Worsening Wenckebach after calcium gluconate injection: not uncommon but frequently missed diagnosis
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American Journal of Emergency Medicine
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Worsening Wenckebach after Calcium gluconate injection: not uncommon but frequently missed diagnosis
Abstract
The objective of the study is to demonstrate a common etiology of hyperkalemia and illustrate a potential iatrogenic errors in treatment.
A 69-year-old woman admitted for worsening nausea and vomiting for 2 days. The patient has a history of end-stage renal disease on hemodialysis and missed her treatment for over a week. Physical examination was unremarkable. Initial laboratories showed a high Anion gap metabolic acidosis with potassium level of 6.4 mmol/dL.
Further Detailed history could not be obtained because the patient was feeling sick and nauseated. First electrocardiogram (ECG) showed second-degree heart block (3:2 conduction) (Fig).
Intravenous Ca gluconate was given to antagonize the effects of potassium on excitable cell membranes. Repeat ECG showed worsening heart block (Mobitz I) (2:1 conduction).
The ratio of extracellular to intracellular potassium (K) concen- tration largely determines the cell membrane resting electrical potential. Its internal balance (equilibrium of K across the cell membrane) is modulated by insulin, catecholamines, acid-base balance, and plasma tonicity. The kidneys are the major modulator of the K external balance (intake and elimination). The gut plays a minor role in the latter balance.
With high potassium, ventricular fibrillation may be the first ECG manifestation; conversely, a normal ECG may be seen even with extreme hyperkalemia. Most patients manifest hyperkalemic ECG changes at plasma K greater than 6.7mmol/L.
Inhibition of the sodium (Na)/potassium (K) ATPase pump results in a reduction in the rate of active Na+ extrusion. The rise in the intracellular Na reduces the transmembrane Na gradient that drives the extrusion of intracellular Ca2 + during myocyte repolarization. This is the basic concept of digoxin mechanism of action. Digoxin also increases the Vagal tone and decreases the sympathetic nervous system activity (desensitization of the baro-reflex arc).
The binding site for digoxin is the phosphorylated ? subunit of the Na/K-ATPase pump that can be dephosphorylated by extracellular K leading to a decrease in the affinity of the enzyme for cardiac glycosides. Although that Ca gluconate is the First-line treatment of hyperka- lemic ECG disturbances, it is contraindicated in digoxin-induced hyperkalemia. The etiology of hyperkalemia should be verified before treatment. High extracellular K is a manifestation of digoxin toxicity.
Digoxin-specific therapy should be used in such instances.
Digoxin toxicity should be suspected, and blood levels should be routinely ordered if the history is unreliable. Our patient’s digoxin level was 2.7 mmol.
Ali Abdul Jabbar MD Abdul Wase MD Cardiology Division
Department of Internal Medicine at the Boonshoft School of Medicine at
Wright State University Dayton, OH 45409, USA
E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2012.12.043
0735-6757/$ - see front matter.
First EKG:
Second EKG [After Ca Gluconate injection]:
Fig. First ECG and second ECG (after Ca gluconate injection).