Effects of PEEP on respiratory mechanics are tidal volume and frequency dependent.

How the effects of frequency, tidal volume (VT) and PEEP interact to determine the mechanical properties of the respiratory system is unclear. Airway flow and airway and esophageal pressures were measured in ten intubated, anesthetized/paralyzed patients during mechanical ventilation at 10-30 breaths/min and VT of 250-800 ml. From these measurements, Fourier transformation was used to calculate elastance (E) and resistance (R) of the total respiratory system (subscript rs), lungs (subscript L) and chest wall (subscript cw) at 5, 10 and 0 cm PEEP. As PEEP increased from 0-5 cmH2O, all elastances and resistances decreased (P < 0.05). Increasing PEEP to 10 cmH2O decreased EL, Rrs, and RL further (P < 0.05). The changes in Ers, EL, Rrs and RL caused by PEEP were less (P < 0.05) as VT increased, while changes in Rrs, RL and Ers were less (P < 0.05) as frequency increased. VT dependences in Ers and Rrs were enhanced (P < 0.05) at 0 cmH2O PEEP. The ratio of EL to chest wall elastance was not affected by PEEP (P > 0.05), but increased (P < 0.05) with increasing VT at 5 and 10 cmH2O PEEP. We conclude that it is critical to standardize ventilatory parameters when comparing groups of patients or testing clinical intervention efficacy and that the differential effects on the lungs and chest wall must be considered in optimizing the application of PEEP.

Effects of Trendelenburg and reverse Trendelenburg postures on lung and chest wall mechanics.

STUDY OBJECTIVE: To test whether the Trendelenburg ("head-down") or reverse Trendelenburg ("head-up") postures change lung and chest wall mechanical properties in a clinical condition. DESIGN: Unblinded study, each patient serving as own control. SETTING: University of Maryland at Baltimore Hospital, Baltimore, Maryland. PATIENTS: 15 patients scheduled for laparoscopic surgery. INTERVENTIONS: Patients were anesthetized and paralyzed, tracheally intubated and mechanically ventilated at 10 to 30 per minute and at a tidal volume of 250 to 800 ml. Measurements were made before surgery in supine, head-up (10 degrees from horizontal) and head-down (15 degrees from horizontal) postures. MEASUREMENTS AND MAIN RESULTS: Airway flow and airway and esophageal pressures were measured. From these measurements, discrete Fourier transformation was used to calculate elastances and resistances of the total respiratory system, lungs, and chest wall. Total respiratory elastance and resistance increased in the head-down posture compared with supine due to increases in lung elastance and resistance (p < 0.05); but chest wall elastance and resistance did not change (p > 0.05). Lung elastance also exhibited a negative dependence on tidal volume while head-down that was not observed in the supine posture. The change in lung elastance compared with supine was positively correlated to body mass index (weight/height2) and negatively correlated to tidal volume. Lung and chest wall elastance and resistance were not affected by shifting from supine to head-up (p > 0.05). CONCLUSIONS: The Trendelenburg posture increases the mechanical impedance of the lung to inflation, probably due to decreases in lung volume. This effect may become clinically relevant in patients predisposed with lung disease and in obese patients.

Changes in lung and chest wall properties with abdominal insufflation of carbon dioxide are immediately reversible.

Previously we have reported that large increases in lung and chest wall elastances as well as lung resistance occur with abdominal insufflation of carbon dioxide during laparoscopic surgery. To examine whether these effects were reversible with abdominal deflation, we calculated lung and chest wall elastances and resistances from measurement of airway flow and pressure and esophageal pressure in 17 anesthetized/paralyzed patients undergoing laparoscopic surgery. Measurements were made immediately prior to abdominal insufflation and after deflation. Lung and chest wall elastances and resistances were not changed from baseline (P > 0.05), although total respiratory elastance remained slightly increased compared to baseline (P < 0.05). The change in total respiratory elastance did not correlate with abdominal insufflation time, surgical site, smoking history, or physical characteristics of the patients. There were no differences in frequency and tidal volume dependences of the elastances and resistances before and after abdominal insufflation (P > 0.5). We conclude that residual changes in respiratory mechanics caused by carbon dioxide insufflation during laparoscopic surgery are minor, and that the reported compromise of respiratory function indicated by pulmonary function tests after laparoscopy does not appear to be due to changes in passive mechanical properties of the lungs or chest wall.

The effects of increased abdominal pressure on lung and chest wall mechanics during laparoscopic surgery.

We tested the hypothesis that increases in pressure in the abdomen (Pab) exerted by CO2 insufflation during laparoscopy would increase elastance (E) and resistance (R) of both the lungs and chest wall. We measured airway flow and airway and esophageal pressures of 12 anesthetized/paralyzed tracheally intubated patients during mechanical ventilation at 10-30/min and tidal volume of 250-800 mL. From these measurements, we used discrete Fourier transformation to calculate E and R of the lungs and chest wall. Measurements were made at 0, 15, and 25 mm Hg Pab in the 15 degrees head-down (Trendelenburg) posture and at 0 and 15 mm Hg Pab in the 10 degrees head-up (reverse Trendelenburg) posture. Lung and chest wall Es and Rs while head-down increased at Pab = 15 mm Hg, and both Es increased further at Pab = 25 mm Hg (P < 0.05). Both Es and Rs also increased while head-up at Pab = 15 mm Hg (P < 0.05), but increases in lung E and R were less than while head-down (P < 0.05). The increase in lung E and R at Pab = 15 mm Hg in either posture were positively correlated to body weight or body mass index, whereas the increases in chest wall E and R were negatively correlated to the same factors (P < 0.05). Lung and chest wall mechanical impedances increase with increasing Pab; the increases depend on body configuration and are greater while head-down.(ABSTRACT TRUNCATED AT 250 WORDS)

Electroconvulsive therapy-induced cardiac arrhythmias during anesthesia with methohexital, thiamylal, or thiopental sodium.

STUDY OBJECTIVE: To determine the frequency of electroconvulsive therapy (ECT)-induced arrhythmias under methohexital, thiamylal, or thiopental sodium anesthesia with and without atropine premedication. DESIGN: A randomized, double-blind study, placebo-controlled for atropine. SETTING: The inpatient psychiatric unit at a university medical center. PATIENTS: Forty-nine patients scheduled for ECT. INTERVENTIONS: Atropine 0.6 mg intravenously (IV) or an equal volume of normal saline IV was given before IV induction of anesthesia with methohexital 0.5 to 1.0 mg/kg, thiamylal 1.5 to 2.5 mg/kg, or thiopental sodium 1.5 to 2.5 mg/kg. MEASUREMENTS AND MAIN RESULTS: Single-lead electrocardiogram (ECG) recordings were made for 1 minute before induction, during induction of anesthesia, and for 5 minutes after the ECT stimulus. Each ECG was evaluated for arrhythmias and evidence of ischemia in a blinded fashion. Blood pressure and ECG evidence of ischemia did not differ among the groups. Seizure duration was significantly (p less than 0.05) prolonged by a mean of 5 seconds during methohexital anesthesia compared with thiopental sodium and thiamylal (47.6 +/- 18.6 seconds, 42.7 +/- 13.2 seconds, and 42.7 +/- 15.2 seconds, respectively). The frequency of sinus bradycardia was decreased (p less than 0.05) with methohexital (8%) compared with thiopental sodium (20%) and thiamylal (20%). The frequency of premature atrial contractions was decreased (p less than 0.05) with methohexital (43%) compared with thiamylal (61%) but not with thiopental sodium (57%). The frequency of premature ventricular contractions was decreased (p less than 0.05) with methohexital (27%) compared with thiopental sodium (44%) but not with thiamylal (40%). Atropine decreased the frequency of bradycardia (9% vs. 24%) and premature atrial contractions (47% vs. 61%) and increased the frequency of sinus tachycardia (88% vs. 75%). CONCLUSIONS: These data suggest that anesthesia for ECT therapy should be induced with methohexital to minimize the possibility of potentially life-threatening cardiac arrhythmias. Atropine premedication may further decrease the frequency of premature atrial contractions and bradycardia, while increasing the frequency of tachycardia.