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Chapter 19: The Heart It’s study = Cardiology. I. Gross Anatomy (A) Cardiovascular System Overview – includes heart and blood vessels. -1- pulmonary circuit connects heart and lungs. -2- systemic circuit connects heart and body’s tissues. (B) Size, Shape & Position location = mediastinum of thoracic cavity. Base and apex (tilts to left). Size of fist. (C) Pericardium – double layered sac, serous membrane. Outer = parietal, inner = visceral. Between is the pericardial cavity with fluid. Inflammation is pericarditis, results in friction rub and cardiac tamponade (interferes with beating). (D) Heart Wall -1- epicardium: visceral pericardium. Serous membrane with fat to fill in grooves. -2- myocardium: thickest layer, cardiac muscle. Contains fibrous skeleton for structural support, anchorage for muscle action, and electrical nonconductivity. -3- endocardium: smooth lining of simple squamous epithelium. (E) Chambers – two atria with auricles, two ventricles. Sulci on surface filled with fat and coronary vessels. Interatrial and interventricular septa, pectinate muscles (line atria) and trabeluae carneae (line ventricles). (F) Valves – prevent backflow. Their flaps = cusps. AV (atrioventricular) valves: tricuspid (right) and bicuspid = mitral (left). These cusps attached to papillary muscles in ventricles by chordae tendinae. Semilunar valves between ventricles and arteries (aorta, pulmonary trunk). Valve malfunctions: -1- valvular insufficiency (incompetence): results in reflux (regurgitation). -2- valvular stenosis: due to stiff scar tissue. Associated with Scarlet Fever, heart murmurs. -3- mitral valve prolapse (MVP). 11 (G) Blood Flow Through Heart – right side with deoxygenated blood, left side with oxygenated. Normally separated. Blood from superior and inferior vena cavae and coronary sinus to right atrium, Through tricuspid valve, into right ventricle, Out pulmonary semilunar valve, into pulmonary trunk, to lungs. Pulmonary veins, with oxygenated blood, to left atrium, Through mitral valve, into left ventricle, Out aortic semilunar valve into aorta. (H) Coronary Circulation through myocardium. Branches of right and left coronary arteries suseptible to MIs (myocardial infarctions) when oxygen deprivation extreme. Less intense = angina pectoris (pain from lactic acid generation). Defense against blockages = anastomoses (connections between vessels). Cardiac veins lead to coronary sinus, returning deoxygenated coronary blood to right atrium. II. Cardiac Muscle and Conduction (A) Cardiac Muscle Anatomy Cells= myocytes; joined by intercalated discs – contain gap junctions for electrical communication. Striated and branched. (B) Cardiac Muscle Metabolism Mostly aerobic. Abundant myoglobin and mitochondria. (C) Cardiac Conduction Autorhythmic. Non-contracting cells form conduction system. SA (sinoatrial = sinus) node is the pacemaker, communicates to AV node, ultimately to Purkinje fibers in ventricles. III. Electrical and Contractile Activity Contraction = systole; relaxation = diastole. Usually refers to ventricles. (A) Cardiac Rhythm – normally sinus (from SA node). Vagus inhibition establishes beat ~ 70-80 BPM. Ectopic focus may be present, e.g. AV nodal rhythm, ~ 40-50 BPM. Arrythmias = abnormal rhythms, often due to heart blocks. -1- atrial flutter – repeated atrial stimulation. -2- PVCs = premature ventricular contractions. -3- ventricular fibrillation: “bag of worms”, corrected with defibrillation. -4- cardiac arrest 12 (B) Physiology of SA Node – cells with pacemaker potentials, leaky Na+ channels. Fast Ca++ channels trigger depolarization. (C) Impulse Conduction to Myocardium Faster in atria than in ventricles. Delay allows atria to contract first. Papillary muscles are stimulated first in ventricles to allow AV valve closure before contraction. (D) Electrical Behavior of Myocardium Action potentials similar to those of neurons. Stimulation opens voltage-regulated Na+ channels, results in depolarization, which spreads to ~ +30mV. Channels then quickly close. Voltage-gated slow Ca++ channels open, results in Ca++ release from sarcoplasmic reticulum, causing the contraction. Relaxation when K+ moves out and Ca++ returned to storage. Long absolute refractory period prevents summation and tetanus, promotes pumping. (E) Electrocardiogram = ECG Electrical currents generated in heart spread to skin. -1- P Wave: atrial depolarization -2- QRS Complex: ventricular depolarization. -3- T Wave: ventricular repolarization. IV. Blood Flow, Heart Sounds, Cardiac Cycle Cardiac cycle – one complete contraction and relaxation of all four chambers. (A) Principles of Pressure & Flow Pressure measured in mm Hg. Fluid moves down pressure gradients, from high to low. (B) Heart Sounds Listening = auscultation. “lubb-dup”, corresponds to blood turbulence caused by valve closures. Triple rhythms common in children. (C) Phases of Cardiac Cycle all within one second -1- ventricular filling: AV valves open. Atrial systole towards end. AV valves close. Ventricles contain EDV (only ~ 1/3 from atrial action). -2- isovolumetric contraction: atria now relaxed. Ventricles depolarize, AV valves close, no ejection of blood yet. BP in aorta and pulmonary trunk still higher than in ventricles. 13 -3- ventricular ejection: when pressure in ventricles exceeds that in arteries. Semilunar valves open. Remaining blood = ESV. SV (stroke volume) = amount ejected. EDV – SV = ESV. Both ventricles with same output – necessary for fluid balance. -4- Isovolumetric relaxation – corresponds to T wave. Ventricular repolarization. Semilunar valves close. Congestive Heart Failure = problems with ventricular ejection. Results in pulmonary or systemic edema (fluid accumulation). V. Cardiac Output Volume/ ventricle/ minute. CO = HR X SV. Works out that heart normally pumps all blood each minute. (A) Heart Rate – measured as pulse. Tachycardia when faster, bradycardia when slower. HR effected by chronotropic factors. -1- ANS chronotropic factors: medullary cardioacceletory and cardioinhibitory (via Vagus) centers communicate to Sa and Av nodes. Receive information from proprioceptors, baroreceptors, chemoreceptors. -2- chemical chronotropic factors: epinephrine, norepinephrine, caffeine, nicotine, K+, Ca++…. (B) Stroke Volume -1- preload: tension in ventricular myocardium. Frank-Starling law: SV related to EDV. Ventricles must fill to contract sufficiently. -2- contractility: for a given preload. Influenced by inotropic factors (e.g. vagus stimulation, Ca++). -3- afterload: pressure in aorta and pulmonary trunk. When high, SV diminished. May be affected by atherosclerosis: fatty plaques in arteries, often coronary. Linked to LDLs (low density lipoproteins in blood), sedentary lifestyle, poor diet, obesity and genetics. Treaments = bypass surgery, balloon or laser angioplasty, stents. (C) Exercise Increases cardiac output. 14