute CO Cardiac output (ml/min) = HR Heart rate (beats/min) X SV Stroke volume (ml/beat) Cardiac Output: Example CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) CO = 5250 ml/min (5.25 L/min) Cardiac reserve is the difference between resting and maximal CO 62 Factors Affecting stroke volume (EDV-ESV) EDV (end diastolic volume) is affected by: Venous return High venous return= high EDV Exercise → ↑Venous return → ↑EDV→ ↑SV ↓Blood volume →↓Venous return→↓EDV→↓SV 63 Factors Affecting stroke volume (EDV-ESV) Filling time Depends on the heart rate ↑ HR → ↓Filling time→ ↓EDV→ ↓SV 64 Factors Affecting stroke volume (EDV-ESV) Preload Stretchiness of the ventricles during diastole Directly proportional to the EDV Frank-Starling principle (“more in = more out”) or increased EDV=increased SV 65 Factors Affecting stroke volume (EDV-ESV) ESV (end systolic volume) is affected by: Contractility Force produced during a contraction Positive inotropic (increases contractility) Increased sympathetic stimuli Certain hormones, some drugs ↑Contractility → ↓ESV→ ↑SV 66 Factors Affecting stroke volume (EDV-ESV) Negative inotropic (decreases contractility) Increased extracellular K+ Calcium channel blockers ↓Contractility → ↑ESV→ ↓SV 67 Heart Contractility and Norepinephrine Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP secondmessenger system Extracellular fluid Norepinephrine b 1-Adrenergic receptor Adenylate cyclase Ca2+ Ca2+ channel Cytoplasm GTP GTP 1 GDP ATP cAMP Active protein kinase A Ca2+ Inactive protein kinase A 3 Ca2+ 2 Enhanced actin-myosin interaction Troponin uptake pump binds to Ca2+ SR Ca2+ channel Cardiac muscle force and velocity Sarcoplasmic reticulum (SR) Factors Affecting stroke volume (EDV-ESV) Afterload The pressure that must be overcome for the ventricles to eject blood (back pressure exerted by blood in the large arteries leaving the heart) Increased by factors that restricts arterial blood flow ↑Afterload→↑ESV →↓SV 69 Preload and Afterload Regulation of Heart Rate: Autonomic Nervous System Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone Atrial (Bainbridge) Reflex Atrial reflex (Bainbridge Reflex) – a sympathetic reflex initiated by increased blood in the atria ↑Venous return→ Stimulates baroreceptors in the atria→ ↑Sympathetic stimulation→ ↑Stimulation of SA node→ ↑HR 72 Chemical Regulation of Heart Rate The hormones epinephrine and thyroxine increase heart rate Intra- and extracellular ion concentrations must be maintained for normal heart function Hypocalcemia depresses the heart and hypercalcemia stimulates the heart Hyperkalemia causes heart block and hypokalemia causes weak and irregular contractions Other factors influencing heart rate Age Exercise Body temperature Tachycardia Bradycardia Figure 20-23 Factors Affecting Stroke Volume Factors Affecting Stroke Volume (SV) Venous return (VR) VR = VR = EDV EDV Filling time (FT) FT = EDV FT = EDV Increased by sympathetic stimulation Decreased by parasympathetic stimulation Increased by E, NE, glucagon, thyroid hormones Contractility (Cont) of muscle cells Cont = Cont = Preload End-diastolic volume (EDV) ESV ESV End-systolic volume (ESV) STROKE VOLUME (SV) EDV = EDV = SV SV ESV = ESV = SV SV Increased by vasoconstriction Decreased by vasodilation Afterload (AL) AL = ESV AL = ESV Congestive Heart Failure (CHF) Congestive heart failure (CHF) is caused by: Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM) Developmental Aspects of the Heart Developmental Aspects of the Heart Fetal heart structures that bypass pulmonary circulation Foramen ovale connects the two atria Ductus arteriosus connects pulmonary trunk and the aorta Examples of Congenital Heart Defects Age-Related Changes Affecting the Heart Sclerosis and thickening of valve flaps Decline in cardiac reserve Fibrosis of cardiac muscle Atherosclerosis