Cardiac Arrhythmias Notes PDF

Image result for cardiac arrhythmia Cardiac Arrhythmias  Normal Cardiac Activity ▪ Mechanical Activity: 4 8 4 Atrial and Ventricular contraction 5 “ The mechanism by which blood is...

Image result for cardiac arrhythmia Cardiac Arrhythmias  Normal Cardiac Activity ▪ Mechanical Activity: 4 8 4 Atrial and Ventricular contraction 5 “ The mechanism by which blood is 5 delivered to tissues” 1 6 ▪ Electrical Activity: ▪ Results in the mechanical activity 7 ▪ The heart possesses an intrinsic 2 electrical conduction system ▪ Depolarization of the atria results 3 in atrial contraction 1 ▪ Depolarization of the ventricles results in ventricular contraction “Malfunction of the heart’s electrical conduction system may result in dysfunctional atrial and/or ventricular contraction “  The Cardiac Conduction System http://washingtonhra.com/resources/AV+block+animation.gif Under normal circumstances: The SA node (the sinus node), serves as the pacemaker of the SA node heart and generates the electrical impulses that subsequently result in atrial and ventricular depolarization. The SA node is the pacemaker because it has the greatest degree of automaticity. The automaticity is: “ The ability of a cardiac fiber or tissue to initiate depolarizations spontaneously”  The Cardiac Conduction System 2 1 Impulse 4B 2 3 4BI 4 4BII 4A 4C  Ventricular Action Potential Na/K ATPase pump maintains relatively high extracellular Na concentrations and relatively low extracellular K concentrations; this keeps the myocyte resting membrane potential between – 70 to –90 mV In a resting cell PHASE - EVENT phase 0 - rapid depolarization phase 1 - rapid initial "repolarization“ phase 2 - "neutral" plateau phase 3 - final repolarization phase 4 - resting membrane potential  Ventricular Action Potential Phase (0) represents ventricular depolarization as a result of rapid Na influx. Phase (1) repolarization occurs primarily as a result of K efflux. Phase (2) repolarization through K efflux continues, but the membrane potential is balanced by an Ca and Na influx, PHASE - EVENT phase 0 - rapid depolarization transported through slow Ca and phase 1 - rapid initial "repolarization“ slow Na channels, resulting in a phase 2 - "neutral" plateau phase 3 - final repolarization plateau. phase 4 - resting membrane potential  Ventricular Action Potential Phase (3) the K efflux greatly exceeds Ca and Na influx, resulting in the major component of ventricular repolarization. Phase (4) Na ions are actively pumped out of the myocyte via the Na/K ATPase pump, resulting in restoration of membrane potential to its resting state. PHASE - EVENT phase 0 - rapid depolarization phase 1 - rapid initial "repolarization“ phase 2 - "neutral" plateau phase 3 - final repolarization phase 4 - resting membrane potential  The Electrocardiogram ▪ The ECG is a non-invasive means of measuring the electrical activity of the heart. The P wave on the ECG represents atrial depolarization The QRS complex “Phase zero” corresponds to ventricular depolarization. T wave represents ventricular repolarization “Phase 3“. Atrial repolarization Not displayed because it occurs during ventricular depolarization and is obscured by the QRS complex.  The Electrocardiogram ▪ QT interval, is used as a non-invasive marker of ventricular repolarization time, measuring 0.32 to 0.4 seconds. ▪ R-R interval represents heart rate.  The Electrocardiogram ▪ PR interval represents the time of conduction of impulses from the atria to the ventricles through the AV node (0.12 to 0.2 seconds in adults). ▪ QRS complex represents the time required for ventricular depolarization (0.08 to 0.12 seconds in adults). ECG tracing File:ECG principle slow.gif Animation of a normal ECG wave  Electrophysiologic properties of cardiac tissue 1. Automaticity 2. Excitability 3. Conduction 4. Refractoriness  1. AUTOMATICITY ▪ The ability of a cardiac fiber to generate action potential (heartbeat) spontaneously, continuously & regularly without external stimulation. ▪ Cardiac cells that are normally automatic include: Intrinsic depolarization rate Sinus (or SA) node 60-100 beats/min AV node 40-60 beats/min Purkinje fibers 30-40 beats/min (Ventricular tissue)  2. EXCITABILITY 3. CONDUCTION The ability to respond to a The ability to spread the cardiac stimulus of adequate strength & impulse (excitation) from cell to cell duration (ie. Threshold) by through the cardiac tissue. generating an action potential. *All cardiac cells are excitable.  4. REFRACTORINESS Period during which cells and fibers CANNOT be depolarized again. Absolute RP: Phase 1, 2, one-third of 3 If there is a premature stimulus, the impulse CANNOT be conducted (tissue is absolutely refractory) Relative RP: Later two-thirds of phase 3 If a new premature stimulus is initiated, it can be conducted abnormally, resulting in arrhythmia.  Arrhythmia Any abnormality in the rate, regularity, or site of origin of the cardiac impulse, or a disturbance in the conduction of that impulse such that the normal sequence of activation of the atria and ventricles is altered. Cardiac arrhythmias are classified into two broad categories: ▪ Supraventricular (those occurring above the ventricles) e.g., Sinus tachycardia, and Atrial fibrillation (AF) ▪ Ventricular (those occurring in the ventricles) e.g., Premature ventricular contractions, and Ventricular fibrillation  Arrhythmia MECHANISMS OF ARRHYTHMIAS: I. Abnormalities of impulse formation a. An alteration of physiological automaticity (enhanced or depressed) b. Development of abnormal automaticity: ectopic pacemakers. II. Abnormalities of impulse conduction a. Conduction delay or block b. Reentry III. Abnormalities of BOTH impulse formation AND conduction Mechanisms of Reentry Arrhythmias Prerequisites for Reentry (Reentrant Arrhythmias) Trigger Reentry substrate Premature beat Two distinctly different An irregular beat arrives at a pathways in conduction critical timing velocity & RP  Normal sinus beat Sinus beat Slow pathway Fast pathway with short RP with long RP No reentry.. No tachycardia  Critically timed premature beat Premature beat To interrupt the loop: - Drugs that slow conduction - Drugs that Slow pathway Fast pathway prolong RP with short RP with long RP Reentry……..tachycardia Please watch this https://www.youtube.com/watch?v=yLI4yj1TZhc&t=177s Reentry Arrhythmia Reentry Arrhythmia Vaughan Williams Classification of anti-arrhythmic drugs (AAD) Class I Na channel blockers Slow conduction velocity & inhibit ventricular automaticity Class IC > Class IA > Class IB Class IA Quinidine, Procainamide, Disopyramide Class IB Lidocaine, Mexiletine, Tocainide Class IC Flecainide, Moricizine, Propafenone Class II -Blockers Acebutolol, Atenolol, Bisoprolol, Carvedilol, Esmolol, Labetalol, Metoprolol, Nadolol. Slow AV nodal conduction & prolong AV nodal refractoriness Class III K channel blockers Amiodarone, Dofetilide, Ibutilide, Sotalol Inhibit ventricular repolarization “Prolong Refractoriness/prolong action potential/prolong QT segment” Class IV CCB Dilitazem, Verapamil Slow AV nodal conduction & prolong AV nodal refractoriness Adverse Effects of Drugs Used to Treat Arrhythmias Penalties of arrhythmias ▪ None ▪ Sudden cardiac death (SCD) ▪ Syncope / near syncope / dizziness ▪ Other symptoms e.g. - palpitation - a choking or pressure sensation during the tachycardia episode - hypotension and confusion with bradyarrhythmias ▪ Stroke / systemic emboli  Long QT ▪ Measured from the onset of the QRS complex to the end of the T wave. ▪ Normally it doesn’t exceed 460ms. ▪ Measured by the following formula QT/√RR interval in sec. ▪ Long QT syndrome could be congenital or acquired. ▪ Acquired long QT can be predisposed by hypokalemia, hypomagnesemia, hypocalcemia, hypothermia, antifungal, macrolides antibiotics, and subarachnoid hemorrhage. ▪ Predisposes to polymorphic VT( Torsades de pointes)  Implantable cardioverter defibrillator (ICD) ICD  Drug induced arrhythmias Torsades de Pointes ▪ Torsades de Pointes (TdP) is a specific polymorphic VT associated with prolongation of the QT interval in the sinus beats that precede the arrhythmia.  Torsades de Pointes ▪ In prolonged QT, repolarization is delayed → membrane remains partially depolarized longer than normal → certain Ca²⁺ and Na⁺ channels don't close completely → inward Ca²⁺ current can reach a threshold that initiates early afterdepolarizations (EADs) during phases 2 and 3 ▪ Not all heart cells experience the same changes in repolarization. This uneven repolarization across cells helps spread the extra beats caused by EADs, which can set off a reentrant loop, keeping the irregular rhythm (like Torsades de Pointes) going Torsades de Pointes  Torsades de Pointes ▪ TdP may be inherited or acquired. ▪ Patients with specific genetic mutations may have an inherited long QT syndrome, in which the QT interval is prolonged, and these patients are at risk for TdP. ▪ Acquired TdP may be caused by numerous drugs ▪ The list of drugs known to cause TdP continues to expand. Torsades de Pointes Several drugs, including terfenadine, astemizole, and cisapride, have been withdrawn from the US market as a result of causing deaths due to TdP. Torsades de Pointes Torsades de Pointes  Algorithm for management of torsades de pointes *Often defined as 1 or more of the following: systolic blood pressure 150 beats per minute, unconscious or losing consciousness, or chest pain. †Polymorphic arrhythmias do not permit synchronization; therefore, defibrillation is recommended, rather than synchronized direct current cardioversion.35,36 Administer sedation when possible. ‡Even if the patient is not hypomagnesemic. IV, intravenous; TdP, torsades de pointes.