ECG of the Month

Giorgia Santarelli Veterinary Hospital, University of Murcia, Campus Espinardo, 30100 Murcia, Spain

Search for other papers by Giorgia Santarelli in
Current site
Google Scholar
PubMed
Close
 DVM, MSc
,
Marco Baron Toaldo Veterinary Hospital, University of Murcia, Campus Espinardo, 30100 Murcia, Spain

Search for other papers by Marco Baron Toaldo in
Current site
Google Scholar
PubMed
Close
 DVM, PhD
, and
M Josefa Fernández del Palacio Department of Veterinary Medical Sciences, Alma Mater Studiorum, University of Bologna, Via Tolara di Sopra 50, 40064 Ozzano Emilia, Italy

Search for other papers by M Josefa Fernández del Palacio in
Current site
Google Scholar
PubMed
Close
 DVM, PhD

A 13-year-old 6-kg (13.2-lb) sexually intact female mixed-breed dog was evaluated because of a 2-week history of lethargy and inappetence. On physical examination, the dog was alert and responsive, with a body condition score of 5 on a scale of 1 to 9. Mucous membranes were slightly pale, capillary refill time was < 2 seconds, and rectal temperature was 38.3°C (100.9°F). Mean heart rate was approximately 128 beats/min, and no femoral pulse irregularities were identified. Mucopurulent vulvar discharge was present, and abdominal distension and signs of pain were detected on palpation. Auscultation of the left hemithorax revealed a grade 3/6 systolic murmur over the cardiac apex.

Survey abdominal radiography revealed a soft tissue opacity (suggestive of a tubular structure) in the caudal portion of the abdomen, and pyometra was strongly suspected. A CBC revealed neutrophilic leukocytosis with a left shift and mild nonregenerative anemia. Serum biochemical abnormalities included hypoalbuminemia, mildly high BUN concentration, and hyperphosphatemia. Transthoracic echocardiographya was performed prior to anesthesia to evaluate the heart murmur; findings revealed myxomatous mitral valve disease (MMVD) without left atrial enlargement (American College of Veterinary Internal Medicine stage B11). Laparotomy was recommended.

During the procedure, pyometra with perforation of the uterus but no apparent signs of diffuse peritonitis were evident, and ovariohysterectomy and peritoneal lavage were performed. The dog recovered uneventfully from anesthesia and was hospitalized for postoperative care. No rhythm disturbances were recorded during anesthesia and surgery. Treatment with cephalexin, marbofloxacin, pantoprazole sodium, lactated Ringer solution, and IV boluses of methadone hydrochloride was initiated. On the day after surgery, signs of severe abdominal pain were detected on palpation, and an IV constant rate infusion of morphine hydrochloride and lidocaine was started; at that time, methadone administration was discontinued. Metronidazole was added to the treatment regimen.

On the third day of hospitalization, rhythm abnormalities were detected on auscultation. At that time, the dog's rectal temperature was 37.6°C (99.7°F), respiratory rate was 36 breaths/min, and systolic arterial blood pressure was 140 mm Hg; signs of moderate abdominal pain were present. A CBC revealed severe neutrophilic leukocytosis with a left shift. Serum electrolyte concentrations were within reference limits, and a rapid immunochromatographic troponin testb revealed high serum cardiac troponin I (cTnI) concentration (detection limit, 1 ng/mL). Abdominal ultrasonographic findings were consistent with uterine stump granuloma and peritonitis, and systemic inflammatory response syndrome was considered likely on the basis of clinical and laboratory findings.2 Six-lead surface ECG was performed (Figure 1).

Figure 1—
Figure 1—

Six-lead surface ECG tracing obtained from a 13-year-old sexually intact female mixed-breed dog with systemic inflammatory response syndrome 2 days after surgical treatment of pyometra and a perforated uterus. Notice the episodes of nonsustained ventricular tachycardia with wide and bizarre QRS complexes of ventricular origin. Paper speed = 25 mm/s; 10 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 247, 9; 10.2460/javma.247.9.1019

ECG interpretation

The ECG examination revealed nonsustained ventricular tachycardia (mean heart rate, 150 beats/min; Figure 1) that was not associated with hemodynamic consequences. The infusion rate of morphine and lidocaine was doubled to control pain. On the fifth day of hospitalization, repeated ECG examination revealed changes in heart rhythm (Figure 2). The repeated 6-lead surface ECG tracing revealed an irregular rhythm with a mean heart rate of 140 beats/min. The P waves and QRS complexes were independent (without a fixed temporal relationship to each other), consistent with atrioventricular (AV) dissociation. The atrial rate was similar to the ventricular rate. When measurable, the atrial cycle length was approximately 0.46 seconds (instantaneous heart rate, 130 beats/min); however, the interval varied slightly from beat to beat, and sometimes P waves were not detected. The PQ intervals were variable (0.02 to 0.28 seconds; reference interval,3 0.05 to 0.09 seconds), and P waves were not consistently observed; when present, they had normal axis (+90°; reference interval,4 −18° to +90°), amplitude (0.3 mV; upper reference limit,3 < 0.4 mV), and duration (0.03 seconds; upper reference limit,3 < 0.04 seconds). The QRS complexes had variable morphology; the prevalent form of QRS complex was wide, bizarre, and splintered (0.22 seconds; upper reference limit,3 < 0.05 seconds) with an rR’ morphology (R'-wave amplitude, 2.2 mV; upper reference limit,3 < 2.5 mV) in the inferior leads, sS’ morphology in the aVr lead, and qRsr’ morphology in the aVL lead (mean electrical axis of the QRS complex on the frontal plane, +52°). The QT intervals were apparently normal (0.2 seconds; reference interval,3 0.07 to 0.2 seconds). A few QRS complexes were negative in the inferior leads (rS morphology), with a mean electrical axis on the frontal plane of −45°, and some fusion complexes were identified. On the basis of these findings, the diagnosis was multiform accelerated idioventricular rhythm coupled to isorhythmic atrioventricular dissociation (IAVD) with type I synchronization. Retrograde conduction to the atria was suspected because P waves were absent and not buried in the QRS complexes. A ladder (Lewis) diagram was created to illustrate the proposed mechanisms (Figure 3).

Figure 2—
Figure 2—

Six-lead surface ECG tracing obtained from the dog in Figure 1 on the fifth day after hospitalization. The heart rhythm is irregular. The P waves (arrows) and QRS complexes are independent, with variable PQ intervals. Wide and bizarre QRS complexes with variable morphology are present, suggesting multifocal ventricular origin. Retrograde conduction to the atria is suspected when P waves are absent and not buried in the QRS complexes. The first, seventh, and twelfth complexes are fusion complexes. Paper speed = 50 mm/s; 10 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 247, 9; 10.2460/javma.247.9.1019

Figure 3—
Figure 3—

Lead II ECG tracing from the ECG recording in Figure 2 and a ladder (Lewis) diagram of the rhythm disturbance in the same dog. In the ladder diagram, the upper zone represents atrial activation (A), the middle zone represents AV conduction (AV), and the lower zone represents ventricular activation (V). Notice that the atrial and ventricular activations are independent. The sixth ventricular beat is a ventricular fusion complex; the seventh ventricular beat conducts retrogradely back to the atria. Paper speed = 50 mm/s; 10 mm = 1 mV

Citation: Journal of the American Veterinary Medical Association 247, 9; 10.2460/javma.247.9.1019

The dog's arrhythmia was still hemodynamically unimportant, and no specific treatment was initiated. Because signs of abdominal pain on palpation were no longer present, the morphine-lidocaine constant rate infusion was discontinued, and analgesia was provided by means of IV boluses of morphine. Furthermore, metronidazole administration was discontinued, and clindamycin administration was initiated. On the sixth day of hospitalization, marked improvement of the dog's general status was noted; morphine administration was interrupted, and buprenorphine and meloxicam were added to the treatment regimen. A repeated ECG examination performed prior to discharge from the hospital 7 days after surgery revealed restoration of sinus rhythm and unremarkable QRS complexes. All previous IV treatments were discontinued, and the dog was administered oral marbofloxacin for 10 days. Fifteen days after discharge from the hospital, the dog had recovered completely and had a stable sinus rhythm. At that time, serum cTnI concentration, as measured by a commercially available immunometrical method,c was normal.

Discussion

Atrioventricular dissociation is a rhythm disturbance characterized by dissociated activity of the atria and ventricles, which are driven by independent pacemakers.5–8 It is always secondary to an underlying rhythm abnormality induced by 1 of 3 factors (or a combination thereof) as follows: slowing of the dominant pacemaker of the heart, which allows escape of a subsidiary pacemaker (either junctional or ventricular); acceleration of a subsidiary or latent pacemaker, which assumes control of the ventricles; or development of a conduction disturbance, generally at the AV junction.5 Isorhythmic atrioventricular dissociation occurs when the rates of the independent atrial and ventricular pacemakers are equal or almost equal over relatively long periods.6–9

During IAVD, 2 patterns of relationship between P waves and QRS complexes may be detected. Type I synchronization is characterized by a rhythmic fluctuation of the PQ interval, and the P waves may oscillate gradually back and forth across the QRS complexes. Type II synchronization is characterized by constant or almost constant PQ intervals, with P waves preceding R waves.9 For the dog of the present report, a diagnosis of multiform accelerated idioventricular rhythm coupled to IAVD with type I synchronization was made.

Accelerated idioventricular rhythm is a common arrhythmia in hospitalized dogs, even those without underlying primary cardiac disease. In fact, it is commonly observed in association with abdominal diseases, following gastric dilatation-volvulus surgery, or secondary to trauma or neurologic diseases.10 In dogs with pyometra, arrhythmias can be the result of direct myocardial damage or a consequence of the systemic release of inflammatory mediators or bacterial constituents (eg, endotoxins) from the infected uterus.2,11

The general status of the dog of this report had deteriorated at the time that the arrhythmia was recognized, and signs of systemic inflammatory response syndrome and peritonitis were present. High serum cTnI concentration was detected when the arrhythmia developed, indicative of myocardial damage. However, preoperative concentration of cTnI was not available, and it cannot be concluded that myocardial damage developed or worsened after surgery. For the dog of this report, a diagnosis of MMVD had been made prior to anesthesia and surgery. Susceptibility to the development of arrhythmias or increased cTnI because of the underlying cardiopathy cannot be ruled out, even though it seems unlikely because of the absence of echocardiographic signs of cardiac remodeling at the time of diagnosis and the postoperative normalization of serum cTnI concentration.

Another possible cause for the development of arrhythmias is cardioactive drug toxicosis. In the case described in the present report, a morphine-lidocaine constant rate infusion was administered for 3 days prior to development of the arrhythmia. Proarrhythmic effects of lidocaine are not common adverse effects in dogs,12 but an idiosyncratic drug reaction to prolonged drug administration cannot be completely excluded. Restoration of sinus rhythm occurred approximately 46 hours after stopping the infusion. Because lidocaine is stored in adipose tissues, and some continues to be released for several hours after cessation of administration,12 the arrhythmia could have resolved when lidocaine had been totally cleared from the body. One might speculate that sinus node depression in the dog of this report could have been the mechanism underlying AV dissociation. Regardless, the dog developed a rare and transient rhythm disturbance as a postsurgical complication (besides peritonitis) after undergoing laparotomy for pyometra and a perforated uterus.

a.

iE33 ultrasound system, Philips Medical Systems, Andover, Mass.

b.

Troponitest+, All Diag, Strasbourg, France.

c.

Immulite, Troponin I, Diagnostic Products Corp, Los Angeles, Calif.

References

  • 1. Atkins C, Bonagura J, Ettinger S, et al. ACVIM Consensus Statement: guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med 2009; 23: 11421150.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2. Fransson BA, Lagerstedt A, Bergstrom A, et al. C-reactive protein, tumor necrosis factor α, and interleukin-6 in dogs with pyometra and SIRS. J Vet Emerg Crit Care 2007; 17: 373381.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3. Tilley LP. Analysis of canine P-QRS-T deflections. In: Tilley LP, ed. Essentials of canine and feline electrocardiography: interpretation and treatment. 2nd ed. Philadelphia: Lea & Febiger, 1985; 58.

    • Search Google Scholar
    • Export Citation
  • 4. Santilli RA, Perego M. Genesi e interpretazione delle onde elettrocardiografiche. In: Elettrocardiografia del cane e del gatto. Milan: Elsevier Inc, 2009; 3946.

    • Search Google Scholar
    • Export Citation
  • 5. Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Libby P, Bonow RO, Mann DL, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. 8th ed. Philadelphia: Saunders Elsevier, 2008; 863932.

    • Search Google Scholar
    • Export Citation
  • 6. Waldo AL, Vitikainen KJ, Harris PD, et al. The mechanism of synchronization in isorhythmic A-V dissociation: some observations on the morphology and polarity of the P wave during retrograde capture of atria. Circulation 1968; 38: 880898.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Levy MN, Zieske H. Mechanism of synchronization in isorhythmic dissociation. I. Experiments on dogs. Circ Res 1970; 27: 429443.

  • 8. Levy MN, Edflstein J. The mechanism of synchronization in isorhythmic A-V dissociation. II. Clinical studies. Circulation 1970; 42: 689699.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Perego M, Ramera L, Santilli RA. Isorhythmic atrioventricular dissociation in Labrador Retrievers. J Vet Intern Med 2012; 26: 320325.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10. Kittleson MD. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: Mosby, 1998; 449494.

    • Search Google Scholar
    • Export Citation
  • 11. Hagman R, Lagerstedt A, Fransson BA, et al. Cardiac troponin I levels in canine pyometra. Acta Vet Scand 2007; 49: 613.

  • 12. Moïse NS. Diagnosis and management of canine arrhythmias. In: Fox FR, Sisson D, Moïse NS, eds. Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia: WB Saunders Co, 1999; 331385.

    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Six-lead surface ECG tracing obtained from a 13-year-old sexually intact female mixed-breed dog with systemic inflammatory response syndrome 2 days after surgical treatment of pyometra and a perforated uterus. Notice the episodes of nonsustained ventricular tachycardia with wide and bizarre QRS complexes of ventricular origin. Paper speed = 25 mm/s; 10 mm = 1 mV.

  • Figure 2—

    Six-lead surface ECG tracing obtained from the dog in Figure 1 on the fifth day after hospitalization. The heart rhythm is irregular. The P waves (arrows) and QRS complexes are independent, with variable PQ intervals. Wide and bizarre QRS complexes with variable morphology are present, suggesting multifocal ventricular origin. Retrograde conduction to the atria is suspected when P waves are absent and not buried in the QRS complexes. The first, seventh, and twelfth complexes are fusion complexes. Paper speed = 50 mm/s; 10 mm = 1 mV.

  • Figure 3—

    Lead II ECG tracing from the ECG recording in Figure 2 and a ladder (Lewis) diagram of the rhythm disturbance in the same dog. In the ladder diagram, the upper zone represents atrial activation (A), the middle zone represents AV conduction (AV), and the lower zone represents ventricular activation (V). Notice that the atrial and ventricular activations are independent. The sixth ventricular beat is a ventricular fusion complex; the seventh ventricular beat conducts retrogradely back to the atria. Paper speed = 50 mm/s; 10 mm = 1 mV

  • 1. Atkins C, Bonagura J, Ettinger S, et al. ACVIM Consensus Statement: guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med 2009; 23: 11421150.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 2. Fransson BA, Lagerstedt A, Bergstrom A, et al. C-reactive protein, tumor necrosis factor α, and interleukin-6 in dogs with pyometra and SIRS. J Vet Emerg Crit Care 2007; 17: 373381.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3. Tilley LP. Analysis of canine P-QRS-T deflections. In: Tilley LP, ed. Essentials of canine and feline electrocardiography: interpretation and treatment. 2nd ed. Philadelphia: Lea & Febiger, 1985; 58.

    • Search Google Scholar
    • Export Citation
  • 4. Santilli RA, Perego M. Genesi e interpretazione delle onde elettrocardiografiche. In: Elettrocardiografia del cane e del gatto. Milan: Elsevier Inc, 2009; 3946.

    • Search Google Scholar
    • Export Citation
  • 5. Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Libby P, Bonow RO, Mann DL, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. 8th ed. Philadelphia: Saunders Elsevier, 2008; 863932.

    • Search Google Scholar
    • Export Citation
  • 6. Waldo AL, Vitikainen KJ, Harris PD, et al. The mechanism of synchronization in isorhythmic A-V dissociation: some observations on the morphology and polarity of the P wave during retrograde capture of atria. Circulation 1968; 38: 880898.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7. Levy MN, Zieske H. Mechanism of synchronization in isorhythmic dissociation. I. Experiments on dogs. Circ Res 1970; 27: 429443.

  • 8. Levy MN, Edflstein J. The mechanism of synchronization in isorhythmic A-V dissociation. II. Clinical studies. Circulation 1970; 42: 689699.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9. Perego M, Ramera L, Santilli RA. Isorhythmic atrioventricular dissociation in Labrador Retrievers. J Vet Intern Med 2012; 26: 320325.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10. Kittleson MD. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: Mosby, 1998; 449494.

    • Search Google Scholar
    • Export Citation
  • 11. Hagman R, Lagerstedt A, Fransson BA, et al. Cardiac troponin I levels in canine pyometra. Acta Vet Scand 2007; 49: 613.

  • 12. Moïse NS. Diagnosis and management of canine arrhythmias. In: Fox FR, Sisson D, Moïse NS, eds. Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia: WB Saunders Co, 1999; 331385.

    • Search Google Scholar
    • Export Citation

Advertisement