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1. Cardiac Arrhythmias (Tachyarrhythmias)

2. Treatment Before pharmacological treatment for sinus tachycardia, precipitating factors must be identified and corrected. Drug therapy required in patients with ischaemic heart disease who develop ST segment changes to prevent further myocardial ischaemia . . Beta-blockers as esmolol is preferred drug for managing its half-life of 10 min with bolus dose of 500 mcg/kg over 1 min, followed by an infusion of 50-300 mcg/kg/min. If continuous use is required, it may be replaced by longer lasting cardio selective drugs such as metoprolol in the dose of 5 to 10 mg given slowly intravenously (IV) at 5 min interval to a total dose of 15 mg. Another drug can be used is propranolol 0.1 mg/kg.

3. Atrial premature beat It represents 10% of all intraoperative arrhythmias. On the ECG they appear as early and abnormal ‘P’ waves and are usually but not always, followed by normal QRS complexes. The duration of QRS wave is normal but wide QRS wave may be present due to aberrant ventricular conduction, which mimics premature ventricular beat. Treatment is not normally required unless the ectopic beats provoke more significant arrhythmias, where blockade may be effective.

4. Atrial tachycardia These arrhythmias are found in 6% of patients undergoing non cardiac surgery. It is nonparoxysmal , narrow QRS rhythm with retrograde or nonapparent P waves and a rate less than 70 beats/min. if faster usually less than 130 beats/min, it is termed as accelerated AV junctional rhythm. Those arrhythmias can lead to fall in blood pressure upto 15% in patients without cardiac disease and upto 30% in diseased heart. Usually no treatment is required; carotid sinus massage and verapamil are often helpful in symptomatic patients. Intravenous adenosine in 6 to 12 mg doses is another alternative. Treatment with class Ia , Ic or III drugs is usually successful e.g. disopyramide 2 mg/kg over 10 min.

5. Atrial flutter This is a rhythm disturbance that is usually associated with organic ischaemic heart disease. The atrial rate varies between 280 and 350 /min but is usually around 300/ min ECG- : The ECG shows regular saw tooth-like atrial flutter waves between QRST complexes. If they are not clearly visible,AV conduction may be transiently impaired by carotid sinus massage or by the administration of AV nodal blocking drugs such as verapamil

6. Treatment- Treatment of an acute paroxysm is electrical cardioversion. Prophylaxis is achieved with class Ia , Ic or III drugs in diseased heart patients.

7. Atrial fibrillation (AF) It accounts for more than 90% of supraventricular tachycardia (SVT) in the perioperative setting. Causes - a raised atrial pressure increased atrial muscle mass atrial fibrosis or inflammation infiltration of the atrium Rheumatic disease is often associated with cardiac causes such as mitral valve disease, myocarditis and coronary artery disease. Systemic diseases include hyperthyroidism, pulmonary embolism and electrolyte imbalance.

8. Clinically the patient has a very irregular pulse, as opposed to a basically regular pulse with an occasional irregularity (extrasystoles) or recurring irregular patterns ECG- Absent P waves Irregularly irregular rhythm Atrial rate of 450-600 Presence of fine “ fibrillatory ” waves which vary in amplitude and morphology

9. Management Electrical cardioversion (Synchronized cardioversion at 100 to 200 J is indicated). It indicated to relieve symptoms of heart failure, to improve cardiac output and to reduce the risk of arterial thromboembolism. Drugs:- i.v. amiodarone, propafenone, ibutilide , diltiazem

10. Paroxysmal Supraventricular Tachycardia (PSVT) A single reentrant ectopic focuses fires in and around the AV node , all of which are conducted normally to the ventricles (usually initiated by a PAC) QRS complexes are almost identical to the sinus beats Rate is usually between 150 and 250 beats per minute The rhythm is always REGULAR Possible symptoms: palpitations, angina, anxiety, syncope Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter May be terminated by carotid massage Treatment: Adenosine, Ca ++ Channel blockers

11. Atrioventricular Nodal Reentrant Tachycardia (AVNRT) Most common SVT (approximately 50 to 60%) Occurs more often in younger women pericarditis, previous myocardial infarction, or mitral valve prolapse Reentry caused by nodal pathways or tract Rate: 120 to 260 bpm Rhythm: regular, narrow QRS complex (< 120 msec); regular, wide QRS complex (≥ 120 msec); may not see any P-wave activity

12. Regular RR interval No P wave Narrow QRS complex

13. Atrioventricular Reentrant Tachycardia (AVRT) The second most common type of SVT. Patients with this arrhythmia typically present at a younger age than those with AVNRT. This SVT is caused by accessory pathways (or bypass tracts) that establishing a reentry circuit. occasionally comorbid with Wolff-Parkinson-White syndrome. Rate: 120 to 250 bpm Rhythm: regular, narrow QRS complex common

14. Wide QRS complex (QRS>0.12) Ventricular premature beat (VPB) / Ventricular extrasystole Ventricular tachycardia Ventricular fibrillation (VF) Torsades de pointes

15. Ventricular premature beat (VPB) / Ventricular extrasystole VPB results from ectopic foci arising from below AV node and give rise to wide (>0.12 sec) bizarre QRS complex. 15% of the observed arrhythmias, more common in anaesthetized patients with pre existing cardiac disease. New onset of VPB, may occur in the presence of coronary artery insufficiency, myocardial infarction, digitalis toxicity with hypokalemia and hypoxaemia .

16. ECG- Premature beat has a broad (>0.125) and bizarre QRS complex because it arises from an abnormal (ectopic) site in the ventricular myocardium. Following the premature beat there is usually a complete compensatory pause because the timing of sinus rhythm is not induced by the premature beat.

17. Treatment- Underlying abnormalities in these patients should be corrected immediately No treatment is generally required for isolated VPB in asymptomatic and healthy patients. VPB with R on T phenomenon associated with haemodynamic disturbance or convert to worse arrhythmias require prompt treatment. Lidocaine with an initial bolus dose of 1.5 mg/kg followed by infusion of 1 to 4 mg/min can be given. Other drugs from class I, II or III are used to treat these types of arrhythmias.

18. Ventricular tachycardia Defined as three or more ventricular beats occurring at a rate of 120 bpm or more. It may be potentially life threatening. Usually there are clinical signs of atrioventricular dissociation i.e. intermittent cannon 'a' waves and variable intensity of the first heart sound ECG- Rapid ventricular rhythm with broad (often 0.14s or more), abnormal QRS complexes. Dissociated P waves activity may be seen and have no fixed relation to wide QRS complex.

19. Types Monomorphic QRS complexes all have same morphology Polymorphic QRS complexes have more than one morphology “ Torsades de Pointes ” “Twisting of the points” Usually > 200 bpm Susceptible if slow repolarization (long QT)

20. Monomorphic VT

21. Polymorphic VT

22. Treatment- If the cardiac output and the blood pressure are very depressed, emergency DC cardioversion must be considered If the blood pressure and cardiac output are well maintained, intravenous therapy with class I drugs is usually advised. First-line drug treatment consists of lidocaine (50-100 mg i.v. over 5 min) followed by a lidocaine infusion (2-4 mg/min i.v. ). Patients with recurrent episodes or unresponsive to lidocaine, may require therapy with procainamide (10-15 mg/kg loading dose followed by an infusion of 2 to 6 mg/min) amiodarone in the dose of 150 mg IV over 10 minutes followed by an infusion of 1 mg/min for 6 hours and 0.5 mg/min.

23. Ventricular fibrillation (VF) It is very rapid and irregular ventricular activation with no mechanical effect. It is usually intiated from an ischaemic myocardium or an aberrant foci (especially in acute perioperative myocardial infarction), ventricular tachycardia or torsades de pointes. On ECG, there are no defined QRS complexes, shows shapeless rapid oscillations and on pulse oximetry, there is acute fall in SpO2 because of low or no cardiac output. Causes include myocardial ischaemia , hypoxaemia , electrolyte imbalance and drug effects.

24. “coarse” ventricular fibrilation “fine” ventricular fibrilation

25. Treatment- Cardiopulmonary resuscitation must be performed as rapidly as possible. Asynchronous external defibrillation should be performed using 200-360J. A precordial thump is occasionally effective in terminating VF, but should be attempted only if a defibrillator is not available immediately. Intravenous bretyium 5-10 mg/kg over 5 min can be useful on some occasion. Supporting pharmacological therapy such as lidocaine, amiodarone and procainamide are used only to prevent recurrence of VF.

26. Torsades de pointes These arrhythmias are usually short in duration and spontaneously revert to sinus rhythm. Occasionally it can change to VF. On ECG, it is characterized by rapid, irregular sharp complexes that continuously change from an upright to an inverted position. Between spells of tachycardia the ECG shows a prolonged QT interval; the corrected QT is equal to or greater than 0.44s.

27. Risk Factors -Female gender -Hypokalemia -Hypomagnesemia -Bradycardia -Congestive Heart Failure -Concurrent Digoxin use . Drugs causing - Terbenafine -Quinidine -Procainamide - Cisapride -Erythromycin

28. Typically initiated by a short-long-short interval Sinus rhythm of 50 beats per minute QT interval > 0.44s

29. Treatment : The arrhythmia is treated as follows Any electrolyte disturbance is corrected. 2. Causative drug and precipitating factors should be stopped and removed. 3. Intravenous isoprenaline may be effective when QT prolongation is acquired. 4. Blockade is advised if the QT prologation is congenital.

30. Anaesthetic considerations

31. Anti arrhythmic drugs Drugs that modify the rhythm and conduction of the heart are used to prevent cardiac arrhythmias

32. Class I drugs These are membrane-depressant drugs that reduce the rate of entry of sodium into the cell. They may slow conduction, delay recovery or reduce the spontaneous discharge rate of myocardial cells. Class Ia drugs (e.g. disopyramide) lengthen the action potential, and Class Ic (flecainide, propafenone) do not affect the duration of the action potential.

33. Class II drugs These antisympathetic drugs prevent the effects of catecholamines on the action potential. Most are beta- adrenergic antagonists. Cardioselective Beta-blockers (1 ) include metoprolol, atenolol, and acebutalol . Class III drugs These prolong the action potential and do not affect sodium transport through the membrane. There are two major drugs in this class; amiodarone and sotalol. Sotalol is also a beta-blocker.

34. Class IV drugs The non-dihydropyridine calcium antagonists that reduce the plateau phase of the action potential are particularly effective at slowing conduction in nodal tissue. Verapamil and diltiazem are the most important drugs in this group.