Acute Right Ventricular Failure

Transcription

1 Acute Right Ventricular Failure Stavros V. Konstantinides, MD, PhD, FESC Professor, Clinical Trials in Antithrombotic Therapy, and Medical Director Center for Thrombosis und Hemostasis, University of Mainz, Germany Professor of Cardiology Democritus University of Thrace, Greece

2 Conflict of Interest - Disclosures below. Affiliation/Financial Relationship Company 1. Honoraria for lectures: Bayer HealthCare, MSD, Squibb, Boehringer Ingelheim, Pfizer Bristol-Myers Servier, BTG 2. Honoraria for advisory board activities: Bayer HealthCare, Daiichi Sankyo, Boehringer Ingelheim, Actelion 3. Participation in clinical trials: United Therapeutics, Actelion, Janssen 4. Research funding (institutional grants): Bayer HealthCare, Actelion, Boehringer Ingelheim, Pfizer

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4 Acute right ventricular failure 1) Right ventricular failure in acute pressure overload a) RV versus LV dynamics b) Causes and pathophysiology c) Diagnosis d) Risk stratification e) General and specific therapy 2) Chronic RV failure, acute decompensation a) Distinguishing between acute and chronic RV overload b) Echo for suspicion and follow-up of PH c) Identifying and treating the decompensation trigger

5 Acute right ventricular failure 1) Right ventricular failure in acute pressure overload a) RV versus LV dynamics b) Causes and pathophysiology c) Diagnosis d) Risk stratification e) General and specific therapy 2) Chronic RV failure, acute decompensation a) Distinguishing between acute and chronic RV overload b) Echo for suspicion and follow-up of PH c) Identifying and treating the decompensation trigger

6 Haddad F, et al. Circulation 2008;117: RV vs. LV physiology RV Elastance (Emax), mm Hg/ ml PVR vs. SVR, dyn.s.cm (20-130) 1100 ( ) End-diastolic compliance high low EF, % 61+7 (47-76) 67+5 (57-78) Stroke work index, g/m²/ beat LV 8+2 (1/6 of LV) Resistance to ischaemia high low Adaptation to disease Better for volume overload Better for pressure overload

7 Implications for causes & pathogenesis of RV failure Secondary to acute LV failure RV ischaemia/infarction Acute pulmonary embolism Exacerbation of chronic lung disease/hypoxia Acute lung injury or ARDS Decompensated chronic pulmonary hypertension Pericardial disease (tamponade) Arrhythmias Congenital heart disease (ASD, VSD, Ebstein s anomaly) Valvulopathies Cardiomyopathies (e.g. ARVD) Myocarditis or other inflammatory disease Cardiac surgery Haematological disorders (e.g. sickle cell disease) PRESSURE PRESSURE PRESSURE PRESSURE PRESSURE PRESSURE PRESSURE PRESSURE

8 Pathophysiology of acute RV failure Harjola VP,, Konstantinides S. Eur J Heart Fail 2016;18:

9 The spiral of RV overload and decompensation Increased RV afterload RV dilatation RV coronary perfusion Systemic BP RV O 2 delivery Low CO LV pre-load Cardiogenic shock Death TV insufficiency RV O 2 demand RV ischaemia RV wall tension Neurohormonal activation Myocardial inflammation RV output RV contractility European Heart Journal (2014):doi: /eurheartj/ehu283

10 Severity spectrum of acute RV failure Courtesy Prof. A. Torbicki, Warsaw, PL

11 Further determinants of prognosis (PE) European Heart Journal (2014):doi: /eurheartj/ehu283

12 Clinical presentation of acute RV failure Harjola VP,, Konstantinides S. Eur J Heart Fail 2016;18:

13 Acute RV failure on echo: diagnosis RV enlargement, paradoxical septum, LV eccentricity RV dysfunction, global and regional Pulmonary hypertension Harjola VP,, Konstantinides S. Eur J Heart Fail 2016;18:

14 RV enlargement -> paradoxical septal wall

15 RV enlargement -> septal shift -> LV eccentricity Eccentricity index of LV >1.0 RV overload

16 RV basal systolic function: TAPSE Upper reference limit (URL) TAPSE: 16 mm

17 Diagnosing the cause/trigger of acute RV failure Schulman S, Ageno W, Konstantinides S. Thromb Haemost 20176;in press Photos: Courtesy K F Kreitner, University Medical Center Mainz, DE

18 Acute RV failure: basis for risk stratification Risk parameters and scores Early mortality risk PESI class III-V or spesi >1 RV dysfunction (imaging) Cardiac laboratory markers Death at 30 days High + + (+) 23/105 22% ( %) Intermediate Interm-high + Both positive Interm-low + One (or none) positive 21/ % ( %) 20/ % ( %) Low Assessment optional; if assessed, both negative 1/ % (0-1.5%) Becattini C,., Konstantinides S. Eur Respir J 2016;48(3):

19 Acute RV failure: general management Assess severity Clinical, biochemical, imaging, invasive parameters Identify triggering factors Ensure cause-specific management Optimize fluid status IV diuretics, RRT; cautious fluid filling if CVP Haemodynamic monitoring, support (ICU) Maintain arterial pressure Norepinephrine Consider inotropes reducing filling pressures Levosimendan, dobutamine, PDE-III inhibitors Further measures for afterload reduction Inhaled NO, prostacyclins Consider transfer for ECMO, mechanical support Harjola VP, et al. Eur J Heart Fail 2016;18:

20 Mechanical circulatory and respiratory support Indications Cardiac arrest Severe haemodynamic compromise Contraindication(s) to systemic thrombolysis Failed systemic thrombolysis Failed catheter-based clot extraction Patient too unstable for catheter-based clot extraction or thrombolysis Severe hypoxaemia Image source: CardiacAssist Weinberg A, Tapson VF, Ramzy D. Semin Respir Crit Care Med 2017;38:66-72

21 Need for multidisciplinary approach (PE) Jaber WA, et al. J Am Coll Cardiol 2016;67:

22 Acute right ventricular failure 1) Right ventricular failure in acute pressure overload a) RV versus LV dynamics b) Causes and pathophysiology c) Diagnosis d) Risk stratification e) General and specific therapy 2) Chronic RV failure, acute decompensation a) Distinguishing between acute and chronic RV overload b) Echo for suspicion and follow-up of PH c) Identifying and treating the decompensation trigger

23 Chronic pulmonary hypertension Pulmonary hypertension WHO Group 1 PAH WHO Group 2 Left heart related WHO Group 3 Lung/hypoxia related WHO Group 4 CTEPH WHO Group 5 Other IPAH Heritable Drug- and toxininduced APAH: CTD HIV infection Portal hypertension CHD Schistosomiasis WHO Group 1 PVOD Pulmonary capillary hemangiomatosis Systolic dysfunction Diastolic dysfunction Valvular disease Congenital/acquired left heart inflow/ outflow tract obstruction COPD ILD Other pulmonary diseases with mixed restrictive and obstructive pattern Sleep-disordered breathing Alveolar hypoventilation disorders Chronic exposure to high altitude Developmental abnormalities Chronic thromboembolic pulmonary hypertension PH with unclear multifactorial mechanisms WHO Group I PPHN modified from Simonneau G et al. J Am Coll Cardiol 2013;62(25 Suppl):D34 41

24 Courtesy Prof. S. Gibbs, London, UK From adaptation to failure of the RV Normal RV LV Compensatory Hypertrophy RV LV Failure RV LV

25 Chronic, preexisting RV failure on echo TR >3.4 m/s Harjola VP,, Konstantinides S. Eur J Heart Fail 2016;18:

26 DD on echo: acute PE or CTEPH?? Management of acute-onchronic RV failure, i.e. acute PE and suspected pre-existing CTEPH: (1) General measures of RV failure management! (2) Treate acute PE, dissolve the fresh thrombus! (3) After stabilization, anticoagulate for at least 3 months (4) Then initiate diagnostic workup for CTEPH Konstantinides S, et al. Eur Heart J 2014; doi: /eurheartj/ehu283 Kim NH, et al. J Am Coll Cardiol 2013;62(25 Suppl):D92 9

27 Echo in the diagnosis of PH Galiè N, et al. European Heart Journal 2016;37:67-119

28 RV-based risk stratification of PH Galiè N, et al. European Heart Journal 2016;37:67-119

29 Decompensation triggers of chronic PH Triggering factors Infection / sepsis Supraventricular arrhythmias Anaemia Non-adherence to treatment Hypoxia, hypercapnia Galiè N, et al. European Heart Journal 2016;37:67-119

30 RV functional status before

31 and after recompensation!!

32 Acute RV failure: Conclusions 1) Acute RV failure is a diagnosis based on history (search for causes/triggers) and clinical examination. 2) Echocardiography and biomarker tests are necessary for accurate assessment and severity-adapted management. 3) Management of acute RV failure demands BOTH general supportive measures and cause-specific treatment, particularly relief of afterload. 4) Decompensated chronic PH must be identified and its triggers treated. 5) Possible acute-on-chronic PE is first treated like acute PE; search for CTEPH is warranted later, after 3 months of therapeutic anticoagulation.

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