1) Anatomy of Heart (refer case 1) Phase 1 Rapid repolarization, Na+ myocardium Discharges 2) Innervation of Heart channel closed, K+ efflux - At the junction of membranous & SA node: 60 -100x/min By cardiac plexus Phase 2 Slow repolarization, muscular part of IVS septum, it AV node: 40-60x/min i. Sympathetic balance of K+ efflux & divides into right & left bundles. Purkinje fibres: 15-40x/min Presynaptic: T5/T6 spinal cord Ca2+ influx plateau Subendocardial branches (Purkinje Pacemaker Postsynaptic: Cervical & superior Phase 3 Final phase of repolarization, fibres) further K+ efflux. Normal: SAN thoracic paravertebral ganglia - Have 1/2 central nuclei Ca is removal - Na+/Ca2+ 2+ Latent: other than SAN cardiopulmonary splanchnic nerve - mitochondria & glycogen exchanger Ectopic: when SA node cant cardiac plexus ends at SA node & - myofibrils restricted at Na+ is removed- Na+/K+ ATPase initiate impulse, latent AV node. periphery of cytoplasm Phase 4 Resting potential pacemaker take over & produce ii. Parasympathetic - Extends at ventricular wall, weaker discharges. Presynaptic: Vagus nerve penetrate 1/3 endocardium. 6) Cardiac rhythmical excitation Controlled by ANS Postsynaptic: Intrinsic ganglia at 5) Action potential (AP) Specialized excitatory & conductive 8) ECG atrial wall & interatrial septum near system of heart Def: Recording of the electrical SA, AV node and along coronary Pacemaker - Initiate impulse & cardiac muscle activity of cardiac cells that artery. cells contracts rhythmically, conduct reaches the body surface. 3) Heart conducting system impulse in normal pathway. Functions SA node atrial muscle AV node - SA node intermodal pathway - Enlargement of chambers AV bundles Bundle branches AV node AV bundle R&L bundle - Arrhythmias Purkinje fibres Ventricular muscles branch Purkinje fibre - Electrolyte abnormality Phase O Depolarization, Ca2+ channel Normal ECG characteristics Mechanism 4) Histology of conducting system opened, Ca2+ influx i. SA node SA node Phase 3 Repolarization, K+ efflux - Self-excitation ability - Small mass of specialized cardiac from cell - Rhythmical period is determined by muscle fibres Phase 4 Resting potential, upward slope (Na+ leakage) AP voltage (ion transport) - Located anterolaterally, at the ii. AV node junction of SVC & RA - Control impulse by delay the AP to - Pacemaker of heart; initiates & allow blood fills efficiently into regulates impulses for heart ventricles. contraction - SA node(0.03s) AV node (0.09s) Vertical axis: voltage AV node AV bundle (0.04s) Purkinje Horizontal axis: time - Smaller than SA node Fibres (0.06s) ventricular muscles - gap junctions - P wave : Atrial depolarization iii. Purkinje fibres - Located at posteroinferior region Cardiac - QRS complex : Ventricular - Faster, via intercalated disks of interatrial septum muscle depolarization cells I Block fast Na+ channel - T wave : Ventricular repolarization ii. Disturbed impulse conduction IA : Qunidine, Disopyramide Adverse effect : - ST segment : Early ventricular - Conduction block IB : Lidocaine Hypertension, repolarization - Unidirectional block & Re-entry IC: Flecainide Arrhythmia - QT interval : Ventricular - Accessory pathway & WPWS II adrenergic receptor v. Lidocaine depolarization + repolarization Bundle of Kent agonists MOA: Class IA Block Method to record ECG Classification III K+ channel blocker fast Na+ channel Placement of 4 basic limb Ex : Amiodarone during phase 0 AP 1. Bradyarrhythmia (<60 bpm) electrodes IV Block L-type Ca2+ channel Adverse effect: Slurred - Sinus bradycardia - Right & left arm Ex : Verapamil speech, dizzy - Right & left leg - Junctional bradycardia (heart vi. Propanolol ECG leads block) 10) PP MOA: Class II - adrenergic i. Standard limb leads a) 1st degree receptor agonists HR, i. Amiodarone I, II, III b) 2nd degree myocardial contractility & BP MOA: Class III prevent K+ ii. Augmented unipolar leads Mobitz I O2 efflux during repolarization aVR, aVL, aVF Mobitz II Adverse effect : Bradycardia prolong AP & effective iii. Precordial leads c) 3rd degree / complete vii. Verapamil refractory period. V1 ICS4, right sternal margin 2. Tachyarrhythmia (>100 bpm) MOA: Ca2+ channel Adverse effect : bradycardia, blocker arterial V2 ICS4, left sternal margin - Sinus tachycardia heart block vasodilation V3 Midway between V2 & V4 - Atrial/Ventricular a) Tachycardia Amiodarone + Digoxin cardiac workload V4 ICS5, midclavicular line, left b) Flatter 250-350 level/effect of digoxin Adverse effect: V5 Left anterior axillary line c) Fibrillation >350 ii. Digoxin Headache, V6 Left mid axillary line MOA: Inhibits Na+/K+ ATPase hypotension - Junctional tachycardia intracellular Na+ Verapamil + Digoxin 9) Arrhythmia Management Ca2+ efflux intracellular toxicity digoxin Def : Abnormality of heart 1. Bradyarrhythmia Ca2+ stored in SR clearance & electrical rhythm Anticholinergic drugs contraction force distribution volume, Mechanism B1 receptor agonist Adverse effect : Severe GI tract absorption i. Altered impulse formation Electronic pacemaker arrhythmias - Altered automaticity 2. Tachyarrhythmia iii. Disopyramide BHP Beneficence & Non * SA node automaticity Anti-arrhythmia (table) MOA: Class IA Block maleficence: Choose patients Na+ medication wisely (/) Vagotonic manuever fast channel * automaticity of latent Electric cardioversion & during phase 0 AP PHOP Educate patient to pacemaker defibrillation Adverse effect : take medication given - Abnormal automaticity Urinary retention regularly. - Triggered activity iv. Epinephrine MOA: Stimulate - CRP Research about adrenergic receptor therapeutic window of digoxin efficacy for treatment.