Perianesthetic Arrhythmias

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Vol. 22, No. 1 January 2000

CE

Refereed Peer Review

FOCAL POINT ★ Arrhythmias are common in the perianesthetic period and should be recognized, thus the electrocardiograph is an important monitoring device that should be used in all anesthetized patients.

KEY FACTS ■ Preanesthetic and induction agents can alter autonomic balance, which can result in a variety of arrhythmias that may or may not be clinically significant. ■ Bradyarrhythmias and heart blocks may often result from opioid and tranquilizer administration but may not be clinically significant if cardiac output is not adversely affected. ■ Anticholinergics may produce such arrhythmias as complex second-degree atrioventricular block and extrasystoles. ■ Ventricular premature complexes can have a variety of noncardiac causes and often do not require specific antiarrhythmic drug administration but may require changes in anesthetic management to prevent serious consequences.

Perianesthetic Arrhythmias Mississippi State University

University of Georgia

Lynne I. Kushner, DVM

Clay A. Calvert, DVM

ABSTRACT: The patients discussed in this article were presented to the Veterinary Teaching Hospital at Mississippi State University for a variety of surgical or medical procedures requiring anesthesia. The electrocardiograms of all patients were monitored during induction and maintenance of anesthesia. A variety of arrhythmias were recorded, including heart blocks, extrasystoles, escape complexes, and accelerated junctional or ventricular rhythms. Noncardiac causes were implicated in all cases. Some arrhythmias may produce hemodynamic instability, whereas others may not. Although specific antiarrhythmic agents were not required, alteration in anesthetic management was necessary in these patients to resolve the arrhythmia and avert serious consequences.

T

he incidence of cardiac arrhythmias in the perioperative period in human patients ranges from 18% to 70%.1,2 Incidence varies with degree of monitoring, type of anesthetic, presence or absence of preexisting disease, and ventilatory status. Although specific statistics are unknown, cardiac arrhythmias are also common in anesthetized veterinary patients.3,4 Causes of arrhythmia during anesthesia and surgery include altered physiologic states, autonomic imbalance, and adverse effects of drugs and drug interactions.2,3 In humans, arrhythmias may be more common when heart disease is present2; in our opinion, most arrhythmias in veterinary patients have a noncardiac cause. Although most arrhythmias are often benign (i.e., causing no physiologic or circulatory impairment), some may result in significant cardiovascular impairment if unrecognized or potentiated by anesthetic agents. The following electrocardiogramsa (ECGs) and case descriptions are of patients presented to the Veterinary Medical Teaching Hospital at Mississippi State University. All patients were either normal and healthy or had only mild systemic disease and were presented for routine medical or surgical procedures. None of the patients had documented cardiac disease. This article describes some common arrhythmias, speculates on their causes, and discusses their relevance and possible treatment.

CASE 1 A 5-year-old Boston terrier required anesthesia for dental cleaning and tooth extraction. The dog was premedicated with acepromazine (0.05 mg/kg intramuscularly [IM]), oxymorphone (0.05 mg/kg IM), and glycopyrrolate (0.01 mg/kg IM) 40 minutes before the preinduction ECG was recorded (Figure 1). aAll

ECGs were recorded in lead II at a paper speed of 25 mm/second; they were not standardized for sensitivity.

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but does not depolarize the atria; sinus arrest occurs because no sinus impulse is formed.5 Electrocardiographically, sinus block and sinus arrest are difficult to differentiate; however, a pause that encompasses exact multiples of R-R intervals suggests sinus Figure 1—Second-degree atrioventricular (AV) block. The atrial and ventricular rates block.5 are 100 and 60 beats/min, respectively. The P-R interval preceding the nonconductIn addition to pathologic conditions ed P wave (0.14 seconds) is slightly longer than the first P-R interval (0.12 seconds) of the atria, sinus arrest/block often of the pair. This describes a Mobitz type 1 (Wenckebach phenomenon) second-de- occurs with sinus arrhythmia caused gree AV block.5 by increased vagal tone.5 The bradycardia (Figure 2A) may be attributed Second-degree atrioventricular (AV) block is characto butorphanol, an opioid with mixed agonist–antagoterized by an interruption of AV conduction that renist activity. Butorphanol produces bradycardia similar sults in one or more P waves that are not followed by a to that caused by oxymorphone in acepromazine-sedatQRS-T complex.5 When found in normal dogs, it is ed dogs.9 Midazolam, a water-soluble benzodiazepine most often associated with sinus arrhythmia and other with twice the potency of diazepam,14 was added in this 5 case to improve the sedative effects of butorphanol. An causes of increased vagal tone. Brachycephalic breeds as well as young or athletic dogs may have hyperactive escape complex occurs when lower pacemakers disvagal reflexes.6,7 Response to anticholinergic drug adcharge to rescue the heart. ministration would verify a vagal cause and an antiAtropine, a competitive muscarinic-receptor antagocholinergic drug is indicated if bradycardia adversely nist, is used to correct vagally mediated bradycardia. affects cardiac output. Although an ECG was not reHowever, atropine often produces initial slowing of HR, corded before premedication in this patient, auscultawith or without AV block, especially at low dosages15; the causative mechanism initially proposed was central tion did not indicate preexisting bradyarrhythmia. stimulatory effects on vagal centers.15,16 Recent evidence, Many drugs, including α2 agonists (e.g., xylazine8) 9 10 and opioids (e.g., oxymorphone, butorphanol ), prohowever, suggests a peripheral mechanism involving duce bradyarrhythmias as a result of increased vagal augmentation of acetylcholine release by high-affinity outflow. Acepromazine may either increase or not have presynaptic muscarinic receptors, followed by blockade a significant effect on heart rate (HR) but may produce of low-affinity postsynaptic muscarinic-receptor subprofound bradycardia in susceptible dogs by increasing types, which results in parasympatholytic effects.17 In 11 addition, current hypotheses include a difference in sencentral cholinergic outflow. Acepromazine’s role in potentiating vagal activity in brachycephalic breeds has sitivity or distribution of muscarinic receptors at the SA been reviewed.12,13 and AV nodes, which may account for the differential Oxymorphone was the most likely cause of the arresponse in SA and AV nodal activity.16,17 A recent study demonstrated this biphasic response rhythmia in this patient, with acepromazine being a in HR after IM and IV administration of atropine.17 potentiating factor. Glycopyrrolate was apparently inefThis effect was also demonstrated in this case. After fective in producing vagal blockade. Although antiseveral minutes, the HR and rhythm improved and incholinergic administration would increase HR and reduction proceeded without complication or further store rhythm, the dog was hemodynamically stable and heart block. induction with thiopental proceeded with no complications. The HR remained around 80 beats/min with no CASE 3 further evidence of heart block. A healthy, 1.5-year-old Labrador retriever was anesCASE 2 thetized for surgical correction of osteochondritis desicAnesthesia and surgery were planned for a healthy, 7cans. After moderate sedation with acepromazine (0.05 year-old dachshund. The patient was premedicated mg/kg IM) and oxymorphone (0.05 mg/kg IM), aneswith butorphanol (0.3 mg/kg IM) and midazolam (0.2 thesia was induced with thiopental (12 mg/kg IV adminmg/kg IM), and a preinduction ECG was recorded istered to effect) and maintained with halothane and (Figure 2A). Because of the low HR, atropine (0.02 oxygen. Approximately 3 to 5 minutes after inhalation mg/kg) was administered intravenously (IV). anesthesia began, an arrhythmia was noted (Figure 3). In sinus block, the sinoatrial (SA) node discharges Ventricular premature complexes (VPCs) arise from SECOND-DEGREE ATRIOVENTRICULAR BLOCK ■ OXYMORPHONE ■ SINUS BLOCK

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Figure 2A

Figure 2B Figure 2—(A) Marked sinus arrhythmia with a ventricular rate of 60 to 80 beats/min. Sinus block/arrest results in long pauses equal to or greater than two R-R intervals. An escape complex, probably either atrioventricular (AV) nodal or high septal in origin, interrupts the block. The P wave can be seen after the QRS complex (arrow). (B) An advanced second-degree AV block occurs. More than one consecutive P wave is not conducted. The atrial rate is 130 beats/min, and the ventricular rate is 60 beats/min. Escape beats, which may be AV nodal or high ventricular in origin, occur independent of the rhythm of sinoatrial node depolarization. P waves occur before, within, and after the QRS of the escape complexes.

ectopic foci in the ventricles and result in bizarre, widened QRS complexes that are not associated with P waves.5 Classification of the severity of VPCs is based on (1) the number of single VPCs per minute; (2) whether they are multiform or uniform in appearance; (3) if they occur early on the preceding T wave (i.e., R-on-T phenomenon); or (4) if they occur in pairs, runs, or paroxysms.5 If VPCs occur frequently enough to produce circulatory impairment, treatment should be instituted. In addition to cardiac disease, VPCs can have numerous noncardiac causes, including electrolyte and acid– base imbalance, autonomic imbalance, hypoxia, and hypercapnia.5 Circulating catecholamines can increase because of stress, pain, and excitement and exert their potential arrhythmogenic effects by binding to α- and β-adrenergic receptors within the myocardium.18 The myocardial sensitization to epinephrine by anesthetic agents has recently been reviewed.19 The arrhythmogenicity of a drug can be measured by determining its effect on the arrhythmogenic dose of epinephrine (ADE). One study determined the receptor mechanism that mediates epinephrine-induced arrhythmias during halothane administration; the ADE was increased the greatest after α1 blockade, suggesting that mediation of sensitization by halothane is predominantly an α1 receptor–effector mechanism.18 Anesthetic agents that have

lowered the ADE include thiobarbiturates, 20,21 propofol,22 and halothane.23 Xylazine and ketamine may or may not enhance arrhythmogenicity.24–27 Thiopental or halothane administration, hypoxia, and hypercapnia are potential precipitating causes in this healthy dog. It is well established that thiopental potentiates halothane-epinephrine–induced arrhythmias.20,21 In addition, the duration of this potentiation can exceed 4 hours, well beyond thiopental’s clinical effects.20,21 This arrhythmia was noticed soon after halothane was administered, but anesthetic concentrations of halothane were not measured. Myocardial epinephrine sensitization may occur with halothane concentrations as low as 0.1%.28 Because oxygen–hemoglobin saturation and partial pressure of arterial carbon dioxide concentrations were not measured, it cannot be stated with certainty whether hypoxia and/or hypercapnia played a role in the genesis of this arrhythmia. The dog was immediately ventilated with several breaths to ensure adequate oxygenation and ventilation, but normal rhythm was not restored and ventricular ectopic beats continued with similar frequency. Because the dog’s mucous membrane color, capillary refill time, pulse quality, and depth of anesthesia were assessed as adequate, surgery proceeded with vigilant monitoring. Halothane was replaced with isoflurane with little response in the frequency of the

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Figure 3—Heart rate is 160 beats/min with ventricular premature complexes (arrows). These complexes are not followed by a

pause and are called interpolated; they do not disrupt the ventricular rhythm.

Figure 4—Ventricular trigeminy (two sinus beats followed by ventricular premature complexes [arrows] in a repetitive pattern).

The ventricular rate is 140 beats/min. The arrhythmia persisted for approximately 10 minutes.

arrhythmia. Although indirect blood pressure remained satisfactory, lidocaine (2 mg/kg IV) was eventually administered and was successful in restoring normal sinus rhythm.

CASE 4 A healthy, 3-year-old, 32-kg rottweiler was presented for ovariohysterectomy. Because of a history of potential aggression, heavy sedation was accomplished with xylazine (0.3 mg/kg IM), butorphanol (0.2 mg/kg IM), and glycopyrrolate (0.015 mg/kg IM). An IV catheter was placed with little physical restraint. A preinduction ECG (not depicted) revealed sinus rhythm with an HR of 140 beats/min. Induction with thiopental was about to begin when an arrhythmia suddenly emerged (Figure 4). In bigeminal or trigeminal rhythms, the interval between the sinus and ectopic beat is constant (fixed coupling). This indicates that the sinus beat controls the discharge of the ectopic focus by a reentry mechanism in the myocardium.29 Noncardiac causes were considered in this normal, healthy dog. Drugs administered to this dog that could be implicated in the genesis of ventricular extrasystoles include glycopyrrolate and xylazine. Dogs receiving glycopyrrolate, xylazine, and butorphanol exhibited decreases in cardiac index with ST segment depression, pulsus alternans, and occasional VPCs.30 Xylazine either decreased 8,24 or did not alter the ADE25 in anesthetized dogs, but differences in methodologies and end points may have accounted for disagreement in the results. Dexmedetomidine, a highly selective α2 agonist, inhibited the arrhythmogenic effect

of epinephrine in halothane-anesthetized dogs.31 Bilateral vagotomy abolished this antiarrhythmogenic effect, suggesting protection from parasympathetic tone.32 Parasympatholytics may induce autonomic imbalance, resulting in extrasystoles. Atropine administration in dogs resulted in a higher frequency of ectopic rhythm disturbances than in control dogs that did not receive atropine.15 However, in a recent study, cholinergic blockade increased the threshold to epinephrine-induced arrhythmias in halothane- and isoflurane-anesthetized dogs.33 In this case, induction was delayed while the ECG, which improved over several minutes, was observed. Because the dog’s mucous membrane color, capillary refill time, and pulses were good, induction was still planned but thiopental was no longer considered because of its potential arrhythmogenicity. Diazepam (0.3 mg/kg IV) followed by ketamine (2 mg/kg IV) was administered, and intubation was easily accomplished. Normal sinus rhythm remained, and no further arrhythmia was observed.

CASE 5 A 13-year-old cocker spaniel required anesthesia for mammary tumor removal. A preoperative radiographic evaluation for possible metastasis revealed no significant abnormalities of the lung fields or cardiac silhouette. The dog was premedicated with oxymorphone (0.05 mg/kg IM), midazolam (0.2 mg/kg IM), and glycopyrrolate (0.015 mg/kg IM). Normal sinus rhythm was noted immediately before induction with thiopental (10 mg/kg IV to effect). During endotracheal intu-

VENTRICULAR TRIGEMINY ■ XYLAZINE ■ PARASYMPATHOLYTICS

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Figure 5A

Figure 5B

Figure 5C Figure 5—(A) Ventricular premature complexes (VPCs; arrows) occur regularly following three sinus complexes. The ventricular

heart rate (HR) is 170 beats/min. (B) There are supraventricular complexes of either atrial or atrioventricular nodal origin (small arrows) occurring in a bigeminal pattern; T waves preceding each supraventricular beat appear deeper, suggesting an additive negative P-wave effect. VPCs are also present (large arrows). (C) Immediately after intubation, the HR is 100 beats/min with no premature complexes.

bation, an arrhythmia was noted and recorded (Figures 5A and 5B). Immediately after intubation, normal sinus rhythm was restored (Figure 5C). Supraventricular premature complexes originate in atrial or AV nodal tissue.5 The P waves, if visible, should differ slightly from the sinus P waves and can occur before, during, or after the QRS complex. The QRS complex should usually have a similar conformation to that associated with sinus beats. When AV nodal premature beats are indistinguishable from those of atrial origin, supraventricular is the appropriate terminology. Atrial premature complexes are often associated with heart disease, although they can occur in normal dogs.5 In one experimental study, atrial arrhythmias preceded ventricular arrhythmias during epinephrine-induced sensitization with halothane and isoflurane.21 The fact that the arrhythmia resolved immediately after intubation argues strongly for laryngeal stimulation as the precipitating cause. Stimulation of the larynx by laryngoscopy and intubation can cause tachycardia, hypertension, and cardiac arrhythmias by an

absolute or relative increase in sympathetic tone. However, parasympathetic stimulation is also possible.1,4 Ectopic complexes resolved after the HR decreased (180 to 100 beats/min), which supports a mechanism of autonomic imbalance from increased sympathetic stimulation. Hypoxia and hypercapnia can induce cardiac arrhythmia indirectly by release of catecholamines or directly by depression of cardiac cells and stimulation of the vasomotor centers of the brain.4 However, manual ventilation was not required to restore the rhythm in this case. If intubation had not been initially successful, ceasing attempts at intubation would have been advisable. Delivery of oxygen via a face mask using high oxygen flow rates before further attempts at intubation may help avoid a more serious arrhythmia and its consequences. After intubation, no further arrhythmia was observed and surgery and recovery were uneventful.

CASE 6 A 10-month-old cat was administered tiletamine–zo-

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reflex or jaw tone, and the vaporizer was turned off temporarily. Because there was no patent airway, the cat was immediately intubated. Sinus rhythm was restored with the administration of one or two Figure 6—The ventricular rate is 170 beats/min. In addition to sinus complexes, there are mulbreaths. Surgery and recovery tiform ventricular complexes with both right (1) and left (2) bundle branch block patterns. proceeded uneventfully. Fusion beats (F) resemble both forms of ventricular premature complexes. Although the cat was neither apneic nor cyanotic, reslazepam (4 mg/kg IM), intubated, and maintained with piration was assumed to be inadequate because the arhalothane for ovariohysterectomy. Approximately 30 rhythmia disappeared immediately after intubation. If an minutes later, during surgery, abnormal complexes were ECG had not been eventually monitored, change in noted on the ECG (Figure 6). management may have been unlikely. Rapidly occurring Fusion beats are the result of simultaneous activation multiform VPCs may lead to ventricular tachycardia and of the ventricle by impulses from the SA node and venfibrillation.5 This case demonstrates the importance of 29 adequate oxygenation, supportive care, and monitoring. tricular ectopic foci. The QRS is intermediate in form between the sinus and ectopic QRS. Ventricular ectopic CASE 8 beats were not noted until the viscera was manipulated. A 10-year-old Labrador retriever with upper airway Catecholamine release from painful stimuli, especially stridor was to be anesthetized for possible laryngoplasty. in the presence of halothane, can result in ventricular After premedication with butorphanol and diazepam, arrhythmias.4,34 Palpebral reflex and jaw tone suggested a light plane of anesthesia. Attempts were made to inthe ECG was monitored in preparation for induction. crease the anesthetic plane by increasing ventilation and An irregular rhythm with abnormal complexes was vaporizer concentration. Because isoflurane was readily recorded (Figure 8). The surgeon’s concern that heart available, halothane was discontinued. The rhythm was disease was present prompted cancellation of surgery quickly restored with no further abnormalities. Disconuntil cardiac evaluation was completed. tinuation of halothane may not have been necessary— Right bundle branch block (RBBB) is a delay or inincreasing halothane concentration has been shown to terruption of conduction through the right bundle result in resolution of ventricular arrhythmias.34 branch. Normally, the right ventricle is activated by an Tiletamine–zolazepam is an unlikely factor in the genimpulse that passes from the bundle of His to the right esis of this arrhythmia. It did not affect ADE in cats bundle branch. With RBBB, the right ventricle is actianesthetized with halothane.35 vated by an impulse that passes from the left bundle branches to the right side of the septum below the CASE 7 block, with delay causing the QRS to be wide and A 1-year-old domestic shorthair cat was given tilebizarre.36 In this case, P-P intervals become progressivetamine–zolazepam (4 mg/kg ly shorter and P-R intervals IM) for castration and onyremain the same. The AV chectomy. Because the anesimpulse enters the conductthetic depth was judged to ing system before the right be inadequate, halothane was bundle branch has a chance administered by face mask. to repolarize, thereby proDuring surgery, an abnormal ducing aberrant conduction. rhythm was noted on the ulThis pattern persisted throughtrasonic Doppler flow detecout the ECG. tor, which was recording pulse Figure 7—In a repetitive pattern, triplets of multiform venCriteria of complete RBBB rhythm at the metatarsal ar- tricular premature complexes (large arrows) can be seen fol- includes a QRS complex tery. An ECG was recorded lowing two possible sinus complexes. However, the second longer than 0.08 seconds; a “sinus beat” (small arrow) may be an atrial premature com- right axis deviation; and (Figure 7). Vital signs and anesthetic plex because, compared with the previous sinus beat, the P deep S waves in leads I, II, depth were quickly evaluat- wave is smaller and there is no S wave on the subsequent III, and aVF. RBBB can be QRS complex. ed. There was no palpebral associated with heart disease FUSION BEATS ■ CATECHOLAMINE RELEASE ■ OXYGENATION

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ing an AV junctional or ventricular focus to take over, increased AV junctional or ventricular automaticity, disturbed AV conduction, or a combination of mechanisms.37 Decreased SA node automaticity and an accelerated ventricular rhythm may be the mechanisms involved in this case. Although AV dissociation may be associated with heart disease, it has been reported in a Figure 8—Intermittent right bundle branch block (RBBB). QRS duration is 39 0.12 seconds with deep S waves (arrows). This is an example of phasic aber- healthy cat during inhalation anesthesia. Isoflurane slows the rate of SA pacemaker rant conduction taking the usual form of rate-dependent RBBB. The R-R intervals preceding the RBBB become progressively shorter until RBBB occurs. discharge by direct and indirect effects on A marked sinus (vagal) arrhythmia is also evident. The ventricular rate is 80 to SA node automaticity.40 In addition, isoflu100 beats/min. rane at increased concentrations lengthens AV nodal conduction time. The depressant effects of anesthetics on AV nodal conducbut also can occur in normal, healthy dogs or as an intion with depression of sinus nodal automaticity could cidental finding in dogs with noncardiac diseases.36 favor an occurrence of AV dissociation.40 RBBB alone does not require treatment, produces no AV dissociation resulting from accelerated junchemodynamic problems, and should not present a contional rhythms can be caused by sympathetic stimulacern for anesthesia. It is important not to confuse tion of AV nodal pacemaker cells or parasympathetic RBBB with VPCs; the former can be distinguished by overriding of the sympathetic nervous system as a repreceding consistent P-R intervals. sult of autonomic imbalance. These arrhythmias have An echocardiogram demonstrated normal cardiac dibeen successfully treated with propranolol41 and atropine.42 Atropine was administered in the cat in this mensions and function. Anesthesia and surgery procase because of the low HR and marginally low sysceeded without complication. tolic pressures. Although atropine increased HR to CASE 9 only 100 beats/min, sinus rhythm was restored (FigA 6-year-old cat was diagnosed with leukocytopenia ure 9C). of undetermined cause. An echocardiogram revealed no CASE 10 significant findings. Months later, the cat was presented A 6-year-old Brittany spaniel was admitted for surgery for an ovariohysterectomy and follow-up bone-marrow 1 day after being hit by a car. The dog, which had an biopsy. There were no significant findings on physical or open fracture of the radius and ulna, was bright and alert. hematologic examination. Ketamine (5 mg/kg), butorRadiographs of the thorax revealed mild changes consisphanol (0.2 mg/kg), and midazolam (0.1 mg/kg ) were tent with heartworm disease; there were no significant administered IM and produced adequate sedation. A findings on abdominal films. Minimal laboratory data, preinduction ECG was not recorded. Thiopental was consisting of packed cell volume, total protein, blood urea administered IV to effect for intubation, and anesthesia nitrogen, and glucose estimation, were within reference was maintained with isoflurane. An ECG was recorded ranges.43 during surgical preparation (Figure 9A). The following day, surgery was scheduled for internal A pararrhythmia is an abnormal rhythm in which fixation of the radius and ulna. The dog was premeditwo pacemakers discharge independently of each other, cated with acepromazine (0.05 mg/kg IM) and oxyand each can activate the ventricle at different times.38 AV dissociation is one example in which the dominant morphone (0.05 mg/kg IM). A preinduction ECG was pacemaker (AV junction or ventricle) controls ventricunormal (not depicted). Anesthesia was induced with lar activation and another pacemaker (SA node or atrithiopental and maintained with isoflurane. Forty-five al) controls the atria. Incomplete AV dissociation ocminutes after surgery began, bradycardia with first- and curs if an impulse from the SA node conducts to the second-degree AV block (not depicted) was noted. HR ventricle, producing a ventricular capture beat. This ocand indirect blood pressure began to drop quickly over curs after every second or third QRS complex (Figure 10 minutes. P waves were no longer recognized (Figure 9A). AV dissociation is a sign of a primary disturbance 10A). Atropine (0.02 mg/kg IV) was administered, and is not an ECG rhythm diagnosis. This disturbance producing electrocardiographic changes (Figure 10B). can result from depressed SA node automaticity allowBlood was collected for electrolyte, chemistry, pH, and RIGHT BUNDLE BRANCH BLOCK ■ ATRIOVENTRICULAR DISSOCIATION ■ ISOFLURANE

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blood gas determinations. Chemistry results that were not within reference ranges43 included potassium (9.89 mEq/L), blood urea nitrogen (90 mg/dL), creatinine (3.9 mg/dL), and albumin (1.4 g/dL). Blood gas re- Figure 9A sults using lingual venous blood were also out of reference range43 and indicated a respiratory and metabolic acidosis (pH, 7.14; partial pressure of carbon dioxide, 66 mm Hg; partial pressure of oxygen, 450 Figure 9B mm Hg; bicarbonate, 23 mEq/L; base deficit, 8.3 mEq/L). Regular insulin (20 units) and 5% dextrose were added to normal saline and administered at a rate of 20 ml/kg IV. Sodium bicarbonate (0.5 mEq/L IV) was administered slowly. Twen- Figure 9C ty minutes after the treat- Figure 9—(A) The ventricular rate is 100 beats/min. The dominant rhythm occurs regularly at ment, P waves were notice- 80 beats/min, with abnormal QRS morphology suggesting a ventricular origin. P waves (arrows), able and a normal ECG was although not clearly visible, may be present and are dissociated from the dominant rhythm. Othrestored 30 minutes there- er leads might better delineate their presence. A P wave is also barely visible (arrow) in the T waves preceding the capture beats (C). Capture beats are sinus impulses that occasionally capture after (not depicted). the ventricles, making this a type of incomplete atrioventricular dissociation.37 (B) After atropine Loss of P-wave morphology with spiked T waves is (0.02 mg/kg IV) is administered, P waves are more clearly evident—demonstrating their occurhighly suggestive of hyper- rence before, within, and after the QRS. The ventricular rate is 80 beats/min, and another capture beat can be seen after the fourth complex. (C) After atropine is readministered, the ventricukalemia. 44,45 The resting lar rate increases to only 100 beats/min but sinus rhythm is restored. membrane potential (RMP) of cardiac muscle depends that the SA node continues to discharge and impulses are on a normal ratio of extracellular:intracellular potassium transmitted to the AV node, and thereby to the ventriconcentration.44 During hyperkalemia, the RMP is raised (becomes less negative). Fewer sodium channels are open, cles, by specialized internodal conducting pathways. The and thus depolarization to threshold potential (TP) is reatria are not activated, and thus no P wave is recorded.45 This is termed sinoventricular conduction. duced. The action potential duration is shortened, and Insulin administration with glucose will result in the rate of repolarization increases. The earliest manifesmovement of potassium into the cells. Sodium bicartations of hyperkalemia on the ECG are peaked, narrowbonate also induces an intracellular potassium shift. based T waves. The RMP decreases with further increasCalcium can be administered in severe cases to restore a es in potassium concentration, which in turn slows normal gradient of RMP to TP and to increase myocarintraventricular conduction and increases the duration of dial conduction and contractility.46 the QRS complex. Automaticity, conductivity, contrac45 The fracture in this patient was quickly repaired. A tility, and excitability are decreased. Various cardiac cells have a differential sensitivity to ruptured bladder was suspected and confirmed by ultrarising extracellular potassium. Purkinje fibers and mysound. Potassium enters the abdominal cavity from a rupocardial cells are the most sensitive, atrial cells more so tured bladder and is reabsorbed, causing serum potassium than ventricular.44,45 Experimental studies have shown to increase. A celiotomy was performed, and approxiHYPERKALEMIA ■ RESTING MEMBRANE POTENTIAL ■ THRESHOLD POTENTIAL

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mately 1 L of fluid was suctioned from the abdomen. A 3-cm rent was observed in the bladder and repaired. Serum potassium was 6.1 mmol/L at the completion of surgery, and recovery occurred with supportive care without further com- Figure 10A plications. A ruptured bladder was not expected either at the time of admission or on the day of surgery because of the dog’s bright attitude and lack of radiographic and clinical signs. More complete hematologic and biochemical evaluation may have induced suspicion of a ruptured bladder. The Figure 10B relatively high fluid rate of 10 Figure 10—(A) The ventricular rate of 50 to 60 beats/min with absence of P waves suggests eiml/kg/hour during anesthesia ther sinoventricular conduction or a junctional rhythm. The QRS morphology is abnormal, most likely produced rapid which could be the result of aberrant conduction from increased serum potassium. T waves urine production and bladder are more than half the size of the R wave. (B) Because of the sudden development of bradydistention to maintain paten- cardia, atropine is administered, after which the complexes are more aberrant, particularly at cy of the tear in the bladder. the faster rates (i.e., S waves are deeper and wider [arrows] ); this may be caused by rate-dependent aberrant conduction in addition to that caused by the increased serum potassium. Atropine was administered for the sudden bradycardia but produced a more aberrant cardiac rhythm. and dogs. JAVMA 185(6):643–646, 1984.

SUMMARY It is hoped that these cases demonstrate the importance of ECG monitoring in anesthetized patients. Although it is not a substitute for simple clinical assessments of pulse quality, mucous membrane color, and respiration, ECG monitoring provides important information not available by any other means. Most of the arrhythmias described in this article did not require specific treatment, but some required alteration in management that may have prevented serious consequences. ACKNOWLEDGMENT

The authors thank Mr. Tom Thompson for his photographic assistance.

REFERENCES 1. Katz RL, Bigger JT: Cardiac arrhythmias during anesthesia and operation. Anesthesiology 23(2):193–213, 1970. 2. Atlee JL: Perioperative cardiac dysrhythmias: Diagnosis and management. Anesthesiology 86(6):1397–1424, 1997. 3. Cohen RB, Tilley LP: Cardiac arrhythmias in the anesthetized patient. Vet Clin North Am Small Anim Pract 9(1): 155–162, 1979. 4. Hubbell JAE, Muir WW, Bednarski RM, Bednarski LS: Change of inhalation anesthetic agents for management of ventricular premature depolarizations in anesthetized cats

5. Tilley LP: Analysis of common canine cardiac arrhythmias, in Tilley LP (ed): Essentials of Canine and Feline Electrocardiography Interpretation and Treatment. Philadelphia, Lea & Febiger, 1992, pp 127–207. 6. Bolton GR: Bradycardia, in Kirk RW (ed): Current Veterinary Therapy VII. Small Animal Practice. Philadelphia, WB Saunders Co, 1980, pp 376–380. 7. Branch CE, Robertson BT, Williams JC: Frequency of second-degree atrioventricular heart block in dogs. JAVMA 36: 925–929, 1975. 8. Muir WW, Werner LL, Hamlin RJ: Effects of xylazine and acetylpromazine upon induced ventricular fibrillation in dogs anesthetized with thiamylal and halothane. Am J Vet Res 36(9):1299–1303, 1975. 9. Cornick JL, Hartsfield SM: Cardiopulmonary and behavioral effects of combinations of acepromazine/butorphanol and acepromazine/oxymorphone in dogs. JAVMA 200(12): 1952–1956, 1992. 10. Trim CM: Cardiopulmonary effects of butorphanol tartrate in dogs. Am J Vet Res 44(2):329–331, 1983. 11. Muir WW: Anesthetics and techniques, in Slatter D (ed): Textbook of Small Animal Surgery. Philadelphia, WB Saunders Co, 1993, pp 2245–2250. 12. Brock N: Acepromazine revisited. Can Vet J 35:458–459, 1994. 13. Dodman NH, Court MH: Questions about ECG interpretations. JAVMA 197(2):169–170, 1990. 14. Reves JG, Fragen RJ, Vinik RH, Greenblatt DJ: Midazolam: Pharmacology and uses. Anesthesiology 62(3):310–324, 1985. 15. Muir WW: Effects of atropine on cardiac rate and rhythm in

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About the Authors At the time this article was submitted for publication, Dr. Kushner was affiliated with the Animal Health Center, Mississippi State University, Mississippi State, Mississippi. Dr. Kushner is currently affiliated with the Veterinary Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania; she is a Diplomate of the American College of Veterinary Anesthesiologists. Dr. Calvert is affiliated with the Department of Small Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, Georgia; he is a Diplomate of the American College of Veterinary Internal Medicine.