William R. Kimball

Autotriggering caused by cardiogenic oscillation during flow-triggered mechanical ventilation.

Objectives: We noticed that in some patients after cardiac surgery, when flow triggering was used, cardiogenic oscillation might be autotriggering the ventilatory support. In a prospective study, we evaluated the degree of cardiogenic oscillation and the frequency rate of autotriggering. We suspected that autotriggering caused by cardiogenic oscillation was more common than clinically appreciated. Design: Prospective, nonrandomized, clinical study. Setting: Surgical intensive care unit in a national heart institute. Patients: A total of 104 adult patients were enrolled after cardiac surgery. Interventions: During the study period, patients were paralyzed and ventilated with intermittent mandatory ventilation at a rate of 10 breaths/min, pressure support of 10 cm H2O, and flow triggering with a sensitivity of 1 L/min. Measurements and Main Results: Because the patients would not be able to breathe spontaneously, we counted pressure‐support (PS) breaths as instances of autotriggering. Then, we classified the patients into two groups according to the number of PS breaths: an “AT group” (PS breaths of >5/min) and a “non‐AT group” (PS breaths of ≤5/min). If autotriggering occurred, we decreased the sensitivity so autotriggering disappeared (threshold triggering sensitivity). The intensity of cardiogenic oscillation was assessed as the flow and airway pressure at the airway opening. A total of 23 patients (22%) demonstrated more than five autotriggered breaths/min. During mechanical ventilation, the inspiratory flow fluctuation caused by cardiogenic oscillation was significantly greater in the AT group than in the non‐AT group (4.67 ± 1.26 L/min vs. 2.03 ± 0.86 L/min; p < .01). The AT group also showed larger cardiac output, higher ventricular filling pressures, larger heart size, and lower respiratory system resistance than the non‐AT group. As the inspiratory flow fluctuation caused by cardiogenic oscillation increased, the level of triggering sensitivity also was increased to avoid autotriggering. In the AT group with 1 L/min of sensitivity, the respiratory rate increased (19.9 ± 2.7 vs. 10 ± 0 breaths/min, p < .01), PaCO2 decreased (30.8 ± 4.0 torr [4.11 ± 0.36 kPa] vs. 37.6 ± 4.3 torr [5.01 ± 0.57 kPa]; p < .01), and mean esophageal pressure increased (7.7 ± 3.0 vs. 6.9 ± 3.0 cm H2O; p < .01) compared with the threshold triggering sensitivity. Conclusions: Autotriggering caused by cardiogenic oscillation is common in postcardiac surgery patients when flow triggering is used. Autotriggering occurred more often in patients with more dynamic circulation. Autotriggering caused respiratory alkalosis and hyperinflation of the lungs.

Diaphragmatic shortening after thoracic surgery in humans. Effects of mechanical ventilation and thoracic epidural anesthesia.

BackgroundDiaphragmatic function is believed to be inhibited after thoracic surgery and may be improved by thoracic epidural anesthesia. MethodsDiaphragmatic function after a thoracotomy was monitored by implanting one pair of sonomicrometry crystals and two electromyogram (EMG) electrodes on the costal diaphragm of six patients undergoing an elective pulmonary resection. Crystals and EMG electrodes remained in place for 12–24 h. ResultsDuring mechanical ventilation, costal diaphragmatic length (as a percent of rest length; %LFRC)decreased passively as tidal volume (VT) Increased (%LFRC = 2.81 + 1.12 × 10-2 VT (ml), r = 0.99). During spontaneous ventilation, the costal shortening (2.1 ± 2.3 %LFRC) was less than during mechanical ventilation (7.9 ± 3.0 %LFRC, P < 0.05) at the same VT. Comparing spontaneous ventilation before and 30 min after thoracic epidural anesthesia, there were Increases of VT (390 ± 78 to 555 ± 75 ml), vital capacity (1.37 ± 0.16 to 1.68 ± 0.21 1), and esophageal (-8.5 ± 1.5 to −10.6 ± 1.7 cmH2O), gastric (-0.7 ± 0.8 to ±0.8 ± 0.8 cmH2O), and transdiaphragmatic (7.7 ± 1.5 to 11.5 ± 1.9 cmH2O) pressures, but diaphragmatic EMG and shortening fraction remained constant. In three of six patients, epidural anesthesia produced paradoxical segment lengthening upon inspiration. ConclusionsThoracotomy and pulmonary resection produce a marked reduction of active diaphragmatic shortening, which is not reversed by thoracic epidural anesthesia despite improvement of other indices of respiratory function.

Nasal ventilation is more effective than combined oral-nasal ventilation during induction of general anesthesia in adult subjects.

Background:The authors hypothesized that nasal mask ventilation may be more effective than combined oral–nasal mask ventilation during induction of general anesthesia. They tested this hypothesis by comparing the volume of carbon dioxide removed per breath with nasal versus combined oral–nasal mask ventilation in nonparalyzed, apneic, adult subjects during induction of general anesthesia. Methods:Fifteen adult subjects receiving general anesthesia were ventilated first with a combined oral–nasal mask and then with only a nasal mask. The patient’s head was maintained in a neutral position, without head extension or lower jaw thrust. Respiratory parameters were recorded simultaneously from both the nasal and oral masks regardless of ventilation approach. Results:The volume of carbon dioxide removed per breath during nasal mask ventilation (median, 5.0 ml; interquartile range, 3.4–8.8 ml) was significantly larger than that during combined oral–nasal mask ventilation (median, 0.0 ml; interquartile range, 0.0–0.4 ml; P = 0.001); even the peak inspiratory airway pressure during nasal ventilation (16.7 ± 2.7 cm H2O) was lower than that during combined oral–nasal ventilation (24.5 ± 4.7 cm H2O; P = 0.002). The expiratory tidal volume during nasal ventilation (259.8 ± 134.2 ml) was also larger than that during combined oral–nasal ventilation (98.9 ± 103.4 ml; P = 0.003). Conclusions:Nasal mask ventilation was more effective than combined oral–nasal mask ventilation in apneic, nonparalyzed, adult subjects during induction of general anesthesia. The authors suggest that nasal mask ventilation, rather than full facemask ventilation, be considered during induction of anesthesia.

Thoracic Epidural Anesthesia Increases Diaphragmatic Shortening after Thoracotomy in the Awake Lamb

BackgroundProlonged inhibition of diaphragmatic function occurs after thoracic and upper abdominal surgery. It was hypothesized that thoracic epidural anesthesia on the day after a thoracotomy could block inhibitory neural pathways and increase the shortening of costal and crural diaphragmatic segments. MethodsPairs of sonomicrometer crystals were implanted into the costal and crural regions of the diaphragm through a right lateral thoracotomy in 14 30-kg, 4–5-month-old lambs. One day after surgery, a thoracic epidural catheter was placed at the T8-T9 level. Regional diaphragmatic shortening normalized to end-expiratory length (%LFRC), was measured by sonomicrometry in these awake lambs. Changes in gastric (ΔPgas), esophageal (ΔPcs,), and transdiaphragmatic (ΔPdi) pressures were measured with transnasal balloon catheters. End-tidal carbon dioxide (FETCO2), costal and crural electromyogram (Edi), and tidal volume (VT) were measured. Inductance plethysmography was used in four lambs to assess relative contributions of the rib cage and abdomen to VT. Control values were obtained during quiet breathing and while rebreathing at up to 10% FETco2 To block thoracic dermatomes, 1% or 2% lidocaine was injected through the epidural catheter. Measurements were repeated after each lidocaine injection. ResultsThere was no change of resting length with 1% lidocaine; costal resting length increased by 22% with 2% lidocaine. After 2% lidocaine, costal %LFRC increased from control both during quiet breathing (8.7 ± 0.7 to 18.1 ± 1, x ± SEM%) and at FETCO2 10% (22.1 ± 2 to 33.7 ± 3%). VT during quiet breathing was unchanged after 1% lidocaine but increased from 235 ± 16 to 283 ± 28 ml after 2% lidocaine. At 10% FeTco2, ΔPdl was unchanged after 1% lidocaine and decreased from 36.5 ± 4.3 to 26.3 ± 4.9 cmH2O after 2% lidocaine. Regional ΔEdl, was unchanged with both 1% and 2% lidocaine at rest and during carbon dioxide rebreathing. Plethysmography in three lambs showed a reduction in rib cage contribution to tidal volume with 2% lidocaine during quiet breathing. ConclusionsImproved postoperative tidal volume and diaphragmatic shortening after thoracic epidural blockade may be due to changes of chest wall conformation and resting length and a shift of the workload of breathing from the rib cage to the diaphragm caused by intercostal muscle paralysis.

Effectiveness of Breathing through Nasal and Oral Routes in Unconscious Apneic Adult Human Subjects: A Prospective Randomized Crossover Trial

Background:The authors hypothesized that mouth ventilation by a resuscitator via the nasal route ensures a more patent airway and more effective ventilation than does ventilation via the oral route and therefore would be the optimal manner to ventilate adult patients in emergencies, such as during cardiopulmonary resuscitation. They tested the hypothesis by comparing the effectiveness of mouth-to-nose breathing (MNB) and mouth-to-mouth breathing (MMB) in anesthetized, apneic, adult subjects without muscle paralysis. Methods:Twenty subjects under general anesthesia randomly received MMB and MNB with their heads placed first in a neutral position and then an extended position. A single operator performed MNB and MMB at the target breathing rate of 10 breaths/min, inspiratory:expiratory ratio 1:2 and peak inspiratory airway pressure 24 cm H2O. A plethysmograph was used to measure the amplitude change during MMB and MNB. The inspiratory and expiratory tidal volumes during MMB and MNB were calculated retrospectively using the calibration curve. Results:All data are presented as medians (interquartile ranges). The rates of effective ventilation (expired volume > estimated anatomic dead space) during MNB and MMB were 91.1% (42.4–100%) and 43.1% (42.5–100%) (P < 0.001), and expired tidal volume with MMB 130.5 ml (44.0–372.8 ml) was significantly lower than with MNB 324.5 ml (140.8–509.0 ml), regardless of the head position (P < 0.001). Conclusions:Direct mouth ventilation delivered exclusively via the nose is significantly more effective than that delivered via the mouth in anesthetized, apneic adult subjects without muscle paralysis. Additional studies are needed to establish whether using this breathing technique during emergency situations will improve patient outcomes.

Continuous positive airway pressure and ventilation are more effective with a nasal mask than a full face mask in unconscious subjects: a randomized controlled trial

IntroductionUpper airway obstruction (UAO) is a major problem in unconscious subjects, making full face mask ventilation difficult. The mechanism of UAO in unconscious subjects shares many similarities with that of obstructive sleep apnea (OSA), especially the hypotonic upper airway seen during rapid eye movement sleep. Continuous positive airway pressure (CPAP) via nasal mask is more effective at maintaining airway patency than a full face mask in patients with OSA. We hypothesized that CPAP via nasal mask and ventilation (nCPAP) would be more effective than full face mask CPAP and ventilation (FmCPAP) for unconscious subjects, and we tested our hypothesis during induction of general anesthesia for elective surgery.MethodsIn total, 73 adult subjects requiring general anesthesia were randomly assigned to one of four groups: nCPAP P0, nCPAP P5, FmCPAP P0, and FmCPAP P5, where P0 and P5 represent positive end-expiratory pressure (PEEP) 0 and 5 cm H2O applied prior to induction. After apnea, ventilation was initiated with pressure control ventilation at a peak inspiratory pressure over PEEP (PIP/PEEP) of 20/0, then 20/5, and finally 20/10 cm H2O, each applied for 1 min. At each pressure setting, expired tidal volume (Vte) was calculated by using a plethysmograph device.ResultsThe rate of effective tidal volume (Vte > estimated anatomical dead space) was higher (87.9% vs. 21.9%; P<0.01) and the median Vte was larger (6.9 vs. 0 mL/kg; P<0.01) with nCPAP than with FmCPAP. Application of CPAP prior to induction of general anesthesia did not affect Vte in either approach (nCPAP pre- vs. post-; 7.9 vs. 5.8 mL/kg, P = 0.07) (FmCPAP pre- vs. post-; 0 vs. 0 mL/kg, P = 0.11).ConclusionsnCPAP produced more effective tidal volume than FmCPAP in unconscious subjects.Trial registrationClinicalTrials.gov identifier: NCT01524614.

Effect of effort pain after upper abdominal surgery on two independent measures of respiratory function

STUDY OBJECTIVE To determine how effort pain interacts with changing pulmonary function after upper abdominal incisions. DESIGN Prospective, case-controlled study. SETTING Academic teaching hospital. PATIENTS 34 ASA physical status I, II, and III patients recovering from elective, major incisional, upper abdominal surgery. MEASUREMENTS Manometry (maximal inspiratory and expiratory pressure) and spirometry (forced vital capacity, forced expiratory volume during the first second, peak expiratory flow) for three postoperative days. Pain scores (Visual Analog Pain Scale; VAS) at rest and after the manometric or spirometric efforts. MAIN RESULTS Effort pain during either manometry or spirometry was greater than pain at rest on the first postoperative day. Maximal respiratory pressure concomitantly recovered with pain during daily efforts (slopes: -0.429 and -0.278% max/mm VAS; P < 0.05). Spirometric measurements showed minimal improvement. CONCLUSION The direct relationship between resolution of pain with effort and direct measures of respiratory muscle effort using manometry, but not those obtained less directly by spirometry, suggests that assessing interactions between pain and effort requires a direct, quantifiable measure of effort.

Effects of digoxin on regional diaphragm function after thoracotomy in awake sheep

The effects of digoxin on diaphragmatic contraction were studied in 12 sheep, within 6 days after a right thoracotomy, during the period of intense diaphragmatic inhibition. Diaphragmatic function was assessed by implanting sonomicrometry crystals and electromyographic (EMG) electrodes in both the costal and crural diaphragmatic regions. Awake sheep were studied before and after intravenous digoxin (0.04 mg/kg) during both quiet breathing (QB) and during CO2 rebreathing, until the fractional concentration of expired CO2 (FETCO2) reached 0.10. After digoxin infusion, during both QB and at FETCO2 of 0.10, esophageal and transdiaphragmatic pressures increased (P < 0.05). After digoxin infusion no changes were measured for end-expiratory resting length, shortening fraction, shortening velocity or EMG activity of either diaphragmatic segment or for respiratory frequency, ventilation, tidal volume and FETCO2. We conclude that intravenous digoxin given to awake sheep after a thoracotomy increases Pdi, but does not alter diaphragmatic shortening nor alter the level of diaphragmatic activation either during QB or at FETCO2 of 0.10.

Effects of Aminophylline on Regional Diaphragmatic Shortening after Thoracotomy in the Awake Lamb

Aminophylline has been reported to augment diaphragmatic contraction, although this remains a controversial finding. We studied the effect of aminophylline on regional diaphragmatic shortening, changes in transdiaphragmatic pressure (delta Pdi), and integrated regional electromyographic (EMG) activity of the diaphragm (Edi) after a right thoracotomy in nine lambs using sonomicrometry, esophageal and gastric balloons, and EMG. Sonomicrometer crystals and EMG leads were implanted into the costal and crural regions of the diaphragm through a right thoracotomy, and a tracheostomy was performed. The animals were studied while awake within 4 days after surgery. Fractional costal and crural diaphragmatic shortening was measured using the sonomicrometer; delta Pdi was calculated from esophageal and gastric pressures. Respiratory variables were measured through the tracheostomy. Data were collected during quiet breathing and during CO2 rebreathing. After control measurements, aminophylline (10 mg/kg) was administered intravenously, producing a serum concentration of 17.7 +/- 1.5 micrograms/ml. Aminophylline did not augment shortening, increase delta Pdi, or overcome postoperative diaphragmatic inhibition acutely in the awake sheep after a right lateral thoracotomy. A small decrease of end-tidal CO2, from 5.2% to 4.9%, was measured at rest during aminophylline infusion, but Edi was unchanged. Although during CO2 rebreathing diaphragmatic shortening increased, the addition of aminophylline did not further augment shortening. Our data in awake lambs suggest that aminophylline does not improve diaphragmatic contraction in the acute postoperative period.

Effects of Paralysis with Pancuronium on Chest Wall Statics in Awake Humans

The influence of tonic inspiratory muscle activity on the relaxation characteristics of the chest wall, rib cage (RC), and abdominal wall (ABW) has been investigated in four highly trained subjects. Chest wall shape and volume were estimated with magnetometers. Pleural pressure (Pes) and abdominal pressure were measured with esophageal and gastric balloons, respectively. Subjects were seated reclining 30 degrees from upright, and respiratory muscle weakness was produced by pancuronium bromide until RC inspiratory capacity was decreased to 60% of control. Only minor changes were observed for Konno-Mead relaxation characteristics (RC vs. ABW) between control and paralysis. Similarly, although RC relaxation curves (RC vs. Pes) during paralysis were significantly different from control (P less than 0.05), the changes were small and not consistent. The differences between paralysis-induced changes in resting end-expiratory position of the chest wall and helium-dilution functional residual capacity (FRC) suggested changes in volume of blood within the chest wall. We conclude that 1) although tonic inspiratory activity of chest wall muscles exists, it does not significantly affect the chest wall relaxation characteristics in trained subjects; 2) submaximal paralysis produced by pancuronium bromide is likely to modify either spinal attitude or the distribution of blood between extremities and the thorax; these effects may account for the changes in FRC in other studies.