End-tidal to Arterial Gradients and Alveolar Deadspace for Anesthetic Agents.

The ventilatory response to acute progressive hypoxia below the carbon dioxide threshold using rebreathing was investigated. Nine subjects rebreathed after 5 min of hyperventilation to lower carbon dioxide stores. The rebreathing bag initially contained enough carbon dioxide to equilibrate alveolar and arterial partial pressures of carbon dioxide to the lowered mixed venous partial pressure (approximately equal to 30 mmHg), and enough oxygen to establish a chosen end-tidal partial pressure (50-70 mmHg), within one circulation time. During rebreathing, end-tidal partial pressure of carbon dioxide increased while end-tidal partial pressure of oxygen fell. Ventilation increased linearly with end-tidal carbon dioxide above a mean end-tidal partial pressure threshold of 39 +/- 2.7 mmHg. Below this peripheral-chemoreflex threshold, ventilation did not increase, despite a progressive fall in end-tidal oxygen partial pressure to a mean of 37 +/- 4.1 mmHg. In conclusion, hypoxia does not stimulate ventilation when carbon dioxide is below its peripheral-chemoreflex threshold.

IS THE END-TIDAL PARTIAL PRESSURE OF ISOFLURANE A GOOD PREDICTOR OF ITS ARTERIAL PARTIAL PRESSURE?

The Big Match: Lung Ventilation and Blood Flow during Inhalational Anesthesia and Recovery-Is There a Winning Combination?

:Background:Both end-tidal carbon dioxide pressure (ETCO2) is used routinely as an indicator of arterial partial pressure of carbon dioxide (PaCO2) and thus adequacy of ventilation. Accurate determination of the PaCO2 level in neuroanesthesia is quite important because of its effect on cerebral blood flow and also hyperventilation is often used to reduce intracranial pressure in neurosurgical patients. This study was aimed to evaluate the relationship between ETCO2 and arterial PaCO2 in neurosurgical patients undergoing craniotomy to assess the predictive value of ETCO2 as an indicator of PaCO2 level.Methods:Forty-five consecutive adult patients with inclusion criteria, scheduled to undergo elective craniotomy surgery were enrolled in this prospective study. Measurements of PaCO2 and ETCO2 were performed at three different intervals: Time 1: 10 min after induction of general anesthesia; time 2: after cranium opening prior to dural incision; and at time 3: start of dural closure. All patients received the same anesthetic agent (propofol, sufentanil, atracurium, oxygen). Data were initially analyzed using Pearson’s Correlation to assess the relationship between PaCO2 and ETCO2 at different stages of the operation. A p-value (P) of less than 0.05 was considered significant. The agreement between the measures of CO2 was assessed using Bland-Altman method, where mean difference and average between PaCO2 and ETCO2 were calculated. The 95% confidence intervals for the lower and upper limits of agreement were presented.Results:A total of 44 patients, aged 18 to 65 years, ASA grades 1 and 2 were participated in the study. Mean difference, standard deviation and correlation coefficient of the parameters were calculated for three time periods. The values for PaCO2, ETCO2, (PaCO2- ETCO2), and correlation coefficient for 10 min after anesthetic induction, prior to dural incision, and start of dural closure were 35.4 ± 3.2, 32.1 ± 3.2, 3.8 ± 2.1, and 0.565, 36.2 ± 3.1, 32.6 ± 3.2,4.8 ± 3.1, and 0.574, and 36.7 ± 2.4, 33 ± 3.2,3.8 ± 2.3, and 0.627, respectively (p less than 0.01 for all analyses). The greatest mean difference occurred just prior to dural incision. The lowest mean difference was observed at 10 min post-anesthetic induction. Conclusions:To the present study was aimed to correlate between End-tidal and arterial carbon dioxide partial pressure in neurosurgical patients undergoing craniotomy. Findings of this study showed that ETCO2 consistently underestimates the value of PaCO2 during craniotomy indicating that ETCO2 value can be used instead of PaCO2.Keywords:End-tidal carbon dioxide pressure, Arterial partial pressure of carbon dioxide, Craniotomy

The aim of this study was to test whether a tidally ventilated homogeneous lung model can correctly describe arterial and end-tidal gas partial pressures and thus the difference in end-tidal and arterial gas partial pressures at rest and during exercise. The implemented mathematical modeling described variations during the breathing cycle in CO2 and O2 fractions, alveolar volume, and pulmonary capillary gas exchange. Experimental data were obtained from measurements performed by 17 healthy subjects at rest and during 40, 50, 65, and 75% exercise .VO(2max) on a cycle ergometer. VO2, VCO2, and PET,CO2 were continuously measured using the MedGraphics CPX/D gas exchange system. Arterial gases were measured in brachial artery blood samples drawn simultaneously with gas exchange. Cardiac output was measured using the CO2 rebreathing method corrected by the blood sample data. The model was driven using experimental data for ventilation, VO2, VCO2, and cardiac output. The mean difference and the upper and lower limits of agreement between measured and simulated data were -0.004, +0.84, and -0.84 Torr for Pa,CO2; -0.06, +0.64, and -0.76 Torr for Pa,O2; -1.96, +2.84, and -6.76 Torr for PET,CO2; and +7.20, +25.80, and -11.40 Torr for PET,O2. Actual PET,CO2-Pa,CO2 difference increased significantly with workload (P < 0.0001) from 0.3 +/- 3 Torr at rest to 4.7 +/- 2.5 Torr at 75% .VO(2max). Model-simulated PET,CO2-Pa,CO2 difference also increased significantly with exercise (P < 0.0001) from 0.7 +/- 1.7 Torr at rest to 9.1 +/- 3.4 Torr at 75% .VO(2max). The lung model described actual arterial CO2 partial pressures better than variations in end-tidal CO2 partial pressures and thus better than the gradient in end-tidal arterial CO2 partial pressures.

Inefficiency of lung gas exchange during general anesthesia is reflected in alveolar (end-tidal) to arterial (end-tidal-arterial) partial pressure gradients for inhaled gases, resulting in an increase in alveolar deadspace. Ventilation-perfusion mismatch is the main contributor to this, but it is unclear what contribution arises from diffusion limitation in the gas phase down the respiratory tree (longitudinal stratification) or at the alveolar-capillary barrier, especially for gases of high molecular weight such as volatile anesthetics. The contribution of longitudinal stratification was examined by comparison of end-tidal-arterial partial pressure gradients for two inhaled gases with similar blood solubility but different molecular weights: desflurane and nitrous oxide, administered together at 2 to 3% and 10 to 15% inspired concentration (FiG), respectively, in 17 anesthetized ventilated patients undergoing cardiac surgery before cardiopulmonary bypass. Simultaneous measurements were done of tidal gas concentrations, of arterial and mixed venous blood partial pressures by headspace equilibration, and of gas uptake rate calculated using the direct Fick method using thermodilution cardiac output measurement. Adjustment for differences between the two gases in FiG and in lung uptake rate (VG) was made on mass balance principles. A 20% larger end-tidal-arterial partial pressure gradient relative to inspired concentration (PetG - PaG)/FiG for desflurane than for N2O was hypothesized as physiologically significant. Mean (SD) measured (PetG - PaG)/FiG for desflurane was significantly smaller than that for N2O (0.86 [0.37] vs. 1.65 [0.58] mmHg; P < 0.0001), as was alveolar deadspace for desflurane. After adjustment for the different VG of the two gases, the adjusted (PetG - PaG)/FiG for desflurane remained less than the 20% threshold above that for N2O (1.62 [0.61] vs. 1.98 [0.69] mmHg; P = 0.028). No evidence was found in measured end-tidal to arterial partial pressure gradients and alveolar deadspace to support a clinically significant additional diffusion limitation to lung uptake of desflurane relative to nitrous oxide.

Objective To analyze the effect of different tidal volume and low levels of end expiratory positive pressure ventilation on respiratory function in laparoscopic surgery under general anesthesia, to provide reference for the selection of ventilation modes of laparoscopic operation in general anesthesia. Methods Ninety-six patients who received general anesthesia were selected from August 2013 to June 2016. According to the random number table method, they were divided into observation group (n=48) and control group (n=48). Mechanical ventilation after tracheal intubation was performed in the two groups, and tidal volume was 9 ml/kg and respiratory frequency was 12 times/min before pneumoperitoneum, after pneumoperitoneum, the tidal volume changed to 6 ml/kg, respiratory frequency changed to 14 times/ min in observation group, but the ventilation parameters of control group were unchanged. The heart rate (HR), mean arterial pressure (MAP), arterial oxygen partial pressure (PaO2), arterial carbon dioxide partial pressure (PaCO2), end expiratory carbon dioxide partial pressure (PetCO2), Alveolar arterial oxygen partial pressure (A-aDO2), oxygenation index and respiratory index, jugular venous oxygen points pressure(PjvO2), internal carotid venous oxygen saturation(SjvO2), jugular venous oxygen content (CjvO2), cerebral arterial venous oxygen content difference (Da-jvO2) index were compared between the two groups before pneumoperitoneum, 30 min after pneumoperitoneum and 60 min after pneumoperitoneum. Results Before pneumoperitoneum, 30 min after pneumoperitoneum and 60 min after pneumoperitoneum, HR and MAP of the two groups had no statistically significant difference(P>0.05); 30 min and 60 min after pneumoperitoneum, PaO2, PaCO2, PetCO2, A-aDO2, oxygen index and respiratory index of observation group were better than those of control group, the differences were significant (P<0.05); 30 min and 60 min after pneumoperitoneum, PjvO2, SjvO2 and CjvO2 of observation group were higher than those of control group, Da-jvO2 was lower than that of control group, and the differences were significant (P<0.05). Conclusions Low tidal volume and low levels of end expiratory positive pressure ventilation can improve the respiratory function and cerebral oxygen metabolism in patients with general anesthesia of laparoscopic surgery, and has a high practical value, it is worth popularization and application. Key words: Anesthesia; Low level of positive end expiratory pressure; Tidal volume; Respiratory function

Cardiorespiratory changes induced by pneumoperitoneum and head-up tilt may generate alveolar ventilation to perfusion ratio changes and increased systemic vascular resistances. The reliability of end-tidal carbon dioxide tension and pulse oximetry in predicting arterial carbon dioxide partial pressure and arterial oxygen saturation may therefore be affected. The 35 ASA 1-2 patients in this study comprised 12 men and 23 women aged 48 (SD 17) years and weighing 71 (SD 14) kg. Twenty-nine were to undergo upper abdominal laparoscopy for cholecystectomy and six hyperselective vagotomy. Intra-abdominal pressure was 1.7 (SD 0.9) kPa and head-up tilt was 5.6 (SD 4.2) degrees. After abdominal insuflation, arterial carbon dioxide partial pressure significantly increased (p < 0.05). However, the arterial carbon dioxide partial pressure-end-tidal carbon dioxide partial pressure gradient remained constant throughout surgery. This gradient was highly correlated with arterial carbon dioxide partial pressure (p < 0.0001), but was not correlated with elapsed time, intra-abdominal pressure or head-up tilt. Arterial oxygen saturation was always greater than 95% in all patients and the arterial oxygen saturation-pulse oximetric saturation gradient was always less than or equal to +4%. In conclusion, end-tidal carbon dioxide partial pressure and pulse oximetric saturation allow reliable monitoring of arterial carbon dioxide partial pressure and arterial oxygen saturation in the absence of pre-existing cardiopulmonary disease and/or acute peroperative disturbance.

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.

Objective To analyze the value of the waveform curve and quantitative value of end-respiratory carbon dioxide partial pressure (PETCO2) in resuscitation monitoring of patients with general anesthesia. Methods One hundred and forty-two patients who performed operation under general anesthesia and entered into the anesthesia recovery room in Zhejiang Xin′an International Hospital from April 2019 to September 2019 were selected. According to the method of random number table, all the 142 cases were divided into control group and observation group, with 71 cases in each group. Routine monitoring during general anaesthesia resuscitation such as blood pressure (BP), respiratory frequency (RR), blood oxygen saturation (SpO2), arterial partial pressure of carbon dioxide (PaCO2) was performed in the control group. On this basis, changes in PETCO2 waveform curve and quantitative value was continuously monitored in the observation group.The abnormal events rate, checkout time, anesthesia resuscitation time and residence time in the anesthesia recovery room of two groups during anesthesia resuscitation were recorded. Besides, the relationship between PETCO2 and PaCO2 was analyzed. Results The levels of RR, BP, SpO2, PaO2 in both groups were in the normal range during general anesthesia resuscitation, and PETCO2 in the observation group was also in the normal range. During general anesthesia resuscitation, the abnormal events rate in the observation group was was higher than that in the control group: 12.68%(9/71) vs. 7.04%(5/71); besides, the checkout time of abnormal events, anesthesia resuscitation time and residence time in the anesthesia recovery room in the observation group were shorter than those in the control group: (1.61 ± 0.52) min vs. (2.11 ± 0.69) min, (35.98 ± 10.66) min vs. (46.75 ± 15.03) min and (62.52 ± 19.63) min vs. (76.97 ± 15.41) min, there were significant differences (P<0.05). PETCO2 was negatively correlated with SpO2 (r=-0.335, P=0.004), while PETCO2 was positively correlated with PaCO2 (r=0.751, P<0.001). Conclusions Monitoring PETCO2 of patients during general anesthesia resuscitation can improve the detection rate and timeliness of abnormal events, promote the recovery of anesthesia and help to reduce the occurrence of adverse events. Key words: Anesthesia resuscitation; Recovery; End-respiratory carbon dioxide partial pressure; Arterial partial pressure of carbon dioxide

Arterial partial pressure alteration of CO2 ((Equation is included in full-text article.)) affects not only the cerebral blood flow velocity but also the systemic arterial blood pressure (BP). At the same time, BP can affect the cerebral blood flow. The objective of the present research is to study the impact of the (Equation is included in full-text article.)level on cerebrovascular CO2 reactivity ((Equation is included in full-text article.)) and BP as well as the impact of BP upon (Equation is included in full-text article.)alteration by hypercapnia and hypocapnia. Cerebral blood flow velocity was recorded by means of transcranial Doppler in both middle cerebral arteries (MCAv left and right). The mean arterial pressure (MAP) was studied using the finger photoplethysmography method, arterial blood oxygen saturation was estimated by the pulse oximetry method, and end-tidal (Equation is included in full-text article.)((Equation is included in full-text article.)) was measured with an infrared capnograph. After a recording of the reference values of all the parameters, all the volunteers underwent a rebreathing as well as a hyperventilation. At rest, (Equation is included in full-text article.)was 33.6 (SD 3.1) mmHg. At rebreathing, MCAv increased at 38 mmHg (Equation is included in full-text article.), MAP - at 43 mmHg (Equation is included in full-text article.). By hyperventilation, MCAv decreased at 28 mmHg (Equation is included in full-text article.), MAP - at 26 mmHg (Equation is included in full-text article.). When (Equation is included in full-text article.)reached 43 mmHg, (Equation is included in full-text article.)increased from 2.3 (SD 1.4) to 3.3 (SD 1.2)%/mmHg (P<0.01). When (Equation is included in full-text article.)decreased to 26 mmHg, (Equation is included in full-text article.)increased from -3.6 (SD 2.5) to -5.9 (SD 3.9)%/mmHg (P<0.01). Within the alteration of (Equation is included in full-text article.)above 43 and under 26 mmHg, BP increased and decreased, respectively, leading to a change in (Equation is included in full-text article.).

The position of the body during surgery may affect the patient's body functions, especially the hemodynamic parameters. We aimed to comparatively analyze the effects of lithotomy and prone position on respiratory mechanics, arterial oxygenation, and hemodynamic parameters in patients who underwent percutaneous nephrolithotomy (PNL).

Multicompartment computer models of heterogeneity in alveolar ventilation-perfusion ratios V̇ A /Q̇ scatter) across the lung explain the significant alveolar-arterial partial pressure gradients and associated alveolar dead-space fractions (V da /V a ) seen in anesthetized patients for both carbon dioxide and for anesthetic gases of different blood solubilities. However, the accuracy of a simpler two-compartment model of V̇ A /Q̇ scatter to do this has not been tested or compared to calculations from the traditional Riley model with "ideal," unventilated (shunt) and unperfused (dead-space) compartments. Measurements of gas partial pressures in inspired and expired gas and arterial and mixed venous blood from 29 patients undergoing inhalational general anesthesia for cardiac surgery were used to compare the accuracy of two simple models of V̇ A /Q̇ scatter and lung gas exchange in predicting measured alveolar and arterial partial pressure differences and the associated alveolar dead-space calculations for the modern anesthetic gases isoflurane, sevoflurane, and desflurane. These models were the Riley model and a two-compartment model with reciprocal proportions of allocation of V̇ A and Q̇, with and without additional true shunt. A multicompartment "log-normal" model was also tested. Mean (95% CI) of the measured alveolar dead-space fraction for the three anesthetic gases G combined (V da /V aG ) was 0.557 (0.523 to 0.592). Mean V da /V aG from the two-compartment model incorporating an additional true-shunt lung compartment (0.539 [0.498 to 0.580]) was similar to the measured value ( P = 0.347) and was 0.501 (0.457 to 0.546) without a true-shunt compartment. The log-normal model outputs were 0.491 (0.453 to 0.529). The Riley model outputs for V da /V aG severely underestimated this (0.327 [0.294 to 0.361]). Satisfactory prediction of the alveolar-arterial partial pressure gradients and alveolar dead space for the modern volatile anesthetic gases measured in vivo requires a model with more than one gas-exchanging lung compartment, which the traditional Riley model lacks. A simple "reciprocal" two-compartment model achieves this.

Inhalational anesthetics depress breathing dose dependently. The authors studied the dynamics of ventilation on changes in end-tidal sevoflurane partial pressure. To learn more about the mechanisms of sevoflurane-induced respiratory depression, the authors also studied its influence on the dynamic ventilatory response to carbon dioxide. Experiments were performed in cats anesthetized with alpha chloralose-urethane. For protocol 1, step changes in end-tidal sevoflurane partial pressure were applied and inspired ventilation was measured. Breath-to-breath inspired ventilation was related to the sevoflurane concentration in a hypothetical effect compartment based on an inhibitory sigmoid Emax model. For protocol 2, step changes in the end-tidal partial pressure of carbon dioxide were applied at 0, 0.5, and 1% end-tidal sevoflurane. The inspired ventilation-end-tidal partial pressure of carbon dioxide data were analyzed using a two-compartment model of the respiratory controller, which consisted of a fast peripheral and slow central compartment. Values are the mean +/- SD. In protocol 1, the effect-site half-life of respiratory changes caused by alterations in end-tidal sevoflurane partial pressure was 3.6+/-1.0 min. In protocol 2, at 0.50% sevoflurane, the central and peripheral carbon dioxide sensitivities decreased to 43+/-20% and 36+/-18% of control. At 1% sevoflurane, the peripheral carbon dioxide sensitivity decreased further, to 12+/-13% of control, whereas the central carbon dioxide sensitivity showed no further decrease. Steady state inspired ventilation is reached after 18 min (i.e., 5 half-lives) on stepwise changes in end-tidal sevoflurane. Anesthetic concentrations of sevoflurane have, in addition to an effect on pathways common to the peripheral and central chemoreflex loops, a selective effect on the peripheral chemoreflex loop. Sevoflurane has similar effects on ventilatory control in humans and cats.

Inert tracer gas exchange across the human respiratory system is simulated in an asymmetric lung model for different oscillatory breathing patterns. The momentary volume-averaged alveolar partial pressure (PA), the expiratory partial pressure (PE), the mixed expiratory partial pressure (PE), the end-tidal partial pressure (PET), and the mean arterial partial pressure (Pa), are calculated as functions of the blood-gas partition coefficient (lambda) and the diffusion coefficient (D) of the tracer gas. The lambda values vary from 0.01 to 330.0 inclusive, and four values of D are used (0.5, 0.22, 0.1, and 0.01). Three ventilation-perfusion conditions corresponding to rest and mild and moderate exercise are simulated. Under simulated exercise conditions, we compute a reversed difference between PET and Pa compared with the rest condition. This reversal is directly reflected in the relation between the physiological dead space fraction (1--PE/Pa) and the Bohr dead space fraction (1--PE/PET). It is argued that the difference (PET--Pa) depends on the lambda of the tracer gas, the buffering capacity of lung tissue, and the stratification caused by diffusion-limited gas transport in the gas phase. Finally some determinants for the reversed difference (PET--Pa) and the significance for conventional gas analysis are discussed.