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Year : 2007  |  Volume : 51  |  Issue : 4  |  Page : 310 Table of Contents     

Management of perioperative arrhythmias

1 M.D., Consultant, Department of Anaesthesiology, Pain & Perioperative Medicine, Sir Ganga Ram Hospital, Sir Ganga Ram Hospital Marg, New Delhi - 110 060, India
2 M.D., D.A., D.Ac., M.Ac.F.I., Emeritus Consultant, Department of Anaesthesiology, Pain & Perioperative Medicine, Sir Ganga Ram Hospital, Sir Ganga Ram Hospital Marg, New Delhi - 110 060, India

Date of Web Publication20-Mar-2010

Correspondence Address:
N Dua
Department of Anaesthesiology, Pain and Perioperative Medicine, Sir Ganga Ram Hospital, Sir Ganga Ram Hospital Marg, New Delhi - 110 060
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Source of Support: None, Conflict of Interest: None

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Keywords: Perioperative, Arrhythmias

How to cite this article:
Dua N, Kumra V P. Management of perioperative arrhythmias. Indian J Anaesth 2007;51:310

How to cite this URL:
Dua N, Kumra V P. Management of perioperative arrhythmias. Indian J Anaesth [serial online] 2007 [cited 2021 Mar 9];51:310. Available from: https://www.ijaweb.org/text.asp?2007/51/4/310/61160

   Definition Top

Arrhythmia is defined as "Abnormality of cardiac rate, rhythm or conduction which can be either lethal (sud­den cardiac death), or symptomatic (syncope, near syn­cope, dizziness, or palpitations) or asymptomatic". Imme­diate diagnosis and intervention with appropriate therapy often will prevent degeneration of an arrhythmia into a life-threatening event.

Cardiac arrhythmias are the most frequent perioperative cardiovascular abnormalities in patients un­dergoing both cardiac and non-cardiac surgery. The oc­currence of arrhythmias have been reported in 70.2% of patients subjected to general anaesthesia for various sur­gical procedures. [1],[2] The incidence of arrhythmias varies from patients undergoing cardiac or non-cardiac surgery as well as on monitoring modality. The incidence has been reported to vary from16.3 to 61.7% with intermittent ECG monitoring [3] and 89% with continuous holter monitoring [4] in patients undergoing non-cardiac surgery, while patients undergoing cardiac surgery are more prone to develop arrhythmia with reported incidence of more than 90%. [5]

Regardless of the terminology (arrhythmia or dys­rhythmia), cardiac rhythm disturbance represents one of the most misunderstood, frustrating and potentially dev­astating problems faced by the general or cardiac anaesthesiologist. The first basic principle of anti-arrhyth­mic therapy is to identify and correct possible precipitat­ing factors related to the administration of anaesthesia. Arrhythmias in the presence of cardiovascular disease are more dangerous and at times may be life threatening unlike those occurring in healthy patients which are usu­ally of little clinical consequence. Pacemakers and im­plantable cardioverter - defibrillators (ICD) are being used in the treatment of tachyarrhythmias and bradyarrhythmias nowadays very frequently. The basic understanding of their perioperative function and management needs to be highlighted. This text will provide a simpler way to diag­nose and manage arrhythmias in the perioperative period.

   Pathogenesis Top

  1. Injury or damage (pathology) to the cardiac con­duction systems.
  2. Re-entry: Reentry is a mechanism that may pre­cipitate a wide variety of supraventricular and ven­tricular arrhythmias.
  3. Automaticity: Abnormal depolarization of atrial or ventricular muscle cell during the periods of action potential can lead to arrhythmias.
  4. Mutations in ion channels: Since these channels are mainly responsible for depolarization, mutation can lead to arrhythmias.
  5. Ectopic foci/ irritable foci
The mechanism of arrthythmogenesis has been il­lustrated [6] in [Figure 1]

  1. Increased automaticity due to reduced threshold po­tential or an increased slope of phase 4 depolariza­tion
  2. Triggered activity due to 'after' depolarizations reach­ing threshold potential
  3. Mechanism of circus movement or reentry. In panel (1) the impulse passes down both limbs of the poten­tial tachycardia circuit. In panel (2) the impulse is blocked in the α pathway but proceeds slowly down the β pathway and returns along the α pathway. In panel (3) the impulse travels so slowly along the β pathway that when it returns along the α pathway to its starting point it is able to travel again down the β pathway, producing a circus movement tachycardia.
Factors and causes- There are several contribut­ing factors. The causes mainly responsible for arrhythmias are listed in [Table 1].

These factors can grossly be divided into following categories:

  1. Patient related factors
  2. Anaesthesia related factors
  3. Surgery related factors
1. Patient related factors

  1. Preexisting cardiac disease - The patients with known cardiac disease (e.g. myocardial ischaemia - MI) have much higher incidence of arrhythmias dur­ing anaesthesia than patients without known cardiac disease [1] . The arrhythmias are more fatal in patients with associated cardiac pathology.
  2. Central nervous system disease - Patients with in­tracranial disease especially sub-arachnoid haemorrhage may show ECG abnormalities such as changes in QT intervals, development of Q waves, ST-segment changes, and occurrences of U waves.
  3. Old age - Postoperative atrial fibrillation (AF) is a fre­quent complication in the elderly patients [3] undergoing thoracic surgery. Aging causes degenerative change in atrial anatomy and is also accompanied by relative changes in atrial pathology. The injury to sympathovagal fibers of cardiac plexus during surgery and preexisting atrial electrical changes in these patients predispose them to postoperative atrial fibrillation

2. Anaesthesia related factors

  1. Tracheal intubation - It is one of the most com­monest causes of arrhythmias during induction as well as during the perioperative period, most often asso­ciated with haemodynamic disturbances.
  2. General anaesthetics - The drugs used for induc­tion, maintenance as well as for reversal of general anaesthesia are not primarily arrhythmogenic, but arrhythmias can be produced in the presence of a variety of triggering agents and clinical situations generating high catecholamines such as light plane of anaesthesia with hypertension and tachycardia, hypoxaemia, hypercarbia, exogenous epinephrine and aminophylline. Halothane or enflurane produces arrhythmias, probably by a reentrant mechanism. [3]
  3. Local anaesthesia - Regional anaesthesia (epidu­ral anaesthesia) followed by central neuraxial block­ade may be associated with pharmacological sym­pathectomy leading to parasympathetic nervous sys­tem predominance causing bradyarrhythmias. It may be mild to very severe in nature. [7]
  4. Electrolyte imbalance and abnormal arterial blood gases - Abnormal blood gases such as hypercarbia, hypoxaemia or electrolyte imbalance produce arrhythmias either by producing reentrant mechanism or by altering phase depolarization of conducting fi­bers. Hypokalemia or hyperkalemia may also lead to arrhythmias.
  5. Central venous cannulation - Stimulation of carotid sinus reflexes may occur due to pressure from fingers during jugular vein cannulation as excess insertion of the central venous catheter into the right atrium during central venous cannulation may also lead to arrhythmias.

3. Surgery related factors

  1. Cardiac surgery - A spectrum of cardiac arrhythmias can be observed during the immediate period following the release of aortic cross clamp when myocardium is recovering from the ischaemic insult and regaining normal sinus rhythm. Surgical manipulation such as retraction of the heart during operation on beating heart, venous cannulation or tak­ing sutures over the atrium can also precipitate arrhythmias.
  2. Non-cardiac surgery - Vagal stimulation due to trac­tion on the peritoneum or direct pressure on the va­gus nerve during carotid artery surgery may produce bradycardia or atrioventricular (AV) blocks, or even asystole. Dental surgery causes profound stimula­tion of both sympathetic and parasympathetic ner­vous stimuli.

1. Bradyarrhythmia

i. Sinus bradycardia -
bradycardia is generally de­fined as a heart rate of less than 60 beats per minute. In patients on chronic beta-blocker therapy such as those suffering from coronary artery disease (CAD), it is defined as a heart rate of less than 50 beats/min.


The causes of sinus bradycardia are as follows:

  1. Drug effects:β blockers, digitalis and other anti-ar­rhythmic drugs
  2. Acute myocardial ischaemia
  3. Hypothermia
  4. Underlying hypothyroidism, cholestatic jaundice or raised intracranial pressure
  5. Chronic degenerative change such as fibrosis of the atrium and sinus node

Asymptomatic bradycardia usually does not require treatment. Symptomatic bradyarrhythmias should be di­agnosed and immediate therapy should follow. In patients who manifest haemodynamic compromise such as hy­potension, atropine is the first line of treatment. It can be used in the dose of 0.5 to 1.0 mg (IV bolus), repeated every 3 to 5 minutes, if required (maximum dose = 0.04 mg.kg -1 ). However, it should be used cautiously in pa­tients with CAD, since excessive increase in heart rate may worsen ischaemia because of increased myocardial oxygen consumption or reduced diastolic filling time. If bradycardia still persists despite treatment, isoprenaline can be administered as an IV bolus of 5 to 10 gg followed by an infusion of 2 to 10µg.min -1 . Other alternative is dopamine infusion 5 to 20gg.min -1 .

While treating sinus bradycardia, various causes or factors contributing should be searched and treatment started. Be ready for percutaneous and transvenous pac­ing. [8] (Flow Chart 1)

Expert cardiologist opinion must be sought for fur­ther management.

ii. Various forms of heart block: Heart blocks (AVHB) are broadly classified into three categories

  1. First degree heart block
  2. Second degree heart block
  3. Complete heart block
Anatomical or functional abnormalities underlie atrio-­ventricular heart block (AVHB). These may be transient or permanent. Transient AVHB can be produced by acute MI and general anaesthetics such as enflurane or hal­othane in patients using calcium channel blocker drug (CCB) or amiodarone. Permanent AVHB, on the other hand is usually idiopathic, other causes include CAD and Lev's or Lenegre disease, where fibrosis of the conduct­ing system occurs.

a) First degree heart block: This is simple prolonga­tion of the PR interval to more than 0.22 sec. Every atrial depolarization is followed by conduction to the ventricle but with delay. The treatment is usually not necessary however, the patients should be carefully observed for progression to a higher degree of block, that requires prompt treatment. [Figure 2] [9]

either broad ( > 0.15) or narrow (< 0.15) QRS complexes. [Figure 5] and [Figure 6] [9]

  • Narrow complex: This is due to disease in the AV node or the proximal bundle of His. The escape rhythm occurs with an adequate rate (50-60 b.p.m.) and is relatively reliable. It occurs because of infe­rior wall MI and toxic concentration of drugs such as digitalis, verapamil or β blockers in perioperative pe­riod.
  • Broad complex: This occurs because of disease in the Purkinje system. The escape pacemaker arises from the distal Purkinje network or the ventricular myocardium. The resulting rhythm is slow (15-40 b.p.m) and relatively insignificant or unharmful. In the elderly, it is usually caused by degenerative fibro­sis and calcification of the distal conduction system (Lenegre's disease) or the more proximal conduc­tion system (Lev's disease). It may occur after clo­sure of ventricular septal defect (VSD) and some­times following aortic valve replacement (AVR). In younger patients, broad complex AV block may be caused by perioperative myocardial ischaemia.
Management: Treatment is not required in narrow complex 3° block except for eradication of toxic causes. Occasionally, permanent pacing is advocated for symp­tomatic, isolated AV block. While in broad complex, pac­ing is indicated to maintain the normal haemodynamics.


The tachycardia can be classified based on the ap­pearance of the QRS complex as tachycardia, narrow complex supraventricular tachycardia (SVT), and wide complex tachycardia. Most wide complex (broad com­plex) tachycardias are ventricular in origin. Symptomatic tachyarrhythmias should be monitored and immediate therapy should be done. [8] (Flow Chart 2) Tachyarrhythmias are classified in two categories depend­ing upon the QRS complexes.

i. Narrow QRS complex (QRS<0.12): In these type of arrhythmias the QRS complex is less than 0.12 sec.

[Additional file 2]

a. Sinus tachycardia: it is defined as an increase in the sinus rate of more than 100 beats/minute. Prolonged tachycardia for long duration can induce ischaemia in coro­nary artery diseased patients.

Causes: It includes

  • Anaemia because of blood loss
  • Pain
  • Inadequate anesthesia
  • Hypovolaemia
  • Fever
  • Hypercarbia
  • Thyrotoxicosis/ thyroid crisis
  • Cardiac failure with compensatory sinus tachy­cardia
  • Catecholamines excess
Treatment: Before instituting pharmacological treatment for sinus tachycardia, precipitating factors must be identified and corrected. Drug therapy is especially required in patients with ischaemic heart disease who develop ST segment changes to prevent further myocar­dial ischaemia. Tachyarrhythmia should be managed ac­cording to Flow Chart 2. Beta-blockers such as esmolol is preferred drug for managing it. It has half-life of 10 min with bolus dose of 500 mcg.kg -1 over 1 min, followed by an infusion of 50-300 mcg.kg -1 .min -1. 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. [10] Another drug can be used is propranolol 0.1 mg.kg -1 .

b. 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 β blockade may be effective. [Figure 7] [9]

c. Atrial tachycardia: These arrhythmias are found in 6% of patients undergoing non cardiac surgery. [2] 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. [11] 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 -1 over 10 min. [Figure 8] [9]

d. 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 -1 but is usually around 300 min -1 .

Most often every second flutter beat conducts giving a ventricular rate of 150 min -1 . Occasionally every beat con­ducts, producing a heart rate of 300 min -1 . More often, espe­cially when patients are receiving treatment, AV conduction block reduces the heart rate to approximately 75 min -1 .

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. [Figure 9] [9]

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

e. Atrial fibrillation (AF)

It accounts for more than 90% of supraventricular ta­chycardia (SVT) in the perioperative setting. It is caused by a raised atrial pressure, increased atrial muscle mass, atrial fibrosis or inflammation and 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. When caused by rheu­matic mitral stenosis, the onset of atrial fibrillation results in considerable worsening of cardiac failure.

Clinically the patient has a very irregular pulse, as opposed to a basically regular pulse with an occasional irregularity (extrasystoles) or recurring irregular pattems. The ECG shows fine oscillations of the baseline (so called fibrillation) and no clear P waves. The QRS rhythm is usually 160-180min -1 but it slows with treatment. ECG changes are more indicative in lead II [Figure 10] [9] . AF may be acute or recent onset (<48 hrs) and chronic. In the recent onset AF, initial treatment is directed towards the control of ventricular response rate with agents that slow AV node conduction. The precipitating or provoking agents should be removed or treated first. Intravenous beta­-blockers or calcium channel blockers produce rapid con­trol of rate, regardless of the level of sympathetic tone. However beta-blockers are preferred over calcium chan­nel blocker (CCB) during intraoperative period due to shorter duration of action and lesser negative inotropic effects. [10],[12] In haemodynamically-compromised patients, DC cardioversion is the most effective method of con­verting AF to sinus rhythm. Chronic AF is often found in patients with rheumatic heart disease undergoing cardiac surgery and may have atrial thrombi, therefore, any at­tempt to restore sinus rhythm by DC cardioversion may be associated with increased risk of systemic or pulmo­nary embolisation. Successful cardioversion is relatively rare in chronic AF. The control of ventricular rate is the preferred approach in these cases. The most useful drug for this purpose is digoxin. The patients with chronic AF undergoing noncardiac surgery should be evaluated for the presence of atrial clot by echocardiogram prior to sur­gery. In the presence of atrial clot, control of ventricular response rate with appropriate medication is instituted during perioperative period, if necessary.

ii. Wide QRS complex (QRS>0.12): In these types of arrhythmias the QRS complex is usually more than 0.12 sec.

a. 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. They account for 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. On the ECG, the 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. [Figure 11] and [Figure 12] [9]

Treatment: Underlying abnormalities in these pa­tients should be corrected immediately. No treatment is generally required for isolated VPB in asymptomatic and healthy patients. However VPB which are multiple (>5 beats/min), multifocal, or bigemminal or occur near the vulnerable period of the preceding ventricular repolarization (the so called 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 -1 followed by infusion of 1 to 4 mg.min -1 can be given. Other drugs from class I, II or III are used to treat these types of arrhythmias.

b. Ventricular tachycardia

This is defined as three or more ventricular beats occurring at a rate of 120 bpm or more. It may be poten­tially life threatening. Examination reveals pulse rate of 120-220bpm. Usually there are clinical signs of atrioven­tricular dissociation i.e. intermittent cannon 'a' waves and variable intensity of the first heart sound. The ECG shows a 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.

Treatment may be urgent depending on the haemodynamic situation. If the cardiac output and the blood pressure are very depressed, emergency DC­ cardioversion must be considered. On the other hand, 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 -1 i.v.). DC-cardioversion may be necessary if medical therapy is unsuccessful. The administration of multiple antiarrhythmic drugs should be avoided.

Patients with recurrent episodes or unresponsive to lidocaine, may require therapy with procainamide (10-15 mg.kg -1 loading dose followed by an infusion of 2 to 6 mg.min -1 ) or bretylium (5 to 10 mg.min -1 over 2 to 5 min then infusion of 1-2 mg.min -1 ) or amiodarone in the dose of 150 mg IV over 10 minutes followed by an infusion of 1 mg.min -1 for 6 hours and 0.5 mg.min -1 thereafter. IV amiodarone has been shown to be as effective as bretylium with added advantage of less hypotension as compared to IV bretylium. [Figure 13] [9]

C. Ventricular fibrillation (VF)

It is very rapid and irregular ventricular activation with no mechanical effect. It is usually intiated from anischaemic 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 SpO 2 because of low or no cardiac output. Causes include myocardial ischaemia, hypoxaemia, electrolyte imbalance and drug effects.

Treatment: Cardiopulmonary resuscitation must be performed as rapidly as possible. Asynchronous external defibrillation should be performed using 200-360J. Apre­cordial 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 -1 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.

d. 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.


The arrhythmia is treated as follows

  1. 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. β Blockade is advised if the QT prologation is con­genital.
Collapse rhythm- There is no ECG rhythm in the case of cardiac arrest or asystole. Immediate manage­ment should be done according to Flow Chart 3.

   Pacemaker Top

New or worse cardiac arrhythmias in the perioperative period are usually temporary occurrences, often due to the result of transient physiologic or pharma­cologic imbalance. Antiarrhythmic drugs have the poten­tial to further aggravate this imbalance. Therefore, early use of temporary pacemaker during perioperative period is preferred nowadays. More than 90% of pacemakers are inserted for the treatment of bradyarrhythmias oc­curring either after tachycardia (bradytachy syndrome) or AV conduction disorders or by themselves (sick sinus syndrome).

Temporary pacemaker may be invasive (epicardial and endocardial) or non-invasive (transcutaneous and transesophageal). The pacing may also be unipolar or bi­polar. Unipolar pacing describes the placement of the negative (stimulation) electrode in the atrium or ventricle and the positive (ground) electrode distant from the heart. Bipolar pacing describes placement of the negative and positive electrode on the cardiac chamber being paced. The combination of wires allows atrial, ventricular, or atrial ventricular sequential pacing when used in combination with a dual output (atrial and ventricular) sequential ex­ternal pacemaker.[13]

Prophylactic transvenous pacing is recommended in patients who are considered at high risk for developing haemodynamically significant bradycardia due to AV heart block or sinus node dysfunction. Whereas, direct cardiac pacing methods are preferred for the patients having car­diac surgery, especially in the post bypass period. In these patients, current output of the pacemaker is slowly in­creased until desired cardiac chamber contraction is cap­tured (usually 5-10 milliamperes), then current output is further increased by 5 more milliamperes to assure con­tinued capture. When atrial ventricular sequential pacing is required, the optimal PR interval will need to be deter­mined. It is generally 150 msec but can vary between 120 to 200 msec so as to optimize ventricular filling and car­diac output. If extensive electrocautery is being used dur­ing the operation, pacemaker may have to be put on asyn­chronous mode to prevent inhibition of the pacemaker by electrocautery radiofrequency current. [Figure 14] [9]

   Anaesthetic considerations Top

All patients undergoing anaesthesia and surgery should have ECG monitoring. Lead II and V 5 are supe­rior for arrhythmia detection and diagnosis before the ap­pearance of physical signs e.g. changes in BP, heart rate or heart sounds. After establishing from ECG that ar­rhythmia is present, it is crucial to evaluate patient's re­sponse to altered rhythm in rate and type of treatment required. Correction of contributing cause and final line of treatment follows thereafter. Routine measures for all intraoperative arrhythmias are as follows [Table 3] & [Table 4]

[Additional file 1]

   Antiarrhythmic drugs Top

Drugs that modify the rhythm and conduction of the heart are used to prevent cardiac arrhythmias. All such drugs may aggravate or produce arrhythmias and they may also depress ventricular contractility and must, there­fore, be used with caution. There are more than 30 anti­arrhythmic drugs. They are classified according to their effect on the action potential (Vaughan Williams' classifi­cation.) [Figure 15] & [Table 5]

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.

Class II drugs

These antisympathetic drugs prevent the effects of catecholamines on the action potential. Most are β-adr­energic antagonists. Cardioselective β-blockers (β1 ) 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 β-blocker.

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.

Another clinical classification [6] is based on the part of the heart that is affected by the antiarrhythmic drug. The features of the major antiarrhythmic drugs are given in [Figure 16].

The main drugs useful for arrhythmia management with dosage are as follows,

[Additional file 3]

   Key points Top

Therapeutic decisions in patients with cardiac arrhythmias are based on an assessment of the haemodynamic impact of the rhythm disturbance, the patient's underlying cardiac function, contributing factors and the correct diagnosis of the arrhythmia. Both clinical examination and the ECG should be considered in making the diagnosis. Incorrect diagnosis can lead, not only to in effective therapy but also to potentially dangerous therapy, especially when wide-QRS tachyarrhythmias are present.

Symptomatic bradyarrhythmia can be treated initially with atropine; in many forms of bradycardia, however, pac­ing, either external or transvenous, is the definitive therapy of choice. In some situations, including Mobitz type II sec­ond-degree block and in wide-QRS, new-onset complete heart block, external pacing can be used temporarily to bridge the patient over to transvenous pacing.

Adenosine is the drug of first choice in treating pa­tients with PSVT. It is therapeutic in over 90% of pa­tients with this tachyarrhythmias, in which AV-nodal re­entry is the most common mechanism. In non-reentrant SVT, such as automatic (ectopic) atrial tachycardia or multifocal atrial tachycardia, adenosine may be useful in unmasking the underlying arrhythmia mechanism, but the 12-lead ECG should first be searched to define the mecha­nism of the arrhythmia. Other pharmacologic options in­clude diltiazem and verapamil, β-blocking drugs, and amiodarone and digoxin. Cardioversion should be consid­ered if drug use is contraindicated or if the arrhythmia is not controlled with drug therapy.

Ventricular tachycardia can be monomorphic or polymorphic. When PVT is accompanied by prolonged repolarization, manifested as QT-interval lengthening on the ECG before or after episodes of tachycardia, the ta­chycardia is torsades de pointes, and its presence man­dates specific diagnostic and therapeutic considerations. If the origin of a wide-QRS tachycardia cannot be con­firmed clinically or electrocardiographically, amiodarone or procainamide, should be used. In all situations, emer­gency cardioversion takes precedence if haemodynamic compromise is present or develops during drug therapy.

Pulseless VT and VF are forms of ventricular tachyarrhythmia that require cardiac arrest therapy with defibrillation and drugs; most importantly epinephrine, for maintenance of myocardial and cerebral blood flow dur­ing external chest compression or open-chest cardiac massage.

   Conclusion Top

Acute-onset cardiac arrhythmia carries the poten­tial of haemodynamic instability, including cardiovascular collapse. Knowledge of both electric and pharmacologic options and an understanding of the therapeutic interven­tion is mandatory. Precipitating factors or causes should be treated or removed immediately. In many situations, cardioversion or defibrillation is the initial intervention of choice, with drug therapy as follow-up in an attempt to prevent recurrence of the arrhythmia. In other more haemodynamically stable situations, drug therapy is used initially.[Table 2] [Figure 3] [Figure 4]

   References Top

1.Forrest J, Cahalan M, Rehder K, et al. Multicenter Study of General Anesthesia II. Results. Anesthesiology 1990; 72:262­-68.  Back to cited text no. 1      
2.Forrest J, Rehder K, Cahalan M, Goldsmith C. Multicenter Study of General Anesthesia III. Predictors of severe perioperative adverse outcomes. Anesthesiology 1992; 76:3-15.  Back to cited text no. 2      
3.Katz RL, Bigger JT Jr. Cardiac arrhythmias during anaesthesia and operation. Anesthesiology 1970; 33:193-213.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Bertrand CA, Steiner NJ, Jameson AG, et al. Disturbances of cardiac rhythm during anesthesia and surgery. JAMA 1971; 216:1615-17.  Back to cited text no. 4      
5.Fisher DM. Preoperative cardiac dysrhythmias; Diagnosis and Management. Anesthesiology 1997; 86:1397-424.  Back to cited text no. 5      
6.Kumar P Clark M. Clinical Medicine. 3rd eds. Cardiac arrhythmias 1994. ELBS 554-555, 566-568.  Back to cited text no. 6      
7.Sokolow M and Mcllroy B (1986) Clinical radiology, 4th eds. New York. Lange. 116-7.  Back to cited text no. 7      
8.The American Heart Association, in collaboration with the Inter­national Liason Committee on Resuscitation Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovas­cular Care. Part 6: advanced cardiovascular life support 7D: the tachycardia algorithms. Circulation 2000; 102:1158-65.  Back to cited text no. 8      
9.Hampton JR (1986). The ECG made easy, 3rd eds. Edinburgh: Churchill Livingstone. 31-34, 59,61,65-68, 79,85.  Back to cited text no. 9      
10.Oxorn D, Knox JW, Hill J. Bolus doses of esmolol for the pre­vention of perioperative hypertension and tachycardia. Can J Anaesth 1990; 37:206-209.  Back to cited text no. 10  [PUBMED]    
11.Atlee J, Bosnjak Z. Mechanisms for cardiac dysrhythmias dur­ing anesthesia. Anesthesiology 1992; 76: 3-15.  Back to cited text no. 11      
12.Das G, Ferris J. Esmolol in the treatment of supraventricular tachyarrhythmias. Can J Cardiol 1988; 4:177-80.  Back to cited text no. 12  [PUBMED]    
13.Salukhe TV. Dob D, Sutton R. Pacemakers and defibrillators: anaesthetic implication. Br J Anaesth 2004; 93; 95-104.  Back to cited text no. 13      


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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