Emergency noninvasive external cardiac pacing

Thirty-seven critical emergency department patients underwent attempts at external cardiac pacing over an 11-month period. Indications for pacing were asystole in 16, complete heart block (CHB) in 4, sinus bradycardia in 2, nodal bradycardia in 1, atrial fibrillation with bradycardia in 2, electromechanical dissociation in 1, idioventricular rhythm (IVR) in 10, and torsades de pointes in 1. Eight patients were successfully paced with improvement in their condition. Two were in asystole, two in CHB, three in sinus rhythm or atrial fibrillation with bradycardia, and one in idioventricular rhythm. Mean systolic blood pressure rise with pacing was 95 +/- 50 mm Hg. Six of these patients were ultimately discharged from the hospital. One asystolic patient survived to discharge. Other survivors presented with either CHB or bradycardia. Of the 29 patients who did not respond to pacing, 5 survived to hospital discharge. Surviving nonresponder presenting rhythms were CHB in one patient, sinus or nodal bradycardia in two, IVR in one, and torsades de pointes in one. External cardiac pacemaking appears to be effective in hemodynamically significant bradycardia. It does not appear to be effective in most instances of asystole or IVR resulting from prolonged cardiac arrest. When applied to patients with a responsive myocardium, it may result in significant hemodynamic improvement and may be lifesaving.     

Fatal hyperkalemia related to combined therapy with a COX-2 inhibitor,ACE inhibitor and potassium rich diet

We describe the case of a 77-year old mildly hypertensive woman with no underlying renal disease who was admitted to the Emergency Department (ED) in a comatose state with fever. The patient had been on low dose enalapril and a potassium rich diet. Five days before admission, rofecoxib, a new selective COX-2 inhibitor nonsteroidal anti-inflammatory drug (NSAID), was added for leg pain. She was found to have severe hyperkalemia and died 90 min after her arrival. We cannot absolutely determine whether the COX-2 inhibitor was the dominant contributor to the development of hyperkalemia or the combination itself, with an intercurrent infection and some degree of dehydration. Physicians should be aware of this possible complication and only prescribe NSAIDs, including the new COX-2 drugs, to the elderly under close monitoring of kidney function and electrolyte tests.     

Hyperkalemia in the elderly

Objective

To review the pathophysiology underlying the predisposition to hyperkalemia in the elderly; the medications that disrupt potassium balance and promote the development of hyperkalemia in the elderly; the prevention of hyperkalemia in elderly patients treated with potassium-altering medications; and the appropriate management of hyperkalemia when it develops.

Methods and main results

A MEDLINE search of the literature (1966–1996) using the terms hyperkalemia, drugs, elderly, and treatment was conducted and pertinent review articles, textbooks, and personal files were consulted. Elderly subjects appear to be predisposed to the development of hyperkalemia on the basis of both innate disturbances in potassium homeostasis and comorbid disease processes that impair potassium handling. Hyperkalemia in the elderly is most often precipitated by medications that impair cellular uptake or renal disposal of potassium. This electrolyte disorder is best prevented by recognition of at-risk physiology in the aged, avoidance of therapy with certain high-risk medications, and monitoring of plasma potassium concentration and renal function at intervals appropriate for the medication prescribed. Management of hyperkalemia entails identification of the clinical manifestations of severe hyperkalemia, stabilization of cardiac tissue, promotion of cellular potassium uptake, and ultimately removal of potassium from the body.

Conclusions

Geriatric patients should be considered at risk of developing hyperkalemia, especially when they are prescribed certain medications. Potassium levels should be monitored at appropriate intervals when these patients are treated with potassium-altering medications. Appropriate management of hyperkalemia in the elderly can avoid life-threatening neuromuscular and cardiac complications.     

血液透析患者高钾血症季节分布特征研究北大核心CSCD

目的分析血液透析患者高钾血症的发生率及其季节分布特征和不同检测次数的高钾检出率,为高钾血症的防治及研究提供重要参考依据。方法纳入四川省2018年至2020年血液透析患者资料,以血钾≥5.0 mmol/L定义为高钾血症,计算高钾血症发生率及时间分布特征。结果(1)共纳入6618例至少有一次血钾检测记录的患者,包含24885次血钾结果,高钾血症发生率为28.2%。(2)第一至第四季度高钾血症发生率分别为30.9%、29.2%、23.7%、28.6%。(3)血钾检测次数越多,高钾血症检出率越高。结论血液透析患者高钾血症发生率较高,存在季节差异,增加检测频率可以显著增加高钾血症患者检出率。     

Intractable hyperkalemia due to nicorandil induced potassium channel syndrome

Nicorandil is a commonly used antianginal agent, which has both nitrate-like and ATP-sensitive potassium (K_ATP) channel activator properties. Activation of potassium channels by nicorandil causes expulsion of potassium ions into the extracellular space leading to membrane hyperpolarization, closure of voltage-gated calcium channels and finally vasodilatation. However, on the other hand, being an activator of K_ATP channel, it can expel K⁺ ions out of the cells and can cause hyperkalemia. Here, we report a case of nicorandil induced hyperkalemia unresponsive to medical treatment in a patient with diabetic nephropathy.     

Ventricular fibrillation in an ex‐premature neonate following reperfusion of ischemic gut incarcerated within an inguinal hernia

We describe the case of a neonate who underwent surgery for bowel obstruction. The child was born at 25 weeks postconception, and at the time of surgery, he had a postconceptual age of 44 weeks. He had undergone two previous laparotomy procedures for necrotizing enterocolitis. At laparotomy, there was unexpected extensive compromise to gut perfusion. The child developed ventricular fibrillation following the reperfusion of a segment of ischemic gut found incarcerated in an inguinal hernial orifice. We discuss the pathophysiology of intestinal ischemia–reperfusion (I‐R) injury. We have reviewed the interventions that may be employed to minimize the systemic impact of I‐R.