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J B Downs

Publications and source records attributed to J B Downs.

At least 19 recordsLinked to original sources
PubMed1999

Cardiopulmonary resuscitation: effect of CPAP on gas exchange during chest compressions.

BACKGROUND: Conventional cardiopulmonary resuscitation (CPR) includes 80-100/min precordial compressions with intermittent positive pressure ventilation (IPPV) after every fifth compression. To prevent gastric insufflation, chest compressions are held during IPPV if the patient is not intubated. Elimination of IPPV would simplify CPR and might offer physiologic advantages, but compression-induced ventilation without IPPV has been shown to result in hypercapnia. The authors hypothesized that application of continuous positive airway pressure (CPAP) might increase CO2 elimination during chest compressions. METHODS: After appropriate instrumentation and measurement of baseline data, ventricular fibrillation was induced in 18 pigs. Conventional CPR was performed as a control (CPR(C)) for 5 min. Pauses were then discontinued, and animals were assigned randomly to receive alternate trials of uninterrupted chest compressions at a rate of 80/min without IPPV, either at atmospheric airway pressure (CPR(ATM)) or with CPAP (CPR(CPAP)). CPAP was adjusted to produce a minute ventilation of 75% of the animal's baseline ventilation. Data were summarized as mean +/- SD and compared with Student t test for paired observations. RESULTS: During CPR without IPPV, CPAP decreased PaCO2 (55+/-28 vs. 100+/-16 mmHg) and increased SaO2 (0.86+/-0.19 vs. 0.50+/-0.18%; P < 0.001). CPAP also increased arteriovenous oxygen content difference (10.7+/-3.1 vs. 5.5+/-2.3 ml/dl blood) and CO2 elimination (120+/-20 vs. 12+/-20 ml/min; P < 0.01). Differences between CPR(CPAP) and CPR(ATM) in aortic blood pressure, cardiac output, and stroke volume were not significant. CONCLUSIONS: Mechanical ventilation may not be necessary during CPR as long as CPAP is applied. Discontinuation of IPPV will simplify CPR and may offer physiologic advantage.

Animals↗
PubMed1998

Intermittent CPAP: a new mode of ventilation during general anesthesia.

BACKGROUND: Airway pressure-release ventilation provides ventilation comparable to controlled mechanical ventilation (CMV), but with lower peak airway pressures and less dead-space ventilation. To obtain these advantages for patients administered general anesthesia, the authors (1) designed a mode similar to airway pressure-release ventilation, intermittent continuous positive airway pressure (CPAPI), and compared its efficiency with that of CMV; and (2) assessed the accuracy of end-tidal carbon dioxide tension (PETCO2) as a monitor of the partial pressure of carbon dioxide in arterial blood (PaCO2) during CPAPI compared with during CMV. METHODS: Twenty anesthetized, tracheally intubated patients received baseline CMV that produced a PETCO2 of approximately 35 mmHg and a pulse oximetry value > 90%. Patients were assigned to undergo alternating trials of CMV and CPAPI. During CPAPI, CPAP was applied to the airway, removed for 1 s, and reapplied at a rate equal to the ventilator rate during CMV. The difference between the carbon dioxide tension in arterial blood and end-tidal gas [P(a-ET)CO2] and the calculation of PaCO2/minute ventilation quantified the efficiency of ventilation. Data were summarized as mean +/- SD and compared using the Student's t-test. RESULTS: Peak airway pressure (13+/-2 vs. 23+/-5 cm H2O; P < 0.001) and minute ventilation (3.5+/-1 vs. 4.6+/-1.2 l/min; P < 0.0001) were lower during CPAPI than during CMV. The value for PaCO2/minute ventilation (11.1+/-2.9 vs. 7.9+/-2.6 mmHg x l(-1) x min(-1); P < 0.0001) was greater during CPAPI. P(a-ET)CO2 was always greater during CMV (6.3+/-1.6 vs. 1.7+/-0.9 mmHg; P < 0.0001) and was never > 3.5 mmHg during CPAPI. CONCLUSIONS: During CPAPI, less ventilation was necessary to produce a PaCO2 comparable to that during CMV. This represents a significant reduction in dead-space ventilation, improved efficiency of ventilation, and a lower value for P(a-ET)CO2. Compared with CMV, CPAPI also improves the accuracy of PETCO2 as a monitor of PaCO2.

Abdomen↗
PubMed1997

Is epinephrine contraindicated during cardiopulmonary resuscitation?

BACKGROUND: Why pulmonary gas exchange deteriorates after administration of epinephrine during cardiopulmonary resuscitation (CPR) is unclear. METHODS AND RESULTS: Forty-four anesthetized swine received an infusion of six inert gases. Animals underwent ventricular fibrillation with CPR and intravenous administration of saline (control), epinephrine (15 microg/kg), or methoxamine (150 microg/kg). Cardiac output, aortic blood pressure, pH, and arterial oxygen saturation were recorded. Distributions of VA and Q were determined by the multiple inert gas elimination technique. Ventricular fibrillation and CPR caused significant decreases in cardiac output, aortic blood pressure, and arterial pH. With epinephrine (versus saline), diastolic blood pressure was significantly higher (23+/-7 versus 8+/-4 mm Hg), but the increase in shunt (from 7+/-4% to 29+/-17%) and the reduction in SaO2 (from 99.7% to 76.8%) were significantly larger. Also, the increase in dead space was greater and elimination of CO2 less. There were no differences between animals given methoxamine or saline, except for increased diastolic blood pressure. CONCLUSIONS: During experimental ventricular fibrillation and CPR, epinephrine increased intrapulmonary shunt approximately 300% more than saline or methoxamine and significantly reduced arterial oxygen saturation. We suspect that the beta-adrenergic receptor activity of epinephrine attenuated hypoxic pulmonary vasoconstriction. Methoxamine is as effective a pressor as epinephrine for CPR and devoid of beta-adrenergic activity. We recommend that such an agent be considered, instead of epinephrine, for CPR.

Adrenergic alpha-Agonists↗
PubMed1997

Does significant arterial hypoxemia alter vital signs?

STUDY OBJECTIVE: To determine the cardiovascular and respiratory effects of arterial hypoxemia in adult volunteers. DESIGN: Prospective, subject-controlled. SETTING: University-affiliated hospital. SUBJECTS: 16 awake, unsedated, unanesthetized adult volunteers. INTERVENTIONS: Inspired oxygen concentration (FIO2) was decreased in decrements to reduce pulse oximeter values to a range of 95% to 90%, 89% to 85%, 84% to 80%, and 79% to 70%. MEASUREMENTS AND MAIN RESULTS: Heart rate (HR), blood pressure (BP), respiratory rate (RR), arterial blood pH, gas tensions, and oxyhemoglobin saturation were determined during normoxia and each level of oxyhemoglobin desaturation. FIO2 was reduced from 21% to 10%. Arterial blood oxyhemoglobin saturation and oxygen tension ranged from 100% to 71% and 103 to 35 mmHg, respectively. There were no significant changes in RR, BP, or HR during the study. CONCLUSIONS: HR, BP, and RR are not reliable indicators of arterial hypoxemia in awake volunteers. If this finding is also true for sedated or anesthetized patients, then continuous monitoring with pulse oximetry should be used whenever patients are at risk for arterial hypoxemia. Stable HR, BP, and RR may not eliminate the possibility of significant arterial hypoxemia and impending catastrophic events.

Adult↗
PubMed1995

Rebreathing improves accuracy of ventilatory monitoring.

OBJECTIVE: Our objective was to determine if rebreathing would reduce the gradient between arterial and end-tidal CO2 tension during positive-pressure ventilation. METHODS DESIGN: Experimental investigation. SETTING: Anesthesiology laboratory. SUBJECTS: A total of 10 dogs of either sex. INTERVENTIONS: Anesthesia (sodium pentobarbital) and muscle relaxation (pancuronium) were induced and animals were tracheally intubated and ventilated with a standard anesthesia ventilator and breathing circuit with CO2 absorber and then with a Mapleson D circuit with a fresh gas flow rate (VF) equal to alveolar ventilation plus the sampling flow rate of two capnometers. Rebreathing was varied by adjusting the respiratory rate (RR) so that minute ventilation (VE) to VF ratio was 1:1, 2:1, 3:1, and 4:1. RESULTS: CO2 production (ATPD) was determined as the product of expired concentration of CO2 and VE (BTPS). Alveolar ventilation (VA) was calculated by dividing the product of CO2 production and barometric pressure corrected for ambient temperature and water vapor pressure at body temperature by PaCO2. Tidal volume, RR, airway gas temperature, concentration of CO2 in gas at the tracheal tube and inlet/outlet of the mechanical ventilator, body temperature, arterial gas tensions and pH, heart rate, arterial blood pressure, and cardiac output were measured. Minute ventilation, mean arterial blood pressure and end-expiratory CO2 tension (PECO2) (BTPS) were calculated. During positive-pressure ventilation, concentration of inspired CO2 was zero with standard circuitry, and significantly increased with Mapleson D when VE:VF ratio was 1:1 (0.56 +/- 0.19%), 2:1 (1.97 +/- 1.30%), 3:1 (2.56 +/- 1.05%), and 4:1 (3.01 +/- 1.45%) (p < 0.05). PECO2 was 34.8 +/- 3.2 mm Hg during ventilation with the standard circuit, and significantly increased during ventilation with Mapleson D when VE:VF ratio was increased from 1:1 (35.4 +/- 2.5 mm Hg) to 2:1 (40.2 +/- 3.6 mm Hg) and was not further increased at a VE:VF ratio of 3:1 (41.8 +/- 2.7 mm Hg) or 4:1 (41.3 +/- 2.4 mm Hg). The selected fresh gas flow rate was appropriate, because PaCO2 remained unchanged regardless of VE:VF ratio, indicating PaCO2 was dependent on VF, not on VE. The gradient between PaCO2 and PECO2 during ventilation with the standard circuit was 6.6 +/- 3.0 mm Hg; during ventilation with Mapleson D, it decreased significantly when VE:VF ratio was increased from 1:1 (6.5 +/- 3.6 mm Hg) to 2:1 (2.9 +/- 1.5 mm Hg), but was not significantly reduced further at 3:1 (1.7 +/- 1.1 mm Hg) or 4:1 (1.8 +/- 0.5 mm Hg) (p < 0.05). CONCLUSIONS: Rebreathing with a Mapleson D circuit and a VF equal to VA permitted normal CO2 elimination. Arterial PCO2 to PECO2 gradient decreased significantly during rebreathing, thus improving the reliability of capnography for estimating arterial PCO2. Consideration should be given to using the Mapleson D as a rebreathing circuit.

Anesthesia, Closed-Circuit↗
PubMed1995

Continuous thermodilution cardiac output: agreement with Fick and bolus thermodilution methods.

OBJECTIVE: Cardiac outputs were determined with continuous thermodilution, bolus thermodilution, and the Fick method during pharmacologically varied hemodynamics. DESIGN: Prospective comparison of techniques. SETTING: University animal laboratory. PARTICIPANTS: Swine. INTERVENTIONS: Swine were anesthetized, tracheally intubated, and instrumented to measure continuous (QTDC) and bolus (QTDB) thermodilution cardiac outputs and sample arterial and mixed venous blood. Continuous thermodilution of blood was facilitated by computer modulation of a thermal filament wrapped around the portion of the pulmonary artery catheter residing in the right atrium and ventricle. QTDC was computed from the thermodilution curve monitored by the thermistor. Bolus thermodilution was performed in triplicate by injecting 10 mL of 5% dextrose in water (0 to 4 degrees C). Oxygen consumption (VO2) was calculated as the averaged minute rate of disappearance of spirometer oxygen over a 6-minute steady state. Cardiac output was determined with the direct Fick method (QF) by dividing VO2 by the difference in arterial and mixed venous oxygen content. Basal QTDC was increased and decreased with an intravenous infusion of dobutamine or labetalol, respectively. Data are summarized as mean +/- SD or 95% confidence interval (CI 95%). Agreement between methods of determining cardiac output was assessed by calculating bias, percent bias, and percent coefficient of determination (100 r2). MEASUREMENTS AND MAIN RESULTS: Eighteen swine (38.9 +/- 1.2 kg) exhibited a range of QTDC from 2.2 to 14.8 L/min. Mean measurement variance of VO2, CaO2, CvO2, and QTDB was 1.5%, 1.5%, 2.0%, and 11.8%, respectively. Mean bias, percent bias, and 100 r2 was 0.004 +/- 1.05 L/min (CI 95%: 0.18 to 0.19 L/min), -0.37 +/- 13.8% (CI 95%: -2.75 to 2.01), and 89% between QTDC and QF, respectively. Bias, percent bias, and 100 r2 was 0.05 +/- 1.09 L/min (CI 95%: -0.14 to 0.23 L/min, 1.21 +/- 13.06% (CI 95%: -1.03 to 3.46%), and 91% between QTDC and QTDB, respectively. Bias, percent bias, and 100 r2 (Fig 6) was -0.04 +/- 0.69 L/min (CI 95%: -0.16 to -.08 L/min), -1.23 +/- 9.17% (CI 95%: -2.8 to 0.35%), and 94% between QTDB and QF, respectively. CONCLUSION: Automatic cardiac output computed with continuous thermodilution appears accurate and reliable. Also, good agreement was confirmed between cardiac output derived by continuous and bolus thermodilution methods and bolus thermodilution and Fick methods.

Adrenergic Agonists↗
PubMed1994

Effect of interfacing between spontaneous breathing and mechanical cycles on the ventilation-perfusion distribution in canine lung injury.

BACKGROUND: Improved matching between ventilation and perfusion (VA/Q) has been proposed to be a major advantage of partial ventilatory support compared with controlled mechanical ventilation. This study was designed to determine whether a difference in gas exchange exists between partial ventilatory support techniques that allow unsupported spontaneous breathing to occur during any phase of the mechanical ventilatory cycle and those that provide mechanical support for each spontaneous inspiratory effort. METHODS: Ten anesthetized dogs with oleic acid-induced lung injury received, in random order, pressure-support ventilation (PSV) and airway pressure-release ventilation (APRV) with and without spontaneous breathing using equivalent airway pressure limits. Gas exchange was assessed by conventional blood gas analysis and by estimating the VA/Q distributions using the multiple inert-gas elimination technique. RESULTS: During APRV, spontaneous breathing accounted for 10 +/- 1% of the total expiratory minute ventilation. Breath-to-breath ventilatory support with PSV resulted in the highest total expiratory minute ventilation (P < 0.05). During spontaneous breathing with APRV, cardiac output increased from 3.9 +/- 0.3 to 4.6 +/- 0.41.min-1 (P < 0.05), arterial oxygen tension from 75 +/- 3 to 107 +/- 8 mmHg (P < 0.05), and oxygen delivery from 567 +/- 47 to 719 +/- 73 ml.kg.min-1 (P < 0.05). PSV did not increase cardiac output, arterial oxygen tension, and oxygen delivery. Spontaneous breathing did not increase oxygen consumption. During APRV spontaneous breathing accounted for a 13 +/- 2% decrease (P < 0.05) in blood flow to shunt units (VA/Q < 0.005) and a 14 +/- 2% increase (P < 0.05) in the perfusion of normal VA/Q units (0.1 < VA/Q < 10). Pulmonary blood flow distribution to shunt and normal VA/Q units was similar during PSV and APRV without spontaneous breathing. Dead space (VA/Q > 100) ventilation decreased by 6% during APRV with spontaneous breathing compared with PSV (P < 0.05). CONCLUSIONS: Spontaneous breathing superimposed on mechanical ventilation contributes to improved VA/Q matching and increased systemic blood flow. Apparently, the spontaneous contribution to a mechanically assisted breath during PSV is not sufficient to counteract the VA/Q maldistribution of positive pressure lung insufflation during acute lung injury.

Animals↗
PubMed1994

Effect of endogenous and inhaled nitric oxide on the ventilation-perfusion relationships in oleic-acid lung injury.

Previous investigations have shown that the ventilation-perfusion (VA/Q) mismatch caused by acute lung injury can be alleviated either by inducing vasodilation in ventilated lung units with inhaled nitric oxide (NO) or by inhibiting the synthesis of endogenous NO, which opposes hypoxic pulmonary vasoconstriction. To determine the effects of a combination of these interventions, we evaluated cardiopulmonary function and VA/Q distributions in 10 dogs with oleic acid-induced lung injury. Each animal received, in random order, zero or 40 ppm of NO in inspiratory gas, with and without intravenous infusion of NG-monomethyl-L-arginine (L-NMMA) (5 mg/kg/h). The multiple inert-gas elimination technique was used to estimate VA/Q distributions. Systemic L-NMMA administration alone did not affect VA/Q inequality and gas exchange, but increased pulmonary and systemic vascular resistance. Inhaled NO improved gas exchange by redistributing blood flow from shunt units to lung units with a nearly ideal VA/Q ratio, without affecting pulmonary or systemic vascular resistance. Improved VA/Q matching and gas exchange was most pronounced when NO was inhaled in the presence of systemic L-NMMA. Inhalation of NO reversed the pulmonary but not the systemic vasoconstriction caused by L-NMMA. These results suggest that endogenous NO release is not limited to hypoxic lung regions in animals with oleic acid-induced lung injury. Inhaled NO reversed L-NMMA-induced pulmonary vasoconstriction and improved VA/Q matching by selectively dilating the pulmonary vasculature in ventilated lung units.

Animals↗
PubMed1994

Continuous positive airway pressure modulates effect of inhaled nitric oxide on the ventilation-perfusion distributions in canine lung injury.

OBJECTIVES: The present study was designed to evaluate if continuous positive airway pressure (CPAP) augments the effect of nitric oxide (NO) inhalation on matching between ventilation and perfusion (VA/Q) during acute lung injury. DESIGN: Prospective, randomized study. SETTING: A research laboratory at a university medical center. SUBJECTS: Ten anesthetized mongrel dogs with oleic acid-induced lung injury. INTERVENTIONS: Zero or 40 parts per million of NO in the inspiratory gas, with and without 10 cm H2O CPAP in random order. MEASUREMENTS AND MAIN RESULTS: Gas exchange was assessed by estimating the VA/Q distributions using the multiple inert gas elimination technique. Application of CPAP decreased blood flow to shunt units by 26 +/- 2 percent (mean +/- SD) and increased the fraction of cardiac output to normal VA/Q units (VA/Q ratio of 0.1 to 10) by 26 +/- 2 percent (p < 0.05). Inhalation of NO during CPAP accounted for a further 10 +/- 2 percent decrease in the blood flow to shunt units and an 8 +/- 2 percent increase in the fraction of the cardiac output to normal VA/Q units (p < 0.05). Inhalation of NO alone had no significant effect on the VA/Q distributions. Inhalation of NO decreased mean transmural pulmonary artery pressure (Ppatm) both without (Ppatm from 30 +/- 2 to 23 +/- 2 mm Hg; PVR from 323 +/- 44 to 228 +/- 43 dynes.s .cm-5; p < 0.05) and with CPAP (Ppatm from 25 +/- 2 to 20 +/- 2 mm Hg; PVR from 255 +/- 30 to 173 +/- 31 dynes.s.cm-5; p < 0.05). CONCLUSIONS: Although pulmonary vascular resistance can be lowered with NO inhalation alone, recruitment of gas exchange units with CPAP is necessary to produce a beneficial effect of NO inhalation on VA/Q matching and oxygenation. When recruitment of gas exchange units with CPAP brings gaseous NO in contact with enough pulmonary blood vessels, NO-induced vasodilation will augment VA/Q matching by a steal mechanism.

Administration, Inhalation↗
PubMed1993

Absence of a capnogram after positive end-expiratory pressure.

OBJECTIVE: The objective of this study was to evaluate the effect of positive end-expiratory pressure (PEEP) on capnography. DESIGN: The study design was experimental and open, and it was performed in the Anesthesiology Experimental Research Laboratory. METHODS: Six dogs (9.8 +/- 0.8 kg) were anesthetized and intubated. The animals' lungs were ventilated with a tidal volume of 137 +/- 34 ml and a respiratory frequency of 34 +/- 10 breaths/min to produce a PaCO2 of 35 to 45 mm Hg. Application of 20 cm H2O of PEEP was initiated for 1 minute, then repeated twice after 10-minute stabilization periods. Arterial pH and gas tensions were measured, and capnogram, airway gas flow, and airway pressure were recorded continuously. Airway gas flow was electronically integrated to calculate tidal volume. RESULTS: Mean values before application of PEEP were as follows: pHa, 7.37 +/- 0.04 mm Hg; PaCO2, 37.1 +/- 3.2 mm Hg; PaO2, 93.4 +/- 1.6 mm Hg; and PETCO2, 32.0 +/- 3.5 mm Hg. Compliance of the ventilator circuit was 3.3 ml/cm H2O. Mean deflation lung-thorax compliance was 41.5 +/- 10.3 ml/cm H2O. After application of PEEP, no capnogram was reported for 1 to 6 breaths, an average of 2.7 +/- 1.8 breaths. CONCLUSION: These results demonstrated that absence of gas flow immediately after the application of PEEP may transiently abolish a capnogram when the lung volume increases.

Anesthesia, Inhalation↗
PubMed1993

Direct or modified Seldinger guide wire-directed technique for arterial catheter insertion.

Percutaneous radial artery cannulation is widely used for direct continuous arterial blood pressure measurement and sampling of arterial blood. We compared the success rate of arterial catheter placement in patients undergoing aortocoronary bypass operations using the direct and the modified Seldinger techniques. The effects of gender and quality of the pulse were also investigated. Our study group consisted of 42 female and 96 male patients. The overall success rate with the guide wire was 82% compared with that of the direct method of 65% (P = 0.02). The success rate for arterial cannulation in male patients was high whether direct cannulation or a guide wire was used. In female patients, on the other hand, the failure rate with the direct technique was high (57%) and was significantly lower (14%) when the guide wire was used (P < 0.001). We conclude that the success rate for cannulation is high in male patients, and patients with a bounding pulse regardless of the use of the direct or guide-wire techniques. The guide wire is recommended as the initial technique for cannulating the radial artery of female patients. In patients with a thready pulse, no significant advantage could be obtained by using a guide wire, but in salvaging an arterial line the guide wire is efficacious.

Adult↗
PubMed1991

Airway pressure release ventilation during acute lung injury: a prospective multicenter trial.

OBJECTIVE: To evaluate the feasibility of airway pressure release ventilation (APRV) in providing ventilatory support to patients with acute lung injury of diverse etiology and mild-to-moderate severity. DESIGN: Prospective, multicenter, nonrandomized crossover trial. SETTING: ICUs in six major referral hospitals. PATIENTS: Fifty adult patients with respiratory failure requiring mechanical ventilation and positive end-expiratory airway pressure. INTERVENTIONS: After optimization of continuous positive airway pressure (CPAP), conventional ventilation and APRV were administered sequentially for 30 mins. During APRV, the CPAP level and airway pressure release level were adjusted to prevent hypoxemia, while the degree of ventilatory support was adjusted by altering the frequency of pressure release. MEASUREMENTS AND MAIN RESULTS: Circulatory and ventilatory pressures, arterial blood gases and pH, heart rate, and respiratory rate were measured. Alveolar ventilation was augmented adequately in 47 of 50 patients by APRV. Adjustment of APRV required an increase in mean CPAP from 13 +/- 3 (SD) to 21 +/- 9 cm H2O and a release pressure of 6 +/- 5 cm H2O. This airway pressure pattern produced a mean airway pressure comparable to that pressure achieved during conventional ventilation. Failure of APRV in three patients could be attributed to an inadequate level of CPAP or an inadequate APRV rate. While maintaining oxygenation of arterial blood and circulatory function, APRV allowed a substantial (55 +/- 17%; p less than .0001) reduction in peak airway pressure compared with conventional positive pressure ventilation adjusted to deliver a comparable or lower level of ventilatory support. CONCLUSIONS: APRV is a feasible alternative to conventional mechanical ventilation for augmentation of alveolar ventilation in patients with acute lung injury of mild-to-moderate severity.

Adult↗
PubMed1991

Distribution of ventilation and perfusion with different modes of mechanical ventilation.

We compared pulmonary gas exchange during synchronized intermittent mandatory ventilation (SIMV), pressure support ventilation (PSV), and airway pressure release ventilation (APRV). Nine subjects aged 56 to 75 yr were studied from 4 to 19 h after cardiac operations. When subjects were ready to be weaned from mechanical ventilation their ventilation-perfusion distribution was estimated using the multiple inert gas elimination technique during SIMV. The subjects then received PSV and APRV during alternating periods on a randomized basis, and the gas-exchange measurements were repeated. Vasoactive infusions and inspired oxygen fraction were held constant throughout the investigation. The results indicated that the major characteristics of the main mode of the VA/Q distributions (mean, standard deviation, and skew) were similar during all three modes. Dead space was lower during APRV (30.1 +/- 1.7% [SEM]) than during SIMV (36.2 +/- 1.5%) and PSV (37.1 +/- 2.7%) (p less than 0.05). Right-to-left shunt was significantly greater during APRV (19.9 +/- 2.3%) than during SIMV (15.4 +/- 1.7%) (p less than 0.05). Peak airway pressure (Paw) was higher during SIMV (32.8 +/- 1.3 cm H2O) than both PSV (19.4 +/- 2.1 cm H2O) and APRV (14.3 +/- 1.0 cm H2O) (p less than 0.05). Minute ventilation was lower during APRV (7.5 +/- 0.07 L/min) than during SIMV (9.4 +/- 0.6 L/min) and PSV (9.0 +/- 0.5 L/min) (p less than 0.05). Hemodynamic variables were similar during all three modes. We conclude that all three modes provide acceptable oxygenation and ventilatory support.

Aged↗