Chapter 19 The Heart PDF

Chapter 19 The Heart Heart Location Layers of the Heart Wall Layers of the Heart Wall 1. Epicardium—visceral layer of the serous pericardium 2. Myocardium – – Spiral bundles of cardiac muscle cells Fibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissue Limits spread of...

Chapter 19 The Heart Heart Location Layers of the Heart Wall Layers of the Heart Wall 1. Epicardium—visceral layer of the serous pericardium 2. Myocardium – – Spiral bundles of cardiac muscle cells Fibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissue Limits spread of action potentials to specific pathways Anchors cardiac muscle fibers Supports great vessels and valves 3. Endocardium is continuous with lining of blood vessels with simple squamous epithelium Cardiac Muscle Bundles Heart Chambers of the Heart Atria: The Receiving Chambers Walls are ridged by pectinate muscles Right atrium receives deoxygenated blood from: – Superior vena cava – Inferior vena cava – Coronary sinus Left atrium receives oxygenated blood from: – Right and left pulmonary veins Chambers of the Heart Ventricles: The Discharging Chambers Walls are ridged by trabeculae carneae Make up the largest part of the heart Deoxygenated blood leaving the right ventricle – Pulmonary trunk (to the lungs) Oxygenated blood leaving the left ventricle – Aorta (to the body) Heart Pathway of Blood Through the Heart The heart is two side-byside pumps – Right side is the pump for the pulmonary circuit Vessels that carry blood to and from the lungs – Left side is the pump for the systemic circuit Vessels that carry the blood to and from all body tissue Blood Flow Through the Heart Pathway of Blood Through the Heart Right atrium → tricuspid valve → right ventricle Right ventricle → pulmonary semilunar valve → pulmonary trunk → pulmonary arteries → lungs Lungs → pulmonary veins → left atrium Left atrium → bicuspid valve → left ventricle Left ventricle → aortic semilunar valve → aorta Aorta → systemic circulation Coronary Circulation The functional blood supply to the heart muscle itself Coronary Arteries – Right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries Coronary Veins – Small cardiac, anterior cardiac, and great cardiac veins Coronary Circulation Heart Valves Ensure unidirectional blood flow through the heart Atrioventricular (AV) valves – Prevent backflow into the atria when ventricles contract – Tricuspid valve (right) – Bicuspid (Mitral) valve (left) Chordae tendineae support valve flaps during ventricle contraction Flaps open during relaxation of the ventricles Heart Valves Heart Valves Semilunar (SL) valves – Prevent backflow into the ventricles when ventricles relax – Aortic semilunar valve – Pulmonary semilunar valve Contraction increases pressure forcing these valves open Relaxation decreases pressure causing these valves to close Heart Physiology: Electrical Events Intrinsic cardiac conduction system – A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart Intrinsic Cardiac Conduction System Heart Physiology: Sequence of Excitation 1. Sinoatrial (SA) node (pacemaker) – Generates impulses about 75 times/minute (sinus rhythm) – Depolarizes faster than any other part of the myocardium 2. Atrioventricular (AV) node – Smaller diameter fibers; fewer gap junctions – Delays impulses approximately 0.1 second – Depolarizes 50 times per minute in absence of SA node input Heart Physiology: Sequence of Excitation 3. Atrioventricular (AV) bundle (bundle of His) – Only electrical connection between the atria and ventricles 4. Right and left bundle branches – Two pathways in the interventricular septum that carry the impulses toward the apex of the heart Heart Physiology: Sequence of Excitation 5. Purkinje fibers – Complete the pathway into the apex and ventricular walls – AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input Heart Electrical Events Autorhythmic cell do not maintain stable resting potentials – Continually depolarizing towards threshold – Pacemaker potentials due to slow open Na⁺ channels – Na⁺ continues to “leak” until threshold is reached – Fast Ca²⁺ channels open – Extracellular Ca²⁺ causes depolarization and action potential Intercalated Discs Membrane Potential (Cardiac Conductive Cells) Membrane Potential (Cardiac Contractile Cells) Extrinsic Innervation of the Heart Heartbeat is modified by the ANS Cardiac centers are located in the medulla oblongata – Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons – Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves Extrinsic Innervation of the Heart 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 Electrocardiograph (ECG) Electrical Current Through the Heart Heart Sounds Two sounds (lub-dup) associated with closing of heart valves – “Lub”: first sound occurs as AV valves close and signifies beginning of ventricular systole – “Dup”: second sound occurs when SL valves close at the beginning of ventricular diastole Heart murmurs: abnormal heart sounds most often indicative of valve problems Mechanical Events: The Cardiac Cycle Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeat – Systole—contraction – Diastole—relaxation Phases of the Cardiac Cycle 1. Ventricular filling—takes place in mid-to-late diastole – AV valves are open – 80% of blood passively flows into ventricles – Atrial systole occurs, delivering the remaining 20% – End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole Phases of the Cardiac Cycle 2. Ventricular systole – – – – Atria relax and ventricles begin to contract Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase (all valves are closed) In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open – End systolic volume (ESV): volume of blood remaining in each ventricle Phases of the Cardiac Cycle 3. Isovolumetric relaxation occurs in early diastole – Ventricles relax – Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure) Phases of the Cardiac Cycle Phases of the Cardiac Cycle Cardiac Output (CO) Cardiac output (CO): volume of blood pumped by each ventricle in one minute CO = heart rate (HR) x stroke volume (SV) – HR = number of beats per minute – SV = volume of blood pumped out by a ventricle with each beat Regulation of Stroke Volume SV = EDV – ESV Example: EDV = 120mL ESV = 50mL SV = 120 – 50 = 70mL/beat Each ventricle pumps ~60% of blood in the chamber with each beat 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 All blood passes through the heart each minute Regulation of Stroke Volume Three main factors affect stroke volume –Preload –Contractility –Afterload 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 – Increased venous return during exercise distends (stretches) the ventricles and increases contraction force which increases stroke volume Regulation of Stroke Volume Contractile strength can be affected by inotropic agents Positive inotropic agents increase contractility – Causes stronger contraction - the heart pumps more blood with each contraction – Increased Ca2+ influx due to sympathetic stimulation – Hormones (thyroxine, glucagon, and epinephrine) Negative inotropic agents decrease contractility – Causes weaker and slower heart contraction – Decreases hypertension and arrhythmia – Calcium channel blockers Regulation of Heart Rate Positive chronotropic factors increase heart rate – Epinephrine Negative chronotropic factors decrease heart rate – Beta-blockers Regulation of Stroke Volume Afterload: the force or resistance against which the ventricles must eject blood during systole. – Increased resistance increases afterload – An increased afterload forces the ventricles to work harder to eject blood against the higher resistance. – Maintaining an appropriate balance between preload and afterload is crucial for optimal cardiac function and efficiency. Summary of Cardiac Output 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) Autonomic Nervous System Regulation Parasympathetic nervous system opposes sympathetic effects – Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels During resting conditions: – The heart exhibits vagal tone (parasympathetic) Chemical Regulation of Heart Rate 1. Hormones – Epinephrine from adrenal medulla enhances heart rate and contractility – Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine 2. Ca2+ and K+ must be maintained for normal heart function – Abnormal potassium levels causes irregular heart rate – Increased calcium levels irregular heart rate – Decreased calcium levels decreases blood pressure and rhythm disorders Other Factors that Influence Heart Rate Age Gender Exercise Body temperature 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 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) Development of the Heart