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Samantha J. Salmon Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, MN 55108.

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Christopher D. Stauthammer Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, MN 55108.

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Caroline F. Baldo Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, MN 55108.

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A 14-month-old 1.31-kg (2.88-lb) spayed female Toy Poodle was evaluated on an emergency basis because of sudden-onset non–weight-bearing lameness of the left forelimb. Radiography of the limb revealed complete, transverse distal diaphyseal fractures of the left radius and ulna with minimal displacement and moderate soft tissue swelling. The dog had previously undergone repair of a radial fracture in the opposite limb, tibial tuberosity transposition, and block recession trochleoplasty. There were no other known comorbidities reported, and the dog was not currently receiving any medications. At the evaluation, the dog was alert, responsive, and adequately hydrated. Its rectal temperature of 38.3°C (100.9°F) and capillary refill time of < 2 seconds were considered normal, but pulse rate (180 beats/min) and respiratory rate (panting) were high. Results of a cardiopulmonary examination were unremarkable. Abnormal physical examination findings included a non–weight-bearing lameness and mild carpal laxity of the left forelimb.

The dog was administered hydromorphone hydrochloride (0.53 mg/kg [0.24 mg/lb], IV) intermittently for pain management. A whole blood biochemical panel revealed high BUN concentration (56 mg/dL; reference interval, 8 to 35 mg/dL) and low concentrations of creatinine (0.4 mg/dL; reference interval, 0.8 to 1.5 mg/dL), potassium (2.7 mmol/L; reference interval, 3.4 to 4.9 mmol/L), and chloride (102 mmol/L; reference interval, 112 to 120 mmol/L). Whole blood total CO2 concentration was high (34 mmol/L; reference interval, 18.6 to 28.4 mmol/L). Anion gap, Hct, and concentrations of glucose, sodium, ionized calcium, and hemoglobin were within reference intervals. In preparation for general anesthesia, the dog was sedated with dexmedetomidine hydrochloride (0.0039 mg/kg [0.0018 mg/lb], IM, once) and methadone hydrochloride (0.46 mg/kg [0.21 mg/lb], IV, once). Anesthesia was subsequently induced with propofol (0.76 mg/kg [0.35 mg/lb], IV, once) and maintained via inhalation (1 L/min) of isoflurane (1% to 2%) in oxygen. Surgical reduction of the dog's fractures was accomplished with application of a T plate and screws.

ECG Interpretation

An initial 6-lead ECG recording (Figure 1) was obtained from the dog after anesthesia was induced. Lead II was used for analysis and revealed a normal mean electrical axis of +60 (reference interval,1 +40 to +100) as well as a normal sinus rhythm with a calculated heart rate of 100 beats/min. With regard to P waves, the duration (0.04 seconds; upper reference limit,1 0.04 seconds) and amplitude (0.4 mV; upper reference limit,1 0.4 mV) were normal and consistent. The PR interval (0.08 seconds; reference interval,1 0.06 to 0.13 seconds) was also normal and consistent. With regard to QRS complexes, the duration (0.035 seconds; upper reference limit,1 0.060 seconds) and amplitude (1.5 mV; upper reference limit,1 3.0 mV) were normal and consistent. However, the QT interval was consistently prolonged at 0.3 seconds (reference interval,1 0.15 to 0.25 seconds). The Van de Water equation2 was used to normalize the QT interval for heart rate and yielded a value of 0.34 seconds.

Figure 1—
Figure 1—

A 6-lead ECG tracing obtained from a 14-month-old Toy Poodle that developed sudden-onset non–weight-bearing lameness of the left forelimb and was subsequently anesthetized for left radius and ulna fracture repair. The dog was hypokalemic (2.7 mmol/L; reference interval, 3.4 to 4.9 mmol/L). In this initial tracing, there is normal sinus rhythm with a calculated heart rate of 100 beats/min. The P-wave, QRS-complex, and PR-interval durations and amplitudes are normal and consistent. However, the QT interval is consistently prolonged, and the corrected QT interval is 0.34 seconds. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 253, 1; 10.2460/javma.253.1.46

Given the ECG and previous clinicopathologic findings, the dog was administered a constant rate infusion of potassium chloride diluted in sterile lactated Ringer solution at a rate of 0.5 mEq/kg/h (0.23 mEq/lb/h) for approximately 75 minutes. Another whole blood biochemical panel performed immediately following potassium chloride administration revealed normalization of the potassium concentration (3.7 mmol/L; reference interval, 3.4 to 4.9 mmol/L). The remaining clinicopathologic abnormalities remained unchanged. A second 6-lead ECG recording was obtained following normalization of the potassium concentration (Figure 2). At this time (approx 100 minutes following the initial ECG assessment), the QT interval was within the reference interval (0.18 seconds); the corrected QT interval was also considered normal at 0.22 seconds.

Figure 2—
Figure 2—

A 6-lead ECG tracing obtained from the dog in Figure 1 during general anesthesia. This tracing was obtained approximately 100 minutes following the initial ECG assessment and immediately following administration of potassium chloride solution, which resulted in normalization of serum potassium concentration at 3.7 mmol/L. There is a normal sinus rhythm with a calculated heart rate of 120 beats/min. The durations and amplitudes of the P waves, QRS complexes, PR intervals, and QT intervals are consistent and normal. At this time, the corrected QT interval is 0.22 seconds. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 253, 1; 10.2460/javma.253.1.46

Discussion

Long QT syndrome (LQTS) is an inherited or acquired disorder that results in prolonged ventricular repolarization identified by increased duration of the QT interval on a surface ECG tracing.3 Inherited LQTS is a result of mutations in genes that encode for the sub-units of cardiac delayed rectifier potassium channels; these mutations are associated with altered outward flow of potassium during repolarization of the cardiac myocyte.3,4 Inherited LQTS is rare among humans5,6 and has been identified in 1 family of English Springer Spaniels.7 Acquired LQTS can be associated with several factors including administration of cardiac and noncardiac drugs3,8,9 as well as electrolyte imbalances (hypokalemia, hypocalcemia, and hypomagnesemia), acid-base disorders, female sex, and bradycardia.8–10 Both inherited and acquired LQTS can lead to syncopal episodes and cardiac-related death through development of arrhythmias such as ventricular tachycardia, ventricular fibrillation, and torsades de pointes.8 Acquired LQTS is more common than inherited LQTS in veterinary patients, and it is thought that multiple acquired factors that predispose animals to LQTS have to be present concurrently to result in development of a fatal arrhythmia.8,9

In a normal ventricular cardiac myocyte action potential, final repolarization (phase 3) is characterized by time-dependent inactivation of calcium channels, which ceases the inward flow of calcium ions while the delayed rectifier potassium channels remain open, thereby allowing potassium out of the cell until the resting membrane potential is restored at −90 mV.3,8,10–12 The delayed rectifier potassium channels' function and stability rely on extracellular potassium concentration; thus, these channels enter a nonconducting state and are rapidly internalized via endocytosis into the cardiac myocyte in the event of hypokalemia.13 This leads to increases in the action potential duration and refractory period as reflected by a prolonged QT interval on surface ECG tracings.

Identification of LQTS on surface ECG tracings is accomplished by measuring the interval between the beginning of the QRS complex and the end of the T wave, which represents the time required for ventricular depolarization and repolarization. The use of the heart rate–corrected QT interval, derived by mean of formulas such as the Van de Water formula, is recommended for clinical evaluation of LQTS because of the heart rate–dependent variance in QT intervals. Other, less well-validated equations for QT interval correction include the Fridericia equation and Bazett equation.2,14 Correction of the QT interval allows for more accurate assessment of the success of treatment of LQTS, although an exact correction of the QT interval is not achievable because of the uncontrollable variance in heart rate and inherent error of mathematical equations.2,14

When individuals have multiple predisposing factors for development of prolonged ventricular repolarization, evaluation for LQTS becomes clinically relevant to avoid development of fatal ventricular arrhythmias. The administration of dexmedetomidine and methadone and the presence of hypokalemia in the dog of the present report prompted initiation of treatment to decrease the likelihood of development of fatal ventricular arrhythmias secondary to LQTS. It should be noted that blockade of the delayed rectifier potassium channels is associated with methadone15 administration and that administration of dexmedetomidine16 is associated with factors that predispose individuals to LQTS, such as bradycardia and possible blockade of the delayed rectifier potassium channels, similar to that described for dexmedetomidine inhibition of vascular ATP-dependent potassium channels.16

References

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  • 14. Soloviev MV, Hamlin RL, Barret RM, et al. Different species require different correction factors for the QT interval. Cardiovasc Toxicol 2006;6:145157.

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  • 16. Kawano T, Yamazaki F, Chi H, et al. Dexmedetomidine directly inhibits vascular ATP-sensitive potassium channels. Life Sci 2012;90:272277.

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