Chest
Volume 60, Issue 4, October 1971, Pages 371-378
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The Lesser Circulation in Pulmonary Fibrosis Secondary to Sarcoidosis and Its Relationship to Respiratory Function

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Fifteen subjects with pulmonary fibrosis due to sarcoidosis were investigated by means of cardiac catheterization and pulmonary function studies. Cardiac output, pulmonary artery pressure, total pulmonary resistance and pulmonary vascular resistance correlated well with diffusing capacity. Exercise pulmonary artery pressure was also correlated well with maximal mid-expiratory flow and one second timed vital capacity. Pulmonary artery pressure, right ventricular end-diastolic pressure, total pulmonary resistance and pulmonary vascular resistance showed good correlation with cardiac output. Correlations between arterial blood gases and pulmonary circulation were very poor. The data suggest that in pulmonary fibrosis secondary to sarcoidosis hemodynamic abnormalities of the lesser circulation are primarily the results of anatomic restriction of the pulmonary vascular bed.

Section snippets

METHODS

The data of all patients who had been seen in this laboratory for the past ten years were reviewed. All patients with pulmonary sarcoidosis who had pulmonary function studies as well as cardiac catheterization were selected. Twenty three such patients were found. Of these, eight patients had data which was either not complete or had other complicating diseases and therefore were discarded. Fifteen patients remained and form the basis of this report. Of these cases the diagnosis of sarcoid was

RESULTS

The results of pulmonary function studies and cardiac catheterization are listed in Table 1 and Table 2, respectively.

PULMONARY FUNCTION

There was wide variation in the severity of respiratory function abnormalities. Some patients were within the normal range for some ventilatory functions. In others, there was significant deterioration in all parameters. The VC was normal in two patients (cases 1, 9) and only moderately impaired for the group. No patient fell within the normal range for DCO, the highest being 61 percent of predicted (case 1). For the group the DCO was severely reduced, averaging 8.7 ml/min/mm Hg, 33 percent of

CARDIAC

Only two patients (cases 1, 3) had normal pulmonary artery pressure (Pa mean ≤ 15 mm Hg) and normal TPR (< 3 units). On 11 of the remaining 13 patients either a normal wedge or left ventricular end-diastolic pressure (≤ 12 mm Hg) was measured and an elevated PVR (> 1.5 units) was calculated.

With one exception (case 1), in none of the nine patients who were exercised did TPR and PVR fall as would be expected in normal subjects.12 Oxygen consumption at rest was within the limits of normal for all

RELATION OF PULMONARY AND CARDIAC FUNCTION

These relationships are shown in FIGURE 3, FIGURE 4, FIGURE 5, FIGURE 6 and the multiple correlations are listed in Table 3. The PCO2, pH and FEV1 did not correlate with any measured parameters of pulmonary circulation. The O2 saturation showed correlations with only resting PAM and TPR and these correlations were poor (Fig 3).

The DCO correlated well with findings in the pulmonary circulation (Fig 4). There was a tendency for the DCO to have a curvilinear relation to PVR and TPR and the use of

DISCUSSION

One of the striking findings in this study, in contradistinction to patients with COPD, is the poor correlation with blood gases (1, 9, 13–15). The O2 saturation showed only a weak relationship with resting PA pressure and total pulmonary resistance (Fig 3).

Of additional interest regarding the blood gases were the findings here which are contrary to the generally held view that oxygen saturation is well maintained until late in the course of the disease. If “late” implies the development of

ACKNOWLEDGMENT

We acknowledge our indebtedness to P. Baskette, C. Doyle, A. Varble, J. Waldie and B. Weinheimer for their valuable assistance.

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  • Cited by (32)

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      Accordingly, perivascular fibrosis or granulomatous pulmonary angiitis has been previously reported in several pathological surveys in these patients [3,4]. Supporting our hypothesis, a significant correlation between DLCO and pulmonary vascular resistance has been widely reported [3,4,7] and a previous study from Nunes and colleagues showed that reduced DLCO values were closely associated to PAH development in patients with sarcoidosis regardless of the presence of pulmonary fibrosis [24]. In the same study, Authors disclosed a close relationship between some HRCT signs, such as ground glass attenuation and septal lines, with pulmonary venous occlusive phenomena in native lungs from transplanted patients [24].

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      However, 31.8 to 50% of patients with sarcoidosis-associated PH develop this complication in the absence of patent pulmonary fibrosis [11,13,14] and a small subset of cases have apparently no underlying lung disease (radiographic stage 0 and I) [6,11,13–15]. Moreover, hemodynamic measurements do not correlate well with spirometric parameters and PaO2 [6,10,13,16] and mPAP is 9 mmHg higher in sarcoidosis than in idiopathic pulmonary fibrosis (IPF) for equivalent respiratory impairment (34.4 versus 25.6 mmHg, P < 0.0001) [17]. Last, the degree of PH is sometimes disproportionate to functional abnormalities [9,11,13,18] and PH may even be more severe when it occurs in patients without fibrotic disease [13].

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    This work was supported by a grant from the Westchester Heart Association.

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