Pulmonary vascular tone improves VA/Q matching in obliterative pulmonary hypertension

Dantzker, David R.; Bower, James S.

doi:10.1152/jappl.1981.51.3.607

Cited by 54 publications

(22 citation statements)

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“…165 Some researchers have suggested that maintaining pulmonary vascular tone could improve V-Q matching in these conditions and have advocated against mitigating the existing vascular tone by vasodilators. In order to decide whether potent vasodilators are use- Figure 6.…”

Section: What Is the Temporal Pattern Of Ph After Apte?mentioning

confidence: 99%

Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?

Tsang

Hogg

2014

Pulm. circ.

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Patients present with a wide range of hypoxemia after acute pulmonary thromboembolism (APTE). Recent studies using fluorescent microspheres demonstrated that the scattering of regional blood flows after APTE, created by the embolic obstruction unique in each patient, significantly worsened regional ventilation/ perfusion (V/Q) heterogeneity and explained the variability in gas exchange. Furthermore, earlier investigators suggested the roles of released vasoactive mediators in affecting pulmonary hypertension after APTE, but their quantification remained challenging. The latest study reported that mechanical obstruction by clots accounted for most of the increase in pulmonary vascular resistance, but that endothelin-mediated vasoconstriction also persisted at significant level during the early phase. More than 30 years ago, Eugene Robin commented on the problems of diagnosing acute pulmonary thromboembolism (APTE) by referring the physicians' attitudes to the emperor's vanity in Hans Christian Andersen's fable. 1,2 Although significant advances have occurred over the years, 3-5 some aspects of its pathophysiology remain puzzling. 6 This report provides an updated review of the literature, published mostly from 1980 onward, specifically addressing the mechanisms of hypoxemia and pulmonary hypertension (PH) after APTE. The emphasis is on the elucidation of the underlying pathophysiological principles and bringing them to the bedside, rather than on presenting meta-analysis or clinical trials. It also allows for occasional personal perspectives but has excluded recent works at the molecular level. GAS EXCHANGE IN APTEHypoxemia is a common and nonspecific feature of APTE. 7,8 It remains mysterious because the patient's arterial oxygen tension (PaO 2 ) is often unpredictable and correlates poorly with embolic load. [9][10][11] It is also associated with very different V/Q (ventilation/perfusion ratio) patterns measured by the multiple inert gas elimination technique (MIGET) among similar subjects 12 or in the same subject over time. 12,13 The roles of anatomical shunts may be important among a minority of patients but are questionable in the rest. These variations in gas exchange are clinically relevant in a negative way, because blood gas results do not contribute to defining pretest probabilities in the interpretation of nuclear scans. 1,14,15 The major purpose of this communication is to discuss the key factors that determine the degree of hypoxemia after APTE and their relevance to 5 commonly asked questions:1. Why do patients with APTE present with such a wide range of hypoxemia? 2. Why do many patients with APTE have relatively clear chest X-rays while severely hypoxic? 3. Can patients with significant APTE present with relatively normal PaO 2 ? 4. Why does hypoxemia worsen when cardiac output is increased? 5. Why do some patients with APTE have pulmonary infarcts and the others do not?

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Section: What Is the Temporal Pattern Of Ph After Apte?mentioning

confidence: 99%

Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?

Tsang

Hogg

2014

Pulm. circ.

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“…(Walmrath et al, 1997) Calcium channel blockers (Barberá andBlanco, 2009) Salbutamol i.v. (Ballester et al, 1989) High fraction of inhaled oxygen (Dantzker and Bower, 1981;Ballester et al, 1989) Inhaled salbutamol in patients with COPD and exacerbation (Polverino et al, 2007) Isoproterenol (Dantzker and Bower, 1981) Nitroprusside (Dantzker and Bower, 1981) Inhaled fenoterol high dose (Viegas et al, 1996) Aminophylline i.v. (Barberá et al, 1992) Sildenafil p.o.…”

Section: General Aspectsmentioning

confidence: 99%

Analysis of V/Q-matching—a safety “biomarker” in pulmonary drug development?

Amen¹,

Becker²,

Truebel³

2011

Biomarkers

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“…Also, in the presence of the increased pulmonary vascular resistance and advanced pulmonary vascular lesions, such as those described in Eisenmenger syndrome (21), perfusion distribution abnormalities in the perfusion distribution are expected. To our knowledge, the / distribution in the lungs of patients with Eisenmenger's syndrome as well as the effect of body position changes on this / distribution has not been prospectively studied, but as mentioned above, abnormalities in / distribution are likely to be present in these patients and they are also likely to be modified as a result of pulmonary hemodynamic changes (i.e., changes in cardiac output and pulmonary vascular resistance with position), as it has been shown in other human models of chronic obliterative pulmonary vascular disease (22,23).…”

Section: Pathophysiologic Mechanismmentioning

confidence: 99%

Effect of Body Position Changes on Pulmonary Gas Exchange in Eisenmenger's Syndrome

Sandoval

Alvarado²,

Martínez-Guerra³

et al. 1999

Am J Respir Crit Care Med

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Preliminary studies on sleep of patients with congenital heart disease and Eisenmenger's syndrome (ES) at our institution demonstrated nocturnal worsening arterial unsaturation, which appeared to be a body position-related phenomenon. To investigate the potential effect of body position on gas exchange in ES, we carried out a prospective study of 28 patients (mean age, 34.8 +/- 11.7 yr) with established ES due to congenital heart disease. In every patient, arterial blood gases were performed during both sitting and supine positions under three different conditions: room air, while breathing 100% oxygen, and after breathing oxygen at a flow rate of 3 L/min through nasal prongs. Alveolar oxygen pressure (PaO2) for the calculation of alveolar-arterial oxygen tension differences (AaPO2) was derived from the alveolar gas equation using PaCO2 and assuming R = 1. We used paired t test, repeated-measures two-way ANOVA with Bonferroni's test, and regression analysis. From sitting to supine position on room air, there was a significant decrease in PaO2 (from 52.5 +/- 7.5 to 47.5 +/- 5.5 mm Hg; p < 0. 001) and SaO2 (from 86.7 +/- 4.6 to 83.3 +/- 4.9%; p < 0.001), both of which were corrected by nasal O2 (to 68.2 +/- 21 mm Hg and to 92 +/- 4%, respectively, p < 0.005). PaCO2 and pH remained unchanged. The magnitude of the change in PaO2 correlated with the change in AaPO2 on room air (r = 0.77; p < 0.01) but not with the change in AaPO2 on 100% oxygen. It is concluded that in adult patients with ES there is a significant decrease in PaO2 and SaO2 when they change from the sitting to the supine position. A ventilation-perfusion (V/Q) distribution abnormality and/or a diffusion limitation phenomenon rather than an increase in true shunt may be the mechanisms responsible for this finding. The response to nasal O 2 we observed warrants a trial with long-term nocturnal oxygen therapy in these patients.

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Pulmonary vascular tone improves VA/Q matching in obliterative pulmonary hypertension

Cited by 54 publications

References 0 publications

Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?

Gas Exchange and Pulmonary Hypertension following Acute Pulmonary Thromboembolism: Has the Emperor Got Some New Clothes Yet?

Analysis of V/Q-matching—a safety “biomarker” in pulmonary drug development?

Effect of Body Position Changes on Pulmonary Gas Exchange in Eisenmenger's Syndrome

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