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

ABSTRACT: 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.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.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).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.

SUBMITTER: Hemnes AR

PROVIDER: S-EPMC4694178 | biostudies-other | 2011 Nov

REPOSITORIES: biostudies-other

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Project description:Pulmonary vascular arterial remodeling is an integral and well-understood component of pulmonary hypertension (PH). In contrast, morphological alterations of pulmonary veins in PH are scarcely described. Explanted lungs (n = 101) from transplant recipients with advanced chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary arterial hypertension (IPAH) were analyzed for venous vascular involvement according to a pre-specified, semi-quantitative grading scheme, which categorizes the intensity of venous remodeling in three groups of incremental severity: venous hypertensive (VH) grade 0 = characterized by an absence of venous vascular remodeling; VH grade 1 = defined by a dominance of either arterialization or intimal fibrosis; and VH grade 2 = a substantial composite of arterialization and intimal fibrosis. Patients were grouped according to clinical and hemodynamic characteristics in three groups: COPD non-PH, COPD-PH, and IPAH, respectively. Histological specimens were examined by a cardiovascular pathologist blinded to clinical and hemodynamic data. Pathological alterations of pulmonary veins were present in all hemodynamic groups, with the following incidences of VH grade 0/1/2: 34/66/0% in COPD non-PH; 19/71/10% in COPD-PH; and 11/61/28% in IPAH. In COPD, explorative correlation analysis of venous remodeling suggested a modest positive correlation with systolic and mean pulmonary artery pressure ( P = 0.032, respectively) and an inverse modest correlation with diffusion capacity for carbon monoxide ( P = 0.027). In addition, venous remodeling correlated positively with the degree of arterial remodeling ( P = 0.014). In COPD-PH and IPAH, advanced forms of pulmonary venous remodeling are present, emphasizing that the disease is not exclusively restricted to arterial lesions. In addition, venous remodeling may be related to the hemodynamic severity, but more rigorous analysis is required to clearly define potential relationships.

Project description:BackgroundPulmonary hypertension is a heterogeneous disease, and a significant portion of patients at risk for it have CT imaging available. Advanced automated processing techniques could be leveraged for early detection, screening, and development of quantitative phenotypes. Pruning and vascular tortuosity have been previously described in pulmonary arterial hypertension (PAH), but the extent of these phenomena in arterial vs venous pulmonary vasculature and in exercise pulmonary hypertension (ePH) have not been described.Research questionWhat are the arterial and venous manifestations of pruning and vascular tortuosity using CT imaging in PAH, and do they also occur in ePH?Study design and methodsA cohort of patients with PAH and ePH and control subjects with available CT angiograms were retrospectively identified to examine the differential arterial and venous presence of pruning and tortuosity in patients with precapillary pulmonary hypertension not confounded by lung or thromboembolic disease. The pulmonary vasculature was reconstructed, and an artificial intelligence method was used to separate arteries and veins and to compute arterial and venous vascular volumes and tortuosity.ResultsA total of 42 patients with PAH, 12 patients with ePH, and 37 control subjects were identified. There was relatively lower (median [interquartile range]) arterial small vessel volume in subjects with PAH (PAH 14.7 [11.7-16.5; P < .0001]) vs control subjects (16.9 [15.6-19.2]) and venous small vessel volume in subjects with PAH and ePH (PAH 8.0 [6.5-9.6; P < .0001]; ePH, 7.8 [7.5-11.4; P = .004]) vs control subjects (11.5 [10.6-12.2]). Higher large arterial volume, however, was only observed in the pulmonary arteries (PAH 17.1 [13.6-23.4; P < .0001] vs control subjects 11.4 [8.1-15.4]). Similarly, tortuosity was higher in the pulmonary arteries in the PAH group (PAH 3.5 [3.3-3.6; P = .0002] vs control 3.2 [3.2-3.3]).InterpretationLower small distal pulmonary vascular volume, higher proximal arterial volume, and higher arterial tortuosity were observed in PAH. These can be quantified by using automated techniques from clinically acquired CT scans of patients with ePH and resting PAH.

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

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