心房颤动伴长R-R间期的临床意义分析

目的探讨心房颤动伴长R-R间期的发生机制及临床意义。心房颤动(Atrialfibrillation)是临床上最常见的心律失常之一。动态心电图监测常发现心房颤动伴长R-R间期(R-R间期≥2.0s),逸搏及逸搏心律现象,以往多认为是房颤合并Ⅱ度、高度,甚至Ⅲ度房室传导阻滞。但以后人们发现许多心房颤动患者复律为窦性心律时并无Ⅱ度或高度房室传导阻滞。方法本研究对门诊及病房心房纤颤患者行动态心电图24h记录到的60例心房颤动伴长R-R间期患者的资料进行相关分析,对长R-R间期与睡眠相关或不相关的情况进行比较。结果 60例患者共出现长R-R间期(≥2.0s)526次,白天65次(12.4%),夜间461次(87.6%);平均心室率<60次/min者37例、≥60次/min者23例;60例患者的长RR间期在2.0～4.6s之间。长R-R间与睡眠相关者46例、不相关者14例。结论心房颤动伴长R-R间期多发生在夜间睡眠状态,与睡眠呈显著相关性(P<0.01),患者无明显自觉症状,为非病理性房室传导阻滞,一般无临床意义,诊断心房颤动伴Ⅱ度房室传导阻滞(AVB)时应慎重。     

急性下壁心梗合并完全性房室传导阻滞抢救成功1例

患者男,68岁。主因心慌伴头、颈部疼痛4小时而入院。查体:血压160/100mmHg,急性痛苦病容,口唇发绀、颈软、心律不齐。心电图示急性下壁心梗、Ⅱ度文氏型房室传导阻滞,室性逸搏。立即给阿托品1.2mg,异丙肾1mg+10%葡萄糖250ml 静滴,以每分钟3～4μg 的速度持续滴入,心率维持在60次/分     

紧急锁骨下静脉穿刺安置临时起搏器的体会

近年来我们在病床旁施行经锁骨下静脉的紧急心脏起搏治疗共32例,现报告如下:1 临床资料及方法1.1病例资料 本组中男22例,女10例,年龄:21～73岁。冠心病(心肌梗死),Ⅲ度房室传导阻滞12例,Ⅱ度Ⅱ型房室传导阻滞5例;窦性停搏,交界性心律3例;病窦综合征6例;病毒性心肌炎,Ⅱ度房室传导阻滞2例;肥厚性心肌病,Ⅱ度Ⅰ型房室性传导阻滞2例;肺源性心脏病,高位截瘫并室性逸搏心     

蟾蜍卵中毒1例报告

患儿,女,2岁.因误服蟾蜍卵30 min后出现频繁呕吐,腹泻4 h以蟾蜍中毒收入院.查体:意识清楚,精神萎靡,面色及口唇,口周轻度紫绀,双肺呼吸音粗,脉搏有力,心率70次/min,节律不整,肠鸣音亢进.心电图示:房室传导阻滞,交界区逸搏心律.立即用1∶5 000高锰酸钾洗胃后注入蛋清,静脉注射速尿加速排毒,静脉滴注维生素C、三磷酸腺苷、辅酶A、地塞米松以保护及恢复心肌功能,应用阿托品缓解房室传导阻滞引起的心动过缓,经以上治疗15 d,患儿痊愈出院.     

阿托品试验诱发高度AVB 1例

患者男性，56岁。因头昏、胸闷2年余，“卖性心动过缓”病史3年。入院时体检：一般情况尚好，两肺（－），心界不扩大、心率54次／分，律齐，第一心音低。心电图示：安律52次／分。进行阿托品试验，静注阿托品1．5mg后策一分钟心电图出现高度房室传导阻滞（AVB）、交界性逸搏，第二、三分钟到1小时均为高度房室传导阻滞。10分钟时给予异丙肾上腺素ling静滴，以每分钟2～3Pg静滴达1小时无效而停网。1小时50分钟时自行恢复窦性心率。讨论本例在进行阿托品试验时发生高度房室传导阻滞，使用异丙肾上腺素无效。而阿托品（抗胆碱能神经药物）和…     

阿奇霉素相关房室传导阻滞

1例86岁女性患者因肺部感染静脉滴注头孢曲松钠2.0 g（1次/d）、阿奇霉素0.5 g （1次/d）和盐酸氨溴索30 mg（2次/d）。第4次静脉滴注阿奇霉素约30 min时,患者突然出现胸闷、憋气。心电图示Ⅲ度房室传导阻滞。立即停止药物输注,给予吸氧。1h后,患者胸闷、憋气消失。5h 后复测心电图示窦性心律。未再应用阿奇霉素,患者未再出现类似症状。     

左氧氟沙星致过敏性休克诱发横纹肌溶解症

1例42岁男性患者因醉酒后摔伤,伤口污染严重,给予盐酸左氧氟沙星注射液0.2 g溶于0.9%氯化钠注射液250 ml静脉滴注预防感染。首次静脉滴注左氧氟沙星约2 min（注入药液约4 ml）时,患者出现呼吸困难,烦躁不安,心率120次/min,呼吸26次/min,血压测不到,血氧饱和度0.80。立即停用左氧氟沙星并给予...     

硝苯吡啶治疗Ⅲ度房室传导阻滞3例报告

例1,男,70岁。以活动后心悸、气促10年,反复晕厥3天为主诉入院。体检:神志清。血压21.2/9kPa。心界向左下扩大,心率32次/分,律整,心前区闻及Ⅲ级收缩期吹风性杂音,A_2>P_2。肺(一)。心电图示左室肥大伴劳损。Ⅲ度房室传导阻滞。临床诊断:冠心病并Ⅲ°房室传导阻滞。住院后给予异丙基肾上腺素、阿托品、麻黄素等治疗1周无效,改为硝苯吡啶20mg口服,每日3次。第三天心律转为窦性,62次/分,住院1个月出院,病情稳定。例2,女,20岁。以1天内晕厥3次为主诉入院。体检:神志清。血压14/9kPa。胸骨左缘第二肋间闻及Ⅲ级收缩期吹风性杂音,P_2亢进、分裂。肺(一)。心电图示Ⅲ°房室传导阻滞。诊断:先天性心脏病房间隔缺损,Ⅲ°房室传导阻滞。入院后以异丙基肾上腺素、阿托品、麻黄素等治疗3天无效,第四天开始口服硝苯吡啶30mg,每日3次。7天后复查心电图示窦性心率,室率68次/分。观察1周病情稳定出院。     

人工心脏起搏心电图(八)

(九)长间隔后起搏性逸搏 1停搏后起搏性逸搏应用抑制型起搏器的患者,在自身心率较快时见不到起搏搏动.只有当发生窦性停搏、窦房阻滞或显著的窦不齐时,起搏器才有机会发放脉冲引起1次或数次起搏性逸搏.如为心房起搏器表现为房性起搏性逸搏.如为心室起搏器则表现为室性起搏性逸搏,见图109.如系双腔起搏器则表现为房室顺序起搏性逸搏.     

重症心肌炎临终前动态心电图1例分析

病人 ,女 ,3 1岁。因胸闷、心悸、气促 3d ,晕厥 4次入院。体检 :病人神志清楚 ,精神软弱 ,呼吸略促 (2 2次 /min) ,口唇无发绀 ,颈静脉无怒张 ,两肺呼吸音清晰 ,未闻及干湿罗音。心律不齐 ,心率 50次 /min ,血压 82 /52mmHg ,心音低钝 ,心浊音界正常范围 ,P2 >A2 ,未闻及明显病理性杂音。腹平软 ,肝脾未及 ,双下肢无浮肿。入院时心电图诊断 :①窦性心律 ;②Ⅲ度房室传导阻滞伴交界性逸搏心律 ,房率 94次/min ,室率 50次 /min ;③不完全左束支传导阻滞 ;④ST T改变。实验室检查 :血钾 3 6mmol/L ,血钠 14 2mmol/L ,血氯96mmol/L ,血钙 …     

倍他乐克注射液治疗急性心肌梗死疗效观察

目的探讨静脉注射倍他乐克治疗急性心肌梗死的有效性及安全性。方法 33例急性心肌梗死患者,排除严重低血压、严重心动过缓、Ⅲ度房室传导阻滞及心源性休克情况,予3支倍他乐克针剂缓慢静脉注射,每支5mg,共15mg,间隔5min,观察心率、血压、心功能、ST段抬值总和、胸痛程度及1周内恶性心律失常、猝死、再发心肌梗死等情况。结果静脉注射倍他乐克后,患者血压、心率及收缩压与心率乘积(SBPHR)、胸痛积分均明显下降,而心梗相关导联ST段抬高值的总和(∑ST)也有明显下降,心功能无明显下降,1周内未发生不断改进性心律失常、猝死、再发心肌梗死。结论早期静脉注射倍他乐克可有效预防急性心肌梗死患者发生心力衰竭和预防猝死、再发心肌梗死。     

The haemodynamic effect of verapamil

Summary The haemodynamic effect of verapamil has been studied in twelve patients during diagnostic cardiac catheterisation. The dose administered was 0.1 mg/kg body-weight given as an i. v. injection followed immediately by continuous infusion of 0.005 mg/kg body-weight per minute for thirty minutes. The total amount of verapamil administered varied between 13.0 and 21.6 mg. Brachial and pulmonary artery pressure, cardiac output, stroke volume, heart rate and peripheral vascular resistance were studied as well as atrioventricular conduction. — In patients in sinus rhythm no significant haemodynamic effects were observed, despite a significant increase in the atrioventricular conduction time. One patient developed second degree atrioventricular block, and several others showed first degree blocks. Two digitalized patients with atrial fibrillation were examined. Their results differed as they showed significant decreases in ventricular rate, blood pressure and cardiac output despite some increase in stroke volume. — On the basis of these results it was concluded that verapamil does not seem to have any haemodynamically unfavourable effects in the doses used. However, until further experience has been gained, verapamil should be used with caution in patients with atrial fibrillation who have already been digitalized. Verapamil should also be used with great care in persons with disturbed atrioventricular conduction and should not be given at all to patients with AV block of the second and third degree.     

The pathophysiological profile of the acute cardiovascular toxicity of sodium fluoride

The intravenous infusion of sodium fluoride (2 mg/kg X min) into anesthetized rats caused a progressive fall in arterial blood pressure, cardiac output, heart rate and peripheral resistance. Respiratory rate increased during the first 20 min of infusion resulting in increased oxygen and decreased carbon dioxide blood concentrations. Total body oxygen consumption decreased after 30 min of NaF infusion by 29%, whereas the respiratory quotient (RQ) increased from 0.8 to 1.06. Death occurred after a mean dose of 79.6 +/- 4.6 mg/kg NaF. The terminal cardiac event before death was atrioventricular block followed immediately by asystole. Artificial ventilation did not influence the cardiovascular and the lethal effects of fluoride infusion. The plasma concentrations of total and ionized calcium decreased upon NaF infusion. The infusion of extra calcium did not prevent NaF-induced cardiovascular failure but decreased plasma fluoride levels and increased the lethal dose of NaF by 17% (not significant). In isolated atria and perfused hearts in vitro, NaF decreased the force of contraction in a dose-dependent manner. In conclusion, cardiovascular failure resulting from the direct cardiodepressive and vasodilatating effects of fluoride (and not from respiratory depression or hypocalcemia) accounts for the lethal outcome of fluoride intoxication.     

Effects of encainide (MJ9067) on the ventricular fibrillation threshold in anesthetized dogs

The right ventricular epicardial ventricular fibrillation threshold (VFT) was determined during paced supraventricular rhythm using 100 Hz trains of stimuli at 15 min intervals in dogs before and during the intravenous administration of encainide, a new antiarrhythmic drug. With each VFT determination, simultaneous blood samples were obtained for determination of drug concentration. In 6 control dogs, VFT determined every 15 min during a 210 administered as a 90 min intravenous infusion at three successive rates (0.01, 0.02 and 0.04 mg/kg/min) for 30 min each. VFT measured at 5 and 20 min of each infusion increased from a mean control of 11.5 +/- 1.5 (+/-SE) to 20.2 +/- 2.2 mA (p less than 0.01) after 20 min of the third infusion. The maximal effect occurred during the second infusion with plasma concentration of 594 +/- 46 ng/ml and then reached a plateau. In group II (n = 6), encainide was administered in four successive sequences, each one including a bolus loading intravenous dose followed by a 45 min intravenous infusion. VFT measured at 30 and 45 min of each infusion when the encainide plasma concentration was close to a steady state increased significantly (p less than 0.01) after the second infusion from 11.8 +/- 2 to 27.3 +/- 4 mA. Two dogs in group II developed transient complete atrioventricular block at an encainide plasma concentration of greater than 800 ng/ml. These results show that the new antiarrhythmic drug encainide increases the VFT in anesthetized dogs.     

硫酸镁救治乌头碱中毒致顽固性室性心律失常

1例46岁男性患者误服生草乌、川乌粉约5 g后3 h出现意识障碍、全身抽搐;心电图检查示心室扑动,心率110次/min。立即电除颤,静脉推注胺碘酮,未复律。再次静脉推注胺碘酮,同时静脉推注利多卡因100 mg和15%硫酸镁8 ml（1 g）,复律。心电监护示频发多源多形性室性期前收缩。继续持续静脉泵入胺碘酮和利多卡因。1 min后,再次出现多形性室性心动过速（室速）,心率180~190次/min。静脉推注胺碘酮和利多卡因以及电复律均无效。再次静脉推注硫酸镁8 ml（1 g）,室速仍存在但频率逐渐降至160~170次/min。遂第3次静脉推注硫酸镁8 ml（1 g）,心率140~150次/min。10 min后,第4次静脉推注硫酸镁8 ml（1 g）,心律转复。1 h后给予患者行血液灌流,最初1 h出现4次多形性室速,每次静脉推注硫酸镁（1~1 g）均有效。次日,患者恢复正常,心电图示窦性心律,心率75次/min。     

静脉滴注莫西沙星致过敏性休克

1例75岁女性患者因腰椎手术后预防感染给予盐酸莫西沙星注射液0.4 g(250ml)静脉滴注。用药约10 min后,患者突感全身不适,皮肤湿冷,大汗,心率130次/min,呼吸26次/min,血压57/37 mmHg(1 mmHg=0.133 kPa)。考虑为莫西沙星导致的过敏性休克,立即停用莫西沙星,给予心电监护、鼻导管吸氧、先后静脉注射盐酸肾上腺素注射液0.5 mg、呋塞米注射液10 mg、硝酸甘油注射液2.5 mg,酒石酸美托洛尔片12.5 mg舌下含服。80 min后症状缓解,心率88次/min、呼吸18次/min,血压95/54 mmHg。     

126例心房颤动合并长R—R间期患者的动态心电图分析

目的采用动态心电图分析心房颤动合并长R—R间期（〉1．5s）、逸搏及逸搏心律患者是否存在房室阻滞。方法对126例心房颤动患者进行24h动态心电图检查，根据患者记录的生活日志，按长R—R间期、逸搏及逸搏心律出现的时间是否与睡眠有关，把患者分为A（睡眠有关组）、B（睡眠无关组）两组。结果A组发生长R—R间期1．5～2．0s，〉2．0s及逸搏及逸搏心律人平均数分别为（26．02±6．03）、（7．39±1．05）、（6．90±1．28）；B组发生长R—R间期1．5—2．0s，〉2．0s及逸搏及逸搏心律人平均数分别为（203．05±41．01）、（35．48±7．52）、（28．10±6．25）；B组明显多于A组（P〈0．01）。结论房颤伴长R—R间期、逸搏及逸搏心律与睡眠有关时，此现象非病理性房室阻滞；而房颤伴长R—R间期、逸搏及逸搏心律与睡眠无关时，应视为病理性房室阻滞。     

频率适应型双腔起搏器对男性Ⅲ度房室传导阻滞患者运动耐量和性生活质量的影响

目的观察频率适应型双腔起搏器（DDDR型起搏器）对男性Ⅲ度房室传导阻滞患者运动耐量和性生活质量的影响。方法选择2008年8月至2012年8月在商丘市第一人民医院住院治疗的Ⅲ度房室传导阻滞患者共计170例。根据有无植入DDDR型起搏器分组为对照组（64例）和DDDR组（106例）。采用国际男性性功能判断指数（IIEF-5）量表观察治疗前后患者性功能评分，调查治疗前及治疗后6个月性功能评分；统计每个月患者性交次数。运动耐量和心功能评价采用6min步行试验和超声心动图，6min步行试验结束时测量患者心率、步行距离，超声心动图测量左心室射血分数，计算心输出量。结果DDDR组较对照组治疗后IIFE-5总评分、性交满意度、性交次数明显增加[（20±6）分比（16±5）分，（4．6±1．3）分比（2．6±1．6）分，（6．1±2．9）次／月比（3．4±1．7）次／月]，差异有统计学意义（P＜0．05）。DDDR组较对照组治疗后6min步行试验步行距离、心率、心输出量明显改善[（528±106）m比（379±75）m，（127±9）次／min比（51±8）次／min，（4．8±0．7）L／min比（3．9±0．5）L／min]，差异有统计学意义（P＜0．05）。结论DDDR型起搏器对于男性Ⅲ度房室传导阻滞患者运动耐量和性生活质量有明显的改善作用，其机制主要是起搏器植人增加雷耍肺器及组织的供向和件毕活时的运动耐量。     

1例头孢曲松钠过敏性休克致持久植物人状态分析

1例47岁女性患者因急性上呼吸道感染就诊,给予静脉滴注头孢曲松钠2.0g。患者静滴约3min时,出现四肢抽搐、口吐白沫,意识丧失、呼吸微弱。立即停药,予以面罩辅助通气给氧、心电监护,患者此时血压测不出,心率50次/min。给予气管插管接呼吸机辅助通气,抗休克药物应用,心率上升至150次/min。收入院急诊ICU继续抢救治疗。入院后患者一直处于昏迷状态,转入神经内科普通病房。入院后49d患者处于持久植物人状态,时有无意识抓握、眨眼等,对声音刺激有反应,意识状态无明显变化,患者家属要求自动出院。     

Cardiovascular effects of histamine infusion in man

Histamine (H) is stored in man in the cardiovascular as well as in other systems, from where it can be released under exposure to immunologic and nonimmunologic stimuli. To understand better the hemodynamic changes produced in man by endogenous H release, we infused H for 3.5-7 min at the rate of 0.4 microgram/kg/min i.v. in four patients with normal left ventricular (LV) function undergoing diagnostic cardiac catheterization. We observed a significant fall in systolic, diastolic, and mean aortic pressure, systemic vascular resistance, LV end-diastolic pressure, and stroke index, and a significant rise in heart rate, cardiac output, and LV dP/dtmax, with small changes in mean pulmonary arterial pressure and pulmonary vascular resistance. During infusion there was also a significant rise in plasma H, epinephrine, and norepinephrine. All hemodynamic changes started 1-2 min after the beginning of H infusion and reverted to normal within 5 min from the end of the infusion. Subjective complaints were mild and transient in all patients. One patient progressed from first- to third-degree atrioventricular block, with prompt recovery of 1:1 atrioventricular conduction at the end of infusion. Thus, exogenous H administration in man at the rate of 0.4 microgram/kg/min produces significant and transient hemodynamic changes, mainly represented by systemic hypotension, tachycardia, and increased LV performance. These latter can be attributed to the associated increase in sympathoadrenergic activity, although a direct cardiac effect of H cannot be excluded.