during the contribution of sympathetic and parasympathetic nervous system imbalance during spinal anesthesia as a mechanism of asystole. They that in a patient with vasovagal syncope, the combination of cardiac sympathetic blockade and vagal stimulation disturbed this autonomic balance even further. It is certainly intuitive to think that the spinal anesthetic blocks cardiac sympathetic efferent nerves and not vagal efferent nerves, ii relative parasympathetic dominance or vagotonic state would result. However, if this was the case, why would severe bradycardia and asystole not occur more often with high-spinal and epidural anesthesia? and or parallel anesthetic and afferent activity has significance in the overall mechanism of cardiac arrest during spinal anesthesia. We think that sympathectomy of the heart after spinal anesthesia should be thought of as a condition with the potential to develop clinically significant vagal dominance or vagotonia. Bradycardia, asystole, and cardiac arrest from autonomic imbalance during spinal anesthesia are more likely to result if precipitccting events resulting in vagal stimulation occur while cardiac sympathetic blockade exists, as reported by lhrush and Downs.’ We agree with these authors that during spinal anesthesia the clinician should have a high index of suspicion for at-risk scenarios that could result in cardiac arrest and a low threshold for the initiation of prophylactic or resuscitative treatment throughout the perioperativc period.

S140 INTRODUCTION: We reported that application of CPAP during precordial compression will provide sufficient tidal ventilation even without intermittent positive pressure ventilation. [1] We have observed increased carotid blood flow and aortic blood pressure during precordial compression and CPAP (CPRCPAP) compared to conventional-CPR (CPRC).2 The objective of this study was to compare the success of defibrillation and restoration of spontaneous circulation during CPRC versus CPRCPAP. METHODS: Twenty-four anesthetized, tracheally intubated pigs (24 +/- 3 kg) underwent appropriate instrumentation to determine aortic blood pressure, arterial blood gas tensions and pH, PETCO2, and minute ventilation. An electromagnetic, in-line flow probe was placed in the left carotid artery to measure blood flow. Ventricular fibrillation was induced by an electric shock, after measurement of baseline data. Animals were given epinephrine (20 mg/kg IV immediately and q5min), then randomly were assigned to receive five or ten min trials of CPRC or CPRCPAP (FIO2=1.0) at a compression rate of 80/minute with a sternal pneumatic compressor. During CPRC, intermittent positive pressure ventilation (12mL/kg) for 1.5sec was given after every fifth compression. During CPRCPAP, CPAP (20 +/- 3 cmH2 O) was adjusted to equal the animal's baseline spontaneous ventilation. Defibrillation was attempted with DC countershock and when successful, data were collected 30min later. Measurement data are summarized as mean +/- 1SD and were compared with a two-factor analysis of variance and Scheffe's test. Defibrillation success rate was compared with Fishers exact test. RESULTS: There were no differences in resuscitation success between animals who received CPRC versus CPRCPAP after five (5/6 vs. 5/5, P=.52) or ten (1/6 vs. 2/7, P=.88) minutes of CPR. There were no intergroup differences in carotid blood flow (CBF), aortic blood pressure during chest compression (BPComp) and relaxation (BPRelax), PETCO2, arterial blood gases or pHa between animals who were or were not resuscitated. There were no intergroup differences in measured variables of the animals who were resuscitated. Variables reflecting cardiovascular function during ventricular fibrillation and CPR are summarized in Table 1 (*p<.06 vs. CPRC at 5min).Table 1DISCUSSION: We observed that defibrillation success during CPR was independent of ventilation technique. Systemic blood pressure was greater after 5min in animals, who received CPRCPAP versus CPRC, which coincides with previous observations that positive airway pressure, applied coincidently with chest compression, increases blood pressure and flow. We conclude that application of CPAP during chest compression obviates the need for intermittent mechanical ventilation, without compromising cardiovascular function or success of resuscitation. This study was supported by the Laerdal Foundation for Acute Medicine.

CARDIAC sequelae after neurologic injury are a welldescribed phenomenon. 1,2 However, most reports focus on electrocardiographic findings as well as pulmonary edema. 3,4 We present two cases of overt cardiac failure after isolated neurologic injury in two previously healthy patients. Case Reports Case 1A 26-yr-old healthy woman fell from a moving golf cart, striking her occiput.She lost consciousness and experienced seizures at the scene.Initial Glasgow coma scale was 6.She was intubated at the scene and transferred to Hermann Hospital.Intravenous mannitol (70 g) was administered in flight.Upon arrival at the hospital, blood pressure BP was 110 -150/75-110 mmHg, and heart rate was 120 -150 beats/min.Intravenous lorazepam and phenytoin were administered to treat seizure activity.Computed tomography scan showed occipital fracture with diffuse cerebral edema, obliteration of basal cisterns, subarachnoid hemorrhage, and contusions in the frontal and temporal areas.In the intensive care unit, BP was 98/57 mmHg, mean arterial pressure was 67 mmHg, heart rate was 140 beats/min, and bladder temperature was 38°C.An intracranial pressure (ICP) monitor was placed, showing an initial ICP of 33-38 mmHg.Efforts to control elevated ICP were immediately instituted.Phenylephrine was started to support mean arterial pressure, and hypothermia to 33°C was instituted for aid in controlling ICP.Status epilepticus was diagnosed on electroencephalogram, for which appropriate anticonvulsant therapy was initiated with phenytoin and lorazepam.A pulmonary artery catheter was inserted.Central venous pressure was 19 mmHg, pulmonary capillary wedge pressure was 22 mmHg, cardiac index was 1.3 l ⅐ min Ϫ1 ⅐ m 2Ϫ1 , systemic vascular resistance index was 2,733 dyne ⅐ s Ϫ1 ⅐ cm 5Ϫ1 , and mixed venous oxygen satu-ration was 66%.Phenylephrine was discontinued, and multiple vasoactive agents (dopamine, dobutamine, norepinephrine, milrinone) were sequentially initiated to treat cardiogenic failure.Electrocardiogram showed sinus tachycardia along with poor R-wave progression anteriorly, associated with elevation of cardiac isoenzymes.A twodimensional transthoracic echocardiogram showed severe depression of systolic function, dilated left ventricle, no valvular abnormalities, and an estimated ejection fraction of 30%.Other complications included rhabdomyolysis with acute renal failure, as well as hepatic dysfunction from hypoperfusion.By hospital day 4, the patient's hemodynamic profile improved, allowing reduction of pharmacologic support to single-agent therapy with dopamine, and thereafter removal of pulmonary artery catheter.Despite a complicated course, metabolic derangements eventually corrected, and she was transferred to a subacute facility approximately 4 weeks after injury.Subsequent functional recovery was good, with no evident lasting cardiac dysfunction. Case 2A 29-yr-old healthy female presented to the Emergency Center with a chief complaint of the worst headache of her life.Her mental status declined quickly to deep coma, with a Glasgow coma scale of 4.She was intubated and transferred to our facility via helicopter.Empirically, 60 g mannitol was administered intravenously.Initial vital signs were BP 80/50 mmHg and heart rate 80 beats/min.A computed tomography scan showed massive intraventricular hemorrhage with associated hydrocephalus, and a ventriculostomy was placed; initial ICP was 18 mmHg.Arteriogram showed a retro-splenial arteriovenous malformation.In the intensive care unit, BP was 100/65 mmHg, and heart rate was 87 beats/min, with phenylephrine infusion in use to support mean arterial pressure.A pulmonary artery catheter was inserted.Cardiac index was 1.2 l ⅐ min Ϫ1 ⅐ m 2Ϫ1 , pulmonary capillary wedge pressure was 18 mmHg, mixed venous oxygen saturation was 54 -67%, and systemic vascular resistance index was 3,720 dyne ⅐ s Ϫ1 ⅐ cm 5Ϫ1 .Profound metabolic acidemia ensued; serum lactate level was 10.7 mM, and phenylephrine was discontinued.Dopamine then dobutamine were begun.A two-dimensional transthoracic echocardiogram demonstrated severely depressed biventricular function with a qualitative ejection fraction of 20 -24%.Afterload reduction was attempted with enalaprilat, as well as additional inotropic support with milrinone.Cardiac index eventually improved to 3.7 l min Ϫ1 ⅐ m 2Ϫ1 , and pharmacologic support was reduced to single-agent therapy.She, too, developed hepatic dysfunction and acute renal failure.Malignant ICP developed; barbiturate coma was induced, and ICP gradually improved.Inotropic support was eventually converted to digoxin, which was continued beyond her stay in the intensive care unit.The patient made a full neurologic recovery and wished to

S141 INTRODUCTION: During CPR, airway pressure and ventilator pattern may have a dramatic effect on arterial blood pressure and flow. This may explain why attempts to define the ideal rate and time of chest compression have led to conflicting results. Thus, we chose to hold airway pressure constant, in order to examine the effect of variable chest compression and rate on hemodynamic function during CPR. METHODS: Sixteen anesthetized, tracheally intubated pigs (28 +/- 3 kg) underwent appropriate instrumentation to determine aortic blood pressure and carotid blood flow. Ventricular fibrillation was induced by an electric shock. Chest compression time (0.25, 0.3 and 0.4s) and rate (40, 60, 80, 100, 120/min) were varied randomly at 30 sec intervals with a computer program driven sternal pneumatic compressor. Compression force was adjusted to result in a sternal displacement of [similar]25% of the anteroposterior diameter. CPAP (20 cmH2 O) was applied with 100% oxygen. Carotid blood flow and aortic blood pressure during chest compression were recorded during each compression time and rate trial. Blood pressure data are summarized as mean +/- 1SD and were compared using a repeated measures analysis of variance. Carotid blood flow values were compared using Friedman's repeated measures ANOVA. RESULTS: There were no differences in BPComp (58 +/- 12 mmHg) and BPRelax (22 +/- 13 mmHg) with varied chest compression time and rate; thus, data were pooled. Carotid blood flow values were similar during CPR and are summarized in Figure 1.Figure 1DISCUSSION: We found that application of CPAP during chest compression will provide sufficient tidal ventilation, even without intermittent positive pressure ventilation.1 We observed greater carotid blood flow and aortic blood pressure during precordial compression and CPAP than during conventional-CPR.2 Assuming the carotid blood flow was a consistent fraction of the total blood flow, we observed no significant advantage of varied chest compression time and rate in the range studied. With a chest compression rate of at least 40/min, blood flow may be more dependent on the filling and emptying time constants of the intrathoracic vasculature.

BACKGROUND:Conventional cardiopulmonary resuscitation (CPR) includes 80-100/min precordial compressions with intermittent positive pressure ventilation (IPPV) after every fifth compression. To prevent gastric insufflation, chest compressions are held during IPPV if the patient is not intubated. Elimination of IPPV would simplify CPR and might offer physiologic advantages, but compression-induced ventilation without IPPV has been shown to result in hypercapnia. The authors hypothesized that application of continuous positive airway pressure (CPAP) might increase CO2 elimination during chest compressions. METHODS:After appropriate instrumentation and measurement of baseline data, ventricular fibrillation was induced in 18 pigs. Conventional CPR was performed as a control (CPR(C)) for 5 min. Pauses were then discontinued, and animals were assigned randomly to receive alternate trials of uninterrupted chest compressions at a rate of 80/min without IPPV, either at atmospheric airway pressure (CPR(ATM)) or with CPAP (CPR(CPAP)). CPAP was adjusted to produce a minute ventilation of 75% of the animal's baseline ventilation. Data were summarized as mean +/- SD and compared with Student t test for paired observations. RESULTS:During CPR without IPPV, CPAP decreased PaCO2 (55+/-28 vs. 100+/-16 mmHg) and increased SaO2 (0.86+/-0.19 vs. 0.50+/-0.18%; P < 0.001). CPAP also increased arteriovenous oxygen content difference (10.7+/-3.1 vs. 5.5+/-2.3 ml/dl blood) and CO2 elimination (120+/-20 vs. 12+/-20 ml/min; P < 0.01). Differences between CPR(CPAP) and CPR(ATM) in aortic blood pressure, cardiac output, and stroke volume were not significant. CONCLUSIONS:Mechanical ventilation may not be necessary during CPR as long as CPAP is applied. Discontinuation of IPPV will simplify CPR and may offer physiologic advantage.

Society of Critical Care Medicine; 28th Educational and Scientific Symposium; San Francisco, California, USA; January 23-27, 1999: Poster Presentations: Poster Hall

S129 We have shown that application of continuous positive airway pressure during chest compressions will result in gas exchange during cardiopulmonary resuscitation even without intermittent positive pressure ventilation. CPAP and precordial compressions (CPRCPAP) provided a ventilation, CO2 elimination and PaO2 comparable to standard CPR (CPRS). Furthermore, carotid blood flow was not effected adversely by the increased intrathoracic pressure which resulted from CPAP. We hypothesized that an increased intrathoracic gas volume and uninterrupted precordial compressions might have a protective effect on cardiopulmonary function during CPR. Therefore, we sought to compare the rate of deterioration in cardiovascular variables during CPRS versus CPRCPAP. METHODS: Sixteen anesthetized pigs (23 +/- 2 kg) underwent tracheal intubation and appropriate instrumentation to determine systemic, pulmonary artery and central venous blood pressures, arterial and mixed venous blood gas tensions and minute ventilation. An electromagnetic in-line flow probe was placed in the left carotid artery to measure blood flow. Ventricular fibrillation was induced by an electric shock of 400 joules after measurement of baseline data. Two minutes later animals were assigned randomly to receive CPRS, or CPRCPAP at a compression rate of 80/min. CPAP was adjusted to produce a ventilation equal to the animal's spontaneous baseline ventilation. Thumper compression force was adjusted to generate a sternal displacement of 4cm in both groups. Data were collected after 10 and 20min of CPR. Findings were summarized as mean +/- 1SD and compared with an analysis of variance and Scheffe's test. RESULTS: There were no significant differences in arterial and mixed venous blood gases, pulmonary artery and central venous pressures between the groups. Aortic blood pressure (BP, mmHg) was higher during CPRCPAP than during CPRS after 10min of resuscitation and remained so through the final data collection at 20min. Carotid blood flow (Qc, mL/min) was much lower after 20min of CPRS, but not during CPRCPAP (Table 1: *P<.05, CPRS v. CPRCPAP).Table 1CONCLUSIONS: These data confirm that precordial compressions with CPAP maintains higher carotid blood flow and aortic blood pressure than standard CPR during 20min of resuscitation. Further studies are needed to determine whether improved cardiovascular performance during CPRCPAP results in improved return of spontaneous circulation and better neurologic outcome after prolonged resuscitation.

S128 We have shown that application of continuous positive airway pressure during precordial compressions provided tidal ventilation even without intermittent positive pressure ventilation. CPAP and precordial compressions (CPRCPAP) provided a minute ventilation, CO2 elimination and PaO2 comparable to standard CPR (CPRS). The objective of this study was to determine whether increased intrathoracic pressure secondary to CPAP compromises carotid blood flow. METHODS: Sixteen anesthetized pigs (23 +/- 2 kg) underwent tracheal intubation and appropriate instrumentation to determine systemic, pulmonary artery and central venous blood pressures, arterial and mixed venous blood gas tensions and pH, and minute ventilation. An electromagnetic in-line flow probe was placed in the left carotid artery to measure blood flow. Ventricular fibrillation was induced by an electric shock of 400 joules after measurement of baseline data. Two minutes later animals were assigned randomly to receive alternate five minute trials of CPRS, or CPRCPAP at a compression rate of 80/minute. Thumper compression force was adjusted to result in a sternal displacement of 4 cm in both groups. The level of CPAP was adjusted to achieve ventilation equal to the animal's baseline spontaneous ventilation. Data were summarized as mean +/- 1SD and compared with Student's t test for paired observations. RESULTS: We found no significant differences in arterial and mixed venous blood gases, or aortic, pulmonary artery and central venous pressures during the different trials. Carotid blood flow was statistically similar during CPRCPAP and CPRS (12.2 +/- 6.7 mL/min vs. 10.2 +/- 5.5 mL/min). CONCLUSIONS: We conclude that the increased intrathoracic pressure secondary to the application of CPAP augments ventilation and oxygenation and does not adversely effect carotid blood flow during CPR. Further studies are needed to determine whether perfusion of other organs and duration of resuscitability are favorably influenced by CPRCPAP.

Background Why pulmonary gas exchange deteriorates after administration of epinephrine during cardiopulmonary resuscitation (CPR) is unclear. Methods and Results Forty-four anesthetized swine received an infusion of six inert gases. Animals underwent ventricular fibrillation with CPR and intravenous administration of saline (control), epinephrine (15 μg/kg), or methoxamine (150 μg/kg). Cardiac output, aortic blood pressure, pH, and arterial oxygen saturation were recorded. Distributions of V̇ a and Q̇ were determined by the multiple inert gas elimination technique. Ventricular fibrillation and CPR caused significant decreases in cardiac output, aortic blood pressure, and arterial pH. With epinephrine (versus saline), diastolic blood pressure was significantly higher (23±7 versus 8±4 mm Hg), but the increase in shunt (from 7±4% to 29±17%) and the reduction in Sa o 2 (from 99.7% to 76.8%) were significantly larger. Also, the increase in dead space was greater and elimination of CO 2 less. There were no differences between animals given methoxamine or saline, except for increased diastolic blood pressure. Conclusions During experimental ventricular fibrillation and CPR, epinephrine increased intrapulmonary shunt ≈300% more than saline or methoxamine and significantly reduced arterial oxygen saturation. We suspect that the β-adrenergic receptor activity of epinephrine attenuated hypoxic pulmonary vasoconstriction. Methoxamine is as effective a pressor as epinephrine for CPR and devoid of β-adrenergic activity. We recommend that such an agent be considered, instead of epinephrine, for CPR.

Study Objective: To determine the cardiovascular and respiratory effects of arterial hypoxemia in adult volunteers.Design: Prospective, subject-controlledSetting: University-affiliated hospital.Subjects: 16 awake, unsedated, unanesthetized adult volunteers. Interventions: Inspired oxygen concentration (FIO2) was decreased in decrements to reduce pulse oximeter values to a range of 95% to 90%, 89% to 85%, 84% to 80%, and 79% to 70%.Measurements and Main Results: Heart rate (HR), blood pressure (BP), respiratory rate (RR), arterial blood PH gas tensions, and oxyhemoglobin saturation were determined during normoxia and each level of oxyhemoglobin desaturation. FIO2 was reduced from 22% to 10%. Arterial blood oxyhemoglobin saturation and oxygen tension ranged from 100% to 71% and 103 to 35 mmHg; respectively. There were no significant changes in RR, BP, or HR during the study.Conclusions: HR BP, and RR are not reliable indicators of arterial hypoxemia in awake volunteers. IS this finding is also true for sedated or anesthetized patients, then continuous monitoring with pulse oximetry should be used whenever patients are at risk for arterial hypoxemia. Stable HR BP, and RR may not eliminate the possibility of significant a arterial hypoxemia and impending catastrophic events. (C) 1997 by Elsevier Science Inc.

NAKE MYOCARDIUM receives its blood supply through a network of channels that communicate directly with ventricle, rather than through epicardial vessels seen in humans. Transmyocardial revascularization (TMR) is an experimental procedure that attempts to duplicate this anatomy in patients with diffuse distal coronary artery disease unamenable to coronary artery bypass grafting (CABG) or angioplasty. For this reason, procedure has been called the snake and was first attempted in 1965 by Sen et al, 1 who used needle acupuncture to create multiple channels through ischemic myocardium. Unfortunately, these channels fibrosed and closed within weeks, offering little long-term benefit. More recently, carbon dioxide (CO2) and holmium:yttrium-aluminum garnet (Ho:YAG) lasers are being used as an alternative to needle perforations in hope that channels created by laser might epithelialize and remain patent longer. 24 If successful, this technique would provide an alternative treatment for patients with coronary artery disease refractory to conventional therapies. The following case is presented to illustrate anesthetic considerations for such a procedure. A 49-year-old, 80-kg man was experiencing class IV (Canadian Heart Association) angina, despite a four-vessel CABG operation 5 years ago and maximal medical therapy. Medical history was significant for an inferior myocardial infarction, and medications included nifedipine (20 mg three times daily), metoprolol (50 mg twice daily), isosorbide dinitrate (40 mg four times daily), amiodipine (10 mg/day), and aspirin (375 mg/ day). Recent cardiac angiography showed small, diffusely diseased coronaries, occluded vein grafts, and a patent internal mammary artery graft. Ejection fraction was 40%, and mild pulmonary hypertension was noted. Persantine-thallium scanning showed, on poststress images, defects in lateral and inferior walls of left ventricle. Reperfusion of lateral wall occurred, but inferior defect was fixed. Wall motion studies showed good motion of septum, but other walls showed considerable dyskinesia. Because patient was not considered an appropriate candidate for repeat CABG or angioplasty and his symptoms were persisting despite medical management, he was enrolled in a protocol for TMR treatment with holmium laser. Inclusion criteria for protocol were as follows: class IV angina (Canadian Heart Association); ejection fraction greater than 25%; greater than 10% reversibility in a myocardial defect located in inferior two thirds of left ventricle; and unsuitable for CABG or angioplasty. Patients were randomly assigned to either a TMR or medical treatment. In TMR group, entire left ventricle was treated with laser, not just areas of reversible ischemia.

OBJECTIVE:Oxygen consumption (VO2) is often measured in critically ill patients using the Fick equation: VO2 = cardiac output x arterial-venous oxygen content difference. To determine if this method is accurate, it was compared with a spirometric technique. DESIGN:Prospective study. SETTING:University laboratory. SUBJECTS:Nineteen large adult pigs. INTERVENTIONS:Cardiac output, measured with bolus thermodilution technique, and arterial and venous oxygen content values, determined with the galvanic fuel cell method, were used to determine VO2 with the Fick equation. The spirometrically determined VO2 was the rate of disappearance of oxygen from a water-sealed spirometer. Dobutamine and labetalol were titrated to vary VO2 (range 204 to 584 mL/min). MEASUREMENTS AND MAIN RESULTS:The bias between the Fick and spirometrically determined VO2 values was 58 mL/min. The precision (SD of the bias) between the Fick and spirometrically determined Vo2 was 35 mL/min. Fick-derived Vo2 was greater than Vo2 measured spirometrically. The correlation coefficient was 0.90. CONCLUSIONS; Despite all attempts to reduce measurement error, there was an unexplained difference in Fick-derived and spirometrically measured Vo2. Therefore, I feel that the two methods are not interchangeable, and that calculations of Vo2 using the Fick method should be used cautiously when therapeutic maneuvers are based on these data.

STUDY OBJECTIVE:To determine if temperature during cardiopulmonary bypass (CPB) has an effect on perioperative and postoperative thyroid function.DESIGN:Prospective study comparing thyroid function during and after hypothermic and normothermic CPB.SETTING:Cardiac surgical unit at a university-affiliated hospital.PATIENTS:Twelve patients scheduled to undergo cardiac operations with normothermic (n = 6) or hypothermic (n = 6) CPB.INTERVENTIONS:Blood was analyzed for serum concentration of total thyroxine (TT4), total triiodothyronine (TT3), free T3 (fT3), reverse T3 (rT3), and thyroid stimulating hormone (TSH) preoperatively, 60 min after CPB was initiated, 30 min after discontinuing CPB, and on postoperative days (POD) 1, 3, and 5.MEASUREMENTS AND RESULTS:Patients who underwent either cold (26 degrees +/- 5 degrees C) or warm (35 degrees +/- 1 degree C) CPB were comparable with regard to age, body weight, duration of CPB, cross-clamp time, use of inotropes, total heparin dose, and length of hospital stay. Incidence of postoperative myocardial infarction, congestive heart failure, and death were similar. In both groups, TT4 and TT3 were reduced below baseline values beginning with CPB and persisting for up to 5 days after CPB (p < 0.05), free T3 was reduced for up to 3 days after CPB (p < 0.05), mean serum rT3 was elevated on POD 1 and POD 3 (p < 0.05), and TSH remained unchanged.CONCLUSION:The results of this study suggest that normothermic CPB does not prevent the development of the "euthyroid sick syndrome" during and after CPB. Despite these changes in thyroid function, most patients in both groups had a normal postoperative recovery.

Oxymetazoline nasal spray is a potent alpha1-adrenergic agonist commonly used to vasoconstrict blood vessels in the nasal mucosa. In this incident, oxymetazoline nasal spray 0.025% was administered to a 2-year-old patient during general anesthesia for nasal endoscopy. Severe hypertension with reflex bradycardia progressed to sinus arrest and was successfully treated with atropine and cardiopulmonary resuscitation. Decreasing the dose of oxymetazoline and pretreatment with an anticholinergic is recommended.