心电图诊断慢性肾衰高钾血症62例分析

目的：探讨心电图对诊断慢性肾衰高钾血症的临床价值。方法：对62例慢性肾衰患者心电图改变与血清钾对比分析。结果：血清钾5．5～6．5mmol／L时心电图诊断高血钾符合率73．3％,血清钾〉6．5mmol／L时心电图诊断符合率94．4％。结论：心电图对诊断高钾血症与血清钾的测定有较好的一致性。     

高钾血症心电图改变的临床意义

目的 探讨心电图对诊断高血钾的临床价值.方法 对45例高血钾患者进行常规心电图描记和血清钾离子浓度测定,比较心电图改变与血清钾浓度的关系.结果 血清钾浓度在5.5～7.0 mmol/L.的34例中,心电图显示有高血钾改变的23例,符合率67.64%.血清钾浓度7.1～8.0 mmol/L的10例中,心电图出现高血钾改变的7例,符合率70%.结论 心电图对高血钾改变的反应比血清钾测定更准确,心电图检查在高血钾的诊断中有重要临床意义.     

心电图在高血钾诊断中的作用

目的探讨心电图在高血钾诊断中的临床价值。方法对49例高血钾患者进行常规心电图描记和血清钾离子浓度测定,比较心电图改变与血清钾浓度的关系。结果心电图在诊断高血钾与血清钾测定符合率为65.3%。血清钾浓度在5.5～7.0mmol/L的37例中,心电图有高血钾改变的25例,符合率67.6%;血清钾浓度在7.0～8.0mmol/L的10例中,心电图有高血钾改变的6例,符合率60.0%。结论随着血清钾浓度的增高,心电图的异常发生率递增,心电图检查在高血钾的诊断中有重要临床价值。     

心电图诊断低血钾症的临床价值

目的探讨低血钾症患者的心电图、血生化诊断价值,进行对比分析。方法本文对192例低钾血症患者的心电图、血生化及两者联合筛查的测定结果及三组低钾血症中不同心电图的表现进行对比分析。结果心电图诊断低钾血症符合率为84.9%,优于血清钾测定（75%）。在重症低钾血症中,心电图和血清钾联合筛查与临床诊断符合率是100%。心电图U波改变、QT间期延长、室性心律失常发生率随血清钾浓度的降低而递增。结论心电图对低钾血症患者诊治及预后具有重要的临床意义。     

不同浓度补钾治疗重度低钾血症的效果评价

目的:探讨不同浓度补钾液治疗重度低钾血症的临床疗效和安全评价.方法:采用中心静脉置管微量泵进行高浓度补钾,根据补钾液浓度不同分成两组,A组20例,采用2％氯化钾溶液;B组25例,采用10％氯化钾溶液原液;两组患者均以氯化钾1g/h匀速泵入,观察两组血清钾≥4.0mmol/L时所需补钾总量、所需液体总量、补钾时间及安全性(高钾血症及恶性心律失常发生例数).结果:两组患者达到目标血清钾所需的氯化钾总量和补钾时间无统计学差异P＞0.05,两组患者补钾期间均无高钾血症及恶性心律失常发生.结论:两组患者均为高浓度补钾,补钾液浓度相差5倍,由于速度未超过传统的20mmol/h其安全性较高,治疗效果明显.     

高钾血症诊断中心电图检查的应用价值评述

目的探究临床上应用心电图检查诊断高钾血症的价值。方法选取2015年6月前在我院就诊的高血钾症患者67例,对所有患者进行心电图检查,观察心电图诊断高血钾症的符合率,并分析心电图的变化与血钾浓度升高的关系。结果 67例高钾血症患者经过心电图检查后,38例患者诊断为高血钾征,符合率为56.71%。心电图的异常与血钾浓度的改变具有一致性。结论心电图诊断高血钾症的符合率高,且随着血钾浓度的升高,患者心电图的异常程度也越来越严重,对临床诊断的意义重大。心电图对高血钾改变的反应比血清钾测定更准确,可作为诊断高血钾、判定其程度和观察疗效的重要指标。     

心电图诊断高钾血症的临床价值分析

目的探讨分析心电图诊断高钾血症的临床价值。方法回顾性分析2011年1月-2013年1月我院收治的100例高钾血症患者的临床资料。结果心电图诊断高钾血症的符合率达54．0％．所有高钾血症患者心电图均表现为直立高耸的T波．但不同程度的高钾血症患者的心电图的T波振幅的高低与患者血清K＋浓度并不呈平行关系．血清K＋浓度增高．心电图显示的P波振幅出现降低、P—R间期发生延长、QRS时限较正常心电图增宽、R波振幅减低、ST段压低、QT间期延长、心电图上可见室内束支或分支传导阻滞。结论高钾血症患者血清钾浓度越高．心电图改变程度越严重．心电图对临床诊断高钾血症具有重要的临床价值。     

急性心肌梗死早期血清钾水平与心律失常关系

目的探讨急性心肌梗死(AMI)早期血清钾水平以及血清钾与心律失常的关系。方法选择确诊为AMI,发病在2~12h之内住院的患者106例,观测发病72h内血清钾,同时对所有患者进行心电监护,监测血压、心率、心律等,并对以上情况进行对比分析。结果入院即测及72h内血清钾≤3.5mmol/L的患者20例,占19%,列为低血钾组;血清钾3.5~4.0mmol/L者71例、占67%,列为正常血钾低值组;血清钾≥4.0mmol/L(4.0~5.0mmol/L)者15例,占14%,列为正常血钾组。前两组心律失常发生率及恶性程度均明显高于正常血钾组。结论AMI早期,密切观测血清钾,并适当补钾,使血清钾维持在4.0~5.0mmo1/L,对提高AMI抢救成功有重要意义。     

Tp-TeTp-Tec及血清钾与术后室性心律异常的相关性

目的 分析心脏瓣膜置换术患者术后室性心律异常与T波峰-末间期(Tp-Te)、经心率校正的波峰-末间期(Tp-Tec)及血清钾的相关性。方法 回顾性分析河南省商丘市第一人民医院2015年9月至2018年9月收治的165例心脏瓣膜病患者的临床资料,根据心功能分级(Ⅱ级组35例、Ⅲ级组64例、Ⅳ级组66例)、主动脉阻断时间(<60 min组60例、60～90 min组68例、>90 min组37例)、术后48小时血清钾水平(<3.5 mmol/L组20例、3.5～4.0 mmol/L组44例、>4.0 mmol/L组101例)、是否发生室性心律失常(异常组95例、非异常组70例)进行分组,比较不同分组患者Tp-Te、Tp-Tec、术后48小时血清钾及室性心律失常发生率,并采用Spearman相关性分析Tp-Te、Tp-Tec及血清钾与室性心律失常发生的相关性。结果 Ⅱ、Ⅲ、Ⅳ级组Tp-Te、Tp-Tec及室性心律失常发生率比较,Ⅳ级组最高,Ⅲ级组次之,Ⅱ级组最低,差异有统计学意义(P<0.05);Ⅳ级组术后48小时血清钾水平低于Ⅱ、Ⅲ级组,Ⅲ级组术后48小时血清钾水平低于Ⅱ级组,差异有统计学意义(P<0.05);主动脉阻断时间<60 min组、60～90 min组、>90 min组Tp-Te、Tp-Tec、室性心律失常发生率比较,>90 min组最高,60～90 min组次之,<60 min组最低;>90 min组术后48小时血清钾水平低于<60 min组、60～90 min组,而60～90 min组术后48小时血清钾水平低于<60 min组,差异均有统计学意义(P<0.05);术后48小时血清钾水平<3.5 mmol/L组、3.5～4.0 mmol/L组、>4.0 mmol/L组Tp-Te、Tp-Tec及室性心律失常发生率比较,>4.0 mmol/L组最高,3.5～4.0 mmol/L组次之,<3.5 mmol/L组最低,差异有统计学意义(P<0.05);室性心律失常组Tp-Te、Tp-Tec高于非异常组,差异有统计学意义(P<0.05),血清钾水平低于非异常组,差异有统计学意义(P<0.05);Tp-Te、Tp-Tec与室性心律失常呈正相关(r=0.565、0.644,P<0.05)。结论 心脏瓣膜置换术后患者Tp-Te、Tp-Tec与室性心律失常呈正相关,还可能受患者心功能分级、主动脉阻断时间、术后血钾水平的影响,应加强上述指标的监测。     

心脏瓣膜替换术后围术期室性心律失常因素探讨及防治研究

目的　探讨心脏瓣膜置换术后围术期室性心律失常的相关因素、规律、量值,以指导临床。方法　将 156 例心脏瓣膜置换术按术式、血清钾浓度、主动脉阻断时间、心胸比例、心功能、体外循环时间等,在术后60h内5个时间段,观察记录室性心律失常例次进行分析对比研究。结果　血钾<3.5mmol/L与>4.1mmol/L组间相比有极显著性差异(P<0.001),主动脉阻断时间>90min与<60min组相比有极显著差异(P<0.01),心胸比>0.8与<0.8组间相比有显著性差异(P<0.05),心功能Ⅳ级与Ⅱ级组相比有极显著性差异(P<0.001)。结论　心脏瓣膜替换术后引起室性心律异常增多的主要因素依次为血清钾<3.5mmoI/L组;主动脉阻断时间>90min组;心功能Ⅳ级组;心胸比>0.8 组;及体外循环时间>150min组;心率<60次/min组;AMP<50mmHg组;CVP>20cmH2O组;异丙基肾上腺素应用>48h组。当室性心律失常频繁发生时,血钾<3.5mmol/L者应给以1% ~1.6%短时、快速补钾,如室性早搏每分钟大于5次,及室性二联律、三联律时,应及时应用利多卡因及快速补钾>4.5mmol/L以上,室性心律失常多会控制。如不能控制可加用心律平、乙胺碘呋酮等多数能够纠正。     

住院精神病人伴发低钾血症105例心电图分析

目的：探讨低钾血症心电图变化特征及与血清钾浓度的关系。方法：将105例患者的心电图特征及血清钾浓度作对比分析。结果：低钾血症的心电图表现为U波明显、T-U融合、Q—T或Q—u间期延长、ST段下移、T波改变和心律失常;心电图与血清钾浓度有较好的一致性,心电图异常表现的发生率与低钾症的严重程度有关。结论：临床上低钾血症心电图的各种异常表现,有助于及时发现低钾血症和指导治疗。     

透析液钾浓度对血液透析患者血钾和心律的影响

目的观察不同透析液钾浓度对血液透析患者血钾和心律的影响,总结钾浓度3．0mmol／L透析液的有效性和安全性。方法对我院50例尿毒症维持性血液透析患者先后应用钾浓度为2．0mmol／L（第一阶段）、3．0mool／L（第二阶段）的透析液各进行3个月血液透析,分别记录并比较临床症状及透析前和透析后血钾、心电图。结果第二阶段患者透析前和透析后血钾水平较第一阶段升高（P〈0．05）,血液透析中心律失常发生率低于第一阶段[（第一阶段429例次,第二阶段137例次）]（P〈0．05）。两阶段透析前高血钾出现率无明显差异（P〉0．05）。结论钾浓度3．0mmol／L透析液能明显减轻血液透析中和血液透析后的低血钾,避免或减轻透析中心律失常的发生。透析间期未发现危及生命的高血钾症。使用钾浓度3．0mmol／L透析液预防血液透析相关心律失常有效、安全。     

过量服用地高辛中毒

1例63岁男性患者因慢性心功能不全致劳累后气喘、夜间睡眠时憋气,口服地高辛0．125mg,1次／d。用药5d后症状缓解,患者自行将地高辛剂量增至0．5mg,2次／d,连续服用7d后气喘症状较前加重,夜间睡眠不能平卧,乏力,食欲差,恶心、呕吐。心电图检查：Ⅲ度房室传导阻滞,频发室性期前收缩,呈二联律,心室率57次／min。实验室检查示血钾2．9mmol／L;地高辛血清浓度〉5．0μg/L。停用地高辛,并给予补钾等对症处理。5d后患者症状明显缓解,心电图及血钾水平恢复正常,再次给予地高辛0．125mg,1次／d口服。5d后实验室检查示血钾4．2mmol／L,地高辛血清浓度1．8μg／L,患者未再出现恶心、呕吐等不适症状。     

Cardiotoxicity after massive amantadine overdose

Introduction

Amantadine hydrochloride is an antiviral medication used as therapy for parkinsonism and as a cognitive enhancer. We report 2 cases of massive, acute ingestion of amantadine hydrochloride confirmed with serial serum levels.

Case Reports

A 47-year-old woman presented to the emergency department (ED) 30 minutes after ingesting 10 g of amantadine (150 mg/kg) by her report. Initial ECG revealed a sinus rhythm with rate of 93 bpm, and a QRS of 84 msec. While in the ED, the patient sustained a pulseless cardiac arrest and the monitor revealed ventricular tachycardia. She was successfully defibrillated. Postdefibrillation ECG showed a sinus rhythm (rate = 82 bpm), QRS of 236 msec, and QTc of 567 msec. The serum potassium was 1.0 mEq/L (1.0 mmol/L). The patient was given 300 ml (300 cc) 3% sodium chloride IV over 10 minutes. Ten minutes after completion of the hypertonic saline infusion, the patient’s ECG abnormalities resolved and the QRS was 88 msec. Her potassium was repleted over the next 11 hours postpresentation, and she also received an IV bolus of 4 g of magnesium sulfate immediately after the cardiac arrest. No further hypotension, dysrhythmia, conduction delay, or ectopy was noted during the patient’s hospital stay. The second case involved a 33-year-old female patient who presented 1 hour after ingesting 100 tablets of amantadine hydrochloride (100 mg/tab). Initial ECG revealed sinus tachycardia with a QRS of 113 msec, an R wave in lead aVR of 4–5 mm and a QTc of 526 msec. Her serum potassium was 3.0 mEq/L (3.0 mmol/L), her serum calcium was 9.4 mg/dl (2.35 mmol/L), and serum magnesium was 2.1 mg/dl (0.86 mmol/L) on labs drawn at initial presentation. The patient was intubated for airway protection, and her potassium was repleted and corrected over the next 9 hours. Her ECG abnormalities improved 8 hours after initial presentation and normalized at approximately 14 hours postingestion. The patient was discharged home 11 days after her ingestion.

Conclusion

Acute amantadine toxicity manifests with life-threatening cardiotoxicity. Concurrent, often profound, hypokalemia may complicate the administration of sodium bicarbonate in the management of cardiac dysrhythmias.

     

Coadministration of estradiol/drospirenone and indomethacin does not cause hyperkalemia in healthy postmenopausal women: a randomized open-label crossover study

The effect of drospirenone on plasma potassium when coadministered with nonsteroidal anti-inflammatory drugs, such as indomethacin, is unknown. An open-label crossover study investigated the effects of estradiol/drospirenone and indomethacin coadministration on plasma potassium levels in 32 postmenopausal women. Each participant received 2 treatments in random order: indomethacin alone for 5 days and estradiol/drospirenone alone for 12 days, then estradiol/drospirenone plus indomethacin for 5 days. Plasma potassium profiles (24 hours) were measured on the first and last days of indomethacin administration. No difference was seen between treatments in the area under the curve or maximum concentration of plasma potassium. No participant experienced hyperkalemia (potassium >5.5 mmol/L). Twenty-seven participants had at least 1 potassium value above the upper limit of normal (4.4 mmol/L), but these occurred during both treatments. Coadministration of estradiol/drospirenone and a nonsteroidal anti-inflammatory drug such as indomethacin is not expected to result in increased plasma potassium or hyperkalemia in healthy postmenopausal women.     

Octreotide- or Trimethoprim-Induced Hyperkalemia?

The article by Sargent et al¹ associating hyperkalemia with octreotide in a 68-year-old, 91-kg trauma victim has little focus on other potential causes of her hyperkalemia. Her medical history was significant for noninsulin-dependent diabetes mellitus. The authors, however, do not state how long she had this disease and whether she had any evidence of end-organ damage. The episode of postoperative hypotension, as well as the assumed oliguria (her serum creatinine increased from 1.5 to 2.3 mg/dl) on day 3 of hospitalization, clearly contributed to renal hypoperfusion and potential renal injury. There was no other mention of renal impairment until the laboratory values revealed a serum creatinine of 2.5 mg/dl and a blood urea nitrogen of 91 mg/dl on day 14 of hospitalization. The patient appeared to be volume depleted (blood urea nitrogen:serum creatinine ratio > 20:1, serum sodium 154 mmol/L), and her potassium may have been lower (4.1 mmol/L) secondary to the effects of aldosterone. Interestingly, on day 11, oral (suspension?) trimethoprim-sulfamethoxazole (TMP-SMX) 180 mg twice/day (4 mg/kg/day TMP) was started for a urinary tract infection. The next day (day 12), this was changed to the intravenous route at a dose of 320 mg every 8 hours (∼11 mg/kg/day TMP) for suspected pneumonia. The patient's serum potassium was already beginning to rise slowly (4.1 to 4.6 mmol/L) even before the start of octreotide on day 16 despite improving serum creatinine (2.5 to 1.2 mg/dl) and serum sodium (154 to 147 mmol/L).     

血钾紊乱心电图异常及临床意义

目的总结血清钾离子紊乱的常见心电图异常并探讨其临床意义。方法回顾分析临床证实血清钾离子紊乱且有心电图异常的78例患者临床资料。结果 69例低血钾患者U波增高者56例,Q-T间期延长者54例,ST-T改变41例,T波改变46例,另有8例患者出现心律失常。9例高血钾患者中6例出现高尖、帐篷状T波改变,4例QRS波明显增宽,3例患者出现窦性心动过缓,1例发生窦-室传导。结论心电图可作为诊断血钾紊乱的重要辅助手段,帮助临床医师及时纠正血钾紊乱、避免血钾紊乱引起的各种严重心律失常。     

复方磺胺甲 唑联合伏立康唑致高钾并低钠血症 3例报告及分析

目的探讨复方磺胺甲唑(SMZ co)联合伏立康唑致高钾并低钠血症的原因及其处置措施。方法收集 2023年 1—2月因重症肺炎入住陕西省人民医院,联合使用了 SMZ co与伏立康唑导致高钾并低钠血症的 3例病人的临床资料并分析。结果 SMZ co联合伏立康唑可增加高钾并低钠血症风险,3例病人血钾最高分别上升至 8.1、6.1、5.6 mmol/L,血钠最低分别下降至 128、134、122 mmol/L,经口服环硅酸锆钠及补钠治疗后,3例病人血钾分别恢复至 4.9、5.1、4.5 mmol/L,血钠恢复至 136、135、 137 mmol/L。结论联合使用 SMZ co与伏立康唑可导致高钾血症及低钠血症风险增加,原因可能为 SMZ co的甲氧苄啶(TMP)成分竞争性抑制远端肾小管和集合管上皮细胞的阿米洛利样敏感钠通道,阻断钠离子(Na+)-氢离子(H+)和 Na+-钾离子(K+)交换,抑制钠的吸收,并减少钾的排泄,从而导致低钠及高钾血症;联合用药可能导致血清伏立康唑水平异常升高而增加高钾血症风险。发生药源性高钾血症时及时停药并口服环硅酸锆钠可有效降钾,低钠血症通过口服及静脉补充高渗盐即可纠正。     

Effectiveness of Sodium Polystyrene Sulfonate for Short-Term Treatment of Hyperkalemia

Background:Sodium polystyrene sulfonate (SPS) is a potassium-binding resin that is commonly used to treat mild hyperkalemia. However, there is limited evidence supporting its effectiveness in the short-term management of hyperkalemia.Objective:To determine whether SPS is effective in reducing serum potassium in general medical patients after a single oral dose.Methods:A retrospective observational study was conducted for patients admitted to the internal medicine service of a tertiary care hospital between January 2011 and May 2012 with documentation of a serum potassium level between 5.0 and 5.9 mmol/L during the hospital stay. Patients eligible for inclusion were adults without chronic or acute renal failure or recent changes in medication or diet that would affect serum potassium level. Propensity score matching was performed to minimize differences between the control group (no treatment) and the treatment group (treatment with oral SPS). Follow-up serum potassium levels (at 6–24 h) were compared with index potassium levels.Results:A total of 138 patients met the inclusion criteria, 72 in the control group and 66 in the treatment group. For most patients in the treatment group, the dose was 15 or 30 g of SPS orally. The difference between the control and treatment groups in terms of mean change in serum potassium at 6 to 24 h after the index potassium measurement was statistically significant (by paired t test) in both an unmatched analysis (−0.41 ± 0.50 and −0.58 ± 0.39 mmol/L, respectively; p = 0.039) and a matched analysis (−0.44 ± 0.29 and −0.58 ± 0.39 mmol/L, respectively; p = 0.026). No difference was observed in terms of mean change in serum potassium between patients who received 15 and 30 g of SPS (−0.51 ± 0.38 and −0.66 ± 0.40 mmol/L, respectively; p = 0.13).Conclusions:In patients with mild hyperkalemia, oral SPS therapy reduced serum potassium by 0.14 mmol/L more than control. Although this difference was statistically significant, the small treatment effect observed in this study may not be clinically important. Furthermore, the cost and potential adverse effects of treatment suggest that routine use of SPS may be inappropriate for patients with mild hyperkalemia. Prospective randomized controlled trials would help in further evaluating the effectiveness and safety of SPS.