Systemic Hyperkalemia Research Articles

Hyperkalemic cardiac arrest triggered by intravenous lidocaine following axillary brachial plexus block for the creation of an arteriovenous fistula -A case report-

Axillary brachial plexus blockade (BPB) is commonly used as an anesthetic method for patients undergoing the creation of an arteriovenous fistula (AVF) during end-stage renal disease (ESRD). Several studies have shown that the combination of intravenous lidocaine and hyperkalemia in ESRD can produce severe conduction disturbance and asystole. Here, we report a case of cardiac arrest in a 41 year old male patient who manifested severe cardiac conduction disturbance during creation of an AVF. Sixty-five minutes after BPB, the intravenous therapeutic doses of lidocaine administered to treat frequent premature ventricular contractions aggravated his heart rhythm and produced a sine wave and ventricular fibrillation. It was assumed that ventricular fibrillation was induced by a combination of local anesthetics administered during BPB and systemic hyperkalemia as a result of the ESRD [ED highlight-please ensure my changes do not alter your intended meaning]. The patient was completely resuscitated 45 minutes after the cardiopulmonary resuscitation and correction of the hyperkalemia.

Hyperkalemia of the blood-primed ECLS circuit does not result in post-initiation hyperkalemia in infants < 10 kg

To assess the risk of hyperkalemia with blood-primed extracorporeal life support (ECLS) circuits in infants < 10 kg. Retrospective cohort study of all neonatal and pediatric patients < 10 kg placed on ECLS from May 1998 to April 2001. Data collection including patient weight, patient potassium levels pre- and post-initiation of ECLS, potassium level of the primed ECLS circuit, age of the packed red blood cell (PRBC) unit, type of preservative, and preservative reduction status. Seventy-six circuits were available for the analysis. The age of the PRBC unit and preservative reduction status significantly affected the potassium level of the primed ECLS circuit. Multivariate linear regression analysis showed no significant effect on the post-ECLS initiation patient potassium level with respect to the PRBC age, the preservative reduction status, the patient potassium level prior to ECLS initiation, and the potassium level of the primed ECLS circuit. Initiation of ECLS in infants < 10 kg should not be delayed unnecessarily to perform preservative reduction or to utilize PRBC units of a specific age, as hyperkalemia of the primed ECLS circuit is not associated with systemic hyperkalemia in the patient post-initiation of ECLS.

Lidocaine-induced conduction disturbance in patients with systemic hyperkalemia

We report 2 cases in which lidocaine, given for wide-complex tachycardia in the presence of hyperkalemia, precipitated profound conduction disturbance and asystole. The electrophysiologic effects of hyperkalemia and its interaction with lidocaine are reviewed. In patients with known hyperkalemia and wide-complex tachycardia, treatment should be directed at hyperkalemia, rather than following treatment algorithms for wide-complex tachycardia. [McLean SA, Paul ID, Spector PS. Lidocaine-induced conduction disturbance in patients with systemic hyperkalemia. Ann Emerg Med. December 2000;36:615-618.]

Ventricular conduction delay and asystole during systemic hyperkalemia

Systemic hyperkalemia was induced in 30 intact dogs to evaluate electrophysiologic and hemodynamic alterations caused by excess of potassium (K +) ion. Sequential changes included atrioventricular junctional delay and block, followed by acceleration of junctional pacemakers and conduction delays in the ventricular specialized tissue and ventricular muscle. These resulted in unusual arrhythmias difficult to interpret in the peripheral electrocardiogram. As the level of potassium progressively rose, terminal Purkinje or Purkinje-muscle block was the dominant mechanism of arrest, with conduction through the ventricular specialized conduction system continuing at a regular rate even after asystole. The duration and amplitude of the intramural complexes were consistently reduced throughout the heart wall, whereas intramural conduction was progressively prolonged with late and inconstant changes in activation sequence. Ventricular pacing thresholds increased progressively, but were attainable even after asystole in some cases. The enhanced plasma K + was associated with accumulation of K + and sodium (Na +) in myocardial tissue. A relatively uniform distribution of these ions from endocardium to epicardium is postulated to be a requirement for progressive conduction delay, lack of ectopic beats and asystole. Systemic arterial pressure and coronary blood flow were maintained until very high levels of K + were reached. Although left ventricular end-diastolic pressure increased progressively, the maximal rate of rise of left ventricular pressure ( dP dt max) was reduced only at a K + level of 11 mEq/liter. Myocardial ischemia was not present, thus suggesting that the abnormal ventricular function may have been secondary to conduction delays.

Systemic hyperkalemia after successful mesenteric embolectomy

Attention is drawn to the rapid development of systemic hyperkalemia after successful superior mesenteric embolectomy. A case illustrating this abnormality is presented. Although the electrolyte shifts indicated in this case were moderate, they point up the need for careful observation of plasma, potassium, and sodium in similar clinical situations. Attention is drawn to the rapid development of systemic hyperkalemia after successful superior mesenteric embolectomy. A case illustrating this abnormality is presented. Although the electrolyte shifts indicated in this case were moderate, they point up the need for careful observation of plasma, potassium, and sodium in similar clinical situations.