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Management of acute right ventricle failure in the ICU. Dr Vincent Ioos Medical ICU Pakistan Institute of Medical Sciences. Introduction. Neglected medical condition RV connected to pulmonary circulation: low pressure system Anatomical specificities of RV: thin wall (1/3 LV), crescent shape
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Management of acute right ventricle failure in the ICU Dr Vincent Ioos Medical ICU Pakistan Institute of Medical Sciences
Introduction • Neglected medical condition • RV connected to pulmonary circulation: low pressure system • Anatomical specificities of RV: thin wall (1/3 LV), crescent shape • RV considered a passive conduit between systemic and pulmonary circulation
Definition « The clinical syndrome resulting from the inability of the right ventricle to provide adequate blood flow to the pulmonary circulation at a normal central venous filling pressure »
Main circumstances in ICU • Severe pulmonary embolism • ARDS • Sepsis induced RV dysfunction • Exacerbation of medical conditions leading to chronic pulmonary hypertension • Right ventricle infarction • Pericardial diseases • RV failure after cardiac surgery • After cardiac transplant
Context • Cardiac versus pulmonary causes • RV previously healthy (Acute) • Chronically impaired RV function (Acute on Chronic): RV hypertrophy / dilatation
Pulmonary hypertension: Venice 2003 classification • Pulmonary arterial hypertension (PAH) • Idiopathic (iPAH) • Familial (FPAH) • Associated with (APAH) : Collagen vascular disease, Congenital systemic-to-pulmonary shunts, Portal hypertension, HIV infection Drugs and toxins, … • Associated with significant venousor capillary involvement • Persistent pulmonary hypertension of the newborn • Pulmonary hypertension with left heart disease • Pulmonary hypertension associated with lung diseases and/or hypoxemia • Pulmonary hypertension due to chronic thrombotic and/or embolic disease • Miscellaneous (Sarciodosis, histiocytosis X, lymphangiomatosis,compression of pulmonary vessels) Simmoneau G, Galiè N, Rubin LJ, et al: Clinical classification of pulmonary hypertension. J Am Coll Cardiol 2004; 43:10S.
Physiology of the normal pulmonary circulation • Low pressure system: Prv (syst) = 25 mmHg / Plv (syst) = 120 mmHg • The pressure in the pulmonary system depends on cardiac ouput, resistance and compliance • The pulmonary vascular resistance has a particular dependency on alveolar oxygen tension, whereby alveolar hypoxia leads to pulmonary arterial vasoconstriction • High compliance of the pulmonary vessels with large diameter and thin wall
O2 requirements and blood supply to the RV • Less O2 requirements than the LV : less myocardic mass, less pre load and after load . • During stress, extraction reserve is greater. • Vascularisation : 2/3 RCA, 1/3 left branches • RV perfused in both systolic and diastolic phases as a result of the low systolic pressure (25 mmHg), which does not occlude the vessel that has a systemic pressure. • If afterload , pressure necessary to contract the RV successfully , partial occlusion of the RCA may occur ischaemia.
Pathophysiology of failing RV Piazza, G. et al. Chest 2005;128:1836-1852
Ventricular interdependence • During systole, LV protrudes in RV • Surrounding pericardium with limited distensibility • Compliance of one ventricle can modify the other = Diastolic ventricular interaction
Right to left shunting • Increase in RA pressure due to RVF • Reopening of patent foramen ovale • Right to left shunting • Secondary hypoxemia • Can be improved by improving RV function • Hypoxemia usually not improved by mechanical ventilation in case of RVF due to pulmonary hypertension due to pulmonary vascular disease (PAH, CTEPH)
Management • Control of trigerring factors • Supportive treatment: • Optimization of preload • Improving contractility • Pulmonary vasodilators • Specific therapies addressing the cause of RVF
Treatment of triggering factors(acute on chronic) • Arrhytmias • Infections • Pulmonary embolism • Thyroïd dysfunction
Optimization of preload Frank-Starling relationship between preload and stroke volume: preload dependance (A) and preload independance (B)
Diuretics • Frequent volume overload • At a point of Frank-Starling curve where there is no more reserve on contractility • Ventricular interdependance • Diuretics to be considered • Sometimes with continuous high dose infusion • If fails, consider CVVHF
Prospective, controlled, randomized, animal study • 22 dogs underwent transient PA constriction (90mn) • Dobutamine 5 and 10 g/kg/mn, norepinephrine 0.1 to 0.5 g/kg/mn • A transient increase in PA pressure persistently worsens PA hemodynamics, RV contractility, RV-PA coupling, and cardiac output. • Dobutamine restores RV-PA coupling and cardiac output better than norepinephrine because of its more pronounced inotropic effect
Dobutamine • 1 adrenergic stimulation • CI PVR at 5 g/kg/mn • At higher dose HR without subsequent in PVR • Experimental models Dobutamine Norepinephrine to improve right-ventricular – pulmonary artery coupling • Improves CI, PVR and PaO2/FiO2 in combination with Inhaled nitric oxyde
Norepinephrine • 1 and 1 adrenergic stimulation • Increases mPAP and PVR • But marked improvement in CO • Useful in combination with Dobutamine for hypotensive patients • Causes less tachycardia than other inotropes • Second choice after Dobutamine in normotensive patients
Levosimendan • Calcium sentitizer: increases the sensitivity of troponin C for Ca2+ within cardiac myocyte • Dilatation of pulmonary vasculature by activation of adenosin tri-phosphate potassium channel • Animal studies and pilot studies support its efficacy in right ventricle failure associated with pulmonary hypertension
35 ICU patients with ARDS and sepsis randomized to receive placebo or levosimendan 0.2g/kg/mn • Mean arterial pressure 80 to 90 mmHg (sustained by norepinephrine infusion) • Improvement of right ventricle performance: • CI (from 3.8 1.1 to 4.2 1.0 L/min/m2) • PAPm (from 29 3 to 25 3 mm Hg) • RVESV, RVEF, SvO2
Addressing the cause of the RV failure, if possible • Treatment of Pulmonary Arterial Hypertension • Pericardiotomy/ drainage • Thrombolysis / embolectomy • Thrombolysis / angioplasty • Thromboendarteriectomy • Atrial septostomy • Transplantation
Inhaled nitric oxyde • Dilate pulmonary vessels in ventilated units of the lung • Reverses hypoxic pulmonary vasoconstriction • In acutely decompensated RV improves PVR, increase CO improve PaO2/FiO2 (Benker KA et Al. Am J Crit Care. 1997 Mar;6(2):127-31) • Beware of methemoglobinemia (high concentraton, prolonged use)
Effect of abrupt discontinuation of NO 2002 Yearbook of Intensive Care and Emergency Medicine, Acute right ventricular failure: physiology and therapy by Renaud E, Karpati P, Mebazaa A
Prostanoids • Intravenous Epoprostenol • Effect on survival in stable patients with PAH • Reduces mPAP and improves CO • Systemic side effects • Worsening PaO2/FiO2 • Systemic effects (hypotension) • Inhaled prostacyclin / nebulized iloprost: case series (Shock associated with PAH, Olschewski H. Intensive Care Med. 1998 Jun;24(6):631-4)
Sidenafil • Phosphodiesterase-5 inhibitor • Approved for treatment of PAH (stable patients) • Only case reports for use in critically ill (RVF after transplant: De Santo LS et Al.Transplant Proc. 2008 Jul-Aug; 40(6): 2015-8) • May be useful for weaning from inhaled nitric oxyde • Effect start 15mn after administration, peak effects within 30-60mn • Systemic hypotension
Effects of mechanical ventilation • Increased RV afterload due to positive pressure ventilation • Hemodynamic failure frequently refractory in PAH patient put on MV • In ARDS increase in mPAP while increasing tidal volume and PEEP • Permissive hypercapnia is deleterious (increase in mPAP)