Periop Arrythmias

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Indian Journal of Anaesthesia, August 2007

Management of Perioperative ArrhythmiasN. Dua1, V.P. Kumra2

Key words Perioperative, Arrhythmias

1. M.D., Consultant, 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. Correspondence to : Naresh Dua, Department ofAnaesthesiology, Pain and Perioperative Medicine, Sir Ganga Ram Hospital, Sir Ganga Ram Hospital Marg, New Delhi - 110 060, INDIA.E mail: [email protected]

DefinitionArrhythmia is defined as “Abnormality of cardiac

rate, rhythm or conduction which can be either lethal (sud-den cardiac death), or symptomatic (syncope, near syn-cope, dizziness, or palpitations) or asymptomatic”. Imme-diate diagnosis and intervention with appropriate therapyoften will prevent degeneration of an arrhythmia into alife-threatening event.

Cardiac arrhythmias are the most frequentperioperative cardiovascular abnormalities in patients un-dergoing both cardiac and non-cardiac surgery. The oc-currence of arrhythmias have been reported in 70.2% ofpatients subjected to general anaesthesia for various sur-gical procedures. 1,2 The incidence of arrhythmias variesfrom patients undergoing cardiac or non-cardiac surgeryas well as on monitoring modality. The incidence has beenreported to vary from 16.3 to 61.7% with intermittent ECGmonitoring3 and 89% with continuous holter monitoring 4

in patients undergoing non-cardiac surgery, while patientsundergoing cardiac surgery are more prone to developarrhythmia with reported incidence of more than 90%. 5

Regardless of the terminology (arrhythmia or dys-rhythmia), cardiac rhythm disturbance represents one ofthe most misunderstood, frustrating and potentially dev-astating problems faced by the general or cardiacanaesthesiologist. The first basic principle of anti-arrhyth-mic therapy is to identify and correct possible precipitat-ing factors related to the administration of anaesthesia.Arrhythmias in the presence of cardiovascular diseaseare more dangerous and at times may be life threateningunlike those occurring in healthy patients which are usu-ally of little clinical consequence. Pacemakers and im-plantable cardioverter - defibrillators (ICD) are being usedin the treatment of tachyarrhythmias and bradyarrhythmiasnowadays very frequently. The basic understanding oftheir perioperative function and management needs to behighlighted. This text will provide a simpler way to diag-nose and manage arrhythmias in the perioperative period.

Pathogenesis1. Injury or damage (pathology) to the cardiac con-

duction systems.

2. Re-entry: Reentry is a mechanism that may pre-cipitate a wide variety of supraventricular and ven-tricular arrhythmias.

3. Automaticity: Abnormal depolarization of atrial orventricular muscle cell during the periods of actionpotential can lead to arrhythmias.

4. Mutations in ion channels: Since these channelsare mainly responsible for depolarization, mutationcan lead to arrhythmias.

5. Ectopic foci/ irritable foci

The mechanism of arrthythmogenesis has been il-lustrated 6 in Fig. 1

Indian Journal of Anaesthesia 2007; 51 (4) : 310-323

Fig 1. Mechanism of arrthythmogenesis

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a) Increased automaticity due to reduced threshold po-tential or an increased slope of phase 4 depolariza-tion

b) Triggered activity due to ‘after’depolarizations reach-ing threshold potential

c) Mechanism of circus movement or reentry. In panel(1) the impulse passes down both limbs of the poten-tial tachycardia circuit. In panel (2) the impulse isblocked in the pathway but proceeds slowly downthe pathway and returns along the pathway. Inpanel (3) the impulse travels so slowly along the pathway that when it returns along the pathway toits starting point it is able to travel again down the pathway, producing a circus movement tachycardia.

Factors and causes- There are several contribut-ing factors. The causes mainly responsible for arrhythmiasare listed in Table 1.

Table 1. Contributing factors and causes

Hypovolemia

Hypoxia

Hypo/Hyperkalemia

Hypomagnesaemia /Hypocalcaemia

Hypoglycemia

Hypothermia

Acidosis

Mechanical

Irritation (e.g. central venous

lines, pulmonary art. catheter,

chest tube)

Cardiac ischaemia

Light plane of anaesthesia/pain

Toxins/ Drugs

Tamponade, Cardiac

Tension pneumothorax

Thrombosis (Coronary or pul-monary)

Trauma

Surgical cause (Traction to intes-tine, oculocardiac reflex, neuro-surgical causes, cardiac compres-sion on beating heart bypass sur-gery etc.)

These factors can grossly be divided into followingcategories:

1. Patient related factors

2. Anaesthesia related factors

3. Surgery related factors

1. Patient related factorsa. Preexisting cardiac disease - The patients with

known cardiac disease (e.g. myocardial ischaemia -MI) have much higher incidence of arrhythmias dur-ing anaesthesia than patients without known cardiacdisease1.The arrhythmias are more fatal in patientswith associated cardiac pathology.

b. Central nervous system disease - Patients with in-tracranial disease especially sub-arachnoidhaemorrhage may show ECG abnormalities such aschanges in QT intervals, development of Q waves,ST-segment changes, and occurrences of U waves.

c. Old age - Postoperative atrial fibrillation (AF) is a fre-quent complication in the elderly patients 3 undergoingthoracic surgery. Aging causes degenerative change inatrial anatomy and is also accompanied by relativechanges in atrialpathology.The injury tosympathovagalfibers of cardiac plexus during surgery and preexistingatrialelectrical changes in thesepatientspredispose themtopostoperative atrial fibrillation

2. Anaesthesia related factorsa. Tracheal intubation – It is one of the most com-

monest causes of arrhythmias during induction as wellas during the perioperative period, most often asso-ciated with haemodynamic disturbances.

b. General anaesthetics – The drugs used for induc-tion, maintenance as well as for reversal of generalanaesthesia are not primarily arrhythmogenic, butarrhythmias can be produced in the presence of avariety of triggering agents and clinical situationsgenerating high catecholamines such as light planeof anaesthesia with hypertension and tachycardia,hypoxaemia, hypercarbia, exogenous epinephrine andaminophylline. Halothane or enflurane producesarrhythmias, probably by a reentrant mechanism.3

c. Local anaesthesia – Regional anaesthesia (epidu-ral anaesthesia) followed by central neuraxial block-ade may be associated with pharmacological sym-pathectomy leading to parasympathetic nervous sys-tem predominance causing bradyarrhythmias. It maybe mild to very severe in nature.7

d. Electrolyte imbalance and abnormal arterial bloodgases – Abnormal blood gases such as hypercarbia,hypoxaemia or electrolyte imbalance producearrhythmias either by producing reentrant mechanismor by altering phase depolarization of conducting fi-bers. Hypokalemia or hyperkalemia may also lead toarrhythmias.

e. Central venous cannulation – Stimulation of carotidsinus reflexes may occur due to pressure from fingersduring jugular vein cannulation as excess insertion ofthe central venous catheter into the right atrium duringcentralvenouscannulationmayalsoleadtoarrhythmias.7

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3. Surgery related factorsa. Cardiac surgery – A spectrum of cardiac

arrhythmias can be observed during the immediateperiod following the release of aortic cross clampwhen myocardium is recovering from the ischaemicinsult and regaining normal sinus rhythm. Surgicalmanipulation such as retraction of the heart duringoperation on beating heart, venous cannulation or tak-ing sutures over the atrium can also precipitatearrhythmias.

b. Non-cardiac surgery – Vagal stimulation due to trac-tion on the peritoneum or direct pressure on the va-gus nerve during carotid artery surgery may producebradycardia or atrioventricular (AV) blocks, or evenasystole. Dental surgery causes profound stimula-tion of both sympathetic and parasympathetic ner-vous stimuli.

Arrhythmias are broadly classified asTable 2 : Classification of arrhythmias1. Bradyarrhythmia

i. Sinus Bradycardia

ii. Various forms ofheart block

a. First degree

b. Second degree

c. complete

2. Tachyarrhythmia

ii. Wide QRScomplextachycardias (QRS >0.12 second)

a. Ventricular prema-ture beat (VPB) / Ven-tricular extrasystole

b. Ventricular tachy-cardia (VT)

c. Ventilation fibrilla-tion

d. Torsades de pointes

i. Narrow QRScomplex (SVT)tachycardias (QRS<0.12 second)

a. Sinus tachycardia

b. Atrial prematurebeat

c. Atrial tachycardia

d. Atrial flutter

e. Atrial fibrillation

1. Bradyarrhythmiai. Sinus bradycardia – bradycardia is generally de-

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

CausesThe causes of sinus bradycardia are as follows:

1. Drug effects: blockers, digitalis and other anti-ar-rhythmic drugs

2. Acute myocardial ischaemia3. Hypothermia4. Underlying hypothyroidism, cholestatic jaundice or

raised intracranial pressure5. Chronic degenerative change such as fibrosis of the

atrium and sinus node

Treatment:Asymptomatic bradycardia usually does not require

treatment. Symptomatic bradyarrhythmias should be di-agnosed and immediate therapy should follow. In patientswho manifest haemodynamic compromise such as hy-potension, atropine is the first line of treatment. It can beused in the dose of 0.5 to 1.0 mg (IV bolus), repeatedevery 3 to 5 minutes, if required (maximum dose = 0.04mg.kg-1). However, it should be used cautiously in pa-tients with CAD, since excessive increase in heart ratemay worsen ischaemia because of increased myocardialoxygen consumption or reduced diastolic filling time. Ifbradycardia still persists despite treatment, isoprenalinecan be administered as an IV bolus of 5 to 10 g followedby an infusion of 2 to 10g.min-1. Other alternative isdopamine infusion 5 to 20g.min-1.

While treating sinus bradycardia, various causes orfactors contributing should be searched and treatmentstarted. Be ready for percutaneous and transvenous pac-ing.8 (Flow Chart 1)

Expert cardiologist opinion must be sought for fur-ther management.ii. Various forms of heart block: Heart blocks

(AVHB) are broadly classified into three categoriesa) First degree heart blockb) Second degree heart blockc) Complete heart block

Anatomical or functional abnormalities underlie atrio-ventricular heart block (AVHB). These may be transientor permanent. Transient AVHB can be produced by acuteMI and general anaesthetics such as enflurane or hal-othane in patients using calcium channel blocker drug(CCB) or amiodarone. Permanent AVHB, on the otherhand is usually idiopathic, other causes include CAD andLev’s or Lenegre disease, where fibrosis of the conduct-ing system occurs.

a) First degree heart block: This is simple prolonga-tion of the PR interval to more than 0.22 sec. Everyatrial depolarization is followed by conduction to theventricle but with delay. The treatment is usually notnecessary however, the patients should be carefullyobserved for progression to a higher degree of block,that requires prompt treatment. (Fig.2)9



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a) Second degree heart block: Thisoccurs whensome Pwavesconduct electrical activationand oth-ers do not. There are several forms of second de-gree AV block

Mobitz Type I Block(Wenckebach’sphenom-enon): Inthis type of AVHB, there isprogressive prolon-

gation of PR interval untila ‘P’wave fails to conduct.The PR intervalbefore the blocked Pwave ismuch longerthan thePR intervalafter theblocked Pwave. Treatmentisusually not necessary exceptin slowventricular rate,where atropine or isoprenaline can be used. (Fig.3) 9

Mobitz Type II Block: There isno progressivelengthening of thePR interval, but occasionally there isan atrialcontraction withouta subsequentventricular con-traction.This iscalled the“Mobitz TypeII” phenomenon.It mayprogresssuddenly and unpredictivelyto completeheart block. Itisclear indication forthe placement of atemporary pacemaker.(Fig.4)9

Flow C hart 1



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either broad ( > 0.15) or narrow (< 0.15) QRS com-plexes. (Fig. 5 & 6)

9

Broad complex: This occurs because of disease inthe Purkinje system. The escape pacemaker arisesfrom the distal Purkinje network or the ventricularmyocardium. The resulting rhythm is slow (15-40b.p.m) and relatively insignificant or unharmful. Inthe elderly, it is usually caused by degenerative fibro-sis and calcification of the distal conduction system(Lenegre’s disease) or the more proximal conduc-tion system (Lev’s disease). It may occur after clo-sure of ventricular septal defect (VSD) and some-times following aortic valve replacement (AVR). Inyounger patients, broad complex AV block may becaused by perioperative myocardial ischaemia.

Management: Treatment is not required in narrowcomplex 3° block except for eradication of toxic causes.Occasionally, permanent pacing is advocated for symp-tomatic, isolatedAV block. While in broad complex, pac-ing is indicated to maintain the normal haemodynamics.

2.TachyarrhythmiaThe tachycardia can be classified based on the ap-

pearance of the QRS complex as tachycardia, narrowcomplex supraventricular tachycardia (SVT), and widecomplex tachycardia. Most wide complex (broad com-plex) tachycardias are ventricular in origin. Symptomatictachy-arrhythmias should be monitored and immediatetherapy should be done. 8 (Flow Chart 2)Tachyarrhythmias are classified in two categories depend-ing upon the QRS complexes.

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

Note

Progressive lengthening of PR interval

One non-conducted P wave

Next conducted beat has a shorter PR interval than the preceding

Fig 3. Second degree heart block (Wenckebach type)

Fig 4. Second degree heart block (Mobitz type 2)

Note

PR interval of the conducted beats is constant

One P wave is not followed by a QRS complex and here seconddegree block is occurring

Note

P wave rate 90/min

QRS complex rate 36/min

No relationship between P waves and QRS complex

Abnormally-shaped QRS complexes because of abnormal spread ofdepolarization from a ventricular focus

Fig 5. Third degree block

Note

Regular P waves (normal atrial depolarization)

P wave rate 145/min

QRS complexes highly abnormal because of abnormal conductionthrough ventricular muscle

QRS (ventricular escape) rate 15/min

No relationship between P waves and QRS complexes

Fig 6. Complete heart block

Narrow complex: This is due to disease in the AVnode or the proximal bundle of His. The escaperhythm occurs with an adequate rate (50-60 b.p.m.)and is relatively reliable. It occurs because of infe-rior wall MI and toxic concentration of drugs such asdigitalis, verapamil or blockers in perioperative pe-riod.



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Flow Chart 3

diltiazem - blockers

Flow Chart 2



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a. Sinus tachycardia: it is defined as an increasein the sinus rate of more than 100 beats/minute. Prolongedtachycardia for long duration can induce ischaemia in coro-nary artery diseased patients.

Causes: It includes

Anaemia because of blood loss Pain

Inadequate anaesthesia

Hypovolaemia

Fever

Hypercarbia Thyrotoxicosis/ thyroid crisis

Cardiac failure with compensatory sinus tachy-cardia

Catecholamines excess

Treatment: Before instituting pharmacologicaltreatment for sinus tachycardia, precipitating factors mustbe identified and corrected. Drug therapy is especiallyrequired in patients with ischaemic heart disease whodevelop ST segment changes to prevent further myocar-dial ischaemia. Tachyarrhythmia should be managed ac-cording to Flow Chart 2. Beta-blockers such as esmololis preferred drug for managing it. It has half-life of 10 minwith bolus dose of 500 mcg.kg-1 over 1 min, followed byan infusion of 50-300 mcg.kg-1.min-1. If continuous use isrequired, it may be replaced by longer lasting cardio se-lective drugs such as metoprolol in the dose of 5 to 10 mggiven slowly intravenously (IV) at 5 min interval to a totaldose of 15 mg.10 Another drug can be used is propranolol0.1 mg.kg-1.

b. Atrial premature beat: It represents 10% of allintraoperative arrhythmias. On the ECG they appear asearly and abnormal ‘P’ waves and are usually but notalways, followed by normal QRS complexes. The dura-tion of QRS wave is normal but wide QRS wave may bepresent due to aberrant ventricular conduction, whichmimics premature ventricular beat. Treatment is not nor-mally required unless the ectopic beats provoke more sig-nificant arrhythmias, where blockade may be effective.(Fig.7) 9

c. Atrial tachycardia: These arrhythmias are foundin 6% of patients undergoing non cardiac surgery. 2 It isnonparoxysmal, narrow QRS rhythm with retrograde ornonapparent P waves and a rate less than 70 beats/min. if

faster usually less than 130 beats/min, it is termed as accel-erated AV junctional rhythm. Those arrhythmias can leadto fall in blood pressure upto 15% in patients without car-diac disease and upto 30% in diseased heart.11 Usually notreatment is required; carotid sinus massage and verapamilare often helpful in symptomatic patients. Intravenous ad-enosine in 6 to 12 mg doses is another alternative. Treat-ment with class Ia, Ic or III drugs is usually successful e.g.disopyramide 2 mg.kg-1 over 10 min. (Fig.8)9

d.Atrial flutterThis is a rhythm disturbance that is usually associated

with organic ischaemic heart disease. The atrial rate variesbetween 280 and 350 min-1 but is usually around 300 min -1.

Most often every second flutter beat conducts giving aventricular rate of 150 min-1. Occasionally every beat con-ducts, producing a heart rate of 300 min-1. More often, espe-cially when patients are receiving treatment,AV conductionblock reduces the heart rate to approximately 75 min-1.

ECG: The ECG shows regular saw tooth-like atrialflutter waves between QRST complexes. If they are notclearly visible,AV conduction may be transiently impairedby carotid sinus massage or by the administration of AVnodal blocking drugs such as verapamil. (Fig.9) 9


Fig 7. Arial premature beat

Note

After one sinus beat the SA node fails to depolarize. After a delay,an abnormal P wave is seen because excitation of the atrium hasbegun somewhere away from the SA node. The abnormal P wave isfollowed by a normal QRS complex, because excitation has spreadnormally down the His bundle. The remaining beats show a returnto sinus arrhythmia.

Fig 8. Atrial tachycardia

Note : After three sinus beats, atrial tachycardia develops at a rate of 150/

min. P waves can be seen superimposed on the T waves of thepreceding beats. The QRS complexes have the same as those of thesinus beats.



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

e.Atrial fibrillation (AF)It accounts for more than 90% of supraventricular ta-

chycardia (SVT) in the perioperative setting. It is caused bya raised atrial pressure, increased atrial muscle mass, atrialfibrosis or inflammation and infiltration of the atrium. Rheu-matic disease is often associated with cardiac causes suchas mitral valve disease, myocarditis and coronary artery dis-ease. Systemic diseases includehyperthyroidism, pulmonaryembolismand electrolyte imbalance. When caused by rheu-matic mitral stenosis, the onset of atrial fibrillation results inconsiderable worsening of cardiac failure.

Clinically the patient has a very irregular pulse, asopposed to a basically regular pulse with an occasionalirregularity (extrasystoles) or recurring irregular pattems.The ECG shows fine oscillations of the baseline (so calledfibrillation) and no clear P waves. The QRS rhythm isusually 160-180min-1 but it slows with treatment. ECGchanges are more indicative in lead II (Fig.10) 9. AF maybe acute or recent onset (<48 hrs) and chronic. In therecent onset AF, initial treatment is directed towards thecontrol of ventricular response rate with agents that slowAV node conduction. The precipitating or provoking agentsshould be removed or treated first. Intravenous beta-blockers or calcium channel blockers produce rapid con-trol of rate, regardless of the level of sympathetic tone.However beta-blockers are preferred over calcium chan-nel blocker (CCB) during intraoperative period due toshorter duration of action and lesser negative inotropiceffects.10,12 In haemodynamically-compromised patients,DC cardioversion is the most effective method of con-verting AF to sinus rhythm. Chronic AF is often found inpatients with rheumatic heart disease undergoing cardiacsurgery and may have atrial thrombi, therefore, any at-tempt to restore sinus rhythm by DC cardioversion maybe associated with increased risk of systemic or pulmo-

nary embolisation. Successful cardioversion is relativelyrare in chronic AF. The control of ventricular rate is thepreferred approach in these cases. The most useful drugfor this purpose is digoxin. The patients with chronic AFundergoing noncardiac surgery should be evaluated forthe presence of atrial clot by echocardiogram prior to sur-gery. In the presence of atrial clot, control of ventricularresponse rate with appropriate medication is institutedduring perioperative period, if necessary.

ii. Wide QRS complex (QRS>0.12): In thesetypes of arrhythmias the QRS complex is usually morethan 0.12 sec.


Fig 9. Atrial flutter

Note

P waves can be seen at a rate of 300 min-1, giving a saw-toothed

appearance. There are four P waves per QRS complex, and ven-tricular activation is perfectly regular at 75min

-1.

Note

No P waves – irregular baseline

Irregular QRS complexes

Normally shaped QRS complexes

In lead V1waves can be seen with some resemblance to those seen inatrial flutter this is common in atrial fibrillation

Fig 10. Atrial fibrillation

a. Ventricular premature beat (VPB) / Ventricularextrasystole

VPB results from ectopic foci arising from belowAV node and give rise to wide (>0.12 sec) bizarre QRScomplex. They account for 15% of the observedarrhythmias, more common in anaesthetized patients withpre existing cardiac disease. New onset of VPB, mayoccur in the presence of coronary artery insufficiency,myocardial infarction, digitalis toxicity with hypokalemiaand hypoxaemia. On the ECG, the premature beat has abroad (>0.125) and bizarre QRS complex because it arisesfrom an abnormal (ectopic) site in the ventricular myo-cardium. Following the premature beat there is usually acomplete compensatory pause because the timing of sinusrhythmis not induced by the premature beat. (Fig.11 & 12) 9

Treatment: Underlying abnormalities in these pa-tients should be corrected immediately. No treatment isgenerally required for isolated VPB in asymptomatic andhealthy patients. However VPB which are multiple (>5beats/min), multifocal, or bigemminal or occur near thevulnerable period of the preceding ventricular repolariza-



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tion (the so called R on T phenomenon), associated withhaemodynamic disturbance or convert to worsearrhythmias require prompt treatment. Lidocaine with aninitial bolus dose of 1.5 mg.kg-1 followed by infusion of 1to 4 mg.min-1 can be given. Other drugs from class I, II orIII are used to treat these types of arrhythmias.

b. Ventricular tachycardiaThis is defined as three or more ventricular beats

occurring at a rate of 120 bpm or more. It may be poten-tially life threatening. Examination reveals pulse rate of120-220bpm. Usually there are clinical signs of atrioven-tricular dissociation i.e. intermittent cannon 'a' waves andvariable intensity of the first heart sound. The ECG showsa rapid ventricular rhythm with broad (often 0.14s ormore), abnormal QRS complexes. Dissociated P wavesactivity may be seen and have no fixed relation to wideQRS complex.

Treatment may be urgent depending on thehaemodynamic situation. If the cardiac output and the

blood pressure are very depressed, emergency DC-cardioversion must be considered. On the other hand, ifthe 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 mgi.v. over 5 min) followed by a lidocaine infusion (2-4mg.min-1 i.v.). DC-cardioversion may be necessary ifmedical therapy is unsuccessful. The administration ofmultiple antiarrhythmic drugs should be avoided.

Patients with recurrent episodes or unresponsive tolidocaine, may require therapy with procainamide (10-15mg.kg-1 loading dose followed by an infusion of 2 to 6mg.min-1) or bretylium (5 to 10 mg.min-1 over 2 to 5 minthen infusion of 1-2 mg.min-1) or amiodarone in the doseof 150 mg IV over 10 minutes followed by an infusion of1 mg.min-1 for 6 hours and 0.5 mg.min-1 thereafter. IVamiodarone has been shown to be as effective as bretyliumwith added advantage of less hypotension as comparedto IV bretylium. (Fig.13)9

Note

The upper trace shows five sinus beats, then an early beat with awide QRS complex and an abnormal T wave: this is a ventricularextrasystole. In the lower trace, the ventricular extrasystole occur(arrows) at the peak of the T waves of the preceding sinus beats:this is the ‘R on T’ phenomenon.

Fig 11. Ventricular extrasystole

Note

Three sinus beats are followed by a ventricular extrasystole. No Pwave is seen after this beat, but the next P wave arrives on time.

Fig 12. Ventricular extrasystoleNote

After two sinus beats, the rate increases to 150/min. The QRScomplexes become broad, and the T waves are difficult to identify.The final beat shows a return to sinus rhythm.

Fig 13. Ventricular tachycardia

C. Ventricularfibrillation (VF)It is very rapid and irregular ventricular activation with

no mechanical effect. It is usually intiated froman ischaemicmyocardium or an aberrant foci (especially in acuteperioperative myocardial infarction), ventricular tachycar-dia or torsades de pointes. On ECG, there are no definedQRS complexes, shows shapeless rapid oscillations and onpulse oximetry, there is acute fall in SpO

2because of low

or no cardiac output. Causes include myocardial ischaemia,hypoxaemia, electrolyte imbalance and drug effects.

Treatment: Cardiopulmonary resuscitation must beperformed as rapidly as possible. Asynchronous externaldefibrillation should be performed using 200-360J.Apre-cordial thump is occasionally effective in terminating VF,but should be attempted only if a defibrillator is not avail-able immediately. Intravenous bretyium 5-10 mg.kg-1 over5 min can be useful on some occasion. Supporting phar-



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macological therapy such as lidocaine, amiodarone andprocainamide are used only to prevent recurrence of VF.

d. Torsades de pointesThese arrhythmias are usually short in duration and

spontaneously revert to sinus rhythm. Occasionally it canchange to VF. On ECG, it is characterized by rapid, ir-regular sharp complexes that continuously change froman upright to an inverted position. Between spells of ta-chycardia the ECG shows a prolonged QT interval; thecorrected QT is equal to or greater than 0.44s.

Treatment:The arrhythmia is treated as follows1. Any electrolyte disturbance is corrected.

2. Causative drug and precipitating factors should bestopped and removed.

3. Intravenous isoprenaline may be effective when QTprolongation is acquired.

4. Blockade is advised if the QT prologation is con-genital.

Collapse rhythm- There is no ECG rhythm in thecase of cardiac arrest or asystole. Immediate manage-ment should be done according to Flow Chart 3.

PacemakerNew or worse cardiac arrhythmias in the

perioperative period are usually temporary occurrences,often due to the result of transient physiologic or pharma-cologic imbalance. Antiarrhythmic drugs have the poten-tial to further aggravate this imbalance. Therefore, earlyuse of temporary pacemaker during perioperative periodis preferred nowadays. More than 90% of pacemakersare inserted for the treatment of bradyarrhythmias oc-curring either after tachycardia (bradytachy syndrome)or AV conduction disorders or by themselves (sick sinussyndrome).

Temporary pacemaker may be invasive (epicardialand endocardial) or non-invasive (transcutaneous andtransesophageal). The pacing may also be unipolar or bi-polar. Unipolar pacing describes the placement of thenegative (stimulation) electrode in the atrium or ventricleand 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 atrialventricular sequential pacing when used in combinationwith a dual output (atrial and ventricular) sequential ex-ternal pacemaker. 13

Prophylactic transvenous pacing is recommendedin patients who are considered at high risk for developinghaemodynamically significant bradycardia due toAV heartblock or sinus node dysfunction. Whereas, direct cardiacpacing methods are preferred for the patients having car-diac surgery, especially in the postbypass period. In thesepatients, current output of the pacemaker is slowly in-creased until desired cardiac chamber contraction is cap-tured (usually 5-10 milliamperes), then current output isfurther increased by 5 more milliamperes to assure con-tinued capture. When atrial ventricular sequential pacingis required, the optimal PR interval will need to be deter-mined. It is generally 150 msec but can vary between 120to 200 msec so as to optimize ventricular filling and car-diac output. If extensive electrocautery is being used dur-ing the operation, pacemaker may have to be put on asyn-chronous mode to prevent inhibition of the pacemaker byelectrocautery radiofrequency current. (Fig.14) 9


Note

Occasional P waves are visible, but are not related to the QRS com-plexes. The QRS complexes are preceded by a brief spike, represent-ing the pacemaker stimulus. The QRS complexes are broad. Becausepacemakers stimulate the right ventricle and cause ‘ventricular’ beats.

Fig 14. Pacemaker

Anaesthetic considerationsAll patients undergoing anaesthesia and surgery

should have ECG monitoring. Lead II and V5

are supe-rior for arrhythmia detection and diagnosis before the ap-pearance of physical signs e.g. changes in BP, heart rateor heart sounds. After establishing from ECG that ar-rhythmia is present, it is crucial to evaluate patient’s re-sponse to altered rhythm in rate and type of treatmentrequired. Correction of contributing cause and final lineof treatment follows thereafter. Routine measures for allintraoperative arrhythmias are as follows (Table 3 & 4)



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Table 3 Routine measures for all intraoperativearrhythmias

Routine measures for all intraoperative arrhythmias

- Assure adequate oxygenation and ventilation

- Alteration in depth of anaesthesia

- Assure optimum PaO2, PaCO

2, acid base, electrolyte and

temperature

- Reevaluate cardiac history/pathology

Get ready for

- Anti-arrhythmic drugs

- Anti-ischaemic drugs

- Pacing and DC shock

Table 4. Management of arrhythmias

Aims

Cure

Prevention (suppression)

Termination

Reduction of ventricular rate

Techniques available

Vagotonic methods

DC cardioversion

Antiarrhythmic drugs

Pacemakers and other electronic devices

Surgery and other ablation methods

Flow Chart 3

g/kg/min

g/min



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Antiarrhythmicdrugs

Drugs that modify the rhythm and conduction of theheart are used to prevent cardiac arrhythmias. All suchdrugs may aggravate or produce arrhythmias and theymay also depress ventricular contractility and must, there-fore, be used with caution. There are more than 30 anti-arrhythmic drugs. They are classified according to theireffect on the action potential (Vaughan Williams’classifi-cation.) (Fig 15 & Table 5)

Class I drugs

These are membrane-depressant drugs that reducethe rate of entry of sodium into the cell. They may slowconduction, delay recovery or reduce the spontaneous dis-charge 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 theaction potential.

Table 5. Vaughan Williams’ classification of antiar-rhythmic drugs

Class I

Ia Quinidine,procainamide,disopyramide

Ib Lidocaine, mexiletine, tocainide

Ic Flecainide, propafenone

Class II -adrenergic blocking drugs

Class III Amiodarone, sotalol, bretylium

Class IV Verapamil, diltiazem

(Other drugs Adenosine, digoxin)

Class II drugs

These antisympathetic drugs prevent the effects ofcatecholamines on the action potential. Most are -adr-energic antagonists. Cardioselective -blockers (

1) in-

clude metoprolol, atenolol, and acebutalol.

Class III drugs

These prolong the action potential and do not affectsodium transport through the membrane. There are twomajor drugs in this class; amiodarone and sotalol. Sotalolis also a-blocker.

Fig.15. Vaughan Williams’ classification, the dotted line indi-cate the effects of antiarrhythmic drugs

Class IV drugs

The non-dihydropyridine calcium antagonists that re-duce the plateau phase of the action potential are particu-larly effective at slowing conduction in nodal tissue.Verapamil and diltiazem are the most important drugs inthis group.

Another clinical classification6 is based on the partof the heart that is affected by the antiarrhythmic drug.The features of the major antiarrhythmic drugs are givenin Fig.16.


Fig.16. Drugs affecting different parts of the heart



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The main drugs useful for arrhythmia managementwith dosage are as follows

Antidysrhythmic drugs useful for ventricular dys-rhythmia

Lidocaine Loading dose 1mg.kg-1, repeat every5min, continuous 30-50g.kg-1.min-1

Phenytoin 50-100mg slowly every 5 min (Max1gm)

Procainamide 20mg.min-1 IV infusion (Max total dose17mg.kg-1; infusion 1-4mg.min-1

Propranolol 0.1mg.kg-1 by slow IV over 10min

Amiodarone 150mgIV over10min;360mg/IV over6hr

Flecainide 2mg.kg-1 at 10mg.min-1 (slowly)

Verapamil 2.5 to 5mg IV bolus over 2 min; 2nd dose5-10mg in 15-30min

Bretylium 5mg.kg-1 IV push, repeat in 5 min at10mg.kg-1, upto max dose of 35 mg.kg-1

Mexiletine 400mg bolus dose followed by 200 mgpo q 8hrly

Tocainide 1200-1800mg PO in divided doses q8-12hr

Digoxin 0.5mg IV single loading dose then 1.0-1.5mg in divided doses over 8-24hrs

Key pointsTherapeutic decisions in patients with cardiac

arrhythmias are based on an assessment of thehaemodynamic impact of the rhythm disturbance, thepatient’s underlying cardiac function, contributing factorsand the correct diagnosis of the arrhythmia. Both clinicalexamination and the ECG should be considered in makingthe diagnosis. Incorrect diagnosis can lead, not only toineffective therapy but also to potentially dangerous therapy,especially when wide-QRS tachyarrhythmias are present.

Symptomatic bradyarrhythmia can be treated initiallywith atropine; in many forms of bradycardia, however, pac-ing, either external or transvenous, is the definitive therapyof choice. In some situations, including Mobitz type II sec-ond-degree block and in wide-QRS, new-onset completeheart block, external pacing can be used temporarily tobridge the patient over to transvenous pacing.

Adenosine is the drug of first choice in treating pa-tients with PSVT. It is therapeutic in over 90% of pa-tients with this tachyarrhythmias, in which AV-nodal re-entry is the most common mechanism. In non-reentrantSVT, such as automatic (ectopic) atrial tachycardia ormultifocal atrial tachycardia, adenosine may be useful inunmasking the underlying arrhythmia mechanism, but the12-lead ECG should first be searched to define the mecha-nism of the arrhythmia. Other pharmacologic options in-clude diltiazem and verapamil, -blocking drugs, andamiodarone and digoxin. Cardioversion should be consid-ered if drug use is contraindicated or if the arrhythmia isnot controlled with drug therapy.

Ventricular tachycardia can be monomorphic orpolymorphic. When PVT is accompanied by prolongedrepolarization, manifested as QT-interval lengthening onthe ECG before or after episodes of tachycardia, the ta-chycardia is torsades de pointes, and its presence man-dates specific diagnostic and therapeutic considerations.If the origin of a wide-QRS tachycardia cannot be con-firmed clinically or electrocardiographically, amiodaroneor procainamide, should be used. In all situations, emer-gency cardioversion takes precedence if haemodynamiccompromise is present or develops during drug therapy.

Pulseless VT and VF are forms of ventriculartachyarrhythmia that require cardiac arrest therapy withdefibrillation and drugs; most importantly epinephrine, formaintenance of myocardial and cerebral blood flow dur-ing external chest compression or open-chest cardiacmassage.

ConclusionAcute-onset cardiac arrhythmia carries the poten-

tial of haemodynamic instability, including cardiovascularcollapse. Knowledge of both electric and pharmacologicoptions and an understanding of the therapeutic interven-tion is mandatory. Precipitating factors or causes shouldbe treated or removed immediately. In many situations,cardioversion or defibrillation is the initial intervention ofchoice, with drug therapy as follow-up in an attempt toprevent recurrence of the arrhythmia. In other morehaemodynamically stable situations, drug therapy is usedinitially.




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References:1. Forrest J, Cahalan M, Rehder K, et al. Multicenter Study of

General Anesthesia II. Results. Anesthesiology 1990; 72:262-68.

2. Forrest J, Rehder K, Cahalan M, Goldsmith C. MulticenterStudy of General Anesthesia III. Predictors of severeperioperative adverse outcomes. Anesthesiology 1992; 76:3-15.

3. Katz RL, Bigger JT Jr. Cardiac arrhythmias during anaesthesiaand operation. Anesthesiology 1970; 33:193-213.

4. Bertrand CA, Steiner NJ, Jameson AG, et al. Disturbances ofcardiac rhythm during anesthesia and surgery. JAMA 1971;216:1615-17.

5. Fisher DM. Preoperative cardiac dysrhythmias; Diagnosis andManagement. Anesthesiology 1997; 86:1397-424.

6. Kumar P Clark M. Clinical Medicine. 3rd

eds. Cardiac arrhythmias1994. ELBS 554-555, 566-568.

7. Sokolow M and Mcllroy B (1986) Clinical radiology, 4th

eds.New York. Lange. 116-7.

8. The American Heart Association, in collaboration with the Inter-national Liason Committee on Resuscitation Guidelines 2000for Cardiopulmonary Resuscitation and Emergency Cardiovas-cular Care. Part 6: advanced cardiovascular life support 7D: thetachycardia algorithms. Circulation 2000; 102:1158-65.

9. Hampton JR (1986). The ECG made easy, 3rd

eds. Edinburgh:Churchill Livingstone. 31-34, 59,61,65-68, 79,85.

10. Oxorn D, Knox JW, Hill J. Bolus doses of esmolol for the pre-vention of perioperative hypertension and tachycardia. Can JAnaesth 1990; 37:206-209.

11. Atlee J, Bosnjak Z. Mechanisms for cardiac dysrhythmias dur-ing anesthesia. Anesthesiology 1992; 76: 3-15.

12. Das G, Ferris J. Esmolol in the treatment of supraventriculartachyarrhythmias. Can J Cardiol 1988; 4:177-80.

13. Salukhe TV. Dob D, Sutton R. Pacemakers and defibrillators:anaesthetic implication. Br J Anaesth 2004; 93; 95-104.

SHORT TERM COURSEDepartment of Anaesthesiology announces short term (3 Months) course in Intraoperative

transesophageal echocardiographyfor post MDAnaesthesiologists working in private or government institu-tion setup starting from 1st March 2008.

For detail:Dr.R.C.RathodProf. & Head ofAnaesthesiaSree ChitraTirunal Institute for Medical Sciences and TechnologyTrivandrum-695011 (Kerala)Ph: 0471-2524643, Fax: (91) 471-2446433Email: [email protected] , [email protected]

MEDICO LEGAL QUERY?Dear Members,

Of late, cases under CPA, against anaesthesiologists, are increasing throughout the country. Though most ofthe cases are dismissed ultimately by the court of law, they are causing lot of tension and worry for theanaesthesiologists and their families. The following members of ISA, are qualified in ‘Law’ and are well versed inmedico-legal aspects. They have kindly volunteered to answer any of the medico legal queries related to ourprofession raised by any of the members of ISA. Please contact any of them, in case of necessity.

Dr. D.N. Upasani Dr. S.C.Parakh Dr. Mahesh S. KapadiaE-mail : [email protected] E-mail : [email protected] E-mail : [email protected]



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Transesophageal Echocardiography and AnaesthesiologistThomas Koshy1, Bhupesh Kumar2, Prabhat Kumar Sinha3

Key words Transesophageal echocardiography, Anaesthesia

Introduction

1. MD, PDCC, Additional Professor, 2.MD, DM Cardiac Anaesthesia Resident, 3. MD, Associate Professor Department of Anaesthesiology,Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala. Correspondence to: Thomas Koshy, Sree ChitraTirunal Institute for Medical Sciences & Technology, Trivandrum-695011, Kerala, India. Email : [email protected]

Echocardiography – the use of ultrasound to exam-ine the heart- is a safe, powerful, non-invasive and pain-less technique. The introduction of transesophagealechocardiography (TEE) has provided a new acousticwindow to the heart and mediastinum. Superior qualityimages of most cardiovascular structures can be obtainedreadily with an ultrasound probe in the esophagus. TEEhas revolutionized cardiac anaesthesia and has also be-come increasingly popular in the management of patientsin the intensive care unit (ICU) and during certain non-cardiac surgical procedures as well.

Although clinical application of TEE is recent,transesophageal application of ultrasonography to assesscardiac function was first reported by Side and Gosling in1971.1 The early transesophageal probes did not attractclinicians because of the problems associated with swal-lowing of the probe in conscious patients and also due tothe logistical difficulties of introducing a rigid endoscope.Transducers were subsequently mounted on flexibleendoscopes, and DiMagno et al first reported the use of alinear phased array flexible endoscope in 1980.2 In 1982,Souquet and co-workers, first produced a clinically usableflexible endoscope with a sector phased array two-dimen-sional echocardiographic transducer having a frequency of2.25 MHz – a frequency equal to that of the standard pre-cordial transducer.3 This represented the definitive break-through for the transesophageal approach. Application ofthese probes took different directions in the United Statesand Europe. The cardiologists in Europe began using TEEto supplement the diagnosis of different cardiac patholo-gies. In the United States on the other hand, increasingnumber of anaesthesiologists started using TEE probes formonitoring patients in the operating rooms (OR). As thepractice expanded it became clear that very few cardiolo-gists were able to spend long period in the OR since cardi-ology has become much more invasive speciality in last 20

yrs. Also the cardiovascular physiology of anaesthetizedpatients is not similar to physiology of awake patients andanaesthesiologists with knowledge and understanding ofthis altered physiology is in better position to interpret theinformation obtained from intraoperative TEE. In currentpractice in the UK, 90 % of the TEEs are performed notby cardiologist but, by cardiac anaesthesiologist.4 As weview the field of echocardiography in the 2000s, it is almostimpossible to conceive of a state-of-the-art cardiac ORwithout TEE machines.

Several authors have described the usefulness ofTEE on cardiac surgical practice.5,6 Kneeshaw and co-workers had showed that in a group of 309 patients whounderwent intraoperative TEE, management changed in26% patients.7 In 6% of patients the changes were ininotrope use and fluid management. However, in 20% ofpatients, TEE resulted in a change in the procedure car-ried out. Among noncardiac surgical procedures it hasbeen found to be useful in management of neurosurgicalpatients for detection of air embolism and other majorsurgical areas where haemodynamic instability may oc-cur. The role of TEE in ICU is also steadily increasing. Itwas found to be of particular value in managinghaemodynamic instability in post cardiopulmonary bypass(CPB) period. Now it is being also used as rapid imagingmodality in the general ICU as an adjunct to other moni-toring modality to provide data in haemodynamically un-stable patients. To summarize, the usefulness of TEE in-cludes, augmentation of preoperative cardiac evaluation,planning of surgery, evaluation of surgical results and dif-ferential diagnosis of haemodynamic instability. TEE isassociated with a long learning curve, because the com-plexities of transducer positioning, imaging sector align-ment and three dimensional cardiac anatomies are notfamiliar to most beginners.

Indian Journal of Anaesthesia 2007; 51 (4) : 324-333



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Periop Arrythmias