ECG of the Month

Michael F. Cocchiaro William R. Pritchard Veterinary Medical Teaching Hospital, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

Search for other papers by Michael F. Cocchiaro in
Current site
Google Scholar
PubMed
Close
 DVM
and
Mark D. Kittleson Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

Search for other papers by Mark D. Kittleson in
Current site
Google Scholar
PubMed
Close
 DVM, PhD, DACVIM

A 12-year-old 39-kg (85.8-lb) castrated male Labrador Retriever was referred for evaluation and surgical correction of a left humeral fracture. The dog had primarily been living outdoors at an equine boarding facility. The dog had been otherwise healthy until non–weight-bearing lameness of the left thoracic limb was noticed by the owner. Although unwitnessed, it was thought that the dog's lameness was the result of being kicked by a horse. Prior to the referral evaluation, the referring veterinarian obtained radiographic views of the left thoracic limb and prescribed medication for pain control.

At the initial referral evaluation, the dog was bright, alert, and panting. Rectal temperature was 38.5°C (101.3°F); mucous membranes were pink, and capillary refill time was 1.5 seconds. The heart rate was 120 beats/min, and the rhythm was regular. No cardiac murmur was ausculted. Femoral pulses were regular, strong, and detected simultaneously in both pelvic limbs.

Initial diagnostic evaluations included a CBC, serum biochemical analyses, urinalysis, thoracic radiography, radiography of the left thoracic limb, and abdominal ultrasonography. Serum biochemical findings included mildly high liver enzyme activities and high creatine kinase activity (802 U/L; reference range, 51 to 399 U/L). Thoracic radiography revealed no cardiovascular or pulmonary abnormalities. Radiography of the left humerus revealed a medial condylar fracture with luxation of the elbow joint. Abdominal ultrasonography revealed large adrenal glands, hepatomegaly, and an incidental renal cyst.

Amputation of the left thoracic limb was elected as the treatment of choice for this dog. Prior to anesthesia, the dog was premedicated with hydromorphone (0.1 mg/kg [0.045 mg/lb], IV) and atropine sulfate (0.04 mg/kg [0.018 mg/lb], IV). Administration of these drugs resulted in marked tachycardia, and the amputation procedure was postponed until the results of a full cardiac evaluation were known. Electrocardiography was performed.

ECG Interpretation

Electrocardiography revealed rapid supraventricular tachycardia with a ventricular rate of approximately 300 complexes/min and an atrial rate of approximately 600 complexes/min (Figure 1). Atrial flutter with a conduction ratio of 2:1 (ie, 2 P or F [flutter] waves for each QRS complex) was suspected on the basis of the regularity of the rhythm and rate of atrial depolarization. It was thought that this arrhythmia was most likely a result of myocardial trauma.

Figure 1—
Figure 1—

Lead II ECG tracing obtained from a 12-year-old Labrador Retriever that was evaluated because of a tachyarrhythmia that had developed following administration of hydromorphone and atropine sulfate in preparation for amputation of an injured thoracic limb. The ventricular rate is 300 complexes/min, the QRS complex duration appears normal, and the rhythm is regular. P waves are present before and also immediately after each QRS complex; thus, the atrial rate is approximately 600 complexes/min. These findings are consistent with atrial flutter. The conduction ratio is 2:1 (ie, 2 P or F waves for each QRS complex). Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 236, 8; 10.2460/javma.236.8.836

The dog was admitted to the hospital's intensive care unit. The treatment plan included arrhythmia management, echocardiography, and thoracic limb amputation. One dose of diltiazem hydrochloride (0.25 mg/kg [0.11 mg/lb]) was administered slowly IV. Electrocardiography (leads I, II, and III) was performed after diltiazem administration. A supraventricular tachyarrhythmia was detected; the ventricular response rate was irregular (40 to 90 QRS complexes/min), and the atrial rate was variable but most commonly approximately 750 complexes/min (Figure 2). Baseline waveforms (shape, duration, amplitude, and direction) were continuously changing during the ECG examination.

Figure 2—
Figure 2—

Lead I, II, and III ECG tracings (upper, middle, and lower tracings, respectively) obtained from the dog in Figure 1 after diltiazem (0.25 mg/kg [0.11 mg/lb]) was administered IV. The ventricular rhythm is irregular with an atrioventricular conduction ratio of 9:1 to 26:1; the atrial rate is 750 complexes/min, and the ventricular rate ranges from 40 to 90 QRS complexes/min. These findings are consistent with atrial fibrillation. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 236, 8; 10.2460/javma.236.8.836

Atrial fibrillation was diagnosed on the basis of the atrial rate, irregular nature of the ventricular rhythm, and continuously changing baseline waveforms.1 Echocardiography performed after achieving heart rate control revealed normal cardiac chamber dimensions with no evidence of underlying cardiac disease. The dog was treated with diltiazem (0.8 mg/kg [0.36 mg/lb], PO, q 8 h); it was planned that electrical cardioversion would be attempted the following day prior to limb amputation.

Following routine induction of anesthesia the next day, the dog was placed in lateral recumbency and the right and left apex beats were located via palpation. The defibrillator output was synchronized to the dog's R wave. A biphasic 30-J shock (0.8 J/kg) was delivered transthoracically at the level of the apex beats via pediatric defibrillator paddlesa (Figure 3). Cardioversion was successful. Sinus rhythm was maintained throughout the duration of the surgical procedure and was evident prior to the dog's discharge from the hospital 2 days later. Electrocardiographic evaluation 1 month after cardioversion revealed sinus rhythm.

Figure 3—
Figure 3—

Continuous lead II ECG tracing obtained from the dog in Figure 1 before and immediately after administration of a biphasic direct current electrical impulse (30 J). The vertical arrows mark the position of a QRS complex, indicating that the cardiac defibrillator appropriately identified the R wave and would deliver the cardioverting electrical shock during ventricular depolarization. The shock was delivered after the second to last arrow on the tracing (middle panel) and resulted in atrial fibrillation with an increased ventricular response rate followed by conversion to sinus rhythm. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 236, 8; 10.2460/javma.236.8.836

Discussion

Cardiac arrhythmias have been reported as a complication of blunt trauma in humans.2 Blunt thoracic trauma can induce various types of arrhythmias including ventricular and supraventricular extrasystoles, atrial fibrillation and flutter, supraventricular and ventricular paroxysmal tachycardias, and ventricular fibrillation.2 Atrial fibrillation, one of the most common cardiac arrhythmias encountered in clinical practice, was found to be the most common arrhythmia that develops after thoracic injury in humans.2

For the dog of this report, it appeared likely that it had trauma-induced atrial flutter as a result of being kicked by a horse. Atrial flutter is the prototypic macroreentrant atrial rhythm. Typical atrial flutter is the result of a reentrant rhythm in the right atrium that is constrained anteriorly by the tricuspid valve annulus and posteriorly by the crista terminalis and Eustachian ridge.3 The flutter can circulate in a counterclockwise direction (typical flutter) or in a clockwise direction (atypical flutter) around the tricuspid valve annulus in the frontal plane. Both typical and atypical atrial flutter involve the same circuit and are therefore constrained by the same anatomic barriers. Several forms of atrial flutter (typically associated with anatomic or functional conduction barriers in the atria) have been identified.3

Atrial flutter is characterized by a very high atrial rate; in dogs, the rate is generally in the range of 450 to 600 depolarizations/min. This high rate results in a rapid succession of P waves called F waves. The F waves appear as atrial complexes of constant morphology, polarity, and cycle length.1 The ventricular response rate to atrial flutter commonly is 2:1 to 4:1 and regular, but it may be irregular.1 The QRS complexes during atrial flutter are most commonly identical to the QRS complexes detected during sinus rhythm because ventricular depolarization occurs via the normal intraventricular pathways.

In the dog of this report, treatment with diltiazem resulted in the degeneration of atrial flutter to atrial fibrillation. Atrial fibrillation is an arrhythmia characterized by disorganized atrial depolarizations without effective atrial contraction.3 During atrial fibrillation, electrical activity of the atrium can be detected in ECG tracings as small, irregular baseline undulations of variable amplitude and morphology (known as fibrillation [f] waves), which occur at a rate of > 600 depolarizations/min.1 The ventricular response rate during atrial fibrillation is always irregular because the refractory period and conductivity of the atrioventricular (AV) node are determinants of ventricular rate. An important property of the AV node is decremental conduction—as the frequency of node stimulation increases, the rate of conduction through the node decreases. If the decrement becomes sufficiently large, conduction through the AV node ceases. Although impulses fail to propagate through the AV node, they still penetrate into the AV node and have an effect on the conduction properties of the AV node. This is called concealed conduction. Concealed conduction affects the refractory period of the AV node. During atrial fibrillation, wherein the AV node is bombarded continuously by rapid depolarizations, this effect on the refractory period varies from beat to beat. As a result, the interval between ventricular depolarizations (ie, QRS complexes) varies as some depolarizations propagate through the AV node and others are filtered out in a highly irregular fashion.4 In humans with atrial flutter, treatment with calcium channel-blocking agents may result in development of atrial fibrillation,3 and a similar treatment effect was evident in the dog of this report.

Proposed mechanisms by which cardiac arrhythmias develop following blunt trauma include abnormal perfusion patterns, vagal sympathetic reflex, decreased PaO2, and aberrant conduction by damaged myocardial cells (myocardial contusion). In a study5 of swine that received a series of low-energy impacts to the thoracic wall, the risk and type of arrhythmia that developed were dependent on when the impact occurred during the cardiac electrical cycle. In addition, the risk of arrhythmia was directly proportional to both the force and speed of the impact and inversely proportional to the size of the contact area. Similar findings were obtained in a study6 of the incidence of and risk factors for atrial fibrillation in 453 humans in a surgical intensive care unit. In that study population, the odds for development of atrial fibrillation were higher (odds ratio, 16.84; 95% confidence interval, 4.00 to 71.20) in patients with blunt thoracic trauma.

Although results of auscultation during the initial referral examination were considered normal, it is possible that the dog of this report did have atrial flutter or atrial fibrillation at that time. Abnormalities were detected via ECG after the dog was premedicated, but there are no reports in the veterinary medical literature describing the development of atrial flutter following administration of atropine, to the authors' knowledge. In a report7 of 2 humans with blunt thoracic trauma, arrhythmias developed within hours to days after the traumatic event. Although atrial flutter in the dog of this report was most likely the result of blunt thoracic trauma, another possible explanation is that administration of hydromorphone induced an increase in vagal tone, which caused the arrhythmia. Increases in vagal tone prolong refractory periods in ventricular muscle and do not promote fibrillation, but such increases have the opposite effects in atrial tissue. In the atria, increases in autonomic tone shorten the refractory period of atrial tissue, thereby promoting the formation of reentrant wavelets and allowing the development and perpetuation of atrial fibrillation.8

It is unknown whether conversion to sinus rhythm would have occurred in the dog of this report if intervention was not performed and the myocardium had time to heal. However, impaired cardiac output associated with atrial flutter may result in decreased ventricular diastolic filling time, and atrial flutter can lead to tachycardia-induced cardiomyopathy and congestive heart failure if allowed to continue at a rapid ventricular response rate.9 Because many dogs may have no clinical signs after the development of supraventricular tachyarrhythmia, it may be beneficial to perform screening procedures for cardiac arrhythmias, such as ECG, in patients with blunt thoracic trauma both at the initial examination and 24 to 48 hours after admission to the hospital.

a.

Zoll M Series cardiac defibrillator, Chelmsford, Mass.

References

  • 1.

    Waldo AL. Atrial flutter. In: Cardiac arrhythmia: mechanisms, diagnosis and management. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2001;501516.

    • Search Google Scholar
    • Export Citation
  • 2.

    Ismailov RM, Weiss HB, Ness RB, et al. Trauma associated with cardiac dysrhythmias: results from a large matched case-control study. J Trauma 2007;62:11861191.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3.

    Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Zipes DP, Libby P, Bonow RO, et al, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. 8th ed. Philadelphia: Saunders, 2008;863920.

    • Search Google Scholar
    • Export Citation
  • 4.

    Mangin L, Vinet A, Pagé P, et al. Effects of antiarrhythmic drug therapy on atrioventricular nodal function during atrial fibrillation in humans. Europace 2005;7(suppl 2):7182.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Link MS, Wang PJ, Pandian NG, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med 1998;338:18051811.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Seguin P, Signouret T, Laviolle B, et al. Incidence and risk factors of atrial fibrillation in a surgical intensive care unit. Crit Care Med 2004;32:722726.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Sakka SG, Huettemann E, Giebe W, et al. Late cardiac arrhythmias after blunt chest trauma. Intensive Care Med 2000;26:792795.

  • 8.

    Maisel WH. Autonomic modulation preceding the onset of atrial fibrillation. J Am Coll Cardiol 2003;42:12691270.

  • 9.

    Umana E, Solares CA, Alpert MA. Tachycardia-induced cardiomyopathy. Am J Med 2003;114:5155.

Contributor Notes

Address correspondence to Dr. Cocchiaro (mfcocchiaro@ucdavis.edu).
  • Figure 1—

    Lead II ECG tracing obtained from a 12-year-old Labrador Retriever that was evaluated because of a tachyarrhythmia that had developed following administration of hydromorphone and atropine sulfate in preparation for amputation of an injured thoracic limb. The ventricular rate is 300 complexes/min, the QRS complex duration appears normal, and the rhythm is regular. P waves are present before and also immediately after each QRS complex; thus, the atrial rate is approximately 600 complexes/min. These findings are consistent with atrial flutter. The conduction ratio is 2:1 (ie, 2 P or F waves for each QRS complex). Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Lead I, II, and III ECG tracings (upper, middle, and lower tracings, respectively) obtained from the dog in Figure 1 after diltiazem (0.25 mg/kg [0.11 mg/lb]) was administered IV. The ventricular rhythm is irregular with an atrioventricular conduction ratio of 9:1 to 26:1; the atrial rate is 750 complexes/min, and the ventricular rate ranges from 40 to 90 QRS complexes/min. These findings are consistent with atrial fibrillation. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 3—

    Continuous lead II ECG tracing obtained from the dog in Figure 1 before and immediately after administration of a biphasic direct current electrical impulse (30 J). The vertical arrows mark the position of a QRS complex, indicating that the cardiac defibrillator appropriately identified the R wave and would deliver the cardioverting electrical shock during ventricular depolarization. The shock was delivered after the second to last arrow on the tracing (middle panel) and resulted in atrial fibrillation with an increased ventricular response rate followed by conversion to sinus rhythm. Paper speed = 25 mm/s; 1 cm = 1 mV.

  • 1.

    Waldo AL. Atrial flutter. In: Cardiac arrhythmia: mechanisms, diagnosis and management. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2001;501516.

    • Search Google Scholar
    • Export Citation
  • 2.

    Ismailov RM, Weiss HB, Ness RB, et al. Trauma associated with cardiac dysrhythmias: results from a large matched case-control study. J Trauma 2007;62:11861191.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3.

    Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Zipes DP, Libby P, Bonow RO, et al, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. 8th ed. Philadelphia: Saunders, 2008;863920.

    • Search Google Scholar
    • Export Citation
  • 4.

    Mangin L, Vinet A, Pagé P, et al. Effects of antiarrhythmic drug therapy on atrioventricular nodal function during atrial fibrillation in humans. Europace 2005;7(suppl 2):7182.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Link MS, Wang PJ, Pandian NG, et al. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med 1998;338:18051811.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Seguin P, Signouret T, Laviolle B, et al. Incidence and risk factors of atrial fibrillation in a surgical intensive care unit. Crit Care Med 2004;32:722726.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Sakka SG, Huettemann E, Giebe W, et al. Late cardiac arrhythmias after blunt chest trauma. Intensive Care Med 2000;26:792795.

  • 8.

    Maisel WH. Autonomic modulation preceding the onset of atrial fibrillation. J Am Coll Cardiol 2003;42:12691270.

  • 9.

    Umana E, Solares CA, Alpert MA. Tachycardia-induced cardiomyopathy. Am J Med 2003;114:5155.

Advertisement