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Cardiac Conducting System Cardiac muscle tissue contracts on its own No neural nor hormonal control “autorhythmicity’ Specialized cells: initiate and distribute depolarization 1. Sinoatrial node (SA node) a. Near entrance of superior vena cava/posterior wall of R. atrium b. “pacemaker cells” establish heart rate c. Connected to AV node via conducting pathways d. Stimulus affects only ATRIA i. Fibrous skeletal separates atria from ventricle 2. AV node: a. Floor of right atrium b. Near opening of coronary sinus c. From AV to bundle of His(bundle branches) which run along interventricular septum d. Delay at AV node allows atria to complete contraction before ventricular contraction begins 3. AV bundle(bundle of His) a. Impulse reaches AV bundle- travels along septum, splits between L & R bundle branches b. Purkinje fibers – where the bundle of His diverge into smaller branches i. Cause ventricular contraction ii. Wave action from apex(bottom) to base(top) iii. Blood is pushed out aortic and pulmonary trunk ELECTROCARDIOGRAM Monitors electrical activity of heart 1. P wave: small, atria contract after start of P wave – depolarization of atria 2. QRS complex: ventricles depolarize – STRONG electrical signal – ventricles contract AFTER peak at R 3. T wave – ventricles relax 4. Do not “see” atrial relaxation due to strong QRS Problems detected: Extension of P-R interval = damage to conducting pathways or damage to AV node Extension of Q-T interval = myocardial damage HEART ATTACK – myocardial infarction Infarct = nonfunctional area of myocardium Enzymes that detect MI= LDH; SGOT; CPK(creatine phosphokinase) Systole – contraction Diastole – relaxation On patient with stethoscope Patients upper area right of sternum – hear pulmonary semilunar valve Lower right of sternum – hear right atrioventricular valve (tricuspid) Upper right of sternum – hear aortic semilunar valve Lower right of sternum – left atrial ventricular valve – bicuspid