Regional cerebrovascular reactivity to carbon dioxide during cardiopulmonary bypass in patients with cerebrovascular disease

In patients with cerebrovascular disease, hypercarbia may cause redistribution of regional cerebral blood flow from marginally perfused to well-perfused regions (intracerebral steal), as evidenced by regional cerebral blood flow studies during carotid endarterectomy. During hypothermic cardiopulmonary bypass, the pH-stat method of acid-base management produces relative hypercarbia. To determine whether pH-stat management produces relative hypercarbia. To determine whether pH-stat management induces intracerebral steals, we investigated nine patients with cerebrovascular disease undergoing coronary artery bypass grafting. During hypothermic cardiopulmonary bypass, arterial carbon dioxide tension was varied in random order between 40 mm Hg and 60 mm Hg (uncorrected for body temperature). Regional cerebral blood flow was measured by clearance of 133 xenon injected into the arterial inflow cannula. Nasopharyngeal temperature (26.8 degrees-28.0 degrees +/- 2.2 degrees-3.0 degrees C), perfusion flow rate (2.14-2.18 +/- 0.70-0.73 L/min/m2), mean arterial pressure (67-68 +/- 6-9 mm Hg), arterial carbon dioxide tension (302-308 +/- 109-113 mm Hg), and hematocrit (23% +/- 4%) were maintained within narrow limits in each patient during arterial carbon dioxide tension manipulation. Global mean cerebral blood flow values were similar to previously reported values in patients free of cerebrovascular disease; patients in this study averaged 15.2 +/- 2.5 ml/100 gm/min at an arterial carbon dioxide tension of 46.1 +/- 8.4 mm Hg and 25.3 +/- 6.1 ml/100 gm/min at an arterial carbon dioxide tension of 71.1 +/- 11.8 mm Hg. Carbon dioxide reactivity, defined as mean global cerebral blood flow (in ml/100 gm/min) divided by arterial carbon dioxide tension (in mm Hg), was similar in the region having the lowest regional cerebral blood flow and in the brain as a whole. No patient developed evidence of an intracerebral steal at the higher arterial carbon dioxide tension. During hypothermic cardiopulmonary bypass, higher levels of arterial carbon dioxide tension, such as those associated with the pH-stat management technique, are apparently not associated with potentially harmful redistribution of cerebral blood flow in patients with cerebrovascular disease.     

Carbon dioxide embolism during laparoscopy: effect of insufflation pressure in pigs.

Carbon dioxide embolism is a rare but potentially devastating complication of laparoscopy. To determine the effects of insufflation pressure on the mortality from carbon dioxide embolism, six swine had intravascular insufflation with carbon dioxide for 30 seconds using a Karl Storz insufflator at a flow rate of 35 mL/kg/min. The initial insufflation pressure was 15 mm Hg. Following recovery from the first embolism, intravascular insufflation using a pressure of 20 mm Hg at the same flow rate was performed in the surviving animals. Significantly less carbon dioxide (8.3 +/- 2.7 versus 16.7 +/- 3.9 mL/kg; p < 0.02) was insufflated intravascularly at 15 mm Hg than at 20 mm Hg pressure. All of the pigs insufflated at 15 mm Hg pressure with a flow rate of 35 mL/kg/min survived. In contrast, 4 of the 5 pigs insufflated at 20 mm Hg pressure died. The surviving pig died when insufflated with 25 mm Hg pressure following an embolism of 15.7 mL/kg. Intravascular injection was often associated with an initial rise in end-tidal carbon dioxide tension, followed by a rapid fall in all cases where the embolism proved fatal. Insufflation should be begun with a low pressure and a slow flow rate to limit the volume of gas embolized in the event of inadvertent venous cannulation. Insufflation should immediately be stopped if a sudden change in end-tidal carbon dioxide tension occurs.     

Continuous arterial and venous blood gas monitoring during cardiopulmonary bypass

A new monitoring technique, based on optical fluorescence chemistry, allows continuous monitoring of all blood gas variables during cardiopulmonary bypass. To evaluate the clinical performance of this monitor, we drew 220 arterial and 216 venous blood samples from 15 patients, and simultaneous blood gas values displayed by the monitor were compared with standard laboratory measurements. The continuous monitor predicted laboratory values with varying degrees of accuracy. (R2 values by linear regression: arterial oxygen tension 0.86, venous oxygen tension 0.36, arterial carbon dioxide tension 0.58, venous carbon dioxide tension 0.72, arterial pH 0.53, venous pH 0.58; pH 0.53, venous pH 0.58; p less than 0.0001). Monitor values of arterial oxygen tension overestimated laboratory values (bias = + 43.5 mm Hg), but the laboratory reference method likely underestimated true arterial oxygen tension in the high range achieved on bypass. Monitoring of venous oxygen tension was imprecise (precision = +/- 6.51 mmHg), regardless of whether stable conditions existed during the sampling period. Monitoring of carbon dioxide tension and pH showed small bias (carbon dioxide tension within 2 mm Hg, pH within 0.03) and good precision (carbon dioxide tension within 3 mm Hg, pH within 0.03). With the development of unstable conditions on bypass, monitor arterial oxygen tension values showed a changing relationship to corresponding laboratory values. In conclusion, arterial and venous carbon dioxide tension and pH monitoring provide acceptably accurate alternatives to laboratory measurement of these variables during cardiopulmonary bypass. Arterial oxygen tension monitoring accurately indicates changes in oxygen tension in the arterial oxygen tension range typically produced during extracorporeal circulation. Oxygen tension monitoring in the venous oxygen tension range is too imprecise for clinical decision-making purposes.     

Hemodynamic effects of carbon dioxide insufflation during endoscopic vein harvesting

BACKGROUND: A prospective study was performed assessing the hemodynamic effects of carbon dioxide (CO2) insufflation during endoscopic vein harvesting (EVH) using the Guidant Vasoview Uniport system. METHODS: Five hemodynamic and respiratory parameters (end-tidal carbon dioxide, arterial partial pressure of carbon dioxide, mean arterial pressure, mean pulmonary arterial pressure, and cardiac output), were measured in 100 consecutive patients undergoing EVH with CO2 insufflation. Data were obtained prior to commencement of EVH, 15 minutes after commencement, and 5 minutes after completion of the vein harvesting. RESULTS: No adverse hemodynamic effects were observed during CO2 insufflation. Specifically, average mean arterial pressure went from 88.77+/-9.64 to 89.13+/-8.60 to 88.24+/-8.71 mm Hg before, during, and after endoscopic vein harvesting (p = 0.291). Likewise, average mean pulmonary artery pressures were 19.76+/-4.75, 20.05+/-4.48, and 20.05+/-4.62 mm Hg (p = 0.547); and average cardiac output was 4.25+/-0.74, 4.22+/-0.73, and 4.23+/-0.69 L/min (p = 0.109) at those three intervals. Additionally, there was no evidence of significant systemic absorption of CO2 as reflected in average arterial PCO2, which remained steady at 37.42+/-5.19, 37.51+/-4.59, and 38.10+/-4.80 mm Hg (p = 0.217); and average end-tidal CO2, which was 32.10+/-3.66, 32.50+/-3.47, and 32.38+/-3.33 mm Hg (p = 0.335). In a subset of 20 patients with elevated pulmonary arterial pressure (more than 32 mm Hg), there was also no significant change in any of the parameters. CONCLUSIONS: Carbon dioxide insufflation during EVH leads to no adverse hemodynamic consequences or systemic CO2 absorption. The technique appears to be safe and well tolerated.     

Effects of altered PaO2 and PaCO2 on left ventricular function and coronary hemodynamics in sheep

The effects of acute changes in arterial carbon dioxide and oxygen tension, produced by altering the inspired gas mixtures while maintaining constant-volume intermittent positive pressure ventilation, on global function, regional left ventricular function, and coronary hemodynamics were studied in eight sheep during halothane anesthesia. Hypercapnia (Paco2, 73.5 +/- 2.3 mm Hg, mean +/- SD) increased heart rate, stroke volume, and cardiac output but decreased systolic shortening in the base of the left ventricle. Hypocapnia (PaO2, 24 +/- 1.5 mm Hg) decreased cardiac output and coronary flow below levels seen with hypercapnia but not below levels seen with normocapnia. Systolic shortening decreased in both apical and basal regions, and left ventricular relaxation was impaired as evidenced by a reduction of the nadir of LV dP/dt. Hypoxemia (PaO2, 39 +/- 1.5 mm Hg) elicited a hyperdynamic response of the circulation, increased coronary blood flow, and exhausted the coronary flow reserve. Neither changes in PaCO2 nor changes in PaO2 caused postsystolic shortening, although hypercapnia caused nonuniformity of contraction in the left ventricle. Thus, marked alterations in oxygen and carbon dioxide tensions do not cause left ventricular dysfunction, even though moderate hypoxia reduces the coronary flow reserve.     

Arterial to end-tidal carbon dioxide tension difference in children under halothane anaesthesia

Using blood gas determinations and capnography, the relationship between arterial and end-tidal PCO₂ was investigated in 20 children under halothane anaesthesia with spontaneous respiration. A median arterial to end-tidal carbon dioxide tension difference of 0.66 kPa (5 mm Hg) was found. There was a close correlation between Pa_co2 and the magnitude of the carbon dioxide difference. Our findings may largely be explained by an increase in Vd/Vt (presumably mainly due to a reduction of Vt) causing admixture of dead space air throughout expiration. It is concluded that though end-tidal carbon dioxide does not exactly reflect Pa_co2 capnography may be of value as a monitor of respiration in paediatric anaesthesia at normal or near-normal values of end-tidal carbon dioxide.     

Brain tissue pH, oxygen tension, and carbon dioxide tension in profoundly hypothermic cardiopulmonary bypass. Comparative study of circulatory arrest, nonpulsatile low-flow perfusion, and pulsatile low-flow perfusion

The pH, oxygen tension, and carbon dioxide tension of canine brain tissue were experimentally examined during profoundly hypothermic cardiopulmonary bypass. After core cooling, a 60-minute period of circulatory arrest was performed in group 1 (n = 8), a 120-minute nonpulsatile low-flow perfusion (25 ml/kg/min) in group 2 (n = 8), and a 120-minute pulsatile low-flow perfusion (25 ml/kg/min) in group 3 (n = 8). When the animal was rewarmed, the core temperature was raised to 32 degrees C. Brain tissue pH kept decreasing in group 1, but it showed a delayed recovery in group 2 and a rapid recovery in group 3 during core rewarming. Brain tissue oxygen tension decreased significantly in group 1. Brain tissue carbon dioxide tension increased irreversibly in group 1, increased to about 100 mm Hg and recovered to 89.9 +/- 15.3 mm Hg in group 2, and reached a plateau of about 85 mm Hg and recovered to 55.4 +/- 6.7 mm Hg in group 3. We concluded that a 120-minute period of nonpulsatile low-flow perfusion provides more protection from brain damage than a 60-minute period of circulatory arrest. Furthermore, pulsatile flow will increase the safety margin of cardiopulmonary bypass even if the flow rate is reduced to 25 ml/kg/min.     

Cerebral perfusion during canine hypothermic cardiopulmonary bypass: effect of arterial carbon dioxide tension

Cerebral blood flow (radioactive microspheres), intracranial pressure (subdural bolt), and retinal histopathology were examined in 20 dogs undergoing 150 minutes of hypothermic (28 degrees C) cardiopulmonary bypass to compare alpha-stat (arterial carbon dioxide tension, 40 +/- 1 mm Hg; n = 10) and pH-stat (arterial carbon dioxide tension, 61 +/- 1 mm Hg; n = 10) techniques of arterial carbon dioxide tension management. Pump flow (80 mL.kg-1.min-1), mean aortic pressure (78 +/- 2 mm Hg), and hemoglobin level (87 +/- 3 g/L [8.7 +/- 0.3 g/dL]) were maintained constant. During bypass, intracranial pressure progressively increased in the alpha-stat group from 6.0 +/- 1.0 to 13.9 +/- 1.8 mm Hg (p less than 0.05) and in the pH-stat group from 7.7 +/- 1.1 to 14.7 +/- 1.4 mm Hg (p less than 0.05), although there was no evidence of loss of intracranial compliance or intracranial edema formation as assessed by brain water content. With cooling, cerebral blood flow decreased by 56% to 62% in the alpha-stat group (p less than 0.05) and by 48% to 56% in the pH-stat group (p less than 0.05). However, 30 minutes after rewarming to 37 degrees C, cerebral blood flow in both groups failed to increase and remained significantly depressed compared with baseline values. Both groups showed similar amounts of ischemic retinal damage, with degeneration of bipolar cells found in the inner nuclear layer in 67% of animals. We conclude that, independent of the arterial carbon dioxide tension management technique, (1) cerebral perfusion decreased comparably during prolonged hypothermic bypass, (2) intracranial pressure increases progressively, (3) ischemic damage to retinal cells occurs despite maintenance of aortic pressure and flow, and (4) a significant reduction in cerebral perfusion persists after rewarming.     

Hypocarbia and spontaneous recovery from vecuronium neuromuscular blockade in anesthetized patients

The effect of hypocarbia on the recovery from the neuromuscular blockade produced by vecuronium was studied in 20 anesthetized patients. Vecuronium was administered until twitch tension was reduced to between 0-15% of control. Neuromuscular function was then allowed to spontaneously recover during continued normocarbia (end-tidal PCO2 5.5 kPa [41 mm Hg]) in half the patients, and in the other half of the patients hyperventilation producing hypocarbia (mean end-tidal PCO2 of 3.1 +/- 0.4 kPa SD [23 +/- 3 mm Hg] at the completion of twitch force recovery) was initiated at the beginning of spontaneous recovery from neuromuscular blockade. The mean vecuronium recovery index (time for spontaneous recovery from 25-75% of control twitch tension) was slightly but not significantly shorter in the hyperventilated patients (8.4 +/- 1.8 min SD) than in the normally ventilated patients (10.4 +/- 3.4 min SD). We conclude the vecuronium recovery index in anesthetized patients is not significantly changed by hyperventilation with hypocarbia when induced at the beginning of recovery from neuromuscular blockade.     

Accuracy of end-tidal carbon dioxide monitoring using the NBP-75 microstream capnometer. A study in intubated ventilated and spontaneously breathing nonintubated patients

Arterial carbon dioxide partial pressure measurements using the NBP-75 microstream capnometer were compared with direct PaCO2 values in patients who were (a) not intubated and spontaneously breathing, and (b) patients receiving intermittent positive pressure ventilation of the lungs and endotracheal anaesthesia. Twenty ASA physical status I-III patients, undergoing general anaesthesia for orthopaedic or vascular surgery were included in a prospective crossover study. After a 20-min equilibration period following the induction of general anaesthesia, arterial blood was drawn from an indwelling radial catheter, while the end-tidal carbon dioxide partial pressure was measured at the angle between the tracheal tube and the ventilation circuit using a microstream capnometer (NBP-75, Nellcor Puritan Bennett, Plesanton, CA, USA) with an aspiration flow rate of 30 mL min(-1). Patients were extubated at the end of surgery and transferred to the postanaesthesia care unit, where end-tidal carbon dioxide was sampled through a nasal cannula (Nasal FilterLine, Nellcor, Plesanton, CA, USA) and measured using the same microstream capnometer. In each patient six measurements were performed, three during mechanical ventilation and three during spontaneous breathing. A good correlation between arterial and end-tidal carbon dioxide partial pressure was observed both during mechanical ventilation (r = 0.59; P = 0.0005) and spontaneous breathing (r = 0.41; P = 0.001); while no differences in the arterial to end-tidal carbon dioxide tension difference were observed when patients were intubated and mechanically ventilated (7. 3 +/- 4 mmHg; CI95: 6.3-8.4) compared to values measured during spontaneous breathing in the postanesthesia care unit, after patients had been awakened and extubated (6.5 +/- 4.8 mmHg; CI95: 5. 2-7.8) (P = 0.311). The mean difference between the arterial to end-tidal carbon dioxide tension gradient measured in intubated and non-intubated spontaneously breathing patients was 1 +/- 6 mmHg (CI95: -11-+13). We conclude that measuring the end-tidal carbon dioxide partial pressure through a nasal cannula using the NBP-75 microstream capnometer provides an estimation of arterial carbon dioxide partial pressure similar to that provided when the same patients are intubated and mechanically ventilated.     

Feasibility of a pumpless extracorporeal respiratory assist device.

BACKGROUND: Our study evaluated the efficacy and feasibility of a pumpless respiratory assist device and determined its capacity for carbon dioxide removal. METHODS: In five adult pigs the left femoral vein and artery were cannulated with a 20F cannula and connected to a low-pressure hollow-fiber artificial lung. After we had obtained baseline values of mean arterial pressure, cardiac output, and blood flow across the artificial lung, the mean arterial pressure was reduced 20% and 40% relative to baseline; in a second phase, it was raised 20% and 40. Cardiac output and artificial lung flow were simultaneously recorded. We determined the carbon dioxide removal capacity of the artificial lung by gradually increasing the arterial partial carbon dioxide tension of the animal. RESULTS: An increase of 10 mm Hg in mean arterial pressure resulted in an increase of flow of 0.14 L/min. The mean pressure drop across the artificial lung was measured at 17 +/- 9 mm Hg. The shunt flow over the artificial lung varied between 14 and 25% of the cardiac output of the animal. Depending on inlet conditions, carbon dioxide removal by the artificial lung was between 62 +/- 22 mL/L/min and 104 +/- 25 mL/L/min. CONCLUSIONS: A pumpless respiratory assist device can remove a significant proportion of the metabolic carbon dioxide production. However, adequate mean arterial pressure is mandatory to maintain sufficient flow across the device. The technique seems attractive because of its simplicity and can be used in acute lung injury in conjunction of apneic oxygenation for prolonged respiratory support.     

Vasopressor response in a porcine model of hypothermic cardiac arrest is improved with active compression-decompression cardiopulmonary resuscitation using the inspiratory impedance threshold valve

During normothermic cardiac arrest, a combination of active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) with the inspiratory threshold valve (ITV) significantly improves vital organ blood flow, but this technique has not been studied during hypothermic cardiac arrest. Accordingly, we evaluated the hemodynamic effects of ACD + ITV CPR before, and after, the administration of vasopressin in a porcine model of hypothermic cardiac arrest. Pigs were surface-cooled until their body core temperature was 26 degrees C. After 10 min of untreated ventricular fibrillation, 14 animals were randomly assigned to either ACD CPR with the ITV (n = 7) or to standard (STD) CPR (n = 7). After 8 min of CPR, all animals received 0.4 U/kg vasopressin IV, and CPR was maintained for an additional 10 min in each group; defibrillation was attempted after 28 min of cardiac arrest, including 18 min of CPR. Before the administration of vasopressin, mean +/- SEM common carotid blood flow was significantly higher in the ACD + ITV group compared with STD CPR (67 +/- 13 versus 26 +/- 5 mL/min, respectively; P < 0.025). After vasopressin was given at minute 8 during CPR, mean +/- SEM coronary perfusion pressure was significantly higher in the ACD + ITV group, but did not increase in the STD group (29 +/- 3 versus 15 +/- 2 mm Hg, and 25 +/- 1 versus 14 +/- 1 mm Hg at minute 12 and 18, respectively; P < 0.001); mean +/- SEM common carotid blood flow remained higher at respective time points (33 +/- 8 versus 10 +/- 3 mL/min, and 31 +/- 7 versus 7 +/- 3 mL/min, respectively; P < 0.01). Without active rewarming, spontaneous circulation was restored and maintained for 1 h in three of seven animals in the ACD + ITV group versus none of seven animals in the STD CPR group (not significant). During hypothermic cardiac arrest, ACD CPR with the ITV improved common carotid blood flow compared with STD CPR alone. Moreover, after the administration of vasopressin, coronary perfusion pressure was significantly higher during ACD + ITV CPR, but not during STD CPR. IMPLICATIONS: New strategies are needed to improve the efficiency of cardiopulmonary resuscitation (CPR) in hypothermic cardiac arrest. Active compression-decompression CPR with the inspiratory threshold valve improved carotid blood flow (and coronary perfusion pressure with vasopressin) compared with standard CPR.     

"Low-pressure" laparoscopic cholecystectomy in high risk patients (ASA III and IV): our experience

The insufflation pressure used for laparoscopic cholecystectomy is usually 12-15 mm Hg, and a pneumoperitoneum with carbon dioxide has a significant effect on both cardiovascular and respiratory function. These effects are transient in young, healthy patients, but may be dangerous in ASA III and IV patients with a poor cardiac reserve. This study was designed to assess the feasibility of performing laparoscopic cholecystectomy at 6.5-8 mm Hg insufflation pressure in "high-risk" patients. Thirteen patients, 10 ASA III and 3 ASA IV, with cholelithiasis, were included in this study The insufflation pressure was 6.5-8 mm Hg, with a 10 degrees anti-Trendelenburg position. The cardiovascular and blood gas variables studied were: mean arterial blood pressure, heart rate, respiratory rate, and end-tidal CO2 pressure. The authors reported no conversions and no intra- or postoperative complications. During insufflation heart rate and mean arterial blood pressure increased minimally if compared with laparoscopic cholecystectomy at 12-15 mm Hg. Pa CO2 increased after insufflation (+5 mm Hg), and the end-tidal CO2 pressure gradient was moderate (3.5 mm Hg) and unchanged during surgery. A low-pressure pneumoperitoneum is feasible for laparoscopic cholecystectomy and minimizes the adverse haemodynamic effects of peritoneal insufflation.     

Cardiopulmonary resuscitation during severe hypothermia in pigs: does epinephrine or vasopressin increase coronary perfusion pressure?

The American Heart Association does not recommend epinephrine for management of hypothermic cardiac arrest if body core temperature is below 30 degrees C. Furthermore, the effects of vasopressin administration during hypothermic cardiac arrest are totally unknown. This study was designed to assess the effects of vasopressin and epinephrine on coronary perfusion pressure in a porcine model during hypothermic cardiac arrest cardiopulmonary resuscitation (CPR). Pigs were surface-cooled until their body core temperature was 26 degrees C. After 30 min of untreated cardiac arrest, followed by 3 min of basic life support CPR, 15 animals were randomly assigned to receive, at 5-min intervals, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 5), epinephrine (45, 45, and 200 microg/kg; n = 5), or saline placebo (n = 5). Compared with epinephrine, mean +/- SEM coronary perfusion pressure was significantly higher (P < 0.05) 90 s and 5 min after the first (35+/-4 vs 22+/-3 mm Hg and 37+/-2 vs 16+/-2 mm Hg) and the second vasopressin administration (40+/-5 vs 26+/-5 mm Hg and 36+/-5 vs 18+/-2 mm Hg, respectively). After the third drug administration, coronary perfusion pressure in the epinephrine group increased dramatically and was comparable to vasopressin. In the saline placebo group, coronary perfusion pressure was significantly lower (P < 0.05) than in the vasopressin and epinephrine groups. Six animals treated with epinephrine or vasopressin had transient return of spontaneous circulation, whereas all placebo animals died (P < 0.05). During CPR in severe hypothermia, administration of both vasopressin and epinephrine resulted in significant increases in coronary perfusion pressure when compared with placebo. IMPLICATIONS: Our study was designed to assess the effects of vasopressin and epinephrine in a porcine model simulating cardiac arrest during severe hypothermia. This study demonstrates that the administration of both emergency drugs results in an increased perfusion pressure in the heart.     

Hemodynamics and gas exchange during carbon dioxide insufflation for totally endoscopic coronary artery bypass grafting

BACKGROUND: In addition to single-lung ventilation (SLV), positive-pressure CO2 insufflation is mandatory for totally endoscopic coronary artery bypass grafting. Studies on the effects of unilateral CO2 insufflation on hemodynamics produced controversial results, and bilateral insufflation has not been studied to our knowledge. The present study sought to investigate hemodynamics and gas exchange during unilateral and bilateral CO2 insufflation in patients who underwent totally endoscopic coronary artery bypass grafting. METHODS: Eleven hemodynamic and gas exchange variables were monitored during 22 totally endoscopic coronary artery bypass grafting procedures with unilateral (n = 17) or bilateral (n = 5) CO2 insufflation at a pressure of 10 to 12 mm Hg. Data were obtained at baseline with double-lung ventilation, after institution of SLV, during insufflation, after cardiopulmonary bypass during SLV, and after return to double-lung ventilation. RESULTS: Arterial oxygen tension decreased significantly during SLV, whereas the peak inspiratory pressure increased. In addition, central venous pressure and heart rate increased significantly during insufflation, but mean arterial pressure remained unchanged. Although the end-tidal CO2 pressure did not change, arterial carbon dioxide tension increased progressively to a maximum of 44.6 +/- 5.9 mm Hg during unilateral insufflation, and 55.7 +/- 14.6 mm Hg during bilateral insufflation (p < 0.05 versus baseline and between groups). Mixed venous oxygen saturation declined during SLV regardless of CO2 insufflation and recovered to baseline once double-lung ventilation was restarted. Left and right ventricular ejection fractions remained unaltered. No patient required inotropic or vasopressor support. CONCLUSIONS: Carbon dioxide insufflation for totally endoscopic coronary artery bypass grafting with SLV had no adverse effects on hemodynamics. In contrast to a moderate increase of arterial carbon dioxide tension during unilateral insufflation, markedly elevated arterial carbon dioxide tension levels remain a cause of concern during bilateral insufflation.     

Respiratory effects of spinal anesthesia: resting ventilation and single-breath CO2 response

The effects of spinal anesthesia with bupivacaine or lidocaine on resting pulmonary ventilation and on the response to the single-breath carbon dioxide test were studied in 11 unpremedicated patients. Resting end-tidal PCO2 decreased from 34.8 +/- 4.5 (mean +/- SD) to 31.6 +/- 4.6 mm Hg after induction of spinal anesthesia (P = 0.002). The decrease in end-tidal PCO2 correlated negatively with patient age (r = -0.67, P = 0.02) and positively with spinal analgesic level (r = 0.58, P = 0.06). Breath-to-breath variability of ventilation increased during spinal anesthesia. Spinal anesthesia was not associated with statistically significant changes in tidal volume, respiratory rate, minute ventilation, mean inspiratory flow rate, inspiratory duty cycle duration, or the response to the single-breath CO2 test.     

Regional low-flow perfusion provides somatic circulatory support during neonatal aortic arch surgery

BACKGROUND: Regional low-flow perfusion has been shown to provide cerebral circulatory support during neonatal aortic arch operations. However, its ability to provide somatic circulatory support remains unknown. METHODS: Fifteen neonates undergoing arch reconstruction with regional perfusion were studied. Three techniques were used to assess somatic perfusion: abdominal aortic blood pressure, quadriceps blood flow (near-infrared spectroscopy), and gastric tonometry. RESULTS: Twelve patients required operation for hypoplastic left heart syndrome, and 3 required arch reconstruction with a biventricular repair. There was one death (7%). Abdominal aortic blood pressure was higher (12+/-3 mm Hg versus 0+/-0 mm Hg), and quadriceps blood volumes (5+/-24 versus -17+/-26) and oxygen saturations (57+/-25 versus 33+/-12) were greater during regional perfusion than during deep hypothermic circulatory arrest (p < 0.05). During rewarming, the arterial-gastric mucosal carbon dioxide tension difference was lower after circulatory arrest than after regional perfusion (-3.3+/-0.3 mm Hg versus 7.8+/-7.6 mm Hg, p < 0.05). CONCLUSIONS: Regional low-flow perfusion provides somatic circulatory support during neonatal arch surgical procedures. Support of the subdiaphragmatic viscera should improve the ability of neonates to survive the postoperative period.     

Blood and brain tissue gaseous strategy for profoundly hypothermic total circulatory arrest

Brain tissue carbon dioxide tension, pH, and oxygen tension were measured in dogs undergoing hypothermic circulatory arrest below 20 degrees C with three types of blood gas manipulation. During core cooling, dogs were given pure oxygen (group I, n = 8), 5% carbon dioxide in oxygen (group II, n = 10), or 7% carbon dioxide in oxygen (group III, n = 4). During core cooling, brain tissue carbon dioxide tension decreased significantly in group I. During circulatory arrest, carbon dioxide tension rose by 21.5 mm Hg in group I, 35.3 mm Hg in group II, and 57.0 mm Hg in group III, nearly doubling in each group. From the last 5 minutes of core cooling to the end of rewarming, carbon dioxide tension was significantly higher in groups II and III than in group I. Brain tissue pH fell by 0.33 to 0.35 during 60 minutes of circulatory arrest and did not recover in groups II and III. Brain tissue oxygen tension decreased significantly during the latter two thirds of the circulatory arrest period in all three groups. To reduce progressive tissue hypercapnia and acidosis during and after circulatory arrest, a more hyperventilatory manipulation of blood gases than that achieved by alpha-stat strategy was thought beneficial for core-cooling perfusion.     

Quantitative assessment of brain microvascular and tissue oxygenation during cardiac arrest and resuscitation in pigs

Cardiac arrest is associated with a very high rate of mortality, in part due to inadequate tissue perfusion during attempts at resuscitation. Parameters such as mean arterial pressure and end‐tidal carbon dioxide may not accurately reflect adequacy of tissue perfusion during cardiac resuscitation. We hypothesised that quantitative measurements of tissue oxygen tension would more accurately reflect adequacy of tissue perfusion during experimental cardiac arrest. Using oxygen‐dependent quenching of phosphorescence, we made measurements of oxygen in the microcirculation and in the interstitial space of the brain and muscle in a porcine model of ventricular fibrillation and cardiopulmonary resuscitation. Measurements were performed at baseline, during untreated ventricular fibrillation, during resuscitation and after return of spontaneous circulation. After achieving stable baseline brain tissue oxygen tension, as measured using an Oxyphor G4‐based phosphorescent microsensor, ventricular fibrillation resulted in an immediate reduction in all measured parameters. During cardiopulmonary resuscitation, brain oxygen tension remained unchanged. After the return of spontaneous circulation, all measured parameters including brain oxygen tension recovered to baseline levels. Muscle tissue oxygen tension followed a similar trend as the brain, but with slower response times. We conclude that measurements of brain tissue oxygen tension, which more accurately reflect adequacy of tissue perfusion during cardiac arrest and resuscitation, may contribute to the development of new strategies to optimise perfusion during cardiac resuscitation and improve patient outcomes after cardiac arrest.     

The effects of propofol or sevoflurane on the estimated cerebral perfusion pressure and zero flow pressure

The zero flow pressure (ZFP) is the pressure at which blood flow ceases through a vascular bed. Using transcranial Doppler ultrasonography, we investigated the effects of propofol or sevoflurane on the estimated cerebral perfusion pressure (eCPP) and ZFP in the cerebral circulation. Twenty-three healthy patients undergoing nonneurosurgical procedures under general anesthesia were studied. After induction of anesthesia using propofol, the anesthesia was maintained with either propofol infusion (n = 13) or sevoflurane (n = 10). Middle cerebral artery flow velocity, noninvasive arterial blood pressure, and end-tidal carbon dioxide partial pressure were recorded awake as a baseline, and during steady-state anesthesia at normocapnia (baseline end-tidal carbon dioxide partial pressure) and hypocapnia (1 kPa below baseline). The eCPP and ZFP were calculated using an established formula. The mean arterial blood pressure decreased in both groups. The eCPP decreased significantly in the propofol group (median, from 58 to 41 mm Hg) but not in the sevoflurane group (from 60 to 62 mm Hg). Correspondingly, ZFP increased significantly in the propofol group (from 25 to 33 mm Hg) and it decreased significantly in the sevoflurane group (from 27 to 7 mm Hg). Hypocapnia did not change eCPP or ZFP in the propofol group, but it significantly decreased eCPP and increased ZFP in the sevoflurane group.