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。     

酮咯酸氨丁三醇致过敏性休克

1例26岁男性患者因腹痛给予酮咯酸氨丁三醇30mg肌内注射。注射完毕后约5min,患者感头晕、乏力,并出现全身出汗、晕厥。血压65／40mmHg（1mmHg=0．133kPa）,心率108次／min。立即予吸氧、静脉给予肾上腺素、地塞米松、间羟胺及肌内注射异丙嗪等治疗。约30min后,患者神志恢复正常,症状逐渐好转,血压105／75mmHg,心率80次／min。其后未再出现不适。     

米力农静脉泵入诱发冠心病患者心房颤动

1例70岁女性患者因冠心病、心力衰竭合并肺部感染入院。入院当天给予米力农5mg加入0.9%氯化钠注射液30ml,8ml/h静脉泵入。约30min后患者诉心慌、胸闷。查体：P128次/min,HR135次/min,心律不齐,脉搏短绌。心电图示心房颤动。立即停用米力农,静脉推入胺碘酮。1h后症状消失,心电监护示心律转为窦性,HR80次/min。     

甲磺酸罗哌卡因致荨麻疹

1例42岁女性患者行右侧甲状腺次全切除术,术前心率80次/min,血压130/80 mm Hg(1 mm Hg=0.133 kPa)。采用利罗合剂(2%利多卡因10 ml+0.894%甲磺酸罗哌卡因10 ml)行双侧颈神经丛阻滞麻醉。10 min后患者胸部出现荨麻疹,心率110次/min,血压155/110 mm Hg,随后腹部与下肢均出现荨麻疹,心率125次/min,血压160/100 mm Hg。即刻给予吸氧,静脉注射地塞米松10 mg,5 min后荨麻疹有所减退。又肌内注射苯海拉明20 mg,5 min后心率95次/min,血压140/90 mm Hg,荨麻疹完全消失。     

Cardiovascular effects of AQ-A 39 in healthy volunteers

Ten healthy male volunteers performed maximal exercise tests on a bicycle ergometer. A control reading was obtained; at a second session propranolol 80 mg was given, and then placebo, 100 mg or 200 mg AQ-A 39 were administered in a randomised double-blind manner. At peak exercise, the heart rate averaged 191.6 beats/min during the control test, 185.8 beats/min after placebo, 172.4 beats/min with 100 mg of AQ-A 39 (-10%), 166.0 (beats/min) with 200 mg of AQ-A 39 (-13.4%); with 80 mg of propranolol, the heart rate averaged 132.8 beats/min and the workload accomplished was substantially lower than that accomplished with AQ-A 39 and placebo which remained the same as in the control test. No effect on blood pressure was observed. The rate pressure product was significantly reduced with AQ-A 39.     

Changes in heart rate associated with nebulized racemic albuterol and levalbuterol in intensive care patients.

The effects of equipotent doses of racemic albuterol and levalbuterol on heart rate (HR) in intensive care patients with and without baseline tachycardia were studied. Patients were included if they were hemodynamically stable and required bronchodilator therapy every four hours; patients were excluded if they were maintained on a beta-blocker. Four hours after the most recent bronchodilator treatment, each patient was randomized to receive at least two consecutive doses of albuterol 2.5 mg or levalbuterol 1.25 mg four hours apart via nebulization. HR was recorded at the end of the second dose and 5, 10, 15, 30, 60, 90, 120, 180, and 240 minutes after treatment. Twenty intensive care patients, including 10 with baseline tachycardia and 10 without baseline tachycardia, were enrolled. In patients with baseline tachycardia, the mean largest HR increase was 1.4 beats/min (1.3%) with albuterol and 2.0 beats/min (2.1%) with levalbuterol (both increases were not significant). In patients without baseline tachycardia, the mean largest HR increase was 4.4 beats/min (6.7%) with albuterol (p = 0.04) and 3.6 beats/min (5.0%) with levalbuterol (p = 0.03). Short-term use of nebulized albuterol and levalbuterol was associated with similar changes in HR in intensive care patients with or without baseline tachycardia.     

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。     

Acute and long-term efficacy of oral propafenone in patients with ventricular tachyarrhythmias.

The class Ic antiarrhythmic agent propafenone was studied by repeated electrophysiologic testing in 54 patients (43 male, aged 54 +/- 10 years, mean ejection fraction of 37.3 +/- 16.9%) with ventricular tachyarrhythmias. Forty patients (74%) had coronary artery disease. Programmed ventricular stimulation (S2, S2S3 during sinus rhythm and/or during S1S1 = 500, 430, 370, and 330 ms) off antiarrhythmic drugs induced sustained ventricular tachycardia, flutter, or fibrillation in all patients. After 450-900 mg of oral propafenone/day for 4-7 days, 51 patients were restudied. In the remaining three patients, spontaneous ventricular tachycardia occurred on drug therapy. Tachycardia induction was suppressed in 9 of 51 patients restudied (18%) and rendered more difficult to induce (basic stimulation drive greater than or equal to 40 beats/min higher than at control study) in another 7 patients (14%) (overall efficacy of 31%). The tachycardia rate decreased from 220 +/- 43 to 177 +/- 44 beats/min (p less than 0.01). The right ventricular effective refractory period increased from 232 +/- 22 to 252 +/- 22 ms (p less than 0.001). Responders to propafenone therapy had higher rates of inducible ventricular tachycardia at control (greater than 230 beats/min: 43%; less than or equal to 230 beats/min: 21%; p less than 0.05), higher ejection fractions, and lower left ventricular end-diastolic pressures than nonresponders. Eleven of the 16 patients showing a positive response to propafenone therapy in electrophysiologic testing were discharged on propafenone alone. During follow-up (17 +/- 12 months), nine patients remained free from ventricular tachycardia, one patient had a relapse, and one patient died of noncardiac death.(ABSTRACT TRUNCATED AT 250 WORDS)     

碘海醇静脉团注致过敏性休克

1例52岁男性患者行CTA检查,给予碘海醇注射液20ml静脉团注后,患者心率由65次/min升至90次/min,并出现咽部不适、咳嗽及手部皮肤瘙痒,遂停用该药。随后出现周身乏力,昏倒,意识不清,脉搏减弱,大汗,血压测不出。立即给予抗过敏、抗休克及对症治疗,患者症状逐渐好转。1周后痊愈。     

复方氨酚那敏颗粒相关室上性心动过速

1例52岁男性患者,因感冒自行服用复方氨酚那敏颗粒2袋（每袋含对乙酰氨基酚250 mg,咖啡因15 mg,马来酸氯苯那敏3 mg,人工牛黄10 mg）。30 min后出现心悸、乏力、全身震颤,大汗。HR 192次/min。心电图示室上性心动过速。给予普罗帕酮70 mg静脉推注,约10 min后震颤停止。此后症状逐渐好转,HR 92次/min。随访3个半月,未再应用该药,上述症状未再发生。     

胺碘酮致心动过缓、低血压及严重肝损害

1例69岁女性患者,因心律失常、阵发性室上性心动过速,HR166次/min,给予胺碘酮150mg静脉推注。30min后,患者出现窦性心动过缓,低血压。HR35次/min,BP81/50mmHg。立即安装临时起搏器,静脉补液,静脉注射多巴胺,1h后缓解。后因心动过速间断发作,再次给予胺碘酮注射液300mg加入5%葡萄糖注射液50ml,以0.6mg/min泵入。次日实验室检查：ALT1770U/L,AST1360U/L,TBil130.20μmol/L,DBil98.40μmol/L;PT17.3s,INR1.45。停用胺碘酮,给予对症、支持治疗。1周后症状好转。     

Cardiovascular effects and risk of syncope related to donepezil in patients with Alzheimer's disease

BACKGROUND: When otherwise unexplained, syncope in patients with Alzheimer's disease may be attributed to bradycardia caused by cholinesterase inhibitors. We studied prospectively the clinical events and cardiovascular changes occurring during treatment with donepezil in patients with Alzheimer's disease. METHODS: Consecutive patients presenting with mild-to-moderate Alzheimer's disease were included in the study. Their clinical characteristics, blood pressure, heart rate and electrocardiogram were recorded before (baseline) and during treatment with donepezil. The drug was administered at a dosage of 5 mg/day for 1 month and 10 mg/day for the following 7 months, as tolerated. We compared the baseline observations with those made at 1, 2 and 8 months of donepezil treatment. We also examined the effects of negatively chronotropic or dromotropic drugs concomitantly administered with donepezil. RESULTS: Thirty patients were included in the study, of whom 43% were taking negatively chronotropic or dromotropic drugs. The first month of therapy (donepezil 5 mg/day) was completed by 26 patients. During the 7-month high-dosage phase (10 mg/day), four patients dropped out of the study; thus, 22 patients completed the full 8 months of the study.The mean heart rate was 66 +/- 8 beats/min at baseline in the overall study population. This decreased significantly to 62 +/- 9, 61 +/- 7 and 62 +/- 8 beats/min at the 1, 2 and 8 month timepoints, respectively (all p = 0.002 vs baseline). Among patients not receiving negatively chronotropic or dromotropic drugs, heart rate decreased significantly over the course of the study (from 67 +/- 8 beats/min at baseline to 62 +/- 8 beats/min at 1 month, 62 +/- 7 beats/min at 2 months and 62 +/- 8 beats/min at 8 months [all p = 0.005 vs baseline]). There was no significant change in heart rate in patients who were receiving negatively chronotropic or dromotropic drugs.The PR interval increased over the course of the study in all patient groups, but these changes were only statistically significant in the group of patients who were not taking negatively chronotropic or dromotropic drugs (155 +/- 23ms at baseline vs 158 +/- 21, 160 +/- 22 and 163 +/- 24ms at the 1, 2 and 8 month timepoints; all p = 0.02 vs baseline).One patient developed syncope due to orthostatic hypotension; there were no cases of bradycardia-induced syncope. Gastrointestinal manifestations were reported in ten of the study patients. Abdominal pain and vomiting were the reasons for study termination in five of the eight patients who did not complete the trial. CONCLUSION: A donepezil-induced decrease in heart rate and increase in PR interval were observed only in patients with Alzheimer's disease who were not treated with negatively chronotropic or dromotropic drugs. These changes were not associated with bradycardia-induced syncope.     

Heart rate in hypertensive patients treated with ACE inhibitors and long-acting dihydropyridine calcium antagonists

Rapid heart rate (HR) has been reported to be a predictor of cardiovascular morbidity and mortality in hypertensive patients. The aim of this study was to evaluate the effect of ACE inhibitors and long-acting dihydropyridine calcium antagonists on clinic and ambulatory HR in patients with essential hypertension. We selected 292 hypertensive patients treated with ACE inhibitors and 198 hypertensive patients treated with dihydropyridine calcium antagonists. Groups were balanced for age, gender, body mass index, baseline blood pressure (BP) and HR, treatment duration and occupation. Patients had been submitted to clinic evaluation and noninvasive monitoring of BP and HR at baseline and during chronic therapy. Clinic and ambulatory BP were significantly and similarly reduced in patients treated with ACE inhibitors and calcium antagonists. Globally, clinic and 24-h HR were significantly reduced in patients treated with ACE inhibitors and remained unchanged in those treated with calcium antagonists. When patients were grouped according to baseline clinic HR (< 65 beats/min, 65-74 beats/min, 75-84 beats/min, and >85 beats/min), ACE inhibitors did not significantly change HR in subjects with baseline clinic HR <74 beats/min but significantly reduced clinic, 24-h, daytime and nighttime HR in those with baseline HR >75 beats/min and particularly in those with baseline HR >85 beats/min. Calcium antagonists did not significantly change clinic, 24-h, daytime and nighttime HR in various subgroups. Our study shows that ACE inhibitors reduce both clinic and ambulatory HR in hypertensive patients with faster HR, who seem to be at higher risk, and that long-acting dihydropyridine calcium antagonists do not induce significant changes in HR during chronic treatment (neither decrease nor increase). Whether this aspect is associated with a better prognostic impact of ACE inhibitors in essential hypertension should be determined in prospective studies.     

Carvedilol overdose with quantitative confirmation

Carvedilol is a non-selective beta-adrenoreceptor antagonist that is also an antagonist at the alpha(1)-adrenoreceptor. This unique pharmacological effect may produce a different toxicodynamic profile compared to other beta-adrenoreceptor antagonists. Only one previous case of carvedilol overdose has been reported. Here, we report massive carvedilol ingestion confirmed by quantitative analysis. The case report deals with an 84-year-old man who chewed a total of 60 (6.25 mg) tablets and rapidly developed symptoms. Vital signs on presentation were systolic blood pressure 70 mmHg; heart rate 45 beats/min.; respirations 18 breaths/min.; temperature 37 degrees . The electrocardiogram showed a junctional rhythm at 49 beats/min. The patient was treated with normal saline boluses, repeated glucagon boluses (2-3 mg each) and a dopamine infusion. At 14 hr after ingestion, he was weaned off vasopressors and was in a normal sinus rhythm. Quantitative confirmation showed a carvedilol serum concentration of 472 ng/ml (steady-state concentration 8.5 ng/ml during 6.25 mg twice daily dosing). Despite its unique pharmacological properties, the clinical manifestations of carvedilol overdose appear similar to other beta-adrenoreceptor antagonists.     

PY 108-068 — Acute effects of a single oral dose in chronic stable angina

Summary PY 108-068 is a dihydropyridine calcium antagonist. In a double-blind, randomised crossover study in 6 patients with chronic stable angina, we compared the acute effects of a single oral dose of placebo with 25 mg and 50 mg of PY 108-068. Investigations were performed on 3 mornings at weekly intervals. Resting supine and erect heart rate and blood pressure were measured before the dose and repeated 75 min later. At approximately 90 min after the dose each patient performed a standardised exercise test on a bicycle ergometer. The mean area (number of points) of ST-segment depression on 16-point precordial exercise maps was 13.1 with placebo, 4.5 with 25 mg of PY 108-068 and 4.3 with 50 mg of PY 108-068 (NS). The rate-pressure product at initial ST-segment depression >1 mm was 15.6×10³ with placebo, 17.8×10³ with 25 mg of PY 108-068 and 18.5×10³ with 50 mg of PY 108-068. Resting supine heart rate was significantly faster with both 25 mg of PY 108-068 (65 beats/min) and 50 mg PY 108-068 (67 beats/min) compared with placebo (59 beats/min). The mean reduction in supine blood pressure from that with placebo was 12/7 mm Hg with 25 mg of PY 108-068 and 10/8 mm Hg with 50 mg of PY 108-068 (NS). These results confirm the modest acute antianginal efficacy of a single oral dose of PY 108-068. The absence of reflex tachycardia found in previous chronic oral dosing studies with this drug appears to take some days to develop in humans.     

单唾液酸四己糖神经节苷脂钠注射液致过敏性休克

1例48岁男性患者因脑脓肿伴继发性癫痫行左侧颞部占位性病变切除术,术后第1天依次静脉滴注单唾液酸四己糖神经节苷脂钠注射液40 mg、青霉素钠320万U（皮肤试验阴性）。药物滴注完毕后约5 min患者出现躁动、口唇发绀、双肺呼吸音粗,可闻痰鸣音,呼吸频率30～40次/min,心率178次/min,血压80～88/48～60 mm Hg（1 mm Hg=0.133 kPa）,血氧饱和度0.60。立即予口咽通气管,吸痰,面罩吸氧,气管插管呼吸机辅助呼吸,静脉滴注多巴胺100 mg、间羟胺40 mg、甲泼尼龙0.5 g,静脉注射去乙酰毛花苷0.2 mg、地塞米松4 mg。2 h后患者心率降至110次/min,呼吸频率降至19次/min,血压升至125～135/70～90 mm Hg,血氧饱和度升至1.00,生命体征趋平稳。怀疑休克与青霉素有关。次日停用青霉素,继续静脉滴注氯化钠注射液100 ml＋单唾液酸四己糖神经节苷脂钠40 mg,10 min后患者再次出现躁动、呼吸急促,心率增快至160次/min,血氧饱和度降至0.85,血压降至77/45 mm Hg。立即停止静脉滴注,给予呼吸机辅助呼吸以及升压、降低心率、抗过敏、抗炎等对症治疗。40 min后,患者心率降至110次/min,呼吸频率降至18次/min,血压升至110～145/60～90mmHg,血氧饱和度0.98,生命体征平稳。     

Assessment of ‘once daily’ verapamil for the treatment of hypertension using ambulatory,intra-arterial blood pressure recording

Summary A new, slow release formulation of verapamil, “verapamil o.d.” was administered to 12 patients with essential hypertension. Drug administration was started at a dose of 240 mg and increased to 480 mg after 2 weeks of treatment if the cuff blood pressure response was unsatisfactory. The drug reduced the daytime intra-arterial blood pressure significantly from 180.7/106.8 mm Hg to 157.3/89.4 mm Hg. The daytime heart rate fell from 88.1 to 71.8 beats/min. The nighttime blood pressure decreased from 155.7/87.2 mm Hg to 140.5/75.3 mm Hg. The nocturnal heart rate decreased from 62.8 to 57 beats/min. Hourly plots of mean systolic and diastolic pressure showed a significant reduction of systolic pressure for 21 of 24 h and of diastolic pressure for all 24 h following a single morning dose. The drug modified the absolute blood pressure and heart-rate response during both forms of exercise, but did not alter the magnitude or rate of blood pressure change. The tilt-test produced no evidence of postural hypotension. Only one patient experienced any side effects whilst taking the drug. These results indicate good 24-h blood pressure control and reduced exercise blood pressure levels during treatment with this new formulation of verapamil. The reduced frequency of drug administration should improve patient complicance with treatment of hypertension.     

Effects of midodrine on experimentally-induced postural hypotension in dogs

Effects of alpha-(2,5-dimethoxyphenyl)-beta-glycinamide-ethanol hydrochloride (midodrine, ST-1085) on experimental postural hypotension was examined in hexamethonium (20 mg/kg s.c.)-treated anesthetized dogs. The dogs were tilted 30 degrees to a head-up position. A 30 degree-tilt caused a significant decrease in blood pressure. Midodrine, 0.3 mg/kg, attenuated the decrease in blood pressure induced by the tilt significantly at 10 and 30 min after administration of the drug. The heart rate increased following the tilt, but the degree of the increase was rather small. Cerebral tissue blood flow significantly decreased by the tilt. Midodrine, 0.3 mg/kg, significantly attenuated the decrease in cerebral tissue blood flow induced by the tilt at 10 and 30 min. Vertebral arterial blood flow significantly decreased by the tilt. Midodrine reduced the decrease in vertebral arterial blood flow induced by the tilt significantly at 10 and 30 min. Cardiac output also decreased significantly by the tilt. Midodrine attenuated the decrease in cardiac output significantly at 10 min. Femoral arterial blood flow decreased significantly by the tilt. Midodrine tended to reduce the decrease in femoral arterial blood flow induced by the tilt at 30 min. Therefore, midodrine via vasoconstriction seems to be useful for the decrease in blood flows due to the postural hypotension.     

别嘌醇致重症药疹和迟发型过敏性休克

1例74岁男性因尿酸增高口服别嘌醇0．1g,2次／d。用药第16天出现全身瘙瘁,第21天胸部及背部皮肤出现针尖样红色皮疹,停药并给予对症处理2d无效,皮疹加重,且出现头昏、胸闷,遂入院。入院后检查心率73次／min,血压70／46mmHg（1mm Hg=0．133kPa）,血清丙氨酸转氨酶124U／L,天冬氨酸转氨酶80U／L,尿素氮22．6mmol／L,肌酐151μmol／L,尿酸738tzmol／L。入院后心率一度降至42次／min。给予对症、支持治疗21d后,患者皮疹基本消退,血压、心率及肾功能正常,肝功能仍异常。     

Transcardiac gradient of aldosterone before and after spironolactone in patients with congestive heart failure

Isoproterenol is widely used as a provocative medium for vasovagal responses during tilt testing. Dose of isoproterenol infusion is generally titrated empirically by increase in resting heart rate before tilt up. To determine the optimal increase in resting heart rate with isoproterenol for tilt-induced vasovagal responses, we studied 97 consecutive patients with unexplained syncope. After the end of a negative baseline tilt (80 degrees for 30 min), the isoproterenol tilt was performed using one of two protocols: two-stage isoproterenol-tilt protocol, with doses of 0.01 and 0.02 microg/kg per min for 10 min each, or one-stage isoproterenol-tilt protocol, with a dose of 1 or 2 microg/min for 10 min. The resting heart rate increase was defined as a percentage increase in the resting heart rate after isoproterenol infusion, compared to the baseline heart rate before the tilt test. In 117 tilt procedures, 28 (93%) of the 30 positive responses occurred with a resting heart rate increase of > or = 21%. With the resting heart rate increase of 60 and 100%, 18 (60%) and 27 (90%) positive responses were observed, respectively. In conclusion, the minimum resting heart rate increase of > or = 21% was required to provoke a vasovagal response during subsequent isoproterenol-tilt (80 degrees for 10 min). Preferably, heart rate should be increased to 60-100% by isoproterenol titration before tilting.