Cardiac Dysrhythmias PDF

Cardiac Dysrhythmias Prof. Dr. A. Altuğ Çinçin Marmara University School of Medicine Department of Cardiology RA LA RV L V RA LA RV L V Ne rvo us sy SN ste m...

Cardiac Dysrhythmias Prof. Dr. A. Altuğ Çinçin Marmara University School of Medicine Department of Cardiology RA LA RV L V RA LA RV L V Ne rvo us sy SN ste m His bundle N RA AV sue LA n d u c tiv e fib rous tis Nonco B BB RV L LB R V  Impulse Conduction Impulses originate regularly at a frequency of 60-100 beat/ min mv Phase 1 Cardiac Action 20 0 Potential Phase 2 Depolarization (Plateau Phase) 20- 40- Phase 0 Phase 3 60- 80- Phase 4 Resting membrane Potential N NN c c N N c Na aa -100 aa+aa +a a++ ++ K Outside + ++ c + + mN K a + + (+) a + ATP + + ase N h KKKK + a İnside ++++ + (-) mv Phase 1 Cardiac Action 20 0 Potential Phase 2 Depolarization (Plateau Phase) 20- 40- Phase 4 only in) Phase 3 pacemaker 60- Phase 0 cells 80- Phase 4 R.M.P N NN c c N N c Na aa aa -100 a +a a++a+ ++ K + ++ c + + mN K a + + a + ATP + + ase N h KKKK + a ++++ + Phases of Cardiac Action Potential Absolute Relative refractory refractory Fig. 35-1  Classification of Anti-Arrhythmic Drugs :Class IV Ca ++ channel - blockers :Class II Phase 2 (Plateau Phase) - Beta blockers - :Class I Phase 1 Na + channel.blockers - Phase 3 Phase 0 Pacemaker potential - Phase 4 :Class III R.M.P K + channel blockers  Classification of Antiarrhythmic Drugs based on Drug Action CLASS ACTION DRUGS.I Sodium Channel Blockers.1A Moderate phase 0 depression and Quinidine, slowed conduction (2+); prolong Procainamide, repolarization Disopyramide.1B Minimal phase 0 depression and slow conduction (0-1+); shorten Lidocaine repolarization.1C Marked phase 0 depression and slow conduction (4+); little effect on Flecainide repolarization.II Beta-Adrenergic Blockers Propranolol, esmolol.III K+ Channel Blockers Amiodarone, Sotalol, (prolong repolarization) Ibutilide.IV Calcium Channel Blockade Verapamil, Diltiazem  Electrocardiography (ECG or EKG*) ⚫ In a conventional 12 lead ECG, ten electrodes are placed on the patient's limbs and on the surface of the chest recorded over a period of time (usually 10 seconds). ⚫ A typical ECG tracing is a repeating cycle of three electrical entities: a. a P wave (atrial depolarization) b. a QRS complex (ventricular depolarization) c. a T wave (ventricular repolarization).  Assessment of Cardiac Rhythm 25mm/sn 25 mm/sec 1 mm = 0.04 sec (40 msec) 5 mm = 0.2 sec (200 msec) Assessment of Cardiac Rate Assessment of Cardiac Rate  Cardiac Arrhythmias An abnormality of the cardiac rhythm is called a cardiac arrhythmia. Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no symptoms at all. There are two main types of arrhythmia: Bradycardia Tachycardia the heart rate is the heart rate is slow (< 60 bpm). fast (> 100 bpm).  Mechanism of Arrhythmias Bradycardia Tachycardia the heart rate is the heart rate is slow (< 60 bpm). fast (> 100 bpm). Mechanisms of bradycardias: Mechanisms generating Abnormally slow tachycardias: automaticity Accelerated automaticity. Abnormal conduction Triggered activity – within the AV node or, Re-entry mechanism – distal AV conduction system.  Cardiac pacemaker cells, particularly in the sinoatrial (SA) node, undergo spontaneous depolarization during ACCELERATED AUTOMATICITY diastole. If the rate of this depolarization increases, it can lead to a faster heart rate. It occurs due to increasing the rate of diastolic depolarization or changing the threshold potential. Abnormal automaticity can occur in virtually all cardiac tissues and may initiate arrhythmias. Such changes are thought to produce sinus tachycardia, escape rhythms and accelerated AV nodal (junctional) rhythms.  TRIGGERED ACTIVITY Oscillations of the transmembrane potential at the end of A patient comes to ER with digoxin the action potential. toxicity, what do you expect to see on his – These oscillations, which are called 'after depolarizations', may ECG? reach threshold potential and produce an arrhythmia. – Myocardial damage (most frequent example) – can be exaggerated by pacing, catecholamines, electrolyte disturbances, and some medications. Examples as atrial tachycardias produced by digoxin toxicity and the initiation of ventricular arrhythmia in the long QT syndrome.  Re-entry (or circus movement) Most frequent way for a tachycardia circuit. The mechanism of re-entry occurs – When a 'ring' of cardiac tissue surrounds an inexcitable core (e.g. in a region of scarred myocardium). – When two ways are evident with different rates or refr. periods. Tachycardia is initiated; – if an ectopic beat finds one limb refractory (α) resulting in unidirectional block and the other limb excitable. – Provided conduction through the excitable limb (β) is slow enough, the other limb (α) will have recovered and will allow retrograde activation to complete the re-entry loop. – If the time to conduct around the ring is longer than the recovery times (refractory periods) of the tissue within the ring, circus movement will be maintained, producing a run of tachycardia. The majority of regular paroxysmal tachycardias are produced by this mechanism.  Reentry Arrhythmias (β) (α) Slow way Fast way Short ref. P. Long ref. P. Normal Early signal (β) (α) Slow way Short ref. Fast way Long ref. Re-enterant P. P. Tachycardia  SA Node RA LA Sinus Sinus Bradycardia Tachycardia Sınusal Arythmia RV L V Sick Sinus Syndrome  Sinus Hypothyroidism causes sinus bradycardia Tachycardia A condition in which the heart rate is 100-160/bpm Symptoms may occur with rapid heart rates including; – weakness, fatigue, dizziness, or palpitations. Sinus tachycardia is often temporary, occurring under stress from; – exercise, strong emotions, fever, dehydratation, thyrotoxicosis, anemia and heart failure.  Sinus Tachycardia  Sinus Tachycardia Treatment Determined by underlying causes Firstly try to eliminate cause… Usually unnecessary β-adrenergic blockers to reduce HR and myocardial oxygen consumption  Sinus Tachycardia before / after slowdown  Sinus Bradycardia Physiological variant due to strong vagal tone or atheletic training. Rate as low as 50 at rest and 40 during sleep. Common causes of sinus bradycardia include: – Extrinsic causes ;Hypothermia, hypothyroidism, cholestatic jaundice and raised intracranial pressure. – Drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs. – Intrinsic causes; Acute ischaemia and infarction of the sinus node (as a complication of acute myocardial infarction). – Chronic degenerative changes such as fibrosis of the atrium and sinus node (sick sinus syndrome).  Sinus Bradycardia  Sinus Bradycardia Carotid sinus massage will lead to bradycardia Clinical Association Occurs in response to Occurs in disease states – Carotid sinus massage – Hypothyroidism – Hypothermia – Increased intracranial – Increased vagal tone pressure – Parasympathomimetic – Obstructive jaundice drugs – Inferior wall MI  In athlets you will not Sinus Bradycardia expect to see hypotension and lower co due to bardycardia Significance Hypotension with decreased CO may occur – Not in physiologic ones. An acute MI may predispose the heart to escape arrhythmias and premature beats  Sinus Bradycardia Treatment Usually not necessary Consists of atropine(inhibits vagal activity….), sempatomimetics(stimulates SA Node. Pacemaker may be required – Transcutaneous – Percutanous  Sınusal Arythmia A condition in which the heart rate varies with breathing. HR increases with insprium and decreases with exprium Usually benign INSP EXP INSP  Sick Sinus Syndrome A condition in which the sinus node sends out electrical signals either too slowly or too fast. – There may be alternation between too-fast and too-slow rate episodes May cause symptoms if the rate becomes too slow or too fast for the body to tolerate. Chronic symptomatic sick sinus syndrome requires permanent pacing (AAI), with additional antiarrhythmic drugs (or ablation therapy) to manage any tachycardia element.  Sick Sinus Syndrome Which one othe statments below is right about sick sinus syndrome ? Thromboembolism is common in tachy-brady In sick sinus syndrome we can see bradycardia and syndrome and patients should be tachycardia there is no need for permeant pacing a trans anticoagulated unless there is a cuatenus one would be enough contraindication. we can see thromboslism very comanly and anticoagulant should be given Treat like Atrial Fibrillation  Supraventricular Tachycardias Which one of below is not a supraventricular tachycardia? AV Nodal Reentran RA Tachycardia LA AV Reentran Tachycardia Atrial Fibrillation RV L Atrial Flutter V Atrial Tachycardia Multifocal Atrial Tachycardia Acclerated Junctional Tachycardia Premature Atrial Contractions (PAC)  AV Nodal Reentran Tachycardia A condition AV Reentran in which an atrial tissue site above the ventricles Tachycardia generates an electrical signal Atrial Fibrillation early than SA node Atrial Flutter – The ventricles Atrial Tachycardia are usually able to respond to this signal, but the result is an irregular heart rhythm. Multifocal Atrial PACs are common and may occur as the result Tachycardia Acclerated Junctional of stimulants Tachycardia such as –Premature coffee,Atrial tea, alcohol, cigarettes, or medications. Contractions (PAC) Treatment is rarely necessary.  Premature Atrial Contractions (PAC)  AV Nodal Reentran Tachycardia Paroxysmal SVTs AV Reentran Tachycardia Atrial Fibrillation Atrial Flutter Atrial Tachycardia Multifocal Atrial Rate is usually between 140-250 /bpm Tachycardia Always regular… Acclerated Junctional Tachycardia They usually begins and ends rapidly, occurring in periods. Premature Atrial Contractions Symptoms(PAC) such as weakness, fatigue, dizziness, fainting, or palpitations if the heart rate becomes too fast.  AV Nodal Reentran Tachycardia Same with beforely described reentry mechanism… Remember the rule: 1- two different pathway 2- an early signal 3- block in fast way In sinus rhythm, the atrial impulse that depolarizes the ventricles usually conducts through the fast pathway. If the atrial impulse (e.g. an atrial premature beat) occurs early when the fast pathway is still refractory, the slow pathway takes over in propagating the atrial impulse to the ventricles. It then travels back through the fast pathway which has already recovered its excitability, thus initiating the most common 'slow-fast', or typical, AVNRT.  Normal propagation  AV Nodal Reentran Tachycardia  AV Nodal Reentran Tachycardia Early activity  AV Nodal Reentran Tachycardia Most frequent cause of continuous palpitations in patients with normal hearts The rhythm is recognized on ECG by normal regular QRS complexes, usually at a rate of 140-240 per minute. Usually narrow QRSs. – Sometimes the QRS complexes will show typical bundle branch block (aberrant conduction) P waves are either not visible or are seen immediately before or after the QRS complex because of simultaneous atrial and ventricular activation.  AVNRT is based on a reentrant mechanism, which requires: Two distinct conduction pathways: A fast pathway and a slow pathway within or adjacent to the AV node. Differential refractory periods: The fast pathway recovers more quickly than the slow pathway. 2. Initiation of AVNRT: Atrial Impulse: Under normal sinus rhythm, the electrical impulse from the atria typically travels down the fast pathway to depolarize the ventricles. Premature Beat: If a premature atrial impulse occurs (such as an atrial premature contraction) while the fast pathway is still in its refractory period, the impulse cannot conduct through the fast pathway. Activation of the Slow Pathway: The impulse then conducts through the slow pathway, which is still excitable. After reaching the ventricles, the impulse travels back to the fast pathway, which has now recovered, thus initiating the reentrant circuit. This process typically results in the most common form of AVNRT known as slow-fast AVNRT. Clinical Features Symptoms: Patients may experience: Palpitations (rapid heart rate) Dizziness or lightheadedness Shortness of breath Chest pain Syncope (in severe cases) ECG Findings: During an episode of AVNRT, the ECG typically shows: A regular narrow-complex tachycardia (heart rate of 150-250 bpm). P waves may be hidden within the QRS complexes or occur just after the QRS due to simultaneous atrial depolarization. DII P wave usually be hidden in QRS. Pseudo r’ or Pseudo S waves, or ST depression (mimic) might be seen…  AV Nodal Reentran Tachycardia AVN AV Reentran Remember the rule: 1- two different pathway Tachycardia 2- an early signal Space in fibroanuler line 3- block in one way Atrial Fibrillation Atrial Flutter In AVRT Atrial Tachycardia there is a large circuit comprising the AV node, the His bundle, the ventricle Multifocaland an abnormal connection from the ventricle back to the Atrial atrium.Tachycardia This abnormal Acclerated connection is called an accessory pathway or bypass tract. Junctional BypassTachycardia tracts result from incomplete separation of the atria and the ventricles Premature during fetal development. Atrial Atrial activation(PAC) Contractions occurs after ventricular activation and the P wave is usually clearly seen between the QRS and T complexes  AVRT there is a large circuit comprising the AV node, the His bundle, ventricle and an abnormal connection from the ventricle back to the atrium This abnormal connection is called an accessory pathway or bypass tract. tracts result from incomplete separation of the atria and the ventricles during fetal development. Atrial activation occurs after ventricular activation and the P wave is usually clearly seen between the QRS and T complexes You can clearly see p wave in AVRT unlike AVNRT  AV Reentran Tachycardia Atrial activation occurs after ventricular activation and the P wave is usually clearly seen between the QRS and T complexes  The Wolf Parkinson White Syndrome (WPW) ►A well known example of AVRT. ►Ventricles stimulates both via AVN and accessory pathway ECG shows: - Short PR interval - Delta wave on the upstroke of the QRS complex ►Drug treatment includes flecainamide, amiodarone or disopyramide. ►Digoxin and verapamil are contraindicated. ►Transvenous catheter radiofrequency ablation is the treatment of choice. WPW syndrome Short PR, Delta wave  AV Nodal Reentran Tachycardia Treatment of AV Reentran Paroxysmal SVTs Tachycardia Acute Management Patients presenting with SVTs and hemodynamic instability require emergency cardioversion. If the patient is hemodynamically stable, vagal manoeuvres, including right carotid massage, Valsalva manoeuvre and facial immersion with cold water can be successfully employed. If not successful, intravenous adenosine (up to 0.25 mg/kg) , verapamil 5-10 mg i.v. over 5-10 minutes, i.v. diltiazem, or beta-blockers should be tried. Long-term management Ablation of an accessory pathway. Verapamil, diltiazem & β-blockers; are effective in 60-80% of patients.  AV Nodal Reentran Tachycardia AV Reentran Tachycardia Atrial Fibrillation Mechanism is set on macro-reentry circuits. Atrial Flutter Atrial rate : 200-400 bpm Atrial Tachycardia – Typical sawtooth pattern Multifocal Ventricle Atrial rate: variable Tachycardia – (150-200) – Magical rate ::150 Acclerated bpm Junctional Tachycardiato Often degenerates fibrillation in time Premature Atrial Management Contractions is similar (PAC) with A.Fibrillation  Atrial Flutter  Atrial Flutter TREATMENT Treatment of the symptomatic acute attack is electrical cardioversion. Patients who have been in atrial flutter more than 1-2 days should be treated in a similar manner to patients with atrial fibrillation and anticoagulated for 4 weeks prior to cardioversion. Recurrent paroxysms may be prevented by class Ic and class III agents The treatment of choice for patients with recurrent atrial flutter is radiofrequency catheter ablation  AV Nodal Reentran Tachycardia AV Reentran Tachycardia A condition in which the c Atrialsignals electrical Fibrillation come from the atria at aFlutter Atrial very fast and erratic rate. The ventricles AtrialinTachycardia contract an irregular manner because Multifocal of the Atrial Tachycardia erratic signals coming from the atria. Acclerated Junctional The ECGTachycardia shows normal but irregular QRS complexes, Premature Atrial fine oscillations of the Contractions (PAC) baseline (so-called fibrillation or f waves) and no P waves.  Atrial Fibrillation Different RR durations Fig. 35-14, B  Atrial Fibrillation Common causes include ; – CAD, – valvular heart disease, – hypertension, – hyperthyroidism and others. In some patients no cause can be found 'lone' atrial fibrillation.  Atrial Fibrillation Either it can be slow or fast… Have to be managed according to patient features  Atrial Fibrillation Management: 1. Look for precipitating something… – Such as alcohol toxicity, chest infection or hyperthyroidism, 2. Look for the need for anticoagulation (anticoagulants) – We decide according to patients risk for SVO. 3. Acute management strategies of AF are – Either ventricular rate control ( block the AV node ) – Or Cardioversion (electrically / class Ic or a class III agent ) 4. Long-term management of atrial fibrillation include; – Either rhythm control: (class Ic or a class III agent ) + OAC – Or rate control: AV nodal slowing agents + OAC  AV Nodal Reentran Tachycardia AV Reentran Tachycardia A rapid, irregular atrial rhythm Atrial arisingFibrillation from multiple ectopic foci within Atrial Flutterthe atria. Rare arrhythmia; most Atrial Tachycardia commonly associated with Multifocal significant chronic Atrial lung disease Tachycardia Multiple Acclerated P waveJunctional Tachycardia morphologies (≥3) and irregular RR intervals Premature Atrial Slowing Contractions AV conduction(PAC) is mainstay for treatment  Multifocal Atrial Tachycardia Rapid irregular rhythm > 100 bpm. At least 3 distinctive P-wave morphologies (arrows)  AV Nodal Reentran Tachycardia AV Reentran Tachycardia Atrial Fibrillation Usually occurs in patients with structural heart disease Atrial Flutter Organized Atrialatrial activity with Tachycardia P wave morphology Multifocal different from sinus Atrial rhythm Tachycardia Acclerated Junctional Tachycardia Premature Atrial Contractions (PAC)  Atrial Tachycardia S,ingle but different p morphology Rapid regular rhythm > 100 bpm.  Causes of SVT Tachycardia ECG features Comment Sinus tachycardia P wave morphology similar to sinus Need to determine underlying cause rhythm AV nodal re-entry tachycardia (AVNRT) No visible P wave, or inverted P wave Commonest cause of palpitations in patients immediately before or after QRS with normal hearts complex AV reciprocating tachycardia (AVRT) P wave visible between QRS and T wave Due to an accessory pathway. If pathway complexes conducts in both directions, ECG during sinus rhythm may be pre-excited Atrial fibrillation Irregularly irregular RR intervals and Commonest tachycardia in patients over 65 absence of organized atrial activity years Atrial flutter Visible flutter waves at 300/min Suspect in any patient with regular SVT at (saw-tooth appearance) usually with 2 : 150/min 1 AV conduction Atrial tachycardia Organized atrial activity with P wave Usually occurs in patients with structural morphology different from sinus heart disease rhythm Multifocal atrial tachycardia Multiple P wave morphologies (≥3) and Rare arrhythmia; most commonly associated irregular RR intervals with significant chronic lung disease Accelerated junctional tachycardia ECG similar to AVNRT Rare in adults  AV and BB Blocks Atrioventricular blocks First Degree AV block Second Degree AV block Type I Type II Third Degree AV block Bundle Brunch Blocks LBBB RBBB  Atrioventricular Blocks First degree AV Block Seldom of clinical significance, and unlikely to progress. ECG shows prolonged PR interval (>200msn) May be associated with acute rheumatic fever, diphtheria, myocardial infarction or drugs as digoxin  Atrioventricular Blocks Second degree AV Block Mobitz type I (Wenchebach phenomenon): Gradually increasing P-R intervals culminating in an omission. If its alone, usually physiological and may due to increased vagal tone and abolishes by exercise or atropine. – PR interval gets longer, up to blocked one. – PR interval is longest immediately before dropped beat – PR interval is shortest immediately after dropped beat – PP intervals are fixed – RR intervals are irregular R R R R R p p p p p p  Atrioventricular Blocks Mobitz type II The P wave is sporadically not conducted. Occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation. Pacing is usually indicated in Mobitz II block, whereas patients with Wenckebach AV block are usually monitored.  Atrioventricular Blocks Mobitz type II Elder age, Drugs, CV surgery… Acute myocardial infarction may produce second-degree heart block. – In inferior myocardial infarction, close monitoring and transcutaneous temporary back-up pacing are all that is required. – In anterior myocardial infarction, second-degree heart block is associated with a high risk of progression to complete heart block, and temporary pacing followed by permanent pacemaker implantation is usually indicated.  Atrioventricular Blocks Third degree A-V Block Common in elderly age groups due to idiopathic bundle branch fibrosis. Other causes include coronary heart disease, calcification from aortic valve, sarcoidosis or congenital. what are the causes of third degree A-V block ECG shows bradycardia, P wave continue, unrelated to regular slow idioventricular rhythm (usually 40 bpm). Treatment is permanent pacing. Third degree A-V Block  Bundle Branch Blocks Interruption of the right or left branch of the bundle of His delays activation of the corresponding ventricle leading to broadening of the QRS complex  Unlike right BBB, left BBB is always associated with an underlying heart disease. Both Rt and Lt BBB show wide deformed QRS complex. In RBBB there is rSR pattern in lead V1, while in LBBB there is a broad monophasic (or notched) R wave in leads V5 and V6. LBBB RBBB Ventricular Tachyarrhytmias Ventricular premature contractions Ventricular tachycardias Torsades de Pointes Ventricular fibrillation  Ventricular Premature Contractions A condition in which an electrical signal originates in the ventricles and causes the ventricles to contract before receiving the electrical signal from the atria. ECG shows uniq wide and bizarre QRS complex PVCs are not uncommon and often do not cause symptoms or problems. Rarely 'R-on-T’ PVC may induce ventricular fibrillation Treated only if symptomatic with beta-blockers or too many in numbers (>5000/day)  Ventricular Premature Continuous PVCs. Contractions Bigeminy: 1 narrow + 1 wide QRS Clinical Associations Stimulants Hypokalemia Exercise Trigeminy: 2 narrow + 1 wide QRS MI Mitral valve prolapse Couplet Triplet  Ventricular Tachycardias A condition in which electrical impulses are sent from the ventricles at a very fast but often regular rate. Wide (often 0.14 s or more), rapid (often >120 bpm), regular rhythm wit abnormal QRS morphology. – 3 to 30 Ventricular beats : Nonsustained VT – >30 Ventricular beats: Sustained VT – Monomorphic: one morphology – Polymorphic: >1 morphology  Ventricular Tachycardias Clinical Associations – Acute MI – Significant electrolyte imbalances – Mitral valve prolapse – Coronary reperfusion after thrombolytic therapy – Congenital arrythmias – Ischemic and nonischemic CMP.  Ventricular Tachycardias  Ventricular Tachycardias 1. First and most Important Question ??? Your patients haemodynamic status is well or not … If VT is monomorphic and patient is hemodynamically stable Procainamide, amiodarone or lidocaine is used (iv therapy) Synchronized cardioversion is used if drug therapy is ineffective If haemodynamically compromised, emergency DC cardioversion. If polymorphic with normal baseline QT interval, therapies include; magnesium infusion, IV β-adrenergic blocker overdrive pacing Ventricular tachycardia without pulse is treated as ventricular fibrillation, rapid defibrillation is necessary.  Ventricular Tachycardias  Torsades de Pointes QRS complexes are irregular and rapid that twist around the baseline. In between the spells of tachycardia, ECG shows prolonged QT interval. This is a type of short duration tachycardia that reverts to sinus rhythm spontaneously. It may be due to: - Congenital - Electrolyte disorders e.g. hypokalemia, hypomagnesemia, hypocalcemia. - Drugs e.g. tricyclic antidepressant, class IA and III antiarrhythmics. It may present with syncopal attacks and occasionally ventricular fibrillation. Treatment includes; – correction of any electrolyte disturbances, – stopping of causative drug, – atrial or ventricular pacing, – Magnesium sulphate 8 mmol (mg2+) over 10-15 min for acquired long QT, – IV isoprenaline in acquired cases and B blockers in congenital types  Torsades de Pointes  Ventricular Fibrillation A condition in which many electrical signals are sent from the ventricles at a very fast and erratic rate. As a result, the ventricles are unable to fill with blood and pump. This rhythm is life-threatening because there is no pulse and complete loss of consciousness. The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes  Ventricular Fibrillation No effective contraction or CO occurs It may cause sudden cardiac death. Immediate initiation of CPR and with use of drug therapy and defibrillation Prompt defibrillation to restore the normal rhythm and function of the heart. ICD’s are needed for patients without identifiable or treatable cause…  Ventricular Fibrillation Clinical Associations During catheterization or with coronary reperfusion after thrombolytic therapy And; – Acute MI – Myocardial ischemia – Chronic diseases such as CAD – Electrical shock – Hyperkalemia – Drug toxicity  Defibrillation Most effective method of terminating ventricular fibrillation Ideally performed within 15 to 20 seconds of onset of arrhythmia Passage of direct current electrical shock through heart to depolarize cells Aim: to allow SA node to resume role Defibrillation Fig. 35-21  Cardioversion Choice therapy for hemodynamically unstable ventricular or supraventricular tachyarrhythmias Delivers countershock during QRS complex Done on non-emergency basis Implantable Cardioverter-Defibrillator Treatment for life-threatening ventricular arrhythmias Lead system placed via subclavian vein to endocardium Pulse generator is implanted over pectoral muscle Implantable Cardioverter- Defibrillator After sensing system defects in lethal arrhythmia, delivers shock to the patient’s heart muscle Initiate overdrive pacing of supraventricular and ventricular tachycardias  Implantable Cardioverter-Defibrillator Fig. 35-22  MANAGEMENT OF ARRHYTHMIAS Pharmacological therapy. Cardioversion. Pacemaker therapy / ICDs Surgical therapy e.g. aneurysmal excision. Interventional therapy “ablation”.