Pulmonary artery pressure and PaO2 in chronic obstructive pulmonary disease

Skjørten, Ingunn; Hilde, Janne Mykland; Melsom, Morten Nissen; Hansteen, V. H.; Steine, Kjetil; Humerfelt, Sjur

doi:10.1016/j.rmed.2013.03.021

Cited by 21 publications

(13 citation statements)

References 31 publications

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“… 7 , 11 , 34 This makes it difficult in daily clinical practice to use predictive models to identify patients with pretest probability of presenting PH. Skjørten et al 37 suggested that PaO 2 values at rest and peak exercise below 71 mmHg and 64 mmHg, respectively, indicate the need for further evaluation of coexisting PH. In our study, we failed to find an adequate model with functional variables that could help to predict the presence of PH.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary hemodynamic profile in chronic obstructive pulmonary disease

Portillo¹,

Torralba²,

Blanco³

et al. 2015

COPD

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IntroductionFew data are available in regards to the prevalence of pulmonary hypertension (PH) in the broad spectrum of COPD. This study was aimed at assessing the prevalence of PH in a cohort of COPD patients across the severity of airflow limitation, and reporting the hemodynamic characteristics at rest and during exercise.MethodsWe performed a retrospective analysis on COPD patients who underwent right-heart catheterization in our center with measurements obtained at rest (n=139) and during exercise (n=85). PH was defined as mean pulmonary artery pressure (mPAP) ≥25 mmHg and pulmonary capillary wedge pressure <15 mmHg. Exercise-induced PH (EIPH) was defined by a ratio of ΔmPAP/Δcardiac output >3.ResultsPH was present in 25 patients (18%). According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification, PH prevalence in GOLD 2 was 7% (3 patients); 25% (14 patients) in GOLD 3; and 22% (8 patients) in GOLD 4. Severe PH (mPAP ≥35 mmHg) was identified in four patients (2.8%). Arterial partial oxygen pressure was the outcome most strongly associated with PH (r=−0.29, P<0.001). EIPH was observed in 60 patients (71%) and had a similar prevalence in both GOLD 2 and 3, and was present in all GOLD 4 patients. Patients with PH had lower cardiac index during exercise than patients without PH (5.0±1.2 versus 6.7±1.4 L/min/m2, respectively; P=0.001).ConclusionPH has a similar prevalence in COPD patients with severe and very-severe airflow limitation, being associated with the presence of arterial hypoxemia. In contrast, EIPH is highly prevalent, even in moderate COPD, and might contribute to limiting exercise tolerance.

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Section: Discussionmentioning

confidence: 99%

Pulmonary hemodynamic profile in chronic obstructive pulmonary disease

Portillo¹,

Torralba²,

Blanco³

et al. 2015

COPD

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“…Severe PH with RHF can present with elevated jugular venous pressure, pulsatile, tender hepatomegaly, and peripheral oedema [66], although the latter is not specific and can be present in patients with CLD without PH [67]. In a study of 95 patients with COPD, PaO 2 < 71 mmHg was also associated with the presence of PH with a sensitivity of 76% [68]. …”

Section: Diagnosismentioning

confidence: 99%

Pulmonary Hypertension and Right Heart Dysfunction in Chronic Lung Disease

Zangiabadi

Pasquale

Sajkov

2014

BioMed Research International

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Group 3 pulmonary hypertension (PH) is a common complication of chronic lung disease (CLD), including chronic obstructive pulmonary disease (COPD), interstitial lung disease, and sleep-disordered breathing. Development of PH is associated with poor prognosis and may progress to right heart failure, however, in the majority of the patients with CLD, PH is mild to moderate and only a small number of patients develop severe PH. The pathophysiology of PH in CLD is multifactorial and includes hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, small vessel destruction, and fibrosis. The effects of PH on the right ventricle (RV) range between early RV remodeling, hypertrophy, dilatation, and eventual failure with associated increased mortality. The golden standard for diagnosis of PH is right heart catheterization, however, evidence of PH can be appreciated on clinical examination, serology, radiological imaging, and Doppler echocardiography. Treatment of PH in CLD focuses on management of the underlying lung disorder and hypoxia. There is, however, limited evidence to suggest that PH-specific vasodilators such as phosphodiesterase-type 5 inhibitors, endothelin receptor antagonists, and prostanoids may have a role in the treatment of patients with CLD and moderate-to-severe PH.

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“…In the study by Chaouat et al [8], severe PH was present in a subgroup of patients with mild airway obstruction and severe hypoxemia with very low diffusing capacity for carbon monoxide. Pulmonary artery vasoconstriction induced by alveolar hypoxia is considered to contribute to mild to moderate PH in COPD [11,12], but cigarette smoke [13] and inflammation (i.e. IL-6) [14] may also play a role.…”

Section: Introductionmentioning

confidence: 99%

Severe Pulmonary Hypertension Associated with COPD: Hemodynamic Improvement with Specific Therapy

Girard¹,

Jouneau²,

Chabanne³

et al. 2015

Respiration

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Background: There is no recommendation for treating pulmonary hypertension (PH) when associated with chronic obstructive pulmonary disease (COPD). Objective: To evaluate the effect of PH-specific therapy in patients with COPD. Methods: All successive patients with severe PH [mean pulmonary arterial pressure (mPAP) ≥35 mm Hg] and COPD, who received specific PH medication and who underwent right heart catheterization at baseline and after 3-12 months of treatment, were analyzed from a prospective database. Results: Twenty-six patients were included with a median follow-up of 14 months. Mean forced expiratory volume in 1 s was 57 ± 20% of predicted, and mean forced expiratory volume in 1 s/forced vital capacity was 47 ± 12%. Dyspnea was New York Health Association classification stage (NYHA) II in 15%, NYHA III in 81% and NYHA IV in 4%. First-line treatments were endothelin receptor antagonists in 11 patients, phosphodiesterase-5 inhibitors in 11 patients, calcium blocker in 1 patient, combination therapy in 3 patients including 2 with a prostanoid. After 6 ± 3 months, pulmonary vascular resistance decreased from 8.5 ± 3 to 6.6 ± 2 Wood units (p < 0.001), with significant improvement of cardiac index from 2.44 ± 0.43 to 2.68 ± 0.63 liters × min × m^-2 (p = 0.015) and mPAP from 48 ± 9 to 42 ± 10 mm Hg (p = 0.008). There was no significant difference in dyspnea, 6-min walking distance, echocardiographic parameters or N-terminal pro-brain natriuretic peptide levels. There was no significant difference in arterial oxygen saturation after 3-12 months of treatment. Conclusions: Specific PH medications may improve hemodynamic parameters in COPD patients with severe PH. Appropriate prospective randomized studies are needed to evaluate the potential long-term clinical benefit of treatment.

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Pulmonary artery pressure and PaO2 in chronic obstructive pulmonary disease

Abstract: In an outpatient COPD population where LV disease was thoroughly excluded, we observed that only PaO2 was a significant predictor of mPAP. PaO2 at rest and peak exercise below 9.5 kPa (71 mmHg) and 8.5 kPa (64 mmHg), respectively, indicates the need for further evaluation of coexisting PH.

Cited by 21 publications

References 31 publications

Pulmonary hemodynamic profile in chronic obstructive pulmonary disease

Pulmonary hemodynamic profile in chronic obstructive pulmonary disease

Pulmonary Hypertension and Right Heart Dysfunction in Chronic Lung Disease

Severe Pulmonary Hypertension Associated with COPD: Hemodynamic Improvement with Specific Therapy

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