Extreme Hyperkalemia

Tran, Huy

doi:10.1097/01.smj.0000149407.51134.77

Cited by 36 publications

(23 citation statements)

References 16 publications

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“…The highest reported hyperkalaemia with cardiac arrest and successful resuscitation was 14 mmol L -1 (12). Other authors reported hyperkalaemia of 9.3 mmol L -1 with lethal outcome (13,14).…”

Section: Discussionmentioning

confidence: 95%

Extreme Hyperkalaemia Caused by Concomitant use of a Nsaid and an Ace Inhibitor in an Elderly Patient

Rogulj¹,

Hauptfeld²,

Iskra³

et al. 2010

Archives of Industrial Hygiene and Toxicology

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Extreme hyperkalaemia is a life-threatening electrolyte disorder. It is relatively common in patients with severe renal insuffi ciency. This report describes a case of extreme hyperkalaemia caused by drugs in an 82-year-old female patient without severe renal insuffi ciency, who was successfully treated without haemodialysis. The patient had been treated for arterial hypertension and type 2 diabetes mellitus for 30 years. Over the last years she had been receiving enalapril and metformin. Three weeks before the admission to the hospital, she was receiving a non-steroidal anti-infl ammatory drug (NSAID) because of the back pain. She was admitted to hospital due to a collapse and weakness in the limbs. Laboratory tests showed extreme hyperkalaemia, high blood sugar, metabolic acidosis, elevated serum creatinine and blood urea nitrogen (BUN), and a slightly elevated serum sodium. On ECG, we noticed typical signs of hyperkalaemia. The patient was treated with a slow intravenous bolus of calcium gluconate and intravenous infusion of sodium chloride with insulin, glucose with insulin and sodium bicarbonte. After the treatment, all laboratory fi ndings normalised together and the patient felt better. This case shows that physicians should be very careful when prescribing NSAIDs to elderly patients treated with drugs that affect renal function.

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Section: Discussionmentioning

confidence: 95%

Extreme Hyperkalaemia Caused by Concomitant use of a Nsaid and an Ace Inhibitor in an Elderly Patient

Rogulj¹,

Hauptfeld²,

Iskra³

et al. 2010

Archives of Industrial Hygiene and Toxicology

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show abstract

“…However, Lisachenko and Ivanova (1999) performed experiments on 25 dogs, and showed that the blood K + value decreased in the prophase (5 min to 9 h). Although high blood K + was thought to be associated with the development of pulseless electrical activity (Tran, 2005), high K + injection could end ventricular fibrillation, resulting in a higher ROSC rate (Liakopoulos et al, 2010). Elevated blood K + during CPR may be attributed to the accumulation of K + from intracellular and damaged cells of the pressed tissue, and has nothing to do with the amount of epinephrine (Lindner et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

β-receptor blocker influences return of spontaneous circulation and chemical examination in rats during cardiopulmonary resuscitation

Zhao

Pen

et al. 2013

J. Zhejiang Univ. Sci. B

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Abstract:Objective: We investigated the influence of β-receptor blocker metoprolol on return of spontaneous circulation (ROSC) during cardiopulmonary resuscitation (CPR) in rats with induced myocardial infarction (MI). Methods: Male Sprague-Dawley rats were randomly divided into three groups: the sham-operated group, the MI group without metoprolol, which was fed the vehicle, and the MI+metoprolol group receiving intragastric metoprolol. Each group was further divided randomly into three subgroups, depending on the dosage of epinephrine administered during subsequent CPR applied after the induction of asphyxial cardiac arrest. Results: The ROSC rate was significantly decreased in the low dose subgroup of MI group, unchanged in the medium dose subgroup of MI group, and significantly decreased in the high dose subgroup of MI group, compared with the same dose subgroup of sham-operated group. MI+metoprolol group had a lower ROSC rate than MI group in the medium dose subgroup, and a higher ROSC rate than MI group in the high dose subgroup. There was no difference in blood K + values of successful rats between MI group and MI+metoprolol group. The rats with successful CPR had lower blood K + values than rats with unsuccessful CPR in each of the three treatment groups. Conclusions: Metoprolol administered to MI rats over a long period significantly improved ROSC rates under an appropriate dose of epinephrine during CPR. An increasing high blood K + value would attenuate the rate of a successful CPR.

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“…A diagnosis of diabetic ketoacidosis with severe hyperkalemia was made (1,2). As his electrocardiogram ( Figure 1b) revealed ventricular fibrillation during resuscitation, electrical defibrillation was conducted, but his electrocardiogram showed pulseless electrical activity.…”

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confidence: 99%

Cardiac Arrest with Extreme Hyperkalemia

Tokuda¹

2017

EAJEM

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A 34-year-old man with type 1 diabetes, which is being treated with a subcutaneous insulin self-injection, presented to the emergency department in a state of coma. The patient had skipped taking the insulin injection for four days and then complained of fatigue and epigastralgia. On the day of hospital arrival, his mother found him unconscious in his room at home and an ambulance brought him to our hospital. At the time of arriving at the emergency department, he had cardiac arrest and his electrocardiogram ( Figure 1a) revealed pulseless electrical activity. Cardiopulmonary resuscitation was immediately performed. His serum glucose concentration was 1.178 mg/dL, arterial blood pH was 6.69, and serum potassium concentration was 10.6 mEq/L.A diagnosis of diabetic ketoacidosis with severe hyperkalemia was made (1, 2). As his electrocardiogram (Figure 1b) revealed ventricular fibrillation during resuscitation, electrical defibrillation was conducted, but his electrocardiogram showed pulseless electrical activity. Calcium gluconate, normal saline, insulin, and bicarbonate were administered. After approximately 1 h of chest compression and artificial ventilation, his potassium concentration reduced to 5.4 mEq/L and his electrocardiogram revealed sinus rhythm restoration (Figure 2) with palpable peripheral pulses. He was discharged home uneventfully after receiving education about the importance of receiving a regular insulin injection during 14 days of admission. DiscussionPatients with diabetic ketoacidosis have a risk of cardiac arrest because of electrolyte imbalance, particularly potassium imbalance. The rapid evaluation of electrocardiograms is key to the immediate diagnosis of life-threatening potassium disorders. As in this case, bradycardia along with an absent P wave, wide QRS complex, and peaked (tentorial) T wave characterize hyperkalemia on the electrocardiogram. Our present case proved that cardiac arrest with extreme hyperkalemia (more than 10 mmol/L) can be reversible by correcting the serum potassium concentration while continuing efforts, such as by providing cardiopulmonary resuscitation. Effective medications include calcium gluconate, insulin, bicarbonate, and saline infusions. Cardiopulmonary resuscitation should be continued in patients with hyperkalemia until serum potassium concentrations are corrected.

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Extreme Hyperkalemia

Cited by 36 publications

References 16 publications

Extreme Hyperkalaemia Caused by Concomitant use of a Nsaid and an Ace Inhibitor in an Elderly Patient

Extreme Hyperkalaemia Caused by Concomitant use of a Nsaid and an Ace Inhibitor in an Elderly Patient

β-receptor blocker influences return of spontaneous circulation and chemical examination in rats during cardiopulmonary resuscitation

Cardiac Arrest with Extreme Hyperkalemia

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