Predictive indices of successful cardiac resuscitation after prolonged arrest and experimental cardiopulmonary resuscitation

To determine if clinically accessible hemodynamic and blood gas measurements are of value in predicting outcome of countershock after prolonged ventricular fibrillation (VF) and artificial cardiopulmonary support, 14 dogs were studied during 30 minutes of VF using two randomly assigned closed-chest techniques. Seven dogs underwent conventional CPR; the other seven were supported with a pneumatic thoracic vest and abdominal binder, which were inflated synchronously with the airway. Ascending aortic (Ao), right atrial (RA), and instantaneous coronary perfusion pressures (Ao - RA) were measured at five-minute intervals. Ao and RA blood samples were analyzed at 10, 20, 25 and 30 minutes for PO2, PCO2, and pH. After 25 minutes, 1 mg epinephrine was given intravenously, and five minutes later defibrillation was attempted. If unsuccessful, repeated countershocks, conventional pharmacologic therapy, and artificial support were continued. If a perfusing spontaneous cardiac rhythm did not result within an additional 30 minutes, the experiment was terminated. Six animals developed a perfusing cardiac rhythm after one or more countershocks (Group 1); eight failed to develop a perfusing rhythm after repeated countershocks and an additional 30 minutes of resuscitative effort (Group 2). Five Group 1 dogs received vest/binder artificial support. When measured values were averaged over the study period, Group 1 was found to have a significantly greater Ao end-diastolic pressure (AoEDP) and peak diastolic coronary perfusion pressure (CPP) when compared to Group 2 (23 +/- 6 vs 14 +/- 8 mm Hg, P less than .05; and 22 +/- 6 vs 5 +/- 10 mm Hg, P less than .01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of continuous abdominal binding during cardiac arrest and resuscitation

Abdominal binding improves arterial pressure and flow during cardiopulmonary resuscitation (CPR). This study was undertaken to assess the mechanisms of improved hemodynamics during cardiac arrest and CPR with continuous abdominal binding in a canine model (n = 8). Carotid and inferior vena caval (IVC) flow probes and cineangiography were used to observe magnitude and direction of blood flow. CPR with binding significantly increased (p < 0.001) systolic aortic (Ao) (49 ± 11 vs 34± 12mm Hg), right atrial (RA) (49 ± 11 vs 31 ± 10 mm Hg) and IVC pressure (50 ± 7 versus 31 ± 11 mm Hg) and common carotid flow (1.1 ± 0.4 vs 0.7 ± 0.4 ml/min/kg, p < 0.05) compared with CPR without binding. Aortic, RA and IVC diastolic pressures increased similarly. Binding decreased the diastolic Ao-IVC pressure difference by 8 ± 12 mm Hg and decreased net IVC flow (0.5 ± 1.4 vs 1.4 ± 1.2 ml/min/kg, p < 0.05). Binding also decreased coronary perfusion pressure (Ao-RA) in 5 of 8 dogs. Cineangiograms showed tricuspid incompetence and reflux from the right atrium to the inferior vena cava during chest compression and IVC-to-right heart inflow during relaxation, which was confirmed by the flowmeter data. Abdominal binding during CPR decreased the size of the perfused vascular bed by inhibiting subdiaphragmatic flow and increased intrathoracic pressure for a given chest compression force, leading to preferential cephalad flow. However, coronary perfusion pressure was often adversely affected. Further studies should be undertaken before the widespread clinical application of continuous abdominal binding during CPR.     

Hemodynamics in humans during conventional and experimental methods of cardiopulmonary resuscitation

High-fidelity hemodynamic recordings of aortic and right atrial pressures and the coronary perfusion gradient (the difference between aortic and atrial pressure) were made in nine patients during cardiopulmonary resuscitation (CPR). Findings during conventional manual CPR were compared with those during high-impulse CPR (rate, 120 cycles/min with a shorter compression:relaxation ratio) as well as during pneumatic vest CPR with and without simultaneous ventilation and abdominal binding. Aortic peak pressure during conventional CPR averaged 61 +/- 29 mm Hg but varied widely (range, 39-126 mm Hg) among patients. Although the magnitude of improvement was modest, the high-impulse method was the only technique tested that significantly elevated both aortic peak pressure and the coronary perfusion gradient during cardiac arrest. During conventional CPR, aortic pressure rose from 61 +/- 29 to 80 +/- 39 mm Hg during high-impulse CPR, and the gradient rose from 9 +/- 11 to 14 +/- 15 mm Hg, respectively; p less than 0.01. The pneumatic vest method significantly improved peak aortic pressure but not the coronary perfusion gradient. Simultaneous ventilation and chest compression created high end-expiratory pressure and lowered the coronary perfusion gradient. Abdominal binding had no significant hemodynamic effects. This evaluation of experimental resuscitation methods in humans shows that the high-impulse chest compression method augments aortic pressure over levels achieved during conventional CPR methods; however, the improvement in pressure is modest and may not be clinically important. Simultaneous ventilation as well as abdominal binding during CPR were associated with no benefit; in fact, simultaneous ventilation appears to adversely affect cardiac perfusion and, therefore, should not be used during clinical resuscitation.     

Aortic and right atrial systolic pressures during cardiopulmonary resuscitation: a potential indicator of the mechanism of blood flow

The absolute difference between aortic and right atrial systolic pressure (systolic pressure gradient) and the difference between the aortic diastolic and right atrial diastolic pressure (coronary perfusion pressure) were evaluated in a series of 63 adult mongrel dogs undergoing five different methods of cardiopulmonary resuscitation (CPR). Fluid-filled pressure monitoring catheters were placed in the ascending aorta and right atrium in each of the animals after induction of anesthesia with morphine sulfate and 1% halothane and oxygen. The animals were then fibrillated with a transvenous electrode catheter that had been introduced into a ventricle. After a "down time" of 3 minutes during which no CPR was performed, the animals' lungs were ventilated, and one of five methods of CPR was initiated. The systolic pressure gradient and coronary perfusion pressure were measured in all animals 1 minute after CPR was begun, and in all but the group undergoing open-chest cardiac massage after 7 minutes and 17 minutes of CPR. The systolic pressure gradient and coronary perfusion pressure were greatest during open-chest cardiac massage (true cardiac compression), intermediate in external mechanical CPR (Thumper) and standard CPR (greater in small dogs than large dogs), and lowest in CPR performed with a combined thoracic and abdominal vest apparatus (predominantly thoracic pump). The observation that the systolic pressure gradient between intrathoracic chambers is largest in open-chest cardiac massage and smallest in vest CPR suggests that similar measurements recorded during the performance of human cardiac resuscitation may be useful in determining the mechanism of blood flow.     

Vest inflation without simultaneous ventilation during cardiac arrest in dogs: improved survival from prolonged cardiopulmonary resuscitation

Myocardial and cerebral blood flow can be generated during cardiac arrest by techniques that manipulate intrathoracic pressure. Augmentation of intrathoracic pressure by high-pressure ventilation simultaneous with compression of the chest in dogs has been shown to produce higher flows to the heart and brain, but has limited usefulness because of the requirement for endotracheal intubation and complex devices. A system was developed that can produce high intrathoracic pressure without simultaneous ventilation by use of a pneumatically cycled vest placed around the thorax (vest cardiopulmonary resuscitation [CPR]). The system was first tested in a short-term study of the maximum achievable flows during arrest. Peak vest pressures up to 380 mm Hg were used on eight 21 to 30 kg dogs after induction of ventricular fibrillation and administration of epinephrine. Microsphere-determined myocardial blood flow was 108 +/- 17 ml/min/100 g (100 +/- 16% of prearrest flow) and cerebral flow was 51 +/- 12 ml/min/100 g (165 +/- 39% of prearrest). Severe lung or liver trauma was noted in three of eight dogs. If peak vest pressure was limited to 280 mm Hg, however, severe trauma was no longer observed. A study of the hemodynamics during and survival from prolonged resuscitation was then performed on three groups of seven dogs. Vest CPR was compared with manual CPR with either conventional (300 newtons) or high (430 newtons) sternal force. After induction of ventricular fibrillation, each technique was performed for 26 min. Defibrillation was then performed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postcountershock pulseless rhythms: response to CPR, artificial cardiac pacing, and adrenergic agonists

Clinically, countershock of ventricular fibrillation (VF) may result in asystole or a pulseless rhythm in more than 50% of attempts. We conducted a study to assess the effects of immediate artificial pacing, CPR, and adrenergic drug therapy in the management of postcountershock pulseless rhythms. Thirty-four episodes of VF followed by countershock were studied in eight anesthetized dogs. Transducer-tipped catheters were positioned in the ascending aorta (Ao) and right atrium (RA). A bipolar pacing catheter was advanced to the apex of the right ventricle and a catheter for measurement of coronary sinus blood flow (CSQ) (continuous thermodilution technique) was positioned in the coronary sinus. VF was induced electrically and a countershock at 400 J was given two minutes later; CPR was not performed during VF episodes. Countershock was followed by asystole or a pulseless rhythm in all animals. Immediate endocardial pacing (0.1 to 5 mA) of bradyarrhythmias produced electrical capture but did not result in arterial pressure pulses in any animal. After pacing, CPR was performed for two minutes or until restoration of spontaneous circulation (ROSC). During CPR, the diastolic coronary perfusion gradient (Ao-RA) was 20 +/- 7 mm Hg (mean +/- SD) and CSQ was 14 +/- 7 mL/min/100 g (53% +/- 43% of control). ROSC followed CPR of less than two minutes duration in 24% of VF study episodes. If ROSC did not follow two minutes of CPR, 1 mg epinephrine, or 50 micrograms or 100 micrograms isoproterenol was given IV.(ABSTRACT TRUNCATED AT 250 WORDS)     

The physiology of external cardiac massage: high-impulse cardiopulmonary resuscitation

In intact chronically instrumented dogs, left ventricular dynamics were studied during cardiopulmonary resuscitation (CPR). Electromagnetic flow probes measured cardiac output and coronary blood flow, ultrasonic transducers measured cardiac dimensions, and micromanometers measured left ventricular, right ventricular, aortic, and intrathoracic pressures. The dogs were anesthetized with morphine, intubated, and fibrillated by rapid ventricular pacing. Data were obtained during manual external massage with dogs in the lateral and supine positions. Force of compression was varied from a peak intrathoracic pressure of 10 to 30 mm Hg, and compression rate was varied from 60 to 150/min. Increasing force of compression increased stroke volume up to a peak intrathoracic pressure of approximately 20 mm Hg, beyond which stroke volume remained constant or declined. Stroke volume appeared to result primarily from direct transmission of manual compression force to the heart rather than from positive intrathoracic pressure because peak cardiac or vascular pressures or the change in these pressures were consistently two to four times greater than the corresponding intrathoracic pressures during manual compression. With increasing compression rate, stroke volume remained relatively constant, and total cardiac output increased significantly: 425 +/- 92 ml/min at 60/min, 643 +/- 130 ml/min at 100/min, and 975 +/- 219 ml/min at 150/min (p less than .05). Left ventricular dimensions decreased minimally at higher manual compression rates. In four patients undergoing CPR, systolic and diastolic arterial blood pressure increased with faster compression rates, correlating well with data obtained in the dog. Dynamic coronary blood flow in canine experiments decreased to zero or negative values during compression. Antegrade coronary flow occurred primarily during noncompression periods and seemed to be related to diastolic aortic perfusion pressure; coronary flow at a compression rate of 150/min averaged 75% of control. Therefore stroke volume and coronary blood flow in this canine preparation were maximized with manual chest compression performed with moderate force and brief duration. Increasing rate of compression increased total cardiac output while coronary blood flow was well maintained. Direct cardiac compression appeared to be the major determinant of stroke volume during manual external cardiac massage.     

Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 +/- 1% to 46 +/- 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 150/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of compression, but not on rates of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression.(ABSTRACT TRUNCATED AT 400 WORDS)     

Comparison of intravenous and intranasal administration of epinephrine during CPR in a canine model.

STUDY OBJECTIVES: Epinephrine improves coronary perfusion pressure during CPR. However, administration of epinephrine during CPR may be delayed or omitted if IV or endotracheal access is not established. Therefore, the objective of this study was to determine if intranasal administration of epinephrine during CPR would provide an alternate route of drug administration that is readily accessible and requires no special technical skills. DESIGN AND SETTING: Randomized blinded study performed in a controlled laboratory environment. TYPE OF PARTICIPANTS: Twenty mongrel dogs weighing 19.5 +/- 4.6 kg. INTERVENTIONS: All dogs received either IV epinephrine 0.015 mg/kg or intranasal epinephrine 14 mg per nostril. Phentolamine (5 mg per nostril) was administered intranasally one minute before nasal administration of epinephrine to improve absorption. Each dog underwent three minutes of ventricular fibrillation followed by seven minutes of CPR with a pneumatic chest compression device. Epinephrine was administered at two minutes into CPR. MEASUREMENTS AND MAIN RESULTS: Seven dogs were excluded because of inadequate baseline coronary perfusion pressure or compression device displacement, leaving a total of 13 dogs for analysis (six IV epinephrine, seven intranasal epinephrine). Baseline coronary perfusion pressure (mean +/- SD) was similar for IV epinephrine and intranasal epinephrine (16.9 +/- 7.1 mm Hg versus 18.2 +/- 13.8 mm Hg, respectively, P = .84). For IV and intranasal epinephrine, coronary perfusion pressure increased to 21.4 +/- 9.2 mm Hg and 24.4 +/- 18.7 mm Hg one minute after epinephrine, respectively (P = .73). Five minutes after epinephrine coronary perfusion pressure was 18.2 +/- 8.7 mm Hg and 24.3 +/- 13.9 mm Hg for IV epinephrine and intranasal epinephrine, respectively (P = .38). The rate of successful resuscitation was similar for both groups, five of seven dogs for intranasal epinephrine and four of six dogs for IV epinephrine (P = .66). CONCLUSION: Intranasal epinephrine has similar effects on coronary perfusion pressure and resuscitation compared with standard-dose IV epinephrine. Therefore, the nasal route for administration of epinephrine appears to be an acceptable alternate method of drug delivery during CPR and compares favorably with standard IV therapy in the canine model. Because of the obvious benefits to human patients, these observations suggest further investigation.     

Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs

Recent studies have demonstrated that for the same chest compression force during mechanical cardiopulmonary resuscitation (CPR), the carotid artery-to-jugular vein pressure gradient and carotid blood flow are increased when the phasic rise of intrathoracic pressure is enhanced by abdominal binding and simultaneous ventilation at high airway pressure with each chest compression (SCV). The objective of the present study was to assess whether cerebral blood flow is also enhanced, since it is known that fluctuations in intrathoracic pressure are transmitted to the intracranial space and affect intracranial pressure (ICP). In two series of pentobarbital-anesthetized dogs, one of two CPR techniques was initiated immediately after inducing ventricular fibrillation. Brain blood flow was measured by the radiolabeled microsphere technique immediately before cardiac arrest and at 1 and 3 minutes after commencing CPR. Evidence of adequate mixing of spheres and lack of sedimentation under these low-flow conditions was verified by correlation with brain venous outflow, comparison of the arterial concentration-time profile of spheres and a nonsedimentary marker (thallium-201 in solution), and use of multiple arterial sampling sites. During SCV CPR with abdominal binding, mean carotid artery pressure (60 +/- 3 mm Hg) was higher than that during conventional CPR (25 +/- 2 mm HG). Pulsations of ICP occurred that were in phase with chest compression and greater than jugular venous pressure. Mean ICP was higher during SCV (46 +/- 2 mm Hg) than conventional CPR (20 +/- 2 mm Hg). However, the net brain perfusion pressure gradient (carotid artery pressure - ICP) was greater with SCV (14 +/- 3 mm Hg) than with conventional CPR (5 +/- 0.4 mm Hg). Cerebral blood flow was significantly greater during SCV CPR (32 +/- 7% of prearrest cerebral flow) than during conventional CPR (3 +/- 2%). We conclude that SCV CPR combined with abdominal binding substantially improved brain perfusion by enhancing cerebral perfusion pressure in this experimental model.     

Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest

BACKGROUND: Blood pressure is severely reduced in patients in cardiac arrest receiving standard cardiopulmonary resuscitation (CPR). Although active compression-decompression (ACD) CPR improves acute hemodynamic parameters, arterial pressures remain suboptimal with this technique. We performed ACD CPR in patients with a new inspiratory threshold valve (ITV) to determine whether lowering intrathoracic pressures during the "relaxation" phase of ACD CPR would enhance venous blood return and overall CPR efficiency. METHODS AND RESULTS: This prospective, randomized, blinded trial was performed in prehospital mobile intensive care units in Paris, France. Patients in nontraumatic cardiac arrest received ACD CPR plus the ITV or ACD CPR alone for 30 minutes during advanced cardiac life support. End tidal CO(2) (ETCO(2)), diastolic blood pressure (DAP) and coronary perfusion pressure, and time to return of spontaneous circulation (ROSC) were measured. Groups were similar with respect to age, gender, and initial rhythm. Mean maximal ETCO(2), coronary perfusion pressure, and DAP values, respectively (in mm Hg), were 13.1+/-0.9, 25.0+/-1.4, and 36.5+/-1.5 with ACD CPR alone versus 19.1+/-1.0, 43.3+/-1.6, and 56.4+/-1.7 with ACD plus valve (P<0.001 between groups). ROSC was observed in 2 of 10 patients with ACD CPR alone after 26.5+/-0.7 minutes versus 4 of 11 patients with ACD CPR plus ITV after 19.8+/-2.8 minutes (P<0.05 for time from intubation to ROSC). Conclusions-Use of an inspiratory resistance valve in patients in cardiac arrest receiving ACD CPR increases the efficiency of CPR, leading to diastolic arterial pressures of >50 mm Hg. The long-term benefits of this new CPR technology are under investigation.     

Use of naloxone during cardiac arrest and CPR: potential adjunct for postcountershock electrical-mechanical dissociation

Naloxone has been shown to increase arterial pressure in hemorrhagic and septic shock. To determine if naloxone has salutary effects during cardiac arrest with conventional closed-chest cardiopulmonary resuscitation (CPR), ten dogs were studied during 20 minutes of ventricular fibrillation (VF) and CPR and during a 30-minute postcountershock period. Central aortic (Ao) and right atrial (RA) systolic and end-diastolic (EDP) pressures, instantaneous Ao-RA pressure difference (coronary perfusion pressure), and electromagnetic Ao flow were measured. Ao and RA samples were analyzed during a control period and at five-minute intervals during CPR for PO2, PCO2, and pH. During VF, a piston-cylinder device was used to perform anteroposterior sternal depressions and positive pressure ventilations (100% O2) at standard rates and ratios. After 15 minutes of CPR, animals were randomized and given either naloxone (5 mg/kg) or epinephrine (1 mg). Defibrillation was attempted five minutes later using 1 J/kg and then, if necessary, 2, 4, 8, 12, and 16 J/kg until VF was terminated or the maximum energy dose was reached. If VF persisted or if countershock resulted in asystole or a nonperfusing rhythm (electrical-mechanical dissociation [EMD]), the alternate drug (naloxone or epinephrine) was then given. Measured systolic pressures, coronary perfusion pressures, aortic flow, and blood gases were not significantly different during the control period or at five, ten, and 15 minutes of VF and CPR between animal groups prior to drug administration. When compared to hemodynamic values measured at 15 minutes, naloxone had no significant effect on pressures or aortic flow measured five minutes after administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of abruptly increased intrathoracic pressure on coronary blood flow velocity in patients

To assess the effects of abruptly increased intrathoracic pressure on coronary blood flow, arterial pressure, heart rate, and intracoronary Doppler blood flow velocity were measured continuously during cough(s) and again during the four phases of the Valsalva maneuver in 14 patients. Coughing significantly increased the systolic pressure (137 +/- 25 to 176 +/- 30 mm Hg), diastolic pressure (72 +/- 10 to 84 +/- 18 mm Hg), and arterial pulse pressure (65 +/- 27 to 92 +/- 35 mm Hg), with no change in heart rate. The mean coronary flow velocity decreased (17 +/- 10 to 14 +/- 12 cm/sec, p less than 0.03). During the Valsalva maneuver, despite marked reduction in the mean arterial pressure during phase III (96 +/- 12 to 68 +/- 14 mm Hg, p less than 0.05), the reduction of coronary blood flow velocity did not achieve statistical significance. These data demonstrate that neither type of abrupt physiologic increase in intrathoracic pressure enhances coronary blood flow. Coughing does not improve coronary perfusion pressures or flow velocity, despite marked increases in arterial diastolic pressure. The Valsalva maneuver, for the most part, does not significantly alter coronary blood flow velocity.     

Comparison of standard external CPR, open-chest CPR, and cardiopulmonary bypass in a canine myocardial infarct model

STUDY OBJECTIVES: After cardiac arrest, open-chest CPR (OCCPR) and cardiopulmonary bypass (CPB) have demonstrated higher resuscitation rates when compared individually with standard external CPR (SECPR). We compared all three techniques in a canine myocardial infarct ventricular fibrillation model. TYPE OF PARTICIPANTS: Twenty-six mongrel dogs were block-randomized to receive SECPR and advanced life support (nine), CPB (nine), or OCCPR (eight). DESIGN AND INTERVENTIONS: All dogs received left anterior descending coronary artery occlusion followed by four minutes of ventricular fibrillation without CPR and eight minutes of Thumper CPR. At 12 minutes, dogs received one of three resuscitation techniques. After resuscitation, all animals received four hours of intensive care. Animals that were resuscitated had histochemical determination of ischemic and necrotic myocardial areas. MEASUREMENTS: Intravascular pressures were measured and coronary perfusion pressure was calculated during baseline, cardiac arrest, resuscitation, and postresuscitation periods. Percent necrotic myocardium, percent ischemic myocardium, and necrotic-to-ischemic ratios were determined for resuscitated animals. Epinephrine dosage and number of countershocks were determined for each group. MAIN RESULTS: Nine of nine CPB and six of nine OCCPR, compared with two of eight SECPR animals, were resuscitated (P less than .01). Three of nine CPB and OCCPR and two of eight SECPR dogs survived to four hours (P = NS). Coronary perfusion pressure two minutes after institution of technique was significantly higher with CPB (75 +/- 37 mm Hg) and OCCPR (56 +/- 31 mm Hg) than in SECPR animals (16 +/- 16 mm Hg, P less than .04). Epinephrine required for resuscitation was significantly less with CPB (0.10 +/- 0.02 mg/kg) than for SECPR (0.28 +/- 0.11 mg/kg, P less than .002). The ratio of necrotic to ischemic myocardium at four hours was significantly lower with CPB (0.15 +/- 0.31) and OCCPR (0.39 +/- 0.25) than for SECPR (1.16 +/- 0.31, P less than .02). CONCLUSION: OCCPR and CPB produce higher coronary perfusion pressures and improved resuscitation rates from ventricular fibrillation when compared with SECPR in this canine myocardial infarct cardiac arrest model. CPB and OCCPR yielded similar resuscitation results, although less epinephrine was required with CPB.     

End tidal carbon dioxide as an haemodynamic determinant of cardiopulmonary resuscitation in the rat

End tidal PCO2 (PETCO2) has been found to be a good prognostic indicator of successful resuscitation from cardiac arrest. To explore the value of this measurement further, we carried out a series of experiments during cardiac arrest and closed chest resuscitation in 14 mechanically ventilated Sprague-Dawley rats. Ventricular fibrillation (VF) was induced by a 10 mA current delivered to the right ventricular endocardium. After 4 min of VF, precordial compression was begun with a mechanical thumper and defibrillation was attempted 2 min later. PETCO2 decreased abruptly during cardiac arrest to 0.3 mm Hg (0.04 kPa). With precordial compression, it increased to 11 mm Hg (1.5 kPa). Within 3 min of successful defibrillation, there was an overshoot in the PETCO2 to 44 mm Hg (5.8 kPa) with return to baseline levels approximating those of the pre-arrest control measurements over the 60 min that followed restoration of spontaneous circulation. The PETCO2 measurement during precordial compression predicted the success of defibrillation with return of spontaneous circulation. When PETCO2 exceeded 9 mm Hg (1.2 kpA), 7 of 8 animals were successfully resuscitated. When PETCO2 was less than 9 mm Hg during precordial compression, none of six animals were successfully resuscitated. The PETCO2 correlated with the mean aortic (r = 0.71) and coronary perfusion pressure (r = 0.80) generated during precordial compression. In corroboration of previously reported observations on pigs, dogs, and human patients, PETCO2 served as a non-invasive monitor of the effectiveness of precordial compression for maintaining coronary perfusion and therefore cardiac viability during CPR. The PETCO2 was also useful in that it promptly signalled restoration of spontaneous circulation.     

Coronary pressure-flow relations in hypertensive left ventricular hypertrophy. Comparison of intact autoregulation with physiological and pharmacological vasodilation in the dog

Coronary pressure-flow relations during autoregulated and vasodilated flow states were compared between eight dogs with renovascular hypertension and left ventricular hypertrophy and 12 normal dogs. Each relation was constructed from serial steady-state measurements of end-diastolic coronary pressure and flow during perfusion of the circumflex artery by an extracorporeal circuit at controlled diastolic pressures of 20-200 mm Hg. Autoregulated pressure-flow relations were compared at three levels of myocardial oxygen demand: resting, high (dobutamine 10 micrograms/kg/min), and low (propranolol 2.5 micrograms/kg/min). Autoregulatory capacity was assessed by calculation of closed-loop flow gain. At each level of myocardial oxygen demand, the lower limit of autoregulation occurred at higher perfusion pressures in the hypertrophy group (rest 65 +/- 3, high 92 +/- 4, low 66 +/- 4 mm Hg) than in the normal group (rest 53 +/- 2, p less than 0.05; high 75 +/- 5, p less than 0.05; low 51 +/- 3 mm Hg) (p less than 0.05). Maximum autoregulatory gain was similar in the normal and hypertrophy groups during resting and low myocardial oxygen demand but was reduced in the hypertrophy group during dobutamine studies. When coronary flow decreased below the lower limit of autoregulation, systolic shortening was reduced in both normal and hypertrophy groups. However, as the autoregulatory limits were at higher pressures in the hypertrophy group, shortening in this group deteriorated at perfusion pressures that did not affect the normal heart. Coronary pressure-flow relations during physiological (peak hyperemia after 15-second flow occlusion) and pharmacologica (intracoronary adenosine 400 micrograms/min) vasodilation was curvilinear and fitted by quadratic regression. During hyperemic vasodilation, maximal conductance per unit mass of myocardium was less in the hypertrophy group over a wide range of perfusion pressures. At a diastolic perfusion pressure of 80 mm Hg, maximum conductance was 4.6 +/- 0.5 ml/min/100 g/mm Hg in the normal group and 3.4 +/- 0.4 ml/min/100 g/mm Hg (p less than 0.05) in the hypertrophy group. Intracoronary adenosine elicited further vasodilation in both groups, but maximum conductance remained less in the hypertrophy group (8.5 +/- 1.7 ml/min/100 g/mm Hg at a perfusion pressure of 80 mm Hg) than in the normal group (13.5 +/- 2.0 ml/min/100 g/mm Hg) (p less than 0.05). Maximal coronary flow reserve is reduced in left ventricular hypertrophy, with a consequent shift of the lower limit of autoregulation to higher perfusion pressures. Thus, as coronary perfusion pressure is decreased, coronary flow and myocardial shortening become impaired at higher     

Continuous transtracheal oxygen delivery during cardiopulmonary resuscitation. An alternative method of ventilation in a canine model

Adequate oxygenation of apneic subjects can be maintained by constant flow transtracheal oxygen (TTO), but this method alone is associated with hypercapnia. The "bellows" effect of external chest compressions (ECC) might prevent this problem if the airway were kept open by TTO. In dogs, we investigated the utility of TTO delivered at 15 L/min by a percutaneously placed intratracheal catheter, plus ECC (TTO/ECC) as an alternative method of ventilation during CPR. TTO was applied to anesthetized, paralyzed dogs in normal sinus rhythm (NSR) at various rates of ECC and during ventricular fibrillation (VF) at an ECC rate of 80/min. During NSR and VF, hypercapnia did not develop and arterial oxygen saturations were maintained above 90 percent. During NSR, the PaCO2 decreased and the pH increased as the ECC rate increased. For many of the animals, coronary perfusion pressure remained above 20 mm Hg during VF, suggesting that these animals could be resuscitated to NSR. In another phase, after 15 min of VF using TTO/ECC, seven of nine animals were defibrillated. We conclude that ventilatory and hemodynamic support adequate to permit successful resuscitation to NSR is provided by the combination of TTO/ECC to apneic dogs during VF.     

Air trapping in the lungs during cardiopulmonary resuscitation in dogs. A mechanism for generating changes in intrathoracic pressure

To test the hypothesis that during cardiopulmonary resuscitation, chest compression with an unobstructed trachea raises and maintains intrathoracic pressure by collapsing airways and trapping air in the lung, we studied 11 dogs (20-32 kg). An inflatable vest compressed the thorax after induction of ventricular fibrillation. First, tracheal airflow was measured by a pneumotachometer during vest inflation and deflation in nine of the dogs. As expected, during the initial phase of vest inflation of cycles after ventilation, air moved out of the lungs, but then airflow stopped. After vest deflation, however, more air moved out of the lungs in eight of the nine dogs; this occurrence indicated that a portion of the inspired tidal volume was trapped during vest inflation. During cycles without prior ventilation, the amount of air expired by chest compression decreased, paradoxically, at higher peak vest pressure (p less than 0.002); this occurrence indicated that air was trapped at the higher vest pressures. The change in right atrial pressure was higher on cycles after ventilation than on cycles without prior ventilation (79 +/- 12 vs. 67 +/- 12 mm Hg [mean +/- SEM], p less than 0.005), and lung volume was higher on cycles after ventilation (p less than 0.001). Next, a 5-Fr micromanometer was advanced down the airway in eight of the dogs. With the tip of the micromanometer 5-8 cm distal to the carina, a zone of high pressure was noted in seven dogs; this high pressure suggested a zone of airway collapse distal to the carina.(ABSTRACT TRUNCATED AT 250 WORDS)     

Low zero-flow pressure and minimal capacitance effect on diastolic coronary arterial pressure-flow relationships during maximum vasodilation in swine

During maximum dilation with adenosine in dogs, the diastolic coronary pressure at which flow ceases (Pzf) has been observed to be up to 27 mm Hg above coronary sinus and right atrial pressures. We studied swine to measure the Pzf and to determine the effects of interventions that change collateral flow and coronary capacitance. In 44 swine, the left anterior descending coronary artery (LAD) was instrumented with two catheters, a hydraulic occluder, and a flowmeter. Late diastolic and mean pressure-flow relationships were constructed at a series of pressures produced by partial LAD occlusions during maximum vasodilation. The late diastolic Pzf was 7.0 +/- 2.2 mm Hg (mean +/- SD), less than 4 mm Hg above right atrial pressure; the mean Pzf was 12.1 +/- 3.1 mm Hg, less than 9 mm Hg above right atrial pressure. The Pzf in the LAD did not change significantly (1) during transient simultaneous occlusion of the right coronary artery (RCA) in seven swine (late diastolic Pzf with the RCA open was 6.6 +/- 1.5 mm Hg and with the RCA closed it was 6.0 +/- 1.5 mm Hg), (2) during increased left ventricular systolic pressure (LVSP) in seven swine (late diastolic Pzf with LVSP of 123 mm Hg was 5.5 +/- 2.2 mm Hg and with LVSP of 184 mm Hg it was 7.3 +/- 2.8 mm Hg), or (3) during increased heart rate in eight swine (late diastolic Pzf at heart rate of 107 per minute was 10.8 +/- 2.9 mm Hg and at 180 per minute it was 12.7 +/- 2.1 mm Hg). Similar results were obtained from analysis of the mean pressure and flow data. The Pzf in the LAD of swine is very close to right atrial pressure, and it did not change significantly during interventions that would modify collateral flow (reduced by RCA occlusion and enhanced by increased LVSP) and coronary capacitance (increased LVSP and increased heart rate). This low Pzf is beneficial in maintaining flow at lower coronary arterial perfusion pressures.     

Interposed abdominal compression-CPR: its effects on parameters of coronary perfusion in human subjects

Recent literature has emphasized the relationship between coronary perfusion during CPR and the success of resuscitation from prolonged arrest. In this study, aortic and right atrial pressures were monitored simultaneously during modifications of CPR. Three parameters associated with survival or coronary blood flow during CPR were measured: diastolic arterial pressure (DAP), diastolic arteriovenous difference (DAVD), and mean AV difference (MAVD). Standard advanced cardiac life support protocol was used although vasopressors were given by continuous infusion. In a series of two-minute trials, standard CPR, interposed abdominal compression (IAC) CPR, high-compression force (HCF) IAC-CPR, and HCF standard CPR were performed, with each patient serving as his own control. The DAP increased from 25 mm Hg during standard CPR to 43 during IAC CPR (P less than .001) and 50 during HC-IAC-CPR (P less than .001). The MAVD increased from 4 to 8 mm Hg during HCF-IAC-CPR (P less than .05). IAC-CPR had inconsistent effects on the DAVD. Three patients had a return of spontaneous circulation during the modifications of CPR after a mean of 43 minutes of asystole with standard CPR. In the seven autopsied patients, no significant abdominal injury was found. All forms of CPR studies produced DAVD in the majority of patients well below the minimum DAVD needed for resuscitation in animal models of prolonged arrest. Although the interposed abdominal compression seems to offer some advantages over standard CPR, these hemodynamic data suggest that it would be unlikely to improve survival rates appreciably.