DR SINHA et al1Sinha P.K. Neema P.K. Unnikrishnan K.P. et al.Effect of lung ventilation with 50% oxygen in air or nitrous oxide versus 100% oxygen on oxygenation index after cardiopulmonary bypass.J Cardiothorac Vasc Anesth. 2006; 20: 136-142Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar have shown that even short-term exposure to 100% inspired oxygen may cause a prolonged decrement in postoperative pulmonary function. The authors provide an acceptable explanation for their findings by using proven physiologic principles. Based on their observations, the authors conclude that provision of 50% inspired oxygen is preferable to a higher FIO2 after cardiopulmonary bypass. Inherent in this suggestion is the basic assumption that some degree of supplementation of inspired oxygen is desirable and/or necessary. Is that so?The rationale for supplementation of inspired oxygen is well known to nearly all healthcare providers. Whether provided in emergency care situations, coronary care units, post-anesthesia recovery areas, or operating rooms, supplemental oxygen is administered in an attempt to provide a safety net and to prevent detrimental hypoxemia and tissue hypoxia. Undoubtedly, the physiologic basis for this clinical decision is based on interpretation of the O2-hemoglobin (Hgb) dissociation curve (Fig 1). I was taught, as were my teachers, that "small changes in oxygen tension will cause a dramatic and marked decrement in oxygen saturation" and further "such a dramatic decrease in oxygen saturation likely will cause tissue hypoxia." Few would dispute the accuracy of these assumptions. However, it is indisputable that there is little or no evidence to support the second part of this assumption. In fact, whether one believes in "intelligent design" or evolution, to accept the accuracy of the assumption would be to admit a gross flaw in design of the Hgb molecule or that the molecule evolved a trait with little or no survival benefit. I believe the clue to solution of this conundrum rests in the methodology used to construct the O2-Hgb dissociation curve. By using a tonometer with known PO2 values, saturation and/or content of blood samples was determined, resulting in the well-known relationship shown in Figure 1. However, it is important to understand that the only organ in humans that acts as a tonometer is the lung (ie, only in lung does PO2 determine oxygen content/saturation). Everywhere else, oxygen extraction by the tissues determines the resultant O2 content/saturation and PO2 is the dependent variable. Had we been taught the relationship between PO2 and O2 content/saturation as a physiologic function, we might draw a different conclusion (Fig 2). Based on this relationship, we would conclude that large amounts of oxygen might be extracted from the Hgb molecule, with minimal change in PO2. Or, as stated by Comroe,2Comroe J.H. Physiology of Respiration. (ed 2). Yearbook Medical Publishers, Chicago, IL1974Google Scholar "… the steep middle and lower parts protect the tissues by enabling them to withdraw large amounts of O2 from blood for relatively small decreases in PO2." Thus, the Hgb molecule serves to protect the organism by maintaining the diffusion gradient from blood to the tissues, even when the Hgb is markedly desaturated.Fig 2The same data as in Figure 1 presented to represent function of the Hgb molecule at the tissue level.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Let us then address the original question. What benefit is provided by maintaining arterial hemoglobin saturation greater than 90% (PaO2 >60 mmHg)? Clearly, we cannot claim a benefit based on increased oxygen delivery (the product of arterial oxygen content and cardiac output) because the increase in oxygen content provided by a few percentage points in arterial oxygen saturation is insignificant relative to Hgb concentration, cardiac output, and the arterial oxygen saturation existent when the patient breathes room air. Therefore, the only remaining rationale must be based on incorrect interpretation of the O2-Hgb curve. For years, this argument has been met with a response similar to "even if there is no proven benefit, supplementation of inspired oxygen should occur until adverse effects of such therapy are proven." In other words, the converse of evidence-based medicine. In the absence of supplemental oxygen, arterial hypoxemia would be detected with a pulse oximeter and would indicate the presence of lung dysfunction. Although arterial hypoxemia might be reversed with supplementation of inspired oxygen, presence of the primary pulmonary derangement would be masked or made worse. In the absence of supplemental oxygen therapy, the clinician likely would direct appropriate therapy toward the primary pulmonary defect, be it hypoventilation, V/Q mismatching, right-to-left intrapulmonary shunt, or diffusion defect.3Fu E.S. Downs J.B. Schweiger J.W. et al.Supplemental oxygen impairs detection of hypoventilation by pulse oximetry.Chest. 2004; 126: 1552-1558Crossref PubMed Scopus (257) Google Scholar, 4Downs J. Has oxygen administration delayed appropriate respiratory care? Fallacies regarding oxygen therapy.Respir Care. 2003; 48: 611-620PubMed Google ScholarAlthough not specifically noted, the authors provide compelling evidence for omission of postoperative supplemental inspired oxygen. For any given right-to-left intrapulmonary shunt fraction, PaO2/FIO2 increases with decrease in FIO2 when saturation falls below 100% (Fig 3). In other words, the Hgb molecule serves to prevent a continued fall in PaO2, as alveolar oxygen tension decreases due to decreasing inspired oxygen concentration. Therefore, the reported PaO2/FIO2 of 300 mmHg to 500 mmHg indicates that the PaO2 of the authors' patient's breathing room air would have been 75 to 80 mmHg!Fig 3PaO2/FIO2 as a function of FIO2, with right-to-left intrapulmonary shunting of blood of 20% to 50%.View Large Image Figure ViewerDownload Hi-res image Download (PPT)If it were not for the physiologically unfounded fear of the "slippery slope" of the oxyhemoglobin dissociation curve, supplementation of inspired oxygen appropriately would be relegated to the treasure trove of physiologically unsound maneuvers, subsequently proven to be of no benefit. Intermittent positive-pressure breathing, blow gloves, incentive spirometry, and leeches all, at one time, were believed to be logical therapeutic maneuvers and were held in great favor until proven to be physiologically unsound. Perhaps, in my lifetime, investigations such as that by Sinha et al1Sinha P.K. Neema P.K. Unnikrishnan K.P. et al.Effect of lung ventilation with 50% oxygen in air or nitrous oxide versus 100% oxygen on oxygenation index after cardiopulmonary bypass.J Cardiothorac Vasc Anesth. 2006; 20: 136-142Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar will lead to the appropriate application of oxygen therapy. DR SINHA et al1Sinha P.K. Neema P.K. Unnikrishnan K.P. et al.Effect of lung ventilation with 50% oxygen in air or nitrous oxide versus 100% oxygen on oxygenation index after cardiopulmonary bypass.J Cardiothorac Vasc Anesth. 2006; 20: 136-142Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar have shown that even short-term exposure to 100% inspired oxygen may cause a prolonged decrement in postoperative pulmonary function. The authors provide an acceptable explanation for their findings by using proven physiologic principles. Based on their observations, the authors conclude that provision of 50% inspired oxygen is preferable to a higher FIO2 after cardiopulmonary bypass. Inherent in this suggestion is the basic assumption that some degree of supplementation of inspired oxygen is desirable and/or necessary. Is that so? The rationale for supplementation of inspired oxygen is well known to nearly all healthcare providers. Whether provided in emergency care situations, coronary care units, post-anesthesia recovery areas, or operating rooms, supplemental oxygen is administered in an attempt to provide a safety net and to prevent detrimental hypoxemia and tissue hypoxia. Undoubtedly, the physiologic basis for this clinical decision is based on interpretation of the O2-hemoglobin (Hgb) dissociation curve (Fig 1). I was taught, as were my teachers, that "small changes in oxygen tension will cause a dramatic and marked decrement in oxygen saturation" and further "such a dramatic decrease in oxygen saturation likely will cause tissue hypoxia." Few would dispute the accuracy of these assumptions. However, it is indisputable that there is little or no evidence to support the second part of this assumption. In fact, whether one believes in "intelligent design" or evolution, to accept the accuracy of the assumption would be to admit a gross flaw in design of the Hgb molecule or that the molecule evolved a trait with little or no survival benefit. I believe the clue to solution of this conundrum rests in the methodology used to construct the O2-Hgb dissociation curve. By using a tonometer with known PO2 values, saturation and/or content of blood samples was determined, resulting in the well-known relationship shown in Figure 1. However, it is important to understand that the only organ in humans that acts as a tonometer is the lung (ie, only in lung does PO2 determine oxygen content/saturation). Everywhere else, oxygen extraction by the tissues determines the resultant O2 content/saturation and PO2 is the dependent variable. Had we been taught the relationship between PO2 and O2 content/saturation as a physiologic function, we might draw a different conclusion (Fig 2). Based on this relationship, we would conclude that large amounts of oxygen might be extracted from the Hgb molecule, with minimal change in PO2. Or, as stated by Comroe,2Comroe J.H. Physiology of Respiration. (ed 2). Yearbook Medical Publishers, Chicago, IL1974Google Scholar "… the steep middle and lower parts protect the tissues by enabling them to withdraw large amounts of O2 from blood for relatively small decreases in PO2." Thus, the Hgb molecule serves to protect the organism by maintaining the diffusion gradient from blood to the tissues, even when the Hgb is markedly desaturated. Let us then address the original question. What benefit is provided by maintaining arterial hemoglobin saturation greater than 90% (PaO2 >60 mmHg)? Clearly, we cannot claim a benefit based on increased oxygen delivery (the product of arterial oxygen content and cardiac output) because the increase in oxygen content provided by a few percentage points in arterial oxygen saturation is insignificant relative to Hgb concentration, cardiac output, and the arterial oxygen saturation existent when the patient breathes room air. Therefore, the only remaining rationale must be based on incorrect interpretation of the O2-Hgb curve. For years, this argument has been met with a response similar to "even if there is no proven benefit, supplementation of inspired oxygen should occur until adverse effects of such therapy are proven." In other words, the converse of evidence-based medicine. In the absence of supplemental oxygen, arterial hypoxemia would be detected with a pulse oximeter and would indicate the presence of lung dysfunction. Although arterial hypoxemia might be reversed with supplementation of inspired oxygen, presence of the primary pulmonary derangement would be masked or made worse. In the absence of supplemental oxygen therapy, the clinician likely would direct appropriate therapy toward the primary pulmonary defect, be it hypoventilation, V/Q mismatching, right-to-left intrapulmonary shunt, or diffusion defect.3Fu E.S. Downs J.B. Schweiger J.W. et al.Supplemental oxygen impairs detection of hypoventilation by pulse oximetry.Chest. 2004; 126: 1552-1558Crossref PubMed Scopus (257) Google Scholar, 4Downs J. Has oxygen administration delayed appropriate respiratory care? Fallacies regarding oxygen therapy.Respir Care. 2003; 48: 611-620PubMed Google Scholar Although not specifically noted, the authors provide compelling evidence for omission of postoperative supplemental inspired oxygen. For any given right-to-left intrapulmonary shunt fraction, PaO2/FIO2 increases with decrease in FIO2 when saturation falls below 100% (Fig 3). In other words, the Hgb molecule serves to prevent a continued fall in PaO2, as alveolar oxygen tension decreases due to decreasing inspired oxygen concentration. Therefore, the reported PaO2/FIO2 of 300 mmHg to 500 mmHg indicates that the PaO2 of the authors' patient's breathing room air would have been 75 to 80 mmHg! If it were not for the physiologically unfounded fear of the "slippery slope" of the oxyhemoglobin dissociation curve, supplementation of inspired oxygen appropriately would be relegated to the treasure trove of physiologically unsound maneuvers, subsequently proven to be of no benefit. Intermittent positive-pressure breathing, blow gloves, incentive spirometry, and leeches all, at one time, were believed to be logical therapeutic maneuvers and were held in great favor until proven to be physiologically unsound. Perhaps, in my lifetime, investigations such as that by Sinha et al1Sinha P.K. Neema P.K. Unnikrishnan K.P. et al.Effect of lung ventilation with 50% oxygen in air or nitrous oxide versus 100% oxygen on oxygenation index after cardiopulmonary bypass.J Cardiothorac Vasc Anesth. 2006; 20: 136-142Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar will lead to the appropriate application of oxygen therapy.

BACKGROUND:Rapid recovery and weaning from ventilatory support and cardiovascular stability are suggested advantages of isoflurane inhalation, in concentrations ranging from 0.1 to 0.6 vol%, for long-term sedation in mechanical ventilated patients. This study was designed to determine whether isoflurane in low concentrations impairs pulmonary gas exchange by increasing ventilation and perfusion (V(A)/Q) mismatch during lung injury.METHODS:Fourteen anesthetized dogs received in random order 0, 0.25, or 0.5 vol% end-tidal isoflurane before and after induction of lung injury with oleic acid. Gas exchange was assessed by blood gas analysis and by estimating the V(A)/Q distributions using the multiple inert gas elimination technique.RESULTS:Administration of oleic acid produced a lung injury with severe V(A)/Q mismatch and 38 +/- 4% intrapulmonary shunting of blood. During lung injury, isoflurane accounted for a dose-related increase in blood flow to shunt units from 38 +/- 4 to 42 +/- 3 (0.25 vol%) and 48 +/- 4% (0.5 vol%) (P < 0.05), dispersion pulmonary blood flow distribution from 0.94 +/- 0.07 to 1.01 +/- 0.09 (0.25 vol%) and 1.11 +/- 0.11% (0.5 vol%) (P < 0.05), and a decrease in perfusion of normal V(A)/Q units from 58 +/- 5 to 55 +/- 4 (0.25 vol%) and 50 +/- 4% (0.5 vol%) (P < 0.05) (mean +/- SE). Isoflurane decreased arterial oxygen partial pressure from 72 +/- 4 to 62 +/- 4 mmHg (0.25 vol%) and 56 +/- 4 mmHg (0.5 vol%) (P < 0.05) and oxygen delivery from 573 +/- 21 to 529 +/- 19 ml. kg. min (0.25 vol%) and 505 +/- 22 ml. kg. min (0.5 vol%) (P < 0.05). Gas exchange, perfusion of shunt and normal V(A)/Q units, and pulmonary blood flow distribution was similar in absence of lung injury with and without isoflurane. Isoflurane 0.5 vol% lowered cardiac output during all conditions (P < 0.05). CONCLUSIONS Inhalation of low concentrations of isoflurane contributed to increased V(A)/Q mismatch and decreased systemic blood flow and oxygen delivery in mechanically ventilated animals with injured lungs.

SOCIETY OF CRITICAL CARE MEDICINE 32ND CRITICAL CARE CONGRESS SAN ANTONIO, TEXAS, USA JANUARY 28-FEBRUARY 2, 2003: ORAL/SANDWICH PRESENTATIONS: Poster Presentation: Basic Science: Neurobiology: PDF Only

Assistant ProfessorProfessor and Chairmanjdowns@com1.med.usf.eduAssociate ProfessorDepartment of Anesthesiology University of South Florida Tampa, FloridaTHE recommended technique of cardiopulmonary resuscitation (CPR) has changed minimally since the 1960s. 1It is intuitive that intermittent positive pressure ventilation should be provided to facilitate the elimination of carbon dioxide and the maintenance of oxygenation while the restoration of spontaneous circulation is attempted. In this issue of Anesthesiology, Saïssy et al. 2present data suggesting that “breathing,” in the classic sense, may not be necessary or desirable during CPR. Furthermore, they suggest that the application of continuous tracheal oxygenation insufflation may provide an alternative to traditional mechanical ventilation. In so doing, the authors provide solid evidence that standard CPR methods provided in out-of-hospital settings show a disappointing success rate (100% mortality in 1 week for a group of patients with asystolic arrests) and that the application of experimental (laboratory) data to the human clinical arena may be warranted. Saïssy et al. 2delivered continuous insufflation of oxygen, which produced continuous positive airway pressure, during precordial compressions. They found that the combination of continuous positive airway pressure and chest compressions during CPR provided gas exchange equivalent to that provided by conventional intermittent positive pressure ventilation. Each technique provided equivalent success, which was measured by the number of patients with spontaneous return of cardiac activity. All patients received significant amounts of intracardiac and intravenous epinephrine, which are proven to cause disruption of ventilation–perfusion relationships and profound postresuscitation arterial hypoxemia. 3The replacement of intermittent positive pressure ventilation by the continuous insufflation of oxygen may have attenuated the development of ventilation–perfusion mismatching, based on results of arterial blood analysis. Of interest is the authors’ presentation of blood gas and oxygen saturation values, which illustrates the inappropriateness of using arterial oxygen tension as a reflection of pulmonary function when intrapulmonary shunting is greater than 20% of cardiac output. Arterial oxygen tension and arterial oxygen saturation have a nonlinear relation secondary to the oxyhemoglobin dissociation curve. This relation is shown by the typical large standard deviation of oxygen tension values, which may skew data and foster misrepresentation (minimization) of the magnitude of pulmonary dysfunction. Use of the arterial oxygen saturation value is desirable not only for the assessment of oxygen delivery, but also for the analysis of pulmonary function.Temporal aspects of this project are of interest. A specialist physician was at the scene of the cardiac arrest within 10 min—an unlikely scenario in the United States. This aspect illustrates a classic philosophical difference of opinion regarding optimal emergency care. Should the patient be transferred promptly to the well-equipped specialty institution or should specialty care be made available at the scene to stabilize the patient before transportation, even if that care causes delays in the hospital-based diagnostic and therapeutic interventions? The average time from cardiac arrest to restoration of spontaneous cardiac activity was more than 25 min in both treatment groups. Although the early application of advanced cardiac life support, including electric shock and drug therapy, is a key to improved survival in any setting; optimizing the techniques of artificial ventilation and circulation also are important. It is reasonable to speculate that enhanced oxygen delivery and carbon dioxide removal during this critical time may improve survival and quality of life for survivors.The issue of human research ethics is raised when performing randomized trials on patients who are unable to provide consent and when obtaining approval from next of kin is not possible. Extensive animal studies have investigated alternative methods of providing gas ex- change during CPR. 4–8Some of these novel approaches were successful in replacing intermittent positive pressure ventilation with other means of manipulating airway pressure. Saïssy et al. 2evaluated an experimental approach for ventilation in humans with asystole or severe bradycardia who were undergoing CPR in the field. Because asystole usually is fatal, it is not likely that these patients were harmed by participation in this research study. However, conducting a similar human study probably would not be possible in the United States. 9French law allows research to be conducted without consent from the patient or the next of kin in emergency situations. The French equivalent of the American institutional review board is a committee that operates independently but is loosely associated with university hospitals. In cases in which patients are unable to give consent, French law allows, in the case of emergency situations (and only in such cases), research to be conducted in individual patients without patient or family consent. The committee is empowered to approve a protocol to be performed anywhere in France (in specified centers) (Personal written communication to the editorial office, Iowa City, Iowa, from Laurent Brouchard, December 1999). This system reflects the progressive philosophy of acting for the “greater good” and without sacrificing an individual’s interest, when a clinical decision is to be made on behalf of an incapacitated patient and when there is reasonable evidence that deviation from the conventional treatment may be beneficial to the patient while furthering science. A comparable decision would be more difficult to make in the United States, where any deviation from the community standard carries tremendous liability, even if the use of the new regimen is supported by extensive laboratory research. Standard care, even if known to provide little chance of survival, becomes the care of choice, not because it will optimize outcome, but because it protects the subjects “rights” as an individual and maintains their status as a “subject” rather than an “object” of the investigation. 10Hence, more promising, albeit “experimental” forms of therapy are denied to the patient. Maintenance of the status quo also protects the caregiver from liability because an expected poor outcome is easier to defend than the possibly premature application of promising, but new, approaches.For more than a decade, numerous alternatives to the recommended standard of ventilation during CPR have been advanced in the experimental research literature. Few investigators have performed controlled trials with human subjects. Replicating experimental CPR research in a clinical or field setting poses significant ethical and liability concerns; however, progress in clinical medicine is impossible without taking this crucial next step.

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.

S177 INTRODUCTION: During general anesthesia, most patients have their ventilation controlled mechanically, in spite of touted advantages of spontaneous breathing. Further, modes of partial ventilatory support ubiquitous in the ICU, have gained little popularity in the operating room. We developed methodology to augment gas exchange of spontaneously breathing, anesthetized patients. METHODS: Twenty-seven adult patients (52 +/- 16 yrs; 75 +/- 16 kg) scheduled to undergo inhalation anesthesia signed a consent form approved by the Institutional Review Board. Anesthesia was induced with IV propofol, a laryngeal mask airway was positioned, and patients were allowed to breathe spontaneously. Anesthesia was maintained with isoflurane, nitrous oxide, oxygen and air. A flow transducer and gas sampling tube were connected to a monitor for determination of respiratory rate (RR), tidal volume (VT), minute ventilation (VE), inspired oxygen concentration, end-tidal carbon dioxide tension (PETCO2) and concentration of anesthetic agents. Heart rate (HR), mean arterial blood pressure (MAP), and SpO2 (%) were recorded. Baseline data were collected after surgical incision and patients breathed spontaneously for 15-min. They then randomly were assigned to undergo alternating 15-min trials of CPAP, or Apneustic Anesthesia Ventilation (AAV). CPAP was titrated to a level that, when released to atmospheric pressure, would produce a VT of 6 mL/kg body weight. The rate of AAV was titrated to reduce spontaneous breathing to [approximate]30% of the baseline value. Data are summarized as mean +/- SD. Data obtained during AAV and CPAP were compared using Student's t test for paired observations and were compared to baseline with Dunnett's test. RESULTS: End-tidal concentration of isoflurane (1.1 +/- 0.4%) and N2 O (62 +/- 11%), FIO2 (0.33 +/- 0.07), HR (73 +/- 14 /min), MAP (78 +/- 16 mmHg) and SpO2 (97 +/- 2%) statistically were comparable throughout the study. Total RR and E during AAV were less than baseline values (P<.001), but VT was significantly greater when generated by decrease in airway pressure than by spontaneous breathing during AAV. Movement of the surgical field was barely detectable. Variables reflecting respiratory function during baseline (Base), CPAP (9 +/- 2 cmH2 O) and AAV (Spont=spontaneous breath, Mech=mechanical breath) are summarized in Table 1 (*P<.001 v. Base; [dagger]P<.001 v. CPAP).Table 1DISCUSSION: Application of AAV in anesthetized, spontaneous breathing patients reduced respiratory rate and minute ventilation, but not alveolar ventilation. Breathing was facilitated with a peak airway pressure much lower than observed during traditional intermittent positive pressure ventilation. We conclude that AAV provides an efficient means of supplementing spontaneous breathing with minimal disruption of the surgical field. Therefore, AAV may be useful in patients who require general anesthesia, who might benefit from lack of paralysis and/or hyperventilation, and who are deemed to benefit from partial ventilatory support.

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

University of South Florida; Tampa, FL Address requests for reprints to: John B. Downs, MD, University of South Florida, College of Medicine, 12901 Bruce B. Downs Blvd., MDC Box 59, Tampa, FL 33612-4799.

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.

S39 INTRODUCTION: Supplemental oxygen is often administered during postanesthesia recovery to prevent hypoxemia. This study was designed to evaluate the incidence of postoperative hypoxemia in patients with and without supplemental oxygen. We also determined the effects of oxygen administration on the ability to detect acute hypoventilation with pulse oximetry (SpO2). METHODS: Preoperatively and at PACU arrival, SpO2 was measured and recorded while consenting patients breathed air. When SpO2 >or=to90%, patients randomly were assigned to breathe air (n=95) or 30% oxygen via face mask (n=96). SpO2 <90% was recorded by a computer every min during the same period. Hypoxemia was defined as a SpO2 <90% for two consecutive min. Intergroup SpO2 values are summarized as mean +/- SD and were compared with a repeated measures ANOVA. To determine the effect of acute hypoventilation on SpO2, minute ventilation during general anesthesia was reduced by 50% in consenting patients who were breathing varied concentrations of oxygen. Patients breathing 21% O2 (n =25) underwent hypoventilation for up to 5 minutes, while patients breathing 25% (n=10) or 30% (n=10) oxygen underwent hypoventilation for ten minutes. End-tidal carbon dioxide tension (PETCO2) and SpO2 were measured every minute. RESULTS: There were no intergroup differences in preoperative (98 +/- 2%) or PACU arrival (97 +/- 3%) SpO2, thus data were pooled. SpO2 was greater in patients who breathed O2 vs. air at 20 (99 +/- 1 vs. 97 +/- 2%, P<.001) and 40 (98 +/- 2 vs. 97 +/- 2, P=.003) min after PACU arrival. The incidence of postoperative hypoxemia was 4.7% (9/191). Seven of the patients were breathing air and two were breathing 30% O2. During acute hypoventilation, every patient had increases in PETCO2. Patients breathing room air had decreases in SpO2 while no significant change in SpO2 occurred in patients breathing 25% or 30% oxygen (Figure 1).Figure 1DISCUSSION: The incidence of postoperative hypoxemia was low, even when patients breathed room air. Administration of supplemental oxygen increased SpO2 overall, but did not prevent the occurrence of arterial hypoxemia. Moreover, a perceptible decrease in SpO2 only occurred when patients breathed room air, during acute hypoventilation. Thus, early detection of hypoventilation only was possible in the absence of supplemental O2. We conclude that administration of oxygen to patients with an SpO2 >or=to90% afforded no physiologic advantage, did not prevent arterial hypoxemia uniformly, and delayed detection of hypoventilation induced arterial hypoxemia. Routine use of postoperative supplemental O2 should no longer be recommended.

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

BACKGROUND:Airway pressure-release ventilation provides ventilation comparable to controlled mechanical ventilation (CMV), but with lower peak airway pressures and less dead-space ventilation. To obtain these advantages for patients administered general anesthesia, the authors (1) designed a mode similar to airway pressure-release ventilation, intermittent continuous positive airway pressure (CPAPI), and compared its efficiency with that of CMV; and (2) assessed the accuracy of end-tidal carbon dioxide tension (PETCO2) as a monitor of the partial pressure of carbon dioxide in arterial blood (PaCO2) during CPAPI compared with during CMV. METHODS:Twenty anesthetized, tracheally intubated patients received baseline CMV that produced a PETCO2 of approximately 35 mmHg and a pulse oximetry value > 90%. Patients were assigned to undergo alternating trials of CMV and CPAPI. During CPAPI, CPAP was applied to the airway, removed for 1 s, and reapplied at a rate equal to the ventilator rate during CMV. The difference between the carbon dioxide tension in arterial blood and end-tidal gas [P(a-ET)CO2] and the calculation of PaCO2/minute ventilation quantified the efficiency of ventilation. Data were summarized as mean +/- SD and compared using the Student's t-test. RESULTS:Peak airway pressure (13+/-2 vs. 23+/-5 cm H2O; P < 0.001) and minute ventilation (3.5+/-1 vs. 4.6+/-1.2 l/min; P < 0.0001) were lower during CPAPI than during CMV. The value for PaCO2/minute ventilation (11.1+/-2.9 vs. 7.9+/-2.6 mmHg x l(-1) x min(-1); P < 0.0001) was greater during CPAPI. P(a-ET)CO2 was always greater during CMV (6.3+/-1.6 vs. 1.7+/-0.9 mmHg; P < 0.0001) and was never > 3.5 mmHg during CPAPI. CONCLUSIONS:During CPAPI, less ventilation was necessary to produce a PaCO2 comparable to that during CMV. This represents a significant reduction in dead-space ventilation, improved efficiency of ventilation, and a lower value for P(a-ET)CO2. Compared with CMV, CPAPI also improves the accuracy of PETCO2 as a monitor of PaCO2.

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.

S532 The manufacturer of the laryngeal mask airway (LMA), recommends that increased airway pressure be limited to 15 cmH2 O, which usually precludes use of mechanical ventilation during general anesthesia. We have previously reported that Apneustic Anesthesia Ventilation (AAV) provides adequate ventilation with a lower peak airway pressure than traditional controlled mechanical ventilation (CMV), in patients undergoing general anesthesia. [1] During AAV, a continuous positive airway pressure (CPAP) is applied. Intermittently, airway pressure is decreased, gas exits the lungs, and lung volume decreases, allowing excretion of carbon dioxide. After a short time ([similar]1 sec), airway pressure and lung volume are rapidly re-established. We sought to determine if AAV would provide full ventilatory support in patients undergoing general anesthesia with a LMA using airway pressures lower than the maximum value (15 cmH2 O) recommended by the manufacturer. METHODS: Patients scheduled to undergo operative procedures and general anesthesia signed an Institutional Review Board approved consent form. General anesthesia was induced with propofol, a LMA was positioned, and patients were allowed to breathe spontaneously. The LMA cuff was inflated with the recommended volume of air. Anesthesia was maintained with isoflurane, nitrous oxide, oxygen and air. A pneumotachometer and gas sampling tube were connected to a monitor for determination of peak airway pressure (Peak Paw), respiratory rate (RR), tidal volume (VT), minute ventilation (VE), inspired oxygen concentration, end-tidal carbon dioxide tension (PETCO2) and concentration of anesthetic agents. Heart rate (HR), mean arterial blood pressure (MAP), and SpO2 (%) were recorded. Baseline data were collected after patients were stable breathing spontaneously. CPAP was titrated to a level that produced a VT of 6 mL/kg body weight when airway pressure was released to atmospheric pressure at a rate adjusted to produce apnea. Data are summarized as mean +/- SD and compared with Student's t test for paired observations. RESULTS: End-tidal concentrations of isoflurane (1.1 +/- 0.1%) and N (2) O (58 +/- 8%), FIO2 (0.31 +/- 0.06), SpO2 (97 +/- 1), HR (78 +/- 14 /min), and MAP (65 +/- 14 mmHg) statistically were comparable throughout the study in 12 patients (47 +/- 16 yrs; 73 +/- 18 kg). Data observed during Baseline and AAV are summarized in Table 1 (*P<.05 v. Baseline).Table 1CONCLUSIONS: We observed that full ventilatory support may be provided with AAV in patients undergoing general anesthesia with LMA. Since peak Paw ranged from 6 to 14 cmH2 O, AAV with LMA may be used for procedures that would normally require placement of a tracheal tube to facilitate ventilation. Conventional mechanical ventilation usually requires greater than 15 cmH2 O to provide effective ventilatory support and may result in airway pressures that increase the risk of aerophagia and regurgitation of gastric contents. We conclude that AAV is a safe and effective method of providing mechanical ventilatory support in patients with laryngeal mask airway.

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.