The Management of Acute Pulmonary Arterial Hypertension

Gan, Hui-Li

doi:10.1111/j.1755-5922.2009.00095.x

Cited by 27 publications

(18 citation statements)

References 180 publications

(194 reference statements)

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“…(13) If enough of the patient’s cardiopulmonary reserve has been compromised, these events can prove to be fatal; particularly if there is associated systemic hypotension (Qs) caused by massive pulmonary artery obstruction from PE resulting in a lack of life sustaining pulmonary perfusion (Qp). This disorder has a very high mortality rate (18%) for hospital in-patients.…”

Section: Acute Phmentioning

confidence: 99%

Magnetic Resonance and Computed Tomography Imaging of the Structural and Functional Changes of Pulmonary Arterial Hypertension

Schiebler

Bhalla

Runo

et al. 2013

Journal of Thoracic Imaging

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The current Dana Point classification system (2009) divides elevation of pulmonary artery pressure into Pulmonary Arterial Hypertension (PAH) and Pulmonary Hypertension (PH). Fortunately, pulmonary arterial hypertension (PAH) is not a common disease. However, with the aging of the first world’s population, heart failure is now an important cause of pulmonary hypertension with up to 9% of the population involved. PAH is usually asymptomatic until late in the disease process. While there are indirect features of PAH found on noninvasive imaging studies, the diagnosis and management still requires right heart catheterization. Imaging features of PAH include: 1. Enlargement of the pulmonary trunk and main pulmonary arteries, 2. Decreased pulmonary arterial compliance, 3. Tapering of the peripheral pulmonary arteries, 4. Enlargement of the inferior vena cava, and 5. Increased mean transit time. The chronic requirement to generate high pulmonary arterial pressures measurably affects the right heart and main pulmonary artery. This change in physiology causes the following structural and functional alterations that have been shown to have prognostic significance: Relative area change of the pulmonary trunk, RVSVindex, RVSV, RVEDVindex, LVEDVindex, and baseline RVEF <35%. All of these variables can be quantified non-invasively and followed longitudinally in each patient using MRI to modify the treatment regimen. Untreated PAH frequently results in a rapid clinical decline and death within 3 years of diagnosis. Unfortunately, even with treatment, less than 1/2 of these patients are alive at four years.

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Section: Acute Phmentioning

confidence: 99%

Magnetic Resonance and Computed Tomography Imaging of the Structural and Functional Changes of Pulmonary Arterial Hypertension

Schiebler

Bhalla

Runo

et al. 2013

Journal of Thoracic Imaging

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“…Thus, dysfunction of the molecular pathways and dysregulation of their production can lead to imbalance between vasodilation and vasoconstriction and between apoptosis and proliferation. These molecular alternations are thought to be the underlying disease mechanisms for chronic pulmonary arterial hypertension [12]. …”

Section: Pathophysiologymentioning

confidence: 99%

“…In acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), both hypoxic vasoconstriction and deposition of intravascular fibrin and cellular debris contribute to vascular obliteration and PH [13]. Endotoxin release in sepsis has been shown in animal studies to cause PH by causing constriction of proximal pulmonary arteries and decreased compliance of the distal pulmonary vasculature [12]. In massive acute pulmonary embolism, the increase in pulmonary vascular resistance is related to the mechanical obstruction from the thrombosis load and subsequent vasoconstriction [14].…”

Section: Pathophysiologymentioning

confidence: 99%

Pulmonary Hypertension in Pregnancy: Critical Care Management

et al. 2012

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Pulmonary hypertension is common in critical care settings and in presence of right ventricular failure is challenging to manage. Pulmonary hypertension in pregnant patients carries a high mortality rates between 30–56%. In the past decade, new treatments for pulmonary hypertension have emerged. Their application in pregnant women with pulmonary hypertension may hold promise in reducing morbidity and mortality. Signs and symptoms of pulmonary hypertension are nonspecific in pregnant women. Imaging workup may have undesirable radiation exposure. Pulmonary artery catheter remains the gold standard for diagnosing pulmonary hypertension, although its use in the intensive care unit for other conditions has slowly fallen out of favor. Goal-directed bedside echocardiogram and lung ultrasonography provide attractive alternatives. Basic principles of managing pulmonary hypertension with right ventricular failure are maintaining right ventricular function and reducing pulmonary vascular resistance. Fluid resuscitation and various vasopressors are used with caution. Pulmonary-hypertension-targeted therapies have been utilized in pregnant women with understanding of their safety profile. Mainstay therapy for pulmonary embolism is anticoagulation, and the treatment for amniotic fluid embolism remains supportive care. Multidisciplinary team approach is crucial to achieving successful outcomes in these difficult cases.

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“…Vasopressin has a unique role in this setting due to its ability to increase systemic pressure while having favourable effects on the pulmonary circulation, possibly via nitric oxide-mediated pulmonary vasodilation. 10 It may be an ideal agent to combine with inotropes with inodilatory properties. Specific operative factors (e.g., coronary air embolism, extrinsic mechanical compression) must be addressed.…”

mentioning

confidence: 99%

“…En raison de sa capacité à augmenter la tension systémique, la vasopressine joue un rôle unique dans ce contexte, tout en ayant des effets favorables sur la circulation pulmonaire, possiblement via la vasodilatation pulmonaire médiée par le monoxyde d'azote. 10 Il pourrait s'agir de l'agent idéal à combiner à des inotropes possédant des propriétés d'inodilatation. Les facteurs spécifiques à l'opération (embolie gazeuse coronarienne, compression mécanique extrinsèque) doivent être pris en charge.…”

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Inhaled milrinone for pulmonary hypertension in high-risk cardiac surgery: silver bullet or just part of a broader management strategy?

Bednarczyk

Strumpher

Jacobsohn

2016

Can J Anesth/J Can Anesth

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Pulmonary hypertension (PH) and right ventricular (RV) dysfunction are common and potentially devastating conditions in patients undergoing cardiac surgery. The prevalence of PH and elevated pulmonary vascular resistance (PVR) in patients with aortic stenosis and regurgitation is 15-30% and C 25%, respectively, and at least 40% in patients with mitral stenosis.1 In certain patients with pulmonary venous hypertension due to valvular cardiac disease, the elevated PVR persists or is slow to regress after valve replacement/repair as a result of remodelling of the pulmonary circulation.2 Preoperative PH is associated with prolonged mechanical ventilation, greater duration of hospital stay, and increased operative and long-term mortality.3 This is likely a consequence of the relationship between PH and the development of perioperative RV failure, a condition that, even with early recognition and treatment, has high morbidity and greater than 30% mortality. 4,5 Despite the critical importance of perioperative PH and RV dysfunction, there is a paucity of high-quality clinical trials addressing the perioperative management of these conditions.Milrinone, a phosphodiesterase-3 inhibitor, acts by augmenting cyclic adenosine monophosphate signalling to induce pulmonary and systemic vasodilation and to increase cardiac contractility -i.e., an inodilator.2,6 Inhaled milrinone (iMil) has attracted attention in view of the preferred route of administration in the setting of PH and RV dysfunction. There is a reduction in systemic vasodilation with this approach when compared with the intravenous route, and there is evidence to suggest that iMil has superior ability to mitigate pulmonary endothelial dysfunction during cardiopulmonary bypass (CPB). 7Lamarche et al. published retrospective data suggesting that the incidence of difficult weaning from CPB was reduced when iMil was administered before vs after CPB. 6 Until now, however, there has been a lack of prospective randomized-controlled trials evaluating the utility of iMil in this setting.In this issue of the Journal, Denault et al. present an important multicentre randomized-controlled trial examining a unique strategy for the management of perioperative PH and RV dysfunction.8 They posed the question: does prophylactic treatment with iMil before CPB facilitate separation from CPB in patients with preoperative PH? The authors studied 124 well-matched adult patients undergoing elective high-risk cardiac surgery with baseline mean pulmonary artery (PA) pressure [ 30 mmHg or a PA systolic pressure [ 40 mmHg. Patients were randomized to receive a single dose of either iMil (5 mg) or placebo through an in-line ultrasonic mesh nebulizer after induction of anesthesia. Detailed hemodynamic measurements and echocardiographic data were collected.

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The Management of Acute Pulmonary Arterial Hypertension

Cited by 27 publications

References 180 publications

Magnetic Resonance and Computed Tomography Imaging of the Structural and Functional Changes of Pulmonary Arterial Hypertension

Magnetic Resonance and Computed Tomography Imaging of the Structural and Functional Changes of Pulmonary Arterial Hypertension

Pulmonary Hypertension in Pregnancy: Critical Care Management

Inhaled milrinone for pulmonary hypertension in high-risk cardiac surgery: silver bullet or just part of a broader management strategy?

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