End tidal CO(2) tension: pulmonary arterial hypertension vs pulmonary venous hypertension and response to treatment

Anna R Hemnes, Meredith E Pugh, Alexander L Newman, Ivan M Robbins, James Tolle, Eric D Austin, John H Newman, Anna R Hemnes, Meredith E Pugh, Alexander L Newman, Ivan M Robbins, James Tolle, Eric D Austin, John H Newman

Abstract

Background: CO(2) excretion is impaired in pulmonary arterial hypertension (PAH) due to underlying vascular obstruction and increased dead space. Our aim was to determine whether resting end tidal CO(2) (Etco(2)) could differentiate patients with PAH from those with pulmonary venous hypertension (PVH) or patients without pulmonary hypertension (PH) and whether successful treatment of PAH resulted in higher Etco(2) values.

Methods: We performed Etco(2) measurements for five breaths at rest and after a 6-min walk test (6MWT) in patients seen at our pulmonary vascular center. Mean Etco(2) values were correlated with 6-min walk distance and right-sided heart catheterization data.

Results: We enrolled 84 patients with PAH, 17 with PVH without left ventricular systolic dysfunction, and seven with no PH and no severe alterations in pulmonary function testing. Etco(2) was significantly lower in patients with PAH than in those with no PH and PVH (P < .0001 PAH vs both groups). Etco(2) correlated with the pulmonary artery diastolic pressure-to-pulmonary artery occlusion pressure gradient (r = -0.50, P = .0002) and pulmonary vascular resistance (r = -0.44, P = .002). Etco(2) after 6MWT correlated with walk distance (r = 0.34, P = .003). In patients with prostaglandin therapy escalation, Etco(2) increased in those who had clinical improvement, whereas in patients who did not improve clinically, Etco(2) failed to rise (P = .04).

Conclusions: Etco(2) is a promising tool to differentiate patients with PAH from those with PVH or no PH, correlates with diagnostic and prognostic hemodynamic indicators, and may increase with successful treatment of PAH.

Figures

Figure 1.
Figure 1.
Etco2 in PAH, PVH, and no PH. Etco2 measurements are shown in PH subcategories and patients with no PH. Data are presented as median with 95% CI. Etco2 = end tidal CO2; PAH = pulmonary artery hypertension; PH = pulmonary hypertension; PVH = pulmonary venous hypertension. *P < .0001 vs no PH and PVH, one-way analysis of variance.
Figure 2.
Figure 2.
Receiver operating characteristic curve for sensitivity and specificity of Etco2 in the diagnosis of PAH. AUC = area under the curve. See Figure 1 legend for expansion of other abbreviations.
Figure 3.
Figure 3.
Correlation of invasive hemodynamics with Etco2. Scatterplots showing correlation of right-sided heart catheterization data with Etco2 measurements in patients with PAH, PVH, or no PH. Pearson test was used to determine correlation. PA = pulmonary artery; PAd = diastolic pulmonary artery pressure; PAOP = pulmonary artery occlusion pressure; PVR = pulmonary vascular resistance. See Figure 1 legend for expansion of other abbreviation.
Figure 4.
Figure 4.
Effect of 6-min walk test on Etco2 in healthy control subjects, subjects with PAH, and subjects with PVH. Bars denote P = .0004; other comparisons were not significant. Data are presented as mean with 95% CI. Pre = before 6-min walk test; Post = after 6-min walk test. See Figure 1 legend for expansion of other abbreviations.
Figure 5.
Figure 5.
Effect of prostaglandin therapy on Etco2. A, Change in Etco2 in the group of patients treated with new or escalating doses of IV or subcutaneous prostaglandins (P = .03 paired t test). B, Change in Etco2 as a function of clinical response (P = .04). See Figure 1 legend for expansion of abbreviation.

Source: PubMed

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