Arrhythmia and its Management.pdf

Phase 4 Resting phase (RMP), Diastole Phase 0 Rapid depolarization Closure of the fast Na+ channels Cardiac Action Potential Phase 1 Initial rapid repolarization Phase 0 and 1 correspond to the R and S waves Sustained by inward movement of Ca+ and outward movement of k+ Phase 2 Plateau pha...

Phase 4 Resting phase (RMP), Diastole Phase 0 Rapid depolarization Closure of the fast Na+ channels Cardiac Action Potential Phase 1 Initial rapid repolarization Phase 0 and 1 correspond to the R and S waves Sustained by inward movement of Ca+ and outward movement of k+ Phase 2 Plateau phase Corresponds to ST segment of the ECG Allows K+ to move out of the cell – repolarize Phase 3 Repolarization Corresponds to T wave on the ECG The SA node (physiologicalpacemaker) starts the sequence by generating an electrical impulse Sequence of pacemakers action potential Resting Phase 4 Action Potentials of the SA/AV Node Upstroke Phase 0 Early repolarization Phase 1 5 Phases of SA node action potential causing the atrial muscles to contract Plateau Phase 2 Repolarization A decline of potential at the end of phase 3 in pacemaker cells, such as the sinus node, is shown as a broken line. Phase 3 PCs Nonpacemaker and Pacemaker cell APs Slow, continuous depolarization during rest Continuously moves potential towards threshold for a new action potential (called a phase 4 depolarization) P Wave Reflects atrial depolarization PR Interval Relationship between phases of the action potential and the electrocardiogram QRS Complex QT Interval The process of initiation of reentry Two pathways for impulse conduction: Mechanisms of Cardiac Arrhythmias Duration potential ventricular action impulse formation Contraction impulse conduction Combination of the two Results of above disturbances Atrial arrhythmia Ventricular depolarization longer refractory period in pathway B Heart condition where disturbances in Heart Rhythm Reflects the conduction velocity through AV node Slowed impulse conduction down pathway A Abnormal Pacemaker Normal rhythm Phase 0 insufficient rate or contraction to maintain normal cardiac output (CO). the top chambers (atria) contract and push blood into the bottom chambers (ventricles). the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles, so you may have four atrial beats to every one ventricular beat. Cardiac ischemia Excessive discharge or sensitivity to autonomic transmitters Electrolyte and pH imbalance Causes of arrhythmias Exposure to toxic substances Mechanical injury overstretching Drug influences including antiarrhythmics Atrial Remodeling Abnormal Conduction Mechanistic Changes Obesity, Hypertension Atrial Enlargement Progressive Substrate Inflammation Arrhythmia and its Management Expression of Endothelin Receptors Atrial Dysfunction Risk factors Modifiable Risk Factors Mechanistic Changes Sleep Apnea, Diabetes, Hyperlipidemia LA Pressure LA Volume Epicardial Fat Vagal Tone Endothelial Dysfunction Cellular Myolysis Alcohol, Smoking Oxidative Stress Mechanistic Changes Conduction Slowing Interstitial Fibrosis Ectopic Triggers Tachycardia Bradycardia Fainting Signs Confusion Dizziness Shortness of breath Profuse sweating Procainamide IA Quinidine Disopyramide Lidocaine Class I Na+ channel blockers IB Mexiletine Direct membrane action Phenytoin Flecainide IC Propafenone Ethmozine Propranolol Class II Sympatholytic agents Esmolol Sotalol also class III Amiodarone Bretylium Classification of AA drugs Class III Prolong repolarization Dofetilide NAPA Verapamil Class IV Ca++ channel blockers Diltiazem Purinergic agonists Digitalis glycosides Based on cellular properties of normal His-Purkinje cells Na+ specific ionic currents Vaughn-Williams Classification K+ Ca2+ lassified on drug’s ability to block: beta-adrenergic receptors Advantage Physiologically based All cells are not normal Disadvantage All cells are not his-purkinje in origin Class I Major site of Action of Anti-arrhythmic Drugs Class II Class III Calss IV Phase 0 Phase 4 Phase 2 Phase 3 Phase 2 Inhibition of Fast depolarization Inhibition of Pacemaker depolarization Inhibition of Plateau phase Inhibition of Rapid repolarization Inhibition of Plateau phase From there, the signal travels to the AV node then through the bundle of His down the bundle branches and through the Purkinje fibers causing the ventricles to contract.