History

An 11-year-old 3.5-kg (7.7-lb) spayed female Himalayan cat was referred to the University of Tennessee College of Veterinary Medicine for evaluation of a 6-day history of lethargy, anorexia, and dyspnea. Examination of thoracic radiographs obtained by the referring veterinarian revealed consolidation of a lung lobe. The cat's condition had not improved with antimicrobial treatment, and the cat was referred for evaluation on an emergency basis.

Physical examination revealed evidence of dehydration and dyspnea; crackles were evident during auscultation of the right hemithorax. No murmurs or arrhythmias were detected. An IV catheter was placed, and 50 mL (14.3 mL/kg [6.5 mL/lb]) of a balanced electrolyte solution was administered as a bolus over 15 minutes, followed by a continuous infusion at a rate of 4 mL/kg/h (1.8 mL/lb/h). Dolasetron (0.5 mg/kg [0.23 mg/lb], IV, q 24 h) and famotidine (0.5 mg/kg, IV, q 12 h) were administered because of presumptive nausea but were discontinued the next day after additional diagnostic testing was completed. Preliminary hematologic testing revealed hemoconcentration (Hct, 54%; total protein, 9.2 g/dL) and normoglycemia (107 mg/dL).

The patient was monitored overnight, and a CBC and serum biochemical panel were performed the next morning. A mild left shift (band neutrophils, 0.37 × 10³ cells/μL; reference range, 0 to 0.3 × 10³ cells/μL) and lymphopenia (0.53 × 10³ cells/μL; reference range, 1.05 × 10³ cells/μL to 8 × 10³ cells/μL) were detected. Biochemical abnormalities included mild hypoalbuminemia (2.4 g/dL; reference range, 2.7 to 4.1 g/dL), hyperglobulinemia (5.8 g/dL; reference range, 2.6 to 4.9 g/dL), hyponatremia (140 mEq/L; reference range, 149 to 160 mEq/L), and hypochloremia (106 mEq/L; reference range, 113 to 121 mEq/L). Results of tests for infection with feline retroviruses were negative. The cat was sedated with butorphanol (0.4 mg/kg [0.18 mg/lb], IV), and thoracic radiography was performed. Moderate pneumothorax that was more severe on the right side and associated with severe right-sided atelectasis was seen (Figure 1). The right cranial lung lobe was of uniform soft tissue opacity, and results of thoracic ultrasonography were suggestive of a right cranial thoracic mass, likely of pulmonary origin. Ultrasound-guided fine-needle aspiration of the mass and therapeutic thoracocentesis were performed. The volume of air removed from the thoracic cavity was not recorded. Cytologic examination of the fine-needle aspirate revealed severe pyogranulomatous inflammation with deeply basophilic, round, thin-walled yeast organisms that exhibited broad-based budding consistent with Blastomyces dermatidis.

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Left lateral and ventrodorsal radiographic views of the thorax of a cat examined because of lethargy, anorexia, and dyspnea. Notice the right cranial lung lobe mass (arrowhead), atelectasis of the remaining right lung lobes (asterisk), and pneumothorax (arrows).

Citation: Journal of the American Veterinary Medical Association 236, 8; 10.2460/javma.236.8.840

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A decision was made to perform exploratory thoracotomy and right cranial lung lobectomy. The goals were to reduce compression of the remaining lung tissue and to improve response to antifungal treatment by debulking grossly diseased tissue. In addition, placement of thoracostomy and esophagostomy tubes was planned.

The cat was premedicated with fentanyl (5 μg/kg [2.3 μg/lb], IV). Approximately 15 minutes later, anesthesia was induced with ketamine HCl (2.9 mg/kg [1.3 mg/lb], IV) and propofol (2.3 mg/kg [1.0 mg/lb], IV). A 5-mm–internal diameter cuffed orotracheal tube was placed, and the cat was connected to a pediatric circle rebreathing circuit. Anesthesia was maintained with a partial IV technique consisting of administration of isoflurane in oxygen (initial isoflurane vaporizer setting, 1.75%; initial oxygen flow rate, 1 L/min) and constant rate infusions of fentanyl (7.7 μg/kg/h [3.5 μg/lb/h], IV) and ketamine (10.5 μg/kg/min [4.8 μg/lb/min], IV).

A dedicated anesthetist monitored the cat continuously; the following variables were measured with a multiparameter anesthesia monitor^a: oxygen saturation as measured with pulse oximetry (SpO₂), end-tidal partial pressure of carbon dioxide (PETCO₂), blood pressure (determined by means of an indirect oscillometric method), and rectal temperature. In addition, a lead II ECG was monitored continuously for heart rate and rhythm and a Doppler ultrasonographic probe was placed over the right palmar digital artery. After anesthetic induction, the cat breathed spontaneously at a rate of 28 to 35 breaths/min. At this time, SpO₂ was 99%, PETCO₂ was 42 mm Hg, heart rate was 165 beats/min, and mean arterial pressure was 172 mm Hg.

The cat was positioned in left lateral recumbency and prepared for surgery. Fifteen minutes after anesthetic induction, an irregularly irregular arrhythmia was noted (Figure 2). Heart rate ranged from 150 to 300 beats/min, SpO₂ was 90%, mean arterial pressure was 162 mm Hg, PETCO₂ was 50 mm Hg, and respiratory rate was 25 breaths/min.

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Lead II ECG obtained 15 minutes after induction of anesthesia in the cat of Figure 1. Heart rate ranges from 150 to 300 beats/min. Multiform ventricular premature contractions and ventricular tachycardia are evident. Capture beats (arrowheads) and ventricular beats occurring after a short pause (asterisks) are evident, along with several ventricular premature contractions that may represent fusion beats (plus signs). An episode of nonsustained ventricular tachycardia consisting of 6 multiform ventricular premature contractions in a row is delineated by the dotted lines. Paper speed = 25 mm/s; 2 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 236, 8; 10.2460/javma.236.8.840

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Question

What is the type of arrhythmia? What is the most likely cause in this patient, and how should the arrhythmia be addressed?

Answer

Multiform ventricular premature contractions (VPCs) and nonsustained ventricular tachycardia are present. Given the documented pneumothorax in combination with a sudden decrease in oxygen saturation, myocardial hypoxia was suspected as the underlying cause of the arrhythmia. Thoracocentesis was performed, and 180 mL of air and 12 mL of fluid were withdrawn from the thoracic cavity. Oxygen saturation improved immediately (SpO₂, 97%); however, runs of ventricular bigeminy and trigeminy developed (Figure 3) . Over a period of a few minutes, more normal beats became apparent. The ventricular arrhythmia resolved completely within 3 minutes after thoracocentesis was performed, and no other arrhythmias were identified during the perioperative period.

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Lead II rhythm strip obtained after therapeutic thoracocentesis in the cat of Figures 1 and 2. The ventricular beats are less multiform in nature, and ventricular trigeminy with every third beat consisting of a ventricular premature contraction (asterisks) is seen. A possible fusion beat is evident (plus sign). Paper speed = 25 mm/s; 2 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 236, 8; 10.2460/javma.236.8.840

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Discussion

Ventricular tachyarrhythmias include isolated or recurrent VPCs, accelerated idioventricular rhythm (heart rate < 180 beats/min), ventricular tachycardia (heart rate > 180 beats/min), and ventricular fibrillation.¹ Ventricular premature contractions occur when ectopic pacemaker impulses within the ventricular conduction system or within the ventricular myocardium itself arise early in relation to the normal sinoatrial rate. With VPCs, the R-R interval is shortened and a P wave is not associated with the QRS complex. Electrical activity spreads outward directly from cell to cell, typically resulting in a wide and bizarre QRS complex. Repolarization is usually abnormal as well, resulting in large and bizarre T waves.¹

Morphology of the QRS complex is determined by the point of origin of the premature complex within the ventricle and subsequent conduction. If the VPC originates in the right ventricle, the QRS complex is typically positive in lead II, but if the VPC originates in the left ventricle, the QRS complex is typically negative. A uniform appearance to the QRS complexes indicates that a single ectopic focus is responsible for the ventricular rhythm, whereas multiform QRS complexes could indicate multiple points of origin or, rarely, a single point of origin with multiple conduction paths.¹ Fusion beats occur when a VPC and a normal sinus beat cause simultaneous depolarization of the ventricular myocardium. On the ECG, a fusion beat is a slightly premature beat with a P wave and hybrid appearance of the QRS complex. Supraventricular premature beats associated with abnormal intraventricular conduction (eg, left bundle branch block) can mimic VPCs¹; however, these supraventricular premature contractions are associated with a P wave.

With ventricular bigeminy, a normal sinus beat alternates with each VPC. This pattern has classically been associated with thiobarbiturate anesthesia.² With ventricular trigeminy, every third beat is a VPC.

Ventricular tachycardia is defined as r 3 consecutive VPCs and can be classified as nonsustained (ie, lasting < 30 seconds) or sustained (ie, lasting > 30 seconds).¹ Morphology of the QRS complexes during ventricular tachycardia can indicate the site of origin and ensuing conduction.

The ECG for the cat described in the present report included multiform VPCs. The multiform nature of the arrhythmia indicated that multiple areas of the ventricles had been damaged, resulting in ectopic impulses of multiple origins. The sinoatrial node continued to depolarize, and intermittent capture beats (ie, normally generated and conducted beats) could be identified. Several beats came after a short pause, but it was difficult to discern whether these beats were escape or premature beats because the normal R-R interval could not be determined. However, on the basis of the R-R interval in the later ECG, these likely were premature complexes. At least 1 episode of nonsustained multiform ventricular tachycardia was documented; this consisted of 6 multiform VPCs in a row. The third QRS complex of this series had a preceding P wave, but the short PR interval and abnormal morphology of the QRS complex indicated that it most likely arose in the ventricle. Atrioventricular dissociation was also evident because several P waves without an associated QRS complex could be identified. Atrioventricular dissociation is a hallmark of ventricular tachycardia and occurs when a normal depolarization arrives coincident with the refractory period of the previous ventricular depolarization so that a normal QRS complex is not generated. A few complexes that may have represented fusion beats were seen; however, no associated P waves were discernible, and these beats may simply have represented separate ventricular foci. The consistent lack of P waves associated with the wide QRS complexes and their multiform nature indicated that the arrhythmia was not a supraventricular tachyarrhythmia combined with a ventricular conduction disturbance.

Causes of ventricular tachyarrhythmias can be divided into those related to primary cardiac disease and those secondary to systemic disorders.³ Patients with cardiac diseases such as hypertrophic or dilated cardiomyopathy, myocarditis, advanced congenital heart defects, and, in dogs, severe valvular disease may have associated myocardial damage that can initiate arrhythmias. Ventricular tachyarrhythmias can also occur secondary to electrolyte derangements, intra-abdominal disease, and alterations in sympathetic tone resulting from pain, hypovolemia, hypercarbia, or hypoxia.^4–6 The authors believe that myocardial hypoxia was the cause of the arrhythmia in the cat described in the present report. No evidence of primary cardiac disease was detected during thoracic auscultation or radiography. However, an echocardiogram was not obtained prior to anesthesia, and the possibility exists that undetected cardiac disease contributed to the development of the ventricular tachyarrhythmia. On the other hand, the fact that the arrhythmia resolved following thoracocentesis and improvement in oxygen saturation makes this scenario less likely. Also, no additional arrhythmias were documented during the remainder of the anesthetic period or during the postoperative period.

Electrophysiologic mechanisms of ventricular tachyarrhythmias include reentry, abnormal automaticity, and triggered activity.^1,3 Reentry involves slowed or blocked conduction through diseased myocardium, which allows a wave of depolarization to return to a portion of the myocardium that has already repolarized, initiating a premature beat. Abnormal automaticity occurs when a portion of infected myocardium depolarizes more frequently than the normal pacemaker as a result of a less negative resting membrane potential. Triggered activity involves oscillations of membrane potential that are associated with a previous action potential.^1,3 It is not possible to discern the underlying mechanism of an arrhythmia without sophisticated electrophysiologic studies. In the case described here, areas of myocardial hypoxia could have caused changes in ventricular myocyte action potentials, resulting in abnormal automaticity, or slowed conduction, resulting in reentry. The arrhythmia was likely sustained through multiple reentrant loops.^7,8

Development of malignant ventricular arrhythmias during general anesthesia is not uncommon, and treatment should be focused on correcting the underlying cause, when possible. Antiarrhythmic agents can be used to control ventricular arrhythmias if necessary. Therapeutic thoracocentesis abolished the ventricular arrhythmia in the cat described in the present report. However, antiarrhythmic drug administration may have been indicated if the ventricular arrhythmia had persisted after thoracocentesis and resolution of hypoxemia. During general anesthesia, administration of antiarrhythmic agents is indicated if the ventricular arrhythmia results in hemodynamic instability, as evidenced by systemic hypotension, prolonged capillary refill time, and pale mucous membranes.³ Such rhythms usually involve fast, sustained ventricular tachycardia (heart rate > 180 beats/min). In addition, use of antiarrhythmic agents should be considered for those rhythms that may be likely to degenerate into ventricular fibrillation, including multiform VPCs and ventricular tachycardia and those that involve the R-on-T phenomenon.³ The R-on-T phenomenon occurs when the QRS complex of a VPC occurs during the T wave of the preceding VPC.

Intravenous administration of lidocaine HCl is the primary pharmacological treatment of ventricular tachyarrhythmias. Lidocaine is a class Ib antiarrhythmic agent that blocks sodium channels, thereby slowing conduction velocity.¹ The therapeutic index of lidocaine in cats is narrow. Therefore, the initial dose should be approximately 0.5 mg/kg, and the total dose should not exceed 2 mg/kg (0.9 mg/lb) in an hour. Esmolol HCl, a short-acting B-adrenoceptor blocker, and procainamide HCl, a class Ia antiarrhythmic agent, can be also administered IV in dogs and cats to control ventricular arrhythmias during anesthesia.

In the case described in the present report, pneumothorax was documented and therapeutic thoracocentesis was performed prior to the induction of anesthesia. Moderate to severe pneumothorax should be corrected prior to the induction of anesthesia. In addition, it may be necessary to repeat thoracocentesis or insert a thoracostomy tube if air continues to accumulate within the pleural space. Because the planned surgical procedure included thoracotomy and thoracostomy tube placement, repeated thoracocentesis was considered adequate in the preoperative period in this case.

Some anesthetic agents, most notably thiobarbiturates and halothane, are associated with the development of arrhythmias,² and in patients with a high likelihood of arrhythmias, these agents should be avoided. Sedative and anesthetic agents used in the cat described in the present report have minimal arrhythmogenic effects, and it is unlikely that they contributed to the ventricular tachyarrhythmia. Ketamine increases sympathetic outflow,⁹ can induce tachyarrhythmias, and could possibly have contributed to initiating or maintaining the ventricular arrhythmia in this cat. However, whereas ketamine lowers the arrhythmogenic dose of epinephrine in halothane-anesthetized cats, this is not true for isoflurane- or sevoflurane-anesthetized cats.¹⁰ In most situations, ketamine is considered antiarrhythmic in nature.¹¹

During anesthesia, compression atelectasis can develop in the dependent lung. After anesthetic induction, the cat was positioned in left lateral recumbency to allow preparation of the right hemithorax for surgery. Although this positioning was necessary for surgical preparation, oxygenation may have been improved if the patient could have remained in sternal recumbency or if the cat had been placed with the more affected lung in a dependent position.

Immediately after anesthetic induction, indirect oscillometric measurement of blood pressure indicated that the patient was hypertensive. In animals undergoing general anesthesia, hypertension can be caused by preexisting disease (eg, renal disease or hyperthyroidism), errors in drug administration (eg, administration of vasopressor drugs), or sympathetic stimulation. Sympathetic stimulation secondary to a light plane of anesthesia, ketamine administration, and hypoxia may all have been causes of hypertension in this cat.

In the cat described in the present report, surgical resection of the right cranial lung lobe proceeded without further complications. Multifocal, raised, white to yellow nodules were seen along the right side of the thoracic wall and mediastinum and were judged to be unresectable. A thoracostomy tube and esophageal feeding tube were placed, and the cat recovered from anesthesia without incident. The fentanyl infusion was continued at a lower rate, titrated to effect (2.0 to 7.5 μg/kg/h [0.9 to 3.4 μg/lb/h]), to provide postoperative analgesia. In addition, meloxicam (0.1 mg/kg [0.045 mg/lb], IV, once) and bupivacaine HCl (1 mg/kg [0.45 mg/lb], administered via the thoracostomy tube, q 6 h) were administered to provide multimodal analgesia. Itraconazole (1 mg/kg, q 24 h) was given via the esophageal tube. The cat developed disseminated intravascular coagulation and required transfusions of fresh frozen plasma and packed RBCs but survived to discharge.