Managing Difficult PE: Trouble with the right ventricle
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1 Managing Difficult PE: Trouble with the right ventricle Stavros V. Konstantinides, MD, PhD, FESC Professor, Clinical Trials in Antithrombotic Therapy Center for Thrombosis und Hemostasis, University of Mainz, Germany Professor of Cardiology Democritus University of Thrace, Greece
2 No disclosures
3 Acute right heart failure Physiology of the right ventricle (RV) and the pulmonary circulation Aetiology and pathophysiology of acute right heart failure Diagnostic assessment or RV function and dysfunction Treatment of right heart failure: general measures Specific management of right heart failure: acute PE
4 The right ventricle pulmonary circulation unit and I ask, as the lungs are so close at hand, and in continual motion, and the vessel that supplies them is of such dimensions, what is the use or meaning of this pulse of the right ventricle? And why was nature reduced to the necessity of adding another ventricle for the sole purpose of nourishing the lungs? -William Harvey, Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus, 1628
5 Haddad, F. et al. Circulation 2008;117: Anatomy of the right ventricle Three components: Inlet trabeculated apex infundubulum/conus Three muscular bands: parietal septomarginal - moderator Shape EDV, mm RV Crescentictriangular (49-101) LV Elliptic (44-89) Mass, g/m (17-34) (64-109) Wall thickness, mm
6 Haddad, F. et al. Circulation 2008;117: Architecture and contraction of the right ventricle Muscle layers: Superficial (circumferential) deep (longitudinal) Contraction pattern: Inward movement of free wall Longitudinal Traction of free wall secondary to LV contraction (contribution to SV and pressure: 20-40%!) Shortening: mainly longitudinal Compared to LV: NO torsion, rotation, thickening Smaller inward motion than LV necessary to eject the same stroke volume
7 Simon, MA. Curr Opin Crit Care 2010;16: Ventricular contraction and interdependence (MRI) normal diastole systole PAH
8 Simon, MA. Curr Opin Crit Care 2010;16: Longitudinal RV contraction (speckle tracking) normal PAH
9 Haddad, F. et al. Circulation 2008;117: RV vs. LV dynamics RV LV 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 8+2 (1/6 of LV) Resistance to ischaemia high low Adaptation to disease Better for volume overload Better for pressure overload
10 Acute right heart failure Physiology of the right ventricle (RV) and the pulmonary circulation Aetiology and pathophysiology of acute right heart failure Diagnostic assessment or RV function and dysfunction Treatment of right heart failure: general measures Specific management of right heart failure: acute PE
11 Lahm T. J Am Coll Cardiol 2010;56:1435 Causes of acute right heart failure LV failure/ Arrhythmia RV ischaemia Afterload Preload Myocardial disease Congenital/ valvular Pericardial RV infarction Secondary to pressure overload (LV) Cardiomyopathies ARVD Cytokines (sepsis) Constrictive pericarditis Most frequent cause Acute PE Pulmonary microthrombi (sepsis) PAH Hypoxic vasoconstriction Mechanical ventilation Post CABG Hypovolemia Capillary leak (sepsis) SVC syndrome RVOT obstruction Mechanical ventilation Tamponade MV disease Ebstein Fallot Transposition ASD TR, PR
12 RL Miller. Chest 1998;113: KM McIntyre und AA Sasahara. Am J Cardiol 1971;28: YM Smulders. Cardiovasc Res 2000;48:23-33 A Torbicki. Eur Heart J 2008;29: Acute RV dysfunction/failure in pulmonary embolism Anatomical obstruction Vasoactive mediators Inotropic (sympathetic) stimulation RV dilation (Frank-Starling) Pressure limit: 40 mm Hg (mean), mm Hg (max) Pulmonary arterial hypertension
13 C Greyson. Cardiovasc Res 1997; Am J Physiol Heart Circ Physiol 2000 Schmitto JD. Eur J Cardiothorac Surg 2009 Acute RV dysfunction/failure in pulmonary embolism PA pressure RV afterload Persistent RV wall stress σ = P x r / h O 2 demand RV dysfunction / myocardial injury RV ischaemia RV ejection Septal shift [RV perfusion??] LV preload LV ejection Hypotension / Shock
14 Mechanisms of right heart failure in the critically ill Lahm T. J Am Coll Cardiol 2010;56:1435
15 Incidence and importance of right heart failure In the ICU, right heart dysfunction/failure can occur: In up to 65% of patients with acute pulmonary embolism In up to 25% of patients with acute lung injury / ARDS on mechanical ventilation (high P plat, high PEEP, hypoxaemia, hypercarbia, acidosis) In up to 50% of patients with sepsis (affecting preload, afterload, contractility). It is independently asociated with increased mortality.
16 Acute right heart failure Physiology of the right ventricle (RV) and the pulmonary circulation Aetiology and pathophysiology of acute right heart failure Diagnostic assessment or RV function and dysfunction Treatment of right heart failure: general measures Specific management of right heart failure: acute PE
17 Noninvasive assesment & monitoring of RV (dys)function Modality Imaging Biomarkers Test Echocardiography CT scan Cardiac troponin T or I Natriuretic peptides Growth differentiation factor-15 H-FABP
18 Imaging of RV dysfunction (echo) Echo criteria: non-standardized; various combinations and thresholds RV dilatation (RV>LV, or RVEDD >30 mm) RV free wall hypokinesia Paradoxical septal wall Pulmonary hypertension (RV-RA gradient >30 mm Hg, or pulm acceleration time <80 ms)
19 Imaging of RV dysfunction (echo) Tricuspid annular plane systolic excursion (M-mode): Established prognostic value (in PAH) TAPSE (n.v.) = mm Forfia et al. AJRCCM,2006; 174 (9):
20 Imaging of RV dysfunction (CT) in PE Prospective multicentre validation (457 pts with PE): RV dilatation: RV:LV >0.9 present in 66% of patients sensitivity, 92%; NPV, 100% Independent predictor of adverse outcome: HR, 3.5; 95% CI, ; P= Becattini C et al. Eur Heart J 2011;eurheartj.ehr108
21 Risk stratification based on RV (dys)function?
22 Acute right heart failure Physiology of the right ventricle (RV) and the pulmonary circulation Etiology and pathophysiology of acute right heart failure Diagnostic assessment or RV function and dysfunction Treatment of right heart failure: general measures Specific management of right heart failure: acute PE
23 Management of acute right heart failure Rhythm stabilisation Lung- and RVprotective MV Haemodynamic support Optimise volume Hypovolaemia Overload Volume challenge: ml ONLY! V T 4-6 ml/kg BW P plat <30 cmh 2 O Use low PEEP Hyperventilate AVOID Acidosis Hypercarbia Hypoxaemia Auto-PEEP Vasopressors / inotropes (low-dose dobutamine, milrinone, levosimendan, NE) COMBINE: Inhaled NO RESCUE: balloon atrial septostomy, LV/RV/ BiVAD, ECMO, Tx Diuretics Continuous / intermittent RRT
24 Thrombolysis for RV failure in PE NP Fam. N Engl J Med 2002; Vol. 347, No. 15
25 Thrombolytic regimens for PE Streptokinase Urokinase Alteplase Reteplase Tenecteplase 250,000 U over 30 min followed by 100,000 U/h over h Accelerated: 1.5 Mio. U over 2 h 4,400 U/kg KG over 10 min, followed by 4,400 U/kg/h over h Accelerated: 3 Mio. U over 2 h 100 mg over 2 h Accelerated: 0.6 mg/kg over 15 min (off-label) in AMI dose: TIPES study
26 RV response to thrombolysis (echo) Normalization of RV/LV end-diastolic dimension ratio 1,40 1,30 p =0.04 p= pes 1,20 1,10 1,00 p = ns TNK Placebo 0,90 0,80 baseline 24 hours 7 days C Becattini Thromb Res 2010;125:e82-e86
27 RV response to thrombolysis (echo) Normalization of paradoxical septal wall rtpa + Heparin Heparin alone S Konstantinides. Am J Cardiol 1998;82:
28 Thrombolysis for PE: recent data on overt RV failure Nationwide Inpatient Sample USA ,110,320 patients discharged with diagnosis of PE (ICD-9-CM) 72,230 (3.4%) unstable (shock, ventilated) 21,390 (30%) received thrombolytics In patients who received thrombolysis: All-cause mortality: RR, 0.31 ( ) PE-related death: RR, 0.20 ( ) PD Stein. Am J Med. 2012;125: Epub 2012 Feb 10.
29 Primary Outcome, Secondary Outcomes S Konstantinides for the PEITHO Steering Committee. Am Heart J 2012;163:33-38.e1 Seconray Outomes, SAE Long-term Follow-up Thrombolysis also for subclinical RV failure? PEITHO Confirmed acute symptomatic PE TNK Absence of hemodynamic collapse UFH infusion UFH, LMWH or Fondaparinux <2 h Confirmed RV dysfunction + myocardial injury DOUBLE BLIND R Placebo VKA UFH infusion UFH, LMWH or Fondaparinux UFH bolus i.v. VKA Day 2 Day 7 Day 30 Day 180
30 Ultrasound-assisted thrombolysis Improvement of RV size Subannular RV/LV ratio Pre to Post RV/LV Ratio N= 24 mean rt-pa dose 33 ± 15 mg over 20 hours P < RV/LV Ratio Ongoing trials in patients without shock: 1.0 NCT in Europe (randomized) NCT in the US (single-arm) Courtesy Prof. Nils Kucher, Bern ± ± 0.13 Pre RV/LV Baseline CT Post RV/LV Follow-up CT at 38 ± 14 hours Engelhardt TC, et al. Thromb Res 2011;128:149-54
31 Summary and Conclusions (1) The RV is particularly vulnerable to changes in afterload. Acute right heart failure occurs in patients with left ventricular / mitral valve disease; acute pulmonary embolism; sepsis, especially with ARDS on mechanical ventilation; pulmonary arterial hypertension, CTEPH, congenital heart disease. It is associated with a poor outcome. Besides clinical and haemodynamic parameters, echocardiography, CT, and biomarkers (alone and in combination) help in its detection and follow-up.
32 Summary and Conclusions (2) General therapeutic measures include: volume status optimisation (NO aggressive volume challenge!); inotropic / vasopressor support (as in LV failure); lung-protective mechanical ventilation, correction of hypoxaemia, hypercarbia and acidosis; pulmonary arterial hypertension, CTEPH, congenital heart disease. Specific measures are particularly effective in acute pulmonary embolism (thrombolysis/surgery/intervention).
33 Thank you
34 Treatment of right heart failure in acute PE Recommendation Class Level Thrombolytic therapy should be used in patients with high-risk PE presenting with cardiogenic shock and/or persistent arterial hypotension Surgical pulmonary embolectomy is a therapeutic alternative if thrombolysis is absolutely contraindicated or has failed Catheter embolectomy or fragmentation of proximal pulmonary arterial clots may be an alternative to surgical treatment when thrombolysis is absolutely contraindicated or has failed I (1) I (2) IIb (2) A (B) C (C) C (C)
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