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December 25, 2015 Category: Canadian Health Care Mall

Baseline Ventilation-Perfusion Distributions

lungThe Va/Q distributions are calculated from the retention-solubility and excretion solubility curves, as described elsewhere. The baseline retention and excretion solubility curves are illustrated for two subjects in Figure 1. The ventilation-perfusion distributions derived from these curves are shown in the same figure. The width of each distribution is measured by the log standard deviation (log SD) of ventilation (Va) and blood flow (Q) and is approximately 0.3 for both Va and 0 in normal subjects; the wider the distribution, the larger the calculated log SD (standard deviation calculated on the logarithmic Va/Q scale, treating the Va or0 as frequency distributions). The log SD of bloodflow is a sensitive indicator of the presence of areas in the lung with a low Va/Q.

In the control state, the subjects had a spectrum of bloodflow distributions from log SD 0.36 to log SD 1.2. Subjects 1-6 had narrow control bloodflow distributions, mean log SD 0.54, range 0.36 to 0.67, while subjects 7-10 had wide control bloodflow distributions, mean log SD 0.98, range 0.82 to 1.2. Spirometry and lung volumes measured on separate occasions (Table 1) and clinical criteria and spirometry measured during the baseline study failed to distinguish between those with narrow or broad control distributions (log SD blood flow, percent predicted FEVi correlation r= -0.18).

The mean log SD of 0.54 in patients 1-6 (Table 2) reflects mild mismatching of ventilation and perfusion homogeneous lungs with the same total ventilation and only. The retention-solubility curves in this group bloodflow (Fig 1). The mean Va/Q of the bloodflow were very close to the ideal curves obtained from distribution was 0.73, very close to normal (0.8 to 1.0).

Only one subject in this group had a measured shunt (perfusion to unventilated lung) greater than 6 percent of the cardiac output. Apart from the small shunts, no subject showed perfusion to lung regions with Va/Q less than 0.1.

The mean log SD of 0.98 in patients 7-10 (Table 2) reflects moderately severe Va/Q mismatching. The measured retention-solubility curves deviated markedly from the ideal curves in the middle range solubility gases (Fig 1). The mean Va/Q of the bloodflow distribution was 0.49, below the normal range (0.8 to 1.0). Two subjects had small shunts, 3.6 percent and 3.2 percent of cardiac cardiac outputoutput, and three subjects had a small amount of blood perfusing units with Va/Q ratio less than 0.1.

There is no close relationship between arterial Po2 and degree of Va/Q inequality as measured by log SD Q(Iable 2, r = 0.56, 0.05 <p<0.1). This is not surprising in view of the well-recognized effects of overall Va and Q and mixed venous gas tensions on PaO£. The inert gas technique allows separation of these influences on the arterial oxygen tension.

Changes in Va/Q Distribution and Retention Solubility Curves while Breathing 100 Percent Oxygen

After breathing 100 percent oxygen for 20 minutes, all six subjects with narrow control distributions (Table 3) demonstrated changes in the retention solubility curves with increased retention of the middle range solubility gases (Fig 2). The bloodflow distributions widened from a mean log SD of bloodflow of 0.54 (range 0.36 to 0.67) to 1.1 (range 0.83 to 1.7) (Fig 3). Since all the narrow bloodflow distributions widened on 100 percent oxygen this is a significant change. The mean Va/Q of the bloodflow dropped to 0.5. The subject with the 13.5 percent shunt increased this to 22.6 percent. In the remaining subjects the shunt fraction remained very small. If you are interested in medical sphere follow the link More info about diseases and hot news with Canadian health&care Mall.

The changes in subjects with wide control distributions were less marked. Two of the four subjects (Table 3) showed small changes in the retention solubility curves with increased retention of the midrange solubility gases (Fig 2). The other two subjects had very minor changes in the retention solubility curves. Overall, subjects 7-10 showed widening of the blood-flow distribution from a mean log SD of 0.98 (range 0.8 to 1.2) to 1.4 (range 1.3 to 1.5) (Table 3, Fig4). However, the mean Va/Q of the bloodflow remained at 0.5 and there was virtually no change in the shunt fraction after oxygen. There was a small increase in the perfusion of Va/Q units between 0.01 and 0.1 (Table 3).

There was a clearly greater change in the Va/Q distributions of the subjects with narrow control distributions. This increase in perfusion to low Va/Q units may be due to a greater maldistribution of ventilation or worse maldistribution of perfusion, or both. A greater maldistribution of ventilation is not likely to be the cause here as the results of spirometry remained unchanged from the control state and high inspired oxygen tensions have not been shown to influence ventilation distribution, apart from inducing atelectasis and shunts. It is likely that the increase in perfusion to low Va/Q units after oxygen administration is due to counteraction of compensatory pulmonary vasoconstriction which was more intense in those patients with the narrow control Va/Q distribution.

Total cardiac output was significantly lower on 100 percent oxygen in the group as a whole (mean air Q = 6.95L, mean 02 Q = 5.63L, p<.005) which is responsible for the rise in mean Va/Q ratio between these two conditions. This would not account for the changes in Va/Q distribution, as much larger changes in Va and Q during exercise have been found to have very little or no effect on Va/Q distribution.

Many of the measured Pa02 values are lower than expected for subjects breathing 100 percent oxygen. The oxygen was administered from a meterologic balloon and no attempt was made to ensure a leak-free circuit, so actual inspired oxygen concentration was somewhat less than 100 percent, although very high.

Changes in Va/Q Distribution and Retention Solubility Curves after Injection of Clemastine

Twenty to 60 minutes after 2 to 4 mg clemastine was injected intravenously, subjects 1-4 (Table 4, Fig 2) showed some broadening of their Va/Q distribution associated with an improvement in spirometry. The bloodflow distribution widened from mean log SD 0.49 (range 0.36 to 0.67) to 0.75 (range 0.54 to 0.9) and the mean Va/Q of the perfusion distribution was 0.56, the same as that oxygen administrationdetermined during oxygen administration. The shunt fraction remained unchanged with no perfusion of lung units with a Va/Q between 0.01 and 0.1. In the other five subjects given clemastine, there were no detectable changes in the retention solubility curves (Fig 2), Va/Q distributions (Fig 3), mean Va/Q of the perfusion distributions, the shunt fractions, or the perfusion to Va/Q units between 0.01 and 0.1 following injection of clemastine (Tables 2, 4).

The Va/Q distributions and retention solubility curves returned toward control configuration in all

subjects 20 minutes after ceasing the 100 percent oxygen; however, the curves for most of those that responded remained broader than the original control measurements. The control points in Figure 5 represent mean values of all three control measurements. No changes were noted in the retention solubility curves or Va/Q distributions five minutes after the injection of clemastine. Only one subject (no. 2) showed increased retention of the midrange solubility gases 20 minutes after clemastine was administered. All the other subjects that had changes in their retention solubility curves had these changes 60 minutes after clemastine was injected.

In the clemastine responders, there was a smaller increase in the log SD of the bloodflow distribution after clemastine administration than during inhalation of 100 percent oxygen. Although a change was not found in the FEV! after breathing 100 percent oxygen, there was a significant (t = 3.44, p<0.05) increase in the FEVi 20 to 60 minutes after clemastine was administered in subjects 1-4. This improvement in spirometry would be expected to improve the distribution of ventilation and thereby improve the Va/Q distribution, masking the possible vasodilation by clemastine. The major bronchodilator effect of the intravenous clemastine was present five minutes after the administration of clemastine, but only small changes in the Va/Q distributions were found at this time (Fig 5).

The Va/Q distributions were widest between 20 and 60 minutes after clemastine administration, but the bronchodilator effect was only slightly greater at this time than at five minutes after clemastine administration. All the subjects (1-4) who had an improvement in spirometric results maintained a widening of the bloodflow distribution. These results suggest that clemastine, given intravenously, has a bronchodilator effect in some patients before a possible effect on the pulmonary vasculature. The early bronchodilator effect, by improving ventilation distribution, may mask the counteraction of compensatory pulmonary vasoconstriction, thereby keeping the bloodflow distribution narrower. At 20 to 60 minutes, when the bronchodilator effect is stable, the clemastine may have its major vasodilator effect and cause a small widening of the bloodflow distribution. Two subjects (7, 9) were shown to have a widening of the bloodflow distributions after oxygen, yet widening was not detected after clemastine. Although these two subjects did not have improvement in the FEVi after clemastine injection, it is possible that the clemastine caused bronchodilata-tion of the small airways and, thereby, improved ventilation distribution. This improvement would narrow the Va/Q distribution and mask any vasodilator effect of clemastine. Alternatively, the small changes in Va/Q distribution measured in these subjects (1-4) could be due simply to worse ventilation distribution associated with bronchodilatation.

Figure-1

Figure 1. The baseline retention and excretion solubility curves with the corresponding derived Va/Q distributions are shown for subject 1 above and subject 10 below. The retention and excretion solubility data points for each gas in subject 1 he very close to the predicted retention and excretion solubility curves for a homogeneous lung with the same total ventilation and cardiac output. The corresponding Va/Q distributions are narrow. In subject 10, the retention and excretion solubility curves (broken lines) deviate from the predicted curves (solid lines) and the corresponding Va/Q distributions are wide.

Figure-2

Figure 2. The measured and predicted retention and excretion solubility curves and the changes after 100 percent Os and clemastine are shown for subject 1 above and for subject 10 below (see text for discussion).

Figure-3

Figure 3. The baseline Va/<J> distributions and the changes induced by 100 percent Oa and clemastine are shown for subject 1 above and subject 10 below. These subjects are the same as shown in Figure 2. The relevant spirometry is shown with each distribution. The symbols only identify every second Va/Q compartment for simplicity.

Figure-4

Figure 4. Changes in log SD of bloodflow (log SD Q), with concomitant changes in the FEVi during oxygen administration are shown. Measurements in each subject are identified by a unique symbol. The broken lines represent subjects who showed a change in their VX/a distribution in response to clemastine.

Figure-5

Figure 5. Changes in log SD Q with concomitant changes in the FEVl after clemastine administration are shown. Symbols identify the same patients as in Figure 4. The control values are the mean of three measurements, two before and one after oxygen administration. The broken lines represent subjects who showed a change in their Va/Q distribution in response to clemastine.

Table 2—Control Data

Subject Logt SD Q at(L/min) (L/min) FEVj(Usee) FEV^pred. Mean Va/0 of blood flow distribution Shunt % Cardiac Output to Va/Q Regions (%) 0-0.1 0.1-1.0 1-10 MeanPAP(mmHg) Pa02(mmHg)
1 0.55 5.9 7.5 0.7 22 0.8 0.6 0 68.0 33.0 14 77
2 0.5 8.4 9.0 1.5 58 0.7 3.0 0 81.6 15.5 18 82
3 0.56 6.5 9.1 1.2 37 0.75 0.2 0 71.6 28.2 12 71
4 0.54 6.0 5.1 1.3 46 0.62 6.1 0 84.8 9.1 78
5 0.55 5.5 7.9 0.8 22 0.8 0.8 0 69.8 29.4 13 75
6 0.67 5.4 6.4 1.4 43 0.7 13.5 0 62.0 23.0 20 80
7 0.82 8.7 9.2 2.1 50 0.47 0 0.5 74.2 24.8 14 87
8 1.1 9.9 11.6 1.1 33 0.49 3.6 1.3 71.9 23.5 65
9 0.8 6.0 7.7 0.6 29 0.52 0 0 76.7 23.3 18 68
10 1.2 7.2 9.3 1.0 32 0.48 3.2 6.9 59.8 30.2 20 67

Table 3—Resubs of 100% Oxygen

Subject Logt SD Q at(L/min) (L/min) FEVj(L/sec) FEV^pred. Mean Va/Q of blood flow distribution Shunt % Cardiac Output to Va/Q Regions (%) 0-0.1 0.1-1.0 1-10 MeanPAP(mmHg) Рa0а(mmHg)
1 1.2 6.1 8.7 0.7 22 0.5 1.3 5.1 68.0 26.0 13 480
2 0.83 7.1 9.8 1.9 50 0.5 3.9 0 85.2 10.6 457
3 1.0 5.2 10.5 1.2 38 0.7 4.0 0 73.2 22.4 12 558
4 1.1 6.0 5.8 1.3 46 0.4 7.2 7.9 68.7 16.2 488
5 0.9 3.5 8.0 0.8 22 1.0 1.4 0 51.6 47.0 11 486
6 1.7 4.6 7.0 0.46 22.7 11.7 38.8 26.3 469
7 1.5 6.7 10.7 2.1 50 0.6 0 21.9 29.8 48.3 15 474
8 1.3 8.0 12.5 1.1 33 0.5 6.1 7.5 66.8 19.6 511
9 1.3 5.5 7.3 0.6 29 0.4 3.4 18.2 53.8 24.6 17 379
10 1.5 3.6 7.4 0.9 29 0.6 3.6 11.8 49.9 34.2 20 395

Table 4—60 Min After Administration of Clemastine

Subject1 LogtSD<?0.8 0*(L/min)7.2 (L/min)7.3 FEVt(L/sec)1.6 FEV^pred.52 Mean Va/Q o blood flow distribution0.5 fShunt ‘ (%)1.8 % Cardiac 0-0.10 Output to V> 0.1-1.084.0 v/Q Regions 1-1014.0 MeanPAP(mmHg)11 PaO*(mmHg)68
2 0.8 7.8 11.5 2.6 68 0.5 3.5 0 89.2 6.9 11 74
3 0.9 6.8 10.2 2.0 63 0.6 2.0 3.9 69.9 24.2 70
4 0.7 6.0 5.6 1.5 54 0.4 5.0 0 84.4 10.6 73
5с 0.54 5.3 7.9 1.0 28 0.8 1.8 0 63.6 34.6 15 82
07 0.8 7.1 9.9 2.1 50 0.7 0 0 64.9 35.1 15 83
8 1.1 9.5 11.5 1.1 33 0.5 3.6 3.0 69.1 24.3 83
9 0.9 7.1 7.9 0.6 29 0.5 6.0 0 72.2 21.8 14 65
10 1.1 8.1 10.2 1.4 45 0.6 7.7 6.3 57.0 29.0 16 64
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