静脉注射美托洛尔、地尔硫卓治疗快速心房纤颤的临床疗效观察

目的:观察美托洛尔注射液和地尔硫卓注射液治疗快速房颤的有效性和安全性。方法:105例符合入选标准的快速房颤患者被随机分为3组,美托洛尔组39例:5mg美托洛尔缓慢静脉注射,观察5min,如无效重复一次,连续用药3次,总量15mg;地尔硫卓35例:地尔硫卓15mg稀释后静脉注射,观察15min,如无效重复1次,继以15mg/h维持。西地兰组31例:西地兰0.2～0.4mg稀释后静脉注射,观察10min,如无效追加0.2～0.4mg,连续用药3次;总量0.6～1.0mg。记录用药前、后心室率和血压变化,并比较在各观察时间点上的有效率。结果:与西地兰相比,美托洛尔和地尔硫卓起效更快[(36.9±11.6)min∶(8.2±4.5)min∶(9.1±3.8)min,P<0.05],心室率下降幅度更明显(25.22%∶33.32%∶37.50%,P<0.05),治疗有效率更高(71.0%∶89.7%∶91.4%,P<0.05)。而美托洛尔组和地尔硫卓组之间无显著性差异。三组均无严重不良反应发生。结论:美托洛尔注射液和地尔硫卓注射液均能快速、安全、有效控制快速房颤的心室率。     

老年肺心病心衰伴快速房颤的临床疗效观察

目的:比较老年肺心病中重度心功能衰竭伴快速房颤的患者静脉注射地尔硫卓及西地兰控制心室率的临床疗效和安全性.方法:采用随机单盲方法,将60例老年肺心病合并中重度心功能衰竭伴快速房颤患者分为2组,分别给予地尔硫卓和西地兰静脉注射,观察控制心室率的有效率及临床症状和体征的变化.结果:地尔硫草组控制心室率有效率为93.6%,西...     

静脉地尔硫(卓)治疗老年人快速心室率房颤、房扑和室上速的临床观察

目的　观察静脉地尔硫艹卓 对老年人快速心室率的房颤、房扑及室上速的疗效与安全性。方法　 1 5例患者 (7例房颤、3例房扑、5例室上速 )静脉注射地尔硫艹卓 1 0～ 1 5mg,有反应者继以 1 0～ 1 5mg/ h浓度持续静点 6～ 1 2 h。结果　用药后心室率比用药前基础心率减少 >2 0 % ;转复为窦性心律或心室率 <1 0 0次 / min为治疗有反应 ,本组 1 5例患者 1 2例 (80 % )有反应 ;用药后心室率下降最大效应时间 1 1 min,心室率下降幅度 42± 1 6次 / min。结论　地尔硫艹卓 能安全地应用于快速心室率的房颤或房扑及室上速的老年人 ,并在大多数病人能迅速有效地达到心率的控制和中止室上速的发作 ,而且不会引起或加重心功能障碍。     

源自右束支的逸搏节律和阵发性心动过速

作者报告1例罕见的起源于右束支的逸搏节律和阵发性心动过速.女性,20岁,无器质性心脏病.心电图呈窦性心律,在窦性停搏后继以室性逸搏节律,呈不完全性左束支传导阻滞型(QRS=110毫秒);偶而伴有QRS形态相似的阵发性心动过速。希氏束电图上:在窦性心律时,PA(房内)、AH(房室结)和HV(希-室)间期分别为10、70和50毫秒;逸搏节律或心动过速时,HV为10毫秒,并逆行激动心房。在超速起搏和心房期前刺激后均有逸搏.     

临床判断足以处理传导障碍

希氏束电图已为复杂心律失常和房室传导疾病的了解作出很大的贡献。在有经验者手中,希氏束电图简单、安全,对于从这些研究所取得的认识,不能有所争论。然而,同所有推广到临床医学中的新技术一样,必须小心地估价其利弊。最后,希氏束电图是否在临床上继续应用或被淘汰,将取决于对病人的治疗能否提供必需的知识、诊断技术和电生理认识。通过区分AH和HV间期以鉴定房室结和希氏-浦顷野传导,已经证实了我们关于房室传导异常的推理。应用心腔内心电图包括希氏束电图,完全有可能测定心房内传导时间、窦房结折返、各分支部位之间的传导和     

随心房率变化的希氏束内阻滞

患者男,56岁,因头晕、胸闷1h急诊。既往无晕厥,有冠心病史。体检:神志清,心率100次/min,呈二联律,未闻病理性杂音,双肺无殊。肝脾未触及。双下肢无浮肿。心电图示:平均心房心室率98次/min,QRS形态及时间正常。有2种P-R间期分别为:0.15s及0.28s,两者交替出现。心电图诊断:间歇性一度房室传导阻滞。心内电生理检查:图1呈交替P-R间期延长;心内电图可见希氏束分裂。当P-R间期150ms,H-H＇间期80ms;P-R间期280ms,H-H＇间期200ms时,每个心房波(A)后均有下传的心室波(V)。A-A间期580ms(心房率103次/min)。H＇在QRS波前30ms。提示传导阻滞在希氏束内。图2示2:1阻滞;心内电图HBEd示下传的A、H-H＇及V电位与图1相同。下传受阻的A波后仅见H,而无H＇及V电位的记录,提示2:1希氏束内阻滞。心内电生理检查结束前的记录(图略),因希氏束记录导管移位,希氏束电位显示不清楚,仅见A及V波,A-A间期888ms(心房率68次/min),心电图可见1:1房室传导,P-R间期170ms,原有的阻滞现象消失。患者安置VVI型人工心脏起搏器。     

刺激左右颈部迷走神经干对犬心脏变时与变传导效应的影响及差异

目的研究犬左右颈迷走交感神经干对心脏变时与变传导效应的影响及差异.方法Mongrel杂种犬20只,静脉麻醉后,气管插管.分别在左右股动、静脉置入电极导管,监测犬血压、体温及心内电图并记录体表心电图;分离并暴露双侧颈迷走交感神经干,植入高频刺激电极,以不同电压强度刺激左右迷走交感神经干,测量心率、AH间期、心房颤动时心室率的变化.结果刺激左右颈迷走交感神经干均可使窦性心率降低、AH间期延长、心房颤动时心室率减慢,且至0.6 V时均达到差异具有统计学意义(P＜0.01);随刺激电流强度的增加,窦性心率进一步下降、AH间期总体呈延长趋势、心室率总体呈减慢趋势;在同一刺激电流强度下,当刺激电流达到一定强度(1.5 V)时,右侧迷走交感神经干刺激减慢窦性心率的程度显著大于左侧(P＜0.01),但刺激左右两侧迷走交感神经干所引起AH间期延长与发生房室传导阻滞的数目及心室率减慢程度差异无统计学意义.结论颈迷走交感神经干对心脏变时与变传导功能的调节属于双侧支配,其中窦房结的变时功能以右侧调节为优势,房室结的变传导功能则受双侧的均衡支配.     

地尔硫(艹卓)在急诊控制心房颤动快速心室率中的应用

目的观察比较静脉注射地尔硫(艹卓)、毛花甙C控制急诊心房颤动快速心室率即时疗效比较及安全性.方法71例急诊心房颤动伴快速心室率患者随机分成2组,分别静脉注射地尔硫(艹卓)或毛花甙C.结果地尔硫(艹卓)、毛花甙C二组控制心房颤动快速心室率总有效率为93.5%,72.9%;心室率平均下降幅度分别为36%、28%;平均起效时间为6.5±3.4min、24±16.5min.地尔硫(艹卓)组有2例出现一过性低血压,可自行恢复.结论静脉注射地尔硫(艹卓)10mg,10～15mg/h维持静脉滴注对心房颤动快速心室率的控制安全、迅速、有效.     

静脉应用地尔硫治疗老年重度心力衰竭伴房颤快速心室率的护理

快速心律失常是诱发和加重心力衰竭的常见因素之一。对心力衰竭伴房颤快速心室率的患者，快速有效地控制房颤的快速心室率，保持血流动力学稳定，是治疗心力衰竭的重要环节。地尔硫革通过直接抑制钙通道，减慢房室结传导和延长房室结有效不应期而发挥控制心室率作用。本文收集2004年至2007年应用地尔硫革治疗老年重度心力衰竭伴房颤快速心室率的患者58例，现将用药过程中的具体护理体会报告如下。     

静脉应用地尔硫革治疗老年重度心力衰竭伴房颤快速心室率的护理

快速心律失常是诱发和加重心力衰竭的常见因素之一。对心力衰竭伴房颤快速心室率的患者，快速有效地控制房颤的快速心室率，保持血流动力学稳定，是治疗心力衰竭的重要环节。地尔硫革通过直接抑制钙通道，减慢房室结传导和延长房室结有效不应期而发挥控制心室率作用。本文收集2004年至2007年应用地尔硫革治疗老年重度心力衰竭伴房颤快速心室率的患者58例，现将用药过程中的具体护理体会报告如下。     

Electrophysiologic effects of propafenone in subjects with pre-existing excito-conduction disorders

Few data are currently available regarding the electrophysiological effects of Propafenon administration in patients with pre-existing excito-conduction system disturbances. We have performed electrophysiological evaluation in 18 patients (15 males and 3 females, mean age 61 +/- 9 years - 4 patients with sinus bradycardia, 5 pts with AVN block, 4 patients with bundle branch block and normal HV and 5 patients with bundle branch block and prolonged HV) before and after intravenous administration of Propafenon (1 mg/Kg B.W. in 5 minutes). Propafenone administration decreased the heart rate, significantly lengthened AH and HV intervals, lengthened atrial, ventricular and, above all, AVN refractory periods. In no cases sinus pauses, marked bradycardia, spontaneous A-V block or additional intraventricular conduction disturbances were observed. We conclude that: due to its marked electrophysiological effects on AVN and His-Purkinje system, Propafenon is electively indicated for the treatment of ventricular arrhythmias and paroxysmal supraventricular tachycardia with AVN reentry; Propafenon intravenous administration appears to be safe also in pts with preexisting excitation and conduction disturbances.     

Electrophysiologic effects of intravenous diltiazem in patients with recurrent supraventricular tachycardias

The electrophysiologic effects of intravenous diltiazem were evaluated in 10 patients with recurrent supraventricular tachycardias. The tachycardia incorporated an accessory pathway in 7 patients and was due to AV nodal reentry in 3 patients. Diltiazem 0.25 mg/kg was administered intravenously over 5 minutes during sustained supraventricular tachycardia. Programmed electrical stimulation was used to restore sinus rhythm if diltiazem failed to terminate the arrhythmia within 10 minutes. Conduction intervals, refractory periods and tachycardia characteristics were evaluated before and immediately after drug administration. Diltiazem did not significantly modify sinus cycle length, AH and HV intervals. Atrial and ventricular effective refractory periods were similar before and after diltiazem. The effective refractory period of the AV node was prolonged by 42 msec after diltiazem (p less than 0.05). Diltiazem increased the tachycardia cycle length from 320 +/- 41 to 353 +/- 36 msec (p less than 0.01) but terminated the arrhythmia in only 2 patients. After diltiazem, supraventricular tachycardia could not be reinitiated in only 2 patients and the tachycardia initiating window was not significantly reduced (56 +/- 26 to 41 +/- 33 msec). The infusion of diltiazem was accomplished without side effects. Thus, 0.25 mg/kg of intravenous diltiazem produces a modest depression of AV nodal function and is not very effective in terminating supraventricular tachycardia or preventing its initiation in this study population. Further studies using higher doses of intravenous diltiazem would be useful to determine its maximal therapeutic benefit in patients with recurrent supraventricular tachycardias.     

Electrophysiologic effects of lidocaine in children.

The effects of intravenous lidocaine on the refractory periods of the atrium, AV node and right ventricular myocardium were studied using His bundle recordings and the extrastimulus technique with and without atrial and ventricular pacing. The drug was administered in an intravenous bolus dose of 1 mg/Kg followed by an infusion of 100 micrograms/Kg/min. The AH, HV intervals and resting sinus cycle length as well as functional and effective refractory periods of atrium, AV node and right ventricle were measured before and 5 min afrer bolus injection of lidocaine. Neither of the refractory periods nor AH and HV intervals changed significantly following administration of lidocaine. The result of this first study in children is in agreement with previous reports of the effects of lidocaine on the cardiac conduction system in adults.     

艾司洛尔、胺碘酮和地尔硫(艹卓)治疗麻醉期间快室率心房颤动的比较

目的 观察静脉注射艾司洛尔、胺碘酮和地尔硫革治疗麻醉期间快室率心房颤动(房颤)的有效性和安全性.方法 将90例快室率房颤患者随机分为艾司洛尔组(Ⅰ组)、胺碘酮组(Ⅱ组)和地尔硫革组(Ⅲ组).Ⅰ组先以艾司洛尔0.5 mg/kg负荷量于1 min内静脉注射,继之以0.05mg·kg-1·min-1静脉泵注射;Ⅱ组以胺碘酮3 mg/kg于10 min内静脉注射,继之以1 mg/min静脉泵注射;Ⅲ组以地尔硫革0.25 mg/kg于5 min内静脉注射.观察用药前及用药后5、10、15、30、60、90min患者的心室率、血压、心律;观察起效时间及不良反应.结果 起效时间Ⅰ、Ⅱ、Ⅲ组分别为(4.3±2.1)min、(19.2±8.5)min、(8.5±3.4)min,组间比较差异均有统计学意义(P＜0.05);有效率在用药后30 min内组间比较差异有统计学意义(P＜0.05),但总有效率(用药后90 min时)三组组间比较差异均无统计学意义(P＞0.05).总不良反应发生率Ⅱ组低于Ⅰ组、Ⅲ组(P＜0.05),Ⅰ组与Ⅲ组组间比较差异无统计学意义(P＞0.05).结论 艾司洛尔、胺碘酮和地尔硫革均可安全有效地治疗麻醉期间的快室率房颤,艾司洛尔起效最迅速,胺碘酮应用最安全.     

Effect of the calcium antagonist diltiazem on atrioventricular conduction in chronic atrial fibrillation

The effect of oral diltiazem treatment on the mean ventricular rate was studied in 10 patients with stable atrial fibrillation (AF). The profile of mean ventricular rate was analyzed by means of 24-hour electrocardiographic recordings. Both single-dose (120 mg) and maintenance therapy (80 mg 3 times daily) reduced the mean ventricular rate significantly. After the single dose, the effect set in after 120 +/- 40 minutes (mean +/- standard deviation) and persisted for 347 +/- 84 minutes. Histograms of RR intervals were plotted and their changes after diltiazem therapy were also analyzed. The shortest and longest atrioventricular (AV) conduction times were defined as 5% and 95% values of the cumulative frequency curve, respectively. There were 2 distinct types of the RR-interval histographic changes: In 50% of the patients, the longest and shortest RR intervals prolonged proportionately; in the other 50%, the longest intervals increased disproportionately. Results indicate that oral diltiazem treatment can significantly decrease the mean ventricular rate in patients with AF by influencing the concealed conduction in the AV node. The changes of the RR-interval histograms suggest that in 50% of the patients, the increase of the concealed conduction was probably caused primarily by the increase of AF rate, and in 50% both increased AF rate and prolonged refractory period in the AV node contributed to the increase of concealed conduction.     

Effect of intravenous and oral calcium antagonists (diltiazem and verapamil) on sustenance of atrial fibrillation

Both verapamil and diltiazem are used to control ventricular response during atrial fibrillation (AF). Their effect on the maintenance of AF is not known. The effects of the intravenous and oral administration of verapamil and diltiazem were investigated in 35 patients, 18 with (group I) and 17 without (group II) documented paroxysmal AF. Programmed electrical stimulation, either extra-stimuli or burst atrial pacing, was used to induce AF. In group I, the mean values of the duration of AF before and after the intravenous and oral administration of the calcium antagonists were 31 +/- 12, 112 +/- 49 and 69 +/- 25 minutes, respectively. For group II, the values were 5 +/- 3.4, 39 +/- 13 and 14 +/- 7 minutes, respectively. The differences were statistically highly significant (p less than 0.001), after both oral and intravenous administration compared with the baseline value in both groups. The data suggest that both intravenously and orally administered calcium antagonists enhance sustenance of electrically induced AF, especially in patients with spontaneous arrhythmia. Thus, in patients with paroxysmal AF, verapamil or diltiazem should be administered cautiously, because these drugs may prolong the duration of arrhythmia. Further studies are warranted to investigate the role of calcium antagonists in spontaneously occurring paroxysmal AF.     

Pharmacological rate control of atrial fibrillation

To control ventricular rate in patients with AF, physicians should seek to control heart rate at rest and with exertion. The goal has to be achieved while minimizing costs and adverse effects. For emergency use, i.v. diltiazem or esmolol are drugs useful because of their rapid onset of action. They have to be used with caution in patients with concomitant left ventricular failure symptoms, however. For most patients with AF, chronic control of the ventricular rate can be achieved with one drug. For the chronic control of ventricular rate in patients with AF and normal ventricular function, diltiazem, atenolol, are metoprolol are probably the drugs of choice. For patients with AF and structurally abnormal hearts, atenolol, metoprolol, or carvedilol are appropriate choices. Adequate ventricular rate control by pharmacological agents should be evaluated by either 24-hour Holter monitoring or a submaximal stress test to determine the resting and exercise ventricular rate. If the mean ventricular rate is not close to 80 beats per minute, or the heart rate on moderate exertion is not between 90 to 115 beats per minute, a second agent to control the rate should be added. Excessive reductions in ventricular rates that could limit exercise tolerance should be avoided.     

Effects of cedilanid-D in combination with metoprolol on exercise tolerance and systolic time intervals in angina pectoris.

The interaction between cedilanid-D and metoprolol, a selective beta receptor blocking agent, on exercise tolerance and systolic intervals was studied in 15 patients with angina pectoris. The patients had been treated with metoprolol for several months in a dose of 50 mg, three times daily (one patient received 25 mg three times daily). Each patient participated in two studies separated by at least 1 week. After arriving at the laboratory each received 50 mg of metoprolol orally; thereafter, either cedilanid-D or placebo was infused intravenously in a double-blind study performed in randomized order. When the effect of the drugs was maximal, the systolic intervals and the heart volume were recorded at rest, and the exercise tolerance was tested with a bicycle ergometer. The mean maximal value of plasma concentrations of metoprolol assessed during the study was about 50 ng/ml but the variation among subjects was great (20 to 187 ng/ml). After administration of cedilanid-D there was a shortening of the pre-ejection period and left ventricular ejection time compared with results after placebo; the reduction was similar to that found after administration of cedilanid-D without beta blocking drugs. The total heart volume decreased by an average of 55 ml, but the individual variation was great. The patients' average work capacity, expressed as total work, was not altered by cedilanid-D when compared with results after placebo. No relation was found between initial heart size and the effect of cedilanid-D on capacity for physical work. It therefore appears that there is no indication for the routine use of digitalis during beta blocking therapy in patients with angina pectoris who do not have cardiac failure.     

Management of the older person with atrial fibrillation

Atrial fibrillation (AF) is associated with a higher incidence of mortality, stroke, and coronary events than is sinus rhythm. AF with a rapid ventricular rate may cause a tachycardia-related cardiomyopathy. Immediate direct-current (DC) cardioversion should be performed in patients with AF and acute myocardial infarction, chest pain due to myocardial ischemia, hypotension, severe heart failure, or syncope. Intravenous beta blockers, verapamil, or diltiazem may be given to slow immediately a very rapid ventricular rate in AF. An oral beta blocker, verapamil, or diltiazem should be used in persons with AF if a fast ventricular rate occurs at rest or during exercise despite digoxin. Amiodarone may be used in selected patients with symptomatic life-threatening AF refractory to other drugs. Nondrug therapies should be performed in patients with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drugs. Paroxysmal AF associated with the tachycardia-bradycardia syndrome should be treated with a permanent pacemaker in combination with drugs. A permanent pacemaker should be implanted in patients with AF and with symptoms such as dizziness or syncope associated with ventricular pauses greater than 3 seconds that are not drug-induced. Elective DC cardioversion has a higher success rate and a lower incidence of cardiac adverse effects than does medical cardioversion in converting AF to sinus rhythm. Unless transesophageal echocardiography has shown no thrombus in the left atrial appendage before cardioversion, oral warfarin should be given for 3 weeks before elective DC or drug cardioversion of AF and should be continued for at least 4 weeks after maintenance of sinus rhythm. Many cardiologists prefer, especially in older persons, ventricular rate control plus warfarin rather than maintaining sinus rhythm with antiarrhythmic drugs. Digoxin should not be used to treat patients with paroxysmal AF. Patients with chronic or paroxysmal AF at high risk for stroke should be treated with long-term warfarin to achieve an International Normalized Ratio of 2.0 to 3.0. Patients with AF at low risk for stroke or with contraindications to warfarin should receive 325 mg of aspirin daily.     

Esmolol versus diltiazem in the treatment of postoperative atrial fibrillation/atrial flutter after open heart surgery

BACKGROUND: Supraventricular tachyarrhythmias are common after open heart surgery. Possible causative factors for these arrhythmias include operative trauma, atrial ischemia, electrolyte imbalances, pericardial irritation, and excess catecholamines. Two agents commonly used to control ventricular rate in atrial fibrillation or atrial flutter (AF/AFL) are beta-blockers and calcium channel blockers. METHODS AND RESULTS: This randomized study was designed to compare the safety and efficacy of intravenous diltiazem versus intravenous esmolol in patients with postoperative AF/AFL after coronary bypass surgery and/or valve replacement surgery. A comparative cost analysis was also performed. Thirty patients received either esmolol (n = 15) or diltiazem (n = 15) for AF/AFL. During the first 6 hours of treatment, 66.6% of esmolol-treated patients converted to sinus rhythm compared with 13.3% of the diltiazem-treated patients (P <.05). At 24 hours, 66.6% of the diltiazem group converted to SR compared with 80% of the esmolol group (not significant). Drug-induced side effects, time to rate control (<90 beats/min), number of patients requiring cardioversion, and length of hospitalization were similar for the two groups. The drug cost/successfully treated patient for esmolol versus diltiazem was $254 versus $437 at 6 hours and $529 versus $262 at 24 hours. CONCLUSIONS: Although this is a small study, it suggests that esmolol is more effective in converting patients to normal sinus rhythm than diltiazem during the initial dosing period. No differences in conversion rates were observed between the two groups after 24 hours. Additional studies are needed to confirm whether esmolol is the initial drug of choice in patients with postoperative AF/AFL after coronary bypass surgery.