Management of perioperative arrhythmias

Management of Perioperative Arrhythmias Thomas W. Feeley, MD Electrocardiography was the first application of electronic monitoring to anesthesia care. The detection of arrhythmias remains the most important use of this technology today. Several predisposing factors tend to emerge when perioperative arrhythmias are evaluated. These are the anesthetic given, the site of surgery, abnormalities of blood gases or electrolytes, tracheal intubation, reflexes such as vagal slowing and the oculo.cardiac reflex, stimulation of the central nervous system, the presence of preexisting heart disease, and the use of intracardiac devices. In the evaluation of cardiac arrhythmias, several facts need to be determined. The most important is to determine if there is an underlying complication of anesthesia and surgery that may explain the arrhythmia. In addition, it is vital to evaluate the heart rate,

the regularity, the number of P waves per QRS, and the configuration of the QRS. The anesthesiologist needs to determine whether the rhythm is dangerous to the patient and whether it requires treatment. Prompt evaluation and management of perioperative arrhythmias reduce anesthetic morbidity and mortality. This article reviews the causes and pharmacological treatment of major abnormalities of atrial and ventricular cardiac arrhythmias occurring in the perioperative period.

NDERSTANDING the cause and treatment of cardiac arrhythmias in the perioperative period is necessary for the safe conduct and outcome of anesthesia. Prompt evaluation and management of perioperative arrhythmias reduce anesthetic morbidity and mortality. The reported incidence of cardiac arrhythmias in both noncardiac and cardiac surgery is high. For noncardiac surgery, it has been reported to be between 60% and 80%,1,2 although most were sinus arrhythmias and premature ventricular contractions and of little clinical significance. Similarly, very high incidences have been reported in patients undergoing coronary artery bypass grafting or valve replacement surgery, particularly in association with the insertion of pulmonary artery catheters and intraoperative aortic dissection in the prebypass perlod.v' In contrast, the reported incidence of serious arrhythmias is less than 1%.5 Nonetheless, cardiac arrhythmias have been shown to have an impact on patient outcome; for example, a recent large multicenter study (n = 17,201) suggested that approximately 5% of patients developed severe perioperative adverse outcomes, with nearly half ofthese attributable to cardiac arrhythmias."

to correlate with the severity of the heart disease and led to a prolonged hospital stay. During surgery, the anesthetic agent influences the development of arrhythmias. The volatile agents halothane, enflurane, and isoflurane reduce the rate of slow diastolic depolarization, increase the threshold potential, and prolong the refractory period.s" The direct influence of this is to slow the heart rate; however, this is only a characteristic of halothane anesthesia. Halothane is more likely to initiate a disturbance in cardiac rhythm than the newer agents. The volatile agents also potentiate the arrhythmogenic effects of circulating endogenous or exogenous catecholamines. Sensitization of the myocardium is most marked with halothane, less pronounced with enflurane, and negligible with isoflurane.!? The newer agents desflurane and sevoflurane have not been shown to sensitize the heart to injected epinephrine.Ui'? Drugs such as cocaine and ketamine increase the frequency of halothane-associated arrhythmias by blocking the reuptake or metabolism of norepinephrine. 13 The [j-blocker esmolol both prevents and suppresses halothaneinduced ventricular arrhythmias. 14 Many other predisposing and interrelated factors are associated with abnormal atrial or ventricular rhythms and conduction disturbances. Abnormalities of the blood gases or electrolytes frequently result in arrhythmias." Myocardial hypoxia, as seen in acute myocardial infarction and with various forms of hypotension, can lead to almost any cardiac arrhythmia. Sinus bradycardia is common in acute infarcts, and ventricular arrhythmias can also be seen. Hypotension causes myocardial ischemia by decreasing blood flow to the myocardium during diastole. Other abnormalities in the patient's vital signs can result in cardiac arrhythmias. Hypertension can produce arrhythmias as myocardial afterload rises and coronary perfusion declines, Hypothermia is frequently associated with ventricular arrhythmias as the temperature declines below 34°C. Ventricular fibrillation threshold is decreased with hypothermia and becomes increasingly likely when the temperature reaches approximately 30°C.15 A low body temperature also makes the termination of catheter-induced arrhythmias more difficult. Tracheal intubation and extubation are well-described causes of cardiac arrhythmias." Many ascribe the increased incidence of arrhythmias around the time of airway manipulation to stimulation resulting in acute hypertension. Direct cardiac stimulation with catheters can result in supraventricular arrhyth-

U

PREDISPOSING FACTORS

Preexisting heart disease is an important clinical condition that predisposes patients to perioperative rhythm disturbances. In 1971, Bertrand et all reported on 100 patients, 84 of whom had intraoperative arrhythmias. Ninety-six percent of the patients in that series who had preexisting heart disease had an intraoperative arrhythmia, leading to a recommendation that all patients with known cardiac disease have electrocardiogram (ECG) monitoring. Early attempts at corrective cardiac surgery again showed that patients with heart disease had many arrhythmias during and after surgery. In the first major review of this subject, Angelini et al? showed that the most dangerous arrhythmias associated with cardiac surgery were those that OCCUlTed in the postoperative period. These arrhythmias tended

From the Department of Anesthesia. Stanford University School of Medicine. Stanford, CA. Address reprint requests to Thomas W, Feeley, MD. Professor of Anesthesia, Stanford University School of Medicine. Department of Anesthesia, 300 Pasteur D,; Stanford, CA 94305-5115. Copyright © 1997 by w'B. Saunders Company 1053-077019711102-1003$3.0010 10

Copyright© 1997 by 1N.8. Saunders Company KEY WORDS: cardiac arrhythmias, anesthesia, pharmacological management

Journal ofCardiothoracic and Vascular Anesthesia, Vo111, No 2, Suppl1 (April). 1997: pp 10-15

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mias, ventricular arrhythmias, as well as conduction abnormalities. In nearly all cases, these catheter-induced arrhythmias are promptly terminated when the catheter is removed from the heart, Reflex bradycardias are commonly reported with surgery. Vagal stimulation can result in bradycardia with direct vagal stimulation such as during carotid surgery, as well as with remote activities such as peritoneal traction. The oculocardiac reflex can also produce bradycardia during eye surgery. The location of the surgery also can influence the development of arrhythmias. Intracranial pathology such as subarachnoid hemorrhage and raised intracranial pressure can result in cardiac arrhythmias because of stimulation of the autonomic nervous system.!" Dental surgery is also associated with arrhythmias because of similar stimulation of the sympathetic and parasympathetic nervous systems." In view of the fact that perioperative arrhythmias can be a warning sign of some correctable blood gas, perfusion, or metabolic abnormality, it is important to look for correctable underlying reasons for an arrhythmia before instituting specific drug therapy that may ordinarily be administered in nonsurgical situations. Whenever an arrhythmia develops in the perioperative period, several preliminary questions should be asked: • Is alveolar ventilation normal? • Is there hypoxemia? • Are there any abnormalities in blood pressure or temperature? • Are electrolyte abnormalities possible? • Could central venous monitoring catheters have changed position? • Is there surgical stimulation that may account for the problem? Pain, light anesthesia, vagal stimulation, or autonomic nervous system stimulation such as raised intracranial pressure? If any of these are encountered, attempts to correct them should be made while continuing to evaluate the arrhythmia. Additional evaluation of the rhythm should be performed in a systematic manner by obtaining a printed rhythm strip if possible and applying the following additional six questions to the situation: • What is the rate? • Is the rhythm regular or irregular? • Is there a P wave for each QRS? • Is the QRS normal or abnormal? • Is the rhythm dangerous or benign? • Is treatment necessary? If so, with what? The remainder of this article reviews the common perioperative arrhythmias and applies these questions to each, with the

aim of establishing a simple approach to rapidly managing arrhythmias as they present. ATRIAL ARRHYTHMIAS

Atrial arrhythmias (Table I) are a common occurrence in the perioperative period.? In fact, sinus tachycardia occurs so frequently that it is not included in most incidence studies. Clinical implications vary tremendously, with both benign events and rhythms that have significant hemodynamic consequences,

Sinus Bradycardia Sinus bradycardia may be a totally benign rhythm secondary to a drug effect. It is common when large doses of narcotics are administered with muscle relaxants that do not stimulate the heart rate. It is the main reason many cardiac anesthesiologists prefer to continue using pancuronium in large-dose narcotic relaxant techniques, The rhythm may also signify a myocardial infarct or may be part of sinus dysfunction called a sick sinus syndrome, in which bradycardia can lead to heart block or tachyarrhythmias." Mild sinus bradycardia is usually harmless. As the rate becomes slower, perfusion becomes impaired, with lower cardiac output and eventually lower blood pressure. The appearance of ventricular escape beats with rates less than 40 beats/min may lead to other more malignant ventricular arrhythmias. Whenever sinus bradycardia is seen, it must be considered a warning of an impending anesthetic catastrophe. In most cases of intraoperative cardiac arrest attributable to problems with ventilation and oxygenation, sinus bradycardia is the rhythm seen before arrest. Management consists of evaluating whether an anestheticrelated problem is responsible for the arrhythmia; if perfusion is impaired, or if there are ventricular escape beats. As the rate becomes slower, treatment progresses from atropine to ephedrine to epinephrine or isoproterenol. In severe cases refractive to pharmacological management, a temporary pacemaker may be necessary.

Sinus Tachycardia Sinus tachycardia usually signifies the presence of some other problem that is ordinarily not of cardiac origin. Nevertheless, sustained tachycardia can result in myocardial ischemia, especially in a patient with underlying coronary artery disease in whom the short times in diastole can result in ischemia. It must be remembered that the higher heart rate is often necessary to sustain the patient's cardiac output and that pharmacologic

Table 1. Diagnostic Features of Atrial Arrhvthrnlas

Sinus bradycardia Sinus tachycardia PACs PAT Atrial flutter Atrial fibrillation Junctional rhythms

Rate

Rhythm

40-60

Regular Regular Irregular Regular Regular Irregularly irregular Regular

110·170 Variable 160-250 250-350 350-500 40·180

P:QRS

1:1 1:1 Usually 1:1

1:1 2:1-8:1 No Pwave Usually 1:1

DRS Complex

Normal Normal Normal Generally normal Normal Normal Generally normal

Abbreviations: MI, myocardial infarction; PACs,premature atrial contractions; PE, pulmonary embolism; PAT, paroxysmal atrial tachycardia,

THOMAS W. FEELEY

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slowing of the rate may result in disastrous reductions in cardiac output, as seen in hypovolemia, sepsis, and congestive heart failure. Slowing the heart rate thus must be weighed against the potential problems created by the high rate, ie, increased myocardial oxygen consumption leading to myocardial ischemia when coronary artery flow is otherwise impaired. There may be significant ST-segment depression during severe sinus tachycardia. This so-called rate-related ST-segment depression mayor may not be related to ongoing myocardial ischemia. It is extremely important to seek the underlying cause of the tachycardia and correct that first. Only when faced with no apparent cause and a persistent sinus tachycardia in a patient with known or suspected cardiac disease should pharmacological methods of slowing the rate be used. The treatment may involve analgesics, volume, or ventilation. Patients with coronary artery disease may be at risk for myocardial infarction, and they can be managed with esmolol for immediate control of the rate. The advantage of esmolol over propranolol is its extremely short duration of action (Table 2). Premature Atrial Contractions

Premature atrial contractions (PACs) can originate from either atrium and provide an impulse with an aberrant P wave that is sometimes hard to locate, being lost in the QRS or the preceding T wave. PACs are usually benign; however, their

Table 2. Intravenous Agents Useful in Management of Perioperative Arrhythmias

Drug Adenosine

Action

Dose

AV nodal blockade

6-12 mg (adults); 0.050.25 mg/kg (children) 5 mg/kg x 20 min; 10-20 Arnlodarone Type-3 antiarrhythmic mg/kg x next 24 h 0.4-1.0 mg (adults); 10-20 Atropine Muscarinic cholinergic antagonist IJg/kg (children) Digoxin Indirect vagomimetic and 0.5-1.0 mg loading (dose 1 50%; 25% at 4 interslows conduction vats): then 0.125-0.25 through AV node mg daily 20 mg x 1 min (0.25 Diltiazem Ca channel antagonist mg/kg); 0.125 mg/kg Esmolol 150-500 IJg/kg x 1 min; Ultrashort-acting 50-200 IJg/kg/min j3-blocker 2-20 IJg/min; (0.02-0.15 Isoproterenol j3-Agonist IJg/kg/min) 1.0-1.5 mg/kg; 1-4 Lidocaine Na channel action mg/min (20-50 IJg/kg/ decreasing duration of min) action potential 0.5-3 mg (10-30 IJg/kg) Propranolol j3-Blocker q 2 min to max of 6-10 mg 5-10 mg (adults) (0.07Verapamil Ca channel antagonist 0.15 mg/kg)

Abbreviations: PAT. paroxysmal atrial tachycardia; VT, ventricular tachycardia; VF, ventricular fibrillation; 5B, sinus bradycardia; VEB, ventricular escape beats; AFib, atrial fibrillation; AFlu, atrial flutter; ST, sinus tachycardia; CHB, complete heart block; PVCs, premature ventricuiar contractions. Data from Stemp and Roy24 and Vlay.36

presence may precede the development of more hemodynamically significant supraventricular arrhythmias. Treatment consists of correcting any underlying cause. Treatment is usually not necessary unless there is hemodynamic instability. In such cases, PACs may respond to digitalis, esmolol, or verapamil. Paroxysmal Atrial Tachycardia

Paroxysmal atrial tachycardia (PAT) is a rapid run of supraventricular beats originating at a site other than the SA node. Rapid rhythms originating at the AV node can also be considered PATs. Rapid supraventricular tachycardias arising from multiple sites are called rnultifocal atrial tachycardia (MAT). PAT is relatively uncommon and typically is rapid in onset and conclusion. The rhythm is usually regular unless it originates from multiple supraventricular foci, in which case it is irregular. PAT can be confused with sinus tachycardia, atrial fibrillation, atrial flutter, and ventricular tachycardia, especially if there is aberrant conduction. If there is severe hypotension, DC cardioversion is the treatment of choice. The most effective drugs are diltiazem, verapamil, and esmolol (Table 2). The rapid termination of esmolol's f3-blocking effect makes it a more attractive agent than propranolol, especially in the postoperative period. MAT is also responsive to esmolol. 2o-22 Adenosine, a rapidly acting endogeuous purine nucleoside, has been used to control PAT under anesthesia (Table 2). Its ultrashort duration of action makes it desirable for rapid conversion and short duration of any side effects. 23•24 Phenylephrine may also be effective if there is mild hypotension in which reflex slowing of the heart occurs as the blood pressure rises. Edrophonium, propranolol, digitalis, and rapid overdrive pacing have also been effective in terminating this arrhythmia. Atrial Flutter

Atrial flutter is a regular atrial arrhythmia at a rapid rate that is usually associated with a conduction block. The regular flutter (F) waves often can be seen in some leads. Atrial flutter usually develops in patients with severe underlying heart disease, although other causes must be ruled out. The most effective treatment is DC cardioversion, which must be performed in any patient who is hypotensive. Patients undergoing general anesthesia are excellent candidates for cardioversion as the first-line treatment. Alternatively, esmolol, digitalis, diltiazem, verapamil, and rapid-overdrive atrial pacing have all been effective. Adenosine may aid in making the diagnosis by briefly slowing the ventricular response. Atrial Fibrillation

Atrial fibrillation is an irregularly irregular rhythm that is often rapid. When the rate is fast, there may be a pulse deficit and hypotension. Patients already receiving digitalis typically have a slower ventricular response. The usual causes of arrhythmias under anesthesia must be ruled out; as with atrial flutter, atrial fibrillation usually indicates the presence of severe underlying heart disease. DC cardioversion is the treatment of choice under general anesthesia when hypotension is present. However, it is not as

PERIOPERATIVE ARRHYTHMIAS

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responsive as atrial flutter. Digitalis is frequently used to control the ventricular response. Esmolol, diltiazem, and verapamil can convert the rhythm as well as slow the rate. Esmolol converts more patients to sinus rhythm on first treatment than does verapamil.v-" One problem with esmolol treatment is that hypotension is a frequent complication of esmolol's rate control. Recent studies suggest that continuous infusions of calcium channel blockers such as verapamil or diltiazem may allow fine tuning of the ventricular response without the high incidence of hypotension seen with esmolol. 27 Chronic management may require quinidine.

Junctional Rhythms Rhythms arising near the AV node are commonly called junctional rhythms. The P wave may be poorly seen located in the following QRS. Junctional rhythms can range from tachycardias to bradycardias. The rate is variable, ranging from 40 to 180 a minute. The rhythm is regular. There is usually one P wave for each QRS; however, the P wave can be high-nodal (short PR interval), mid-nodal (P wave not visible), and low-nodal, where the P wave follows the QRS. The QRS is usually normal in appearance. Junctional rhythms are common under anesthesia, with an incidence as high as 20%. They are especially common when halogenated anesthetics are used. Junctional rhythms can result either in no change in hemodynamics or in reductions in cardiac output of up to 30%.28 Usually no treatment is necessary; however, if there is significant reduction in blood pressure, management can include decreasing the halogenated anesthetic dose as well as increasing the rate of the SA node using atropine, ephedrine, or isoproterenol. If a rapid junctional rhythm is present, a l3-blocker such as esmolol may be effective.

VENTRICULAR ARRHYTHMIAS Ventricular arrhythmias are more common during anesthesia in patients with preexisting cardiac disease, and their occurrence must be considered life threatening (Table 3).

caine as a bolus of 1.0 to 1.5 mg/kg, followed by a continuous infusion at 1 to 4 mg/min. Second-line drugs are procainamide and bretylium. If the PVCs occur in the context of sinus bradycardia, speeding up the SA node may be effective with drugs such as atropine or isoproterenol or with the use of pacing.

Ventricular Tachycardia Ventricular tachycardia is two or more ventricular ectopic beats in succession. It may be constant and associated with adequate perfusion or it may be associated with shock and rapidly degenerate to ventricular fibrillation. This is clearly a life-threatening rhythm requiring immediate assessment and management. Correction of underlying causes is immediately sought. Blood pressure is assessed. If there is adequate perfusion, pharmacological interventions may be tried. If there is hypotension, immediate DC cardioversion is required, followed by cardiopulmonary resuscitation (CPR) if perfusion is inadequate. Pharmacological therapy is similar as for PVCs: lidocaine, procaine, and bretylium. Magnesium may be useful in torsade de pointes ventricular tachycardia. Intravenous amiodarone can be used in recurrent life-threatening ventricular tachycardia."

Ventricular Fibrillation Ventricular fibrillation is a serious, life-threatening rhythm because there is no ventricular output during the arrhythmia. CPR must be undertaken with closed-chest cardiac massage; it is followed by immediate DC cardioversion with 200 to 400 W-s. Pharmacological therapy is not effective until a regular rhythm is established. Lidocaine, bretylium, and procaine are usually used. A recent study showed the efficacy of esmolol in converting ventricular fibrillation when lidocaine and procaine had failed.t? Epinephrine may convert a fine ventricular fibrillation to a coarse ventricular fibrillation that may be more conducive to DC cardioversion.P Amiodarone has also been used in refractory ventricular flbrillation."

Asystole PrematureVentricular Contractions Premature ventricular contractions (PVCs) are ectopic beats originating from below the AV node. PVCs can be unifocal, multifocal, or they can alternate with sinus beats in an every second (bigeminy) or every third (trigeminy) beat pattern. Frequent PVCs, multifocal PVCs, and PVCs occurring on the T wave render the patient more likely to develop ventricular tachycardia and ventricular fibrillation. However, the use of antiarrhythmic drugs to suppress ventricular ectopy is controversial.P-" Management should be to first assess the patient for correctable underlying problems such as hypoxemia, hypotension, hypoventilation, hypokalemia, and hypothermia. Pharmacological treatment should include lido-

Asystole is the absolute absence of cardiac electrical activity. There is no cardiac output, and CPR must be instituted immediately. There is no heart rate and a straight line is on the ECG; there are no P waves or QRS complexes. Asystole is resistant to treatment, and continual CPR is needed during efforts to develop fibrillation or some regular rhythm. Epinephrine may stimulate fibrillation, and other agents would include isoproterenol. A transvenous pacemaker may be effective, but CPR must be continued throughout efforts to regain a rhythm.

HEART BLOCK There are several varieties of heart block: block originating at the SA node, at the AV node, and in the conduction system.

Table3. Diagnostic Features of Ventricular Arrhythmias

Premature ventricular contraction Ventricular tachycardia Ventricular fibrillation

Rate

Rhythm

Variable 100·200 Rapid, grossly disorganized

Irregular Regular Irregular

P:ORS

No Pwave No fixed relationship None seen

ORS Complex

Wide <0.12 s & bizarre Wide <0.12 s Not present

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THOMAS W. FEELEY

Blocks in theAV node can be the most life threatening. They are first-degree block where there is merely slowing of the PR interval. Second-degree block is the conduction of some but not all of the atrial beats and is of two types. In Mobitz's block type 1, also called Wenckebach's block, there is progressive lengthening of the PR interval before a beat is dropped; in Mobitz's type 2, there is no progressive lengthening. Type 2 is the more serious, with more frequent degeneration into type 3, or complete heart block. In complete heart block, the atrial contractions are not sent down the conduction system, and QRS complexes originate from the ventricle. There can be reductions in cardiac output and blood pressure, and immediate treatment is often needed. Isoproterenol can temporize the situation until transvenous or external pacemaking can be established. Bundle-branch blocks are usually indicative of significant cardiac or pulmonary disease. Left bundle-branch block is usually associated with cardiac disease. A right bundle-branch block CRBBB) may have no clinical significance or it may be associated with pulmonary disease or atrial septal defects. Hemiblocks are blocks of one of the two bundles of the left-sided conduction system. Hemiblocks may exist along with RBBB. When that is the case, the concern is whether the patient will progress to complete heart block. Patients with RBBB and left posterior hemiblock are more likely to proceed to complete heart block, whereas patients with RBBB and left anterior hemiblock only progress to complete heart block in 10% of

cases. Trifascicular block is a bifascicular block in association with a prolonged PR intervaJ.34.35 In all of these situations, the patient should be monitored carefully for the development of complete heart block and treated as necessary. There is no evidence that any of these patient groups require prophylactic placement of a temporary transvenous pacemaker in the peri operative period.

SUMMARY Perioperative arrhythmias are important causes of anesthetic morbidity and mortality. In many instances, they are signs of more significant anesthetic complications that often require emergency management. Conditions such as hypoxemia, hypercapnia, acidosis, shock, and electrolyte and temperature abnormalities can precipitate arrhythmias and often must be corrected to successfully manage the arrhythmia. Some arrhythmias appearing in the perioperative period are benign, and others are malignant and life threatening. In all situations, the condi tion of the patient must be evaluated in terms of the adequacy of ventilation and perfusion. When ventilation is inadequate, it must first be corrected. When perfusion is impaired, CPR must be instituted when appropriate and rhythms responsive to DC cardioversion should be so managed. Prompt recognition and management of peri operative arrhythmias improve anesthetic morbidity and mortality.

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