Introduction to Perioperative Arrhythmias
While the incidence of perioperative arrhythmias is extremely high (the Multicenter Study of General Anesthesia reported a 70.2% incidence of tachycardia, bradycardia, or dysrhythmias in 17,201 patients having general anesthesia), only 1.6% of these will require clinically-significant management (antidysrhythmic drugs, electrical devices, or cardiopulmonary resuscitation) [Forrest J et al. Anesthesiology 72: 262, 1990; Forrest J et al. Anesthesiology 76: 3, 1992]
Evaluation of the EKG using the RARIS method (rate, axis, rhythm, intervals, ST changes/TWI/Qwaves/LVH) allows one to cover most of the important check points
Common occurrence following cardiac surgery. Perioperative beta blockade has been shown to reduce the incidence of this side effect. More recently, the PAPABEAR Trial (n = 601) showed that perioperative amiodarone administration can also reduce the incidence of AF following cardiac surgery, although mortality is not affected [Mitchell et al.].
Sick Sinus Syndrome
SA node degeneration leading to bradycardia and often complicated by intermittent SVT. Initially treated pharmacologically, however artificial pacemakers may be required. These patients also have an increased incidence of pulmonary emboli.
Ventricular Premature Beats
Characterized by an abnormally-shaped QRS complex with no preceding P wave. Also look for the absence of a T wave, as well as a compensatory pause following the premature beat. Considered significant if > 6/min, > 2 in a row (if HR > 120/min, this is technically V-tach), are multifocal, or infringe on an existing T wave (R on T phenomena, potential for malignant arrhythmia), in which case treat with lidocaine 1-2 mg/kg while trying to determine the underlying pathology (MI? hypoxemia, hypercapnea, HTN, hypokalemia, mechanical irritation).
Three or more ventricular beats occurring at a HR > 120/min. Stable V-tach is treated with lidocaine 1-2 mg/kg, amiodarone 150 mg over 10 minutes, or procainamide 35-100 mg/min. Unstable V-tach is treated with shock (200 J biphasic x 3).
Can be classified geographically, as follows (above the AV node to below), with those above the AV node generally being benign and often transient, and those below the AV node being more serious, more permanent, and progressive.
1st degree AV block 2nd degree AV block (type I and II) Unifasicular block (L anterior hemiblock, L posterior hemiblock) RBB LBB Bifasicular block (RBB + L anterior hemiblock, RBB + L posterior hemiblock) 3rd degree block
There is no evidence that surgery will push a bifasicular block into a 3rd degree block, and prophylactic pacemaker placement is unnecessary [Stoelting RK. Basics of Anesthesia, 5th ed. Elsevier (China) p. 377, 2007]. Existing 3rd degree blocks, however, require the placement of a pacemaker. In an urgent situation, isoproteronol (used by electrophysiologists to initiate arrhythmias) can be used as a pharmacologic pacemaker.
Pre-Excitation Syndromes (Wolff-Parkinson-White)
WPW occurs in 0.3% of the population, and is identified by a short PR (< 0.12s), wide QRS complex, and delta wave, often resulting in paroxysymal atrial tachycardia – do NOT give beta blockers, calcium channel blockers, digoxin, or any other junctional slowing medications to WPW patients, as it will increase transmission through the aberrant pathway, increasing ventricular rate. The goal of anesthesia should be to minimize sympathetic stimulation (which increases sinus rate). Short-term treatment is with procainamide (lengthens the refractory period of the accessory pathway) and possibly adenosine (prolongs the refractory period of the AV node). Long-term treatment us usually accomplished by catheter ablation.
Prolonged QT Syndrome
QTc > 0.44 is caused by an imbalance of cardiac innervation, which decreases the relative amount of sympathetic nervous system activity in the right heart, leading to an association with ventricular arrhythmias, syncope, and sudden death. Anesthetic management should focus on minimizing SNS activity, minimizing drugs which further prolong QTc, and availability of beta-blockers and cardioversion pads. Long term treatment is with beta-blockers and/or stellate ganglion blockade. Note that while volatile anesthetics have been shown to prolong QTc in normal patients [Schmeling WT et al. Anesth Analg 72: 137, 1991], enflurane may be QTc neutral in long QTc patients [Brown M et al. Anesthesiology 55: 586, 1981], and isoflurane may actually decrease QTc in long-QTc patients [Medak R and Benumof J. Br J Anaesth 55: 361 1983]. A case report of QTc prolongation in a patient with long-QTc following sevoflurane [Gallagher JD et al. Anesthesiology 89: 1569, 1998] makes it difficult to make any generalizations about QTc prolongation by volatile anesthetics on patients with long QTc syndrome.