A 3-year-old 5-kg (11-lb) neutered male domestic shorthair cat was evaluated because of lethargy of 1 week's duration and decreased appetite and episodes of vomiting of 2 days' duration. One year earlier, the cat had developed urethral obstruction because of struvite calculi and had since been fed a calculolytic diet. On physical examination, the cat had a dull attitude. Rectal temperature was 37.5°C (99.5°F), and mucous membranes were pale. On cardiac auscultation, no murmur was detected; the heart rhythm was regular, but heart rate was low (80 beats/min). The femoral pulse was of normal intensity and synchronous with the heart beat. Lung auscultation revealed no abnormalities.
A CBC, serum biochemical analysis, and urinalysis were performed. The CBC revealed eosinophilia (2.7 × 103 cells/μL; reference interval, 0 × 103 cells/μL to 1.5 × 103 cells/μL), relative neutropenia (absolute number, 3.2 × 103 cells/μL [reference interval,1 2.5 × 103 cells/μL to 12.5 × 103 cells/μL]; fraction, 40.8% [reference interval, 60% to 70%]), and relative lymphocytosis (absolute number, 4.4 × 103 cells/μL [reference interval,1 1.5 × 103 cells/μL to 7.0 × 103 cells/μL]; fraction, 55.8% [reference interval, 12% to 30%]). Serum biochemical abnormalities included high concentrations of creatinine (7.87 mg/dL; reference interval, < 2.0 mg/dL), BUN (> 300 mg/dL; reference interval, < 30 mg/dL), and potassium (8.78 mEq/L; reference interval, 3.5 to 5.5 mEq/L). Serum glucose concentration was considered low-normal (71 mg/dL; reference interval, 64 to 120 mg/dL), and alanine aminotransferase activity was high (51.9 mg/dL; reference interval, 6 to 40 mg/dL). Urine specific gravity was low (1.015), and no struvite crystals or signs of inflammatory cystitis were identified on sediment evaluation. The cat was hospitalized, and an ECG examination was performed (Figure 1).
Initial lead I, II, and III ECG tracings obtained from a cat that was evaluated because of lethargy of 1 week's duration and decreased appetite and episodes of vomiting of 2 days' duration. Notice the atrial standstill with absence of P waves and sinus bradycardia. Most QRS complexes appear normal in amplitude and duration; however, 2 isolated premature beats with wide QRS complexes are present (arrows), compatible with hyperkalemia-induced ventricular premature complexes. Paper speed = 50 mm/s; 1 cm = 2 mV.
Citation: Journal of the American Veterinary Medical Association 244, 1; 10.2460/javma.244.1.45
ECG Interpretation
Surface 3-lead ECG tracings of 5 minutes' duration were obtained (Figure 1). The tracings revealed low heart rate (80 beats/min) with a regular rhythm, regular R-R intervals, absent P waves, and QRS complexes of normal amplitude (0.25 mV; reference range, 0.0 to 0.9 mV) and duration (0.02 seconds; reference range, 0.0 to 0.04 seconds), with a few single premature beats with wide QRS complexes. The diagnosis was atrial standstill with isolated ventricular premature beats secondary to hyperkalemia.
The cat was administered a bolus of calcium gluconate solution (1 mL/kg [0.45 mL/lb]) IV, and the ECG examination was repeated 10 minutes after treatment (Figure 2). At this time, P waves were present in the ECG tracings. The PR intervals were prolonged (0.14 seconds; reference range, 0.05 to 0.09 seconds), indicative of first-degree atrioventricular (AV) block.
Lead I, II, and III ECG tracings obtained from the cat in Figure 1 ten minutes after IV administration of a bolus of calcium gluconate solution. Notice that P waves (arrows) are present and the PR intervals are prolonged (PR interval, 0.14 seconds; reference range, 0.05 to 0.09 seconds [ie, first-degree atrioventricular block]). Paper speed = 50 mm/s; 1 cm = 2 mV.
Citation: Journal of the American Veterinary Medical Association 244, 1; 10.2460/javma.244.1.45
Once the cat was more stable, radiographic and ultrasonographic examinations of the abdomen were performed to determine whether urethral or bladder calculi or evidence of acute kidney failure was present. Abdominal radiographic views were unremarkable. On abdominal ultrasonography, both kidneys appeared to have increased hyperechogenicity of the cortex and a decreased corticomedullary rim sign, in contrast to expected ultrasonographic findings in healthy cats. No calculi were detected in the urinary bladder or ureters during the abdominal ultrasonographic examination.
The cat received fluid therapy (saline [0.9% NaCl] solution at twice the maintenance rate) for a period of 12 hours, after which serum creatinine concentration (5.5 mg/dL) and BUN concentration (281 mg/dL) remained high. The serum sodium-to-potassium concentration ratio was 13.7:1 (reference interval, > 27:1) as a result of high potassium concentration (9.5 mEq/L) and low sodium concentration (130 mEq/L; reference interval, 140 to 155 mEq/L); serum chloride concentration was 107 mEq/L (reference interval, 114 to 125 mEq/L). These results were compatible with hypoadrenocorticism. An ACTH stimulation test was performed, and results confirmed hypoadrenocorticism; basal serum cortisol concentration was 0.4 ng/dL (reference interval, 0.5 to 5.4 ng/dL), serum cortisol concentration at 30 minutes after stimulation was 0.5 ng/dL, and serum cortisol concentration at 60 minutes after stimulation was 0.6 ng/dL.
Treatment with dexamethasone (1 mg/kg) and hydrocortisone (10 mg/kg [4.5 mg/lb]) IV 3 times daily was initiated. Regular insulin (0.25 U/kg [0.11 U/lb]) and a bolus of 25% dextrose solution (2 g of dextrose for each unit of regular insulin) were administered IV every 8 hours. Unfortunately, despite an initial response to treatment, the cat did not have marked improvement in demeanor, renal variables, or serum potassium concentration; the owner requested euthanasia.
Discussion
Atrial standstill is an arrhythmia characterized by failure in atrial depolarization, with an absence of P waves and QRS complexes of generally normal amplitude and duration.2,3 Permanent atrial standstill is a condition typically associated with severe end-stage cardiomyopathy or atrial myopathy.2,4,5
Hyperkalemia is the most common cause of transient atrial standstill and is reversible if the primary disease is identified and treated. It has been shown that increasing concentrations of serum potassium induce a wide variety of ECG alterations.2,3,6 The underlying disease, duration of hyperkalemia, and presence of concurrent electrolyte or metabolic abnormalities alter myocyte membrane potential and threshold; thus, ECG alterations detected in patients with hyperkalemia are not accurate predictors of serum potassium concentration. Attempts to characterize ECG alterations associated with increasing serum concentration of potassium in cats and dogs have been made.6 Even if this classification is helpful in understanding hyperkalemia-related conduction disturbances, serum potassium concentration is not always associated with predictable ECG alterations in mammals.
In general, mildly high serum potassium concentrations (5.6 to 6.5 mEq/L) are associated with greater cell membrane permeability, which induces faster re-polarization of cardiac myocytes (ie, short QT interval and tented T wave).2 Higher serum potassium concentrations (mild to moderate hyperkalemia, 6.6 to 7.5 mEq/L) reduce heart rate and interfere with cell-to-cell transmission for both atrial and ventricular myocytes by decreasing the phase 4 slope of diastolic depolarization. This can lead to sinus bradycardia and QRS complex widening.2 With moderate to severe hyperkalemia (7.0 to 8.5 mEq/L), the most frequent abnormalities detected include PR interval prolongation (Figure 2) or, most commonly, absent P waves (Figure 1). These findings are related to the decreased negativity of atrial resting membrane potentials, which induces a persistent depolarization of atrial myocytes. This rhythm can also be defined as sinoventricular; atrial activation fails, but the sinoatrial node fires normally and the electrical impulse reaches the AV node through internodal pathways. Thus, the QRS complexes are normal in appearance and the RR intervals are regular.2,3 Very high serum potassium concentrations (> 11.6 mEq/L) can depress the sinoatrial node, resulting in a junctional or paradoxical ventricular rhythm with low heart rate, wide QRS complexes, and T waves. This condition can be considered as preagonal and precedes ventricular fibrillation and death.
In the case described in the present report, the ECG alterations were variable. A sinoventricular rhythm associated with isolated premature beats with wide QRS complexes was detected initially; following treatment for hyperkalemia with calcium gluconate solution, first-degree AV block was apparent. Sinoventricular rhythm and first-degree AV block are typically associated with hyperkalemia. The presence of isolated premature beats with wider-than-normal QRS complexes suggested a ventricular origin, which could have been triggered by hyperkalemia-induced variation in resting membrane potentials of cardiac myocytes.
To the authors' knowledge, this is the first report of a cat with hypoadrenocorticism and multiple arrhythmias. Arrhythmias associated with hypoadrenocorticism in cats are infrequently reported, in contrast to dogs with hypoadrenocorticism, in which arrhythmias are frequently encountered.7–9 In a study7 of 10 cats with hypoadrenocorticism, the only arrhythmias identified were sinus bradycardia and atrial premature complexes. However, the mean ± SD serum potassium concentration among the 10 cats was lower (6.2 ± 0.6 mEq/L) than the value for the cat of the present report.
There are 2 components to the elimination of hyperkalemia-induced ECG alterations: decrease serum potassium concentration and treat the underlying disease.2,3,8,9 Various disorders are associated with hyperkalemia, and it is of outmost importance to identify and treat the underlying disease. The most common causes of hyperkalemia in cats are acute kidney failure, urethral obstruction, severe tissue damage or reperfusion injury, metabolic acidosis, and hypoadrenocorticism.10–12 Persistently high serum potassium concentration in a patient without clinical signs of postrenal obstructive disease or reperfusion injury, together with increasing values of renal variables despite intensive fluid therapy, should prompt a clinician to consider hypoadrenocorticism as a differential diagnosis.
Hypoadrenocorticism is an uncommon endocrine disorder in dogs and a very rare condition in cats. It is a result of deficient secretion of both mineralocorticoids and glucocorticoids. Primary hypoadrenocorticism can be induced by immune-mediated disease or neoplastic infiltration of both adrenal glands.7–9,13 Secondary hypoadrenocorticism can be iatrogenic or caused by insufficient secretion of ACTH from the pituitary gland.9 The clinical signs of acute hypoadrenocorticism are variable, and the diagnosis can be challenging.7–9,14 For the cat of the present report, the ECG alterations, hyperkalemia that was unresponsive to fluid therapy, and concurrent hyponatremia generated a suspicion of hypoadrenocorticism. For this cat and other animals with hypoadrenocorticism, results of an ACTH stimulation test, namely low basal serum cortisol concentration associated with a low increase in serum cortisol concentration after ACTH stimulation, provide a definitive diagnosis.7–9
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