University of KwaZulu-Natal



05 April 2019

No.05

THE TRUTH IN THE FIBS:

MANAGING ATRIAL FIBRILLATION IN THE PERI-OPERATIVE SETTING

DR P. SEWBUCKUS

Moderator: Dr P. Gokal

School of Clinical Medicine

Discipline of Anaesthesiology and Critical Care

CONTENTS

INTRODUCTION 3

DEFINITION 4

CLASSIFICATION 4

PATHOPHYSIOLOGY 5

RISK FACTORS 7

RISK STRATIFICATION 7

MEDICAL MANAGEMENT 11

CONTROVERSIES IN MANAGEMENT STRATEGIES 13

2019 FOCUSED UPDATE ON THE 2014 AHA GUIDELINE FOR THE MANAGEMENT OF PATIENTS WITH ATRIAL FIBILLATIN (10) 14

ANAESTHEITC CONSIDERATIONS FOR AF IN THE PERI-OPERATIVE SETTING 15

SPECIAL SUBGROUPS (2,5,6) 20

CONCLUSION 22

REFERENCES 23

THE TRUTH IN THE FIBS: MANAGING ATRIAL FIBRILLATION IN THE PERI-OPERATIVE SETTING

INTRODUCTION

Atrial fibrillation (AF) has been described as the most common arrhythmia that an anaesthetist is likely to encounter in the peri-operative setting[pic](1-4). Surgical conditions, anaesthetic related pharmacological agents and non-pharmacological stimuli can produce new onset AF or worsen chronic AF. Knowledge of the disease process and associated complications is therefore crucial to the anaesthestist in order to prevent significant morbidity and mortality.

The incidence of supraventricular tachyarrhythmias is on the rise with an increase in the age of the population and AF, in particular, has been quoted as 1-2% of the population in developing countries(1). In South Africa, studies have shown that AF is prevalent at 7% in the black urban population(4). AF most often presents in the elderly operative population, estimated at 5% of UK patients above the age of 65, and 10% of UK patients above the age of 75 years (2). The incidence in the postoperative cardiac population is estimated to be approximately 30%. Once AF has occurred it has been linked with increased mortality, increased hospital duration, and an increased burden on the healthcare sector.

With advances in medical technology, the incidence of AF is predicted to increase as the age of the population increases. (Fig. 1)

[pic]

Figure 1. The ATRIA study from the United States puts forth a projection of predicted cases by the year 2050. This study focuses on the risk factors associated with atrial fibrillation.

DEFINITION

AF is classified as a supraventricular tachycardia that features disorganized and uncoordinated electrical activity in the atria resulting in ventricular conduction that is rapid and irregular. This manifests as absent P waves on ECG, and P waves are replaced with fibrillatory waves prior to narrowed, irregularly irregular QRS complexes. Atrial rates range between 300-600 beats per minute, while ventricular rates range between 100 - 160 beats per minute.

[pic]

Figure 2. Comparison of normal cardiac conduction and conduction occurring in atrial fibrillation with associated ECG manifestation.

CLASSIFICATION

Classification of AF is required to assist with management strategies and prevent the associated risk of morbidity and mortality.

Classification can be made according to the occurrence of AF in the peri-operative period ie. pre-operatively, intra-operatively or post-operatively.

AF can be further catergorised according to the onset of the disease, the duration of the event, and the response to treatment [pic](1-3, 5, 6). Definitive classification does not exist, but most literature favour classification based on onset and duration.

1. New onset AF – this is the first presentation of AF, that is present for less than 48 hours in duration. These episodes can be symptomless, and the patient can be unaware of their condition.

2. Paroxysmal AF – this consists of recurrent episodes of AF that can be present for any amount of time and revert to sinus rhythm spontaneously within 7 days of onset. Intervention may be required in some cases. Two or more attacks are considered as recurrent. Symptoms that can occur at the time of presentation include dizziness, palpitations, dyspnea, chest pain and fatigue.

3. Persistent or chronic AF – there is no self-termination of the attacks. Pharmacological or electrical intervention is required to ensure restoration of a regular rhythm.

4. Permanent AF – intervention has not been attempted as yet, or there is no response to all modalities of intervention.

5. Non-valvular AF – this is used to describe AF that occurs outside the setting of mitral stenosis due to rheumatic disease or mitral valve repair, and in the absence of mechanical or prosthetic valves.

PATHOPHYSIOLOGY

There have been many postulations regarding the mechanisms of AF. Normally, the initiation of electrical conduction occurs in the sino-atrial node of the right atrial wall. In AF, multiple trigger points occur in both atria or adjacent pulmonary veins and propagate repetitively and in a continuous fashion. The general theories of AF are described as: [pic](2, 5, 7) (Fig. 3)

a) Enhanced automaticity of atrial tissue that produce multiple ectopics. These focal points can extend to pulmonary veins and vena cava junctions.

b) Multiple colliding re-entrants maintaining chaotic electrical firing in chronic AF.

c) Atrial remodeling both structurally and chemically in chronic AF which can produce shortened refractory periods. This can result in difficulty in restoration of sinus rhythm. Remodeling can occur in the settings of fibrosis, ischemia, dilatation and hypertrophy.

d) Dysfunction of ion channels resulting in an increased outward potassium movement and decreased inward calcium flux that results in accelerated repolarization and promoting re-entry.

e) Abnormal calcium handling via enhanced phosphorylation of calcium handling proteins.

When left untreated AF results in significant morbidity and mortality:

|Table 1. Morbidity and mortality associated with Atrial Fibrillation [pic](8) |

|Quality of life reduction |Palpitations, dyspnea, fatigability, decreased level of exercise tolerance |

|Thromboembolism |20-30% increased risk |

| |Reduced cognitive function from micro emboli |

| |Prothrombotic state |

|Affected hemodynamics |Diminished atrial kick |

| |Irregular ventricular contractions |

| |Heart failure |

| |Tachycardia induced cardiomyopathy |

|Hospitalisations |Most common arrhythmia requiring admission |

|Mortality |2 times increased risk of cardiovascular disease |

| |Sudden death in heart failure and hypertrophic cardiomyopathy |

[pic]

Figure 3. Proposed pathophysiological principles for the development of AF [pic](7).

RISK FACTORS

There are numerous associated risks of AF. Attempts to classify these risks according to systems have been made and are listed in the table below.

When faced with new onset AF in the peri-operative scenario, it is essential to exclude all correctable causes of AF such as those listed under the heading “Other” in Table 2.

|Table 2. Associated risk factors of AF [pic](1, 2, 5, 6, 9) |

|Associated cardiovascular |Respiratory associations |Postoperative risk factors |Other |

|disease | | | |

|Hypertension |Hypoxia |Increasing age |Low/high Potassium |

|Coronary artery disease |Pneumonia |Electrolyte shifts post |Low magnesium |

| | |operatively | |

|Cardiomyopathy |Effusions |Pericarditis |Low calcium |

|Valvular heart disease (Mitral) |Thromboembolic disease |Preoperative AF |Acidosis |

|Cardiac surgery |Pulmonary embolism |Atrial distension |Increasing age |

|Myocarditis |OSA |History of CCF |Hypovolemia |

|Pericarditis |Thoracic/ esophageal surgery |COPD |Sepsis |

|Wolff-Parkinson-White syndrome | |Increased catecholamines |Alcohol |

|Sick sinus syndrome | |Hyperthyroidism |Hyperthyroidism |

| | |Diabetes Mellitus |Familial |

| | |Alcohol ingestion |Neurogenic (high vagal or |

| | | |sympathetic tone) |

RISK STRATIFICATION

AF that persists beyond 48 hours produces an escalated likelihood of stroke due to an increased chance of thrombus formation in the atria from incomplete blood ejection and resulting stagnation. Anticoagulation is suggested to manage this risk.

A few scoring systems have been developed to estimate the probability of stroke and guide anticoagulation therapy, the most popular consisting of the CHADS2 and CHA2DS2-VASc scoring systems, the latter of which comprises of additional risk factors and subsequently greater predictive value. They are included in the European Society of Cardiology guidelines as well as the American College of Cardiology/American Heart Association Task Force on Practice Guidelines on AF management [pic](6, 8).

The scoring criteria include risk factors for stroke, with one point per risk factor with the exception of age criteria in the CHADS2 system, and age and prior stroke criteria in the CHA2DS2 – VASc system (Table 3). Adjusted stroke rate percentage per year according to the points in the scoring systems are listed in Table 4 (6).

Scoring risks and the need for anticoagulation is summarized in Table 5.

In an emergency situation where a patient is on anticoagulation, the likelihood of thromboembolism versus the risk of bleeding needs to be made on an individual basis. It is suggested to bridge to low molecular weight heparin (LMWH) in patients at an elevated risk of thrombosis, and unaltered anticoagulation therapy for surgeries with a low chance of bleeding. Patients with high thrombotic risk for surgeries with an increased risk of bleeding require bridging a week before surgery, and correct management of anticoagulation prior to surgery [pic](1, 6).

The 2014 AHA guidelines on the management of AF for thromboembolic risk and treatment suggest the following: (6)

• Individualised management outlining all benefits and harm of stroke and bleeding to the patient.

• Anticoagulation is initiated on the basis of thromboembolic risk irrespective of the classification of AF (eg. new onset AF, paroxysmal AF etc.).

• The CHA2DS2-VASc system can be utilized for nonvalvular AF. Omission of anticoagulants is acceptable with CHA2DS2-VASc scores of or equal to 2. Oral anticoagulation achieved with warfarin, direct thrombin inhibitors (dabigatran), or factor Xa inhibitors (apixaban).

• Initiation of warfarin requires INR measurements on a weekly basis and thereafter on a monthly basis once established.

• In cases of contraindication to warfarin, or inability to establish therapeutic levels of warfarin, direct thrombin inhibitors and/or factor Xa inhibitors are acceptable. Renal function is investigated before initiation, as these agents are not advocated in end stage chronic kidney disease.

• It is recommended that unfractionated heparin or low-molecular weight heparin (LMWH) be utilized as bridging agents in patients with AF and mechanical valves for operations that require warfarin interruption. The risk of bleeding and stroke should be balanced on an individualised basis.

The 2014 ACC/AHA Guidelines on perioperative cardiovascular evaluation and management of patients undergoing non-cardiac surgery states that asymptomatic arrhythmias do not increase the risk of cardiac complications but should be adequately investigated. Modification of medical management of controlled AF is not required, but anticoagulation should be adjusted as thrombus formation can occur in thoracic procedures (12).

|Table 3. CHADS2 and CHA2DS2-VASc criteria and scoring systems [pic](1, 6) |

|CHADS2 SCORE |CONDITION |POINTS |CHA2DS2-VASc |CONDITION |POINTS |

| |Congestive cardiac failure | |C |Congestive cardiac failure or LV | |

|C | |1 | |systolic dysfunction |1 |

| |Hypertension – BP | |H |Hypertension | |

|H |consistently >140/90 |1 | | |1 |

|A |Age > 75 years |1 |A (2) |Age >75 years |2 |

|D |Diabetes Mellitus |1 |D |Diabetes Mellitus |1 |

| |Prior stroke or TIA | |S (2) |Prior stroke or TIA or | |

|S (2) | |2 | |Thromboembolism |2 |

| | | |V |Vascular disease |1 |

| | | |A |Age 65-74 years |1 |

| | | |Sc |Sex category (female sex) |1 |

|Table 4. Adjusted stroke rate percentage per year associated with point scoring of CHADS2 and CHA2DS2-VASc scoring systems (6) |

| | | | |

|CHADS2 |ADJUSTED STROKE RATE |CHA2DS2VASc SCORING SYSTEM |ADJUSTED STROKE RATE |

|SCORING SYSTEM |% / YEAR | |% / YEAR |

|0 |1.9 |0 |0 |

|1 |2.8 |1 |1.3 |

|2 |4.0 |2 |2.2 |

|3 |5.9 |3 |3.2 |

|4 |8.5 |4 |4.0 |

|5 |12.5 |5 |6.7 |

|6 |18.2 |6 |9.8 |

| | |7 |9.6 |

| | |8 |6.7 |

| | |9 |15.2 |

|Table 5. Anticoagulation recommendations according to CHADS2 and CHA2DS2-VASc point scoring (1) |

|CHADS2 SCORE |RISK |ANTICOAGULATION |CONSIDERATIONS |

| | | | |

| 48 hours or undetermined duration |Anticoagulation - warfarin to INR 2 – 3 for 3 weeks prior to and 4 weeks |

| |following elective cardioversion irrespective of CHA2DS2-VASc score. |

| |If no anticoagulation was given prior to cardioversion then transthoracic |

| |echocardiography is recommended to exclude left atrial thrombus. |

|AF > 48 hours or unknown duration with hemodynamic |Direct current cardioversion with initiation of anticoagulation timeously and |

|instability |continuation for 4 weeks following cardioversion. |

|AF < 48 hours with increased probability of stroke |Intravenous heparin, low-molecular weight heparin, direct thrombin inhibitor |

| |or factor Xa inhibitor before and immediately after cardioversion with chronic|

| |anticoagulation therapy. |

|AF < 48 hours with low probability of stroke |Anticoagulation may not be considered for cardioversion, and post procedural |

| |oral anticoagulation not required. |

CONTROVERSIES IN MANAGEMENT STRATEGIES

• Rate vs rhythm control – Wyse and colleagues assessed rate and rhythm control in patients over 5 years. 60% of rhythm control patients reverted to sinus rhythm, while 35% of patients in the rate control group displayed regular rhythm at the end of 5 years. Mortality comparison showed no significant difference, but the control group undergoing rhythm therapy displayed more drug side effects, frequent hospitalisations, and showed a greater risk for a stroke.

Ven Gelder et al did a similar study and found 39% of the rhythm control group to be in sinus rhythm after 2.5 years, compared to 10% of the group receiving rate therapy. The rhythm therapy group showed increased exercise tolerance, more drug side effects, increased hospitalisations, and an increased thromboembolic risk.

• Esmolol vs Diltiazem – a study done by Balser et al compared the response of new onset SVT to intravenous esmolol or diltiazem. 59% of patients reverted to regular sinus rhythm within two hours in the esmolol group compared to 33% in the diltiazem group. After 12 hours of treatment conversion rates increased in both groups with no statistical difference between the two drugs.

Mooss et al found similar results with patients presenting in AF following major cardiac surgery. 67% converted to sinus rhythm within 6 hours of esmolol management compared to 13% in the diltiazem group.

• Sotalol vs amiodarone vs digoxin – Joseph at al compared the conversion rate of these 3 agents within 48 hours of new onset AF, and the results showed that sotalol and amiodarone demonstrated shorter conversion times compared to digoxin. In addition, digoxin displayed higher adverse events with use.

• Diltiazem vs amiodarone – Karth et al compared the rate control efficacy of diltiazem and amiodarone in critical patients displaying new-onset tachyarrhythmias. Diltiazem achieved a better rate reduction over time compared to amiodarone. Hypotension due to diltiazem use resulted in premature drug discontinuation, and it was recommended that amiodarone may be the primary choice of drug in hemodynamic compromise.

2019 FOCUSED UPDATE ON THE 2014 AHA GUIDELINE FOR THE MANAGEMENT OF PATIENTS WITH ATRIAL FIBRILLATION (10)

|Table 9. 2019 Focused update on the 2014 AHA Guideline for the management of patients with atrial fibrillation (10) |

| |-Non-valvular AF no longer a classification. |

| | |

| |-Oral anticoagulation recommended for CHA2DS2-VASc score of 2 or more in men or 3 or more in females. |

| | |

| |-Anticoagulants include: Warfarin, dabigatran, rivaroxaban, apixaban and edoxaban which is a new factor |

| |Xa inhibitor. |

| | |

| |-NOACs are preferred over warfarin in eligible patients, with the exception of mitral stenosis that is |

| |graded above moderate or mechanical heart valves. Renal and hepatic function should be investigated |

|Thrombo-embolic risk: |prior to initiation. |

| | |

| |-Warfarin is still recommended for AF with mechanical heart valves. Dabigatran should not be used in |

| |these situations. |

| | |

| |-High risk CHA2DS2-VASc scoring in end stage chronic kidney disease suggests anticoagulation with |

| |warfarin or apixaban. Dabigatran and rivaroxaban are not recommended due to lack of displayed benefit |

| |over risk in clinical trials. |

| | |

| |-Percutaneous left atrial appendage occlusion can be performed in patients with an elevated risk of |

| |stroke and in whom long-term anticoagulation is contraindicated. Surgical left atrial appendage |

| |occlusion or excision may be an option in patients undergoing cardiac surgery. |

| |-Patients with mechanical heart valves and undergoing procedures that necessitates anticoagulation |

| |interruption should be bridged to unfractionated heparin or LMWH. |

| | |

| |-In the absence of mechanical heart valves interruption of warfarin should have a balanced risk |

|Bridging for interruption of |assessment of stroke versus bleeding. |

|anti-coagulation | |

| |-Idarucizumab, a monoclonal antibody that binds dabigatran, reverses the effects of dabigatran in the |

| |event of severe bleeding or urgent procedures. |

| | |

| |-Rivaroxaban and apixaban effects can be reversed with andexanet, which is a factor Xa recombinant. |

| | |

| | |

| | |

| | |

| |AF > 48 hours or unknown duration |

| |Warfarin INR 2 – 3, or direct thrombin inhibitor or factor Xa inhibitor for 3 weeks before and 4 weeks |

| |after cardioversion, irrespective of CHA2DS2-VASc scoring or method of restoration of sinus rhythm. |

| | |

| |If anticoagulation has not been initiated 3 weeks before planned cardioversion – echocardiography should|

| |be done to exclude left atrial thrombus and thereafter proceed with anticoagulation and cardioversion |

| |once excluded. |

| | |

|Anti- coagulation |AF > 48 hours or unknown duration with hemodynamic instability |

| | |

| | |

| |Initiate anticoagulants timeously and continue for 4 weeks post cardioversion. |

| | |

| |AF < 48 hours with high CHA2DS2-VASc score |

| | |

| |Initiate heparin, factor Xa inhibitor or direct thrombin inhibitor urgently prior to cardioversion |

| |followed by chronic therapy. |

| | |

| |AF < 48 hours with low CHA2DS2-VASc score |

| | |

| |Anticoagulation may be considered pre-cardioversion, and not required post cardioversion. |

| | |

| | |

| |-High atrial rate recordings in cardiac implantable electronic devices should be further investigated |

|AF Device detection |for guidance of treatment options. |

| | |

| |-Consideration of insertion of implanted cardiac monitor in cryptogenic shock to detect silent AF. |

| | |

|Weight loss |Lifestyle and risk modification are recommended for overweight or obese patients. |

ANAESTHETIC CONSIDERATIONS FOR AF IN THE PERI-OPERATIVE SETTING

The anaesthetist will encounter AF in a variety of scenarios. From acute AF on table as a first presentation, to a patient with chronic controlled AF requiring an unrelated procedure, to delivering anaesthesia for correction of AF. Assessment of these patients involves meticulous examination and investigation, as well as implementation of the appropriate management strategies to limit significant morbidity and mortality.

History-taking

Look for suggested symptoms of AF such as dyspnea, reduced exercise tolerance, fatigue, palpitations, chest pains, and syncope. Determine if this is a recurring problem, and if the patient is on current treatment for this condition. It is important to note if the patient is taking any anti-arrhythmic agents, anticoagulants or had any interventions to manage persistent AF. Take note of any other concurrent cardiovascular disease. A systems review will reveal symptoms of risk factors for AF such as obstructive sleep apnoea, hyperthyroidism, alcohol use or family history of AF (5, 11).

Examination

Assessment of the pulse reveals an irregularly irregular rate. A controlled rate is considered to be a resting rate of 60-80 bpm, and an exercise-induced rate of 90-115 bpm. A jugular venous pulsation can also be expected. Assess for any associated cardiovascular disease (5).

Investigations

A standard 12 lead ECG confirms the suspicion of AF. Fibrillatory waves in the place of p-waves with rapid, irregular QRS complexes will be visualized. Note if there are any associated strain patterns, pre-excitation syndromes, bundle branch blocks or abnormal Q waves. Assess RR, QRS and QT intervals if the patient is currently on anti-arrhythmic agent therapy (5, 11).

Blood panels will reveal electrolyte abnormalities of which hypokalemia and hypomagnesaemia are the most common disturbances to produce AF (5).

A chest radiograph will assist to assess the lung fields and cardiac size and shape.

An echocardiogram can be done in light of delayed presentation of AF with the suspicion of thrombus formation if the patient is hemodynamically stable and adequately anticoagulated. The left atrial appendage is assessed for a thrombus, while special note of any regional wall motion abnormalities or valvular pathology is made. Volume status and ejection fraction can also be assessed with this modality [pic](3, 10, 11).

Premedication

In chronic AF, any anti-arrhythmic agents that have been initiated should be administered in the pre-operative period.

Patients undergoing elective cardiac surgery can prevent postoperative AF with prophylactic oral beta blocker therapy [pic](5, 6).

Acute onset AF management in the peri-operative setting (5, 9)

New onset AF can occur before a scheduled procedure or while on-table during the procedure. In the event of elective cases, risk factors should be identified and corrected, and the patient should be optimised before the procedure – goals include rate control with heart rate 90mmHg, consider rate conversion with intravenous beta blocker, digoxin or amiodarone. Amiodarone is administered as a bolus of 300mg within 10-20 minutes and a 900mg infusion over 24 hours.

If the patient is unstable and presents with a systolic blood pressure of < 90mmHG, reduced level of consciousness or in heart failure, then attempt synchronized direct cardioversion – if using a biphasic defibrillator, it is suggested to start between 120-150 joules, or at 200 joules with monophasic defibrillators. Incremental increases of energy with the initial three attempts. If the rhythm does not revert to regular sinus rhythm, amiodarone should be started 300mg over 10-20 minutes, and cardioversion re-attempted. The patient should be observed in a high care unit if hemodynamically stable post-operatively, or conversely in an intensive care unit if hemodynamically unstable. A cardiology consult can be ordered post-operatively and anticoagulation guidelines followed if the AF is present for greater than 48 hours (Fig. 4 and 5).

[pic]

Figure 4 Algorithm outlining the management of tachycardia by the Resuscitation Council of the UK (5)

[pic]

Figure 5 An algorithm highlighting the management of AF in surgical patients drawn up by the Department of Surgical Education, Orlando, USA (9)

Chronic AF management in the peri-operative setting (1)

According to NICE guidelines an ECG should be done for patients above 40 years of age assessed as ASA 2 and above or have a history of cardiovascular disease. Patients with established AF require a transthoracic echocardiogram to assess ejection fraction, significant valvular abnormalities, regional wall motion abnormalities, and exclude thrombus in the left atrial appendage.

Assess rate control by monitoring the heart rate of the patient. A controlled rate is considered to be a resting heart rate of 60-80 bpm, and an exercise-induced rate of 90-115 bpm. It is safe to proceed provided there are no other cardiac abnormalities. Heart rates > 110 beats per minute require further optimization if the surgical case is an elective case. In the event of an emergency, the acute onset AF algorithm may be followed, and post-operative consideration of high care unit and monitoring can be made.

Chronic therapy for AF should be continued pre-operatively. Diltiazem and verapamil may be omitted on the day of surgery due to the risk of hypotension and bradycardia with anaesthesia (1).

Anticoagulation continuation is established on the CHADS2 and CHA2DS2-VASc risk stratification models, as well as balancing the probability of bleeding over the risk of thrombosis on an individualized basis as stated in the above section on risk stratification. Low likelihood of bleeding and intermediate probability of thromboembolism requires no interruption of anticoagulation. High likelihood of bleeding and high risk of thromboembolism will necessitate bridging of anticoagulation to unfractionated heparin or LMWH.

Paroxysmal AF management in the peri-operative setting(1)

Paroxysmal AF refers to episodes that occur spontaneously and self-terminate without precipitating events or intervention.

These patients are managed in the same way as pre-existing or chronic AF is managed. Conversion to sinus rhythm must not be attempted until echocardiography has excluded any emboli.

Anaesthetic management for elective cardioversion (2)

Elective cardioversion can be performed as a day case procedure. Patients should be thoroughly examined, pre-medicated and fasted as per normal nil per os guidelines.

Anticoagulation is suggested for 3-4 weeks prior and following cardioversion. Procedural rooms should be well equipped with emergency resuscitation equipment as well as adequate anaesthesia equipment.

Numerous combinations of drugs may be used including induction agents, sedatives or inhalational agents. Preferred anaesthetic agents include short acting agents where propofol is the preferred induction agent in stable patients. Sedative agents such as diazepam and midazolam can also be used.

Adequate preoxygenation should be performed before cardioversion for the risk of apnoea or difficult airway.

Analgesia is not recommended due to the absence of post-procedural pain, the risk of nausea and vomiting and the risk of respiratory depression.

Cardioversion risks include arrhythmias, asystole, thromboembolism, ischemia and pulmonary oedema, myocardial necrosis, rhabdomyolysis and renal failure.

Anaesthetic management for ablation of AF(11)

Radiofrequency catheter ablation is used for drug resistant AF and aims to ablate the excess focal initiation points. It is advised as the first line of treatment for paroxysmal AF with minimal associated cardiac disease, and second line of treatment for refractory AF. Treatment areas include pulmonary veins, additional linear lesions (posterior left atrium, superior aspect of the left atrium and along the mitral isthmus) and non-pulmonary vein triggers (e.g. Coronary sinus, superior vena cava). Access is achieved via femoral sheaths inserted into the right and left femoral veins. Catheters are passed into the right atrium, across the septum via echocardiography and fluoroscopic guidance and into the left atrium. Once completed, a pharmacological challenge with isoproterenol at 2-10(g/min and adenosine in 6mg boluses is given to interrogate the resulting sinus rhythm. If AF recurs, then further ablation is performed.

Preoperatively the patient is thoroughly examined, investigated and risk stratified accordingly. Exclusion of thrombus as well as anticoagulation is explored.

Anaesthesia conduct – this procedure can be successfully carried out under conscious sedation, regional anaesthesia or general anaesthesia. However, factors that may guide the appropriate choice of anaesthetic include: remote location anaesthesia, limited access to airway, prolonged procedure duration, patient discomfort and movement, intra-procedural use of anticoagulation, and the possibility of on-table arrhythmias, cardiovascular collapse and arrest.

Monitoring – standard ASA monitoring by the way of 5-lead electrocardiogram, non-invasive blood pressure monitoring, temperature, and pulse oximetry. Invasive blood pressure monitoring is based on patient’s comorbidities and functional status.

Intra-operative conduct - Large bore intravenous access is sufficient. Defibrillator pads are placed on the chest prior to induction. Anticoagulation is given intra-operatively as passage through the septum can produce thromboembolism. This is achieved with a heparin bolus of 100U/kg prior to septal puncture, aiming for activated clotting time of 300-400 seconds, followed by a heparin infusion, and protamine to reverse the effect of heparin.

Complications of ablation – cardiovascular collapse, cardiac tamponade, arrhythmias, cardiac arrest, sepsis, air emboli, phrenic nerve injury, retroperitoneal injury, and thermal injury to the oesophagus resulting in atrial-oesophageal fistula formation.

Post-operative care – in the cases of general anaesthesia extubation is encouraged unless the patient has cardiac instability or is a bleeding risk then ventilation is advised in an intensive care facility. Atrial stunning post ablation carries the risk of thrombi formation therefore necessitating the need for post-operative anticoagulation. Anticoagulation can only be started 4-6 hours post removal of femoral sheaths.

SPECIAL SUBGROUPS (2,5,6)

• Acute coronary syndrome – immediate electrical cardioversion is suggested for hemodynamic instability and ongoing ischemia or ineffective rate control. Digoxin or amiodarone can assist with left ventricular function in cardiac failure. Beta blockers achieve rate control in those without left ventricular dysfunction, atrio-ventricular block, hemodynamic instability or bronchospasm. Calcium channel blockers are used only if there is lack of significant heart failure and hemodynamic instability. Anticoagulation with warfarin recommended in CHA2DS2-VASc 2 or more.

• Hypertrophic cardiomyopathy – anticoagulation is initiated regardless of CHA2DS2-VASc score. Anti-arrhythmic agents can prevent AF recurrence. Ablation is considered when medical therapy has failed.

• Pre-excitation syndrome – In Wolff-Parkinson-White syndrome conduction through accessory pathways results in rapid ventricular rates that can become unstable. Digoxin, calcium channel blockers and beta blockers are avoided as they do not block accessory pathways. Electrical cardioversion for unstable patients is advised, while chemical cardioversion and cardiology referral is suggested for stable patients. Ablation therapy is suitable in symptomatic patients where the refractory period is shortened.

• Pregnant patient – AF occurs mostly in pregnant patients with pre-existing cardiac disease. Rate control in chronic AF and pregnancy can be accomplished with digoxin, beta blockers or calcium channel blockers, although the safety profile of the latter have not been well documented. Atenolol is avoided due to risks of intra-uterine growth retardation. Electrical cardioversion is used for hemodynamically unstable patients. Anticoagulation is continued during pregnancy; however oral anticoagulation has the risk of teratogenicity in the first and third trimesters and bridging to low molecular weight heparin is advised.

• Hyperthyroidism – in hyperthyroidism beta blockers control the rapid ventricular rate. If contraindicated, verapamil, diltiazem or calcium channel blockers can be used. Anticoagulation is advocated.

• Pulmonary disease –hypoxemia and acidosis amendment can result in resolution of AF in this subgroup. Rate control is accomplished with calcium channel blockers, verapamil or diltiazem. Beta blockers, sotalolol and adenosine are not recommended due to the risk of bronchospasm. Chronic amiodarone administration can cause pulmonary fibrosis.

• Post cardiac surgery – prophylaxis for high risk AF with pre-operative amiodarone. Post-operative AF is treated with beta blockers or calcium channel blockers if beta blockers are contra-indicated. Direct current cardioversion is advocated for unstable patients.

CONCLUSION

AF is a common disorder to occur in the peri-operative setting. Adequate knowledge of the pathophysiology and underlying mechanisms as well as the correct management of the type of AF can prevent significant morbidity and mortality.

Insight into the risk and benefit of each treatment modality can be used to make informed decisions by anaesthetists’ acting as the patient’s advocate intra-operatively. Keeping up to date on new guidelines and drug therapies can result in change of practice and improve patient care.

REFERENCES

1. Sokhi J, Kinnear J. Atrial fibrillation (AF). Perioperative management for non-cardiac surgery. Anaesthesia Tutorial of the Week. 2014.

2. Bajpai A, Rowland E. Atrial fibrillation. Continuing Education in Anaesthesia Critical Care & Pain. 2006;6(6):219-24.

3. Parida S, Thangaswamy CR. Cardiac tachyarrhythmias and anaesthesia: General principles and focus on atrial fibrillation. Indian J Anaesth. 2017;61(9):712-20.

4. Jardine RM, Fine J, Obel IWP. A survey on the treatment of atrial fibrillation in South Africa. South African Medical Journal. 2014;104(9).

5. Theron DA. Atrial fibrillation and Anaesthesia. Royal Devon and Exetr Hospital resource. 2006;UK.

6. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary. Journal of the American College of Cardiology. 2014;64(21):2246-80.

7. Andrade J, Khairy P, Dobrev D, Nattel S. The clinical profile and pathophysiology of atrial fibrillation: relationships among clinical features, epidemiology, and mechanisms. Circ Res. 2014;114(9):1453-68.

8. Kirchhof P, Benussi S, Kotecha D, Ahlsson A, Atar D, Casadei B, et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur J Cardiothorac Surg. 2016;50(5):e1-e88.

9. Department of Surgical Education ORMC. Acute atrial fibrillation treatment in the surgical patient. Orlando Regional Medical Center resource. 2002.

10. January CW, Samuel. 2019 AHA/ACC/HRS Focused update of the 2014 Guideline for management of patients with atrial fibrillation. American College of Cardiology. 2019.

11. Malladi VN, Payam; Razavi, Mehdi; Collard, Charles; Anton, James; Tolphin, Daniel. Endovascular ablation of atrial fibrillation. Anesthesiology. 2014;V 120(No. 6):1513-9.

................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download