Changes In Carbon Dioxide Tension Research Articles

Respiratory Changes under Spinal Anaesthesia for Laparoscopic Gynaecological Procedures- a comparison with General Anaesthesia

Background: Laparoscopic surgery has become a frequently applied technique for a wide field ofindications. The procedure has become the gold standard for many procedures, with some of the mostcommon being gynecological procedures and appendectomy. Laparoscopic procedures that are widelyused in gynecological surgery are commonly applied under general anesthesia (GA). Now a days spinalanaesthesia (SAB) has become a routine technique for healthy patients. It is currently presumed thatspinal anaesthesia can compromise respiratory muscle function during carbon dioxide (CO2)pneumoperitoneum and causes some respiratory changes. Objective: This study was designed to compare the respiratory effects of CO2 pneumoperitoneumunder spinal anaesthesia with general anaesthesia for short duration (<1hr) laparoscopicgynaecological procedures. Methods: A total number of sixty female patients, thirty in each group of ASA grade I & II wereenrolled for the study. Group I patients received lumber SAB with 15 mg heavy bupivacaine and 25mcg fentanyl. Group II patients received standard general anaesthesia with propofol, halothane andfentanyl. Baseline heart rate, blood pressure, respiratory rate, ETCO2 & SPO2 were noted in allpatients. Arterial blood gas analysis was done at time 0, 20 and 40 min after initiation ofpneumoperitoneum. Continuous ECG, pulse oximetry, noninvasive blood pressure, and ETCO2 weremonitored during the procedure. Any per operative and post-operative side effects were recorded andmanaged. Results: There were no observed changes in the respiratory rate. In group I, ETCO2 increased in astepwise manner over the first 10 min and reached a plateau between 15th and 30th min and declinedafter deflation of pneumoperitoneum. Arterial CO2 tension also increased at 20 min with significantchanges (p=0.000) in arterial to end tidal carbon dioxide tension. ETCO2 and arterial carbon dioxidetension changes were almost similar in both groups. Conclusion: Arterial and end-tidal CO2 tension changes during lower abdominal laparoscopicsurgery under SAB remain within physiological limits and comparable to the CO2 tension under GA.SAB may be adopted in ASA physical status I and II patients with proper preoperative counseling.Hence it is a safe alternative to GA with minimum respiratory alterations. JBSA 2021; 34 (2) : 10-15

Arterial and end-tidal Carbon Dioxide Tension Changes during Spinal Anaesthesia in Upper Abdominal Laparoscopic Surgeries: A Comparison with General Anaesthesia


 Nowadays, laparoscopic surgeries are being performed under subarachnoid block (SAB) safely.
 Aims: This study was to compare the arterial and end-tidal carbon dioxide (CO2) tension changes during spinal and general anaesthesia (GA) in CO2 pneumoperitoneum for upper abdominal laparoscopic surgeries.
 Settings and Design: This was a prospective randomized comparative clinical study.
 Materials and Methods: Eighty patients posted for upper abdominal laparoscopic surgeries were randomly allocated to two groups either to receive standard GA or lumbar SAB.
 Results: The demographic profiles of both the groups were comparable. The PaCO2 was increased gradually and sustained at its peaks within 20±4.37 minutes in both the groups. The mean±SD revealed to be higher in Group B (41.5500±2.1315) than Group A (40.8460±2.1136), but the difference between the two was not statistically significant (P=0.6142). There was a gradual increase in ETCO2 over the initial 10±2.07 minutes and reached a plateau within 20±5.74 minutes in both the groups and declined faster after deflation of pneumoperitoneum in SAB group. The mean±SD was found to be higher in Group B (33.923±1.642) than Group A (33.408±1.772), but it was also not statistically significant (P=0.4492). The difference of the arterial blood pH between the groups was not statistically significant. Three (7.5%) patients developed transient urinary retention and 2 (5%) patients suffered from post-dural puncture headache in SAB group.
 Conclusions: Arterial and end-tidal CO2 tension changes during upper abdominal laparoscopic surgery under SAB remain within physiological limit and comparable to the CO2 tensions under GA. However, per-operative complications in SAB are greater, while it is lesser in postoperative period in comparison to GA. SAB may be adopted in ASA physical status I patients with proper preoperative counselling.
 J Bangladesh Coll Phys Surg 2019; 37(1): 13-18
 

Anatomy, physiology, and genetics of paragangliomas

Paragangliomas arise from an extra-adrenal paraganglionic cells, derived from the neural crest of the autonomic nervous system and make up the most common class of benign vascular neoplasms of the neck. PGLs of the head and neck originate most commonly from the paraganglia within the carotid body, the jugular foramen, the middle ear and the vagus nerve. Knowledge of the embryology, anatomy and genetics of these rare tumors is paramount to successful diagnosis and treatment of head and neck paragangliomas.

Cerebral vasomotor reactivity: steady-state versus transient changes in carbon dioxide tension.

New FindingsWhat is the central question of this study?The relationship between changes in cerebral blood flow and arterial carbon dioxide tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady-state and transient increases in carbon dioxide tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia.What is the main finding and its importance?The cerebrovascular response is similar between steady-state and transient hypercapnia. However, hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.Cerebral vasomotor reactivity (CVMR) to changes in arterial carbon dioxide tension () is assessed during steady-state or transient changes in . This study tested the following two hypotheses: (i) that CVMR during steady-state changes differs from that during transient changes in ; and (ii) that CVMR during rebreathing-induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end-tidal carbon dioxide tension () middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versus ) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady-state increases in of 5 and 10 Torr above baseline; and (ii) rebreathing-induced transient breath-by-breath increases in . The linear regression for CBFV versus (P = 0.65) and CVCI versus (P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versus (P < 0.01) and CVCI versus (P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in is similar regardless of the employed methodology to induce changes in and that hyperventilation-induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing-induced hypercapnia.

Cerebral Oxygen Saturation: Graded Response to Carbon Dioxide with Isoxia and Graded Response to Oxygen with Isocapnia

BackgroundMonitoring cerebral saturation is increasingly seen as an aid to management of patients in the operating room and in neurocritical care. How best to manipulate cerebral saturation is not fully known. We examined cerebral saturation with graded changes in carbon dioxide tension while isoxic and with graded changes in oxygen tension while isocapnic.Methodology/Principal FindingsThe study was approved by the Research Ethics Board of the University Health Network at the University of Toronto. Thirteen studies were undertaken in healthy adults with cerebral oximetry by near infrared spectroscopy. End-tidal gas concentrations were manipulated using a model-based prospective end-tidal targeting device. End-tidal carbon dioxide was altered ±15 mmHg from baseline in 5 mmHg increments with isoxia (clamped at 110±4 mmHg). End-tidal oxygen was changed to 300, 400, 500, 80, 60 and 50 mmHg under isocapnia (37±2 mmHg). Twelve studies were completed. The end-tidal carbon dioxide versus cerebral saturation fit a linear relationship (R2 = 0.92±0.06). The end-tidal oxygen versus cerebral saturation followed log-linear behaviour and best fit a hyperbolic relationship (R2 = 0.85±0.10). Cerebral saturation was maximized in isoxia at end-tidal carbon dioxide of baseline +15 mmHg (77±3 percent). Cerebral saturation was minimal in isocapnia at an end-tidal oxygen tension of 50 mmHg (61±3 percent). The cerebral saturation during normoxic hypocapnia was equivalent to normocapnic hypoxia of 60 mmHg.Conclusions/SignificanceHypocapnia reduces cerebral saturation to an extent equivalent to moderate hypoxia.

Secondary Responses to Altered Acid-Base Status

Each of the four canonical acid-base disorders expresses as a primary change in carbon dioxide tension or plasma bicarbonate concentration followed by a secondary response in the countervailing variable. Quantified empirically, these secondary responses are directional and proportional to the primary changes, run a variable time course, and tend to minimize the impact on body acidity engendered by the primary changes. Absence of an appropriate secondary response denotes the coexistence of an additional acid-base disorder. Here we address the expected magnitude of the secondary response to each cardinal acid-base disorder in humans and offer caveats for judging the appropriateness of each secondary response.

Lingual, Splanchnic, and Systemic Hemodynamic and Carbon Dioxide Tension Changes During Endotoxic Shock and Resuscitation

Lingual, Splanchnic, and Systemic Hemodynamic and Carbon Dioxide Tension Changes During Endotoxic Shock and Resuscitation

Lingual, splanchnic, and systemic hemodynamic and carbon dioxide tension changes during endotoxic shock and resuscitation.

Sublingual and intestinal mucosal blood flow and Pco(2) were studied in a canine model of endotoxin-induced circulatory shock and resuscitation. Sublingual Pco(2) (Ps(CO(2))) was measured by using a novel fluorescent optrode-based technique and compared with lingual measurements obtained by using a Stowe-Severinghaus electrode [lingual Pco(2) (Pl(CO(2)))]. Endotoxin caused parallel changes in cardiac output, and in portal, intestinal mucosal, and sublingual blood flow (Q(s)). Different blood flow patterns were observed during resuscitation: intestinal mucosal blood flow returned to near baseline levels postfluid resuscitation and decreased by 21% after vasopressor resuscitation, whereas Q(s) rose to twice that of the preshock level and was maintained throughout the resuscitation period. Electrochemical and fluorescent Pco(2) measurements showed similar changes throughout the experiments. The shock-induced increases in Ps(CO(2)) and Pl(CO(2)) were nearly reversed after fluid resuscitation, despite persistent systemic arterial hypotension. Vasopressor administration induced a rebound of Ps(CO(2)) and Pl(CO(2)) to shock levels, despite higher cardiac output and Q(s), possibly due to blood flow redistribution and shunting. Changes in Pl(CO(2)) and Ps(CO(2)) paralleled gastric and intestinal Pco(2) changes during shock but not during resuscitation. We found that the lingual, splanchnic, and systemic circulations follow a similar pattern of blood flow variations in response to endotoxin shock, although discrepancies were observed during resuscitation. Restoration of systemic, splanchnic, and lingual perfusion can be accompanied by persistent tissue hypercarbia, mainly lingual and intestinal, more so when a vasopressor agent is used to normalize systemic hemodynamic variables.

Cerebral Vascular Responses to Changes in Carbon Dioxide Tension in Term and Preterm Infants with Apnea

Carbon dioxide (CO₂) plays important roles in regulating both respiratory drive and cerebral blood flow. These effects are mediated, in part, by activity of the sympathetic nervous system. We hypothesized that the presence of acute life-threatening events or apnea in term or preterm infants, respectively, would serve as a marker for immaturity of cerebral autonomic innervation and that such infants would display a reduced cerebral vascular response to elevated pCO₂. Therefore, we evaluated the cerebral vascular response during CO₂ challenge tests in groups of term and preterm infants with primary apnea. In term infants (39 ± 2 weeks gestation) with acute life-threatening events, elevated pCO₂ was accompanied by decreasing pulsatility index and increasing mean anterior cerebral blood flow velocity. However, in preterm infants (29 ± 2 weeks’ gestation) with apnea, pulsatility index and anterior cerebral artery flow velocity did not significantly change in response to CO₂ supplementation. We conclude that preterm, but not term, infants with apnea exhibit impaired vascular responses to hypercarbia.

Dissociation between respiratory effort and dyspnoea in a subset of patients with stroke.

Dyspnoea is not a prominent complaint of resting patients with recent hemispheric stroke (RHS). We hypothesized that, in patients with RHS presenting abnormalities in respiratory mechanics, increased respiratory motor output could translate into an increased perception of dyspnoea. We studied eight wheelchair-bound patients with RHS (mean age 62.4 years), previously evaluated by computerized tomography scanning, and a control group of normal subjects, matched for age and sex. We assessed routine spirometry, inspiratory and expiratory muscle pressures, breathing pattern and dyspnoea using a modified Borg scale. In six patients, we also measured oesophageal pressure during the maximal sniff manoeuvre and tidal inspiratory swing, and mechanical characteristics of the lung in terms of dynamic elastance during both quiet breathing and a hypercapnic/hyperoxic rebreathing test. During room air breathing, ventilation and tidal volume were similar in patients and controls, while tidal inspiratory swings of oesophageal pressure, an index of inspiratory motor output, were greater in patients ( P =0.005). Patients also exhibited a greater dynamic elastance ( P =0.013). During rebreathing, dynamic elastance remained higher ( P =0.01) and a greater than normal inspiratory motor output was found ( P =0.03). Responses of ventilation and tidal volume to carbon dioxide tension were normal, and in all patients but one a lower Borg score for the unit change in carbon dioxide tension and ventilation was found. In conclusion, a higher than normal inspiratory motor output was unexpectedly associated with a blunted perception of dyspnoea in this subset of RHS patients. This is likely to be due to the modulation of the integration process of respiratory sensation.

Ventilatory and cerebrovascular responses in normocapnic and hypercapnic COPD patients.

This study investigated the hypothesis that hypercapnia in some chronic obstructive pulmonary disease (COPD) patients may be related to a high cerebrovascular response to carbon dioxide (CO2). The relationship between responses of ventilation and of cerebral blood volume (CBV) to acute changes in carbon dioxide tension in arterial blood (Pa,CO2) was measured in 17 chronic hypercapnic (Pa,CO2 >6.0 kPa) and 16 normocapnic (Pa,CO2 < or = 6.0 kPa) COPD patients, who were matched for degree of airway obstruction (forced expiratory volume in one second 27% predicted). Results were compared with 15 age-matched healthy subjects. CBV was measured using near infrared spectroscopy during normo- and hypercapnia and related to inspired minute ventilation (V'I) and mouth occlusion pressure (P0.1). Hypercapnia (end-tidal pressure of carbon dioxide (deltaPET,CO2) > 1 kPa) was induced by giving adequate amounts of CO2 in the inspired air. During normocapnia, CBV (mL x 100 g(-1)) was 2.41+/- 0.66 and 2.90 +/- 0.60 (mean +/- SD) in the normocapnic and chronic hypercapnic patients, respectively, which was significantly lower compared to healthy subjects (3.53 +/- 0.77). All slopes of CO2 responsiveness (deltaCBV/deltaPa,CO2, deltaV'I/deltaPa,CO2, deltaP0.1/deltaPa,CO2) were significantly lower in both COPD groups relative to healthy subjects, but were not significantly different between the COPD groups. A poor but positive correlation between ventilatory and cerebrovascular CO2 responsiveness (deltaCBV/deltaPa,CO2 and deltaV'I/deltaPa,CO2) was found in COPD patients and healthy subjects. The findings do not support the hypothesis of abnormal cerebrovascular responses to carbon dioxide in hypercapnic chronic obstructive pulmonary disease patients.

Society of Neurosurgical Anesthesia and Critical Care

Society of Neurosurgical Anesthesia and Critical Care

Changes in carbon dioxide tension and oxygen saturation during deep sedation for paediatric cardiac catheterization.

The purpose of this observational study was to determine whether hypercarbia or oxygen desaturation occurred during our current regimens of deep sedation or general anaesthesia of infants and children undergoing cardiac catheterization. Data were gathered prospectively from 50 consecutive infants and children aged 4 months to 12 years undergoing cardiac catheterization. Several anaesthetists used the following regimens, which were not randomized: 1) propofol. 1.5-2.0 mg.kg-1 and fentanyl 1 microgram.kg-1 IV over 2 min for induction, followed by propofol infusion of 100-150 micrograms.kg-1.min-1; 2) fentanyl 2-3 micrograms.kg-1 and midazolam 0.1-0.2 mg.kg-1 IV over 10-15 min; 3) ketamine 8 mg.kg-1 IM, or 4) same as regimens 1 or 2, plus pancuronium, intubation and controlled ventilation. Regimens 1, 2, and 3 were associated with spontaneous ventilation through the natural airway. End-tidal carbon dioxide tension (PetCO2), SpO2, and respiratory rate were monitored for 60 min. The three regimens employing spontaneous ventilation through the natural airway were associated with both statistically and clinically significant increases in PetCO2 and decreases in SpO2. This raises the possibility that acute exacerbation of PAP and PVR may occur in pulmonary hypertensive patients. In contrast, PetCO2 and SpO2 did not change significantly from baseline in the controlled ventilation group.

Epinephrine-mediated changes in carbon dioxide tension during reperfusion of ventricular fibrillation in a canine model

Previous studies suggest that epinephrine may alter the correlation of perfusion with measures of PCO2 during cardiopulmonary resuscitation. This study investigated the effects of epinephrine on PaCO2 and mixed venous PCO2 in a high-flow reperfusion model of cardiac arrest. Prospective, block randomized, blinded, placebo-controlled, laboratory study. Thirty mixed breed canines. After a 12-min ventricular fibrillation cardiac arrest, 30 mixed breed canines were reperfused with standardized (3200 revolutions/min) cardiopulmonary bypass and were given placebo (n = 10), standard dose epinephrine (0.02 mg/kg; n = 10), or high-dose epinephrine (0.2 mg/kg; n = 10). Arterial and mixed venous blood gases, coronary perfusion pressure, pump flow and peripheral vascular resistance were compared between groups during the early reperfusion period using analysis of variance with a post hoc Tukey's multiple comparison test. Baseline variables were similar between groups. With reperfusion, the high-dose epinephrine group had higher coronary perfusion pressures (p < .002), lower systemic pump flow (p < .01), and higher peripheral vascular resistance (p < .001). In the high-dose epinephrine group, both PaCO2 (high-dose epinephrine, 40 +/- 6 torr [5.3 +/- 0.8 kPa]; standard dose epinephrine, 45 +/- 7 torr [6.0 +/- 0.9 kPa]; placebo, 54 +/- 4 torr [7.2 +/- 0.5 kPa]; p < .01) and mixed venous PCO2 (high-dose epinephrine, 55 +/- 10 torr [7.3 +/- 1.3 kPa]; standard dose epinephrine, 57 +/- 9 torr [7.6 +/- 1.2 kPa]; placebo, 67 +/- 4 torr [8.9 +/- 0.5 kPa]; p < .05) were significantly decreased, and arterial pH, PaO2, and mixed venous PO2 were significantly increased compared with the placebo group. In this model, when ventilation and CO2 production are constant, the decrease in PaCO2 with epinephrine is due to decreased pulmonary blood flow (flow to membrane oxygenator) and peripheral shunting.

End-tidal carbon dioxide tension during laparoscopic cholecystectomy. Correlation with the baseline value prior to carbon dioxide insufflation.

An investigation of end-tidal carbon dioxide tension changes was carried out in 19 healthy adult patients undergoing laparoscopic cholecystectomy. Following induction of anaesthesia, and throughout surgery, the end-tidal carbon dioxide tension was continuously monitored by capnography. The value following carbon dioxide insufflation increased with time to reach a maximum value after 40 min. Correlation of the individual maximum end-tidal carbon dioxide tension during laparoscopy with the corresponding baseline value prior to carbon dioxide insufflation showed a positive linear relationship (correlation coefficient 0.86). The correlation showed that an end-tidal carbon dioxide tension of 5.32 kPa (40 mmHg) can be achieved during laparoscopy when the baseline value is adjusted to around 4.0 kPa (30 mmHg).

Cerebral blood volume response to changes in carbon dioxide tension before and during cardiopulmonary bypass in children, investigated by near infrared spectroscopy

Neurological impairment may occur following cardiopulmonary bypass (CPB) and the effect of CPB on cerebrovascular control may be important in the mechanism of cerebral injury. We have used near infrared spectroscopy (NIRS) to observe cerebral haemodynamics non-invasively before and during CPB. We measured the change in cerebral blood volume (CBV) associated with changing PaCO2 (CBVR). Patients (n = 19) were aged from 1 to 135 (median 14) months. The cerebral blood volume response was determined pre-operatively at normothermia under the influence of standardised anaesthesia employing isoflurane (up to ET conc 0.5%) and during steady-state hypothermic bypass (22-32 degrees C) at an arterial pump flow rate of 1.9-2.4 lm-2.min-1. Complete data was available for 10 patients. The relation between CBV, arterial carbon dioxide tension (PaCO2), mean arterial pressure (MAP) and central venous pressure (CVP) was examined using analysis of covariance (P < or = 0.05) was accepted as significant). The change in CBV associated with changing PaCO2 was corrected for the effects of MAP and CVP. Preoperatively the median CBVR was 0.130 (25th-75th percentile 0.079-0.243) ml.100 g-1.kPa-1 and during hypothermic bypass the median CBVR was 0.093 (25th-75th percentile 0.026-0.255) ml.100 g-1.kPa-1. These values were compared with our reference range derived for normal conscious children using the Kruskal-Wallis test. There was not statistically significant difference between the three groups (P = 0.35). These results, indicating preservation of CBVR during the conditions of anaesthesia and bypass used, are consistent with the observations of previous authors who measured cerebral blood flow response to carbon dioxide by a variety of other methods. Near infrared spectroscopy is proving to be a reliable, non-invasive technique for the investigation of cerebral haemodynamics during CPB.

Changes in cerebral oxygenation and cerebral blood volume during endotracheal suctioning in ventilated neonates.

The effect of endotracheal suctioning on cerebral haemodynamics was investigated in 29 newborn infants with a mean gestational age of 31 weeks (range 25-40 weeks). Prior to one of two suctioning procedures, the inspiratory fraction of oxygen was increased by 10%. Brain oxygenation and total haemoglobin concentration were estimated continuously by near infrared spectroscopy. Mean arterial blood pressure, arterial blood oxygen saturation and carbon dioxide tension were recorded simultaneously. Brain oxygenation decreased in parallel with arterial oxygen saturation during suctioning. Preoxygenation ameliorated the decrease in brain oxygenation and arterial oxygen saturation whereas there was no benefit with regard to the changes in total haemoglobin concentration, carbon dioxide tension or mean arterial pressure. Changes in total haemoglobin concentration were related closely to concomitant changes in carbon dioxide tension (p less than 0.0001) but unrelated to changes in mean arterial pressure or arterial oxygen saturation. Our findings suggest that cerebral blood volume may react to changes in carbon dioxide tension during endotracheal suctioning in mechanically ventilated neonates. Apparently, preoxygenation prior to suctioning does not ameliorate the stress in normoxic infants.

Differential contractile effects of changes in carbon dioxide tension on rat mesenteric resistance arteries precontracted with noradrenaline

The pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5(and -6)-carboxyfluorescein (BCECF) was used to measure intracellular pH (pHi) in rat mesenteric resistance arteries (internal diameter 152-289 microns) mounted in an isometric myograph for simultaneous measurements of force. Extracellular pH was measured using a pH-sensitive electrode. Experiments were designed to test contractile electrode. Experiments were designed to test contractile effects of changes in carbon dioxide tension (PCO2) on vessels precontracted with noradrenaline. An acute increase in PCO2 caused acute intracellular acidification and potentiation of contractility. The longer-term effect, however, was recovery of intracellular pH and vaso-relaxation. Opposite changes in tension and intracellular pH were observed by decreasing PCO2. Qualitatively similar changes in contractility were observed in response to changes in pHi induced by NH4Cl. Thus, effects on vessels precontracted with noradrenaline were biphasic. In another set of experiments, the amplitude of the transient responses to 50 microM noradrenaline in calcium-free media was significantly augmented by an increase in the PCO2, whereas the response to 5 microM noradrenaline 1 min after readdition of calcium to the medium was depressed by the rise in PCO2. These data suggest that acute intracellular acidification causes acute tension development and are consistent with the possibility that the biphasic response to changes in noradrenaline-induced contractility caused by changes in PCO2 may be ascribed to differential effects on calcium mobilisation processes.

Transcranial Doppler-estimated versus thermodilution-estimated cerebral blood flow during cardiac operations: Influence of temperature and arterial carbon dioxide tension

The ability of the noninvasive continuous transcranial Doppler technique to reflect changes in cerebral blood flow during cardiac operations was evaluated in seven adults. Middle cerebral artery blood flow velocity changes were compared with simultaneous thermodilution measurements of venous blood flow in the ipsilateral internal jugular vein during 11 preset stages of the procedure. Cerebral blood flow was varied by changes in arterial carbon dioxide tension and temperature. High-dose fentanyl-droperidol anesthesia and alpha-stat pH management were employed. To facilitate comparisons between the two methods, the individual awake values of middle cerebral artery flow velocity (45.1 +/- 3.3 cm/sec, mean +/- standard error of the mean) and jugular venous blood flow (382 +/- 37 ml/min) were normalized (100%). Cerebral metabolic rate for oxygen was calculated as the product of jugular arteriovenous oxygen content difference and middle cerebral artery flow velocity or jugular venous blood flow, respectively. The individual correlations between the two flow estimates varied between 0.76 and 0.87 (median 0.83), and the correlation of the combined data from all seven patients was 0.77 (p less than 0.0001). Variations in arterial carbon dioxide tension induced significant changes in the two flow estimates both during normothermia before cardiopulmonary bypass and at deep hypothermia (20 degrees C) during cardiopulmonary bypass. The significant arterial carbon dioxide tension changes had no significant effects either on Doppler- or thermodilution-estimated cerebral metabolic rate for oxygen. Deep hypothermia (20 degrees C) reduced Doppler- and thermodilution-estimated cerebral metabolic rate for oxygen to 22.0% +/- 3.9% and 20.6% +/- 6.9% of the awake levels, respectively. The study supports the validity of using middle cerebral arterial flow velocity changes as an estimate of changes in volume flow through the brain during cardiac operations.

Effect of Pco2-adjusted pH on the neonatal heart during hypothermic perfusion and ischemia

The effect of pH regulation on the function of the isolated neonatal heart during continuous hypothermic perfusion and arrest was tested in 3- to 6-day-old piglet hearts. Three groups of hearts were perfused from an adult support pig, with pH varied by a carbon dioxide/oxygen gas exchanger and temperature controlled by a heat exchanger. After control function studies were obtained at normothermia with a pH of 7.4, the hearts were cooled over 15 minutes to 10 degrees C. Hypothermic perfusion was maintained for 1 hour, followed by rewarming to 37 degrees C. In group 1 (n = 5), the alpha stat (neutral) model, the blood perfusate was maintained at a pH of 7.4 (calculated at 37 degrees C). In group 2, the alkaline model, the pH was maintained at 7.9, and in group 3, the pH-stat (acid) model, the pH was maintained at 7.0. In addition, the effect of 1 hour of hypothermic ischemia after hypothermic perfusion at a pH of 7.0 was evaluated in five hearts (group 4). After rewarming no significant difference was noted in functional recovery (group 1 = 93% +/- 5%, group 2 = 92% +/- 6%, group 3 = 96% +/- 5%, and group 4 = 95% +/- 2%), oxygen consumption, coronary resistance, lactate extraction, and myocardial extravascular water content. We conclude that neonatal heart function is resistant within the range of this study to changes in pH caused by changes in carbon dioxide tension during hypothermic perfusion and ischemia.