不同频率插入式腹部按压心肺复苏对室颤犬血流动力学的影响

目的对不同频率插入式腹部按压心肺复苏及标准心肺复苏产生的血流动力学参数进行比较,探讨IAC-CPR的最佳按压频率。方法选12条健康杂种犬,每条实验犬均接受S-CPR和80IAC-CPR、100IAC-CPR、120IAC-CPR四种复苏方法,每只犬四种复苏方法的顺序由随机法确定,每种按压方法进行5min。体外电击法制作犬室颤模型,采用6F猪尾导管及压力换能器,测量中心静脉压(CVP)、升主动脉收缩和舒张压、颈动脉收缩(CAS)和舒张压(CAD),并通过公式计算获得冠状动脉灌注压(CPP)、平均主动脉压(MAP)及平均颈动脉压(CMAP)。结果100IAC-CPR产生的MAP、CMAP、CVP均大于其他三种按压方法(P<0·05),产生的CPP和120IAC-CPR相当(P>0·05),优于其余两种按压方法(P<0·05)。结论100IAC-CPR能产生最好的血流动力学效果,主要表现为能产生更好的CPP和CMAP,预示可能产生更好的复苏成功率,而且易于操作和维持。     

有创动脉血压监测在综合评价医务人员胸外按压质量中的价值

[目的]通过PHILIPS MP60中央监护仪调查重症监护室(ICU)病人发生心搏骤停时,医务人员胸外心脏按压质量指标与病人有创动脉血压的情况。[方法]采用回顾性研究方法,调查2016年初入住ICU发生心搏骤停病人61例,根据有创动脉血压是否达到80mmHg水平分为达标组与非达标组,比较两组病人在心肺复苏阶段的有创动脉血压、按压频率、胸外按压分数、通气频率、自主循环恢复率(ROSC)等指标。[结果]达标组的有创动脉收缩压83.65mmHg±6.63 mmHg、舒张压33.96 mmHg±2.89 mmHg、按压频率(112.83/min±16.45/min)、自主循环恢复率84.0%,分别高于非达标组有创动脉收缩压72.74mmHg±5.09mmHg、舒张压26.03mmHg±2.65mmHg、按压频率(88.07±15.70)/min、自主循环恢复率36.1%,差异均有统计学意义(均P0.01)。[结论]ICU病人在心肺复苏时有创动脉血压水平偏低是胸部按压质量下降主要体现,我们必须及时核查并调整我们胸外按压操作,保证有创动脉血压在80/30mmHg以上水平,维持高质量的胸外按压状态,提高自主循环恢复率。     

新型双泵复苏术的基础研究:以胸骨按压为主体的双泵复苏术的血液动力学研究

胸部按压放松期辅以体外膈肌起搏（EDP）和增强型体外反搏（EECP）的双泵复苏木（EDCPR）对8条犬室颤1分钟后，随机先后予以标准心肺复苏术（SECPR）与EDCPR进行自身对照实验研究。实验结果：EDCPR较SECPR显著提高升主动脉收缩压（P＜0．05），舒张压（P＜0．01）。而右房舒张压平均值来显著性升高（P＞0．05）。冠脉有效灌流压（CPP）显著增加（P＜0．01）。提示EECP使动脉血运流升高舒张压，EECP的促进静脉回流与EDP的胸腔负压形成配合，静脉回流血吸入肺循环并流向左心，不升高右房压又增加前负荷，主动脉压收缩压升高。EDCPR既产生了有效的人工通气、调动了大小循环；又较好地改善了心肌血供。     

心性猝死患者院前三种复苏方法的初期复苏效果比较

目的　回顾比较分析院前三种复苏方法对心性猝死患者的疗效 ,探讨院前心性猝死患者复苏的最佳方法。方法　回顾分析 1996 - 11～ 2 0 0 3- 0 7现场抢救心性猝死患者 10 8例 ,随机采取标准CPR气管插管通气法、气囊 -面罩通气法及单纯胸外肺心同步按压复苏法 (ECPC)三种复苏方法的自主循环恢复率 (ROSC)及平均恢复时间。结果　经统计分析 ,ECPC组与气囊 -面罩通气组的ROSC明显高于气管插管组 (P <0 0 5 ) ,并且平均恢复时间也明显少于气管插管组 (P <0 0 5 )。结论　在院前抢救心性猝死患者时 ,ECPC可提供良好的肺通气换气作用 ,因试图气管插管等呼吸支持措施而中止心脏体外按压 ,对自主循环的恢复有害无益。     

心脏泵用于院前心肺复苏109例患者疗效观察

胸外心脏按压是心博骤停时用人工维持患者血液循环的主要急救方法,临床有着统一的操作标准,即心肺复苏术(标准CPR).近年出现的心脏泵则是在胸外心脏按压时,不但主动按压,而且也主动提拉胸部减压,即主动加压减压心肺复苏术(ACD-CPR).2004年6月-2007年6月,本院急救中心在心搏骤停患者的院前急救中应用ACD-CPR进行复苏,报告如下.     

心脏泵用于院前心肺复苏109例患者疗效观察

胸外心脏按压是心博骤停时用人工维持患者血液循环的主要急救方法,临床有着统一的操作标准,即心肺复苏术(标准CPR).近年出现的心脏泵则是在胸外心脏按压时,不但主动按压,而且也主动提拉胸部减压,即主动加压减压心肺复苏术(ACD-CPR).2004年6月-2007年6月,本院急救中心在心搏骤停患者的院前急救中应用ACD-CPR进行复苏,报告如下.     

心脏泵用于院前心肺复苏109例患者疗效观察

胸外心脏按压是心博骤停时用人工维持患者血液循环的主要急救方法,临床有着统一的操作标准,即心肺复苏术(标准CPR).近年出现的心脏泵则是在胸外心脏按压时,不但主动按压,而且也主动提拉胸部减压,即主动加压减压心肺复苏术(ACD-CPR).2004年6月-2007年6月,本院急救中心在心搏骤停患者的院前急救中应用ACD-CPR进行复苏,报告如下.     

心脏泵用于院前心肺复苏109例患者疗效观察

胸外心脏按压是心博骤停时用人工维持患者血液循环的主要急救方法,临床有着统一的操作标准,即心肺复苏术(标准CPR).近年出现的心脏泵则是在胸外心脏按压时,不但主动按压,而且也主动提拉胸部减压,即主动加压减压心肺复苏术(ACD-CPR).2004年6月-2007年6月,本院急救中心在心搏骤停患者的院前急救中应用ACD-CPR进行复苏,报告如下.     

与胸外心脏按压同时和非同时机械通气对心肺复苏影响的比较

目的：探讨与胸外心脏按压同时和非同时机械通气在心肺复苏中应用的效果。方法：将12例心跳呼吸骤停患者随机分为与胸外心脏按压同时控制机械通气组和与胸外按压非同时手控机械通气组。采用控制通气模式机械通气与持续循手胸外心脏按压同时进行;后者采用手控通气模式机械通气（MAMV）与间断徒手胸外心脏按压非同时配配合进行心肺复苏,胸外心脏按压每5次后暂停1次,在暂停间期给予MAMV1次,之后通气与按压依此比例进行。2组均进行无创动脉血压、心电、经皮氧饱和度（SpO2)、潮气量（VT)、气道峰压（Ppeak)等监测。结果：与胸外心脏按压非同时手控机械通气组的SpO2、VT均明显高于与胸外心脏按压同时模式通气组的SpO2和VT,P均＜0．05;而peak则明显低于后者,P＜0．05;2组的平均动脉压无显著差别。结论：与胸外心脏按压非同时手控机械通气在提高SpO2、VT,降低Ppeak,恢复窦性心律及提高心肺复苏成功率等方面明显优于与胸外心脏按压同时控制机械通气。     

心脏泵用于院前心肺复苏109例患者疗效观察

胸外心脏按压是心博骤停时用人工维持患者血液循环的主要急救方法,临床有着统一的操作标准,即心肺复苏术(标准CPR).近年出现的心脏泵则是在胸外心脏按压时,不但主动按压,而且也主动提拉胸部减压,即主动加压减压心肺复苏术(ACD-CPR).2004年6月-2007年6月,本院急救中心在心搏骤停患者的院前急救中应用ACD-CPR进行复苏,报告如下.     

Observations of hemodynamics during human cardiopulmonary resuscitation

To evaluate hemodynamics during human CPR, 32 patients with witnessed cardiac arrest were studied during manual and mechanical conventional CPR. In eight patients during manual conventional CPR, peak systolic radial artery, right atrial (RAP), and pulmonary artery pressures were found to be similar (59.8 +/- 4.3, 70.8 +/- 4.7, 71.2 +/- 8.2 mm Hg) and higher than external jugular venous pressure (33.8 +/- 1.9 mm Hg, p less than .0001). The diastolic radial artery to RAP gradient was found to be only 10.7 +/- 2.1 mm Hg. In four patients, maneuvers that avoid chest compression and thus obviate cardiac compression, i.e., rhythmic compression of the abdomen, yielded arterial pressures comparable to those generated by conventional CPR (48 +/- 6.4 vs. 52.8 +/- 3.4 mm Hg, NS). In 13 other patients during mechanical conventional CPR at constant chest compression force, radial artery pressure was higher during the first compression after ventilation as compared with subsequent chest compressions (67.5 +/- 5.0 vs. 61.9 +/- 4.8 mm Hg, p less than .007). These hemodynamic observations are similar to those reported in large dogs during CPR and support the generation of vascular pressures during CPR by an increase in intrathoracic pressure. They also suggest that despite anatomic differences, the similarity of hemodynamics in dogs and humans justifies the use of large dogs as a human model during acute resuscitation studies.     

Use of an inspiratory impedance threshold valve during chest compressions without assisted ventilation may result in hypoxaemia

INTRODUCTION: Although the concept of intermittent airway occlusion with the inspiratory impedance threshold valve (ITV) is a well-recognised strategy for improving efficiency of cardiopulmonary resuscitation (CPR), little is known about possible pulmonary side effects. METHODS: After a baseline chest CT-scan, 24 pigs with beating hearts undergoing apnoeic oxygenation received an injection of a contrast medium and were then assigned randomly to either active compression-decompression CPR with ITV (ACD ITV CPR), ACD CPR alone, or standard-CPR with ITV (standard-ITV CPR), or standard-CPR alone. After a maximum of 5 min of chest compressions or if oxygen saturation dropped below 70%, the experiment was stopped, haemodynamic variables and blood gas values were measured, and another CT-scan was performed; all animals underwent a 30 min recovery-period and a third subsequent CT-scan. RESULTS: At baseline arterial oxygen saturation by pulse oxymetry was 99% in all four groups; in both the ACD ITV CPR and the standard-ITV CPR groups, arterial oxygen saturation dropped below 70% within 126+/-9s, whereas chest compressions in all ACD CPR and standard-CPR pigs were performed over 5 min (P<0.001). Before stopping chest compressions arterial oxygen pressure decreased in the ACD ITV CPR group from 426+/-96 to 42+/-8 mmHg while it decreased in the ACD CPR group only from 415+/-116 to 197+/-127 mmHg (P<0.001 between groups); in the standard-ITV CPR group arterial oxygen partial pressure decreased from 427+/-109 to 34+/-5 mmHg while oxygen partial pressure decreased only from 467+/-44 to 144+/-98 mmHg in the standard-CPR group (P<0.004 between groups). After the second CT scan arterial oxygen partial pressure decreased further to 19+/-2 mmHg in the ACD ITV CPR versus 210+/-41 mmHg in the ACD CPR group; to 20+/-2 mmHg in the standard-ITV CPR versus 148+/-33 mmHg in the standard-CPR group. Lung-density values (Hounsfield units) were significantly higher in the ACD ITV CPR versus ACD CPR group (-134+/-54 versus -330+/-77) and standard-ITV CPR versus standard-CPR group (-98+/-50 versus -387+/-42). After a 30 min recovery-period, there were no significant differences in arterial oxygen partial pressure (ACD ITV CPR 275+/-110 mmHg versus ACD CPR 379+/-111 mmHg and standard-ITV CPR 265+/-138 mmHg versus standard CPR 367+/-55 mmHg). Furthermore, there were no differences in lung density values between groups after 30 min of recovery. CONCLUSION: In this animal model with a beating heart, intermittent airway obstruction through an ITV combined with apnoeic oxygenation and without active ventilation resulted in hypoxaemia due to transiently impaired lung function.     

Comparison of mechanical techniques of cardiopulmonary resuscitation: survival and neurologic outcome in dogs

Three currently available mechanical devices for cardiopulmonary resuscitation (CPR) were compared using a canine cardiac arrest model. Twenty-four-hour survival without neurologic deficit was the goal. A group of 30 large mongrel dogs was divided equally among Thumper CPR, simultaneous compression and ventilation (SCV) CPR, and vest CPR. Ventricular fibrillation was induced electrically, and after 3 minutes of no intervention, one of the three types of mechanical CPR was performed for 17 minutes. SCV CPR and vest CPR produced significantly greater aortic and right atrial systolic pressures than Thumper CPR (P less than .03). The SCV CPR technique also produced significantly higher aortic diastolic pressure and right atrial diastolic pressure than either of the other methods (P less than .03). However, coronary perfusion pressure was not different among the three mechanical methods. No differences in immediate resuscitation, 24-hour survival, or neurologic deficit scores at 24 hours were found. Neither SCV nor the vest techniques of CPR appear better for survival or neurologic outcome than standard cardiopulmonary resuscitation performed with the Thumper.     

Optimizing ventilation in conjunction with phased chest and abdominal compression-decompression (Lifestick) resuscitation.

The best method for employment of phased chest and abdominal compression-decompression (Lifestick) cardiopulmonary resuscitation (CPR) has yet to be determined. Of particular concern with using this technique is the combining of ventilation with the phased compressions and decompressions. Twenty domestic swine (50+/-1 kg) were equally divided into four groups. Following 10 min of untreated VF, CPR was begun. Group 1 received Lifestick (LS) CPR with only passive ventilation ('passive'); Group 2 received LS-CPR with synchronized positive pressure ventilations (ppv) at a chest compression ratio of 15:2 (15:2 S); Group 3 had LS-CPR with synchronized ppv at 5:1 (5:1 S); and Group 4 received LS-CPR with asynchronous ppv at 5:1 (5:1 A). Endpoints included hemodynamics, blood gases, minute ventilation, and 24 h outcome. Asynchronous ventilation (5:1 A) had significantly worse hemodynamics including aortic and right atrial systolic, aortic diastolic, and coronary perfusion pressures than the other groups (P<0.05). Passive ventilation had the poorest arterial and mixed venous blood gases (P<0.05), but did not differ from 15:2 S in minute ventilation produced (8 vs 10 l/min). No differences in outcome were seen. The ventilation technique combined with LS-CPR can make a significant difference in hemodynamics as well as ventilation. Optimizing other forms of basic and advanced cardiac life support through different ventilation methods deserves new consideration, including a re-examination of the current single rescuer recommendation of a 15:2 ratio. Optimal ventilation strategy when using the LS device at 60 compressions per min appears to be 5:1 S. Such data is important for conducting clinical trials with this new CPR adjunct.     

Effect of interposed abdominal compression during CPR on central arterial and venous pressures

Despite the problems inherent in estimating blood flow from pressure, determination of systolic arterial pressure during cardiopulmonary resuscitation (CPR) is common and probably valuable as an indicator of potential systemic flow. The addition of interposed abdominal compression (IAC) to closed-chest CPR has been promoted because of its potential to increase systolic arterial pressure during CPR. Interposed abdominal compressions have also reportedly increased diastolic arterial-central venous pressure difference (DA-DCVP) and, thus, have the potential to increase coronary vascular flow. Two distinct methods of CPR were studied in conjunction with IAC. In six humans, there was no significant increase late in the resuscitative process in systolic arterial pressure or in DA-DCVP difference with IAC as compared with the two methods of CPR studied without IAC.     

Combination of active compression decompression cardiopulmonary resuscitation and the inspiratory impedance threshold device: state of the art

PURPOSE OF REVIEW: Over the past decade, the combination of active compression decompression (ACD) cardiopulmonary resuscitation (CPR) and an impedance threshold device (ITD) has been shown to significantly increase vital organ perfusion pressures and survival rates in animals and humans. The purpose of this review article is to summarize the recent advances with this new technology. RECENT FINDINGS: Building upon animal studies that demonstrated the benefit of the ITD used with either ACD CPR or standard CPR (S-CPR), four prospective, randomized clinical trials with ACD/ITD CPR have been recently completed. One blinded, out-of-hospital cardiac arrest trial (n = 21 patients) demonstrated that systemic blood pressures and coronary perfusion pressures were markedly higher when ACD/ITD CPR was used when compared directly with ACD CPR alone. The second blinded trial demonstrated that the combination of ACD/ITD CPR was effective with both a facemask and an endotracheal tube (n = 15 patients). A third randomized clinical trial (n = 210 patients) demonstrated that 24-hour survival rates for out-of-hospital cardiac arrest were more than 65% higher with ACD/ITD CPR than with S-CPR (P < 0.01). Neurologic function after cardiac arrest trended higher in patients with witnessed arrest who received ACD/ITD CPR than in those who received S-CPR(P < 0.07). In addition, when ACD/ITD CPR was applied later in the course of treatment, short-term survival rates were threefold higher in patients receiving ACD/ITD CPR (44%) than in those receiving S-CPR (14%)(P < 0.05). In that study, patients with the greatest chance for survival-those with witnessed cardiac arrest and an initial rhythm of ventricular fibrillation-had a 23% 24-hour survival rate with S-CPR versus a 58% 24-hour survival rate with ACD/ITD CPR (P < 0.01). It should be noted that this trial was performed in a city where an earlier study found no difference in outcomes between ACD CPR alone and S-CPR. The fourth clinical trial was a randomized, double-blinded study of 400 patients with out-of-hospital cardiac arrest treated by advanced life support personnel. All patients received ACD CPR: half were treated with a sham ITD and the other half were treated with an active ITD. Twenty-four hour survival, the primary endpoint, was 32% in the active ITD group versus 22% in the sham group (P < 0.05). SUMMARY: On the basis of the cumulative findings of these studies, it is concluded that ACD/ITD CPR provides superior vital organ blood flow and results in significantly higher short-term survival rates than do ACD CPR alone or S-CPR. Use of the ACD/ITD CPR technology optimizes perfusion of the heart and brain during cardiac arrest and results in the highest reported survival rates of any CPR device technology. Use of this technology should be encouraged while additional studies are under way to examine the potential long-term impact of this new technology.     

经膈肌下抬挤心脏方法对心脏停搏兔复苏的实验研究

目的 比较标准胸外按压心肺复苏(S-CPR)与经膈肌下心脏按压心肺复苏(D-CPR)对复苏循环效应的影响;评价D-CPR用于CPR的可行性.方法 健康新西兰白兔20只,经呼气末窒息8 min造成心脏停搏(CA)模型.随机分两组,每组10只,分别实施S-CPR和D-CPR;于窒息前平静5 min后开始连续记录升主动脉收缩压(AOS)和舒张压(AOD)、经皮血氧饱和度(Sp02)、右心房收缩压(RASP)和舒张压(RADP)、心电图(ECG)等直至实验结束;计算升主动脉平均动脉压(MAP)、冠状动脉灌注压(CPP);分别观察两组动物的自主循环恢复(ROSC)率及6 h存活率.结果 S-CPR组有5只、D-CPR组有8只动物获得ROSC(ROSC率分别为50%和80%,P=20.05);S-CPR组6 h存活率为40%,D-CPR组为50%.D-CPR组复苏1 rain和5 rain时AOS、AoD、MAP和CPP均高于S-CPR组(P均<0.05);D-CPR组复苏1 rain时MAP、CPP分别是其基础值的54.1%、33.4%.5 min时为60.0%、41.8%,而S-CPR组复苏1 min时AOS、AOD为基础值的37.3%、16.5%,5 min时为38.5%、17.1%#且D-CPR组ROSC后动物血流动力学较S-CPR组变化平稳.结论 D-CPR方法可产生较高的动脉血压和心排血量,并能增加实验动物的ROSC率和短期存活率.D-CPR方法优于S-CPR.     

心肺复苏后猪各主要脏器组织和超微结构的变化及对血流动力学的影响

目的 通过建立心搏骤停室颤-心肺复苏模型,观察心肺复苏后猪心肌、大脑、肺脏、肝脏及肾脏组织普通病理和超微结构的变化及对血流动力学的影响.方法 16头北京长白猪(29～35kg)随机(随机数字法)分为正常组(n=8)与复苏组(n=8).前组动物仅进行麻醉及气管插管,不予致室颤及心肺复苏.后组动物在建立心搏骤停室颤模型4 min后给予标准心肺复苏术,恢复自主循环(ROSC)10 min后以0.5 mL/(h·kg)的速度持续静脉泵入生理盐水直至复苏后6 h,并分别于致颤前,ROSC后0.5 h,2 h,4 h,6 h监测心排血量(CO)、左心室收缩期压力最大上升速率(+dp/dtmax)、左心室舒张期最大下降速率(-dp/dtmax)、心率(HR)、平均动脉压(MAP),两组动物均于复苏6 h后静脉麻醉下处死,速取其左心室心尖、大脑顶叶皮层、左肺、肝右叶、右肾上极组织行普通病理学及透射电镜检查.对实验数据用t检验的方法进行统计学分析.结果 复苏组在ROSC后各时间点,左心室收缩期压力最大上升速率、左心室舒张期最大下降速率、心排血量与致颤前相比均明显降低,差异具有统计学意义(P＜0.05),复苏组ROSC后各时间点HR较致颤前明显增加(P＜0.05),各时间点MAP之间比较差异无统计学意义(P＞0.05);通过对苏木精-伊红(HE)染色切片及透射电镜切片的观察,进行正常组与复苏组动物各主要脏器组织病理学比较,心搏骤停室颤-心肺复苏模型中猪的心肌、大脑、肺脏、肝脏及肾脏组织均存在不同程度的病理损伤,以心肌、大脑、肺脏的损伤更为严重.结论 心搏骤停-心肺复苏对机体各主要脏器均可以造成不同程度的形态学损伤及血流动力学影响,在ROSC成功6 h的模型中,以心肌、大脑及肺的损伤较重,肝、肾的损伤较轻.     

Reducing ventilation frequency during cardiopulmonary resuscitation in a porcine model of cardiac arrest

INTRODUCTION: American Heart Association/American College of Cardiology guidelines recommend a compression-to-ventilation ratio (C/V ratio) of 15:2 during cardiopulmonary resuscitation (CPR) for out-of-the-hospital cardiac arrest. Recent data have shown that frequent ventilations are unnecessary and may be harmful during CPR, since each positive-pressure ventilation increases intrathoracic pressure and may increase intracranial pressure and decrease venous blood return to the right heart and thereby decrease both the cerebral and coronary perfusion pressures. HYPOTHESIS: We hypothesized that reducing the ventilation rate by increasing the C/V ratio from 15:2 to 15:1 will increase vital-organ perfusion pressures without compromising oxygenation and acid-base balance. METHODS: Direct-current ventricular fibrillation was induced in 8 pigs. After 4 min of untreated ventricular fibrillation without ventilation, all animals received 4 min of standard CPR with a C/V ratio of 15:2. Animals were then randomized to either (A) a C/V ratio of 15:1 and then 15:2, or (B) a C/V ratio of 15:2 and then 15:1, for 3 min each. During CPR, ventilations were delivered with an automatic transport ventilator, with 100% oxygen. Right atrial pressure, intratracheal pressure (a surrogate for intrathoracic pressure), aortic pressure, and intracranial pressure were measured. Coronary perfusion pressure was calculated as diastolic aortic pressure minus right atrial pressure. Cerebral perfusion pressure was calculated as mean aortic pressure minus mean intracranial pressure. Arterial blood gas values were obtained at the end of each intervention. A paired t test was used for statistical analysis, and a p value < 0.05 was considered significant. RESULTS: The mean +/- SEM values over 1 min with either 15:2 or 15:1 C/V ratios were as follows: intratracheal pressure 0.93 +/- 0.3 mm Hg versus 0.3 +/- 0.28 mm Hg, p = 0.006; coronary perfusion pressure 10.1 +/- 4.5 mm Hg versus 19.3 +/- 3.2 mm Hg, p = 0.007; intracranial pressure 25.4 +/- 2.7 mm Hg versus 25.7 +/- 2.7 mm Hg, p = NS; mean arterial pressure 33.1 +/- 3.7 mm Hg versus 40.2 +/- 3.6 mm Hg, p = 0.007; cerebral perfusion pressure 7.7 +/- 6.2 mm Hg versus 14.5 +/- 5.5 mm Hg, p = 0.008. Minute area intratracheal pressure was 55 +/- 17 mm Hg . s versus 22.3 +/- 10 mm Hg . s, p < 0.001. End-tidal CO(2) with 15:2 versus 15:1 was 24 +/- 3.6 mm Hg versus 29 +/- 2.5 mm Hg, respectively, p = 0.001. Arterial blood gas values were not significantly changed with 15:2 versus 15:1 C/V ratios: pH 7.28 +/- 0.03 versus 7.3 +/- 0.03; P(aCO(2)) 37.7 +/- 2.9 mm Hg versus 37.6 +/- 3.5 mm Hg; and P(aO(2)) 274 +/- 36 mm Hg versus 303 +/- 51 mm Hg. CONCLUSIONS: In a porcine model of ventricular fibrillation cardiac arrest, reducing the ventilation frequency during CPR by increasing the C/V ratio from 15:2 to 15:1 resulted in improved vital-organ perfusion pressures, higher end-tidal CO(2) levels, and no change in arterial oxygen content or acid-base balance.     

Intravenous nitroglycerin in acute respiratory failure of patients with chronic obstructive lung disease,secondary pulmonary hypertension and cor pulmonale

We have studied the hemodynamic effects of an intravenous single dose of nitroglycerin in 13 patients with secondary pulmonary hypertension and Cor Pulmonale, during the acute course of respiratory failure and under assisted ventilation. We observed a significant decrease in systolic, diastolic and mean pulmonary arterial pressures, and in pulmonary resistance and systolic right ventricular work index, without any change in right or left pre-loads. The systolic arterial pressure decreased slightly, without any change in cardiac index or diastolic pressure. The arterial and mixed venous oxygen contents, and the pulmonary shunting (Qs/Qt) were unchanged. These results suggest that nitroglycerin may be a useful therapy in patients in the acute stages of pulmonary hypertension resulting from chronic lung disease and under assisted ventilation. In addition, the lack of change in cardiac index, intrapulmonary shunting and oxygen content suggests that this decrease in pulmonary resistance is not linked with any deleterious effect in oxygen transfer.