Cardiac Arrhythmias Lecture Notes PDF

Cardiac Arrhythmias ILOs At the end of this session, the student will be able to:  To understand the anatomy and physiology of the normal conduction system  To know the basic mechanisms of cardiac arrhythmias.  To Identify the different types of cardiac arrhythmias....

Cardiac Arrhythmias ILOs At the end of this session, the student will be able to:  To understand the anatomy and physiology of the normal conduction system  To know the basic mechanisms of cardiac arrhythmias.  To Identify the different types of cardiac arrhythmias.  To know the basics of management of management of cardiac arrhythmias.  To know the classification, clinical presentation and management of atrial fibrillation.  Anatomy of the conduction system of the heart:  The cardiac conduction system is formed by specialized myocytes capable of generating action potential and propagating cardiac impulse to the rest of the myocytes to allow cardiac muscle contraction in a synchronized fashion.  Electrical signal arises in the sinoatrial (SA) node (located in the right atrium), then travels through the interatrial tracts stimulate the atria to contract, then the signal travels to the atrioventricular (AV) node. The AV node delays impulse propagation to allow time for ventricular filling. Afterwards, The electrical signal travels very rapidly down the bundle of His into the left and right bundle branches and finally the respective Purkinje fibers for each side of the heart. (Figure 1) Figure 1: The normal cardiac conduction system 1   Cardiac Muscle Action Potential:  The resting potential of the contractile myocardial fibers is stable at about -90 mv with sodium and calcium ions dominantly outside the cell membrane and potassium dominantly inside. A stimulus would initiate an action potential by opening of the voltage-gated Na channels and Na influx into the cell causing depolarization (figure 2).  The pacemaker cells are characterized by having unstable resting membrane potential in the form of spontaneous leakage of Na ions leading to spontaneous depolarization. This occurs independently from the connection to the CNS. This property is termed “automaticity” (figure 3).  Normally, the SA node generates the highest frequency of impulses which makes it the normal pacemaker of the heart. Figure 2: The cardiac action potential. Note the stable membrane potential (phase 4) which needs a stimulus for depolarization to occur 2  Figure 3: The pacemaker cells action potential. Note the spontaneous depolarization initiated by leakage of sodium ions into the cell  Mechanisms of cardiac arrhythmias:  All cardiac arrhythmias occur due to abnormal impulse initiation or abnormal impulse conduction.  Abnormal impulse initiation could be: enhanced automaticity, suppressed automaticity or triggered activity. Abnormal impulse conduction could be: re- entry or conduction block.  The main mechanisms for cardiac tachyarrhythmias are: enhanced automaticity, re-entry and triggered activity.  The main mechanisms for cardiac bradyarrhythmias are: suppressed automaticity and conduction block 3  1. Enhanced automaticity:  Enhanced normal automaticity: the SA nodes fires at a rate higher than normal (sinus tachycardia)  Enhanced abnormal automaticity: another focus fires at a rate faster than the SA node (atrial premature beats, ventricular premature beats, junctional tachycardia, atrial tachycardia, ventricular tachycardia) 2. Re-entry:  It is the most common mechanism of clinically important arrhythmias,  Re-entry is defined as a continuous repetitive propagation of an excitatory wave travelling in a circular path (reentrant circuit) returning to its site of origin to reactivate that site as an electrical circle loop.  3 requirements for reentry are (Figure 4): o A pathway with slow conduction and short refractory period. o Unidirectional block. o Trigger (e.g a premature beat). Figure 4: The mechanism of re-entry. During sinus rhythm the impulse utilizes the fast pathway. (1) In case of occurrence of a premature beat, the fast pathway is refractory so the impulse utilizes the slow pathway. (2) By the time the impulse is conducted through the slow pathway, the fast pathway would have recovered so the impulse is conducted retrogradely thought the fast pathway and (3) again down the slow pathway and so on causing reentrant tachycardia. 4  3. Triggered Activity  Under certain conditions, an action potential can trigger abnormal depolarizations which take place when the first action potential causes instability of the membrane voltage known as after depolarization. It is an uncommon mechanism of arrhythmias (e.g Torsades de pointes and digitalis- induced arrhythmias) 4. Suppressed automaticity:  The SA node has a slower rate of depolarization than normal (sinus bradycardia) or stops firing (sinus arrest). 5. Conduction block:  Block of conduction of the impulse: at the AV node (heart block) or at one of the bundle branches (bundle branch block).  Clinical manifestations of cardiac arrhythmias: A. Symptoms:  Can be asymptomatic, accidentally discovered (e.g. Atrial fibrillation).  Palpitations: usually rapid or “racing” heart beats, with or without a sense of irregularity, are reported by patients with tachyarrhythmias. The palpitations may be chronic or paroxysmal. The onset may be gradual (sinus tachycardia, some forms of atrial tachycardia) or sudden (supraventricular tachycardia).  Symptoms of low cardiac output: dizziness, shortness of breath, fatigue, chest discomfort and syncope in severe forms of arrhythmias. These symptoms may occur at rest or during exertion and may be chronic or paroxysmal. 5  B. Signs:  Rapid (>100 bpm) or slow (100 bpm (figure 8). It is of gradual onset and is usually physiological in response to exercise, anxiety, emotional upset or pregnancy, or secondary to other medical conditions such as 10  hyperthyroidism, anemia, fever or drugs (e.g sympathomimetics). Rarely it is a primary arrhythmia.  Reassurance and treatment of the cause are the mainstay of treatment. Figure 8: sinus tachycardia. The rate is >100 bpm with characteristic P wave similar to sinus rhythm (upright in lead II and inverted in aVR) 2. Supraventricular tachycardias (SVT):  These include atrioventricular nodal reciprocating tachycardia (AVNRT, the most common) and atrioventricular reciprocating tachycardia (AVRT).  They usually occur in patients with structurally normal hearts.  They present with attacks of rapid regular palpitations of sudden onset and offset that usually last for a few minutes up to a few hours. Patients may also complain of symptoms of low cardiac output but syncope rarely occurs.  AVNRT: o The most common SVT. o The mechanism is reentry between the slow and fast pathways of the AV node (figure 4) o The ECG shows narrow-complex tachycardia at rate of 160-220 bpm, the P waves are not visible or may be hidden just after the QRS complex (figure 9) 11   Management of SVTs:  Termination of tachycardia: o In case of hemodynamic instability: Synchronized cardioversion is recommended. o If stable: Vagal maneuvers, IV adenosine are recommended as first line. If not terminated then IV beta blockers, verapamil or diltiazem are recommended and finally synchronized cardioversion if not terminated by the abovementioned methods.  Long-term management: catheter ablation is the mainstay of treatment. Beta blockers, calcium channel blockers or antiarrhythmic drugs can be used if catheter ablation is not available or not desired Figure 9: AVNRT, narrow complex tachycardia with P waves hidden after the QRS complex (arrows) 12 3. Tachyarrhythmias conducted over an accessory pathway (AVRT)  What is an accessory pathway? They are abnormal conducting fibers between the atria and the ventricles other than the AV node (figure 10).  Most pathways do not conduct during sinus rhythm, but may be involved in tachycardia (AVRT). These are termed “concealed accessory pathways” and the ECG during sinus rhythm is normal.  Some pathways conduct during sinus rhythm and are termed “manifest accessory pathways”. The impulse during sinus rhythm bypasses the AV nodal delay resulting in a short PR interval, would “pre-excite” a part of the ventricles before the rest of the ventricular tissue resulting in delta wave at the beginning of the QRS complex, and since the ventricles are not stimulated through the normal conduction system, the QRS complex becomes wide. The triad of (1) short PR interval, (2) wide QRS complex and (3) delta wave in addition to tachycardia is termed Wolff-Parkinson-White (WPW) syndrome (figure 11).  Patients with an accessory pathway o may be asymptomatic o may suffer from AVRT (regular tachycardia between the AV node and an accessory pathway). o may suffer from atrial fibrillation conducted over the accessory pathway (irregular), termed “pre-excited AF” which is potentially life- threatening (figure 12). 13  Figure 10: a diagram representing an accessory pathway. Figure 11: manifest accessory pathway. Note the short PR interval, wide QRS complex and delta wave (arrows) 14   Precautions with some drugs in WPW: o Drugs that block the AVN (beta blockers, verapamil, diltiazem, digoxin) are contraindicated in patients with WPW specially in pre- excited AF, as they will enhance the conduction over the AP leading to worsening of the tachycardia. o If WPW is suspected, synchronized DC cardioversion is the safest method to terminate the tachycardia o Catheter ablation of the accessory pathway is the definitive treatment Figure 12: pre-excited AF. Note the irregular rhythm, wide QRS complex and absent P waves 15  4. Atrial flutter  Is a re-entrant tachycardia in the right atrium with area of slow conduction at the cavotricuspid isthmus (CTI), which is located between the tricuspid valve and the inferior vena cava.  Atrial flutter can occur in the presence or absence of a structural heart disease.  Clinical manifestations are similar to AF except for a regular pulse usually at 150 bpm.  ECG shows Narrow complex tachycardia with atrial rate (p waves) at 300 bpm with loss of isoelectric baseline giving the “saw-tooth appearance”. The ventricular rate is usually 150 bpm due to 2:1 block by the A node but may be slower if the patient is taking A nodal blocking drugs. (figure 13) Figure 13: atrial flutter. Note the saw-tooth appearance in leads II, III, aVF Management of Atrial Flutter:  Anticoagulation follows the same rules as in AF (see later).  Rate control with AV blocking agents like betablockers and calcium channel blockers can be attempted.  If not controlled, rhythm restoration is either pharmacologic or via synchronized DC cardioversion, after TEE evaluation to exclude possible LAA thrombi.  Radiofrequency ablation of the CTI is recommended to prevent recurrence. 16 5. Monomorphic ventricular tachycardia (WCT):  It is a life-threatening arrhythmia characterized by Regular wide QRS complex tachycardia of ventricular origin at a rate more than 100 bpm (Figure 14).  The mechanism of VT can be abnormal automaticity (idiopathic VT), reentry (scar-related VT in ischemic heart disease) or triggered activity (Torsades de pointes).  VT is either Non-sustained VT (lasts less than 30 seconds and does not cause hemodynamic instability) or Sustained VT (lasts more than 30 seconds and or causes hemodynamic instability).  VT morphologically is divided into either monomorphic VT (all QRS complexes have the same morphology) or polymorphic VT (QRS complexes have different morphologies). In the last type, the tachyarrhythmia will be irregular.  Ischemic heart disease is the most common cause of ventricular tachycardia. However, VT may be idiopathic like outflow tract VT  Other causes of VT include (Ischemic and non-ischemic dilated cardiomyopathy – Adult and congenital structural heart disease- inherited genetic disorders - Electrolyte disorders as hypokalemia, hypocalcemia - drugs as digitalis toxicity). Figure 14: sustained monomorphic VT. Note the wide QRS complex and regular rhythm 17  Management of VT  VT is usually symptomatic, leads to hemodynamic instability and may lead to cardiac arrest. In this case emergency cardioversion and advanced cardiac life support is recommended. In other cases, managing using antiarrhythmic drugs (AAD) according to underlying cardiac disease.  Long term treatment should include 1. Correction of precipitating factors like ischemia, electrolyte disturbance. 2. Use of beta blockers and other AAD (e.g amiodarone). 3. Catheter ablation is especially useful in idiopathic VT. 4. Implantable cardiac defibrillator (ICD) implantation in hemodynamically unstable VT, survivors of cardiac arrest and in those with reduced LV systolic function.  B- Irregular Tachyarrhythmias 1. Atrial fibrillation (AF) The most common sustained arrhythmia. It is characterized by disorganized atrial electrical activity and contraction. The atrial rate is very fast (400-600 bpm) with no efficient atrial contraction. The AV node blocks the conduction of most of the atrial impulses resulting in a slower, irregular ventricular rate. The incidence and prevalence of AF is increasing. Lifetime risk over the age of 40 years is ~25%. AF is more common in males and increases with advancing age. Mechanism of AF is multifactorial and depends on the underlying structural heart disease. Triggers originating from foci located in the pulmonary veins and tachycardia is maintained by micro-reentry within the left atrium are responsible for AF in the absence of structural heart disease. 18   Classification of atrial fibrillation according to clinical presentation o First diagnosed: AF not diagnosed before, regardless of the duration. o Paroxysmal: AF episodes lasting less than 7 days. o Persistent: AF episodes lasting 7days to 12 months. o Long-standing persistent: AF lasting for more than 12 months when the desire to return to sinus rhythm is still present. o Permanent: AF is accepted by both the patient and the physician with no desire for further attempts to return to sinus rhythm.  Etiology of AF: AF is multifactorial and almost any form of structural heart disease can result in AF The most common causes are:  Systemic hypertension  Mitral Valve disease  Coronary artery disease  Thyroid disorders  Atrial septal defects (ASD)  Constrictive pericarditis  Lone (AF with no apparent cause) Other medical condition that can cause AF are CKD, obesity, sleep apnea, COPD. Aging, genetic predisposition, gender and ethnicity (non-caucasian) also play a role.  Consequences of AF: o Structural changes: progressive atrial dilatation, fibrosis, cellular necrosis and apoptosis. These changes are responsible for the progression from paroxysmal to permanent AF. o Hemodynamic consequences: loss of atrial contraction results in loss of 15- 20% of the cardiac output. Patients with diastolic dysfunction and mitral 19  stenosis are especially prone to the hemodynamic effect of AF since the atrial kick contributes significantly to the cardiac output in those patients. o Thrombosis: due to atrial dilatation and blood stagnation, patients with AF are prone to thrombus formation specially inside the left atrial appendage. Thromboembolism can occur with resultant cerebrovascular stroke or other forms of systemic embolization.  Diagnosis and workup: o Patients with AF may be asymptomatic or complain of paroxysmal or chronic palpitations. Other symptoms include fatigue, dyspnea, chest tightness, effort intolerance. Patients may present with hemodynamic instability like acute heart failure, ongoing ischemia and shock. Clinical examination reveals irregularly irregular pulse and pulsus deficit (the apical rate is faster than the radial rate) o ECG: typically shows irregular heartbeats with absent P waves. The heart rate may be rapid (>110 bpm), controlled (60-110 bpm) or slow (