Diagnosis and management of pulmonary hypertension

2016 ◽  
Author(s):  
Philip Marino ◽  
Laura Price
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Critical Illness ◽  
Management Strategies ◽  
Haemodynamic Monitoring ◽  
Vasoactive Agents ◽  
Non Invasive ◽  
Pulmonary Vasodilators ◽  
Surgical Options ◽  
Pulmonary Arterial

The diagnosis of pulmonary hypertension (PH) and associated right ventricular (RV) dysfunction or failure in the setting of critical illness relies on the use of non-invasive tools including echocardiography, and in some cases invasive haemodynamic monitoring. The management for PH and RV failure in the ICU may be challenging, and is dependent on local expertise and drug availability.Systemic vasoactive agents and pulmonary vasodilators play an important role. Patients with pulmonary arterial hypertension, pulmonary embolism or chronic thromboembolic PH should be anticoagulated; those with haemodynamically unstable PE may require thrombolysis.The characteristics of individual agents must be considered and monitored carefully.Few clinical studies or ICU-specific guidelines exist. Surgical options exist for patients with PH and RV failure. This chapter reviews the diagnostic and management strategies of PH and RV failure in the ICU setting.

scholarly journals Effect of Coronavirus Disease 2019 in Pulmonary Circulation. The Particular Scenario of Precapillary Pulmonary Hypertension

Diagnostics ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 548 ◽  
Author(s):  
Jorge Nuche ◽  
Teresa Segura de la Cal ◽  
Carmen Jiménez López Guarch ◽  
Francisco López-Medrano ◽  
Carmen Pérez-Olivares Delgado ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Respiratory Infections ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
The Elderly ◽  
Angiotensin Converting Enzyme 2 ◽  
Common Features ◽  
Pulmonary Vasodilators ◽  
Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
Low Incidence

The Coronavirus Disease of 2019 (COVID-19) has supposed a global health emergency affecting millions of people, with particular severity in the elderly and patients with previous comorbidities, especially those with cardiovascular disease. Patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) could represent an especially vulnerable population because of the high mortality rates reported for respiratory infections. However, the number of COVID-19 cases reported among PAH and CTEPH patients is surprisingly low. Furthermore, the clinical picture that has been described in these patients is far from the severity that experts would expect. Endothelial dysfunction is a common feature between patients with PAH/CTEPH and COVID-19, leading to ventilation/perfusion mismatch, vasoconstriction, thrombosis and inflammation. In this picture, the angiotensin-converting enzyme 2 plays an essential role, being directly involved in the pathophysiology of both clinical entities. Some of these common characteristics could explain the good adaptation of PAH and CTEPH patients to COVID-19, who could also have obtained a benefit from the disease’s specific treatments (anticoagulant and pulmonary vasodilators), probably due to its protective effect on the endothelium. Additionally, these common features could also lead to PAH/CTEPH as a potential sequelae of COVID-19. Throughout this comprehensive review, we describe the similarities and differences between both conditions and the possible pathophysiological and therapeutic-based mechanisms leading to the low incidence and severity of COVID-19 reported in PAH/CTEPH patients to date. Nevertheless, international registries should look carefully into this population for better understanding and management.

Pulmonary arterial hypertension and acute and chronic thromboembolism

ESC CardioMed ◽  
2018 ◽  
pp. 406-409
Author(s):  
Thomas Henzler
Keyword(s):  
Computed Tomography ◽  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Imaging Modality ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Right Ventricular Dysfunction ◽  
Chronic Pulmonary Embolism ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) and acute and chronic pulmonary embolism represent severe cardiovascular diseases with a high mortality if left undiagnosed and untreated. Computed tomography of the chest plays a pivotal role in the diagnosis of all three disorders. In acute pulmonary embolism, computed tomography pulmonary angiography has become the gold-standard imaging modality due to its high diagnostic accuracy, cost-effectiveness, 24-hour availability at most institutions, as well as the ability to diagnose alternative chest pathologies and right ventricular dysfunction within a single examination. In PAH, computed tomography of the chest is also deeply embedded within the diagnostic algorithm in order to exclude other causes of pulmonary hypertension, such as structural lung disease and chronic thromboembolic pulmonary hypertension of left heart disease. This article intends to provide a short overview on imaging techniques and characteristic findings in PAH, as well as acute and chronic pulmonary embolism.

Pathophysiology and causes of pulmonary hypertension

2016 ◽  
Author(s):  
Laura Price ◽  
S. John Wort
Keyword(s):  
Pulmonary Hypertension ◽  
Critical Illness ◽  
Positive Pressure Ventilation ◽  
Massive Pulmonary Embolism ◽  
Positive Pressure ◽  
Vasoactive Drugs ◽  
Acute Decompensation ◽  
Prognostic Feature ◽  
Pulmonary Arterial ◽  
Poor Prognostic Feature

Pulmonary hypertension (PH) in the setting of critical illness may reflect the acute syndrome itself (such as acute massive pulmonary embolism or acute lung injury), and/or pre-existing ‘chronic’ causes of PH. To compound this, iatrogenic factors may also contribute to PH including the effects of positive pressure ventilation and certain vasoactive drugs. The presence of PH, especially when complicated by resulting right ventricular (RV) dysfunction and failure, is a poor prognostic feature in all settings. This chapter reviews the pathophysiology of acute PH in critical illness, and pre-existing chronic causes of PH, including acute decompensation in patients with pre-existing pulmonary arterial hypertension.

Effect of selective embolization of various sized pulmonary arteries in dogs

1963 ◽  
Vol 204 (4) ◽  
pp. 619-625 ◽  
Author(s):  
John W. Hyland ◽  
George T. Smith ◽  
Lockhart B. McGuire ◽  
Donald C. Harrison ◽  
Florence W. Haynes ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Internal Diameter ◽  
Polystyrene Spheres ◽  
Selective Embolization ◽  
Blood Clots ◽  
Pulmonary Arterial ◽  
The Right

Pulmonary embolism was produced in 30 closed-chest 8-kg dogs with polystyrene spheres, glass beads, or blood clots of precise graded size. The sizes matched selectively the internal diameter of pulmonary arteries from lobar branches (5–6 mm) down to atrial arteries (0.17 mm). Emboli were injected into the right atrium until the pressure in the pulmonary artery rose 5–10 mm Hg. The number of emboli of a given size required to produce this incipient pulmonary hypertension was compared with the number of vessels of that same size as determined from the literature as well as by postmortem injection with Schlesinger mass. The number of emboli bore a constant relation to the number of vessels of that same size. With each size, the majority of vessels had to be occluded before pulmonary hypertension appeared. This was true even in the absence of anesthesia. The results support the thesis that mechanical blockade rather than vasoconstriction is the mechanism by which pulmonary hypertension is produced by emboli occluding pulmonary arterial (as opposed to arteriolar) vessels.

scholarly journals Classification of Pulmonary Hypertension

2014 ◽  
Vol 13 (1) ◽  
pp. 17-20
Author(s):  
Rogerio Souza ◽  
Gerald Simonneau
Keyword(s):  
Pulmonary Hypertension ◽  
Task Force ◽  
Management Strategies ◽  
Pathological Findings ◽  
Clinical Classification ◽  
Current Classification ◽  
Pulmonary Arterial ◽  
Current Classification System ◽  
Group 1

Classification of pulmonary hypertension groups patients with similar pathological findings, hemodynamic profiles, and management strategies. Minor modifications have been made to the current classification system, particularly within Group 1 pulmonary arterial hypertension. This article summarizes the published conclusions of the Fifth World Symposium of Pulmonary Hypertension task force that addressed the updated clinical classification of pulmonary hypertension.

Starling resistor vs. distensible vessel models for embolic pulmonary hypertension

1995 ◽  
Vol 268 (2) ◽  
pp. H817-H827 ◽  
Author(s):  
C. Melot ◽  
M. Delcroix ◽  
J. Closset ◽  
P. Vanderhoeft ◽  
P. Lejeune ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Left Atrial ◽  
Glass Bead ◽  
Inflection Point ◽  
Pulmonary Arterial Pressure ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Closing Pressure

We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065–1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15–26, 1991) best describes pulmonary vascular pressure-flow (Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (Ppa)-Q plots at constant left atrial pressure (Pla) and Ppa-Pla plots at constant Q were investigated in seven dogs before and after 500-micron glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P(i)) of Ppa-Q plots and increased the inflection point of Ppa-Pla plots, above which an increase in Pla is transmitted to Ppa in a ratio of approximately 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the Ppa-Q and Ppa-Pla coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of Ppa-Pla plots and P(i). We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.

scholarly journals Children with Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension Treated with Pulmonary Vasodilators—The Pediatric Cardiologist Point of View

Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 326
Author(s):  
Anna Migdał ◽  
Anna Sądel-Wieczorek ◽  
Edyta Ryciak ◽  
Alicja Mirecka-Rola ◽  
Grażyna Brzezińska-Rajszys ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Prognostic Factors ◽  
Bronchopulmonary Dysplasia ◽  
Pressure Ratio ◽  
Point Of View ◽  
Term Outcome ◽  
Pulmonary Vasodilators ◽  
Long Term Effect ◽  
Postmenstrual Age ◽  
Pulmonary Arterial

Pulmonary hypertension in children with bronchopulmonary dysplasia (BPD-PH) significantly worsens the prognosis. Pulmonary vasodilators are often used in BPD-PH but the short-term outcome of treatment is not well described. The aim of this study was to evaluate BPD-PH children diagnosed beyond 36 weeks postmenstrual age treated with pulmonary vasodilators (sildenafil, bosentan, or both) and to assess the short and long-term effect of oral pulmonary vasodilators treatment. Twenty patients were included in the study. Cardiology evaluation (WHO-FC, NTproBNP, oxygen saturation, pulmonary to systemic pressure ratio PAP/SAP) was performed at diagnosis and after treatment initiation. In the majority of patients improvement in all evaluated factors was observed. No side effects of vasodilators were observed. PH resolved in 10 patients after a mean of 21.4 months of treatment. Six patients died. The number of poor prognostic factors commonly used to assess patients with pulmonary arterial hypertension (PAH) decreased significantly during BPD-PH treatment. The influence of BPD-PH perinatal risk factors on prognosis was considered but was not confirmed. In conclusion, the treatment of BPD-PH with pulmonary vasodilators was well tolerated and led to a clinical improvement with the possibility of discontinuation without recurrence of PH. Prognostic factors used in pediatric PAH risk stratification also seem to be useful in assessing treatment efficacy and prognosis in patients with BPD-PH.

scholarly journals The Efficacy and Safety of Pulmonary Vasodilators in Pediatric Pulmonary Hypertension (PH): A Systematic Review and Meta-analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Tingting Shu ◽  
Huaqiao Chen ◽  
Lu Wang ◽  
Wuwan Wang ◽  
Panpan Feng ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Pulmonary Hypertension ◽  
Meta Analysis ◽  
Control Group ◽  
Efficacy And Safety ◽  
Pulmonary Vasodilators ◽  
Ventilation Duration ◽  
Mechanical Ventilation Duration ◽  
Pulmonary Arterial

Background: We performed a meta-analysis to evaluate the efficacy and safety of pulmonary vasodilators in pediatric pulmonary hypertension (PH) patients.Methods: We searched electronic databases including PubMed, EMBASE, and the Cochrane Library up to May 2020, and conducted a subgroup analysis for pulmonary vasodilators or underlying disease.Results: Fifteen studies with 719 pediatric PH patients were included in the meta-analysis. Adverse events did not differ (p = 0.11, I2 = 15%) between the pulmonary vasodilators group and the control group, neither in the subgroups. In total, compared with the control group treatment, pulmonary vasodilators significantly decreased the mortality (p = 0.002), mean pulmonary artery pressure (mPAP, p = 0.02), and mechanical ventilation duration (p = 0.03), also improved the oxygenation index (OI, p = 0.01). In the persistent pulmonary hypertension of the newborn (PPHN) subgroup, phosphodiesterase type 5 inhibitors (PDE5i) significantly reduced mortality (p = 0.03), OI (p = 0.007) and mechanical ventilation duration (p = 0.004). Administration of endothelin receptor antagonists (ERAs) improved OI (p = 0.04) and mechanical ventilation duration (p < 0.00001) in PPHN. We also found that in the pediatric pulmonary arterial hypertension (PPAH) subgroup, mPAP was pronouncedly declined with ERAs (p = 0.006). Systolic pulmonary artery pressure (sPAP, p < 0.0001) and pulmonary arterial/aortic pressure (PA/AO, p < 0.00001) were significantly relieved with PDE5i, partial pressure of arterial oxygen (PaO2) was improved with prostacyclin in postoperative PH (POPH) subgroup (p = 0.001). Compared with the control group, pulmonary vasodilators could significantly decrease PA/AO pressure (p < 0.00001) and OI (p < 0.00001) in the short-term (duration <7 days) follow-up subgroup, improve mPAP (p = 0.03) and PaO2 (p = 0.01) in the mid-term (7–30 days) follow-up subgroup, also decrease mortality, mPAP (p = 0.0001), PA/AO pressure (p = 0.0007), duration of mechanical ventilation (p = 0.004), and ICU stay (p < 0.00001) in the long-term follow subgroup (>30 days).Conclusion: Pulmonary vasodilators decrease the mortality in pediatric PH patients, improve the respiratory and hemodynamic parameters, reduce the mechanical ventilation duration.

scholarly journals Overview of WHO Group 2 Pulmonary Hypertension Due to Left Heart Disease

2015 ◽  
Vol 14 (2) ◽  
pp. 70-78 ◽  
Author(s):  
Christopher F. Barnett ◽  
Van N. Selby
Keyword(s):  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Patient Outcomes ◽  
Left Heart ◽  
Pulmonary Vasodilators ◽  
Poor Patient ◽  
Left Heart Disease ◽  
Pulmonary Arterial ◽  
Transplant Evaluation ◽  
Group 2

Background: Left heart disease (LHD) is the most common cause of pulmonary hypertension (PH) and is associated with poor patient outcomes, especially among patients undergoing heart transplant evaluation. Implications for clinicians: Left heart disease should be considered in all patients undergoing an evaluation for PH. Correct management of PH from LHD is to optimize treatment of LHD. Pulmonary vasodilators used to treat pulmonary arterial hypertension should not be used in patients with PH from LHD. Conclusions: Additional research is needed to better understand how PH develops in patients with LHD and to investigate the role for treatment targeting PH in these patients.

Sign in / Sign up

Export Citation Format

Share Document