key: cord-0010738-dw2gceks
authors: Weldon, Alan D.; Moise, N. S.; Rebhun, W. C.
title: Hyperkalemic Atrial Standstill in Neonatal Calf Diarrhea
date: 2008-06-28
journal: J Vet Intern Med
DOI: 10.1111/j.1939-1676.1992.tb00354.x
sha: 369d67bfbbceb33db6b1a0d9b5fa2766b217bdc5
doc_id: 10738
cord_uid: dw2gceks

Hyperkalemia has been associated with cardiac abnormalities and muscular disorders. Hyperkalemia is a common problem associated with the acid‐base and electrolyte disturbances that occur in neonatal calves having acute diarrhea. Occasional calves with acute neonatal diarrhea, metabolic acidosis, and hyperkalemia have cardiac rate or rhythm abnormalities. Bradycardia observed in three such calves was found to represent atrial standstill and was attributed to hyperkalemia. (Journal of Veterinary Internal Medicine 1992; 6:294–297)

cine as a representative of a recent farm outbreak of neonatal calf diarrhea during which seven calves had died. The calf had received colostrum, an E. coli bacterin, and a selenium injection at birth. Before amval, this calf had been treated with scour boluses, oral electrolytes, and penicillin.

At initial examination, the calf was recumbent, dehydrated (-8%), hypothermic (T = 97.OoF/36. 1 1 "C), and had profuse watery diarrhea of 12 hours duration. Auscultation revealed bradycardia (heart rate = 88 beats/ min), poor pulse quality, and occasional pulse deficits. Electrocardiographic analysis showed an irregular rhythm, no P-waves, and inconsistent supraventricular premature complexes with aberrant ventricular conduction ( Figure 1A) . A serum biochemical profile indicated marked hyperkalemia (K = 9.6 mEq/L), azotemia (BUN = 105.0 mg/dL), increased creatinine concentration (6.1 mg/dL), and an increased anion gap (34.0 mEq/L).

An intravenous catheter was placed in the jugular vein and therapy with 5% dextrose and 150 mEq NaHC03/L was instituted. Electrocardiographic tracings were done every 15 minutes until a normal sinus rhythm was recorded 45 minutes later, at which point the calf was able to stand. Two heavily encapsulated species of E. coli and Clostridium perfingens were isolated from the feces. Fecal electron microscopy for viruses and blood cultures were negative. Fluid therapy was maintained until the serum potassium and creatinine were normal.

A 2-week-old Holstein heifer weighing 84 kg was presented because of diarrhea of 48 hours duration. Six other neonatal calves on the farm also were affected. Before admission, the calf had been treated with gentomi-HYPERKALEMIC ATRIAL STANDSTILL 295 FIG. I . Base apex electrocardiograms recorded from two calves (strips A and C: I cm = I mv; strips B and D Y2 cm = I mv 25 mm/second). A: Electrocardiogram recorded from calf with plasma potassium of 9.6 mEq/L. Atrial standstill (absence of P-waves) and negative spiked Twaves are seen. Arrows point to narrow premature complexes that are either superventricular or high ventricular in origin. The curved arrow points to either a premature ventricular complex or a supraventricular impulse conducted with aberrancy. B: Electrocardiogram recorded from same calf as in A after therapy. Plasma potassium was 5 . I mEq/L. Sinus rhythm is evident, P-waves (p) are visible, and the T-wave has changed polarity and is no longer spiked. A 60-cycle artifact is also recorded. C: Electrocardiogram recorded from a calfwith plasma potassium of 7.6 mEq/L. Atrial standstill with a supraventricular premature complex (arrow) and tall spiked T-waves are seen as well as variable R-R interval and S-T segment elevation. D: Electrocardiogram recorded from the same calfas C after therapy. Plasma potassium was 4. I mEq/L. Sinus rhythm with normal T-waves can be seen. cin,* trimethoprimt and sulfadiozine and a commercial scour preparation. All calves had a K-99 E. coli bacterin at 2 days of age. Upon admission to the clinic, the calf was febrile (T = 103.2"F/39.56"C), depressed, recumbent, and approximately 8% dehydrated. On physical examination, an arrhythmia, weak peripheral pulses, and a slightly thickened umbilicus were found. Electrocardiography revealed bradycardia (heart rate = 89 beats/min) with no P waves present. Biochemical abnormalities included hyponatremia (Na+ = 122 mEq/L), hyperkale-

t Tribrissen, Burroughs Wellcome, Co., Kansas City, MO. mia (K+ = 8.7 mEq/L), metabolic acidosis (pH = 7.27; HCO, = 10 mm/L; pC0, = 23 mmHg), an increased anion gap (2.5 mEq/L), and azotemia (BUN = 83 mg/ dL; creatinine = 8.1 mg/dL).

Intravenous fluid therapy with 2 L of 5% dextrose with 1 50 mEq/L NaHCO, was given over a 1 -hour period and ceftiofurt therapy ( 1 mg/lb twice daily) was instituted.

Electrocardiograms (not shown) were obtained at 15-minute intervals until a normal sinus rhythm was obtained approximately 1 hour later. Serum potassium was 5.4 mEq/L at this time. Fluid therapy was changed to lactated Ringer's solution to maintain a normal serum potassium concentration because of the possibility of total body potassium depletion associated with diarrhea.

Fecal culture yielded Clostridium perfringens and fecal flotation revealed Cryptosporidium spp. Electron microscopy was negative for viral particles.

A 12-day-old Holstein heifer weighing 30 kg was presented with diarrhea of 48 hours duration and a patent urachus. All calves on the premises had received an E. coli bacterin at birth, and this calf was the only one affected. The calf was recumbent, approximately 10% dehydrated, hypothermic (T = 98.6"F/37.OoC), and had an irregular heart rate (HR = 98 beats/min). A serum biochemical profile revealed hyponatremia (Na+ = 124.0 mEq/L), hyperkalemia (K+ = 7.5 mEq/L), hypochloremia (C1= 93.0 mEq/L), an increased anion gap (23 mEq/L), and azotemia (BUN = 80.0 mg/dL) with increased creatinine concentration (2.6 mg/dL). The electrocardiogram showed an irregular rhythm and the absence of P-waves ( Figure 1C ).

Intravenous fluid therapy consisting of 2 L of 5% dextrose with 150 mEq/L NaHCO, was given over a 45-min-Ute period. Electrocardiograms were performed at 15-minute intervals. A normal sinus rhythm was recorded after 30 minutes of therapy. Serum potassium normalized at 4.1 mEq/uL, at which time a balanced electrolyte solution was given.

A heavily encapsulated E. coli was isolated from the feces. Culture of the umbilicus, resected on the second day of hospitalization, yielded a different E. coli, as well as Actinornyces pyogenes, and CIostridiurn spp. Results of blood cultures, fecal flotation, and electron microscopy were negative.

Cardiac arrhythmias in calves are not common; when they are detected, septicemia, endotoxemia, white muscle disease, congenital anomalies, ingestion of toxins, hypoglycemia, and electrolyte aberrations must be considered. 13, 24 Changes in serum potassium concentrations,

Internal Medicine particularly hyperkalemia, can profoundly affect myocardial Typically, this is viewed electrocardiographically as a combination of broadening, flattening, or disappearance of the P-wave. A tall spiked Twave usually is o b~e r v e d .~' -~~~~' It must be emphasized, however, that the T-wave is a highly variable component of the electrocardiogram and that T-wave changes alone cannot accurately predict h~perkalemia.~',~~ T-wave changes can occur with normal serum Kf concentrations.6J2

As serum K+ concentration increases (>7.0 mEq/L), the atrial myocardium becomes refractory to activation. However, conduction of impulses from the S-A and A-V nodes continues as these specialized fibers are relatively resistant to hypercal~emia.~~~~~.~',~~ This differential effect on cardiac tissues is due to an increased sensitivity of atrial myocardium when compared with the ventricular myocytes and specialized tissues to depolarization by excess K+. The increase in extracellular K+ and subsequent drop in intracellular K+ reduces the resting membrane potential, shortens the duration of the action potential,20 and eventually decreases the excitability of the atrial myocyte. Continued increase in serum K+ leads to ventricular conduction disturbances, as evidenced by widening or axis deviation of the QRS. Other ECG alterations, such as ST segment elevation, irregular R-R intervals, and premature complexes also have been d e~c r i b e d . '~,~~ These changes also were evident in Figure 1C . The St-T change could be indicative of myocardial ischemia or could develop secondary to 'QRS alterations. Bundle of His studies in the dog have shown that A-V conduction failure does occur at higher K" concentration^,'^,",^^ indicating progressive A-V nodal block.20 It has been shown that the cardiotoxic effects of hyperkalemia can be exacerbated by concurrent hyponatremia and/or hypocalcemia. 12, 20, 30 This, in conjunction with decreased intracellular K+ concentrations could possibly explain the clinical finding of hyperkalemic atrial standstill in diarrhetic calves at lesser K+ concentration than in experimentally induced hyperkalemic atrial ~t a n d s t i l l .~' -~~,~' Arrhythmia and/or bradycardia in a diarrhetic calf should alert the examiner to the possible presence of hyperkalemia. Assessment of acid-base status, serum electrolyte concentrations, and renal function can assist the diagnosis and management of the hyperkalemic patient. Hydration status, however, is best assessed clinically in calves2 because of the wide variations in PCV and TP during the neonatal p e r i~d .~,~~ Furthermore, electrocardiographic analysis can provide rapid insight into the cause of an arrhythmia and supports a diagnosis of hyperkalemic atrial standstill. Treatment is directed at reducing serum K+ concentration and increasing volume, and correcting concurrent metabolic derangement.

Intravenous fluid therapy is paramount. The use of 5% dextrose and sodium bicarbonate is an effective initial treatment for hyperkalemia. Both dextrose and bicar-bonate promote transcellular potassium transport from extracellular fluid.'1, '6,33 Insulin also can be used to expedite potassium transfer into cells because it increases sodium potassium ATPase activity at the cell membrane level, a process independent of glucose uptake into the cell. However, due to the frequent presence of concurrent hypoglycemia, caution must be exercised when using insulin.

Calcium can also be used in severe life-threatening hyperkalemia because it antagonizes the cardiotoxic effects of p o t a~s i u m .~~,~~ However, this is a transient effect, and further therapies must be employed to decrease serum potassium. Recent reports have suggested the efficacy of p2 adrenergic agents such as salbutamol in treating hyperkalemic patient^.^^-^' These reports suggest results similar to treatment with dextrose, alkalinizing agents, and insulin. Consideration should be given to these agents in animals with hyperkalemia.

Arrhythmias, although uncommon in calves, should signal the possibility of hyperkalemia when associated with signs of diarrhea, dehydration, and recumbency in neonatal calves. Electrocardiographic analysis can provide a rapid indication of hyperkalemia in situations in which serum electrolyte determination is unavailable or delayed. Electrocardiography can be further used to assess the effectiveness of therapy.

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