Pre-oxygenation using high-flow nasal oxygen in parturients undergoing caesarean section in general anaesthesia: A prospective, multi-centre, pilot study.

BACKGROUND: Parturients undergoing caesarean section in general anaesthesia have an increased risk of desaturating during anaesthesia induction. Pre- and peri-oxygenation with high-flow nasal oxygen prolong the safe apnoea time but data on parturients undergoing caesarean section under general anaesthesia are limited. This pilot study aimed to investigate the clinical effects and frequency of desaturation in parturients undergoing caesarean section in general anaesthesia pre- and peri-oxygenated with high-flow nasal oxygen and compare this to traditional pre-oxygenation using a facemask. METHODS: In this prospective, non-randomised, multi-centre study we included pregnant women with a gestational age ≥30 weeks undergoing caesarean section under general anaesthesia. All parturients were asked to participate in the intervention group consisting of pre-oxygenation using high-flow nasal oxygen. Parturients declining participation were pre-oxygenated with a traditional facemask. Primary outcome was the proportion of parturients desaturating below 93% from start of pre-oxygenation until 1 min after tracheal intubation. Secondary outcomes investigated end-tidal oxygen concentrations after tracheal intubation and the proportion of parturients with signs of regurgitation. RESULTS: A total of 34 parturients were included, 25 pre- and peri-oxygenated with high-flow nasal oxygen and 9 pre-oxygenated with facemask. No difference in patient or airway characteristics could be seen except for a higher BMI in the high-flow nasal oxygen group (31.4 kg m-2 [4.7] vs. 27.7 kg m-2 [3.1]; p = .034). No woman in any of the two groups desaturated below 93%. The lowest peripheral oxygen saturation observed, in any parturient, was 97%. There was no difference detected in end-tidal oxygen concentration after tracheal intubation, 87% (6) in the high-flow nasal oxygen group vs 80% (15) in the facemask group (p = .308). No signs of regurgitation, in any parturient, were seen. CONCLUSION: Pre- and peri-oxygenation with high-flow nasal oxygen maintain adequate oxygen saturation levels during induction of anaesthesia also in parturients. Regurgitation of gastric content did not occur in any parturient and no other safety concerns were observed in this pilot study.

Cardiopulmonary haemodynamic effects and gas exchange during apnoeic oxygenation with high-flow and low-flow nasal oxygen: A large animal study.

BACKGROUND: Apnoeic oxygenation with high-flow nasal oxygen prolongs the safe apnoeic period during induction of general anaesthesia. However, central haemodynamic effects and the characteristics of central gaseous exchange remain unexplored. OBJECTIVE: To describe mean pulmonary arterial pressure along with arterial and mixed venous blood gases and central haemodynamic parameters during apnoeic oxygenation with low-flow and high-flow nasal oxygen in pigs. DESIGN: Experimental crossover study. SETTING: Animal study of 10 healthy Swedish landrace pigs at Karolinska Institutet, Sweden, April-May 2021. INTERVENTION: The pigs were anaesthetised, their tracheas intubated and their pulmonary arteries catheterised. The animals were preoxygenated and paralysed before apnoea. Apnoeic periods between 45 and 60 min were implemented with either 70 or 10 l min -1 100% O 2 delivered via nasal catheters. In addition, seven animals underwent an apnoea without fresh gas flow. Cardiopulmonary parameters and blood gases were measured repeatedly. MAIN OUTCOME MEASURES: Mean pulmonary arterial pressure during apnoeic oxygenation with high-flow and low-flow oxygen. RESULTS: Nine pigs completed two apnoeic periods of at least 45 min with a Pa O 2 not lower than 13 kPa. The mean pulmonary arterial pressure increased during 45 min of apnoea, from 18 ±â€Š1 to 33 ±â€Š2 mmHg and 18 ±â€Š1 to 35 ±â€Š2 mmHg, at 70 and 10 l min -1 O 2 , respectively ( P  < 0.001); there was no difference between the groups ( P  = 0.87). The Pa CO 2 increased by 0.48 ±â€Š0.07 and 0.52 ±â€Š0.04 kPa min -1 , at 70 and 10 l min -1 O 2 , respectively; there was no difference between the groups ( P  = 0.22). During apnoea without fresh gas flow, the SpO 2 declined to less than 85% after 155 ±â€Š11 s. CONCLUSION: During apnoeic oxygenation in pigs, the mean pulmonary arterial pressure increased two-fold and Pa CO 2 five-fold after 45 min, while the arterial oxygen levels were maintained over 13 kPa, irrespective of high-flow or low-flow oxygen.

Biomarkers for oxidative stress and organ injury during Transnasal Humidified Rapid-Insufflation Ventilatory Exchange compared to mechanical ventilation in adults undergoing microlaryngoscopy: A randomised controlled study.

BACKGROUND: Apnoeic oxygenation using Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE) during general anaesthesia prolongs the safe apnoeic period. However, there is a gap of knowledge how THRIVE-induced hyperoxia and hypercapnia impact vital organs. The primary aim of this randomised controlled trial was to characterise oxidative stress and, secondary, vital organ function biomarkers during THRIVE compared to mechanical ventilation (MV). METHODS: Thirty adult patients, American Society of Anesthesiologists (ASA) 1-2, undergoing short laryngeal surgery under general anaesthesia were randomised to THRIVE, FI O2 1.0, 70 L min-1 during apnoea or MV. Blood biomarkers for oxidative stress, malondialdehyde and TAC and vital organ function were collected (A) preoperatively, (B) at procedure completion and (C) at PACU discharge. RESULTS: Mean apnoea time was 17.9 (4.8) min and intubation to end-of-surgery time was 28.1 (12.8) min in the THRIVE and MV group, respectively. Malondialdehyde increased from 11.2 (3.1) to 12.7 (3.1) µM (P = .02) and from 9.5 (2.2) to 11.6 (2.6) µM (P = .003) (A to C) in the THRIVE and MV group, respectively. S100B increased from 0.05 (0.02) to 0.06 (0.02) µg L-1 (P = .005) (A to C) in the THRIVE group. No increase in TAC, CRP, leukocyte count, troponin-T, NTproBNP, creatinine, eGFRcrea or NSE was demonstrated during THRIVE. CONCLUSION: While THRIVE and MV was associated with increased oxidative stress, we found no change in cardiac, inflammation or kidney biomarkers during THRIVE. Further evaluation of stress and inflammatory response and cerebral and cardiac function during THRIVE is needed.

Lung volume changes in Apnoeic Oxygenation using Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE) compared to mechanical ventilation in adults undergoing laryngeal surgery.

BACKGROUND: Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE) using high-flow 100% oxygen during apnoea has gained increased use during difficult airway management and laryngeal surgery due to a slower carbon dioxide rise compared to traditional apnoeic oxygenation. We have previously demonstrated high arterial oxygen partial pressures and an increasing arterial-alveolar carbon dioxide difference during THRIVE. Primary aim of this study was to characterise lung volume changes measured with electrical impedance tomography during THRIVE compared to mechanical ventilation. METHODS: Thirty adult patients undergoing laryngeal surgery under general anaesthesia were randomised to THRIVE or mechanical ventilation. Subjects were monitored with electrical impedance tomography and repeated blood gas measurement perioperatively. The THRIVE group received 100% oxygen at 70 l min-1 during apnoea. The mechanical ventilation group was intubated and normoventilated with an FiO2 of 0.4. RESULTS: Mean age were 48.2 (19.9) and 51.3 (12.3) years, and BMI 26.0 (4.5) and 26.0 (3.9) in the THRIVE and mechanical ventilation group respectively. Mean apnoea time in the THRIVE group was 17.9 (4.8) min. Mean apnoea to end-of-surgery time was 28.1 (12.8) min in the mechanical ventilation group. No difference in delta End Expiratory Lung Impedance was seen between groups over time. In the THRIVE group all but three subjects were well oxygenated during apnoea. THRIVE was discontinued for the three patients who desaturated. CONCLUSIONS: No difference in lung volume change over time, measured by electrical impedance tomography, was detected when using THRIVE compared to mechanical ventilation during laryngeal surgery.

Upper Airway Collapsibility during Dexmedetomidine and Propofol Sedation in Healthy Volunteers: A Nonblinded Randomized Crossover Study.

BACKGROUND: Dexmedetomidine is a sedative promoted as having minimal impact on ventilatory drive or upper airway muscle activity. However, a trial recently demonstrated impaired ventilatory drive and induction of apneas in sedated volunteers. The present study measured upper airway collapsibility during dexmedetomidine sedation and related it to propofol. METHODS: Twelve volunteers (seven female) entered this nonblinded, randomized crossover study. Upper airway collapsibility (pharyngeal critical pressure) was measured during low and moderate infusion rates of propofol or dexmedetomidine. A bolus dose was followed by low (0.5 µg · kg · h or 42 µg · kg · min) and moderate (1.5 µg · kg · h or 83 µg · kg · min) rates of infusion of dexmedetomidine and propofol, respectively. RESULTS: Complete data sets were obtained from nine volunteers (median age [range], 46 [23 to 66] yr; body mass index, 25.4 [20.3 to 32.4] kg/m). The Bispectral Index score at time of pharyngeal critical pressure measurements was 74 ± 10 and 65 ± 13 (mean difference, 9; 95% CI, 3 to 16; P = 0.011) during low infusion rates versus 57 ± 16 and 39 ± 12 (mean difference, 18; 95% CI, 8 to 28; P = 0.003) during moderate infusion rates of dexmedetomidine and propofol, respectively. A difference in pharyngeal critical pressure during sedation with dexmedetomidine or propofol could not be shown at either the low or moderate infusion rate. Median (interquartile range) pharyngeal critical pressure was -2.0 (less than -15 to 2.3) and 0.9 (less than -15 to 1.5) cm H2O (mean difference, 0.9; 95% CI, -4.7 to 3.1) during low infusion rates (P = 0. 595) versus 0.3 (-9.2 to 1.4) and -0.6 (-7.7 to 1.3) cm H2O (mean difference, 0.0; 95% CI, -2.1 to 2.1; P = 0.980) during moderate infusion of dexmedetomidine and propofol, respectively. A strong linear relationship between pharyngeal critical pressure during dexmedetomidine and propofol sedation was evident at low (r = 0.82; P = 0.007) and moderate (r = 0.90; P < 0.001) infusion rates. CONCLUSIONS: These observations suggest that dexmedetomidine sedation does not inherently protect against upper airway obstruction.

Sedation with Dexmedetomidine or Propofol Impairs Hypoxic Control of Breathing in Healthy Male Volunteers: A Nonblinded, Randomized Crossover Study.

BACKGROUND: In contrast to general anesthetics such as propofol, dexmedetomidine when used for sedation has been put forward as a drug with minimal effects on respiration. To obtain a more comprehensive understanding of the regulation of breathing during sedation with dexmedetomidine, the authors compared ventilatory responses to hypoxia and hypercapnia during sedation with dexmedetomidine and propofol. METHODS: Eleven healthy male volunteers entered this randomized crossover study. Sedation was administered as an intravenous bolus followed by an infusion and monitored by Observer's Assessment of Alertness/Sedation (OAA/S) scale, Richmond Agitation Sedation Scale, and Bispectral Index Score. Hypoxic and hypercapnic ventilatory responses were measured at rest, during sedation (OAA/S 2 to 4), and after recovery. Drug exposure was verified with concentration analysis in plasma. RESULTS: Ten subjects completed the study. The OAA/S at the sedation goal was 3 (3 to 4) (median [minimum to maximum]) for both drugs. Bispectral Index Score was 82 ± 8 and 75 ± 3, and the drug concentrations in plasma at the sedation target were 0.66 ± 0.14 and 1.26 ± 0.36 µg/ml for dexmedetomidine and propofol, respectively. Compared with baseline, sedation reduced hypoxic ventilation to 59 and 53% and the hypercapnic ventilation to 82 and 86% for dexmedetomidine and propofol, respectively. In addition, some volunteers displayed upper airway obstruction and episodes of apnea during sedation. CONCLUSIONS: Dexmedetomidine-induced sedation reduces ventilatory responses to hypoxia and hypercapnia to a similar extent as sedation with propofol. This finding implies that sedation with dexmedetomidine interacts with both peripheral and central control of breathing.