Atrial Fibrillation in the Perioperative Period

Congestive Heart Failure History

Arterial Hypertension History

A₂

Age ≥75 years

Diabetes

S₂

Stroke/TIA/Thromboembolism History

Vascular Diseases History (i.e., obliterating arteriopathy, myocardial infarctum, coronary artery disease)

Age 65–74 years

Female Sex

The final score is obtained by adding partial scores. The zero value corresponds to low-risk; the value of one corresponds to low-moderate risk; values of two or greater correspond to moderate-high risk (modified from [2])

5.4.2 Rate Control vs Rhythm Control Strategies

Apart from the thromboembolic risk, AF poses two main problems: the loss of the atrial pump to ventricular filling and the onset of too high or low ventricular rates. These alterations are particularly damaging in patients with left ventricle diastolic dysfunction or mitral stenosis. The therapeutic goal can be limited to maintain ventricular rate within an acceptable range (rate control) or aimed to restore sinus rhythm (rhythm control). Although the second approach may appear as the best one, it should be considered that 50% of recent-onset AFs spontaneously convert to the sinus rhythm and that from the point of view of survival and morbidity, no significant difference has been observed between the two strategies.

5.4.2.1 Rate Control

In AF, the average ventricular rate depends on the length of the refractory period of the atrioventricular node, which blocks most of the electrical impulses that arrive from the atria at a frequency greater than 300 bpm. A too high rate may compromise ventricular filling and cause myocardial ischemia. On the other hand, bradycardia can interfere with the function of the left ventricle both in systolic and diastolic dysfunction. In the former, tachycardia represents a compensation mechanism; in the latter, diastolic stiffness limits the volume of blood that the left ventricle can accept in diastole. The rate control strategy aims to keep the average ventricular rate at rest below 80 bpm. In acute cases with good hemodynamic compensation, an initial goal may be to maintain the rate below 110 bpm. In order to control ventricular rate, the refractory period of the atrioventricular node is increased to reduce the number of atrial excitations transmitted through the conduction system. For this purpose, some drugs can be used:

Beta-blockers act by reducing the effects of sympathetic hyperactivity; furthermore, they are particularly effective to prevent myocardial ischemia. Their prophylactic activity against AF has been proved in at least two conditions: paroxysmal AF induced by sympathetic hyperactivity and postoperative AF that occurs in 30% of patients after cardiac surgery. Main contraindications are the severe systolic dysfunction of the left ventricle and bronchial obstruction. Several molecules are used, including atenolol, bisoprolol, carvedilol, metoprolol, nadolol, propranolol, and timolol. Metoprolol is administered acutely at the dosage of 2.5–5 mg every 5 min up to 10–15 mg; oral dosage varies from 25 to 100 mg every 12 h. A special role is played by esmolol, which is particularly valuable in critically ill patients because of its short half-life of about 10 min. The dosage is 0.05–0.2 mg/kg/min after an initial bolus of 0.5 mg/kg.
Non-dihydropyridine calcium antagonists (verapamil, diltiazem) prolong atrioventricular node conduction and refractory period. They have negative inotropic and vasodilator effects, which contraindicate their use in ventricular systolic dysfunction and in arterial hypotension. They should also be avoided in patients with Wolff–Parkinson–White (WPW) syndrome. Verapamil can be administered intravenously as a bolus, 5–20 mg, and in rare cases as an infusion, at a rate of 5–10 mg/h. Orally, the dosage is 40–80 mg every 8 h.
Amiodarone is a class III antiarrhythmic drug (K channel blockers) according to Vaughan Williams classification, and is effective both to reduce mean ventricular rate and to restore sinus rhythm. This drug is particularly useful in patients with cardiovascular instability and/or systolic dysfunction because of its modest negative inotropic effect; the vasodilator effect is also mild and is clinically apparent only during rapid intravenous infusion. Amiodarone may cause phlebitis and prolongation of QT with potential induction of polymorphic ventricular tachycardia (torsades de pointes); it is also contraindicated in WPW syndrome. Intravenously, an initial injection of 300 mg is given as a slow injection in 10 min (risk of hypotension by vasodilatation) or as an infusion in 2 h, followed by a 5-h infusion at a rate of 75 mg/h, and finally by a constant-rate infusion at 18 mg/h. Orally, the dosage is 200–400 mg daily.
Digitalis slows down the average ventricular rate in the presence of AF because it increases the parasympathetic tone. For this reason, it may be ineffective in conditions characterized by an increased activity of sympathetic hyperactivity, as is often the case in the perioperative period. Digoxin is contraindicated in WPW syndrome. In the attack phase, the loading dose is 0.5–1 mg iv, followed by a maintenance dose of 0.25 mg orally.

The choice of the drugs to be used for heart rate control is partly based on associated pathologies. For instance, beta-blockers and calcium antagonists are indicated for the presence of coronary heart disease and arterial hypertension, digitalis in the presence of heart failure. A particular case is that of patients with WPW syndrome. Drugs such as calcium antagonists, amiodarone, and digitalis increase the refractory period of the atrioventricular node. In case the refractory period of the accessory bundle is shorter than the atrioventricular node, electric impulses can be transmitted from the atria to the ventricles through the former and high ventricular rates can occur. In patients with WPW, rate control approach is therefore based on the administration of beta-blockers, but rhythm control is recommended.

5.4.2.2 Rhythm Control

The decision to pursue AF conversion to sinus rhythm in emergency conditions is generally based on the presence of hemodynamic instability, too high or low ventricular rates, and myocardial ischemia. Otherwise, it is reasonable to follow the rate control strategy and to shift to the rhythm control only after a few days, when a spontaneous cardioversion becomes unlikely. The sinus rhythm can be restored by an electrical or pharmacological cardioversion. The former is recommended in patients with WPW syndrome.