Perioperative Cardiac Arrhythmias

For every affection ... that is attended with either pain or pleasure, hope or fear, is the cause of an agitation whose influence extends to the heart.
Sir William Harvey, 1628

That emotion and stress may affect the heart was recognized by William Harvey over three centuries ago. Stresses encountered by surgical patients predispose them to a variety of cardiac rhythm disturbances. Because these rhythm disturbances can contribute to morbidity and mortality, it is important to anticipate and avoid them when possible. When not possible, early recognition and intervention are usually advantageous. Monitoring heart rate and rhythm during and after surgery is, consequently, of utmost importance. Anesthesiologists and surgeons must be aware of normal variations of rate and rhythm in healthy anesthetized animals. In addition, they must be familiar with specific pathologic arrhythmias and appropriate treatment interventions for clinically significant rhythm perturbations. This chapter provides an overview of the identification and management of common perioperative arrhythmias. Other sources should be consulted for a discussion of arrhythmogenic properties of various preanesthetic and anesthetic agents [1].

Risk Factors

Animals with a history of arrhythmia are at increased risk for recurrence or exacerbation of the arrhythmia during the perioperative period. Similarly, patients with preexisting structural heart disease are at risk of developing significant intraoperative and postoperative cardiac rate and rhythm abnormalities. The preoperative assessment of these animals should, therefore, include a complete cardiac evaluation, including Doppler/echocardiography, electrocardiography (ECG), thoracic radiographs, and blood pressure measurement. The data obtained from this evaluation is critical for choosing the safest anesthetic protocol and the most appropriate antiarrhythmic agents. A preoperative ECG in cats older than seven years of age is helpful for detecting the presence of left anterior fascicular block, which is a silent ECG abnormality often associated with myocardial disease in this species.

In people, risk factors identified for development of supraventricular tachyarrhythmias include advancing age, a previous history of supraventricular arrhythmia, type of surgery (intraabdominal, intrathoracic, or major vascular surgery), and preexisting congestive heart failure or chronic lung disease [2]. Risk factors for development of supraventricular arrhythmia in dogs during the perioperative period include atrial enlargement and a history of previous supraventricular ectopy. Furthermore, giant breeds and Labrador retrievers are predisposed.

Perioperative ventricular arrhythmias are strongly associated with underlying myocardial dysfunction or contusion, splenic surgeries, pheochromocytoma, hyperthyroidism, and surgery to correct gastric dilation/volvulus. Patients with preoperative ventricular tachyarrhythmias are also at high risk for intraoperative and postoperative ventricular ectopy. Animals receiving β-adrenergic antagonists preoperatively may develop either supraventricular or ventricular tachyarrhythmias associated with β-blocker withdrawal if these agents have been recently and abruptly discontinued.

An important bradyarrhythmia that must be anticipated preoperatively is the development of increasing severity of atrioventricular (AV) block in animals with conduction system disease. Bradyarrhythmias resulting from enhanced vagal tone occur frequently in animals with upper airway obstruction, those undergoing surgery of the cervical spine, and animals with increased intracranial pressure.

General Approach for Management of Perioperative Arrhythmias

Abnormalities of cardiac rate and rhythm that occur while the patient is anesthetized are often the result of alterations in depth of anesthesia. Arrhythmias may also occur under anesthesia as a result of autonomic imbalance and catecholamine release; direct effects of anesthetic agents including analgesics, muscle relaxants, and reversal agents; hypothermia (and rarely hyperthermia); and mechanical stimulation secondary to invasive procedures and surgical manipulation. All of these factors must be considered and specific interventions taken to alleviate the causative mechanism(s). Other factors involved in arrhythmogenesis during the intraoperative period include electrolyte abnormalities, acid-base disturbances, volume depletion, release of toxic metabolites, and myocardial ischemia. Again, these factors must be specifically treated to appropriately manage the resulting arrhythmias.

Although cardiac arrhythmias are common in the postoperative period, most are clinically benign, such as sinus bradycardia, sinus pauses, accelerated idioventricular rhythm, isorhythmic AV dissociation, and isolated ventricular premature contractions (VPCs). Tachycardia in the immediate postoperative period may reflect the sympathetic activation associated with recovery. However, in addition to anesthetic emergence, both supraventricular and ventricular tachyarrhythmias in the postoperative period may reflect hypoxemia, hypercarbia, acidosis, toxemia, hypovolemia, blood loss, electrolyte imbalances, fear, pain, or a combination of these factors. Residual effects of anesthetic agents such as ketamine may also play a role. Again, treatment should be directed at identification and reversal of underlying causative factors; however, antiarrhythmic therapy may be needed when the primary cause of a potentially fatal arrhythmia cannot be identified or quickly corrected. In summary, the following general approach for management of perioperative arrhythmias is proffered:

1. Have a precise ECG diagnosis for the arrhythmia, if possible.
2. Specifically treat noncardiac causes (e.g., electrolyte abnormalities, hypothermia, acidosis, hypovolemia, hypoxemia, pain, fear) before using an antiarrhythmic medication unless hemodynamic or electrical instability are present.
3. Consider discontinuing drugs that may be causing or contributing to the arrhythmia.

Identification and Management of Common Perioperative Tachyarrhythmias

Sinus Tachycardia

Post-anesthetic sinus tachycardia (canine > 180 beats/minute; feline > 240 beats/minute) may often result from the anesthetic agents used, including atropine, glycopyrrolate, ketamine, or adrenergic agonists. Sinus tachycardia in the perioperative period is rarely, if ever, a true cardiac arrhythmia, but, rather, a reflection of increased sympathetic tone, which may arise from a wide variety of pathologic and/or physiologic causes. Physiologic causes include excitement, stress, and fear. Pathologic causes include pain, hypovolemia, anemia, acidosis, hypoxemia, fever, hyperthermia, toxemia, cardiac failure, hypercapnia, hypotension, acute hemorrhage, and hyperthyroidism.

Treatment of sinus tachycardia should be directed at identification and correction of the underlying cause of the heightened adrenergic tone. Antiarrhythmic agents are rarely indicated and are often detrimental.

Atrial Fibrillation and Atrial Flutter

Atrial fibrillation and atrial flutter are common postoperative arrhythmias in human patients [3], but development of either of these arrhythmias postoperatively is less common in dogs and extremely rare in cats. When atrial fibrillation and atrial flutter are noted in animals in the perioperative setting, these arrhythmias are usually present preoperatively. Nonetheless, both arrhythmias are clinically important because both may decrease cardiac output secondary to inappropriately fast heart rates that reduce stroke volume. Furthermore, atrial fibrillation abolishes the atrial contribution to ventricular filling and may, thereby, decrease cardiac output by as much as 39% while increasing left atrial pressure by as much as 9.5 mm Hg in otherwise healthy dogs [4].

On ECG, atrial fibrillation is recognized by absence of P waves and completely irregular R-R intervals (Fig. 18-1). Rapid, irregular fibrillatory waves that vary in size, shape, and timing are often visible. The QRS complexes are normal unless an intraventricular conduction abnormality is also present (e.g., right or left bundle branch block). The ventricular rate will depend on conduction velocity and refractoriness of the AV node and may be normal in dogs without structural heart disease. However, heart rate is typically very rapid in dogs and cats with heart failure as well as those with high circulating levels of catecholamines. In animals with atrial fibrillation that have been receiving oral medication for rate control, the heart rate often drops significantly following induction of anesthesia.

Figure 18.1. An ECG rhythm strip recorded during direct current (DC) cardioversion of atrial fibrillation in a dog with laryngeal paralysis. Atrial fibrillation is recognized as the underlying cardiac rhythm in the initial portion of the ECG by absence of P waves and completely irregular R-R intervals. Fibrillatory waves are present in the baseline. Prior to delivery of the synchronized electrical shock (at large arrow), the cardioversion device identifies QRS complexes with small arrows. As a result of the shock, normal sinus rhythm is restored. (lead II; 25 mm/s).

Management of atrial fibrillation is initially aimed at controlling heart rate. Intravenous calcium channel blockers or β-blockers are effective for slowing conduction through the AV node and can rapidly provide control of the ventricular response in patients with atrial fibrillation (Table 18-1). These drugs may be administered by bolus injection but require maintenance infusions or follow-up oral dosing to maintain adequate rate control. When continuous infusions are administered, blood pressure and heart rate should be closely monitored because these medications may cause hypotension and bradycardia. Because of the negative inotropic effects of β-blockers or calcium channel blockers, patients with myocardial systolic dysfunction may develop congestive heart failure or worsening of congestive heart failure after administration of these agents. Oral digoxin is used extensively for chronic heart rate control in dogs with atrial fibrillation because this drug will increase parasympathetic tone to the AV node with a resultant slowing of AV nodal conduction. However, in the postoperative period, sympathetic tone is often excessive, rendering this drug less effective in this setting. Furthermore, digoxin toxicity can cause nearly every known cardiac rhythm disturbance, and animals receiving digoxin may develop digoxin-induced arrhythmias in the perioperative setting if hypovolemia, hypoalbuminemia, or electrolyte depletion is induced by surgery or anesthesia.

Restoration of sinus rhythm with a synchronized direct current shock (DC cardioversion) has several advantages over heart rate control for management of atrial fibrillation in animals needing surgery. The cardioversion may be done immediately after induction of anesthesia, obviating the need to administer negative inotropic agents for rate control. Also, restoring sinus rhythm immediately after induction of anesthesia will improve cardiac performance and reduce ventricular filling pressures throughout the remainder of the anesthetic period and recovery.

Although similar to atrial fibrillation, atrial flutter is less common in veterinary patients. With atrial flutter the ECG recorded will show rapid, organized atrial activation with an abnormally rapid ventricular rate unless the patient is receiving medication to control heart rate or unless AV conduction block is also present. Unlike atrial fibrillation, the ventricular rate is usually regular. Although a "saw-toothed" pattern of flutter waves is typically described, this pattern of atrial activation may be difficult to appreciate when 2:1 AV conduction is present, and the arrhythmia may, therefore, be difficult to distinguish from other types of supraventricular arrhythmia. With administration of calcium channel blockers or β-blockers, or with induction of anesthesia, the flutter waves usually become easily visible. Management of atrial flutter is similar to management of atrial fibrillation, although rate control is often more difficult. DC cardioversion of atrial flutter is usually achieved at lower energy levels than those needed for cardioversion of atrial fibrillation.

Occasionally, atrial fibrillation and atrial flutter will develop in the postoperative period as a result of autonomic imbalance. This is recognized most frequently in patients that have had surgery on or trauma to the cervical spine. In this situation, the arrhythmias are often self-limiting with no treatment required (Fig. 18-2).

Figure 18.2. Continuous ECG rhythm strips obtained from a Labrador retriever during the early postoperative period following hemilaminectomy. Initially, the rhythm strip (A) shows sinus arrhythmia with brief paroxysms of atrial flutter. Ultimately (B), the rhythm degenerates to atrial fibrillation. This dog spontaneously converted to sinus rhythm within 24 hours, suggesting that the arrhythmias resulted from autonomic imbalance caused by surgical manipulation and stress. (lead II; 25 mm/s).

Paroxysmal Supraventricular Tachycardias

Although the term supraventricular tachycardia (SVT) in its broadest sense refers to any tachycardia originating above the ventricles, this term is generally reserved to describe supraventricular tachyarrhythmias other than sinus tachycardia, atrial fibrillation, or atrial flutter.

Paroxysmal SVT owing to impulse reentry in the AV node, impulse reentry within atrial tissue, or impulse reentry via an accessory atrioventricular conduction pathway has a similar ECG appearance, namely a rapid tachycardia with narrow (normal) QRS complexes (Fig. 18-3). The QRS complexes will be abnormally wide, however, if there is intraventricular conduction delay such as right or left bundle branch block or when conduction from atria to ventricles occurs over an accessory conduction pathway. Regardless of the anatomic location of the reentry pathway, any of these SVTs may occur in the perioperative setting, causing a very rapid heart rate with hypotension. SVTs may occur in any age group and often are not associated with structural heart disease. These tachycardias are usually associated with enhanced adrenergic tone as well as with triggers such as premature atrial contractions or premature ventricular contractions. When paroxysmal, these SVTs begin and terminate abruptly (lack of gradual rate acceleration and deceleration).

Figure 18.3. A lead II ECG rhythm strip obtained from a 1–year-old golden retriever. The ECG shows supraventricular tachycardia with a rate of 300 beats/minute. Abrupt conversion to sinus rhythm resulted from intravenous administration of diltiazem (0.25 mg/kg). Note that the QRS complexes during the arrhythmia are normal and identical to those during sinus rhythm. (lead II; 25 mm/s).

The specific type of paroxysmal SVT can theoretically be identified from a multiple lead ECG (including chest leads) by evaluating P' wave morphology and timing. However, P' waves may be extremely difficult to identify with certainty during a rapid SVT. Furthermore, during anesthetic induction, surgery, or in the immediate recovery period, available ECG monitoring equipment is often not conducive to examination of multiple-lead ECG recordings. While vagal maneuvers may be helpful both diagnostically and therapeutically, many animals do not respond to them. Furthermore, aggressive vagal maneuvers may, on occasion, produce ventricular fibrillation. Therefore, administration of intravenous antiarrhythmic agents is generally a safer, more effective means of differentiating and treating SVTs. Ideally, blood pressure and ECG monitoring are done as antiarrhythmic agents are administered. Diltiazem is the drug of choice for initial treatment because of its ability to rapidly slow the ventricular response to atrial tachyarrhythmias, and for terminating most AV nodal and AV reciprocating tachycardias (see Table 18-1). Diltiazem has a negative inotropic effect and must be used cautiously in animals with myocardial failure; however, diltiazem has a less potent negative inotropic effect than verapamil or esmolol [5]. Although adenosine is used to terminate SVT in human patients, this agent does not appear to be effective for this purpose in dogs. Procainamide, a class IA antiarrhythmic, may also be administered intravenously for management for supraventricular tachyarrhythmias in dogs (see Table 18-1). This agent is most appropriately used after administering diltiazem and is useful for terminating atrial reentrant tachycardias and atrioventricular reentrant tachycardias.

Ventricular Tachyarrhythmias

Perioperative ventricular ectopy may include relatively benign conditions such as ventricular premature contractions (VPCs) and accelerated idioventricular rhythm or potentially lethal arrhythmias such as sustained ventricular tachycardia (VT) and ventricular fibrillation (VF). The appearance of ventricular ectopy of any type should prompt measures to eliminate inciting factors such as hypoxemia, hypercarbia, electrolyte deficiencies, drug toxicities, and catecholamine excess. Antiarrhythmic therapy is indicated when the inciting cause cannot be identified or immediately reversed and the arrhythmia is responsible for hemodynamic compromise. Antiarrhythmic treatment is also indicated in animals at risk for sudden death triggered by fatal electrical instability [6,7]. In one postoperative study of 230 consecutive human patients with frequent VPCs or VT, adverse outcomes were not associated with the arrhythmias [8]. The adverse effects of ventricular arrhythmias in veterinary surgical patients has also been questioned, and the empiric use of antiarrhythmic agents has been challenged [6,7]. The decision that a ventricular arrhythmia is dangerous and should be suppressed with antiarrhythmic medication is based on the presence of weakness, syncope, hypotension, pallor, or exacerbation of heart failure directly attributable to the arrhythmia. Ventricular tachycardias vary in rate, morphology, and duration, and rate is generally the most important determinant of hemodynamic consequences. In general, the slower the rate of VT, the more benign the arrhythmia will be. In absence of clinical signs linked to the arrhythmia, the following characteristics of VT justify suppression with antiarrhythmic agents: rapid VT (rate appreciably greater than underlying sinus rate), sustained VT (> 30 seconds), VT with a short coupling interval to preceding sinus complex, and polymorphic VT. Furthermore, because of the known tendency for sudden death from ventricular ectopy, suppression of VPCs and VT is justified in boxers, Doberman pinschers, German shepherds, dogs with subaortic stenosis, and animals with significant myocardial dysfunction.

Ventricular premature contractions (VPCs) are identified on the ECG as wide QRS complexes that differ from the sinus complexes and occur prematurely (Fig. 18-4). VPCs are frequently followed by a compensatory pause caused by retrograde conduction of the VPC into the His-Purkinje system with either block of the subsequent sinus beat or with retrograde conduction to the atrium resetting the sinus node. Ventricular ectopic complexes are classified as monomorphic or polymorphic according to whether the QRS complexes are uniform or variable. Ventricular tachycardia is defined as three or more consecutive ventricular premature beats (see Fig. 18-4). VPCs may be difficult to distinguish from aberrantly conducted supraventricular beats; however, the presence of P waves that are not associated with QRS complexes or the presence of fusion beats indicates ventricular ectopy. It is also helpful to recall that ventricular tachycardia occurs much more frequently than supraventricular tachycardia with aberrancy. Ventricular tachycardia, particularly VT that is rapid, sustained, and polymorphic, may degenerate to ventricular fibrillation which is a rapid, chaotic, wide complex rhythm with absence of adequate cardiac output.

Figure 18-4. Simultaneous ECG rhythm strips recorded from a 7-year-old Irish wolfhound presented for collapse. Initial narrow complex, irregular rhythm consistent with atrial fibrillation is interrupted by isolated ventricular premature contractions (arrows). However, the rhythm abruptly deteriorates to sustained ventricular tachycardia with a dangerously rapid rate of 350 beats/minute. (lead AVL (top strip) and lead AVF (bottom strip); 25 mm/s; 5 mm/mV).

Ventricular tachycardia resulting in hemodynamic compromise (hypoperfusion or hypotension) should be treated immediately with DC cardioversion. Antiarrhythmic therapy can be administered to prevent a recurrence or as the initial therapy to terminate the VT in hemodynamically stable patients at risk for progression to hemodynamic instability. For veterinary patients, the antiarrhythmic agent of choice for immediate suppression of ventricular ectopy is lidocaine. This agent is highly effective with few side effects [3] (see Table 18-1). If lidocaine is not effective, substitution or addition of intravenous procainamide may provide arrhythmia suppression. Procainamide administration is particularly appealing when the ECG diagnosis of a wide complex tachycardia is uncertain. For refractory ventricular arrhythmias during the perioperative period, β-adrenergic blockers are often effective, particularly when combined with a class IA or IB antiarrhythmic agent, because the β-blockade antagonizes increased circulating catecholamines caused by stress. Regardless of the underlying mechanism of the ventricular arrhythmia, increased sympathetic tone can trigger the arrhythmia. Furthermore, adrenergic stimulation can render many antiarrhythmic drugs ineffective. Similarly, most antiarrhythmic agents are ineffective in the presence of hypokalemia or hypomagnesemia.

Amiodarone is now available for intravenous treatment of life-threatening VT and is recommended as a first line treatment for pulseless VT in people [9]. However, the most readily available intravenous preparation of amiodarone (Cordarone, Wyeth Laboratories Inc, Philadelphia, PA) contains polysorbate 80 and benzyl alcohol, both of which cause severe hypotension in dogs [10,11]. A newer aqueous formulation of amiodarone (Amio-Aqueous, Academic Pharmaceuticals Inc, Lake Bluff, IL) does not contain these agents and is better suited for dogs. Ventricular fibrillation should be managed by immediate DC defibrillation.

Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm develops frequently in dogs and cats during the intraoperative and postoperative periods. This arrhythmia is actually slow ventricular tachycardia, ventricular tachycardia at a rate slower than the sinus rate in a normal animal. Therefore, by heart rate criteria alone, this rhythm is not a tachycardia. Yet, because the ectopic ventricular focus responsible for the arrhythmia is depolarizing at a rate faster than a normal ventricular escape focus can depolarize, this rhythm is truly a ventricular tachycardia. Nonetheless, because the rate is slow, this form of VT is often referred to as accelerated idioventricular rhythm. The clinical importance of this terminology is that an accelerated idioventricular rhythm is usually benign whereas rapid VT is often malignant. The specific rates at which accelerated idioventricular rhythm becomes "true" ventricular tachycardia have not been precisely defined for dogs and cats. However, heart rates exceeding 180 beats/minute in dogs with VT and heart rates greater than 240 beats/minute in cats are most likely to be harmful.

Accelerated idioventricular rhythm often occurs in the perioperative setting in animals without underlying cardiac disease. This arrhythmia is frequent in dogs after gastric dilation/volvulus surgery, in dogs following splenic surgery, and in dogs with any type of abdominal disease (e.g., pancreatitis, prostatitis, enteritis, colitis). Accelerated idioventricular rhythm is also common in dogs with neurologic disease and with trauma [12]. Accelerated idioventricular rhythm in animals without underlying primary cardiac disease is nearly always benign, and antiarrhythmic treatment, in most cases, is unjustified.

On ECG, accelerated idioventricular rhythm is recognized as intermittent ventricular tachycardia that has a rate similar to or slightly greater than the sinus rate. The ventricular rhythm competes for the cardiac rhythm, meaning that the ventricular rhythm is apparent when the sinus rate slows or during sinus pauses (Fig. 18-5a and Fig. 18-5b). Although accelerated idioventricular rhythm usually has a uniform morphology, multiform ventricular complexes may occasionally be present.

Figure 18-5a. ECG rhythm strips recorded after splenectomy from a canine patient. A sinus arrhythmia is present with wandering pacemaker during which the sinus rate varies from 83 to 107 beats/minute. The sinus arrhythmia is usurped intermittently by a wide QRS complex rhythm with a regular rate of 79 beats/minute. This wide complex rhythm is a slow ventricular tachycardia referred to as accelerated idioventricular rhythm. The idioventricular rhythm is evident only when the sinus rate drops below the ventricular ectopic rate. P waves unassociated with the QRS complexes are visible intermittently during the ventricular rhythm (arrows). Occasional fusion beats are present (arrow heads). (lead II; 25 mm/s)

Figure 18-5b. ECG rhythm strip recorded from an anesthetized cat showing accelerated idioventricular rhythm. The cat was undergoing a subtotal colectomy. Initially a wide complex rhythm is seen with a regular rate of 142 beats/minute, during which P waves, unassociated with QRS complexes, are intermittently seen (arrows). Between the episodes of idioventricular rhythm is sinus rhythm with a similar rate (142 beats/minute). The accelerated idioventricular rhythm competes with the sinus rate as the dominant rhythm. (lead II; 25 mm/s)

Identification and Management of Perioperative Bradyarrhythmias

Bradyarrhythmias seldom cause significant problems in the perioperative period, and antiarrhythmic treatment is rarely indicated. Patients with symptomatic bradycardia resulting from disease of the cardiac pacing or conduction system should be evaluated for permanent pacemaker implantation prior to elective surgery. For patients with AV block or sinus node dysfunction without clinical signs or for those needing emergency surgery, temporary transvenous or transcutaneous pacing should be available. In the intraoperative and postoperative settings, bradycardia may signify a potentially serious underlying problem that requires specific intervention such as hypoxemia, hypothermia, surgical manipulation of the autonomic nervous system, excessive anesthetic depth, cardiac ischemia, hyperkalemia, increased intrathoracic pressure associated with pneumothorax, or drug toxicity (e.g., from opioids, α-adrenergic agonists, digoxin, β-adrenergic antagonists, calcium channel blockers, halothane, or vagomimetic agents) [2,13,14]. Profound sinus bradycardia and asystole have been described in association with spinal anesthesia in humans [2].

Sinus bradycardia (sinus rhythm with rate < 60 beats/minute in dogs), sinus arrhythmia, and sinus pauses are common in healthy large and giant breed dogs with strong vagal tone. These physiologic, vagally mediated arrhythmias are often observed in dogs in the perioperative setting, particularly during sleep. Vagally mediated rate and rhythm alterations may also be associated with enhanced vagal tone caused by chronic airway diseases (particularly upper airway obstruction), chronic gastrointestinal diseases, increased intraocular pressure, increased intracranial pressure, and cervical spinal injuries or surgery [14].

High-grade second-degree AV block and complete (third-degree) AV block often reflect intracardiac disease, and animals with these arrhythmias may require temporary or permanent heart rate support. Second-degree AV block is recognized on ECG by the presence of intermittent nonconducted P waves; whereas with complete AV block, the atrial and ventricular activity are completely dissociated, and the ventricular rate is slower than the atrial rate. Causes of high-grade AV conduction block in dogs and cats include degenerative disease of the conduction system, primary or secondary myocardial diseases, trauma, endocarditis, neoplasia, drug toxicity, and surgery or catheters within the heart. Transient third-degree AV block is occasionally due to vagal surges caused by pain, hypoxemia, or suctioning [2].

Other than correcting reversible underlying causes, treatment of bradycardia is needed only if the rate is slow enough to cause hypoperfusion. Atropine may be administered intravenously at a dose of 0.02 to 0.04 mg/kg IV or IM. Intravenous infusion of isoproterenol(0.01-2.0 µg/kg/min) or dopamine (5-8 µg/kg/min) may also be considered. Temporary pacing for bradycardia may be performed transcutaneously in anesthetized patients; however, not all patients can be effectively paced in this manner because of high chest wall impedance. The discomfort induced by this pacing method limits its use to anesthetized or comatose patients. Transvenous pacing is more reliable and may be utilized as a bridge to permanent pacing in conscious or unconscious patients. However, temporary transvenous pacing is associated with risks including sepsis and sudden death from lead displacement. It should be recognized that any type of temporary pacing may produce pacemaker dependence.

Arrhythmias Associated with Specific Surgical Procedures

Instrumentation and Monitoring

Tracheal intubation may be associated with tachyarrhythmias caused by reflex sympathetic stimulation, and anxious patients with high adrenergic tone are particularly susceptible. Pretreatment with opioids, lidocaine, or β-blockers will reduce the cardiovascular responses to intubation [1]. Transient supraventricular or ventricular tachyarrhythmias have also been noted during placement of central venous pressure (CVP) monitoring catheters as the guide wire is passed into the right atrium or right ventricle [1,15]. Similar arrhythmias may occur from catheters passed through the right side of the heart into the pulmonary artery. Usually, these arrhythmias are transient and insignificant, but ventricular fibrillation has been reported [16]. Complete AV block has also occurred with guide-wire insertion during CVP cannulation [17]. To avoid these potential arrhythmias, it is recommended that guide-wire insertion be limited to the length necessary to reach the junction of the cranial vena cava with the right atrium. It is also important to monitor the patient's ECG or pulse and to have resuscitative drugs and equipment readily available during insertion of central venous or pulmonary artery catheters.

Acute Gastric Dilation and Gastric Dilation with Volvulus

A high incidence of ventricular arrhythmias (VT and VPCs) has been noted in dogs during and after surgery for acute gastric dilation (AGD) and gastric dilation with volvulus (GDV) [18]. Continuous ECG monitoring is, therefore, recommended, and management of ventricular arrhythmias should be considered when formulating the anesthetic plan. The cause of ventricular ectopy associated with gastric dilation most likely is multifactorial. Ischemia almost certainly plays an important role [19]. Release of myocardial depressant factors from the pancreas has also been implicated [20]. Reperfusion injury is known to occur with GDV and will produce cardiac compromise and irritability [21]. Finally, the acid-base and electrolyte abnormalities in affected dogs undoubtedly play a contributing role. Ventricular ectopy in dogs with AGD and GDV rarely produces hemodynamic instability, and the value of antiarrhythmic treatment is unproven [22]. However, dogs with polymorphic VT, frequent pulse deficits, rapid VT, underlying heart disease, or hypotension associated with the arrhythmia should receive antiarrhythmic agents. Spontaneous resolution of the arrhythmia typically occurs within a few days with successful treatment of the underlying disease.

Splenectomy

Ventricular arrhythmias are also common in dogs undergoing splenectomy for neoplasia, torsion, or immune-mediated disease [23,24]. These arrhythmias may occur in the pre-, intra-, and postoperative periods, but arrhythmias most commonly develop 5 to 12 hours after surgery [24]. Therefore, continuous ECG monitoring throughout the perioperative period is advised. Proposed causes of the ventricular ectopy include release of emboli during manipulation of the spleen, arterial hypotension, anemia, free radical-induced myocardial damage, transient ischemia, and the effect of myocardial depressant factors [23-25]. Treatment should consist of restoring normal blood volume and red cell mass, treatment of hypotension, and correction of metabolic abnormalities. As with gastric dilation/volvulus, the ventricular arrhythmias associated with splenectomy are usually hemodynamically stable, and contribution of the ventricular ectopy to postoperative death is unlikely.6 Monitoring cardiac rhythm and arterial blood pressure without administration of antiarrhythmic medication is a reasonable course of action in many patients. However, dogs with polymorphic VT, frequent pulse deficits, rapid VT, underlying heart disease, or hypotension associated with the arrhythmia should receive antiarrhythmic agents. In most dogs, ventricular arrhythmias associated with splenectomy resolve without antiarrhythmic treatment within 2 to 3 days following successful treatment of the underlying noncardiac abnormalities.

Thoracic Surgery

Cardiac surgical procedures frequently result in arrhythmias owing to direct stimulation of the myocardium. VPCs are a common manifestation of surgical manipulation or incision of the myocardium, and ventricular ectopy in this setting should be suppressed to prevent unstable VT or VF [14]. Preventive measures include discontinuing arrhythmogenic drugs (e.g., digoxin) in the preoperative period if possible; reversing electrolyte depletion caused by chronic diuretic administration; avoiding the use of halothane; and administration of lidocaine prior to and during manipulation, incision, or suturing of the myocardium.

Arrhythmias also occur frequently during thoracic surgeries that do not directly involve the heart. The etiology of these arrhythmias typically includes one or several factors including increased pulmonary vascular resistance, mediastinal shift, autonomic imbalance (vagal surges and release of catecholamines), hypoxemia, electrolyte and acid-base imbalance, and preexisting cardiac disease [26].

Pheochromocytoma

Pheochromocytomas are functional tumors of the adrenal medulla that produce norepinephrine, epinephrine, and occasionally, dopamine. Large amounts of catecholamines may be released into the central circulation as a result of intraoperative tumor manipulation. This catecholamine release may cause or aggravate potentially fatal tachyarrhythmias. Direct monitoring of the ECG, arterial blood pressure, and central venous pressure throughout the perioperative period is advised. Supraventricular and ventricular tachycardias should be suppressed with intravenous administration of a β-adrenergic blocking agent such as esmolol or propranolol (Table 18-1). In addition, intravenous administration of phentolamine to control hypertension may indirectly mitigate ventricular tachyarrhythmias. Administration of lidocaine immediately prior to tracheal intubation has also been suggested [27].

Thyroidectomy

Functional thyroid tumors (adenomatous thyroid hyperplasia) are common in older cats. In one series of 85 cats undergoing thyroidectomy, 10% had tachyarrhythmias during surgery [28]. When surgery on cats with this condition is necessary, intraoperative and postoperative cardiovascular complications, including supraventricular and ventricular tachyarrhythmias, can be minimized by medical induction of a euthyroid state prior to surgery. If this is not possible, recommendations for minimizing arrhythmia include administration of acepromazine prior to induction, avoidance of anticholinergic agents and α2-adrenergic agonists, and avoidance of halothane [27].