05 Jun

Addition of Nitric Oxide to Oxygen Improves Cardiopulmonary Function in Patients With Severe COPD: Results

Mean values of hemodynamic variables are shown in Table 2. Inhaled NO did not significantly alter the systemic circulatory indexes HR, MAP, pulmonary capillary wedge pressure, or SVRI at any level of NO concentration. However, Cl, which remained unchanged with 5 ppm NO, did increase by 9% at 10 ppm and by 12% at 20 ppm NO. There were significant changes in the pulmonary circulation. Addition of 5 ppm and 10 ppm NO to LTOT decreased MPAP by 14% and 17%, respectively, compared with control (p<0.05). No further improvement was observed at 20 ppm NO. At the same time, PVRI decreased by 19% and 26%, respectively (p<0.05). Calculated REF improved by 9% at 5 ppm and by up to 12% at 10 ppm NO.
The effect of the addition of NO to oxygen on gas exchange is given in Table 3. Both arterial oxygenation and the Pa02/FIo2 ratio were significantly improved by the application of NO. There was a ceiling effect on the Pa02, which increased by 26% of control at 5 ppm NO, but no further at higher concentrations. The Pa02/FIo2 ratio improved by 24% of control at all NO concentrations. The Qs/Qt decreased to a minimum value of 17% at 20 ppm NO. The N02 concentration measured by the chemoluminescence detection analyzer was always <1 ppm. Methemoglobin concentration was 0.37±0.17% at control, and 0.37±0.13% at 5 ppm, 0.38±0.15% at 10 ppm, and 0.42±0.16% at 20 ppm NO, demonstrating no significant increase during the duration of the study.
Individual responses with respect to PVRI and Pa02 are illustrated in Tables 4 and 5. Of note, although the FIo2 during the study varied from patient to patient, within each individual patient, the FIo2 was kept constant. Therefore, individual changes in Pa02 were not related to changes in FIo2. canadian health mall

Discussion
Chronic hypoxemia has a major detrimental impact on the quality of life, exercise tolerance, overall morbidity, and survival in patients with COPD. This is directly related to hypoxemia-induced pulmonary hypertension, which is substantially worsened by physical exertion or acute bronchial or bronchopulmonary infections. Nocturnal oxyhemoglobin desaturation, which occurs during episodes of rapid eye movement sleep, also increases pulmonary vascular resistance. Chronic elevation of right ventricular afterload ultimately results in decompensation, with repeated episodes of right ventricular failure and multifocal atrial tachycardia.
Table 3—Oxygenation Variables

ppm NO
Variable LTOT Control 15 10 i20
Pa02, mm 73±11 74±11 93±20f 95±22f 92±17f
Hg
Pv02, mm 39±2 39±3 42±3 43±3 42±3
Hg
PaC02, 50±7 50±8 50±8 50±8 50±8
mm Hg
Sv02, % 72 ±5 72 ±5 74±4f 74±4 75±4
Qs/Qt, % 23±5 23±6 18±6f 18±5t 17±5f
Pa02/FIo2 244±37 303±59f 308±62f 304±53*

Table 4—PVRI: Individual Responses

ppm NO
Patient LTOT Control 5 10 20
1 736 733 585 626 600
2 301 291 180 193 111
3 457 500 368 476 378
4 400 533 414 400 361
5 330 249 274 173 239
6 272 208 161 180 195
7 439 417 533 356 386
8 195 189 173 130 114
9 1,180 1,175 1,000 867 933
10 1,005 989 800 691 588
11 1,840 1,467 1,520 1,400 1,200
12 246 253 147 122 178
13 284 287 310 291 189
14 297 165 110 105 137
15 998 1,077 543 480 461
16 267 250 222 212 178
17 838 840 557 522 500
18 469 543 361 314 300

Table 5—Arterial Oxygenation: Individual Responses

ppm NO
Patient LTOT Control 5 10 20
1 82 79 76 78 71
2 55 57 82 88 81
3 95 99 101 105 103
4 86 88 99 98 98
5 75 77 171 170 146
6 72 77 69 69 70
7 64 66 151 154 117
8 92 94 95 96 101
9 91 89 115 143 132
10 65 68 96 84 87
11 67 63 79 73 107
12 68 72 92 90 90
13 63 66 77 75 73
14 74 76 75 75 75
15 54 54 65 71 79
16 94 92 93 99 93
17 55 54 57 56 60
18 69 69 73 81 80

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