Atrial Flutter in anesthesia
Atrial flutter is characterized by
an organized atrial rhythm with an atrial rate of 250–350 bpm with varying degrees of AV block.
Atrial flutter is a type of supraventricular tachycardia caused by a re-entry circuit within the right atrium. The length of the re-entry circuit corresponds to the size of the right atrium, resulting in a fairly predictable atrial rate of around 300 bpm (range 200-400).
The rapid P waves create a sawtooth appearance on ECG and are called flutter waves.
Flutter waves are particularly noticeable in leads II, III, aVF, and V1.
The flutter waves are not separated by an isoelectric baseline.
The ventricular rate may be regular or irregular depending on the rate of conduction.
Most commonly, patients have 2:1 AV conduction; an atrial rate of 300 bpm with 2:1 conduction, for example, results in a ventricular rate of 150 bpm. Characteristically the ventricular rate is about 150 bpm.
Atrial flutter frequently occurs in association with other dysrhythmias such as AF. It occurs in approximately 30% of patients with AF and may be associated with more intense symptoms than AF because of the more rapid ventricular response.
About 60% of patients experience atrial flutter in association with an acute exacerbation of a chronic condition such as
Chronic pulmonary disease
Inflammatory condition affecting heart
After cardiothoracic surgery
In many instances, treatment of the underlying disease process restores sinus rhythm.
Ventricular response rates as high as 180 bpm can occur in patients with normal AV node function.
Extremely rapid ventricular responses in excess of 180 bpm can be seen in patients with accessory AV nodal bypass tracts. In this situation the QRS complex is often wide, and the ECG can resemble ventricular tachycardia or ventricular fibrillation.
Types of atrial flutter:
Anticlockwise Reentry: Commonest form of atrial flutter (90% of cases). Retrograde atrial conduction produces:
Inverted flutter waves in leads II,III, aVF
Positive flutter waves in V1 – may resemble upright P waves
Clockwise Reentry. This uncommon variant produces the opposite pattern:
Positive flutter waves in leads II, III, aVF
Broad, inverted flutter waves in V1
Initial history and physical examination include the following:
Documentation of clinical type of atrial flutter
Assessment of precipitating factors (eg, exertion, sleep, caffeine, alcohol use)
Assessment of modes of termination (eg, vagal maneuvers)
Documentation of prior use of antiarrhythmics and rate-controlling agents
Assessment of presence of underlying heart disease
Documentation of any previous surgical or percutaneous ablation procedures
Airway, breathing, and circulation (ABCs)
Vital signs (particularly heart rate, blood pressure, respiratory rate, and oxygen saturation)
Evaluation of head and neck, lungs, heart, abdomen, lower extremities, and nervous system
Ventricular rate control should be the initial goal of therapy. This is done to prevent deterioration in AV conduction from 2:1 to 1:1, which would represent a doubling of the heart rate. Such an increase in heart rate can cause severe hemodynamic instability.
If there is 1:1 conduction with a ventricular rate of 300 bpm or faster, reentry is the most likely mechanism and procainamide administration should be considered.
Drug therapy for ventricular rate control includes amiodarone, diltiazem, and verapamil. All these drugs are helpful in controlling the ventricular rate, but none of them is likely to convert atrial flutter to sinus rhythm.
For acute ventricular rate reduction with atrial flutter has been satisfactory with either esmolol or edrophonium.
Drugs of choice include
beta blockers such as esmolol (0.5 mg/kg IV bolus followed by 50-300 ucg/kg/min) and
propranolol, or calcium channel blockers such as verapamil (5-10 mg IV) or diltiazem.
Beta blockers and CCB are effective in prophylactic prevention of atrial flutter after postoperative thoracic or cardiac surgery.
Pharmacologic control of the ventricular response and conversion to sinus rhythm can be challenging in patients with atrial flutter.
If atrial flutter is hemodynamically significant, the treatment is cardioversion. Often less than 50 J (monophasic) is adequate to convert the rhythm to sinus.
If the patient is hemodynamically stable, overdrive pacing using transesophageal or atrial electrodes may be helpful to convert atrial flutter to sinus rhythm.
Ibutilide, a class III antiarrhythmic (1 mg in 10 mL saline infused slowly over 10 minutes) is effective in converting new-onset atrial flutter patients to normal sinus rhythm 90% of the time. It may be repeated once, but the provider should be aware it has a potential risk of inducing torsades de pointes, so the patient needs to be monitored carefully for 4-8 hours after drug administration.
Amiodarone (150 mg IV loading dose infused over 10 minutes, followed by 1 mg/min infusion for 6 hours, a 0.5-mg/min infusion for 18 hours, and then a reduced IV dose or oral dose) is also effective in converting atrial flutter to normal sinus ryhthm.
Patients with atrial flutter lasting longer than 48 hours should receive anticoagulant therapy.
If atrial flutter occurs before induction of anesthesia, surgery should be postponed if possible until control of the dysrhythmia has been achieved.
Management of atrial flutter occurring during anesthesia or surgery depends on the hemodynamic stability of the patient.
If the atrial flutter is hemodynamically significant, treatment requires cardioversion. Synchronised cardioversion starting at 50J (monophasic) is indicated.
Pharmacologic control of the ventricular response may be attempted if vital signs are stable.
The choice of drug depends on the co-existing medical conditions of the patient.
Digoxin alone is not recommended for acute ventricular rate reduction.
CCBs or beta-blockers, alone or with digoxin, are more reliable, safer, and faster.
Class IA, IC, and III antidysrhythmics are used to prevent recurrences of atrial flutter, except that IA and IC drugs are contraindicated in patients with coronary disease and left ventricular dysfunction (ventricular prodysrhythmia).
Further, class IA drugs can accelerate AV conduction during atrial flutter as a result of antimuscarinic effects.
Atrial flutter with 2:1 block: regular narrow-complex tachycardia at 150 bpm — particularly when the rate is extremely consistent.
Rate in sinus tachycardia typically varies slightly from beat to beat, while in AVNRT/AVRT the rate is usually faster (170-250 bpm).
To tell the difference between these rhythms, vagal manoeuvres or a test dose of adenosine — AVNRT/AVRT will often revert to sinus rhythm, whereas slowing of the ventricular rate will unmask the underlying atrial rhythm in sinus tachycardia or atrial flutter.
Source: Stoelting’s ANESTHESIA AND CO-EXISTING DISEASE