Anaesthesia and Atrial Fibrillation

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THE PERIOPERATIVE MANAGEMENT OF ATRIAL FIBRILLATION

Clinical Scenarios What is atrial fibrillation? Why is atrial fibrillation important? How is Atrial Fibrillation Managed. Suggested Treatment Protocol Preoperative assessment The Effects of Anaesthesia on Atrial Fibrillation Atrial Fibrillation following Cardiothoracic Surgery Key Points

Clinical Scenarios
CASE 1 A 74 year old female presents for cystoscopy for TURBT. She has a history of hypertension and an irregular pulse. She complains of dyspnoea on moderate exertion. Current medications are Dyazide one table mane, Methyldopa one tab mane and Digoxin 0.0625mg mane. On examination, her blood pressure is 150/90, apex rate 144, irregularly irregular. JVP is raised 4cm. No murmurs. Lung fields are clear. Palpable liver, saccral and pedal oedema. How would you manage this patient? CASE2 A 53 year old male was admitted through the accident and emergency department (A&E) last night. He has been complaining of intermittant palpitations for 3 weeks. He had a particularly distressful episode ladt night, lasting 3 hours. He has no background medical problems. Family history is non contributary. He is on no medications. On examination, his blood pressure is 140/60, pulse rate is 110 radially, and 150 apically. His lung fields are clear. There are no other clinical signs. The medical registrar contacts you, requesting an anaesthetic for cardioversion of this patient. How would you manage this patient? CASE 3

A 68 year old female undergoes a right upper lobectomy for neoplasm. The perioperative course was uncomplicated. She has a history of COPD, 50 pack year history of smoking. Current medications: salbutamol 2 puffs prn, uniphyllin 300mg bd. On the second post-operative day, in the high dependency unit, the patient suddenly develops atrial fibrillation with an apical rate of 140 to 170 beats/min. Blood pressure remains stable. How would you manage this patient?

What is Atrial Fibrillation?

Background and Aetiology

Atrial Fibrillation [AF] is a common cardiac arrhythmia. Incidence is 5 10% in the over 65 years. AF may be paroxysmal (i.e. intermittent) or sustained. AF is characterized by rapid atrial contraction, >400 beats/min, with minimal mechanical activity. Only a small proportion of atrial impulses are conducted into the ventricles.

Aetiology:
Mnemonic "ARITHMIC" A Alcohol R Rheumatic Heart Disease I Ischaemic Heart Disease T Thyrotoxicosis H Haemochromatosis M Mitral Valve Disease I Infection (e.g. pneumonia or systemic sepsis) C Cardiomyopathy

The other important causes are: chronic lung disease, hypertension, ASD, WPW, pericarditis, pulmonary embolism, electrolyte or acid-base abnormalities, hypovolaemia, surgical manipulation of the thorax & "Lone" a. fib, which is idiopathic.
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Clinical Features
Clinical Features:

History of palpitations. History of risk factors (ARITHMIC) Irregularly Irregular Pulse. Absent "a" wave on JVP. The irregularity of the pulse is maintained through exercise. Variable pulse pressures in carotid pulse. Variation in intensity of first heart sound. Variation in pulse rate measured at apex and wrist (apex rate>wrist). Rate is not slowed by carotid sinus massage.

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Electrocardiograph

Discrete "p" waves are not seen. Atrial activity manifests itself as an undulating baseline. The ventricular response is variable: The most important determinant of the ventricular response is the functional refractory period of the AV node. A large number of atrial responses bombard the AV node, which is, consequently, from beat to beat, at varying levels of refractoriness ["concealed conduction"]. If AF converts to A. Flutter, because the atrial rate is slower, the ventricular response may actually increase. In Atrial Flutter, the atrial rate is 300 beats/min, and the ventricular response is usually a division of this: 150 (with 2:1 AV block), 100 (with 3:1 block), 75 (with 4:1 block). A. Flutter has a "sawtooth" baseline, with a regular rate. If the heart rate becomes regular and slows to 30 40, consider complete heart block, or if the patient develops a new tachycardia, consider digitalis toxicity.

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Why is Atrial Fibrillation Important?

Why is A. Fib Important to the Anaesthetist?
1. It is an indicator of significant systemic disease (e.g. undiagnosed thyrotoxicosis). 2. The loss of the atrial component to systole may lead to a decease in cardiac output. 3. An excessive ventricular rate may lead to angina, ischaemia, hypotension, pulmonary oedema. 4. Development of left atrial thrombus leads to systemic embolisation. 5. The patient may develop anxiety secondary to palpitations. 6. Treatment with digoxin may cause toxicity, particularly in the presence of hypokalaemia. 7. Treatment with warfarin may lead to bleeding complications.
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The "Atrial Kick"

In patients with ischaemic heart disease, the loss of the atrial component may lead to a 50% derease in cardiac output & blood pressure. If there is impaired LV function, then the heart may be more dependent than normal on the atrial component. The loss of the atrial kick may only be apparent during exercise.

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Irregular Ventricular Response

The irregularity, per se, of the ventricular response, does not cause any problems. The ventricular rate, however, is critical:

Rapid ventricular rates are associated with decreased ventricular filling, and consequently reduced cardiac output.

In Mitral Stenosis ventricular filling time is critical, onset of AF causes a sudden deterioration in the disease process.

Rawles BHJ 1990; 63: 157-61 "What is meant by "controlled" ventricular rate in atrial fibrillation": The optimum ventricular rate, at rest, in AF is 90 b/min (increasing with exercise) the higher than normal rate being required to overcome the loss of the atrial "kick"
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HOW IS ATRIAL FIBRILLATION MANAGED?

Up to 50% of cases of recent onset atrial fibrillation revert spontaneously to sins rhythm. Comparative studies of antiarrhythmics are consequently unreliable. Treatment plan: 1. Treat the cause. 2. Return to sinus rhythm. 3. Control the ventricular rate. 4. Prevent thromboembolism

Step 1: correct any electrolyte imbalance

Replace Potassium and Magnesium*

Step 2: consider cardioversion3.2

Synchronized direct current cardioversion (SDDC) is the gold standard for management of acute onset AF.

SDDC is the treatment of choice in acute onset AF with cardiovascular compromise. The electrical current causes a generalized depolarization of excitable myocardium, a period of asystole follows, allowin the sinus node to reassert itself as the pacemaker. A DC current of 25 to 100J is usually required (synchronized with the QRS complex to prevent V. Fib). The success rate depends on the duration of the arrhythmia; shorter=better. Large left atrial size (on TOE) >4.5cm suggests difficulty in cardioversion. AF secondary to rheumatic heart disease rarely cardioverts. The risk of thromboembolism is high: if the AF is of >3 days duration, the patient should be anticoagulated for 3 weeks before cardioversion is attempted.

Pharmacologic cardioversion can be attempted with a number of agents, class 1a (disopyramide), class 1c (propafenone) or class 3 (amiodarone). These are, at best, only partially effective, but may be efficacious in the maintenance of sinus rhythm post cardioversion Moreover, conversion to and maintenance of sinus rhythm with antiarrhythmic drug therapy has not shown any improvement in mortality. For most patients, control of the ventricular response is the most effective therapy.

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Step 3: control the ventricular response.

A variety of agents have been used, but the most effective are digoxin, calcium channel blockers, beta blockers and amiodarone.

CALCIUM CHANNEL BLOCKERS (Verapamil & Diltiazem).

Ca channel blockers block the inward movement of calcium into the cells of the conducting system, thereby they: Reduce automaticity Reduce conduction velocity Increase the refractory period

These agents do not promote conversion to sinus rhythm, but merely control the ventricular rate. Negative inotropic effect (verapamil>diltiazem). May be effectively combined for synchronous activity with digoxin, but should not be combined with beta blockers.

BETA BLOCKERS

These agents are ineffective in terminating atrial fibrillation. They are, however, useful for slowing the ventricular response, used alone or in combination with digoxin. Most effective agents in slowing the ventricular response in hyperadrenergic states (thyrotoxicosis). b -Blockers have a negative inotropic effect. Esmolol is an ultrashort acting agent, with rapid onset time to control the rate, although it may cause hypotension. The theraputic effect is lost within 30 mins of stopping the infusion. b -Blockers have been shown by two meta analyses to have a protective effect in the prevention of a. fib in cardiac surgery. Withdrawl of b -Blockers post operatively is associated with a higher incidence of tachyarrhythmias.

AMIODARONE

Complex potent antiarrhythmic agent with class I, II, III, IV activity and antifibrillatory effects. Effective against supra- and ventriculartachyarrhythmias. In atrial fibrillation its main action is to decrease nodal conduction. A number of recent studies have shown it to be ineffective in returning the patient to sinus rhythm in the acute phase; but it may be effective in the longer term (days/weeks). Amiodarone is more effective than quinidine & flecainide for maintaining sinus rhythm post DC cardioversion. Amiodarone increases ejection fraction in patients with congestive heart failure and arrhythmias (probably from its vasodilatory effect). The onset of action for Amiodarone compared to digoxin is more rapid, assuming adequate loading doses of each are given.

DIGITALIS
Digoxin has two effects:

1. Stimulation of activity in vagal tissue / baroreceptors leading to an increase in vagal tone:

Decreased automaticity in the sinoatrial node. Increased refractory period and decreased conduction in the AV node. Decreased refractory period in atrial muscle

2. Digoxin inhibits the Na-K ATPase on the membrane of the myocyte; to maintain electical neutrality the Na-Ca pump reverses its flow, thereby increasing the intracellular concentration of calcium. This has an inotropic and proarrhythmic effect.

Digoxin is relatively ineffective in controlling the ventricular response in situations where the sympathetic tone is high (thyrotoxicosis, phaeo, sepsis). Digoxin has a narrow theraputic window, and toxicity can cause every known arrhythmia. Theraputic onset time is slow, requiring several hours to control vent. rate. ECG: flattened or inverted T waves

Pharmacokinetics

Volume of distribution (Vd) 500L in 70 kg man Plasma protein binding = 30% 80% eliminated unchanged in the urine T1/2 is 36 hours Loading dose required: 1mg iv or 1.5 mg po (oral bioavailability is 67%) Theraputic level is 1 - 2 ng/l Toxicity is likely in: Renal failure, Elderly patients, Hypothyroidism, Hypokalaemia

Side Effects

CARDIAC: all forms of dysrhythmias, particularly ectopics / heart block GASTROINTESTINAL: anorexia and vomiting VISUAL: blurring, and abnormalities of colour vision (yellow vision) MENTAL: confusion, nightmares OTHER: gynaecomastia in males

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Step 4: Anticoagulation
Risk of embolic stroke is increased with:

Large left atrial size (>4.5 cm) Valvular heart disease

Congestive cardiac failure. With warfarin anticoagulation, the risk of stroke is reduced by about 60% (3% vs 8%) The risk of intracranial haemorrhage is about 0.3% per year. Patients <65y with lone a. fib have a low incidence of thromboembolism, and aspirin is recommended. Patients >75y with a. fib & diabetes, previous CVA/TIA/RIND, hypertension, should be anticoagulated, unless haemorrhagic risks are deemed unacceptably high.

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SUGGESTED TREATMENT PROTOCOL

RECENT ONSET ATRIAL FIBRILLATION
1. Haemodynamically unstable with rapid ventricular rate: Immediate synchronized D.C. shock 2. Haemodynamically stable, symptomatic, with depressed LV function: Semi-urgent DC shock or drug therapy to control ventricular rate until spontaneous cardioversion occurs: amiodarone infusion 5-7mg/kg over 30mins, the 50mg/hr or digoxin 15m g/kg over 1h. 3. Haemodynamically stable, symptomatic, with normal LV function: Control the ventricular rate with amiodarone, digoxin, verapamil, esmolol. 4. Haemodynamically stable, asymptomatic: No immediate treatment, most cases will revert spontaneously within 24h.
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CHRONIC ATRIAL FIBRILLATION

Control the ventricular rate and prevent embolic stroke. Digoxin remains the gold standard for controlling the rate, but is ineffective during exercise: b -Blockers or verapamil may be added.

For patients who do not respond to antiarrhythmic therapy, radiofrequency ablation of the his-bundle, with permenant pacing, may be necessary. Anticoagulation with warfarin, as discussed earlier.
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THE PREOPERATIVE ASSESSMENT Take a history and examine the patient

Historical information of interest.

Background history of cardiovascular disease: Coronary Heart disease Angina (quantified) Previous Revascularization (PTCA or CABG) CCF (quantify dyspnoea / orthopnoea / PND, exercise tolerance) Rheumatic Fever (did anyone ever tell you that you had a murmur?) Hypertension.

Think about the other causes:

Thyrotoxicosis (heat intolerance, weight loss etc). Haemochromatosis. Alcohol ingestion.

Family History.

Vascular diseases, sudden death. Endocrine diseases.

Medications:

Antiarrhythmics, warfarin, diuretics, other cardiac medications.

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Physical Examination.

Pulse rate, apical and radial. Look for raised JVP.

Listen carefully to heart sounds: are there any murmurs? Look for saccral / pedal oedema.

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Investigations.

Look at the ECG, CXR (cardiomegaly, enlarged left atrium, LV aneurysm) Haemoglobin (O2 carring capacity). Electrolytes (particularly K, Mg, Ca) deficiencies should be corrected pre op. Digoxin levels theraputic / toxic? T4 & TSH if AF newly diagnosed.

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Preoperative medication.
1. Anxiolytic, as required. 2. Continue all cardiac medications (except diuretics) up to and including the day of surgery. 3. Stop warfarin a week pre op, and do not heparinize (the risk of stroke is low).
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ANAESTHESIA & ATRIAL FIBRILLATION

Nathanson and Gajraj, Anaesthesia 1998; 53 665-676

Halothane sensitizes the myocardium to catecholamines, and this may drive atrial fibrillation. Other volatile agents appear to have a protective effect, with antifibrillatory effects on the myocardium following ischaemia or reperfusion similar to calcium channel blockers. Isoflurane depresses sinus node automaticity and AV nodal conduction, and has antifibrillatory effects on canine atrial tissue. Temporary conversion of a. fib to normal sinus rhythm, during anaesthesia, has been reported.

Most anaesthetic agents have minimal effect on a.fib, except pancuronium, whose vagolytic properties may increase the ventricular rate. Likewise, sympathetic stimulation or exogenous catecholamines may drive up the ventricular response. AF may be induced by some procedures for which anaesthesia is given: ECT, Cardiac & Thoracic surgery.

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ATRIAL FIBRILLATION FOLLOWING CARDIOTHORACIC SURGERY

From Ommen et al "Atrial arrhythmias after Cardiothoracic Surgery" NEJM 1997 336; 20, 1429-34

Incidence of atrial tachyarrhythmias is 11 to 40% after CABG and >50% following valvular surgery. Incidence has not decreased over the last 20 years. Cause unknown: associations include pericardial inflammation/effusion, excessive catecholamines/autonomic imbalance.

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Risk Factors:

Age 5% < 40 years, 30% > 70 years. Probably due to age related changes in atrial tissue dilatation, muscular and conducting system atrophy. Concomitant valvular heart disease. Cardiopulmonary bypass: although long cross-clamp times/bypass times are not associated with a higher incidence of a. fib. Myocardial protection strategies have not been found to decrease the inciudence of a.fib. Atrial Arrhythmias most commonly occur during the first 3 days post op. Usually transient, but may recur. Long term these patients have not been studied. AF increases the incidence of stroke in the peri-op period.

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Prevention Strategies
Preoperative digitalisation: has not been shown to decrease the incidence of arrhythmais; theoretically may increase it (digoxin decreases atrial refractoriness). b -Blockers may have a protective effect, as does diltiazem.
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Preoperative amiodarone as prophylaxis against atrial fibrillation after heart surgery.

Daoud EG. N Engl J Med 1997 Dec 18;337(25):1785-1791

124 patients were given either oral amiodarone (64 patients) or placebo (60 patients) for a minimum of seven days before elective cardiac surgery. Therapy consisted of 600 mg of amiodarone per day for seven days, then 200 mg per day until the day of discharge from the hospital. Postoperative atrial fibrillation occurred in 16 of the 64 patients in the amiodarone group (25 percent) and 32 of the 60 patients in the placebo group (53 percent) (P=0.003). Patients in the amiodarone group were hospitalized for significantly fewer days than were patients in the placebo group (6.5+/-2.6 vs. 7.9+/-4.3 days, P=0.04). Conclusion: Preoperative oral amiodarone in patients undergoing complex cardiac surgery is well tolerated and significantly reduces the incidence of postoperative atrial fibrillation and the duration and cost of hospitalization.
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Treatment:
Treatment protocols as described earlier, with particular attention given to the use of Magnesium Sulphate.
The New England Journal of Medicine -- September 18, 1997 -- Volume 337, Number 12 William J.C. Hobbs, M.B., Ch.B. Manchester Heart Centre

Hypomagnesemia is frequent after diuresis in patients who have undergone cardiopulmonary bypass, and it is a risk factor for atrial and ventricular arrhythmias. Intravenous magnesium therapy avoids the proarrhythmic effects associated other drugs. Magnesium reduces ventricular rates rapidly. This effect is thought to be due both to direct action on the atrioventricular node and to a reduction in the sympathetic input to that node. Similar effects are noted in patients with hypomagnesemia and those without it, which suggests that magnesium has a pharmacologic action. Magnesium used alone has been shown to be better than digoxin in controlling the ventricular response rate in atrial fibrillation, and the two agents control the rate better than either in isolation. Magnesium has an efficacy similar to that of intravenous amiodarone in controlling the ventricular rate, and it may be superior with respect to cardioversion in atrial tachyarrhythmias. Cardioversion of atrial arrhythmias after parenteral magnesium therapy has been reported in several small studies.

There is also evidence for the prophylactic use of magnesium in preventing atrial arrhythmias after bypass surgery. Fanning et al. reported a double-blind, placebo-controlled trial in 99 patients that showed a reduction in atrial fibrillation from 42 episodes in 14 patients in the control group to 12 episodes in 7 patients in the magnesium group (P<0.02). "When patients have new atrial fibrillation after bypass surgery, it is our practice to seek reversible causes of atrial arrhythmias actively and then use an intravenous bolus of 12 mmol of magnesium over a period of 1 hour, followed by an infusion of 60 mmol over a 24-hour period, before using other antiarrhythmic agents".

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KEY POINTS
1. Atrial fibrillation is a common cardiac arrhythmia characterised by an atrial

rate >400beats/min, and a variable ventricular response.

2. There is loss of atrial mechanical activity leading to reduced cardiac output .

This is more apparent on exercise, in LV dysfunction and in mitral stenosis.

3. In most cases atrial fibrillation signifies significant systemic disease. 4. There is a history of palpitations, an irregularly irregular pulse, and varying

pulse pressure, leading to an apex-radial pulse deficit. 5. Treatment is necessary to control the ventricular rate and maintain cardiac output, and prevent systemic embolisation of thrombus. 6. Treatment involves correcting the cause, cardioverting to sinus rhythm, controlling the ventricular rate and anticoagulation. 7. The ideal ventricular rate is 90 beats/min 8. Cardioversion is indicated for acute onset AF (<3 days). If the duration is longer, anticoagulation is essential. Mechanical activity may take weeks to normalize. Cardioversion may be ineffective in rheumatic AF or if the LA size >4.5cm 9. The ventricular response may be controlled with digoxin, beta blockers, calcium channel blockers, amiodarone, or other antiarrhythmics. 10. Digoxin remains the gold standard, but is limited by its narrow theraputic range, slow onset time and potential toxicity. 11. Digoxin is ineffective in controlling the ventricular response in thyrotoxicosis (where sympathetic tone is high) and probably in sepsis. 12. Beta blockers and calcium channel blockers are effective for slowing the ventricular response, but they do not restore sinus rhythm and are negatively inotropic. 13. Amiodarone has rapid onset time, has negligable effect on the myocardium, and is useful for maintaining NSR post cardioversion.A loading dose is required, and long term therapy is associated with a myriad of complications. 14. Anticoagulation significantly reduces the incidence of stroke in patients >65 years with AF. 15. When assessing a patient with AF for theatre, it is essential to examine the patient looking for the potential cause of the disease. 16. Watch out for the undiagnosed thyrotoxic patient.

17. Volatile agents, with the exception of Halothane, have anti fibrillatory

properties. Vagolytics and sympathomimetics may drive up the ventricular response 18. New onset AF is associated with cardiothoracic surgery and ECT. 19. AF occurs at a rate of 11-40% following CABG, >50% following valvular surgery, and insreases with age. 20. Most of these cases are self limiting. 21. Initial treatment with magnesium and normalisation of serum potassium is indicated. 22. Diltiazem, Beta blockers and Amiodarone probably have a protective effect (reducing the incidence of AF). The significance of this is unknown. Preoperative digitalisation is ineffective.