Apnea testing for the determination of brain death: a modified protocol. Technical note.

The absence of spontaneous respirations at a PaCO2 of 60 mm Hg or above has traditionally been accepted as the respiratory criteria for the determination of brain death. The testing of patients for the presence or absence of apnea has been complicated because the rate of PaCO2 elevation may vary substantially from patient to patient, and a nonlinear relationship exists between the rate of PaCO2 increase and the duration of apnea. In an attempt to refine the apnea test and to further elucidate the physiology of hypercapnia in humans, 11 patients who met all but the respiratory criteria for brain death were evaluated using a modification of a previously utilized apnea testing protocol. All patients were brought to a PaCO2 of 40 mm Hg or above prior to the apnea test. Baseline PaCO2 ranged from 40 to 45 mm Hg in six patients (Group I) and from 46 to 51 mm Hg in five patients (Group II). The mean rate of PaCO2 increase was 5.1 +/- 1.4 mm Hg/min in Group I and 6.7 +/- 3.1 mm Hg/min in Group II. No problems with cardiovascular instability or hypoxia were encountered during testing in this series. This refinement of the apnea test allows for a streamlined and safe approach to brain death detection.     

The apnea test for the determination of brain death

By conventional criteria, an apneic patient's PaCO2 must be greater than 60 mm Hg before apnea can be attributed to brain death. The rate of a PaCO2 increase in the apneic patient traditionally has been thought to be in the range of 3 mm Hg/min. In order to assess the validity of these data and the validity of the "apnea test" for determination of brain death, the results of this test were reviewed in 20 patients. In all patients, arterial blood samples were drawn for blood gas measurements every 2 minutes following the cessation of volume ventilation (with an oxygen cannula at 6 liters O2/min passed into the tracheobronchial tree). The rate of PaCO2 increase was noted to be very erratic. The average rate of rise was 3.7 +/- 2.3 mm Hg/min (+/- standard deviation). This, however, varied from 0.5 to 10.5 mm Hg/min and was not predictable from the variables evaluated. The rate of PaCO2 increase was noted to decline throughout the duration of the test. This ranged from 3.9 +/- 1.2 mm Hg/min (for patients with baseline PaCO2 less than or equal to 30 mm Hg) and 4.5 +/- 1.9 mm Hg/min (for patients with baseline PaCO2 greater than or equal to 30 mm Hg) in the first 4 minutes of the test to an average of 0.92 mm Hg/min for patients with test lasted longer than 12 minutes. These unpredictable results might be related to CO2 washout, atelectasis, cardiac ventilations, or other yet-undefined parameters. The nonlinear relationship between rate of PaCO2 increase and time following onset of apnea resulted in the test being prolonged in several patients. In these patients, the PaCO2 approached 60 mm Hg in an asymptotic fashion. These lengthy tests could have been avoided by utilizing a standardized apnea test with a baseline PaCO2 of 40 mm Hg or greater. The observation that a high baseline PaCO2 greatly augments the efficiency and safety of the test allows criteria that have previously been based on conjecture to be documented and applied clinically. A standardized apnea test, utilizing these principles, may satisfy many of the criticisms regarding brain-death testing that have been raised by neurologists, neurosurgeons, and transplant surgeons.     

Frequency of spinal reflex movements in brain-dead patients

Spontaneous and reflex movements may occur in brain-dead patients. These movements originate from spinal cord neurons and do not preclude a brain-death diagnosis. In this study, we sought to determine the frequency and characteristics of motor movements in patients who fulfilled diagnostic criteria for brain death.Patients admitted to our department between January 2000 and March 2003 and diagnosed as brain-dead were prospectively evaluated in terms of spinal reflexes. Clinical brain death was diagnosed according to our national law. We also prefer to document the diagnosis of brain death with an EEG and/or TCD. Spinal reflex movements were observed in 18 out of 134 (13.4%) brain-dead patients during the study period. Lazarus sign, the most dramatic and complex movement seen in brain-dead patients, was observed a few times in two patients during an apnea test, an oculocephalic test, after a painful stimulus, and after removal of a ventilator. The other reflex movements observed in our brain-dead patients were finger and toe jerks, extension at arms and shoulders, and flexion of arms and feet.The occurrence of spinal reflexes in brain-dead patients may certainly delay decision making, such as starting a transplantation procedure, because of difficulties in convincing the family or even a physician taking part in the diagnosis of brain death. An awareness of spinal reflexes may prevent delays in and misinterpretations of the brain-death diagnosis.     

An evaluation of capnography monitoring during the apnoea test in brain-dead patients

BACKGROUND AND OBJECTIVE: Diagnosis of brain death usually requires the absence of spontaneous respiratory movements during the apnoea test and an arterial carbon dioxide partial pressure above 60 mmHg. On the other hand, although capnography (end-tidal CO(2)) is currently monitored in intensive care unit patients, it has not been evaluated during the apnoea test in brain-dead patients. Therefore, the aim of this prospective study was first to investigate the usefulness of capnography monitoring, and secondly to evaluate the variation of the carbon dioxide partial pressure-end-tidal CO(2) gradient during the apnoea test in clinically brain-dead patients. METHODS: After local Ethics Committee approval, 60 clinically brain-dead patients were investigated. End-tidal CO(2) was continuously recorded before, during and after the apnoea test. Arterial blood gases were sampled immediately before and after the apnoea test for calculation of the carbon dioxide partial pressure-end-tidal CO(2) gradient. RESULTS: The apnoea test was clinically positive in 58 patients, whereas end-tidal CO(2) was equal to 0 during the apnoea. During the 20-min apnoea test, carbon dioxide partial pressure increased from 40 +/- 7 to 97 +/- 19 mmHg (P < 0.001) with a rate of 2.8 +/- 0.9 mmHg min(-1), end-tidal CO(2) increased from 31 +/- 6 to 68 +/- 17 mmHg (P < 0.001) and carbon dioxide partial pressure-end-tidal CO(2) gradient increased from 9 +/- 4 to 29 +/- 10 mmHg (P < 0.001). In two patients, the apnoea test was clinically negative because of the occurrence of spontaneous respiratory movements, whereas capnography showed contemporaneously significant increases in end-tidal CO(2). CONCLUSIONS: End-tidal CO(2) should be systematically monitored and recorded, at least for medico-legal considerations, during the apnoea test in brain-dead patients. The high variability in the carbon dioxide partial pressure-end-tidal CO(2) gradient increase precludes any extrapolation of the carbon dioxide partial pressure from the end-tidal CO(2) at the end of the apnoea test.     

Monitoring patients in the anesthesia recovery room. Continuous transcutaneous O2 and CO2 measurements]

To establish whether continuous transcutaneous O2 and CO2 measurement in the recovery room is suitable for non-invasive monitoring of spontaneous respiration in patients newly operated upon, comparative transcutaneous and arterial pO2 and pCO2 investigations were carried out on 35 adults. There was a correlation coefficient of 0.66 between paO2 and tcpO2. The transcutaneous pO2 values measured were 45.3 mm Hg under the arterial values. When the transcutaneous CO2 values were compared with the arterial values, the correlation coefficient was 0.906. The mean transcutaneous pCO2 values measured lay around 0.7 mm Hg above the arterial values. On the basis of this slight deviation in CO2 values, the method appears to be suitable for continuous non-invasive determination of pCO2. The very large deviations in the O2 values indicate that transcutaneous measurement of oxygen partial pressure in this specific examination situation is not sufficiently reliable, which makes questionable the practice of using one piece of equipment for both measurements. In the clinical setting presented, transcutaneous O2 monitoring does not represent an alternative to close clinical observation and pulse oximetry.     

The status of arterial and mixed venous blood gases in the initial phase of intubation apnea. Studies on the Christiansen-Douglas-Haldane effect

The Christiansen-Douglas-Haldane effect describes the reduced CO2 binding capacity of oxygenated as compared to deoxygenated hemoglobin on the basis of its increased acidity. This study describes the development of the above effect during the first 2 min of hyperoxic intubation apnea. METHODS. After institutional approval 12 patients (NYHA III, ASA IV) scheduled for coronary-artery bypass grafting were studied after written informed consent. Routine monitoring measures included invasive arterial and pulmonary-arterial pressure monitoring. Pulse oximetry (Nellcor N 101) was also used during intubation apnea. Premedication consisted of flunitrazepam 2.0 mg p.o. the evening before operation and another 2.0 mg p.o. 90-120 min before induction of anesthesia. Following standardized preoxygenation induction of anesthesia was performed with 20-25 micrograms/kg fentanyl and 0.1 mg/kg pancuronium. After cessation of spontaneous respiration, controlled ventilation was continued with 100% oxygen until intubation. Thirteen arterial (a) and mixed-venous (v) blood samples were drawn sequentially immediately before and during the first 2 min of apnea and analyzed using Corning 150 pH/blood gas analyzer and a Corning 2500 CO-oximeter. RESULTS. As shown in Table 1 and Fig. 1, paO2 decreased from 485 +/- 100 mmHg before apnea to 376 +/- 68 mmHg after 2 min of apnea while pvO2 remained constant at 47-50 mmHg. Arterial oxygen saturation (saO2) showed stable values greater than 97% while svO2 slightly increased from 81.9% to 82.4% until the end of apnea. A biphasic increase was observed in paCO2 from 41.2 +/- 3.4 mmHg before to 54.5 +/- 3.9 mmHg at the end of apnea. An increase in pvO2 during apnea was linear from 45.7 +/- 3.9 mmHg to 51.9 +/- 4.0 mmHg. After 28.5 s of apnea paCO2 exceeded pvCO2 due to the Haldane effect ("pCO2 reversal"). During apnea, pHa decreased biphasically from 7.40 +/- 0.03 to 7.31 +/- 0.02. The speed of decrease was 0.106 pH units/min (5-35 s) in the 1st and 0.023 pH units/min in the 2nd min of apnea; pHv decreased almost linearly from 7.37 +/- 0.03 mmHg (5s) to 7.33 +/- 0.02 mmHg (115s). After 20.66 s of apnea pHa exceeded pHv ("pH reversal"); pH-reversal occurred earlier than pCO2 reversal (p less than = 0.05). CONCLUSIONS. During early hyperoxic apnea, venoarterial pH and pCO2 reversal can be observed due to the Christiansen-Douglas-Haldane effect. pH reversal starts earlier than pCO2 reversal. Reversal time is dependent on arterial-mixed-venous pCO2 difference (avDpCO2) before apnea, arterial-mixed-venous O2 saturation difference (avDsO2) and cardiac output. The amount of reversal is dependent on avDsO2, i.e. the pH difference of arterial and m     

Videoendoscopic endotracheal intubation in the rat: a comprehensive rodent model of laparoscopic surgery

BACKGROUND: Peritoneal absorption of CO(2) during abdominal insufflation in laparoscopy may disrupt the acid-base equilibrium and alter the physiological response to stress. Current nonventilated rodent models of laparoscopy do not manage the CO(2) load of pneumoperitoneum, but ventilated surgical rodent models are invasive (tracheotomy) and may independently induce the inflammatory response. MATERIALS AND METHODS: A comprehensive rodent model of laparoscopy was developed. Rats were randomized to receive anesthesia alone, anesthesia plus CO(2) pneumoperitoneum, or anesthesia plus CO(2) pneumoperitoneum with videoendoscopic intubation and mechanical ventilation. Arterial blood-gas analysis was performed at baseline and after 30 min of intervention. RESULTS: Baseline pH, pCO(2), and HCO(3)(-) arterial blood gas parameters were normal for all rats. After 30 min, pCO(2) and pH changed slightly but remained normal among rats receiving anesthesia alone (pCO(2) = 46.5 +/- 1.9; pH = 7.365 +/- 0.009) whereas animals receiving anesthesia plus CO(2) pneumoperitoneum that were dependent on spontaneous respiration for ventilation developed significant hypercarbic acidosis (pCO(2) = 53.2 +/- 1.9, P < 0.05; pH = 7.299 +/- 0.011, P < 0.001). This acidosis was completely corrected with increased minute ventilation in intubated rats receiving mechanical ventilation (pCO(2) = 36.8 +/- 1.5, P < 0.001; pH = 7.398 +/- 0.011, P < 0.001). CONCLUSIONS: CO(2) pneumoperitoneum induces significant hypercarbic acidosis in nonventilated rats. Noninvasive endotracheal intubation is feasible in the rat with videoendoscopic assistance. Our noninvasive rodent model of laparoscopic surgery controls for anesthesia- and capnoperitoneum-related acid-base changes and provides an environment in which the biological response to pneumoperitoneum can be studied precisely.     

Target-controlled versus manually-controlled infusion of propofol for direct laryngoscopy and bronchoscopy

Few studies have compared the clinical profile of target-controlled infusions of propofol with that of manually-controlled infusions. Fifty-four ASA physical status I or II patients scheduled for an elective otorhinolaryngology endoscopy performed under general anesthesia with spontaneous ventilation were enrolled in this prospective randomized study to compare the clinical outcome of such administrations. Before induction, all patients received a single alfentanil bolus dose (10 microg/kg). Propofol administration was adapted to maintain absence of movement, hemodynamic stability, and efficient spontaneous ventilation. When compared with the Manually-Controlled Infusion group, in the Target-Controlled Infusion group there were fewer movements at insertion of the laryngoscope (14.8% vs. 44.4%), improved hemodynamic stability (largest variations of mean arterial blood pressure <10% of control values, versus 20%), fewer episodes of apnea, and less respiratory acidosis after endoscopy (pH = 7.37 +/- 0.05 and PaCO(2) = 50 +/- 7 mm Hg versus pH = 7.28 +/- 0.06 and PaCO(2) = 58 +/- 9 mm Hg); the recovery was also shorter (time to opening eyes or verbal response, 4.6 +/- 2.0 min and 6.8 +/- 2.5 min versus 10.8 +/- 7.3 min and 15.7 +/- 7.1 min). Propofol consumption was comparable in the two groups. Targeting the effect-site concentration improved the time course of the propofol drug effect during direct laryngoscopy performed during spontaneous ventilation when compared with manual infusion. IMPLICATIONS: This study compares the clinical profile of propofol anesthesia for direct laryngoscopy with spontaneous ventilation when the drug is administered either as a manually controlled infusion or by targeting the effect-site concentration through a target-controlled infusion (TCI) device. TCI improves the time course of propofol effects.     

国际标准化脑死亡供肺的临床应用3例报告

目的总结适应我国国情的国际标准化脑死亡供体肺的获取以及应用于肺移植的经验。方法 3例机械通气分别达到3d、16d、12d的志愿捐献者经脑死亡和供体器官功能评估后,行国际标准化肺获取术。获取的双侧供肺分别为32岁、34岁、61岁的终末期肺病患者进行了双肺移植。结果利用3例脑死亡供肺成功进行了3例双肺移植,1例患者手术后第9日死于多器官功能衰竭,另外2例双肺移植患者术后恢复良好,顺利出院,术后随访生活质量良好,肺功能极大改善。结论在我国的条件下,严格按国际标准化获取脑死亡供肺,可作为肺移植的主要供肺来源之一。     

The effect of insufflation pressure on CO(2) pneumoperitoneum and embolism in piglets

We conducted this study to investigate the effect of insufflation pressure on the pathophysiology of CO(2) pneumoperitoneum and embolism in an infant model. Twenty anesthetized piglets had stepwise intraperitoneal insufflation with CO(2) for 15 min at pressures ranging from 5 to 20 mm Hg. The piglets were ventilated to baseline normocarbia (ETCO(2) = 30 mm Hg, PaCO(2) = 38 mm Hg) before beginning each insufflation. CO(2) was then insufflated IV in 15 of these piglets at the same pressures. There was no reduction of blood pressure or cardiac output with intraperitoneal insufflation, but the stroke volume declined significantly (*P < 0.05) from (mean +/- SE) 10.6 +/- 1.3 mL to 8.5 +/- 1.3* mL and from 10.0 +/- 1.4 mL to 7.2 +/- 1.2* mL at 15 and 20 mm Hg insufflation pressure, respectively. Abdominal insufflation at 5, 10, 15, and 20 mm Hg caused an increase in ETCO(2) to 31.7 +/- 0.8 mm Hg, 35.6 +/- 1.2* mm Hg, 37.5 +/- 1.5* mm Hg, and 40.1 +/- 1.8* mm Hg and in PaCO(2) to 41.1 +/- 1.3* mm Hg, 44.2 +/- 1.4* mm Hg, 49.9 +/- 1.8* mm Hg, and 53.0 +/- 2.1* mm Hg, respectively. In contrast, the ETCO(2)decreased to 19.4 +/- 1.5* mm Hg, 20.4 +/- 1.4 mm Hg, 15.2 +/- 2.1* mm Hg, and 10.6 +/- 2.0* mm Hg with IV insufflation using the same pressures. IV insufflation caused marked hypotension and mortality. As the insufflation pressure increased, the mortality increased (0 in 15, 1 in 15, 1 in 14, and 6 in 13* at 5, 10, 15, and 20 mm Hg; *P < 0.05 vs 0 in 15, 1 in 15, and 1 in 14). This study suggests that although intraperitoneal insufflation up to 20 mm Hg may be tolerated hemodynamically, the lowest possible pressure should be used to reduce hypercarbia. A low insufflation pressure may also prevent mortality from CO(2) embolism. IMPLICATIONS: The lowest pressure possible should be used when inflating the abdomen with CO(2) to perform a laparoscopy in babies. A low pressure allows better ventilation and may prevent mortality if CO(2) is accidentally injected into a vein.     

Second place-resident clinical science award 1999: laryngeal chemoreflex severity and end-apnea PaO(2) and PaCO(2).

OBJECTIVE: The laryngeal chemoreflex (LCR) is a model for investigating the sudden infant death syndrome. The severity of the LCR-induced response may vary. This study examines the conditions under which recovery from the LCR-induced apnea occurs. METHODS: Twenty-five piglets underwent normoxic laryngeal stimulation (Pao(2) > 70 mm Hg); 11 then underwent hypoxic stimulation (Pao(2) 50-65 mm Hg). Cardiovascular and respiratory responses were recorded. RESULTS: Recovery Pao(2) was lower during profound responses (Pao(2) = 45.9 +/- 12.8 mm Hg) than during moderate (Pao(2) = 54.9 +/- 7.5 mm Hg) and mild (Pao(2) = 60.6 +/- 10.3 mm Hg) responses (analysis of variance [ANOVA], P = 0.05). Recovery PaCO(2) did not vary (ANOVA, P > 0.05). Blood pressure and O(2) saturation declined at faster rates with increasing severity of response (ANOVA, P < 0.05 for both). CONCLUSIONS: Resumption of respiration after LCR-induced apnea is associated with a consistent level of PaCO(2). The severity of the response is associated with recovery PaO(2) levels.     

Volume ventilation of infants with congenital heart disease: a comparison of Dräger, NAD 6000 and Siemens, Servo 900C ventilators

We compared the ventilation and pulmonary mechanics produced by a new anesthesia ventilator (NAD 6000) using a circle system with that produced by a critical care ventilator (Servo 900C) using a nonrebreathing circuit in infants with congenital heart disease. Twenty patients, aged 1 day to 7 mo, weighing 2.1 to 4.6 kg, were studied. The NAD 6000 had improved alveolar ventilation: PaCO(2) 43 +/- 8 vs 47 +/- 5 mm Hg (P = 0.005), end-tidal CO(2) 34 +/- 7 vs 37 +/- 5 mm Hg (P = 0.042); larger inspired tidal volumes 12.9 +/- 2.8 vs 11.3 +/- 2.2 mL/kg (P < 0.001), but with higher mean airway pressures 9.7 +/- 1.6 vs 8.6 +/- 1.3 cm H(2)O (P < 0.001). These differences in ventilation and airway pressures were not clinically significant. Although there were differences in observed ventilatory variables, both machines provided adequate ventilation when set in the volume control mode. Implications: We compared two ventilators for use in infants. Twenty infants undergoing surgery for congenital heart defects were randomized to receive ventilation first with one ventilator, then with the other. Although there were differences in observed ventilatory variables, both machines provided adequate ventilation when set in the volume control mode.     

A comparative evaluation of transcutaneous and end-tidal measurements of CO2 in thoracic anesthesia

We performed this study to assess the accuracy of transcutaneous CO(2) (PTCCO(2)) monitoring compared with end-tidal CO(2) (PETCO(2)) in thoracic anesthesia. Twenty-six patients undergoing pneumonectomy with thoracotomy for which a long period of one-lung ventilation (OLV) was required were studied. The lungs were mechanically ventilated in the lateral decubitus position. PTCCO(2), PETCO(2), and arterial CO(2) (PaCO(2)) were simultaneously measured during two-lung ventilation (TLV) and during OLV at intervals of 15 min. All patients completed the study protocol. Bland-Altman analysis revealed a bias of -0.4 mm Hg with a precision of +/-2.5 mm Hg during OLV and 1.4 mm Hg with +/-4.3 mm Hg during TLV when PTCCO(2) and PaCO(2) were compared and revealed a bias of -5.8 mm Hg with a precision of +/-4.1 mm Hg during OLV and -7.1 mm Hg with +/-4.6 mm Hg during TLV when PETCO(2) and PaCO(2) were compared. We conclude that PTCCO(2) monitoring is accurate for evaluating CO(2) levels during thoracic anesthesia.     

Does continuous mucosal partial carbon dioxide pressure measurement predict leakage of intrathoracic esophagogastrostomy?

BACKGROUND: Gastroplasty after esophagectomy is associated with relevant morbidity due to anastomotic leakage of the esophagogastrostomy. The aim of this study was to find out whether continuous partial carbon dioxide pressure (pCO2) measurement of the gastric mucosa is an adequate method of monitoring the gastric tube during the postoperative course and of detecting patients with an anastomotic leakage. METHODS: Forty-seven patients with esophageal cancer underwent esophagectomy and gastric tube formation with intrathoracic esophagogastrostomy. Postoperatively, mucosal pCO2 of the gastric tube (pCO2i) was measured using continuous tonometry (TONOCAP, Datex Ohmeda). pCO2i was related to the arterial pCO2 (delta pCO2 = pCO2i - pCO2a). RESULTS: A total of 4,338 delta pCO2 measurements were recorded. On average, the pCO2i of each patient was monitored over a period of 92 hours. In 5 patients an anastomotic leakage of the esophagogastrostomy developed. The mean delta pCO2 of this group was 31.7 mm Hg (+/-19.3 SD) and significantly higher (p < 0.0001) than that of patients without anastomotic leakage (20.7 mm Hg +/- 12.8 SD). With a delta pCO2 cut-off point of 56 mm Hg measured for 5 hours, the sensitivity was 0.8, the specificity 0.9, and the positive predictive value 0.5. In patients with anastomotic leakage, the peak delta pCO2 preceded clinical symptoms. False positive delta pCO2 measurements (n = 4) were mainly due to severe pneumonia with long-term ventilation. CONCLUSIONS: Mucosal pCO2 measurement of the gastric tube can be used as an early indicator of a complicated postoperative course predicting anastomotic leakage of the esophagogastrostomy.     

The effect of air embolization from the femoral canal on hemodynamic parameters during hip arthroplasty

A canine laboratory and clinical study was designed to determine the effect of air embolism during hip arthroplasty. Canine femurs were pressurized with air to 250-300 mm Hg or with low-viscosity cement to 300-900 mm Hg. Pressurization with low-viscosity cement from distal to proximal with a plugged femur revealed no change in pO2, pCO2, pulmonary artery pressure, or end-tidal CO2. Air pressurization resulted in significant increases in pCO2, pulmonary artery pressure, and end-tidal CO2, and a decrease in pO2. Pressurization of the medullary canal with xenon-labeled air was used to document pulmonary embolism. In a clinical setting, two different femoral cementing techniques during total hip arthroplasty were studied to determine their effect on hemodynamic parameters associated with embolic phenomenon. Five patients had a plugged femoral canal filled from proximal to distal with a vent tube, followed by finger-packing. Three of the patients demonstrated a significant drop in pO2 and blood pressure and a rise in pCO2 and end-tidal CO2. Five other patients had their plugged femoral canals filled from distal to proximal, three with regular cement and two with low-viscosity cement, with no significant cardiopulmonary changes. The adverse cardiopulmonary effects reported during hip arthroplasty appear to be avoided by eliminating air during the cementing procedure, by filling a plugged canal from distal to proximal.     

Cardiopulmonary effects of pressure support ventilation

Pressure support ventilation (PSV) is a newer mode of ventilatory support that augments the patient's spontaneous inspirations to a preselected peak inspiratory pressure. We studied the effects of adding low levels of PSV (5 to 10 cm H2O) in conjunction with intermittent mandatory ventilation (IMV) on 15 patients who required mechanical ventilation for flail chest and pulmonary contusion. Patients were selected for the study if, during weaning from IMV, the following criteria were met: (1) a PaCO2 level greater than 45 mm Hg, (2) a spontaneous respiratory rate (RR) greater than 30 breaths per minute, (3) a minute ventilation (VE) greater than 9.0 L/min, and (4) spontaneous tidal volumes (VT) of less than 2 mL/kg. The PSV was added to the IMV at a level that augmented spontaneous VT to greater than 4 mL/kg. An average of 9 +/- 3 cm H2O of pressure support resulted in a fall in the level of PaCO2 (50 +/- 4 to 43 +/- 5 mm Hg), spontaneous RR (36 +/- 5 to 16 +/- 3 breaths per minute), VE (12 +/- 2 to 8.4 +/- 1.5 L/min), and dead space-tidal volume ratio from (0.68 +/- 0.1 to 0.47 +/- 0.05). Mean airway pressure and PaO2 both increased, but these changes were not statistically significant. Oxygen consumption was also unchanged. These results suggest that in patients who are difficult to wean due to respiratory muscle fatigue (characterized by increasing RR and decreasing VT), PSV normalizes lung volumes, improves ventilation, and may expedite the weaning process.     

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

Profound arterial hypotension is a commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.     

Regulation of respiration in assisted ventilation

Based on knowledge of the control of external respiration, the physiological reactions are discussed which should be evoked proprioceptively and chemoreceptively by an assisting respirator's disturbances of spontaneous breathing movements. The following possible states are discriminated: 1. "no adaption": the respiratory motor system does not remain passive during the machine's stroke; 2. "passive adaption": the respiratory motor system remains passive during the respirator's stroke; to changes of the blood gas-status, only the breathing frequency responds, but in just the same manner as during spontaneous ventilation; 3. "active adaption": the ventilatory motor apparatus remains passive during the respirator's operation; changes of the blood gases are responded to by the breathing frequency only, but in a manner different to spontaneous breathing and which compensates for the invariability of the fixed stroke-volume. - Related to these 3 states, consequences concerning the efficiency of chemical respiratory control can be derived which should reveal themselves during experimental manipulation of the blood gas partial pressures. Accordingly, the CO2-response curves of minute ventilation, breathing frequency and tidal-volume generated in 9 healthy, awake and cooperative subjects during spontaneous breathing and assisted (stroke-volume controlled) respiration with gas mixtures of 0, 3 and 6% CO2 were investigated and compared. (In each subject assisted ventilation with 2 or 3 different stroke-volumes was performed. The smallest stroke-volume equalled the medium tidal-volume of spontaneous ventilation. Every stroke-volume produced its particular CO2-response curve). Hence it follows that with assisted ventilation, using a stroke-volume larger than the spontaneous tidal-volume, the subjects maintain a state between "passive" and "active adaption".(ABSTRACT TRUNCATED AT 250 WORDS)     

Miniature intravascular pCO2 sensors in neurosurgery.

In this study the authors compared PaCO2 measurements from a newly developed miniature intravascular pCO2 sensor for continuous on-line monitoring with those from a Radiometer bench instrument. In 10 patients undergoing craniotomy procedures, 84 paired comparisons were made. At the same time it was possible to follow continuously the trend of PaCO2 during deliberate hyperventilation, during the apneic period following hyperventilation, and during spontaneous respiration in the postoperative period. The comparisons showed an average difference in pCO2 of 1.62 +/- SE 0.15 torr. The apneic threshold for PaCO2 after passive hyperventilation was lower than in the awake patient. After the period of apnea no hypoxemia occurred. In the recovery room the PaCO2 increased and the PaO2 decreased. The latter decreased to subnormal levels in two patients more than an hour postoperatively.