Arterial blood gases during cardiac arrest: markers of blood flow in a canine model.

Measures of CO2 have been shown to correlate with coronary perfusion pressure and cardiac output during cardiac arrest. We evaluated arterial pH (pHa) relative to blood flow during cardiac arrest in a canine electromechanical dissociation (EMD) model of cardiac arrest using different resuscitation techniques. Following 15 min of cardiac arrest, 24 mongrel dogs received epinephrine with continued CPR or closed-chest cardiopulmonary bypass. Central arterial blood gases, end-tidal carbon dioxide (PetCO2), coronary perfusion pressure and cardiac output were measured. During CPR, prior to epinephrine or bypass, there was no correlation of pHa, PACO2 and PetCO2, with cardiac output or coronary perfusion pressure. Immediately after instituting the resuscitation techniques, both pHa and PaCO2 showed a significant correlation with cardiac output (pHa; R = -0.78, P less than 0.001 and PaCO2; R = 0.87, P less than 0.001) and with coronary perfusion pressure (pHa; R = -0.75, P less than 0.001 and PaCO2; R = 0.75, P less than 0.001). Eventual survivors (n = 15) had an early significant decrease in pHa, base excess and a significant increase in PaCO2 which was not present in non-survivors (n = 9). Neither pHa nor PaCO2 correlate with blood flow under low flow conditions of CPR. However, with effective circulatory assistance, pHa and PaCO2 reflect systemic blood flow and reperfusion washout.     

Diltiazem improves resuscitation from experimental ventricular fibrillation in dogs.

OBJECTIVE: To determine the effect of diltiazem on survival immediately after cardiac arrest and cardiopulmonary resuscitation (CPR) in dogs. DESIGN: Prospective, double-blind, randomized trial. SETTING: Laboratory at a large, university-affiliated medical center. SUBJECTS: Twenty-eight mongrel dogs, weighing 12 to 16 kg. INTERVENTIONS: After the administration of anesthesia, catheters were placed in the pulmonary artery, aortic arch, left ventricle, right ventricle, and great cardiac vein (12 dogs) for sample collection, pressure determinations, and induction of ventricular fibrillation. Dogs were randomized to receive either diltiazem, calcium chloride, or placebo (saline) either before or early during CPR. Dogs underwent 3 mins of unassisted fibrillatory arrest followed by 10 mins of standard CPR using a pneumatic device. After 13 mins of ventricular fibrillation, defibrillation was attempted repeatedly for less than or equal to 10 mins. Successful resuscitation was defined as an organized rhythm with an unassisted systolic BP of greater than 60 mm Hg for greater than or equal to 2 mins. MEASUREMENTS AND MAIN RESULTS: The resuscitation rate was significantly greater in diltiazem-treated animals (100%) than in those dogs receiving calcium (57%) or placebo (29%). Diltiazem-treated animals were resuscitated faster and required fewer defibrillation attempts than did dogs in the other groups. During CPR, coronary artery perfusion pressure and blood gases (arterial, venous, and myocardial) were similar among treatment groups. CONCLUSIONS: Diltiazem improves the resuscitation from experimentally induced ventricular fibrillation when administered before or early during CPR. This response may have important clinical implications in the treatment of patients undergoing cardiac arrest and CPR.     

Adenosine during cardiac arrest and cardiopulmonary resuscitation: a placebo-controlled, randomized trial.

BACKGROUND AND HYPOTHESIS TESTED: The effects of adenosine (100 micrograms/kg/min; n = 7) were examined during rodent cardiopulmonary resuscitation (CPR). Change in coronary artery perfusion pressure, end-tidal PCO2, and arterial acid-base status of anesthetized, male, Sprague-Dawley rats were compared with CPR controls (0.9% sodium chloride; n = 7) and with sham controls (n = 9). Sustained ventricular fibrillation was induced and precordial chest compression was followed by defibrillation. RESULTS: After 6 mins of cardiac arrest, six (86%) of seven adenosine-treated animals were resuscitated after adenosine infusion and four (57%) of seven control animals were resuscitated after sodium chloride infusion. During chest compression, coronary artery perfusion pressure was 7 +/- 2 mm Hg after adenosine, but was 22 +/- 3 mm Hg in the controls (p less than .01). Parallel decreases were observed in mean aortic pressure. Arterial and end-tidal PCO2 significantly (p less than .01) decreased after adenosine. These changes contrasted with a second control group of nine identically prepared animals which, in the absence of ventricular fibrillation and subsequent chest compression, demonstrated no changes in hemodynamic, respiratory, or blood gas variables. CONCLUSIONS: Adenosine decreased coronary artery perfusion pressure. However, despite marked reductions in coronary artery perfusion pressure, survival was not compromised after adenosine infusion in this rodent model of CPR.     

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.     

Simultaneous sternothoracic cardiopulmonary resuscitation: a new method of cardiopulmonary resuscitation

No existing device for cardiopulmonary resuscitation (CPR) is designed to exploit both the "cardiac pump" and the "thoracic pump" effect simultaneously. The purpose of this study was to measure the haemodynamic effect of a new simultaneous sternothoracic cardiopulmonary resuscitation (SST-CPR) device that could compress the sternum and constrict the thoracic cavity simultaneously in a canine cardiac arrest model. After 4 min of ventricular fibrillation, 24 mongrel dogs were randomized to receive standard CPR (n=12) or SST-CPR (n=12). SST-CPR generated a new pattern of the aortic pressure curve presumed to be the result of both sternal compression and thoracic constriction. SST-CPR resulted in significantly higher mean arterial pressure than standard CPR (68.9+/-16.1 vs. 30.5+/-10.0 mmHg, P<0.01). SST-CPR generated higher coronary perfusion pressure than standard CPR (47.0+/-11.4 vs. 17.3+/-8.9 mmHg, P<0.01). End tidal CO(2) tension was also higher during SST-CPR than standard CPR (11.6+/-6.1 vs. 2.17+/-3.3 mmHg, P<0.01). In this preliminary animal model study, simultaneous sternothoracic cardiopulmonary resuscitation generated better haemodynamic effects than standard, closed chest cardiopulmonary resuscitation.     

Simultaneous sterno-thoracic cardiopulmonary resuscitation improves short-term survival rate in canine cardiac arrests

We have reported previously that simultaneous sterno-thoracic cardiopulmonary resuscitation (SST-CPR) using a device that compresses the sternum and constricts the thorax circumferentially during a compression systole that can be achieved using standard cardiopulmonary resuscitation (STD-CPR). This study was designed to assess whether SST-CPR improves the survival rate of dogs with cardiac arrest compared with STD-CPR. Twenty-nine mongrel dogs (19-31 kg) were enrolled in this study. After 4 min of ventricular fibrillation induced by an AC current, animals were randomized to be resuscitated by either STD-CPR (n=15) or SST-CPR (n=14). Defibrillation was attempted 10 min after the induction of cardiac arrest. Standard advanced cardiac life support was started if defibrillation was unsuccessful. Aortic blood pressure, coronary perfusion pressure, and end tidal CO(2) tension were measured during CPR and the post-resuscitation period. Survival was determined 12 h after the induction of cardiac arrest. SST-CPR resulted in a significantly (P<0.001) higher systolic arterial pressure (91+/-47 vs 47+/-24 mmHg), diastolic pressure (43+/-24 vs 17+/-10 mmHg), coronary perfusion pressure (35+/-25 vs 13+/-9 mmHg), and end tidal CO(2) tension (9+/-4 vs 3+/-2 mmHg). Two of 15 animals (13%) resuscitated by STD-CPR and seven of 14 animals (50%) resuscitated by SST-CPR survived for 12 h after cardiac arrest (P<0.05). In conclusion, SST-CPR improves the short-term survival rate in canine cardiac arrest compared with STD-CPR.     

Venous and arterial blood gases during and after cardiopulmonary resuscitation in dogs

This study was undertaken to characterize blood gas, pH, and lactate changes during and after cardiopulmonary resuscitation (CPR) in arterial and venous samples. Blood samples were withdrawn from the brachial artery, aortic arch, pulmonary artery, coronary sinus, and either the right or left cardiac ventricle of 24 anesthetized dogs. Ventricular fibrillation (VF) was induced electrically, and mechanical CPR was begun. Blood samples were withdrawn before CPR, at 2, 5, 7, and 9 minutes during CPR, and at 1, 3, 10, 30, and 60 minutes after defibrillation. Control arterial and venous samples indicated mild metabolic acidosis. During CPR, there was a significant arteriovenous difference in pH, PCO2, and PO2. With ventilation onset, arterial pH increased 0.25 units, PCO2 decreased 22 mm Hg, and PO2 increased 200 mm Hg. Venous blood gases exhibited gradual changes during the CPR period. With the re-establishment of circulation and spontaneous respirations, both the arterial and venous pH levels decreased to nearly 7.1, and PCO2 approached 40 mm Hg. Lactate increased to 32 mg/dl during 9 minutes of CPR and did not significantly differ after defibrillation. Blood gases and pH returned to control values within an hour. This study suggests that arterial blood gases are sensitive to rapid changes occurring in the pulmonary capillary bed, while venous blood gases reflect changes occurring in the systemic capillary bed.     

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.     

复苏后心功能不全犬的心肌组织病理学变化

目的:观察犬心跳骤停复苏后存在复苏后心功能不全的犬心肌组织的病理变化。方法:体外电击诱发犬室颤,3min后复苏,12只犬随机分为心肺复苏组(CPR组)和空白对照组,每组6只,采用Swan-Ganz漂浮导管监测复苏前后6h的平均动脉压(MAP)、心输出量(CO)和肺毛细血管楔压(PAWP),6h后取心肌组织,TUNEL法检测心肌组织凋亡的形态学改变以及心肌病理学检查。结果:MAP和CO在恢复自主循环后随时间延长而下降,6h降至最低,复苏后各观察点均低于空白对照组。CPR组心肌细胞凋亡指数明显高于空白对照组(P<0.01),CPR组心肌的病理损害大于空白对照组。结论:电击诱发室颤犬复苏成功后存在着心肌细胞的坏死和凋亡增加,可能是复苏后心功能不全的原因之一。     

Inhibition of nitric oxide improves coronary perfusion pressure and return of spontaneous circulation in a porcine cardiopulmonary resuscitation model

OBJECTIVE: During spontaneous circulation, nonspecific inhibition of nitric oxide synthase by N(G)-nitro-L-arginine methyl ester (L-NAME) increases systemic vascular resistance and, therefore, mean arterial pressure. If this effect can be extrapolated to cardiopulmonary resuscitation (CPR), administering L-NAME during CPR may be beneficial by maintaining or even improving coronary perfusion pressure, and hence successful defibrillation. DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for hemodynamic variables, blood gases, and defibrillation attempt. SETTING: University medical center experimental laboratory. SUBJECTS: Ten domestic pigs. INTERVENTIONS: After 4 mins of ventricular fibrillation, ten animals were randomly assigned to receive L-NAME (25 mg/kg; n = 5) or saline placebo (n = 5) (given in two doses) after 3 and 13 mins of CPR, respectively. Defibrillation was provided 5 mins after the second dose of active drug or placebo. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem coronary perfusion pressure was significantly (p < .05) higher 90 secs (27 +/- 3 vs. 17 +/- 3 mm Hg), 10 mins (28 +/- 3 vs. 14 +/- 2 mm Hg), and 15 mins (21 +/- 5 vs. 7 +/- 3 mm Hg) after the first L-NAME administration compared with saline placebo. Mean +/- sem coronary perfusion pressure remained significantly higher 90 secs and 5 mins after the second L-NAME vs. saline placebo administration (19 +/- 4 vs. 6 +/- 4 mm Hg, and 17 +/- 3 vs. 4 +/- 4 mm Hg). After 22 mins of cardiac arrest, including 18 mins of CPR, four of five pigs in the L-NAME group were successfully defibrillated, and survived the 60-min postresuscitation phase. In the placebo group, none of five pigs could be defibrillated successfully (p < .05). CONCLUSIONS: Nonspecific blockade of nitric oxide synthase with L-NAME during CPR was associated with an increase in coronary perfusion pressure and resulted in significantly better initial resuscitation when compared with saline placebo.     

The effect of cardiopulmonary bypass resuscitation on cardiac arrest induced lactic acidosis in dogs

The adequacy of end organ blood flow following a cardiac arrest varies depending on the artificial reperfusion technique utilized and may critically affect patient outcome. Both oxygen consumption (VO2) and arterial lactate values have previously been used to assess tissue perfusion. Cardiopulmonary bypass resuscitation (CPB) is a reperfusion technique capable of providing near normal end organ blood flow. The purpose of this investigation was to study the effect of femoro-femoral veno-arterial CPB resuscitation compared to standard CPR on VO2 and arterial lactic acid values after a prolonged cardiac arrest. Ten mongrel dogs were electrically fibrillated and left in cardiopulmonary arrest without therapy for 12 min. Resuscitation was attempted according to a standardized protocol utilizing either CPB (n = 5) or standard external CPR (n = 5). Oxygen consumption values and arterial lactic acid samples were obtained at baseline, at timed intervals throughout resuscitation and after return of spontaneous circulation in successfully resuscitated dogs. Baseline hemodynamic and biochemical measurements were similar in both treatment groups (P greater than 0.05). Oxygen consumption (440 +/- 50 ml/min/M2) and mean arterial lactic acid values (7.44 +/- 2.25 mmol/l) were significantly higher at 1 min of resuscitation in CPB-treated dogs compared to dogs treated with CPR (60 +/- 10 ml/min/M2) (3.16 +/- 0.69 mmol/l) respectively (P less than 0.05). Mean arterial lactic acid values rose significantly at each sampling interval during CPR (P less than 0.05) but began to decrease after 5 min of resuscitation in the CPB animals and were not significantly different than baseline after 60 min of bypass (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

A comparison of cardiopulmonary resuscitation with cardiopulmonary bypass after prolonged cardiac arrest in dogs. Reperfusion pressures and neurologic recovery.

Resuscitability and outcome after prolonged cardiac arrest were compared in dogs with standard external cardiopulmonary resuscitation (CPR) vs. closed-chest emergency cardiopulmonary bypass (CPB). Ventricular fibrillation (VF) was with no blood flow from VF 0 min to VF 10 min. Subsequent CPR basic life support (BLS) was from 10 min to VF 15 min. Then, group I (n = 13) received CPR advanced life support (ALS) from VF 15 min until restoration of spontaneous circulation to occur not later than VF 40 min. Group II (n = 14) received CPR-ALS from VF 15 min to VF 20 min without defibrillation, and then total CPB to defibrillation attempts started at VF 20 min, followed by assisted CPB to 2 h. Total ischemia time (no-flow time plus CPR time of MAP less than 50 mmHg) was unexpectedly shorter in group I (14.3 +/- 2.5 min) than in group II (18.6 +/- 2.3 min) (P less than 0.01). During CPR-BLS, coronary perfusion pressures were 25 +/- 9 mmHg in group I and 18 +/- 8 mmHg in group II (NS). Epinephrine during CPR-ALS, before countershock, raised coronary perfusion pressure to 40 +/- 10 mmHg in group I and 27 +/- 10 mmHg in group II (NS). In group II, coronary perfusion pressure increased during total CPB to 58 +/- 16 mmHg (P less than 0.01 vs. group I). Spontaneous normotension was restored in 11/13 dogs of group I and all 14 dogs of group II (NS). Ten dogs in each group followed protocol and survived to 96 h. Five of ten in group I and six of ten in group II were neurologically normal (NS). We conclude that: (1) Reperfusion with CPB yields higher coronary perfusion pressures than reperfusion with CPR-ALS; and (2) even after no blood flow for 10 min, optimized CPR can result in cardiovascular resuscitability and neurologic recovery, similar to those achieved by CPB.     

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.     

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.     

Effects of different dosages and modes of sodium bicarbonate administration during cardiopulmonary resuscitation.

Systemic acidosis occurs during cardiac arrest and cardiopulmonary resuscitation (CPR). The present study investigated the effect of different modes of sodium bicarbonate administration on blood gas parameters during CPR. Arterial and venous blood gases were obtained during 10 minutes of CPR which was preceded by 3 minutes of unassisted ventricular fibrillation in 36 dogs. Following 1 minute of CPR, the animals received one of four treatments in a randomized and blinded manner: normal saline (NS), sodium bicarbonate bolus dose 1 mEq/kg (B), sodium bicarbonate continuous infusion 0.1 mEq/kg/min (I), and sodium bicarbonate bolus dose (0.5 mEq/kg) plus continuous infusion 0.1 mEq/kg/min (L+I). Eleven dogs completed NS, 8 B, 8 I, and 9 L+I protocol. Following NS infusion, both arterial and venous pH declined consistently over time. Significant differences compared with NS treatment in venous pH were observed at 12 minutes of ventricular fibrillation (L+I, 7.27 +/- 0.05; NS, 7.15 +/- 0.05; B, 7.20 +/- 0.05; I, 7.24 +/- 0.04, each bicarbonate treatment versus NS, and L+I versus B, (P < .05). The B group had an elevated venous PCO2 (mm Hg) concentration following 6 minutes of ventricular fibrillation compared with NS, L+I, and I groups (81 +/- 14 versus 69 +/- 10 versus 68 +/- 10 versus 71 +/- 8, respectively, (P = .07). Arterial pH and PCO2 values showed a similar trend as the venous data with the L+I group demonstrating arterial alkalosis (pH > 7.45) at 12 minutes of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium bicarbonate improves the chance of resuscitation after 10 minutes of cardiac arrest in dogs.

The likelihood of successful defibrillation and resuscitation decreases as the duration of cardiac arrest increases. Prolonged cardiac arrest is also associated with the development of acidosis. These experiments were designed to determine whether administration of sodium bicarbonate and/or adrenaline in combination with a brief period of cardiopulmonary resuscitation (CPR) prior to defibrillation would improve the outcome of prolonged cardiac arrest in dogs. Ventricular fibrillation (VF) was induced by a.c. shock in anaesthetised dogs. After 10 min of VF, animals received either immediate defibrillation (followed by treatment with bicarbonate or control) or immediate treatment with bicarbonate or saline (followed by defibrillation). Treatment with bicarbonate was associated with increased rates of restoration of spontaneous circulation. This was achieved with fewer shocks and in a shorter time. Coronary perfusion pressure was significantly higher in NaHCO3-treated animals than in control animals. There were smaller decreases in venous pH in NaHCO3-treated animals than in controls. The best outcome in this study was achieved when defibrillation was delayed for approximately 2 min, during which time NaHCO3 and adrenaline were administered with CPR. The results of the present study indicate that in prolonged arrests bicarbonate therapy and a period of perfusion prior to defibrillation may increase survival.     

Postcountershock pulseless rhythms: hemodynamic effects of glucagon in a canine model

Defibrillation after prolonged ventricular fibrillation (VF) is frequently followed by asystole or electromechanical dissociation (EMD) which are usually fatal. We studied the effects of glucagon, a known inotropic and chronotropic agent, during 19 episodes of postcountershock asystole/EMD in nine dogs. Systolic and diastolic aortic (Ao), left ventricular, pulmonary arterial, and right atrial (RA) pressures were recorded as was the instantaneous Ao-RA difference (coronary perfusion pressure) and coronary sinus blood flow (CSF) during closed-chest CPR. VF was induced electrically; 2 min later, a 400-J transthoracic shock was given. Countershock was always followed by asystole (n = 12) or EMD (n = 7). Conventional closed-chest CPR with a mechanical device was begun 30 to 60 sec after countershock and continued for 2 to 3 min. If a perfusing rhythm did not occur, glucagon (1 mg) was given iv and CPR continued for 2 to 3 min more. Glucagon had no significant effect on intravascular pressures, the coronary perfusion gradient, or CSF when compared to CPR alone. However, in 14 or 19 postcountershock episodes unresponsive to CPR alone, glucagon restored effective spontaneous circulation, i.e., successful cardiac resuscitation, due to its effects on the intrinsic pacemaker discharge rate. Glucagon has been previously shown to stimulate myocardial adenyl cyclase via nonadrenergic mechanisms. We conclude that when postcountershock asystole/EMD occurs, glucagon has a direct and favorable effect on cardiac resuscitation outcome due to its effects on pacemaker discharge rate which is not mediated by changes in myocardial blood flow or coronary perfusion pressure.     

复苏后心功能不全与炎症因子关系的实验研究

目的:观察犬心跳骤停复苏后血流动力学和细胞因子的变化及其关系。方法:体外电击诱发犬室颤,3min后复苏,12只犬随机分为2组,常规治疗组(CPR组)和正常对照组,每组6只,采用Swan-Ganz漂浮导管监测复苏前和复苏后6h的心输出量(CO)和肺动脉楔压(PAWP),同时抽血检测血清肿瘤坏死因子-α(TNF-α),白介素-6(IL-6)和白介素-10(IL-10)水平(放免法)。结果:两组各血流动力学指标在心跳骤停前差异无统计学意义,CPR组的MAP在复苏成功即时高于正常对照组,随后开始下降,在复苏后4、6h低于正常对照组。CPR组的PAWP从心跳骤停前的(5.0±1.26)mmHg一直上升,到复苏后达高峰(28.83±4.79)mmHg,各观察点均高于正常对照组,CO在复苏成功后随时间延长而下降,6h降至最低,复苏后各观察点均低于正常对照组和电击前。TNF-α、IL-6浓度在复苏后即时和2h开始出现明显的升高,并随时间的延长而增高,与本组电击前及同时间的正常对照组比较差异有统计学意义。在整个实验过程均未能检测到IL-10的浓度。细胞因子TNF-α和IL-6与CO之间呈负相关。结论:电击诱发室颤犬复苏成功后存...