Applied Therapeutics Lec 5: Arrhythmia Ther PDF 2024

Arrhythmia Arrhythmia is a term which refers to any change in the normal rate or rhythm of the heart. Normal activity of the heart. Four structures are key to the conduction of electrical impulses through the heart muscle: The sinoatrial (SA) node located in the right atrium. The atrio...

Arrhythmia Arrhythmia is a term which refers to any change in the normal rate or rhythm of the heart. Normal activity of the heart. Four structures are key to the conduction of electrical impulses through the heart muscle: The sinoatrial (SA) node located in the right atrium. The atrioventricular (AV) node located between the right atria and ventricles. The bundle of His (or AV bundle) and bundle branches, which carry current from the AV node to the ventricles. The Purkinje fibers, which conduct the current throughout the ventricular tissue. In the healthy heart the SA node acts as the cardiac pacemaker, generating electrical impulses which are then conducted via the atria to the ventricles, hence the term "sinus rhythm". The normal resting heart rate is approximately 70 beats per minute and is maintained by electrical impulses arising from within the SA node. Etiology Arrhythmias result from abnormal impulse formation or abnormal impulse conduction. These changes may be brought about in several ways.: 1. An infarction may cause the death of pacemaker cells or conducting tissue. 2. A cardiac tissue disorder, e.g. fibrosis or rheumatic fever, disrupts the conduction network. 3. Sympathetic or parasympathetic control changes, e.g. stress, anxiety, exercise, or smoking. 4. Circulating drugs, e.g. antiarrhythmics or inotropes or other substances, e.g. caffeine, or alcohol. 5. Hypothyroidism, hyperthyroidism, hyperkalaemia and hypokalemia or other electrolyte disturbances may predispose the heart to arrhythmias. Patients who have pre-existing cardiac disorders including heart failure, hypertension or a recent infarction are at greater risk of arrhythmias. 1 Description of arrhythmias All cardiac rhythms can be described by a phrase which includes terms that relate to rate, origin, and pattern. (Table 22.1) Paroxysmal refers to self-terminating episodes of up to 7 days, although in practice they are usually less than 1 day in duration. Pathogenesis of arrhythmias Arrhythmias develop by one of two mechanisms: 1- Altered impulse generation, for example, changes in ability of the pacemaker cells in the SA node to generate electrical impulses spontaneously, or through the occurrence of action potentials from sites other than the SA node. 2- Altered impulse conduction, for example, complete or partial block of conduction pathways within the myocardium. Classification of Arrhythmias 1- Supraventricular arrhythmias All arrhythmias originating above the bundle of His 2- Ventricular arrhythmias. Arrhythmias originating below the bundle of His 3-An alternative method of classifying arrhythmias is based on the rate: Bradyarrhythmia (100 beats/minute). Signs and consequences of arrhythmias 1-Arrhythmias are associated with increased morbidity and mortality. Atrial fibrillation (AF) roughly doubles the risk of a person having a stroke, triples the risk of heart failure and doubles mortality risk. 2- Bradycardias tend to cause symptoms that reflect low cardiac output: fatigue, 2 lightheadedness, and syncope (syncope: is a sudden loss of consciousness due to reduced cerebral perfusion). 3-Tachycardias cause rapid palpitation, dizziness, chest discomfort or breathlessness. Extreme tachycardias can cause syncope because the heart is unable to contract or relax properly at extreme rates. 4-Palpitations are the awareness of one's heartbeat; they may range from a minor sensation to a distressing problem. 5- Extreme bradycardias or tachycardias can precipitate sudden death or cardiac Arrest. 6-Since these signs are not unique to arrhythmias, arrhythmias are not always easy to diagnose, and 24- hour recordings of the ECG (Holter monitoring) may be used. Diagnosis of Arrhythmia 1-Electrocardiogram (ECG) 2-Holter monitoring: Ambulatory, portable ECG monitor that can record the electrical activity of the heart for 1 to 2 days at a time to detect episodes of arrhythmia. Bradycardia A heart rate of less than 60 beats per minute is considered a bradycardia. If the heart rate slows but the rhythm remains unchanged (i.e, is still controlled by impulses generated in the SA node) this is known as sinus bradycardia. It can be entirely normal, for example in athletes (well-conditioned heart and large stroke volume) or during sleep, but it may also occur secondary to acute myocardial infarction, sick sinus syndrome (sinoatrial disease e.g. fibrosis of the SA (sinus) node) or drug therapy, particularly beta-blockers. The condition is characterized by a variety of arrhythmias including: 3 A-Sinus bradycardia due to a reduction in the frequency of impulse generation within the nodal pacemaker cells (reduced automaticity). B-Sinus arrest if the node completely fails to generate an action potential. Bradycardias can also be of neurocardiogenic origin, for example, they can be due to excessive vagal tone or can arise during carotid sinus massage which results in stimulating vagal activity. (Carotid: The two main arteries in the neck). Heart block Bradycardias can be caused by heart block, where there is a failure to conduct the electrical signal. AV nodal block is the most commonly identified in clinical practice. In this situation, the electrical impulse generated by the SA node travels across the atria but is blocked at the level of the AV node before it can be conducted to the ventricles. AV block may be classified into three types. 1-First degree AV block : describes instances where all beats are conducted through the AV node, but with some delay. This does not require treatment but may be a warning to avoid drugs that would worsen the block, such as β-blockers and class IV agents (verapamil, diltiazem). 2-Second degree AV block: implies that some, but not all, beats are conducted through the AV node. Second-degree AV block is further distinguished into two types: Mobitz type I (also known as Wenckebach) and Mobitz type II (3). The need for treatment depends upon whether a satisfactory ventricular rate and output can be maintained. 3-Third degree or complete heart block implies that there is no conduction of sinus or atrial beats through the AV node. (The ventricles initiate their own depolarizations). Treatment is usually required. Bundle branch blocks (BBB) Right bundle branch block (RBBB) occurs in normal healthy individuals and heart diseases (e.g. Ischemic heart diseases) while Left Bundle branch block (LBBB) indicates underlying cardiac pathology. Tachycardias A heart rate of more than 100 beats per minute is considered a tachycardia. 4  They can be divided into: Supra-ventricular arrhythmias and Ventricular arrhythmias. 1-Supra-ventricular arrhythmias (supra-ventricular tachycardias) A-Sinus tachycardia Sinus tachycardia occurs if the heart rate increases but the rhythm remains unchanged. It is usually due to an increase in sympathetic activity. Sinus tachycardia is common during exercise or excitation but may also occur during infection, hypovolaemia, anaemia, thyrotoxicosis, and shock. It can also occur as a side effect of many drugs, such as beta 2 agonists, thyroxine and aminophylline. B-Atrial ectopic beats (extrasystoles, premature beats) These usually cause no symptoms but can give the sensation of a missed beat or an abnormally strong beat (due to the increased output of the post-ectopic beat). In most cases these are of no consequence. Treatment is rarely necessary. C-Atrial flutter (regular irregularity): Atrial flutter occurs less frequently than atrial fibrillation (AF). The atrial rate is approximately 300/min. The resulting ventricular rate is usually regular, but slower than the atrial rate as the AV nodal delay prevents these rapid atrial impulses from being conducted to the ventricles in a 1:1 ratio. Conduction may be 2:1 (one ventricular depolarization for every two atrial impulses), 3:1 or 4: 1). The rapid atrial rate and disturbance of conduction pathways in atrial flutter increases the risk of localized thrombus formation and secondary embolic events (ie, thrombotic stroke) in this group of patients. D-Atrial fibrillation (AF) (irregular irregularity): AF is one of the most common arrhythmias and it is a major cause of morbidity and mortality. AF incidence increases with age and is more common in patients with hypertension, coronary artery disease and heart failure. Other causative factors include hyperthyroidism and high alcohol consumption. The inappropriate electrical signals lead to repetitive and chaotic ‫ﻓﻮﺿ ﻮي‬ 5  depolarization of the atrial myocardium. The ventricular rate is usually rapid (around 100-180 beats per minute) and irregular. (In general ,when compared with Atrial flutter, AF is associated with higher atrial rates, a slower ventricular rate, and an irregular ventricular rhythm). The condition can lead to the formation of local thrombi. As a result, one of the most important complications of AF is the increased risk of thromboembolic stroke. E. Paroxysmal Supraventricular Tachycardias (PSVTs) AV nodal re-entry tachycardias (AVNRT) and AV re-entry tachycardias (AVRT) Wolff-Parkinson-White (WPW) syndrome is the best-known type of AVRT in which there is an accessory pathway between atria and ventricles. 2-Ventricular arrhythmias (OR Ventricular tachyarrhythmias) A-Ventricular ectopic beats (extrasystoles, premature beats) Ventricular ectopic beats in otherwise healthy subjects: Treatment is not necessary unless the patient is highly symptomatic, in which case ß-blockers can be used. Ventricular ectopic beats associated with heart disease (e.g. recent MI or heart failure): Treatment is usually needed. B-Ventricular tachycardias (VT) VT is defined as three or more consecutive ventricular ectopic beats. VT is defined as non-sustained if it lasts less than 30 seconds and terminates spontaneously; sustained VT lasts greater than 30 seconds and does not terminate spontaneously, but rather requires therapeutic intervention for termination. Torsades de pointes (TdP) is a specific form of VT with prolongation of the QT interval secondary to drug therapy, particularly anti-arrhythmics Torsades de pointes can rapidly degenerate into ventricular fibrillation and must therefore be treated as a medical emergency. 6 C-Ventricular fibrillation -Ventricular fibrillation (VF) is a rapid and uncoordinated contraction of the ventricular tissue. It severely compromises cardiac output (resulting in no cardiac output) to the extent that patients usually lose consciousness within 10-20 seconds of onset. It is responsible for most deaths caused by myocardial infarction and there is high risk of VF in patients with severe ischaemic heart disease. Vf is a medical emergency, because without prompt treatment irreversible cerebral and myocardial damage will occur. The options for treatment 1-Nonpharmacologic therapy of bradyarrhythmias: Cardiac pacemakers Artificial cardiac pacemakers are devices that deliver a small electrical impulse to a localized region of the heart, thus initiating an action potential that then spreads to the remainder of the heart. Permanent pacemaker systems are implanted in a skin "pocket" below the collar bone. Leads are inserted via a vein into the heart. 2-Nonpharmacologic therapy of tachyarrhythmias A-Direct current cardioversion and defibrillation Cardioversion refers to the process of restoring the heart's normal rhythm. This can be done chemically using drugs (chemical or pharmacological cardioversion) or by application of an electric shock across the chest (electrical cardioversion). B-Radiofrequency Catheter Ablation and Implantable Cardioverter-Defibrillators 7 3-Pharmacologic therapy Classification of antiarrhythmic drugs A-Vaughn Williams classification The most frequently used classification system is the Vaughn Williams classification, which categorizes these drugs on the basis of their in vitro electrophysiologic effect on normal Purkinje fibers. There are four antiarrhythmic drug classes. Class I drugs, Na-channel blockers, Class II drugs β-adrenergic blockers, class III drugs K-channel blockers, and class IV drugs Ca-channel blockers (4, 5). B-Classification according to site of action A more simple classification system used in clinical practice is to consider the principal site or sites of action of anti-arrhythmic drugs Ventricular fibrillation 1- hemodynamically unstable, due to the absence of pulse and blood pressure. 2-Initial management includes initiation of cardiopulmonary resuscitation (CPR). 3-Oxygen should be administered as soon as it is available. 4- The only means of successfully terminating VF and restoring sinus rhythm is electrical defibrillation (DCC). 5-The vasopressor agents epinephrine or vasopressin are administered initially, 8 9