Pulmonary Vascular Hemodynamics in Chronic Lung Disease Patients: Awake Data

These data are compatible with two hypotheses. First, it is possible that the groups differ because of functional characteristics of the lung parenchyma that cause worsened ventilation/perfusion (V/Q) matching, daytime hypoxemia, and a greater propensity toward NOD. The recurrent nocturnal transient elevation of Ppa* and to some extent, the relative daytime hypoxemia, may then lead to daytime pulmonary hypertension through hypoxic vasoconstriction and subsequent vascular changes. Secondly, differences in daytime Pa02 could indicate structural or anatomic differences between the groups that adversely affect both V/Q relationships as well as pulmonary hemodynamics. in detail

It is generally agreed, in part because of the shape of the oxyhemoglobin dissociation curve, that the lower the Pa02 at sleep onset, the more likely that REM desaturation will occur. Thus, by the second hypothesis, REM desaturation and daytime hypoxemia could be a marker for structural lung abnormalities rather than a cause of pulmonary hypertension. If the two groups had equivalent daytime Pa02 levels as well as PFT results, it would be less likely that structural differences existed between them that could account for the observed hemodynamic differences (eg, more parenchymal destruction causing both hypoxemia and vessel destruction or obliteration in NOD subjects). With equivalent daytime Pa02 levels, it would be more likely that NOD resulted from transient “functional” changes in gas exchange present only at night, which secondarily caused hemodynamic differences (chronic vasoconstriction, vascular smooth muscle hypertrophy).
To examine this possibility, we selected by computer 13 of the 36 NOD subjects which most closely matched the 13 non-NOD subjects in age, FEV!, and daytime Pa02. Using these three parameters, the matched groups were equivalent in age, FEV!, and Pa02 (Table 5). There were no differences between groups in other parameters of pulmonary function including spirometry, plethysmography (not all depicted in the table), or Deo. There were no differences between the groups in PaC02, Pa02, P(A-a)02, or a/A ratio, indicating similar gas exchange parameters.
Table 5—Selected Awake Data on 13 Non-NOD and 13 Matched NOD Subjects

Group 1 (NOD, N = 13) Group 2 (Non-NOD, N = 13) P
Mean SD Mean SD
Selection parameters:
Age, yr 61.6 4.9 64.4 4.2 NS
Pa02, mm Hg 76.5 8.1 82.4 7.6 NS
FEV,, L 1.28 0.51 1.25 0.50 NS
Pulmonary function parameters:
FVC, L 3.1 0.6 3.2 0.6 NS
FEV/FVC, % 47.3 17.6 40.0 11.1 NS
Deo, ml/min/mm Hg 13.7 7.3 15.3 6.7 NS
Dco/VA, ml/min/mm Hg/L 3.3 2.1 2.9 1.9 NS
Gas exchange parameters:
PaC02, mm Hg 38.6 5.0 36.4 3.8 NS
Pa02, mm Hg 98.8 6.2 101.6 4.7 NS
P(A-a)Oa, mm Hg 20.3 7.0 19.1 7.8 NS
a/A Ratio 0.78 0.08 0.81 0.07 NS
Barometers of chronic hypoxia:
Hemoglobin, g/dL 15.4 1.5 14.4 0.8 <0.04
RBC Mass/kg, ml/kg 27.8 2.4 25.2 1.7 <0.004
Hemodynamic parameters:
Sys/Dia Ppa, mm Hg 31/18 7/6 26/17 4/4 <0.03/NS
Mean PpA, mm Hg 22.6 5.9 20.4 4.2 NS
Mean Pew, mm Hg 11.8 4.6 13.1 3.6 NS
Cardiac output, L/m 5.94 1.70 5.74 0.81 NS
Mean PVR, d#s*cm-5 160.0 42.6 101.8 27.6 <0.0004

Category: Lung Disease

Tags: chronic lung disease, Pulmonary function, pulmonary vascular hemodynamics