Post on 29-Mar-2020
Acute Right Ventricular Failure
Professor of Cardiology Democritus University of Thrace, Greece skonst@med.duth.gr
Stavros V. Konstantinides, MD, PhD, FESC Professor, Clinical Trials in Antithrombotic Therapy, and Medical Director Center for Thrombosis und Hemostasis, University of Mainz, Germany stavros.konstantinides@unimedizin-mainz.de
Conflict of Interest - Disclosures
below. Affiliation/Financial Relationship Company 1. Honoraria for lectures: Bayer HealthCare,
Boehringer Ingelheim, MSD, Pfizer – Bristol-Myers Squibb, 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
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
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
Acute right ventricular failure
RV LVElastance (Emax), mm Hg/ml
1.30+0.84 5.48+1.23
PVR vs. SVR, dyn.s.cm-5 70 (20-130) 1100 (700-1600)
End-diastolic compliance high low
EF, % 61+7 (47-76) 67+5 (57-78)
Stroke work index, g/m²/beat
8+2 (1/6 of LV) 50+20
Resistance to ischaemia high low
Adaptation to disease Better for volume overload
Better for pressure overload
RV vs. LV physiology
Haddad F, et al. Circulation 2008;117:1436-1448
• 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)
Implications for causes & pathogenesis of RV failure
PRESSURE
PRESSURE
PRESSURE
PRESSURE
PRESSURE
PRESSURE
PRESSURE
PRESSURE
Pathophysiology of acute RV failure
Harjola VP, …, Konstantinides S. Eur J Heart Fail 2016;18:226-241
European Heart Journal (2014):doi:10.1093/eurheartj/ehu283
Increased RV afterload
Cardiogenicshock
Death
RV O2 delivery
RV coronaryperfusion
Systemic BP
Low CO
LV pre-load
RV output RV contractility
RV ischaemia
RV O2 demand
Myocardialinflammation
Neurohormonalactivation
RV wall tension
TV insufficiency
RV dilatation
The spiral of RV overload and decompensation
Courtesy Prof. A. Torbicki, Warsaw, PL
Severity spectrum of acute RV failure
Further determinants of prognosis (PE)
European Heart Journal (2014):doi:10.1093/eurheartj/ehu283
Clinical presentation of acute RV failure
Harjola VP, …, Konstantinides S. Eur J Heart Fail 2016;18:226-241
Harjola VP, …, Konstantinides S. Eur J Heart Fail 2016;18:226-241
Acute RV failure on echo: diagnosis
RV enlargement, paradoxical septum, LV eccentricity
Pulmonary hypertension
RV dysfunction, global and regional
RV enlargement -> paradoxical septal wall
RV enlargement -> septal shift -> LV eccentricity
Eccentricity index of LV >1.0 ➔ RV overload
RV basal systolic function: TAPSE
Upper reference limit (URL) TAPSE: 16 mm
Schulman S, Ageno W, Konstantinides S. Thromb Haemost 20176;in press Photos: Courtesy K F Kreitner, University Medical Center Mainz, DE
Diagnosing the cause/trigger of acute RV failure
Becattini C, …., Konstantinides S. Eur Respir J 2016;48(3):780-786
Early mortality risk
Risk parameters and scores
Death at 30 days PESI class
III-V or sPESI >1
RV dysfunction
(imaging)
Cardiac laboratory markers
High + + (+) 23/105 22% (14-29.8%)
IntermediateInterm-high + Both positive 21/272
7.7% (4.5-10.9%)
Interm-low + One (or none) positive 20/333 6.0% (3.4-8.6%)
Low − Assessment optional;if assessed, both negative
1/196 0.5% (0-1.5%)
Acute RV failure: basis for risk stratification
Acute RV failure: general management
Haemodynamic monitoring, support
(ICU)
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↑
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;18:226-241
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
Weinberg A, Tapson VF, Ramzy D. Semin Respir Crit Care Med 2017;38:66-72
Mechanical circulatory and respiratory support
Image source: CardiacAssist
Need for multidisciplinary approach (PE)
Jaber WA, et al. J Am Coll Cardiol 2016;67:991-1002
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
Acute right ventricular failure
Chronic pulmonary hypertension
● COPD ● ILD ● Other pulmonary
diseases with mixed restrictive and obstructive pattern
● Sleep-disordered breathing
● Alveolar hypoventilation disorders
● Chronic exposure to high altitude
● Developmental abnormalities
WHO Group 3 Lung/hypoxia related
Pulmonary hypertension
● IPAH ● Heritable ● Drug- and toxin-
induced ● APAH: ● CTD ● HIV infection ● Portal hypertension ● CHD ● Schistosomiasis
WHO Group 1′ ● PVOD ● Pulmonary capillary
hemangiomatosis WHO Group I′′
● PPHN
● Systolic dysfunction ● Diastolic dysfunction ● Valvular disease ● Congenital/acquired left
heart inflow/ outflow tract obstruction
Chronic thromboembolic
pulmonary hypertension
PH with unclear multifactorial mechanisms
WHO Group 1 PAH
WHO Group 2 Left heart related
WHO Group 4 CTEPH
WHO Group 5 Other
modified from Simonneau G et al. J Am Coll Cardiol 2013;62(25 Suppl):D34–41
RV
RV
RV
LV
LV
LV
Normal
Compensatory Hypertrophy
Failure
From adaptation to failure of the RV
Courtesy Prof. S. Gibbs, London, UK
Chronic, preexisting RV failure on echo
TR >3.4 m/s
Harjola VP, …, Konstantinides S. Eur J Heart Fail 2016;18:226-241
DD on echo: acute PE or CTEPH??
Konstantinides S, et al. Eur Heart J 2014; doi:10.1093/eurheartj/ehu283 Kim NH, et al. J Am Coll Cardiol 2013;62(25 Suppl):D92–9
Management of “acute-on-chronic” 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
Galiè N, et al. European Heart Journal 2016;37:67-119
Echo in the diagnosis of PH
Galiè N, et al. European Heart Journal 2016;37:67-119
RV-based risk stratification of PH
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
RV functional status before…
…and after recompensation!!
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.
Acute RV failure: Conclusions