Pulmonary hypertension at exercise in COPD: does it matter?

Naeije, Robert; Boerrigter, Bart

doi:10.1183/09031936.00173512

Cited by 20 publications

(14 citation statements)

References 22 publications

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“…While normal respiratory cycle-ventricular filling interactions are complex [22, 23], the most significant factor influencing respirophasic wedge pressure variation appears to be intrathoracic pressure variation. Previous work in COPD has supported a close relationship between variable intrathoracic pressure and measured wedge pressures [19-21, 24, 25]. Rice et al ., for example, demonstrated very tight correlation (slope 1.04, r=0.98) between changes in esophageal and wedge pressures during respiration in COPD patients [19].…”

Section: Discussionmentioning

confidence: 84%

“…During catheterization, use of end-expiratory PAWP assumes that intrathoracic pressure is approximately equal to atmospheric pressure at end-exhalation, and thus that measured PAWP reflects a transmural left ventricular filling pressure. In the setting of mechanical ventilation [14, 15], obesity [16], or chronic obstructive pulmonary disease (COPD) [17-21], end-expiratory intrathoracic pressure can be significantly greater than atmospheric. In these scenarios, use of end-expiratory PAWP overestimates true transmural PAWP (as well as RAP).…”

Section: Discussionmentioning

confidence: 99%

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Reliance on end-expiratory wedge pressure leads to misclassification of pulmonary hypertension

2014

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Current guidelines recommend measurement of pulmonary artery wedge pressure (PAWP) at end-expiration. However, this recommendation is not universally followed and may not be physiologically appropriate. We investigated the performance of end-expiratory wedge pressure (eePAWP) in the evaluation of precapillary pulmonary hypertension patients. Three hundred and twenty-nine spontaneously breathing patients undergoing right heart catheterization were retrospectively classified as having precapillary, postcapillary, or mixed phenotype based on standardized clinical criteria. Tracings were reviewed to compare eePAWP with PAWP averaged throughout the respiratory cycle; these values were correlated with the clinical classifications. Predictors of large respirophasic excursion in PAWP were determined. Elevated eePAWP (>15 mm Hg) occurred in 29.0% of subjects with precapillary phenotype. There were no differences in demographics or clinical history between those with elevated and normal eePAWP. Those with elevated eePAWP had greater right atrial pressure and respirophasic PAWP variation. Among all subjects, the magnitude of respirophasic variation in PAWP was positively correlated with body mass index and respirophasic variation in left ventricular end diastolic pressure. A significant proportion of precapillary pulmonary hypertension patients have eePAWP >15 mm Hg. Spontaneous positive end-expiratory intrathoracic pressure may contribute; in those cases, PAWP averaged throughout respiration may be a more accurate measurement.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Reliance on end-expiratory wedge pressure leads to misclassification of pulmonary hypertension

2014

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“…Negative intrathoracic pressure during OSA might additionally cause PAP to rise by increased pulmonary vascular resistance [40]. A similar mechanism has recently been documented in patients with COPD experiencing major increases in pleural pressure swings during exercise that were accompanied by rises in PAP [41]. …”

Section: Mechanisms Linking Precapillary Ph and Sdbmentioning

confidence: 96%

Precapillary Pulmonary Hypertension and Sleep-Disordered Breathing: Is There a Link?

2016

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Among patients with sleep apnea the reported prevalence of precapillary pulmonary hypertension (PH) has varied largely, depending on patient selection, disease definition, and associated conditions, in particular chronic pulmonary disease. However, in the absence of comorbidities, PH seems to be rare in patients with sleep apnea. Conversely, sleep-related breathing disorders have been commonly found in patients with PH and they have been associated with an impaired quality of life. Since sleep-related breathing disorders may affect the pulmonary circulation and vice versa, patients with sleep-related breathing disorders should be evaluated for risk factors, symptoms and clinical signs of PH and right ventricular heart failure and patients with PH should be evaluated for sleep apnea. Therapeutic options for patients with sleep apnea and PH may include supplemental oxygen, drugs and positive pressure ventilation. Both nocturnal oxygen administration and acetazolamide have been shown to improve sleep apnea in patients with PH. In addition, oxygen therapy also improved exercise performance. Further studies are needed to corroborate the efficacy of these and other treatments.

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“…Negativer intrathorakaler Druck bei OSA könnte zusätzlich zur PAP-Erhöhung führen, indem der pulmonale Gefäßwiderstand erhöht wird [40]. Ein ähnlicher Mechanismus wurde kürzlich bei COPD-Patienten dokumentiert, bei denen deutlich verstärkte pleurale Druckschwankungen unter Belastung in Begleitung von PAP-Anstiegen gemessen wurden [41]. …”

Section: Mechanismen Die Präkapilläre Ph Und Sbas Verbindenunclassified

Präkapilläre pulmonale Hypertonie und schlafbezogene Atmungsstörungen: Gibt es einen Zusammenhang?

2018

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Zur Prävalenz der präkapillären pulmonalen Hypertonie (PH) bei Patienten mit Schlafapnoe liegen sehr unterschiedliche Angaben vor, je nach Auswahl der Patienten, Krankheitsdefinition und Begleiterkrankungen, insbesondere chronische Lungenerkrankungen. Wenn keine Komorbiditäten vorliegen, scheint PH bei Patienten mit Schlafapnoe jedoch selten zu sein. Umgekehrt kommen schlafbezogene Atmungsstörungen bei PH-Patienten häufig vor und gehen mit einer Beeinträchtigung ihrer Lebensqualität einher. Da sich schlafbezogene Atmungsstörungen auf den Lungenkreislauf auswirken können und umgekehrt, sollten Patienten mit schlafbezogenen Atmungsstörungen auf Risikofaktoren, Symptome und klinische Anzeichen für PH und rechtsventrikuläre Herzinsuffizienz untersucht werden, und Patienten mit PH sollten im Hinblick auf Schlafapnoe evaluiert werden. Mögliche Therapieoptionen für Patienten mit Schlafapnoe und PH sind zum Beispiel Sauerstoffgabe, Medikamente und Überdruckbeatmung. Sowohl nächtliche Sauerstoffgabe als auch Acetazolamid bewirken nachweislich eine Besserung der Schlafapnoe bei PH-Patienten. Eine Sauerstofftherapie verbesserte außerdem die körperliche Belastbarkeit. Weitere Studien sind erforderlich, um die Wirksamkeit dieser und anderer Behandlungsmaßnahmen zu unterfüttern. Übersetzung aus Respiration 2017;93:65-77 (DOI: 10.1159/000452957)

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Pulmonary hypertension at exercise in COPD: does it matter?

Cited by 20 publications

References 22 publications

Reliance on end-expiratory wedge pressure leads to misclassification of pulmonary hypertension

Reliance on end-expiratory wedge pressure leads to misclassification of pulmonary hypertension

Precapillary Pulmonary Hypertension and Sleep-Disordered Breathing: Is There a Link?

Präkapilläre pulmonale Hypertonie und schlafbezogene Atmungsstörungen: Gibt es einen Zusammenhang?

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