Chest
Volume 127, Issue 5, May 2005, Pages 1637-1646
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Clinical Investigations
End-tidal Pco2 Abnormality and Exercise Limitation in Patients With Primary Pulmonary Hypertension

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Objectives

Primary pulmonary hypertension (PPH) is a pulmonary vasculopathy resulting in exercise intolerance, usually due to dyspnea. We hypothesized that ventilation is increased during exercise in PPH relative to normal because the ventilated lung is underperfused, cardiac output increase is restricted, and arterial hypoxemia may develop. Our aim was to determine the size of the reduction in end-tidal Pco2 (Petco2) as a reflection of the abnormality in ventilatory efficiency and ventilatory drive in PPH patients.

Methods

We performed cardiopulmonary exercise testing (CPET) in 52 PPH patients. All had hemodynamic measurements to confirm the diagnosis of PPH. A subgroup of 29 patients who underwent right-heart catheterization within 50 days of CPET were studied to compare their CPET responses to resting hemodynamics. Nine healthy volunteers matched for age and gender served as CPET control subjects.

Results

In PPH patients, the percentage of predicted peak oxygen uptake ( V.o2) correlated significantly with mean pulmonary artery pressure (mPAP) [r = − 0.59, p = 0.0007, n = 29]. Petco2 values at rest, anaerobic threshold (AT), and peak V.o2 were proportionately reduced as percentage of predicted peak V.o2 decreased (r = 0.66 to 0.72, p < 0.0001, n = 52). Petco2 values at rest, AT, and peak V.o2 were also reduced as mPAP increased (r = − 0.51 to − 0.53, p < 0.005, n = 29). In contrast to normal subjects in whom Petco2 increased from rest to AT, Petco2 decreased in PPH patients, except for two patients with mild PPH in whom there was no change. Also, Petco2 increased rather than decreased further at the start of recovery, in contrast to normal. Although usually normal at rest, oxyhemoglobin saturation decreased during exercise in most PPH patients.

Conclusions

In patients with PPH, Petco2 at rest and exercise is significantly reduced in proportion to physiologic disease severity. The range of values is unusually low. Furthermore, the directional changes of Petco2 during exercise and early recovery are in the opposite direction of normal.

Section snippets

Materials and Methods

We retrospectively investigated the exercise pathophysiology in 52 patients with PPH referred for evaluation and treatment to our Pulmonary Hypertension Referral Clinic, and 9 healthy volunteers of similar distribution in age and gender (3 men and 6 women; mean age, 39.9 ± 4.8 years [mean ± SE]). The diagnosis of PPH was based on clinical findings and the diagnostic criteria described by the National Institutes of Health registry for PPH and the World Health Organization.1 The Human Subjects

Subject Characteristics

Patient and control subject characteristics are shown in Table 1. There were 7 men and 45 women (age, 43.5 ± 1.8 years) enrolled in the patient group and 3 men and 6 women enrolled in the control group. The patient group was further divided into four groups according to the physiologic grade of severity defined by percentage of predicted peak V.o2.12 The percentage of predicted AT and V.e/ V.co2 at AT were progressively more abnormal as physiologic severity increased (Table 1

Discussion

Normal subjects dwelling near sea level have progressively increased Petco2 by approximately 5 mm Hg above resting values at the AT (Fig 2). In contrast, Petco2 decreases rather than increases from rest to AT in PPH, except for the two subjects with mildest disease, in whom Petco2 did not change. This directional change in Petco2 from rest to AT is greater for a greater reduction in percentage of predicted AT (Fig 4).

The reduction in Petco2 seen in PPH may be accounted for by mechanisms that

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Supported in part by a grant from the American Heart Association (0160126Y).

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