Arterial PCO2 as an indicator of systemic perfusion during cardiopulmonary resuscitation

End-tidal PCO2 (PetCO2) is a quantitative indicator of pulmonary blood flow generated by precordial compression and therefore predicts resuscitability during CPR. A striking increase in PetCO2 follows return of spontaneous circulation. Since PaCO2 is closely related to alveolar PCO2 (PACO2) and therefore PetCO2, we hypothesized that PaCO2 may itself serve as an indicator of the blood flow generated during CPR. In a porcine model of cardiac arrest, PaCO2 during precordial compression was highly correlated with PetCO2 (r = .89), cardiac output (r = .72), and coronary perfusion pressure (CPP) (r = .74). In 14 successfully resuscitated animals, PaCO2, PetCO2, and CPP during precordial compression were significantly higher than in nine nonresuscitated animals. After restoration of spontaneous circulation, there was a marked increase in PaCO2 to levels exceeding control values, which corresponded to the sharp increase in PetCO2 that is characteristic of successful resuscitation. We therefore confirm that both PetCO2 and PaCO2 correspond to the pulmonary blood flow and therefore cardiac output which is generated by precordial compression during CPR. Moreover, both serve as prognosticators of cardiac resuscitability and early indicators that spontaneous circulation has been restored.     

Factors influencing variable outcomes after ventricular fibrillation cardiac arrest of 15 minutes in dogs

Animal experiments with cardiac arrest and cardiopulmonary resuscitation (CPR) despite controlled insult and postinsult life support, have yielded variable individual outcomes. This report concerns 10 dog experiments with a standardized model of VF cardiac arrest with no flow for 10 min followed by CPR basic life support (BLS) from VF 10 to 15 min and then CPR advanced life support (ALS) with epinephrine at 15 min. Defibrillating countershocks began at 17 min, for restoration of spontaneous circulation. After controlled ventilation to 20 h and intensive care to 96 h, outcome was evaluated using the overall performance category (OPC) 1 (normal) (n5) vs. OPC 2-4 (impaired) (n5) (P less than 0.001). We searched for correlations between normal vs. impaired outcome in various prearrest, arrest and postarrest factors that are suspected to influence postarrest neurologic deficit. Prearrest variables were similar in the normal and impaired groups. Resuscitation variables were similar in both. Coronary perfusion pressure during CPR-ALS was higher in the normal outcome group (P = 0.03). Among postarrest variables, postarrest reperfusion pressure pattern (initial hypertensive bout), blood glucose, cardiac output, Hct, pHa, PaO2 and PaCO2 were the same. Our data support the importance of maximizing coronary perfusion pressure not only for restoration of heart beat but also as a possible predictor of improved cerebral outcome.     

Arterial pH and carbon dioxide tension as indicators of tissue perfusion during cardiac arrest in a canine model.

BACKGROUND AND METHODS: Previous studies have shown that Paco2 and end-tidal CO2 reflect coronary artery perfusion pressures during cardiac arrest. We investigated the relationship of coronary artery perfusion pressure to central arterial pH and Paco2 values during resuscitation from cardiac arrest in a canine model. Twenty-four mongrel dogs were block randomized to three different resuscitation groups after induction of ventricular fibrillation and cardiac arrest: a) standard cardiopulmonary resuscitation (CPR) and advanced life support (n = 8); b) cardiopulmonary bypass (n = 8); or c) open-chest CPR (n = 8). Central arterial blood gases and perfusion pressures were monitored during cardiac arrest and during resuscitation. RESULTS: Prearrest blood gases and hemodynamic values were similar between groups. Sixteen dogs from all three groups were successfully resuscitated. Survivors had significantly higher coronary artery perfusion pressure (p = .03), Paco2 (p = .015), and lower pH (p = .01) values than nonsurvivors. There was no correlation of pH and Paco2 during mechanical external CPR. However, after institution of the different resuscitation techniques, pH and Paco2 each showed a statistically significant correlation (r2 = .50 and .33, respectively) with coronary artery perfusion pressure. CONCLUSIONS: Central arterial pH and Paco2 monitoring during cardiac arrest may reflect the adequacy of tissue perfusion during resuscitation and may predict resuscitation outcome from ventricular fibrillation.     

The beneficial effect of basic life support on ventricular fibrillation mean frequency and coronary perfusion pressure.

BACKGROUND AND OBJECTIVE: Chest compressions before initial defibrillation attempts have been shown to increase successful defibrillation. This animal study was designed to assess whether ventricular fibrillation mean frequency after 90 s of basic life support cardiopulmonary resuscitation (CPR) may be used as an indicator of coronary perfusion and mean arterial pressure during CPR. METHODS AND RESULTS: After 4 min of ventricular fibrillation cardiac arrest in a porcine model, CPR was performed manually for 3 min. Mean ventricular fibrillation frequency and amplitude, together with coronary perfusion and mean arterial pressure were measured before initiation of chest compressions, and after 90 s and 3 min of basic life support CPR. Increases in fibrillation mean frequency correlated with increases in coronary perfusion and mean arterial pressure after both 90 s (R=0.77, P<0.0001, n=30; R=0.75, P<0.0001, n=30, respectively) and 3 min (R=0.61, P<0.001, n=30; R=0.78, P<0.0001, n=30, respectively) of basic life support CPR. Increases in fibrillation mean amplitude correlated with increases in mean arterial pressure after both 90 s (R=0.46, P<0.01; n=30) and 3 min (R=0.42, P<0.05, n=30) of CPR. Correlation between fibrillation mean amplitude and coronary perfusion pressure was not significant both at 90 s and 3 min of CPR. CONCLUSIONS: In this porcine laboratory model, 90 s and 3 min of CPR improved ventricular fibrillation mean frequency, which correlated positively with coronary perfusion pressure, and mean arterial pressure.     

Effects of diaspirin cross-linked hemoglobin (DCLHb) during and post-CPR in swine

The purpose of the study was to test the hypothesis that diaspirin cross-linked hemoglobin (DCLHb) can produce improved resuscitation during cardiac arrest. DCLHb, a derivative of human hemoglobin, has previously been demonstrated to produce a vasopressor response that is associated with increased blood flow to vital organs. In addition, it is an oxygen carrier. These effects may be beneficial to extreme low flow states, such as that during cardiac arrest and cardiopulmonary resuscitation (CPR). Experimental cardiac arrest and CPR were carried out in 32 anesthetized immature pigs. In each animal, ventricular fibrillation was induced for 5 min, followed by 10 min of standard CPR with a pneumatic device and room air ventilation. High (15 ml/kg) and low (5 ml/kg) doses of DCLHb or equivalent volume of normal saline were infused at the beginning of CPR in a random and blind manner. Cardiac output, organ blood flow, aortic pressure, coronary perfusion pressure, blood gases, and lactate concentrations were obtained before and during CPR. Following the 10-min CPR, the animals were defibrillated and the return of spontaneous circulation (ROSC) determined. DCLHb treatment achieved 75% ROSC compared with 25% in the saline group (p < 0.05). In addition, a better (p < 0.05) myocardial O(2) delivery, venous blood O(2) content, and myocardial and cerebral perfusion pressure were observed in the DCLHb group. DCLHb treatment during cardiac arrest and CPR significantly improves ROSC. This is most likely related to its improvement in coronary perfusion and myocardial oxygen delivery.     

A model for regional blood flow measurements during cardiopulmonary resuscitation in a swine model

Recent reports examining regional blood flow during cardiopulmonary resuscitation (CPR) have been criticized for several reasons: (1) cardiac arrest times of 5 min or less are not reflective of the prehospital setting, (2) anesthetic agents may significantly influence autonomic control of regional blood flow, (3) canine cardiac anatomy and coronary blood supply are not reflective of humans and (4) precise validation data for blood flow measurements have not been reported. This study presents a methodology and model for measuring regional blood flow during CPR after a prolonged cardiac arrest. Fifteen swine weighing 15-25.4 kg were instrumented for regional blood flow measurements using tracer microspheres. Regional cerebral and myocardial blood flow were measured during normal sinus rhythm (NSR) and during CPR following a 10-min cardiopulmonary arrest. Regional blood flow (ml/min/100 g) to the cerebral cortices averaged less than 3% of baseline flow (NSR: right cortex = 41.2 +/- 13.8; left cortex = 41.2 +/- 12.2; CPR: right cortex = 1.3 +/- 1.2; left cortex = 1.3 +/- 1.3). Total myocardial blood flow averaged less than 5% of baseline flow (NSR = 211.5 +/- 104.9; CPR = 9.5 +/- 14.9). The flow data demonstrates minimal cardiac and cerebral perfusion with standard CPR following a 10-min arrest. The variability in the pilot data may be used in determining sample sizes for future studies.     

Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs

BACKGROUND: A new device, the intrathoracic pressure regulator (ITPR), was developed to generate continuous negative intrathoracic pressure during cardiopulmonary resuscitation (CPR) and allow for intermittent positive pressure ventilation. Use of the ITPR has been shown to increase vital organ perfusion and short-term survival rates in pigs. The purpose of this study was to investigate the hemodynamic and blood gas effects of more prolonged (15 min) use of the ITPR during CPR in a porcine model of cardiac arrest. METHODS: After 8 min of untreated ventricular fibrillation (VF), 16 female pigs were anaesthetized with propofol, intubated, and randomized prospectively to 15 min of either ITPR-CPR or standard (STD) CPR. Compressions were delivered at a rate of 100/min with a compression to ventilation ratio of 15:2. Ventilations were delivered with a resuscitator bag. Tracheal, aortic, right atrial, intracranial pressures (ICP), common carotid blood flow and respiratory variables were recorded continuously. Arterial and venous blood gases were collected at baseline, and after 5, 10, and 15 min of CPR. Coronary perfusion pressure (CPP) was calculated as diastolic aortic pressure-right atrial pressure. Cerebral perfusion pressure (CerPP) was calculated as mean arterial pressure (MAP)-intracranial pressure. Statistical analysis was performed with unpaired t-test and Friedman's Repeated Measures Analysis. RESULTS: ITPR-CPR when compared to STD-CPR resulted in a significant decrease in mean decompression phase (diastolic) tracheal pressure (-9+/-0.6 mmHg versus -3+/-0.3 mmHg, p<0.001), diastolic right atrial pressure (DRAP) (-0.1+/-0.2 mmHg versus 2.3+/-0.2 mmHg, p<0.001) and intracranial pressure (20.8+/-0.6 mmHg versus 23+/-0.5 mmHg, respectively, p=0.04) and a significant increase in total mean aortic pressure, coronary and cerebral perfusion pressures and end tidal carbon dioxide (ETCO(2)), (p<0.001). Common carotid artery blood flow was increased by an average of 70%, p<0.001. ABGs showed progressive metabolic acidosis in the ITPR-CPR group, but PaCO(2) remained stable at 34 mmHg for 15 min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO(2) values remaining <20 mmHg (p<0.001). PaO(2) was not different between groups. Following 23 min of cardiac arrest (15 min of CPR) ROSC was achieved in 5/8 ITPR-CPR animals versus 2/8 STD-CPR animals p=0.3. CONCLUSION: ITPR-CPR significantly improved hemodynamics, vital organ perfusion pressures and common carotid blood flow compared to STD-CPR in a porcine model of prolonged cardiac arrest and basic life support. The beneficial hemodynamic effects of ITPR-CPR were sustained at least 15 min without any compromise in oxygenation.     

Vasopressin versus continuous adrenaline during experimental cardiopulmonary resuscitation

OBJECTIVE: To evaluate the effects of a bolus dose of vasopressin compared to continuous adrenaline (epinephrine) infusion on vital organ blood flow during cardiopulmonary resuscitation (CPR). METHODS: Ventricular fibrillation was induced in 24 anaesthetised pigs. After a 5-min non-intervention interval, CPR was started. After 2 min of CPR the animals were randomly assigned to receive either vasopressin (0.4 U/kg) or adrenaline (bolus of 20 microg/kg followed by continuous infusion of 10 microg/(kg min)). Defibrillation was attempted after 9 min of CPR. RESULTS: Vasopressin generated higher cortical cerebral blood flow (P < 0.001) and lower cerebral oxygen extraction (P < 0.001) during CPR compared to continuous adrenaline. Coronary perfusion pressure during CPR was higher in vasopressin-treated pigs (P < 0.001) and successful resuscitation was achieved in 12/12 in the vasopressin group versus 5/12 in the adrenaline group (P = 0.005). CONCLUSIONS: In this experimental model, vasopressin caused a greater increase in cortical cerebral blood flow and lower cerebral oxygen extraction during CPR compared to continuous adrenaline. Furthermore, vasopressin generated higher coronary perfusion pressure and increased the likelihood of restoring spontaneous circulation.     

Epinephrine versus methoxamine in survival postventricular fibrillation and cardiopulmonary resuscitation in dogs

Previous studies have indicated that methoxamine (an alpha adrenergic receptor agonist) may provide an advantage compared to epinephrine (a mixed alpha and beta adrenergic agonist) during cardiac arrest and CPR. To test this theory, we compared the effects of bolus injections of epinephrine vs. methoxamine on survival, hemodynamic variables, blood gases, and blood lactate concentrations during ventricular fibrillation and CPR in 12 dogs. Each dog underwent a 3-min fibrillatory arrest followed by 10 min of fibrillation and CPR, at which time the animals were defibrillated. Epinephrine (0.05 mg/kg, n = 6) or methoxamine (2 mg/kg, n = 6) was administered at the start of CPR. Both epinephrine and methoxamine produced identical survival rates (5/6) with no differences in coronary perfusion pressure gradients or blood gases (aortic, venous, or great cardiac venous pH, PaO2, or PaCO2) during CPR. Also, there were no differences between the two study groups in myocardial lactate or oxygen extraction ratios during CPR. We conclude that in the dosages tested in our experimental model, epinephrine and methoxamine produce similar results in the variables which we measured.     

The effects of epinephrine/norepinephrine on end-tidal carbon dioxide concentration, coronary perfusion pressure and pulmonary arterial blood flow during cardiopulmonary resuscitation

End-tidal CO2 concentration correlates with pulmonary blood flow during cardiopulmonary resuscitation and has been claimed to be a useful tool to judge the effectiveness of chest compression. A high concentration of end-tidal CO2 has been related to a better outcome. However, most authors have noticed a decrease in end-tidal CO2 concentration after administration of epinephrine, concomitant with an increase in coronary perfusion pressure and an increased incidence of return of spontaneous circulation. This study was performed to evaluate changes in end-tidal CO2 concentration after injection of vasopressors during cardiopulmonary resuscitation and to investigate the time-course of the response and possible explanations for it. After 1 min of electrically induced cardiac arrest and 5 min of chest compressions, 18 pigs were randomly assigned to receive 0.045 mg kg(-1) epinephrine, 0.045 mg kg(-1) norepinephrine or no drug. After another 4 min of chest compressions the pigs were defibrillated. End-tidal CO2, pulmonary blood flow and coronary perfusion pressure decreased immediately after the induction of cardiac arrest, increased slightly during chest compressions and increased initially to supernormal levels after the return of spontaneous circulation. Injection of epinephrine or norepinephrine during chest compressions decreased end-tidal CO2 51 +/- 2%, (mean +/- S.E.M.), and 43 +/- 1%, respectively, and pulmonary blood flow by 134 +/- 13 and 125 +/- 16%, respectively, within 1 min, simultaneously increasing coronary perfusion pressure from 10 +/- 2 to 45 +/- 5 mm Hg and from 11 +/- 1 to 38 +/- 5 mm Hg, respectively. The coronary perfusion pressure slowly fell, but the effects on end-tidal CO2 and pulmonary blood flow were prolonged. In conclusion, vasopressors increased coronary perfusion pressure and the likelihood of a return of spontaneous circulation, but decreased end-tidal CO2 concentration and induced a critical deterioration in cardiac output and thus oxygen delivery in this model of cardiopulmonary resuscitation.     

The dynamic pattern of end-tidal carbon dioxide during cardiopulmonary resuscitation: difference between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest

Introduction  

Partial pressure of end-tidal carbon dioxide (PetCO2) during cardiopulmonary resuscitation (CPR) correlates with cardiac output and consequently has a prognostic value in CPR. In our previous study we confirmed that initial PetCO2 value was significantly higher in asphyxial arrest than in ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) cardiac arrest. In this study we sought to evaluate the pattern of PetCO2 changes in cardiac arrest caused by VF/VT and asphyxial cardiac arrest in patients who were resuscitated according to new 2005 guidelines.     

Combination drug therapy with vasopressin,adrenaline (epinephrine) and nitroglycerin improves vital organ blood flow in a porcine model of ventricular fibrillation

There is increasing evidence that the combination of epinephrine (adrenaline) with vasopressin may be superior to either epinephrine or vasopressin alone for treatment of cardiac arrest. However, the optimal combination, and dosage of cardiovascular drugs to minimize side effects, and to improve outcome has yet to be found. We therefore evaluated whether the combination of vasopressin plus epinephrine plus nitroglycerin (EVN), would improve vital organ blood flow during cardiopulmonary resuscitation (CPR) when compared with epinephrine (EPI) alone. After 4 min of ventricular fibrillation (VF) and 4 min of standard CPR, pigs were randomized to the combination of epinephrine (45 microg/kg) plus vasopressin (0.4 U/kg) plus nitroglycerin (7.5 microg/kg; n=12), or epinephrine (40 microg/kg; n=12) alone. Cerebral and myocardial blood flow was measured with radiolabeled microspheres. Defibrillation was attempted after 19 min of VF including 15 min of CPR. Mean+/-SEM coronary perfusion pressures were significantly (P < 0.01) higher 5 min after EVN vs. EPI alone (34+/-3 vs. 24+/-3 mmHg, respectively). At the same time, mean+/-SEM left ventricular, and global cerebral blood flow was also significantly (P < 0.05) higher after EVN vs. EPI alone (0.78+/-0.11 vs. 0.48+/-0.08 ml/min/g; and 0.37+/-0.05 vs. 0.22+/-0.0 3 ml/min/g, respectively). Spontaneous circulation was restored in 11 of 12 animals in the EVN group vs. 6 of 12 swine after EPI alone (P = N.S.). In conclusion, the combination of EVN significantly improved vital organ blood flow during CPR compared with EPI alone. Addition of nitroglycerin to the combination of low dose epinephrine with vasopressin during cardiac arrest may be beneficial.     

Intra-aortic administration of epinephrine above an aortic balloon occlusion during experimental CPR does not further improve cerebral blood flow and oxygenation

Balloon occlusion of the descending aorta during cardiopulmonary resuscitation (CPR) improves coronary and cerebral blood flow. In comparison with an equivalent dose administered through a central venous catheter it has been suggested that epinephrine administration above the aortic occlusion might produce a more rapid increase in coronary perfusion pressure and a shorter time to restoration of spontaneous circulation (ROSC). In a recent study, however, outcome was not improved after intra-aortic epinephrine administration. We hypothesised that epinephrine administered above the aortic occlusion could impose adverse effects on cerebral blood flow and oxygenation, possibly because of an alpha-adrenergic mediated vasoconstriction in the cerebral vascular beds. Twenty-six piglets underwent 5 min of non intervention cardiac arrest followed by 8 min of closed-chest CPR. They were randomised to receive bolus doses of 45 microg/kg epinephrine either above the aortic occlusion or through a central venous catheter. Cerebral cortical blood flow was continuously measured using laser-Doppler technique. Cerebral tissue pH and PCO(2) were also measured using a multi-parameter fiberoptic device and cerebral oxygen extraction was calculated. Balloon inflation resulted in an immediate enhancement of cerebral cortical blood flow. Each of the epinephrine boluses through the central venous catheter resulted in a transient increase in cerebral cortical blood flow. When administered above the aortic balloon occlusion, epinephrine did not result in a further increase in cerebral cortical blood flow, though a significant increase in cerebral perfusion pressure was recorded throughout the CPR period. Cerebral tissue pH monitoring revealed severe acidosis during CPR and long after ROSC, which was refractory to buffering. No differences in the cerebral oxygen extraction ratio were observed between the groups. In conclusion, epinephrine administration above an aortic balloon occlusion was unable to improve cerebral blood flow and oxygenation. In fact, it may even attenuate the beneficial effects of aortic balloon occlusion on cerebral blood flow due to an alpha-adrenergic mediated cerebral vasoconstriction. Further studies, including dose-response and volumes of distribution, are needed to identify the effective beneficial dosage of epinephrine during aortic occlusion with the least possible adverse effects.     

Hemodynamic effects of the intra-aortic balloon pump during experimental cardiac arrest

The low flow states and limited coronary perfusion provided by conventional cardiopulmonary resuscitation (CPR) have prompted investigations into alternative, more invasive, methods of resuscitation. Previous case reports and limited animal evidence have suggested that the intra-aortic balloon pump (IABP) may have a role in resuscitation. We used a canine cardiac arrest model to study the hemodynamic effects of the IABP during closed-chest CPR. A sensor attached to the chest plate of a Thumper was used to time a Datascope Model 3520 ventricular assist console such that the balloon inflated on the upstroke and deflated on the downstroke of the Thumper. There was no increase in systolic blood pressure with the balloon pump. Diastolic blood pressure and coronary perfusion pressure were significantly higher with the IABP. Circulation times were shorter and end-tidal CO2 was higher with the IABP. It was concluded that the IABP improves hemodynamic parameters during experimental cardiac arrest.     

Effects of epinephrine in a pig model of hypothermic cardiac arrest and closed-chest cardiopulmonary resuscitation combined with active rewarming

OBJECTIVE: The aim of the current study was to assess the effects of epinephrine in a pig model of hypothermic cardiac arrest followed by closed-chest cardiopulmonary resuscitation combined with active rewarming, simulating the clinical management of an arrested hypothermic patient in a hospital without cardiopulmonary bypass facilities. DESIGN: Prospective, randomized animal study. SETTING: University research laboratory. SUBJECTS: Twelve 12- to 16-week-old domestic pigs. INTERVENTIONS: Pigs were surface cooled to a body core temperature of 28 degrees C. After 4 min of untreated cardiac arrest, manual closed-chest CPR and thoracic lavage with 40 degrees C warmed fluid were started. After 3 min of external chest compression animals were randomly assigned to receive epinephrine (45, 45 and 200 microg/kg) or saline placebo in 5-min intervals. MEASUREMENTS AND MAIN RESULTS: Coronary perfusion pressure was about 15 mmHg in placebo group pigs. Coronary perfusion pressure was significantly higher after epinephrine, but restoration of spontaneous circulation was not more frequent (one of six epinephrine versus three of six saline placebo pigs, P=0.34). After 45 microg/kg epinephrine the arterial PO(2) was significantly lower when compared to the saline placebo. The third 200 microg/kg epinephrine dose resulted in a significantly enhanced mixed venous hypercarbic acidosis. CONCLUSIONS: After a short 4-min period of hypothermic cardiac arrest, epinephrine may not be necessary to maintain coronary perfusion pressure around the threshold usually correlating with successful defibrillation, even during prolonged closed-chest CPR combined with active rewarming. The enhanced mixed venous hypercarbic acidosis in epinephrine-treated animals may support the argument against repeated or high dose epinephrine administration during hypothermic CPR.     

Resuscitation from cardiac arrest in cats: influence of epinephrine dosage on brain recovery

The quality of brain recovery after cardiac arrest depends crucially on the speed of cardiac resuscitation because the low cerebral perfusion pressure during the resuscitation procedure facilitates the development of no-reflow. To accelerate return of spontaneous circulation, high dose epinephrine has been recommended but the effect on the dynamics of early brain recovery is still unknown. We, therefore, studied the dynamics of brain resuscitation after cardiopulmonary resuscitation (CPR) with standard and high dose epinephrine using non-invasive NMR techniques. Fifteen min cardiac arrest was induced in normothermic cats by ventricular fibrillation. CPR was performed using an inflatable pneumatic vest for cyclic chest compression. With the beginning of CPR the standard dose group received 0.02 mg/kg epinephrine (n = 6) and the high dose group received 0.2 mg/kg (n = 8). Brain recovery was monitored by magnetic resonance imaging of the apparent diffusion coefficient (ADC) of water for 3 h. Although high dose epinephrine treatment led to a significantly higher blood pressure during early reperfusion, rapidly changing heterogeneities of early brain recovery were observed in both groups. High dose epinephrine thus does not improve the quality of post-cardiac arrest brain recovery during the first 3 h of reperfusion.     

潮气末二氧化碳分压对心肺复苏结果的指导和预测作用

目的 探讨潮气末二氧碳(PetCO2)监测在心肺复苏(CPR)期间的临床意义并寻求定值以指导临床抢救.方法 采用回顾性研究方法,选择2003年5月至2009年3月解放军第四五一医院急诊科院内外非外伤性心搏骤停已明确原因的患者124例,监测心搏骤停患者在CPR过程中PetCO2的变化.结果 ①恢复自主循环(ROSC)的71例与未恢复的53例气管插管后性别、年龄、抢救时间比较P值分别为＜0.05,＜0.05,＜0.01,差异具有统计学意义,说明上述因素与复苏成功正相关,但性别和年龄与最终存活率无相关性.②最终存活者PetCO2水平高于未复苏成功者和虽复苏成功但最终院内死亡者,并与施救时间相关.③经过20 min的高级生命支持没有恢复自主循环者PetCO2平均水平在(6.7±1.2) mmHg(1mmHg =0.133 kPa),恢复自主循环者在(33.9±7.8) mmHg (P＜0.01),以20 min高级生命支持后PetCO2水平高于14.4 mmHg作为参考值预期死亡,阳性率和阴性率均为100％.结论 CPR过程中PetCO2的监测对复苏有指导和预测作用.     

Dye circulation times during cardiac arrest

Dye dilution curves have been used to calculate cardiac output under conditions of normal circulation. Unfortunately, these curves cannot be integrated easily to determine cardiac output under the low flow states of CPR. The time to initial dye appearance (circulation time), may be useful in judging relative changes in flow when studying experimental resuscitation techniques. The purpose of this study was to investigate the relationship between dye circulation times and other hemodynamic measures during CPR. Repeated measurements of coronary perfusion pressure, dye circulation times, blood gases, and end-tidal CO2 (ETCO2) were made in dogs undergoing CPR. Dye circulation time was significantly associated with the systolic, diastolic, and coronary perfusion pressures. The correlation between circulation time and ETCO2 was -0.70 (P less than 0.0001). There was no correlation with the arterial-venous PO2 gradient. There were significant correlations between the circulation time and both the A-V PCO2 and the A-V pH gradients. We conclude that dye circulation times may be used to gauge relative changes in blood flow during CPR, particularly in laboratory investigations involving repeated measurements.     

The clinical rationale of cardiac resuscitation

After failure of external defibrillation, return of cardiac activity with spontaneous circulation is contingent on rapid and effective reversal of myocardial ischemia. Closed-chest cardiopulmonary resuscitation (CPR) evolved about 30 years ago and was almost universally implemented by both professional providers and lay bystanders because of its technical simplicity and noninvasiveness. However, there is growing concern since the limited hemodynamic efficacy of precordial compression accounts for a disappointingly low success rate; especially so if there is a delay of more than 3 minutes before resuscitation is started. There is also increasing concern with the lack of objective hemodynamic measurements currently available for the assessment and quantitation of the effectiveness of resuscitation efforts. Accordingly, the resuscitation procedure proceeds without confirmation that it increases systemic and myocardial blood flows to levels that would be likely to restore spontaneous circulation. Continuous monitoring of end-tidal carbon dioxide (PETCO2) now appears to be a practical measurement which provides a noninvasive quantitative indication of both systemic blood flow and coronary perfusion pressure. Consequently, PETCO2 predicts the likelihood of successful resuscitation and guides the operator who may modify the technique of precordial compression to improve systemic and myocardial perfusion. Among the large polypharmacy for cardiac resuscitation, only alpha-adrenergic agents (which increase coronary perfusion pressure) and especially epinephrine are of proven benefit. Neither buffer agents nor calcium salts appear to improve outcome except under unique conditions. To the contrary, there is increasing awareness of adverse effects of pharmacologic interventions such that they may hinder the return of viable myocardial and cerebral function. This has constrained the routine use of all drugs except for the use of alpha-adrenergic agonists. More invasive interventions by which blood flow is restored such as open-chest cardiac massage or extra-corporeal pump oxygenation (ECPO) are consistently more effective than conventional CPR. Experimentally, both methods promptly restore systemic and myocardial perfusion to viable levels and thereby increase the likelihood that spontaneous circulation is restored even after prolonged cardiac arrest or failure of conventional CPR.     

Effect of phased chest and abdominal compression-decompression cardiopulmonary resuscitation on myocardial and cerebral blood flow in pigs

OBJECTIVE: This study was designed to assess the effects of a phased chest and abdominal compression-decompression cardiopulmonary resuscitation (CPR) device, Lifestick, vs. standard CPR on vital organ blood flow in a porcine CPR model. DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for measurement of hemodynamic variables, vital organ blood flow, blood gases, and return of spontaneous circulation. SETTING: University hospital research laboratory. SUBJECTS: Twelve domestic pigs. INTERVENTIONS: After 4 mins of untreated ventricular fibrillation, either the Lifestick CPR device (n = 6) or standard CPR (n = 6) was started and maintained for an additional interval of 6 mins before attempting defibrillation. MEASUREMENTS AND MAIN RESULTS: During CPR, but before epinephrine, use of the Lifestick CPR device resulted in significantly higher (p < .05) mean (+/- SD) coronary perfusion pressure (23+/-9 vs. 10+/-7 mm Hg), cerebral perfusion pressure (29+/-11 vs. 18+/-10 mm Hg), mean arterial pressure (49+/-10 vs. 36+/-13 mm Hg), end-tidal carbon dioxide (32+/-11 vs. 20+/-7 mm Hg), left ventricular myocardial blood flow (44+/-19 vs. 19+/-12 mL x min(-1) x 100 g(-1)), and total cerebral blood flow (29+/-10 vs. 14+/-12 mL x min(-1) x 100 g(-1)). After 45 microg/kg epinephrine, hemodynamic and vital organ blood flow variables increased to comparable levels in both groups. CONCLUSIONS: Compared with standard CPR, the Lifestick CPR device increased significantly hemodynamic variables and vital organ blood flow during CPR before epinephrine administration.