Chapter 19 Cardiovascular System: Heart Cardiac Anatomy 1 • Pericardial sac: 3 layers – fibrous, parietal, and visceral endothelium (pericardium) surrounds the heart; visceral & parietal endothelium form pericardial cavity (potential space) which contains serous fluid • Location: Thorax (mediastinum), left of midline with apex antero-inferior and base postero-superior; the right ventricle rests on the superior border of the diaphragm. The heart sits between the right & left lung. Cardiac Anatomy 2 • Four chambered pump: Atria (right and left) - superior to and smaller than the ventricles. On the outer surface they are separated from the ventricles by a groove (coronary sulcus). Ventricles (right and left) - On the outer surface anteriorly & posteriorly, they are separated from each other by a sulcus (anterior and posterior interventricular sulcus, respectively). Fig. 19.6 Cardiac Anatomy 3 • Anterior external view Great vessels arise superiorly (from rt to lt) 1) superior vena cava to the rt. atrium 2) ascending aorta from the left ventricle (giving rise to coronary arteries which travel along coronary sulcus); branches to form systemic circulation 3) pulmonary trunk from the right ventricle (giving rise to pulmonary arteries); branches to form pulmonary circulation. 4) inferior vena cava to the rt. atrium from inferior aspect. Cardiac Anatomy 4 Branches from Aorta to supply the heart muscle. • Right coronary artery: travels along the rt. coronary sulcus. It branches to rt. marginal artery (runs along the inferior surface of rt. ventricle) • Left coronary artery: branches to circumflex art. (travels posteriorly in coronary sulcus) and LAD(Left Anterior Descending)/Anterior Interventricular art. (traveling inferiorly within the anterior interventricular sulcus) Cardiac Anatomy 5 • Coronary arts.: supply the very active muscles of the heart wall. They are functional end arteries (anastomoses are ineffective in supply needs). • Cardiac veins : (great, middle & small) run alongside LAD, posterior interventricular & marginal arts respectively. drain into the coronary sinus (posterior surface) which drains into right atrium. Fig. 19.13 Cardiac Function 1 • Two pump structure: left (A) and right (B) sides A) systemic – circulates oxygenated to body’s cells; removes metabolic wastes from the cells. B) pulmonary – circulates deoxygenated blood to lungs for oxygenation and removal of CO2. Each pump has a receiving chamber, atrium, and a pumping chamber, ventricle. • Perfusion: the delivery of blood (ml) to tissues (gm) per unit time (min.): ml/gm/min. Requires a healthy heart and blood vessels for adequate perfusion for healthy tissues and body. Fig. 19.3 Cardiac Function 2 Cardiac Anatomy 6 • Interior view Cardiac muscle wall structure: (outer to inner) epicardium, myocardium, and endocardium Epicardium – visceral layer of pericardium. It is simple squamous epithelium with underlying layer of adipose connective tissue. Myocardium – muscular layer of the wall of the heart; thickest layer; contraction of the myocardium forces the blood through the circulatory system. Endocardium – inner lining; simple squamous epithelium; covers the surface of heart valves and is continuous with blood vessel endothelium. Fig. 19.8 Cardiac Anatomy 7 Ventricular walls are thicker than atrial walls. Left ventricle is thicker than rt. ventricle. Septae separate the atria and ventricles, respectively. • Rt. atrium: pectinate muscles; fossa ovalis; tricuspid valve (rt. AV valve) opens to Rt. Ventricle; coronary sinus • Rt. ventricle: papillary muscles; chordae tendineae pulmonary semilunar valve; trabeculae carneae • Lt. atrium: pectinate muscles; bicuspid valve (Lt. AV/Mitral valve) opens to Lt. Ventricle • Lt. ventricle: papillary muscles; chordae tendineae aortic semilunar valve; trabeculae carneae; Cardiac Anatomy 8 Cardiac Valves Heart valves 1 • Heart Valves two categories of valves ensure one-way flow of blood through the heart. AV valves – permits flow from atria to ventricles; right AV is tricuspid valve (3 leaflets); left AV is bicuspid/Mitral valve (2 leaflets). Semilunar valves – permits flow from left & right ventricles to aorta and pulmonary trunk, respectively. Each valve contains 3 ‘half moonshaped’ leaflets. Heart valves are flexible & made of fibrous connective tissue covered by endothelial lining. Heart valves 2 Myocardium 1 • • • • • • Cardiac muscle anatomy Relatively short, branched, striated muscle cells sarcolemma (plasma membrane) forms T-tubules to SR (sarcoplasmic reticulum) Endomysium: areolar connective tissue surrounds muscle fiber; supports cellular structure sarcomere : Z disc to Z disc; unit of muscle structure intercalated discs (gap junctions, desmosomes) mechanical & electrical link between cells T-tubules: invaginations of sarcolemma, overlying Zdiscs; one ‘t-tubule /sarcomere; extends to SR. Fig. 19.11 Heart pathology 1 • Coronary arteries: atherosclerosis, coronary muscle spasm causes: Angina pectoris: workload exceeds blood supply Myocardial Infarction: cellular death due to sudden, complete occlusion; myocardial tissue replaced by nonfunctional scar tissue; • Valvular disorders: murmurs: heard on ascultation; back flow of blood; insufficiency stenosis (Streptococcal infections) Fig. 19.14 Fibrous Skeleton • Dense irregular connective tissue structural & mechanical support of heart anchor for heart muscle attachment; fibrous rings anchor heart valves; forms septa electrical insulation of conduction system action potentials do not leak from atria to ventricles or vice versa; independent contraction • Cardiac muscle arranged in spiral bundles causing inward compression of heart chambers; ventricular contraction starts at the apex moving superiorly Cardiac function 1 • Perfusion: delivery of blood per tissue per time ml/ min/gm. Exchange of gases, nutrients and wastes take place at level of the capillary network. • Circulation: a) arteries – blood away from the heart b) veins – blood towards the heart c) capillaries – joins arterioles to venules; exchange of nutrients, gases, wastes • Cardiac cycle: systole & diastole (contract/relax) Cardiac output: HR x SV = CO Heart rate x Stroke volume Cardiac function 2 • Conduction system: regulates heart pumping action: rate (chronotropic) and/or force (inotropic) SA (sinoatrial) node: pacemaker AV node, AV bundle, Purkinje fibers (larger); ANS Cardioaccelaratory Center: Sympathetic (T1-5) Cardioinhbitory Center: Parasympathetic (Vagus n.:CN X); Vagal tone Atrial reflex (Bainbridge reflex) stretch of atrial wall stimulates sympathetic response; protection from overfilling. Cardiac function 3 • SA Node: generates action potential RMP: - 60mV; (Na+/K+) pumps; (Na+) leak channels; (K+) leak channels. (Ca2+) pumps: > conc. Ca2+ extracellular. *Na+ channels: slow voltage-gated Ca2+channels: fast voltage-gated K+ channels: voltage-gated Threshold: -40mV; Pacemaker potential: RMP (-) Threshold (20mV) *autorhythmic; self regulating; Cycle: 0.8 secs; SA nodal rhythm: ~100/min Vagal tone: parasympathetic (ANS): 75beats/min Heart pathology 2 • Conduction: Ectopic pacemaker – focus other than SA node; SA node inherent rhythm of ~100/min; AV node rhythm of ~45/min; Cardiac muscle cells: 20-40/min Arrhythmias Flutter: regular atrial contractions 200-400/min; Fibrillation: irregularly irregular rate; chaotic disturbances in heart rate; atrial or ventricular; atrial bombardment causes ventricular irregularity. V. fibrillation- twitching/fibrillary movement replaces regular contractions; incompatible with life (cardiac arrest) treated with defibrillation. Heart pathology 3 • PVC: single/bundles; initiated in AV node or ventricular conduction; caused by stress/stimulants. Usually not problematic if they don’t occur in large numbers. • Heart block – AV block 1st degree: delayed ventricular depolarization 2nd degree: some atrial AP’s are blocked 3rd degree: no SA nodal AP’s reach AV node; life threatening requiring medical intervention. Bradycardia: less than 60beats/min, resting HR Tachycardia: 100+ beats/min. resting HR. Cardiac Muscle 1 • Electrical Events Depolarization of sarcolemma RMP: -90mV stimulated by action potential in SA/AV node, fast voltage gated Na+ channels open; sarcoplasm become relatively positive; K+ channels open, initiating repolarization; simultaneously, slow voltage-gated Ca2+channels open prolonging depolarization (*plateau). Ca2+channels close, K+ channels remain open, the sarcolemma repolarizes. *Refractory period is extended preventing tetany. Cardiac muscle 2 Cardiac muscle 3 • Muscle contraction (mechanical events) Ca2+ enters sarcoplasm (on depolarization) Ca2+ binds troponin initiating crossbridge cycling. Sarcomeres shorten as thin filaments slide past thick filaments (reference slide #41), cardiac muscle contracts (systole). Voltage gated Ca2+ channels close, reuptake of Ca2+ from sarcoplasm by SR, and release of Ca2+ from troponin causes cardiac muscle relaxation (diastole). Cardiac muscle contraction Electrocardiogram • EKG/ECG: reflect electrical changes in myocardium P wave – depolarization of atria QRS complex – depolarization of ventricles; atrial repolarization is masked by ventricular activity T wave - repolarization of ventricles. P, QRS, and T wave sequence indicate one heart cycle Fig. 19.20 Cardiac Cycle 1 • One cycle includes: the start of one heart beat to the next; it is the contraction and relaxation of the two sets of heart chambers (atria & ventricles) & includes five phases: atrial systole, early ventricular systole, late ventricular systole, early ventricular diastole, late ventricular diastole (ref. slide # 46 for details). Systole is the contraction of a heart chamber. Diastole is the relaxation of a heart chamber. Cardiac Cycle 2 • Ventricular contraction and relaxation along with the pressure changes within the heart chambers are the primary cause of unidirectional blood flow and valve function preventing back flow. Cardiac output 1 • The amount of blood pumped in one minute by either the left or right ventricle. It is determined by heart rate and stroke volume and expressed in liters/minute: HR x SV = CO (L/min) 75beats/min x 70ml = 5250 ml/mi Exertion demands require an increase in CO (both HR & SV increase). Cardiac Reserve: an increase in CO beyond the heart’s resting level. May increase to four fold (20L) in a healthy individual; to seven fold (35L) in an athlete. Cardiac output 2 • CO is influenced by variables which affect either HR or SV or both (chronotropic or ionotropic, respectively). • Chronotropic influences: affect SA/AV node ANS – Positive chronotropic agents cause an increase in HR include: sympathetic pathways and hormonal stimulants. Norepinephrine, Epinephrine bind β1 receptors releasing Ca2+ to nodal cells, increasing AP rate. Thyroid hormone increases # of β1 receptors, increasing response to sympathetic stimulation. Caffeine, nicotine & cocaine increase HR. Cardiac output 3 • Chronotropic influences: Negative chronotropic agents: cause a decrease in HR include: parasympathetic pathways and β blockers. Acetylcholine binds voltage-gated K+ channels releasing K+ from the nodal cells, hyperpolarizing nodal cells and delaying threshold, slowing HR. β blockers stop NE & Epi binding and block nodal cells from reaching threshold, decreasing action potentials and slowing HR. β blockers are generally used to treat high blood pressure (HBP). Cardiac output 4 • Stroke volume influences (SV is the amount of blood pumped each heart beat) venous return, ionotropic agents, and afterload Venous return determines EDV : the amount of blood in the ventricle prior to contraction. This determines the preload: the stretch on the cardiac wall due to filling capacity prior to contraction. • Frank Starling law: increasing venous return, increases preload, resulting in a more forceful contraction, due to increased overlap of thick & thin filaments, increasing crossbridging. A more forceful contraction increases SV. Cardiac output 5 • Stroke volume influences Decrease in venous return, decreases preload, decreasing overlap & crossbridging. The force of contraction is thereby decreased, decreasing SV. Venous return is influenced by: 1) an increase or decrease in venous pressure; 2) an increase or decrease in filling time. • Ionotropic agents: increase/decrease the force of contraction (positive/negative respectively). This is due to the concentration of Ca2+ in the sarcoplasm. Ca2+ forms the crossbridging by binding troponin. Cardiac output 6 • Ionotropic agents: Positive ionotropic agents – increase the [Ca2+] in the sarcoplasm, include: sympathetic axon release of NE, adrenal medulla release of NE & Epi., thyroid hormone, digitalis. Negative ionotropic agents - decrease the [Ca2+] in the sarcoplasm, include: electrolyte imbalances increases of K+ and H+, Ca2+; channel blockers (Nifedipine/Procardia) used to treat HBP. • Afterload: arterial resistance to ventricular ejection; increases with aging as the arterial lumen size decreases. The pericardial cavity is located between the a) fibrous pericardium and the parietal layer of the serous pericardium. b) parietal and visceral layers of the serous pericardium. c) visceral layer of the serous pericardium and the epicardium. d) myocardium and the visceral layer of the serous pericardium. During the recycling of components following the normal destruction of erythrocytes, globin is broken down, and its components are: a) used to synthesize new proteins. b) stored as iron in the liver. c) eliminated from the body in the bile. d) removed in the urine.