A 9-year-old spayed female Doberman Pinscher was referred to the small animal clinic of the University of Berne because of severe apathy, weakness, anorexia, and diarrhea of 4 days' duration. On physical examination (day 0), the dog's weight was considered normal (27 kg [59.4 lb]). Heart rate, respiratory rate, and rectal temperature were within reference limits. The dog was dehydrated (estimated to be 8%). Mucous membranes were pink and dry, and the capillary refill time was prolonged (> 2 seconds). On initial auscultation, the dog had a regular cardiac rhythm with a heart rate of 110 beats/min. A grade 2/6 systolic heart murmur was detected over the mitral valve. Diagnostic procedures included a CBC, serum biochemical analyses, and thoracic radiography. The CBC revealed a slight leukocytosis (16.2 × 109 WBCs/L; reference range, 6 × 109 to 12 × 109 WBCs/L) with a left shift (1.46 × 109 band neutrophils/L; reference range, 0 to 0.3 × 109 band neutrophils/L). Serum biochemical analyses revealed low concentrations of sodium (122.0 mmol/L; reference range, 144 to 155 mmol/L) and chloride (96.0 mmol/L; reference range, 106 to 135 mmol/L). Serum potassium concentration was high (7.9 mmol/L; reference range, 4.1 to 5.3 mmol/L), and the sodium-to-potassium concentration ratio was 15.4:1. Thoracic radiography revealed evidence of hypovolemia, microcardia, aerophagia, and a mild reticular lung pattern.
Because of the low sodium-to-potassium concentration ratio, an ACTH stimulation test was performed. On the basis of the test result, a diagnosis of primary hypoadrenocorticism was made. Intravenous fluid therapy (30 mL/kg/h [13.6 mL/lb/h] during the first 4 hours and then 10 mL/kg/h [4.5 mL/lb/h]) and treatment with glucocorticoids were initiated; dexamethasone (0.75 mg/kg [0.34 mg/lb], IV) was administered once, followed by administration of prednisolone (0.22 mg/kg [0.1 mg/lb], PO) daily. Desoxy-corticosterone pivalate (1.9 mg/kg [0.86 mg/lb]) was administered IM once. Serum potassium concentration was within reference limits 10 hours after treatment was started. The dog responded well to treatment during the initial 24-hour period, and the rate of IV fluid administration was tapered to 2 mL/kg/h (0.9 mL/lb/h). Forty hours after initial evaluation, auscultation revealed that the dog had an irregular cardiac rhythm with a heart rate of 220 beats/min; an ECG was recorded with the dog in right lateral recumbency.
ECG Interpretation
Initial 3-lead ECG tracings obtained from the dog revealed atrial fibrillation with a mean heart rate of 190 beats/min (Figure 1). The duration of the QRS complexes was 0.06 seconds (upper reference limit, 0.05 seconds). The R-wave amplitude in lead II was 1.1 mV, which is borderline hypovoltage. Because of the tachycardic atrial fibrillation, treatment with digoxin (0.22 mg/m2, PO, q 12 h) was begun and echocardiography was performed.
Initial ECG tracings (leads I, II, and III) in a 9-year-old spayed female Doberman Pinscher that was evaluated because of severe apathy, weakness, anorexia, and diarrhea of 4 days' duration. The ECG was performed 40 hours after initiation of treatment for acute hypoadrenocorticism. Notice the tachycardic atrial fibrillation. Paper speed 50 mm/s; 20 mm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 229, 12; 10.2460/javma.229.12.1890
Twelve hours after initiation of antiarrhythmic treatment with digoxin, another ECG was performed and revealed sinus rhythm with a mean heart rate of 120 beats/min. Another 12 hours later, an ECG revealed atrial fibrillation with a mean heart rate of 230 beats/min. The heart rhythm converted spontaneously back and forth between sinus rhythm and atrial fibrillation during the ECG recording. On a rhythm strip obtained during normal sinus rhythm, a few isolated ventricular premature complexes with compensatory pauses were observed (Figure 2). All waveform intervals and amplitudes were within reference ranges. In the lead III and aVL tracings (data not shown), notching of the QRS complex was evident and interpreted as indicative of minor intraventricular conduction disturbance.
Electrocardiographic tracings (leads I and II [2 lower tracings]) obtained from the dog in Figure 1 2.5 days after initiation of treatment for acute hypoadrenocorticism. Notice the normal sinus rhythm. Isolated ventricular premature complexes and notching of the QRS complexes are evident. Paper speed = 50 mm/s; 10 mm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 229, 12; 10.2460/javma.229.12.1890
At the time echocardiography was performed, the dog had atrial fibrillation. The cardiac dimensions (ratio of the left atrial dimension to the aortic diameter, 0.95; end-systolic volume index, 19 mL/m2) and the fractional shortening (38.8%) were within reference limits. Thick mitral valve leaflets and mild mitral regurgitation were detected; these findings were considered indicative of mild myxomatous mitral valve disease. There was no evidence of occult dilated cardiomyopathy.
Four days after initial evaluation, there was no evidence of weakness or rhythm disturbances; serum electrolyte concentrations were within reference ranges. Maintenance treatment with fludrocortisone acetate (0.4 mg/d) was initiated, and the dog was discharged from the hospital.
On day 11 after the initial evaluation, the dog was reexamined. The sodium-to-potassium concentration ratio was 26.5. Therefore, the dosage of fludrocortisone acetate was increased to 0.45 mg/d. The ECG tracings obtained at this time revealed sinus rhythm with a heart rate of 95 beats/min; overall, the ECG findings were similar to those obtained 24 hours after initiation of antiarrhythmic treatment with digoxin. Five weeks later, the referring veterinarian reexamined the dog. Serum electrolyte concentrations were within reference limits, and ECG tracings revealed respiratory sinus arrhythmia with a heart rate of 90 beats/min. No ventricular premature complexes were detected electrocar-diographically. Serum digoxin concentration assessed 6 hours after administration of the drug was 0.95 ng/mL (reference range, 0.8 to 2.1 ng/mL). Two years after the Addisonian crisis, the dog was reported to be well and there was no evidence of rhythm disturbances or cardiac disease.
Discussion
Hypoadrenocorticism is a rare but well-known endocrine disorder in dogs and humans.1 Although hypoadrenocorticism can be diagnosed in dogs of any age, it is a disease that more commonly affects young and female dogs. 1 The dog of this report was a spayed female Doberman Pinscher that was 9 years old. The typical serum electrolyte alterations associated with hypoadrenocorticism (eg, hyponatremia, hypochloremia, and hyperkalemia) were evident in the dog of this report.
The ECG findings did not directly relate to serum potassium concentration alone because coexistent hyponatremia, hypocalcemia, and acidosis can influence ECGs. Arrhythmias were recorded in 46 of 100 dogs with hypoadrenocorticism in 1 study,2 and these included sinoventricular rhythm, brady- and tachycardia, conduction disturbances, ventricular fibrillation, and asystole.2 In a larger study2 that evaluated ECGs obtained prior to treatment in 122 dogs with hypoadrenocorticism, atrial standstill was detected in approximately 47%, bradycardia in 29%, atrial or ventricular extrasystoles in 6%, and atrioventricular block (second or third degree) in 5%.
The principal detrimental effect of hyperkalemia is its electrical effect on the transmembrane potential of the myocardial cell. Generally, the earliest sign of hyperkalemia detected electrocardiographically is narrowing of T waves, followed by a progressive increase of the T-wave amplitude, widening of the QRS complex, and progressive loss of P waves. The atrial conduction is reported to continue silently (without obvious deflections on a body surface ECG) via internodal pathways. With severe hyperkalemia, a sinusoidal wave pattern consisting of QRS complexes and T waves may be evident on an ECG tracing and can be followed by ventricular fibrillation and cardiac arrest.3 Unfortunately, only an approximate correlation exists between the serum concentration of potassium and ECG abnormalities. Increased concentration of potassium in the extracellular space partially diminishes the intracellular-to-extracellular gradient and partially depolarizes the cell (ie, the cell's transmembrane potential is decreased from a range of −60 to −90 mV toward 0 mV). The reduced transmembrane potential of a stimulated myocardial cell slows the upstroke of phase 0 of the single cell action potential. This results in decreased impulse propagation velocity because of the so-called membrane responsiveness.3 These changes are also evident on a body-surface ECG, wherein all action potentials of the single myocardial cells are summed.
Hyperkalemia slows intraventricular conduction and widens the QRS complex; in the atria, the P-wave amplitude decreases and then becomes isoelectric. The other major effect of hyperkalemia on the action potential is the uniform reduction of the total duration of depolarization, especially through shortening phase 3 of the action potential.3
Atrial fibrillation is a common and important arrhythmia in dogs,2,4,5 horses,6,7 and humans.3,8 It represents 14% of all arrhythmias in dogs, and the incidence of atrial fibrillation among cases of dilated cardiomyopathy is 50%.4 Atrial fibrillation in dogs is most often caused by primary, underlying cardiac disease. However, atrial fibrillation may also develop in individuals with structurally normal hearts (eg, during anesthesia or in association with hypothyroidism, pericardiocentesis, gastrointestinal tract disease, or volume overload causing atrial stretch).4 Atrial fibrillation is usually persistent in untreated dogs.4 Paroxysmal or intermittent atrial fibrillation in dogs is usually of short duration and, in most instances, progresses to persistent atrial fibrillation because of severe underlying cardiac disease.2,4,5 In the dog of this report, heart dimensions (especially those of the left atrium) and fractional shortening were within reference limits. Two years after the Addisonian crisis, the dog did not appear to have any cardiovascular disturbance; therefore, the possibility that occult dilated cardiomyopathy was a contributory factor in arrhythmogenesis is considered less likely.
Atrial fibrillation in horses may be paroxysmal or sustained and is most often detected in adult horses. In horses, paroxysmal atrial fibrillation is often associated with a single episode of poor performance (such as sudden deceleration during a race). The arrhythmia usually resolves spontaneously within 24 to 48 hours after the race.6,7
Administration of desoxycorticosterone pivalate in therapeutic dosages has not been associated with effects on systolic and diastolic blood pressure and electrical cardiac conduction in dogs.9 Desoxy-corticosterone pivalate treatment is well tolerated, even when a dosage that is 15 times as great as the therapeutic dosage of 2.2 mg/kg (1 mg/lb) every 25 days is administered.9 To date, atrial fibrillation has not been reported as a complication of desoxycorticosterone pivalate administration.
Ischemia-reperfusion injury, which is a complex process involving the generation and release of inflammatory cytokines, accumulation and infiltration of neutrophils and macrophages, release of oxygen free radicals, activation of proteases, and generation of nitric oxide, may result in myocardial dysfunction and possible injury to other major organs.10 Among dogs with gastric dilatation-volvulus, approximately 40% develop ventricular arrhythmias.11 Numerous factors have been implicated in the initiation and maintenance of cardiac arrhythmias in dogs with gastric dilatationvolvulus, including myocardial ischemia, autonomic imbalance, myocardial reperfusion injury, and acidbase and electrolyte disturbances.11 After spontaneous gastric dilatation-volvulus, microhemorrhages are evident in the myocardium and resolution of these hemorrhages into microinfarcts is proposed to predispose the dog to delayed onset of ventricular arrhythmia.11 Reperfusion injury and stunning of the myocardium are also implicated in delayed onset of ventricular arrhythmia. Spontaneous arrhythmias have been reported to develop approximately 12 to 24 hours after decompression of gastric dilatation-volvulus.11 In the dog of this report, atrial fibrillation developed 40 hours after initial evaluation. It is possible that this delayed onset may be attributable to the fact that cardiovascular depression resolves fast after decompression of gastric dilatation-volvulus.
We speculate that a combination of serum electrolyte imbalance, mild acidosis, and myocardial reperfusion injuries as a result of hypotension and hypovolemia influenced the ionic intra- and extracellular myocardial milieux considerably, facilitating conduction abnormalities and rhythm disturbances in the dog of this report. Atrial fibrillation resolved after several days of digoxin administration. Whether the atrial fibrillation resolved because a therapeutic serum concentration of digoxin had been reached, myocardial reperfusion injuries had regenerated, or the intra- and extracellular ionic milieux had normalized cannot be determined.
References
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