Carbon Dioxide Changes during High-flow Nasal Oxygenation in Apneic Patients: A Single-center Randomized Controlled Noninferiority Trial

Background Anesthesia studies using high-flow, humidified, heated oxygen delivered via nasal cannulas at flow rates of more than 50 l · min–1 postulated a ventilatory effect because carbon dioxide increased at lower levels as reported earlier. This study investigated the increase of arterial partial pressure of carbon dioxide between different flow rates of 100% oxygen in elective anesthetized and paralyzed surgical adults before intubation. Methods After preoxygenation and standardized anesthesia induction with nondepolarizing neuromuscular blockade, all patients received 100% oxygen (via high-flow nasal oxygenation system or circuit of the anesthesia machine), and continuous jaw thrust/laryngoscopy was applied throughout the 15-min period. In this single-center noninferiority trial, 25 patients each, were randomized to five groups: (1) minimal flow: 0.25 l · min–1, endotracheal tube; (2) low flow: 2 l · min–1, continuous jaw thrust; (3) medium flow: 10 l · min–1, continuous jaw thrust; (4) high flow: 70 l · min–1, continuous jaw thrust; and (5) control: 70 l · min–1, continuous laryngoscopy. Immediately after anesthesia induction, the 15-min apnea period started with oxygen delivered according to the randomized flow rate. Serial arterial blood gas analyses were drawn every 2 min. The study was terminated if either oxygen saturation measured by pulse oximetry was less than 92%, transcutaneous carbon dioxide was greater than 100 mmHg, pH was less than 7.1, potassium level was greater than 6 mmol · l–1, or apnea time was 15 min. The primary outcome was the linear rate of mean increase of arterial carbon dioxide during the 15-min apnea period computed from linear regressions. Results In total, 125 patients completed the study. Noninferiority with a predefined noninferiority margin of 0.3 mmHg · min–1 could be declared for all treatments with the following mean and 95% CI for the mean differences in the linear rate of arterial partial pressure of carbon dioxide with associated P values regarding noninferiority: high flow versus control, –0.0 mmHg · min–1 (–0.3, 0.3 mmHg · min–1, P = 0.030); medium flow versus control, –0.1 mmHg · min–1 (–0.4, 0.2 mmHg · min–1, P = 0.002); low flow versus control, –0.1 mmHg · min–1 (–0.4, 0.2 mmHg · min–1, P = 0.003); and minimal flow versus control, –0.1 mmHg · min–1 (–0.4, 0.2 mmHg · min–1, P = 0.004). Conclusions Widely differing flow rates of humidified 100% oxygen during apnea resulted in comparable increases of arterial partial pressure of carbon dioxide, which does not support an additional ventilatory effect of high-flow nasal oxygenation. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Ventilatory Effect of Midazolam in Propofol Deep Sedation for Hepatic Tumor Patients Undergoing Percutaneous Radiofrequency Ablation Procedure

Objective: The aim of the study was to compare the ventilatory effect between propofol deep sedation technique with and without midazolam in hepatic tumor patients undergoing radiofrequency ablation procedure. Methods: Three hundred and seventy-four patients who underwent radiofrequency ablation procedure in a single year were randomly assigned to the deep sedation without midazolam group (A, n = 187) and deep sedation with midazolam group (B, n = 187). Patients in group A received normal saline, and those in group B received 0.02 mg/kg of midazolam intravenously in equivalent volume. All patients were oxygenated with 100% O2 via nasal cannula and sedated with intravenous fentanyl and the titration of intravenous propofol. Ventilatory parameters, including oxygen saturation, end tidal carbon dioxide, and respiratory rate every five minutes, during and after the procedure, as well as the duration of sleep and sedation score in the recovery room, were recorded. Results: There were no significant differences in the patients’ characteristics, duration of procedure, total dose of propofol, ventilatory parameters including oxygen saturation, end tidal carbon dioxide, and respiratory rate, as well as sedation score at 20, 25, 30, 35, and 40 min after the procedure, between the two groups. However, mean sedation score at 5, 10, and 15 min after the procedure, in group B, was significantly lower than in group A. In addition, the duration of sleep after the procedure, in group B, was significantly greater than in group A. No serious ventilatory adverse effects were observed either group. Conclusion: Propofol deep sedation with and without midazolam for hepatic tumor patients who underwent radiofrequency ablation procedure was safe and effective. A low dose of midazolam in propofol deep-sedation technique did not create serious ventilatory effects.

Effects of Pleural Effusion on Respiratory Function

The accumulation of pleural effusion has important effects on respiratory system function. It changes the elastic equilibrium volumes of the lung and chest wall, resulting in a restrictive ventilatory effect, chest wall expansion and reduced efficiency of the inspiratory muscles. The magnitude of these alterations depends on the pleural fluid volume and the underlying disease of the respiratory system. The decrease in lung volume is associated with hypoxemia mainly due to an increase in right to left shunt. The drainage of pleural fluid results in an increase in lung volume that is considerably less than the amount of aspirated fluid, while hypoxemia is not readily reversible upon fluid aspiration.

Dopaminergic modulation of respiratory motor output in peripherally chemodenervated goats

We examined the ventilatory effects of exogenous dopamine (DA) and norepinephrine (NE) administration in chloralose-anesthetized, paralyzed, artificially ventilated adult goats before and after carotid body denervation (CBD). Intravenous (iv) DA bolus injections and slow iv infusions caused dose-dependent inhibition of phrenic nerve activity (PNA) in carotid body (CB)-intact animals during normoxia and hyperoxia but not during hypercapnia. NE administration in CB-intact goats caused dose-dependent inhibition of PNA of similar magnitude to DA trials. The DA D2-receptor agonists quinelorane and quinpirole inhibited PNA, whereas the DA D1-receptor agonist SKF-81297 had no effect. After CBD, the ventilatory depressant effects of DA persisted, but responses were significantly attenuated compared with CB-intact trials. CBD abolished the inhibitory effect of low-dose NE administration but did not alter ventilatory responses to high-dose NE injection. The peripheral DA D2-receptor antagonist domperidone substantially attenuated the inhibitory effects of DA bolus injections and infusions and reversed the inhibitory ventilatory effect of high-dose DA administration to excitation in some animals. The α-adrenoceptor antagonist phentolamine had no effect on DA-induced ventilatory depression. β-Adrenoceptor stimulation with isoproterenol produced similar hemodynamic effects to DA administration but had no effect on PNA. We conclude that DA and NE exert both CB-mediated and non-CB-mediated inhibitory effects on respiratory motor output in anesthetized goats. The ventilatory depressant effects that persist in peripherally chemodenervated animals are DA D2-receptor mediated, but their exact location remains speculative.

Ventilatory effects of specific carotid body hypocapnia and hypoxia in awake dogs

Smith, Curtis A., Craig A. Harms, Kathleen S. Henderson, and Jerome A. Dempsey. Ventilatory effects of specific carotid body hypocapnia and hypoxia in awake dogs. J. Appl. Physiol. 82(3): 791–798, 1997.—Specific carotid body (CB) hypocapnia in the −10-Torr (less than eupneic) range reduced ventilation in the awake and sleeping dog to the same degree as did CB hyperoxia [CB [Formula: see text]([Formula: see text]); >500 Torr; C. A. Smith, K. W. Saupe, K. S. Henderson, and J. A. Dempsey. J. Appl. Physiol. 79: 689–699, 1995], suggesting a powerful inhibitory effect of hypocapnia at the carotid chemosensor over a range of[Formula: see text] encountered commonly in physiological hyperpneas. The primary purpose of this study was to assess the ventilatory effect of CB hypocapnia on the ventilatory response to concomitant CB hypoxia. The secondary purpose was to assess the relative gains of the CB and central chemoreceptors to hypocapnia. In eight awake female dogs the vascularly isolated CB was perfused with hypoxic blood (mild,[Formula: see text]≅ 50 Torr or severe,[Formula: see text]≅ 36 Torr) in a background of normocapnia or hypocapnia (10 Torr less than eupneic arterial [Formula: see text]) in the perfusate. The systemic (and brain) circulation was normoxic throughout, and arterial Pco 2 was not controlled (poikilocapnia). With CB hypocapnia, the peak ventilation (range 19–27 s) in response to hypoxic CB perfusion increased 48% (mild) and 77% (severe) due to increased tidal volume. When CB hypocapnia was present, these increases in ventilation were reduced to 21 and 27%, respectively. With systemic hypocapnia, with the isolated CB maintained normocapnic and hypoxic for >70 s, the steady-state poikilocapnic ventilatory response (i.e., to systemic hypocapnia alone) decreased 15% (mild CB hypoxia) and 27% (severe CB hypoxia) from the peak response, respectively. We conclude that carotid body hypocapnia can be a major source of inhibitory feedback to respiratory motor output during the hyperventilatory response to hypoxic carotid body stimulation.

Effects of the combination of skin cooling and hyperpnea of frigid air in asthmatic and normal subjects

McDonald, James S., Joann Nelson, K. A. Lenner, Melissa L. McLane, and E. R. McFadden, Jr. Effects of the combination of skin cooling and hyperpnea of frigid air in asthmatic and normal subjects. J. Appl. Physiol. 82(2): 453–459, 1997.—To investigate whether reducing integumental temperatures influences pulmonary mechanics and interacts with inhaling cold air, 10 normal and 10 asthmatic subjects participated in a three-part trial in which cooling the skin of the head and thorax and isocapnic hyperventilation of frigid air were undertaken as isolated challenges and then administered in combination. Integumental cooling for 30 min caused airway obstruction to develop in both populations [change in 1-s forced expiratory volume (ΔFEV1) asthmatic subjects = 10%; normal subjects = 6%)]. Hyperventilation, however, only affected the asthmatic subjects (ΔFEV1 asthmatic subjects = 18%; normal subjects = 3%). In contrast to expectations, the combined challenge did not produce a summation effect (ΔFEV1 asthmatic subjects = 21%; normal subjects = 7%). These data demonstrate that the skin of the trunk and head is cold sensitive and when stimulated causes similar degrees of bronchial narrowing in both normal subjects and patients with airway disease independent of any ventilatory effect. They also indicate that cooling of the skin does not add to the obstructive consequences of hyperpnea.