Instantaneous electrocardiographic changes and transient sinus rhythm restoration in severe hyperkalaemia (original) (raw)
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Electrographic alterations induced by hyperkalaemia simulating acute myocardial infarction
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 1989
In general, severe hyperkalaemia produces classic electrocardiographic manifestations including tenting of T waves, widening of the QRS complex, loss of P waves, and eventually, sine waves and asystole. This report concerns a patient with chronic renal failure on maintenance haemodialysis who developed a severe hyperkalaemia associated with chest pain, manifested electrocardiographically by elevation of the S-T segment resembling acute myocardial infarction. After haemodialysis, serum potassium decreased and the electrocardiogram returned to normal. We review the literature and discuss the possible physiology of this electrocardiographic alteration.
Hyperkalemia Presenting as Sinus Bradycardia, Junctional Rhythm and Atrial Bigeminy
Cureus, 2019
The spectrum of electrocardiographic changes seen with hyperkalemia is known to progress gradually with increasing serum levels of potassium. Initial changes are limited to peaked T waves and QT shortening, which subsequently progress to prolonged QRS/QT intervals, and finally sinus arrest, sinus bradycardia and asystole. We report a unique case of severe sinus bradycardia with atrial bigeminy and junctional rhythm in the setting of moderate hyperkalemia, a rarely reported electrocardiographic finding.
Hyperkalaemia Induced Narrow QRS Complex Complete Heart Block
2020
Potassium is an important extracellular ion with an important role in the myocardial cells function. Hyperkalaemia is a potentially life-threatening electrolyte disturbance which can impair cardiac conduction. Here, we report a case of a 72-year-old woman with past medical history of chronic kidney disease secondary to insulin dependent diabetes, who was brought to the Emergency Department with unresponsiveness 15 minutes after acute dyspnea. On arrival, the patient was in asystole without any cardiac output. Cardiopulmonary resuscitation (CPR) was commenced immediately. In addition to the resuscitation guideline during the CPR, with the presumed Hyperkalemia, treatment was started empirically while awaiting point of care electrolyte result. After treatment and during 3rd cycle of CPR, ECG demonstrated sinoventricular rhythm with ROSC. QRS subsequent narrowed down in her ECG followed by narrow QRS complete heart block within 15 minutes. Minutes later, she gained consciousness. Patho...
Atrioventricular and intraventricular conduction in hyperkalemia
The American Journal of Cardiology, 1975
Electrophysioiogic studies using His bundle recording and atriai pacing in one patient revealed intraatrial conduction delay and marked prolongation of conduction time in the His-Purkinje system. it is concluded that conduction defects in the specialized intraventricuiar conduction system are common in hyperkaiemia and result in electrocardiographic patterns of fascicular block.
Marked Symptomatic Bradycardia Associated with Profound Hyperkalemia
Emergency Medicine: Open Access, 2012
Background and objectives: Hyperkalemia is a common disorder presents to Emergency Department (ED) with different type of presentations, one of them is cardiac dysrythmia which can be lethal if potassium level is not normalized quickly and cardiac cells stabilized by calcium in appropriate manner. We hypothesize that administration of calcium and potassium lowering drugs will prevent the need for aggressive intervention for patient with sever hyperkalemia and very slow heart rate with decrease level of consciousness. Design and setting: Prospective, patient presented to academic emergency department. Patient and method: On arrival to the emergency department, patient was confused with a lethargic mental status and pulse rate of 41 beat per minute. Blood samples were sent for immediate determination of venous blood gas (VBG) concentrations, which showed potassium concentration of 7.85 mmol/L. The patient was immediately started on hyperkalemia treatment including 2 g calcium chloride was administered intravenously (IV) over 5 minutes. The patient started to regain consciousness and recognize her family with 10 minutes of these treatments. Results: A repeat ECG showed atrial fibrillation, which is similar to the patient's baseline ECG before this admission. Repeat VBG results 90 minutes later showed pH 7.22, Pco 2 39.8 mm Hg, Po 2 26.5 mm Hg, HC0 3 15.9 mmol/L, and potassium 6.00 mmol/L. These interventions led to an almost immediate resolution of the sever bradycardia without the need for temporary cardiac pacing. Conclusion: Life-threatening hyperkalemia should be suspected in any patient with acute onset bradycardia who presents to the emergency department. Blood potassium concentration should be determined immediately by rapid point-of-care tests for an early diagnosis and appropriate medical treatment. Sufficient agreement is found in potassium levels obtained from a chemistry laboratory analyzer and a VBG analyzer.
ECG alterations suggestive of hyperkalemia in normokalemic versus hyperkalemic patients
BMC Emergency Medicine
Background: In periarrest situations and during resuscitation it is essential to rule out reversible causes. Hyperkalemia is one of the most common, reversible causes of periarrest situations. Typical electrocardiogram (ECG) alterations may indicate hyperkalemia. The aim of our study was to compare the prevalence of ECG alterations suggestive of hyperkalemia in normokalemic and hyperkalemic patients. Methods: 170 patients with normal potassium (K +) levels and 135 patients with moderate (serum K + = 6.0-7.0 mmol/l) or severe (K + > 7.0 mmol/l) hyperkalemia, admitted to the Department of Emergency Medicine at the Somogy County Kaposi Mór General Hospital, were selected for this retrospective, cross-sectional study. ECG obtained upon admission were analyzed by two emergency physicians, independently, blinded to the objectives of the study. Statistical analysis was performed using SPSS22 software. χ 2 test and Fischer exact tests were applied. Results: 24% of normokalemic patients and 46% of patients with elevated potassium levels had some kind of ECG alteration suggestive of hyperkalemia. Wide QRS (31.6%), peaked T-waves (18.4%), Ist degree AV-block (18.4%) and bradycardia (18.4%) were the most common and significantly more frequent ECG alterations suggestive of hyperkalemia in severely hyperkalemic patients compared with normokalemic patients (8.2, 4.7, 7.1 and 6.5%, respectively). There was no significant difference between the frequency of ECG alterations suggestive of hyperkalemia in normokalemic and moderately hyperkalemic patients. Upon examining ECG alterations not typically associated with hyperkalemia, we found that prolonged QTc was the only ECG alteration which was significantly more prevalent in both patients with moderate (17.5%) and severe hyperkalemia (21.1%) compared to patients with normokalemia (5.3%). Conclusions: A minority of patients with normal potassium levels may also exhibit ECG alterations considered to be suggestive of hyperkalemia, while more than half of the patients with hyperkalemia do not have ECG alterations suggesting hyperkalemia. These results imply that treatment of hyperkalemia in the prehospital setting should be initiated with caution. Multiple ECG alterations, however, should draw attention to potentially life threatening conditions.
Severe hyperkalemia with minimal electrocardiographic manifestations
Journal of Electrocardiology, 1999
Severe hyperkalemia with minimal or nonspecific electrocardiographic (ECG) changes is unusual. We report data on seven patients with renal failure, metabolic acidosis, and severe hyperkalemia (K + -> 8 mmol/L) without typical ECG changes. Initial ECGs revealed sinus rhythm and PR and QT intervals in the normal range. QRS intervals were slightly prolonged in two patients (110 ms), and incomplete right bundle branch block was evident in one. Thus, the absence of typical ECG changes does not preclude severe hyperkalemia.
Journal of Clinical Cardiology and Cardiovascular Interventions, 2020
Bradycardia is commonly encountered in emergency department. Hyperkalemia may sometime cause bradycardia with block and also synergize with AV node blockers to cause bradycardia and hypoperfusion. We report a 53 years old male with history of hypertension, congestive heart failure and coronary artery disease was admitted to hospital for sudden onset of breathlessness. He underwent percutaneous coronary intervention (PCI) to left anterior descending (LAD) artery and left circumflex (LCx) artery one year ago and taking Aspilet 80 mg for daily, Clopidogrel 75 mg daily, Ramipril 5 mg daily, Atorvastatin 20 mg daily, Metoprolol 25 mg daily, Spironolactone 25 mg daily and Frusemide 40 mg daily. Significant physical examination was remarkable for a temperature 97.5'F, blood pressure of 110/70 mmHg, heart rate of 40 beats per minute, oxygen saturation was 99% on air and both lung were full with audible crepitation by auscultation. He was given atropine 0.6 mg bolus and transcutanaeous pacing with unimproved heart rate and then a transvenous pacing was immediately placed before the blood investigation results were returned. His relevant laboratory values were significant for a potassium of 7.99 mmol/L(ref range : 3.5-5.2 mmo/l) , creatinine of 458 micmol/L (ref range : 59-104 micmol/L) , Urea of 33.9 mmol/L (ref range : 2.7-8.0 mmol/l), random blood glucose of 233mg/dl , sodium 126.8 mmol/L (ref range 135-145 mmol/L) , anion gap of 13.5 mmol/? (ref range : 3.6-11.0 mmo/L) and bicarbonate of 15.6 mmil/L (ref range: 22-29 mmol/L). He was given calcium glucoronate , insulin with dextrose , kaexylate , nebulizer salbutamol with significant improvement in his potassium levels to 4.6 in 24 hours. In Cardiac intensive care unit his heart rate was improved and the transvenous pacemaker was turned off the next day.