Continuous Positive Airway Pressure Modulates Effect of Inhaled Nitric Oxide on the Ventilation-Perfusion Distributions in Canine Lung Injury: Statistical Analysis

Continuous Positive Airway Pressure Modulates Effect of Inhaled Nitric Oxide on the Ventilation-Perfusion Distributions in Canine Lung Injury: Statistical AnalysisResults are expressed as mean ± standard error of the mean (SE). Data were normally distributed and analyzed by using an analysis of variance for repeated measures to determine if inhaled NO concentration and the CPAP level had significant effects on the measured and calculated variables. The relationship between measured and predicted Pa02 was assessed with a linear regression analysis; p<0.05 was considered to be statistically significant.
The effects of NO inhalation and CPAP on cardiovascular function are shown in Table 1. Mean Ppatm and PVR decreased during inhalation of 40 ppm NO with and without CPAP. In the absence of NO inhalation, mean Ppatm and PVR decreased during CPAP compared to ambient airway pressure. Inhalation of NO (p<0.05), CPAP (p<0.05), and the combination of CPAP and NO inhalation (p<0.05) decreased mean Ppatm and PVR significantly. Heart rate, mean Psa, SVR, CO, Pcvtm, and Paotm remained unchanged. Minute ventilation and respiratory rate were lowered by CPAP (p<0.05) (Table 2). Application of CPAP (p<0.05), the combination of CPAP and NO inhalation (p<0.05) but not NO inhalation alone, increased Pa02 and PVO2 significantly (Table 2). The highest Pa02 was observed during NO inhalation with CPAP. Arterial pH, PaC02, and methemoglo-bin remained essentially unchanged.

Changes reflecting the Va/Q distributions are summarized in Table 3 and illustrated for a representative dog in Figure 1. Application of CPAP decreased blood flow to shunt units and increased the fraction of CO to units with a normal Va/Q (0.1 <Va/Q <10) ratio. Inhalation of NO with CPAP accounted for a further 10 ± 1 percent decrease in the blood flow to shunt units and an 8 ± 1 percent increase in the fraction of the CO to normal Va/Q units. Application of CPAP (p<0.05), the combination of CPAP and NO inhalation (p<0.05) but not NO inhalation alone, had a significant effect on the blood flow to shunt and normal Va/Q units.

Table 1—Hemodynamic Variables

Ambient Pressure CPAP Main Effects Interaction NO, CPAP
N0=0 ppm N0=40 ppm N0=0 ppm N0=40 ppm NO CPAP
HR, beats/min 131 ±15 131 ±21 129 ±21 122 ±15 NS NS NS
Psa, mm Hg 111 ± 15 113 ± 12 103 ±12 107 ±4 NS NS NS
Ppatm, mm Hg 30 ±5 24 ±6 25 ±6 20 ±5 p<0.05 p<0.05 NS
Pcvtm, mm Hg 7±2 7 ±2 5±2 5 ± 2 NS NS NS
Paotm, mm Hg 9±2 9 ±2 10±2 9±2 NS NS NS
CO, L/min 5.2 ± 1.4 5.0± 1.1 4.8± 1.4 4.7 ± 1.7 NS NS NS
SVR, dynes-s/cm 1,673 ±480 1,712 ±580 1,678 ±420 1,759 ±428 NS NS NS
PVR, dynes-s/cm 323 ±120 228 ±115 255 ±90 173 ±92 p<0.05 p<0.05 NS

Table 2—Physiologic Gases and Ventilatory Variables

Ambient Pressure CPAP Main Effects Interaction NO, CPAP
N0=0 ppm N0=40 ppm N0=0 ppm N0=40 ppm NO CPAP
FIo2 0.30 0.30 0.30 0.30 NS NS NS
РаОг, mm Hg 62 ±8 64 ± 9 92 ±8 111 ± 14 p<0.05 p<0.05 p<0.05
РаСОг, mm Hg 50 ±6 51 ±6 51 ±6 50 ±6 NS NS NS
pHa, units 7.26 ±0.09 7.28 ±0.09 7.25 ±0.09 7.26 ±0.09 NS NS NS
Pv02, mm Hg 50 ±6 51 ±5 57 ± 3 57 ±5 NS p<0.05 NS
Met Hb, g/dl 0.8 ±0.3 1.1 ±0.6 0.9 ±0.6 1.0±0.5 NS NS NS
RR, breaths/min 39 ±15 40 ±17 16± 12 17±6 NS p<0.05 NS
Ve, ml/min 5,767 ±1,606 6,189 ±1,732 4,308 ±1,205 4,662 ±1,345 NS p<0.05 NS

Table 3—Inert Gas Data

Ambient Pressure CPAP Main Effects Interaction NO, CPAP
N0=0 ppm N0=40 ppm N0=0 ppm N0=40 ppm NO CPAP
RSS 0.71 ±0.94 0.60 ±0.74 1.20 ±0.75 1.10±0.67 NS NS NS
Shunt (Va/Q<0.005), %Qt 48.3 ±7.2 45.2 ±7.8 20.9 ±9.1 12.1 ±5.1 NS p<0.05 p<0.05
0.005<Va/Q<0.1, %Qt 2.1 ±2.4 2.1 ±3.7 2.9±5.2 2.7±5.7 NS NS NS
0.1<Va/Q<10, %Qt 50.2 ±8.2 51.9±9.4 78.4± 11.3 85.8 ±8.8 NS p<0.05 p<0.05
10<Va/Q<100, %Ve 8.4 ±4.3 8.5 ±5.3 8.5 ±6.3 7.3 ±6.3 NS NS NS
Dead space (Va/Q>100), %Ve 71.1 ±7.2 69.9 ±8.5 64.0 ±12.1 62.9 ±12.3 NS p<0.05 NS
Q 0.51 ±0.03 0.49 ±0.09 0.38 ±0.11 0.43 ±0.12 NS NS NS
log SDq 0.82 ±0.3 0.87 ±0.3 0.73 ±0.3 0.72 ±0.3 NS NS NS
V 3.21 ±1.64 3.60 ±2.20 2.27 ±1.70 2.10± 1.54 NS p<0.05 NS
log SDv 1.92±0.6 1.79 ±0.6 1.75 ±0.9 1.67 ±0.9 NS NS NS
DISPr-e* 38.8 ±7.2 35.9 ±9.8 25.5 ±12.9 20.7 ±11.8 NS p<0.05 NS

Figure-1

Figure 1. Continuous distributions of ventilation and blood flow plotted vs the ventilation-perfusion (Va/Q) ratio for a representative dog with oleic acid-induced acute lung injury while breathing at ambient airway pressure and continuous positive airway pressure (CPAP) with and without 40 ppm nitic oxide (NO) in the inspiratory gas.

This entry was posted in Lung injury and tagged acute lung injury, continuous positive airway pressure, Nitric oxide, pulmonary gas exchange, ventilation-perfusion distribution.