Management strategies for patients with pulmonary hypertension in the intensive care unit*

Zamanian, Roham T.; Haddad, François; Doyle, Ramona L.; Weinacker, Ann

doi:10.1097/01.ccm.0000280433.74246.9e

Cited by 188 publications

(179 citation statements)

References 162 publications

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“…The basic principles of ICU management of patients with PH and RV failure include the treatment of triggering factors (such as anaemia, arrhythmias, infections or other co-morbidities), optimization of fluid balance (usually with i.v. diuretics), reduction of RV afterload (usually with parenteral prostacyclin analogues, but sometimes also with other PAH drugs), improvement of CO with inotropes (with dobutamine being the preferred inotrope to treat RV failure) and maintenance of systemic blood pressure with vasopressors, if necessary [258][259][260]. Intubation should be avoided in patients with RV failure, as it frequently results in haemodynamic collapse.…”

Section: 37mentioning

confidence: 99%

2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension

et al. 2015

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Guidelines summarize and evaluate all available evidence on a particular issue at the time of the writing process, with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate.

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Section: 37mentioning

confidence: 99%

2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension

et al. 2015

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“…Vigorous fluid administration should be avoided, since it can decrease LV output because of further RV dilation and a leftward shift of the intraventricular septum (13). Norepinephrine is beneficial in hypotensive and tachycardic patients with compromised RV coronary perfusion, but in patients with RV failure and preserved arterial pressure dobutamine or levosimendan is preferred (14)(15)(16). RV afterload can be decreased by inhalation of nitric oxide or use of prostacyclins, endothelin receptor antagonists and inhibitors of phosphodiesterase.…”

Section: Treatment Of Right Ventricular Failurementioning

confidence: 99%

Right ventricular function in critically ill patients

2017

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The right ventricular function is crucial for maintaining hemodynamic stability in critically ill patients who suffer from sudden increases of right ventricular pressure overload and/or severely decreased right ventricular contractility. The morphological and functional assessment of the right ventricle is usually performed by bedside echocardiography and hemodynamic measurements with a pulmonary artery catheter. The therapeutic approach to patients with right ventricular failure includes measures to decrease right ventricular afterload and to improve its coronary perfusion and contractility.Key words: right ventricle, failure, systolic function BASIC ANATOMIC, PHYSIOLOGIC AND PATHOPHYSIOLOGIC DATA Sixty years ago, the right ventricle (RV) was considered a passive conduit for blood flow and only a "weak sister" of the strong and powerful left ventricle (1). More than thirty years later, the RV function was revisited and it became clear, that RV failure is responsible for shock in patients with massive pulmonary embolism and RV myocardial infarction (2-4). The thin free wall of the RV forms the anterior and inferior part of the RV and the posterolateral wall represents the intraventricular septum, which normally bulges into the RV. The RV blood supply occurs during systole and diastole; the oxygen extraction is very high, and ATP amount is lower than in the LV. The free wall is very compliant and is capable of maintaining low systemic pressure and preventing pulmonary edema in the case of LV failure. These characteristics make the RV very sensitive to hypoxia. The geometry of the RV is quite complex with clearly separated inflow and outflow tracts. Because of the complex geometry, the LV models are not valid for the RV. The contraction of the RV is less synchronous than that of the LV and occurs as a peristaltic wave starting in the inflow tract and propagating through the apex to the outflow tract. In physiologic conditions, when the pulmonary vascular resistance is low, RV function is indeed of secondary importance. On the other hand, in pathologic conditions with increased pulmonary vascular resistance and/or severely impaired RV contractility, RV function becomes essential for maintaining adequate pulmonary blood flow. The basic consequence of the sudden increase of RV afterload and/ or decreased contractility is RV dilation. Since a dilated RV reduces the LV volume in the rigid pericardial sac, the LV filling is reduced with consequently decreased LV stroke volume and mean arterial pressure. Arterial hypotension provokes RV ischemia that further reduces RV systolic function (5). The RV function is therefore relevant in patients with chronic lung diseases, primary pulmonary vascular disease, pulmonary thrombembolic disorders, sepsis related acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) and after cardiac surgery. Patients with chronic lung diseases frequently present with chronic cor pulmonale, which is characterized by RV free wall hypertrophy and various degrees of dilation w...

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“…Few studies have addressed the value of vasopressors and pulmonary vasodilators in critically ill PAH patients, as well as in patients successfully resuscitated after sudden cardiac death, but dobutamine, milrinone, inhaled nitric oxide, and intravenous prostacyclin are commonly utilized. 114 …”

Section: Syncope In Pahmentioning

confidence: 99%

Complications Leading to Sudden Cardiac Death in Pulmonary Arterial Hypertension

Demerouti

Manginas²,

Athanassopoulos

et al. 2012

Respir Care

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SummaryPulmonary arterial hypertension (PAH) is a disease of small pulmonary arteries, characterized by vascular proliferation and remodeling. Progressive increase in pulmonary vascular resistance ultimately leads to right ventricular heart failure and death. PAH-specific drug therapy has improved clinical outcomes and survival. While the survival is better, progression of pulmonary vasculopathy contributes to pulmonary artery dilatation. Left main compression syndrome, pulmonary artery dissection, pulmonary artery rupture, and severe hemoptysis are reported as complications leading to sudden cardiac death, an event encountered more often in PAH patients. The advent of PAHtargeted drug therapy has reduced referral for lung transplantation; however, severe complications require rapid diagnosis, decision making, and possible registration on a lung transplantation waiting list. PAH referral centers provide multidisciplinary emergency care and specific therapeutic management, contributing to improved quality of life and survival for PAH patients. We review the complications leading to sudden death in PAH. Key words: pulmonary hypertension; pulmonary artery dissection; pulmonary artery rupture; left main compression syndrome. [Respir Care 2013;58(7):1246 -1254.

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Management strategies for patients with pulmonary hypertension in the intensive care unit*

Cited by 188 publications

References 162 publications

2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension

2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension

Right ventricular function in critically ill patients

Complications Leading to Sudden Cardiac Death in Pulmonary Arterial Hypertension

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