ECG Interpretation

The initial ECG tracing revealed sinus tachycardia with a heart rate of 190 beats/min (Figure 1). There was evidence of P waves of normal duration (duration, 0.03 seconds; upper reference limit,² 0.04 seconds) and amplitude (amplitude, 0.05 mV; upper reference limit,² 0.4 mV) that were partially merged with prominent T waves. The PR interval was 0.13 seconds (reference range,² 0.06 to 0.13 seconds). The QRS complexes were equivocally prolonged (0.07 seconds; upper reference limit,² < 0.07 seconds). The corrected QT interval (QTc) was calculated by use of the Bazett formula³ (QT interval/[RR interval]^0.5) and was 0.39 seconds (reference range,² 0.15 to 0.24 seconds). Mild ST segment depression (depression, 0.2 mV; upper reference limit,² < 0.1 mV) was evident. Variable high-voltage T waves were evident (0.7 to 1.3 mV; upper reference limit,² 1 mV), which partially merged into the subsequent P waves.

Initial treatment included administration of butorphanol (0.2 mg/kg, IM, once), ampicillin (20 mg/kg [9.1 mg/lb], IV, q 8 h), and saline (0.9% NaCl) solution (6 mL/kg/h [2.7 mL/lb/h], IV) with supplemental potassium chloride (80 mEq/L). The betamethasone and albuterol treatments were discontinued. Blood gas analyses and ECGs were repeated at 6- to 12-hour intervals during hospitalization. After 6 hours, the dog's hypokalemia was less pronounced (3 mEq/L). At this time, a second ECG examination revealed sinus tachycardia with a heart rate of approximately 180 beats/min (Figure 2). Compared with the initial ECG findings, there were reductions in the PR interval (0.11 seconds), QT interval (0.33 seconds), QRS complex duration (0.05 seconds), and T-wave amplitude (0.2 mV) and normalization of the ST segment. Thirty-six hours after admission, the dog's serum potassium concentration (4.4 mEq/L) was within the reference range; the normalization of ECG changes was maintained, and the heart rate had decreased to 150 beats/min.

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Lead I, II, and III ECG tracings obtained from the dog in Figure 1 six hours after IV administration of saline (0.9% NaCl) solution with supplemental potassium chloride. At this time, hypokalemia was less pronounced (3 mEq/L). Sinus tachycardia (heart rate, approx 170 beats/min) is evident. Notice the reduction of the PR interval (0.11 seconds), QT interval (0.33 seconds), and QRS complex duration (0.05 seconds) as well as reduction of the T-wave amplitude (0.2 mV) and normalization of the ST segment. Paper speed = 50 mm/s; 1 cm = 1 mV

Citation: Journal of the American Veterinary Medical Association 243, 8; 10.2460/javma.243.8.1108

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In accordance with the owner's wishes, the dog was discharged from the hospital on day 3, although the respiratory signs were only mildly improved but with complete remission of weakness and resolution of acid-base, electrolyte, and ECG abnormalities. On the basis of historical, clinical, hematologic, radiographic and ultrasonographic findings, gastrointestinal and urinary tract causes for potassium loss or reduced potassium intake were unlikely. Rather, the owner had administered high dosages of albuterol, which could explain the very low serum potassium concentration as a result of β-adrenoreceptor agonist-mediated potassium translocation. This mechanism for hypokalemia was further supported by the resolution of hypokalemia on discontinuation of albuterol administration.

Discussion

The dog of this report had bronchial disease, and the ECG abnormalities were caused by severe hypokalemia as a result of oral overdosing with albuterol over a 2-year period. Albuterol is a selective β₂-adrenoreceptor agonist used in humans, dogs, cats, and horses for the treatment of airway disease, particularly bronchospasm. Albuterol administration has been associated with mild to severe hypokalemia and ECG alterations in human⁴ and veterinary medicine.⁵ The electrophysiologic effects of hypokalemia include decreased conduction velocity, shortening of the effective refractory period, prolongation of the relative refractory period, increased automaticity, and presence of early afterdepolarizations.⁶ The ECG changes related to hypokalemia are a result of its effects on repolarization and on conduction.⁶ Electrocardiographic abnormalities can include a prolonged QT interval, T-wave abnormalities, prominent U waves, and ST segment depression.⁶ Conduction abnormalities include increased QRS complex duration without a concomitant change in QRS complex configuration, increased P-wave amplitude and duration, slightly prolonged PR interval, bradycardia, atrioventricular block, and cardiac arrest.⁶

For the dog of the present report, the initial ECG tracing was obtained when the dog's serum potassium concentration was 1.7 mEq/L. That tracing revealed sinus tachycardia with marked prolongation of the QT interval, prolongation of QRS complex duration without morphological abnormalities, high-normal (slightly less than the upper reference limit) PR interval, depression of the ST segment, and variable high-voltage T waves that were partially merged into the subsequent P waves (a consequence of QT interval prolongation). Sinus tachycardia was probably a response to the dog's hypovolemic state; indeed, after fluid therapy, the heart rate and blood pressure normalized. Most other ECG findings were similar to those commonly detected in animals with hypokalemia. Under physiologic or pathological conditions, the T wave is variable in shape; in humans and dogs, positive, negative, diphasic, flat, and dome-dart–shaped T waves have been reported.^6,7 Therefore, a correct ECG interpretation of T waves could present a diagnostic challenge, especially in cases of pathological conditions that affect repolarization gradients, such as hypokalemia.

At the time of admission of the dog of the present report, the initial ECG tracing revealed variable high-voltage T waves with an unusual bifid appearance. Explanations for this finding included T waves that were partially merged with a subsequent U wave, dome-dart T waves, and P waves that were superimposed on the preceding T waves.^6–8

A U wave is an extra deflection at the end of the repolarization sequence, the origin of which remains controversial.⁹ In dogs, U waves begin 40 milliseconds after the end of T waves and have low amplitude (not detectable or < 0.05 mV) and long duration (70 to 90 milliseconds).² Intake of some drugs and various electrolyte imbalances, such as hypokalemia, result in prominent U waves that are partially superimposed on the T waves (simulating a bifid T wave),⁸ but very seldom do they equal or exceed T-wave amplitude. Thus, U waves were less likely an explanation for the deflections following the T waves in the case described in this report.

With dome-dart T waves, the ST segment and the first portion of the T wave form a convex upward curve followed by the terminal portion of the T wave, which forms a second positive peak separated from the first by a low-amplitude negative deflection (hence the descriptive term).⁶ It has been reported that dome-dart T waves are a result of asynchronous repolarization of the left and right ventricles. The first peak of a dome-dart T wave is produced by repolarization of the left ventricle and the second peak is produced by repolarization of the right ventricle; delay of repolarization at the inter-ventricular groove is thought to be the cause of the dip between the 2 peaks.⁶ Atypical configurations of the dome-dart pattern have been seldom reported,⁶ but the morphology of the deflections on the first ECG tracing obtained from the dog of this report did not completely match the classic morphological appearance of the dome-dart T wave. Moreover, lead I and III tracings had positive deflections that were partially merged with the descendent limb of previous T waves, with a constant distance to the QRS complexes. This finding is best explained by an incomplete fusion between T and P waves, such as occurs when nonconducted P waves are superimposed on preceding T waves, the QT interval is prolonged, or heart rate is high.^8,10 In the dog of the present report, no atrial extrasystole was detected and no bifid T wave was followed by a pause, as might be expected if P waves had fused with preceding T waves as a result of premature atrial depolarization. Instead, both extensive QT interval prolongation and sinus tachycardia were evident. Therefore, it seems most likely that the T-wave appearance in the initial ECG tracing was the result of superimposition of sinus P waves on the preceding T waves because of QT interval prolongation and high heart rate.¹⁰

In dogs, the contour, slope, and deviation from the isopotential line of the ST segment are quite variable and change spontaneously from recording to recording obtained at different times.⁷ Deviation of the ST segment is one of the ECG hallmarks of hypokalemia.⁷ Deviation of the ST segment is usually measured at its junction with the end of the QRS complex (called the J point) and referenced against the TP or PR segment.² Some authors prefer to measure the level of the ST segment in relation to the end of the PR segment, not the TP segment.¹¹ In this way, ST segment deviation can still be detected accurately, even if the TP segment is not present because the P wave is superimposed on the T wave.¹¹ In the initial ECG tracing obtained from the dog of the present report, the ST segment deviation was evident by referencing the J point against the end of the PR segment; afterward, when the dog's serum potassium concentration was within the reference range, the ST segment normalized.

For the dog of this report, the presumptive diagnosis for depletion in potassium concentration was albuterol-induced hypokalemia, according to the dog's medical history and because all other causes of hypokalemia were ruled out. It is important to consider that albuterol administration even at clinically relevant dosages (0.05 mg/kg [0.023 mg/lb], PO, q 8 to 12 h in dogs¹) can induce hypokalemia.¹² Although hypokalemia and ECG abnormalities as a result of albuterol administration are well known in human medicine, albuterol-associated adverse effects in veterinary clinical practice are not yet completely known. Three cases of spontaneous acute albuterol intoxication in dogs^1,5,13 have been published, and ECG abnormalities (ventricular tachycardia) were evident in 1 case⁵; however, the long-term administration of albuterol in the case described in the present report appears to be unique. Special precautions must be taken during treatment of dogs with albuterol because ECG abnormalities may develop. Cardiac evaluation, electrolyte disturbance correction, and appropriate treatment should be considered in the management of adverse effects induced by albuterol in dogs.