The use of inhaled aerosolized prostacyclin (IAP) in the treatment of pulmonary hypertension secondary to pulmonary embolism

Webb, Sally A.; Stott, S; Heerden, Peter Vernon van

doi:10.1007/bf01700458

Cited by 61 publications

(29 citation statements)

References 6 publications

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“…However, inhaled iloprost did not result in acute improvements in hemodynamics in patients immediately before PEA in another study [26]. Previously, several case reports of inhaled iloprost in CTEPH have been reported [27, 28]. In one study by Ulrich et al [29],acute vasoreactivity testing with inhalative nitric oxide and iloprost was performed in patients with IPAH and CTEPH showing similar pulmonary artery reactivity.…”

Section: Introductionmentioning

confidence: 99%

Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension

Krug¹,

Hammerschmidt²,

Pankau³

et al. 2007

Respiration

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Background: Chronic thromboembolic pulmonary hypertension (CTEPH) is a potential consequence to pulmonary embolism. The histologic picture is similar to idiopathic pulmonary hypertension (IPAH) suggesting that vascular remodeling also contributes to CTEPH. The treatment of choice is pulmonary endarterectomy. However, this treatment option is not adequate for all patients with CTEPH. Currently, no data exist on standard vasodilative therapy for CTEPH. Intravenous and oral prostanoids, both well-known vasodilators in IPAH, have been used with promising results, whereas the same has not been consistently observed for inhaled iloprost. Objective: In this study, we examined acute hemodynamic effects of inhaled iloprost in patients with CTEPH. Methods: In a prospective study, right heart catheterization was performed in 20 patients (mean age 56 years, New York Heart Association class II–IV) at the time of diagnosis of CTEPH. Pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (mPAP), cardiac output (CO), mean systemic arterial pressure (MAP) and oxygen partial pressure (PaO₂) were obtained before and 20 min after inhaling 5 µg iloprost. Subsequently, all patients were evaluated for pulmonary endarterectomy. Six patients were eligible for surgery. Results: Significant changes in pulmonary and systemic hemodynamics were observed following the inhalation of iloprost (before to after inhalation): PVR: 1,057 ± 404.3 to 821.3 ± 294.3 dyn·s·cm^–5, p < 0.0001; mPAP: 50.55 ± 8.43 to 45.75 ± 8.09 mm Hg, p = 0.0002; CO: 3.66 ± 1.05 to 4.05 ± 0.91 l/min, p < 0.0106. MAP and PaO₂ decreased significantly (MAP: 94.15 ± 11.58 to 89.45 ± 14.29 mm Hg, p = 0.0111; PaO₂: 7.33 ± 1.17 to 6.64 ± 1.25 kPa, p = 0.0260). Conclusions: Hemodynamic changes directly following inhalation of iloprost suggest a significant contribution of a reversible component of vasoconstriction to pulmonary arterial hypertension in patients with CTEPH.

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Section: Introductionmentioning

confidence: 99%

Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension

Krug¹,

Hammerschmidt²,

Pankau³

et al. 2007

Respiration

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“…Inhaled aerosolised prostacyclin has been used in severe pulmonary hypertension secondary to massive PE, resulting in transient improvement in pulmonary haemodynamics and gas exchange. 83 …”

Section: Pulmonary Vasodilatorsmentioning

confidence: 99%

Pulmonary Embolism in the Mechanically-Ventilated Critically Ill Patient: Is it Different?

Zochios

Keeshan

2013

Journal of the Intensive Care Society

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Acute PE results in increased right ventricular (RV) afterload. If the afterload is severely increased, RV enlargement, hypokinesis, ischaemia and RV failure may ensue. 13,14 The concomitant release of vasoactive and bronchoactive humoral factors such as serotonin from platelets, thrombin from plasma and histamine from tissue, have all been implicated in both pulmonary oedema and the ventilation-perfusion mismatch seen. 15 Experimental data suggest that the main mechanisms involved in hypoxaemia and the increase in the alveolararterial oxygen tension gradient are shunt, low ventilationperfusion ratio (V/Q), decrease in the mixed venous partial Pulmonary embolism in the mechanicallyventilated critically ill patient: is it different? 2C03, 3C00VA Zochios, A Keeshan Pulmonary embolism (PE) confers significant in-hospital morbidity and mortality, and critically ill patients remain at risk for venous thromboembolism despite thromboprophylaxis. Recognition of the clinical manifestations and immediate management of PE are of paramount importance. Despite diagnostic advances, PE is often undiagnosed and untreated in patients receiving mechanical ventilation, as these patients do not exhibit the common clinical features of the condition, making the diagnosis very challenging. Computed tomographic pulmonary angiography is probably the reference standard for the diagnosis of acute PE in the haemodynamically stable, ventilated patient. In the setting of circulatory collapse, bedside echocardiography may be used to risk stratify these patients, based on the presence or absence of right ventricular dysfunction, and guide further management. Treatment options include anticoagulation alone, anticoagulation plus thrombolysis, surgical or catheter embolectomy. Inotropes, vasopressors and pulmonary artery vasodilators may be considered after initial resuscitation of the right ventricle. Few studies have focused on estimating the prevalence of PE among mechanically-ventilated intensive care unit (ICU) patients and there is notable lack of data assessing predictive factors, prevention, diagnostic strategy and management of PE in the ICU setting.

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“…Ähnlich wie NO führt ᭤Prostacyclinaerosol bei akuter Lungenembolie ebenfalls zu einer selektiven Senkung des pulmonalarteriellen Drucks [62]. Prostacyclin ist ein natürlicher Antagonist des Thromboxans.…”

Section: Hämodynamische Stabilisierung Beatmungunclassified

Die akute Lungenarterienembolie

Walther

Böttiger

2002

Anaesthesist

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Der Anaesthesist 5•2002 | 427 Weiter-und Fortbildung Lungenarterienembolie Trotz nachgewiesener Vorteile verschiedener prophylaktischer Maßnahmen zur Vermeidung einer akuten Thromboembolie der Lunge zählt die Lungenembolie in Deutschland mit etwa 20.000 Todesfällen pro Jahr nach wie vor zu den Haupttodesursachen hospitalisierter Patienten [2]. Die Prävalenz der Lungenembolie bei Autopsien ist in den letzten drei Jahrzehnten unverändert hoch und liegt bei 12-15% der zuvor stationären Patienten [58]. Nur in etwa 30% der autoptisch gesicherten Fälle wird die Diagnose zu Lebzeiten gestellt [42]. Unbehandelt beträgt die Mortalität der Lungenembolie ca. 30%. Unter adäquater Therapie lässt sich die Mortalitätsrate auf 2-8% senken [10, 17, 60]. Der Häufigkeitsgipfel der perioperativen Lungenembolie liegt am 3. postoperativen Tag für gefäßchirurgische Patienten und am 9. postoperativen Tag in der Allgemeinchirurgie [53]. Charakteristisch für die Lungenembolie ist eine hohe Frühletalität. Innerhalb von 1-2 h nach Symptombeginn ereignen sich 45-90% aller Todesfälle [3,58].Werden embolische Ereignisse überlebt, besteht das Langzeitrisiko in der Manifestation einer pulmonalen Hypertonie. Diese entsteht durch rezidivierende, oft klinisch inapparent verlaufende kleinere Lungenembolien und/oder durch unzureichende Reperfusion der pulmonalen Strombahn nach Lungenembolie [43]. Die medizinischen Anforderungen, die sowohl die Diagnose als auch die Therapie der Lungenembolie betreffen, können nur interdisziplinär in enger Zusammenarbeit zwischen den Fachdisziplinen und unter genauer Kenntnis der pathophysiologischen Veränderungen bewältigt werden. Unter einer Lungenarterienembolie versteht man den embolischen Verschluss eines Lungenarterienastes, wobei sich der Verschluss entweder zentral im Bereich der A. pulmonalis, eines Hauptastes oder peripher im Bereich der Segment-bis Subsegmentarterien manifestieren kann. Die häufigste ᭤Ursache einer Lungenembolie ist die tiefe Beinvenenthrombose auf dem Boden bestehender Risikofaktoren.Auch andere Embolieursachen wie Luft, Fett, Knochenmark, Palacos oder Amnionflüssigkeit Lungenarterienembolie=embolischer Verschluss im Bereich der Lungenarterien ᭤ Ursache für Lungenembolie Die Beiträge der Rubrik "Weiter-und Fortbildung" sollen dem Facharzt als Repetitorium dienen und dem Wissenstand der Facharztprüfung für den Arzt in Weiterbildung entsprechen.Die Rubrik beschränkt sich auf gesicherte Aussagen zum Thema.

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The use of inhaled aerosolized prostacyclin (IAP) in the treatment of pulmonary hypertension secondary to pulmonary embolism

Abstract: We describe a patient with massive pulmonary embolism for whom the addition of IAP to his therapy appeared to result in a transient improvement in pulmonary haemodynamics and gas exchange.

Cited by 61 publications

References 6 publications

Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension

Acute Improved Hemodynamics following Inhaled Iloprost in Chronic Thromboembolic Pulmonary Hypertension

Pulmonary Embolism in the Mechanically-Ventilated Critically Ill Patient: Is it Different?

Die akute Lungenarterienembolie

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