Anesthesia for the cardiac compromised patient Right ventricular failure
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1 Anesthesia for the cardiac compromised patient 26th International Winter Symposium Steffen Rex Update in Cardiothoracic Anesthesia January 7th - 8th, 2011 Leuven, Belgium Dept. of Anesthesiology University Hospital, RWTH Aachen Germany srex@ukaachen.de
2 Significance of the right ventricle Starr I, Jeffers WA, Meade RH The absence of conspicuous increments of venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease. Am Heart J 1943; 26:
3 Significance of the right ventricle Fontan-Surgery Paul Khairy, Nancy Poirier and Lise-Andrée Mercier Univentricular Heart. Circulation 2007;115;
4 Significance of the right ventricle RV-function independent predictor of morbidity und mortality in patients with: COPD Burgess MI: Comparison of echocardiographic markers of right ventricular function in determining prognosis in chronic pulmonary disease. J Am Soc. Echocardiogr 2002; 15: PPH D'Alonzo GE: Survival in patients with primary pulmonary hypertension. Results from a national prospective registry. Ann Intern Med 1991; 115: Left-sided valvular heart disease Nagel E: Importance of the right ventricle in valvular heart disease. Eur.Heart J 1996; 17: Inferior myocardial infarction Chronic Heart Failure Mehta SR: Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction. J Am Coll.Cardiol 2001; 37: de Groote P: Right ventricular ejection fraction is an independent predictor of survival in patients with moderate heart failure. J.Am.Coll.Cardiol 1998; 32: Congenital Heart Disease Graham TP: Long-term outcome in congenitally corrected transposition of the great arteries: a multi-institutional study. J Am Coll Cardiol 2000; 36: Pulmonary Artery Embolism Ghaye B: Severe pulmonary embolism:pulmonary artery clot load scores and cardiovascular parameters as predictors of mortality. Radiology 2006 Jun;239(3): ARDS Monchi M: Early predictive factors of survival in the acute respiratory distress syndrome. A multivariate analysis. Am J Respir.Crit Care Med 1998; 158: Cardiothoracic Surgery Reichert CL: Prognostic value of biventricular function in hypotensive patients after cardiac surgery as assessed by transesophageal echocardiography. J Cardiothorac Vasc Anesth 1992; 6: Liver Transplantation Le Pavec J: Portopulmonary Hypertension: Survival and Prognostic Factors. Am J Respir Crit Care Med 2008; 178:
5 Epidemiology of RV failure in the perioperative period Cardiac Surgery Few prospective data 48% of LCOS, mortality 44% Davila-Roman, Ann Thor Surg 1995 Heart transplant: 50% of early complications; 42% of perioperative mortality Haddad, CanJCardiol 2008 LVAD-implantation: 30-50%; mortality: 46% Matthews, JACC 2008 ARDS Few prospective data 25-30% using modern ventilation strategies (mortality: 30-40%) Vieillard-Baron, CCM 2001; Jardin, ICM 2007; Osman, ICM2009
6 Right ventricular paradoxon Passive Conduit Active part of circulatory homeostasis Low RV Afterload Increased
7 Anatomy of the right ventricle The right ventricle is not just a small left ventricle! Shape: triangular/crescent (LV: ellipsoid) Thin-walled (2-5mm vs. LV: 7-11mm): poor contractile reserves LV RV LV
8 Pathophysiology of the right ventricle Consequences of an increase in afterload Specific anatomy Poor contractile reserves Increased susceptibility to elevations of afterload 1) RV Output Haddad F et al. The Right Ventricle in Cardiac Surgery, a Perioperative Perspective: I. Anatomy, Physiology, and Assessment Anesth Analg 2009;108:407 21
9 Pathophysiology of the right ventricle Consequences of an increase in afterload 2) LV Output Ventricular Interdependence Diastolic ventricular interaction: Leftward septal shift LV preload Systolic ventricular interaction: Leftward septal shift LV contractility
10 Pathophysiology of the right ventricle Consequences of an increase in afterload 3) Septal dysfunction RV Output Ventricular Interdependence Systolic ventricular interaction: Leftward septal shift LV contractility RV output
11 Pathophysiology of the right ventricle Consequences of an increase in afterload 4) RV Coronary Perfusion Normal Systole Diastole Systole PHT Diastole Van Wolferen et al. Right coronary artery flow impairment in patients with pulmonary hypertension. European Heart Journal (2008) 29,
12 Pathophysiology of the right ventricle Consequences of an increase in afterload 5) Activation of apoptotic pathways RV and septal expressions of Bcl-2 (antiapoptotic) No changes in expressions of Bax (proapoptotic) Bax/Bcl-2 ratio (proapoptotic) RV caspase-8, caspase-9 and caspase-3 (proapoptotic) Dewachter C et al. Activation of apoptotic pathways in experimental acute afterload-induced right ventricular failure Crit Care Med 2010; 38:
13 Pathophysiology of the right ventricle The vicious cycle of RV failure A. RV Preload B. RV Afterload Tricuspid Regurgitation RV Output Acute RV Failure and Dilation Leftward septal shift RV wall tension RV contractility Right-Left- Shunting LV contractility LV compliance RV O 2 Supply/Demand LV preload RV coronary perfusion Cardiac output Systemic hypotension
14 Pathophysiology of the right ventricle The vicious cycle of RV failure RV afterload RV dilatation RV dysfunction Tricuspid Regurgitation RV contractility RV ischemia RV wall tension RV diastolic dysfunction Venous Congestion Liver Failure Renal Failure Gaynor et al. Right Atrial and Ventricular Adaptation to Chronic Right Ventricular Pressure Overload. Circulation. 2005;112[suppl I]:I-212 I-218
15 Etiology of RV failure in the perioperative period RV Contractility Ischemia Postoperative contractile dysfunction (Stunning, Air embolism) Sepsis Cardiac Surgery RV Afterload PHT CPB Pulmonary Embolism Mechanical Ventilation ALI/ARDS Pulmonary Valve Stenosis Adult congenital heart disease Intracardiac shunt Tricuspid regurgitation Pulmonary regurgitation RV Preload
16 Etiology of RV failure Post-Cardiotomy Arterial Endothelin (fmol/ml) Air Embolism (RCA!) Suboptimal myocardial protection (Stunning) RV Ischaemia Protamine CPB-associated PHT Release of pulmonary vasoconstrictors Depression of pulmonary vasodilators CPB and NO CPB Off Pump Courtesy P. Wouters 2 0 CPB and Endothelin Baseline Pre-CPB Post-CPB 6h ICU 24h ICU
17 Monitoring the right ventricle in the perioperative period Pulmonary Artery Catheter CVP RVP PAP
18 Monitoring the right ventricle in the perioperative period Echocardiography RV Shape Relative Size IVS IAS RVSP RVEDA < 0.7 LVEDA RVFAC > 40%
19 Monitoring the right ventricle in the perioperative period Echocardiography: Longitudinal Function! TAPSE = Tricuspid Anular Plane Systolic Excursion Tissue Doppler Imaging IVA Vogel et al. Validation of Myocardial Acceleration During Isovolumic Contraction as a Novel Noninvasive Index of Right Ventricular Contractility. Circulation. 2002;105: Misannt, Rex et al. Load-sensitivity of Regional Tissue Deformation in the Right Ventricle: Isovolumic versus Ejection-phase Indices of Contractility. Eur Heart J 2008
20 Therapy/Prevention of RV failure in the perioperative period Maintain RV intrinsic protective mechanism: Homeometric Autoregulation: Adaptation of RV contractility to match an increase in afterload Avoid/Stop 14 Sympathicolysis 12 Control TEA * RV 5 4 Control TEA * Mw (mwatt s ml -1 ) Mw (mwatt s ml -1 ) Baseline Hypoxia Baseline 0 Hypoxia Rex et al. Thoracic epidural anesthesia impairs the hemodynamic response to acute pulmonary hypertension by deteriorating right ventricular pulmonary arterial coupling. Crit Care Med 2007; 35:
21 Therapy/Prevention of RV failure in the perioperative period Maintain Homeometric Autoregulation: Avoid/stop cardiac sympathicolysis Missant C., Rex S. et al. Differential effects of lumbar and thoracic epidural anaesthesia on the haemodynamic response to acute right ventricular pressure overload. British Journal of Anaesthesia 104 (2): (2010)
22 Therapy/Prevention of RV failure in the perioperative period RVP (mmhg) SR Avoid Hypoxia cadp-ribose β-nadh Hypoxia Ca ++ Ca ++ - Channel Ca ++ Contraction (+) (-) Ca ++ K ATP K + Depolarization FiO 2 40% 21% 15% Hypoxic Pulmonary Vasoconstriction RVV (ml)
23 Therapy/Prevention of RV failure in the perioperative period Pulmonary Vascular Resistance Adjust the ventilator HPV PEEP Total PVR Alveolar vessels Compression by overinflation Avoid high airway pressures/ high tidal volumes Extra-alveolar vessels Avoid hypoxia RV FRC TLC Lung Volume
24 Pharmacological Therapy of RV failure in the perioperative period Vasodilation Inodilators Inotropy RV Afterload RV Dilatation RV Dysfunction RV contractility RV Ischemia RV wall tension RV VO 2 RV DO 2 RV Output Vasopressors Leftward septal shift RV diastolic dysfunction Coronary perfusion pressure LV Preload Venous Congestion Shunt (R-L) Vasopressors CO Optimization Preload Hypotension
25 Therapy of RV failure in the perioperative period No RCT s! Therapeutic concepts derived from LV failure Volume: Caution! Tricuspid regurgitation Wall tension Inotropy Poor contractile reserves of RV Inodilator (levosimendan, milrinone) vs. Inopressor (epinephrine) Vasoconstriction Coronary artery perfusion pressure Optimization of ventricular interdependence Caution: PVR Vasodilation Caution: Systemic hypotension / oxygenation Selective pulmonary vasodilation (ino, iloprost)
26 Therapy of RV failure Selective pulmonary vasodilation Inhaled NO Problems: Non-Responders Toxic metabolites (NO 2-, NO x ) Sophisticated monitoring (NO, NO 2- ) Met-Hemoglobinemia Inhibition of platelet-aggregation Rebound-effects (PHT, Hypoxia) Extremely short duration of action Not approved Costs No proven impact on outcome (ARDS) Haddad E. et al. Use of Inhaled Nitric Oxide Perioperatively and in Intensive Care Patients. Anesthesiology 2000; 92(6): Dosing: 20 (bis zu 40) ppm, weaning!
27 Therapy of RV failure Selective pulmonary vasodilation Clinical experience suggests that in acute RV dysfunction and elevated PVR, use of ino may result in haemodynamic improvement when used during or after cardiac surgery Prior to ino administration RV function should be optimised with conventional treatment
28 Therapy of RV failure Selective pulmonary vasodilation: Iloprost Advantages Disadvantages Stable carbacyclin derivative of PGI 2 Half-life: 6-9 mins Duration of action: mins Intermittent nebulization Solution stable at room temperature Solution stable at physiologic ph Light-stable Special nebulizer required Ill-defined dose-responserelationship Non-responders Costs No impact on outcome Dosing: 20 (up to 40) µg, every h
29 Therapy of RV failure Selective pulmonary vasodilation: Iloprost 25µg iloprost vs. 0.5 µg/kg/min NTG 25µg iloprost vs. 0.5 µg/kg/min NTG SVI (ml/m²) Iloprost Control 25µg iloprost vs. 0.5 µg/kg/min NTG *# Rex et al. T1 T2 T3 T4 T1 T2 T3 T4 Inhaled iloprost to control pulmonary artery hypertension in patients undergoing mitral valve surgery: a prospective, randomized-controlled trial. Acta Anaesthesiol Scand 2008; 52: PVRI/SVRI µg iloprost vs. 0.5 µg/kg/min NTG 0.4 Iloprost Control
30 Therapy of RV failure Selective pulmonary vasodilation Sildenafil Advantages: selective inhibition of PDE-V cgmp Low costs Inotropic effects in RV hypertrophy Disadvantages: Few experience Systemic vasodilation Indications: Mitigation of rebound-pht during weaning from ino Chronic therapy of PHT Combination therapy with inhaled iloprost Dosing: Start: 3x12.5mg p.o., then increase to up to 3x50mg, Caution: SVR!!!
31 Therapy of RV failure Inodilators Levosimendan Mw (mwatt.s.ml -1 ) RV-Contractility C L * * * F : P : AUC Mw (mwatt.s.ml -1.min) P : C L Emax / Ea RV-Coupling C L F : P : * * AUC Emax / Ea (min) P : C L PA-Ea (mmhg.ml -1 ) BL I/R T15 T60 T120 BL I/R T15 T60 T120 RV-Afterload C L * * * * * * F : P : AUC Ea (mmhg.ml -1.min) P : C L Tau (Fraction of RR - interval) RV Diastolic Function L C * * * * F : NS P : NS AUC Tau (min) C P : NS L 0.0 BL I/R T15 T60 T120 BL I/R T15 T60 T Missant C, Rex S, Segers P, Wouters P Levosimendan improves right ventriculovascular coupling in a porcine model of right ventricular dysfunction. Crit Care Med 2007; 35:
32 RV failure Summary o Neglected problem in anaesthesia and intensive care medicine o Poor prognosis o Unique (patho)physiological characteristics o Necessitate tailored prophylaxis and therapy o Therapy: Selective pulmonary vasodilation, vasopressors, inodilators o Need for RCT s
33 Thank you very much for your attention
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