Ventriculo-arterial coupling and diastolic elastance MasterclassIC Schiermonnikoog 2015
Ventriculo-arterial coupling Dynamic interaction between heart and systemic circulation (modulation of compliance / stiffness / resistance) allowing the system to provide adequate CO and arterial pressures necessary for sufficient organ perfusion under different circumstances Optimizes cardiovascular performance and cardiac energetics
Ventriculo-arterial coupling Cardiac contractility End-systolic arterial pressure Cardiac contractility End-systolic arterial pressure EDV Low ESV EDV Low ESV EDV Normal ESV EDV High ESV EDV High ESV EDV Normal ESV
Diastole Systole Baseline LVEF 70% Norepinephrine LVEF 40% Veillard-Baron A. Ann Int Care 2011;1:6
Ventriculo-arterial coupling Ratio of arterial- to ventricular elastance (Ea/Ees) Ea/Ees approximating unity is optimal for the system (adequate SV with lowest possible energetic consumption) Ees is the slope of the end-systolic pressure-volume relationship Ea represents the total afterload of LV and is the capability of the arterial vessels to increase pressure when LV stroke volume increases
LVESP Ees Ea LVEDP ESV EDV
Ea1 Ea2
Effects of increased afterload in normal and failing heart 120" 100" Stroke'volume'(mL)' 80" 60" 40" 20" 0" 0" 25" 50" 75" 100" 125" 150" Mean'arterial'pressure'(mmHg)'
1 Stroke Volume End-systolic pressure = 0.9 systolic blood pressure 3 2 Pressure at onset of injection = diastolic blood arterial pressure Ees Ea 4 End-Diastolic pressure = 11.96 + (0.596 E/e )? V0 5 ESV Single beat method by Chen (Stroke volume, SBP, DBP, isovolumic contraction time and ejection time) EDV E e Chen CH. J Am Col Cardiol 2001;38:2028-2024
V-A decoupling (Ea/Ees > 1) Due to decreased Ees Due to decreased Ea Acute heart failure Acute systemic hypertension Cardiac surgery Acute systemic hypotension Could be an additional clue what is wrong and how it should be treated
Levosimendan and V-A coupling Bolus Levosimendan of 12 μg followed by 0.1 μg/kg/min 3 Ea/Ees 2,5 2 1,5 1 0,5 0 Before After Ischemic cardiomyopathy Guarracino F. Acta Anaesthesiol Scand 2007;51:1217-1224
V-A decoupling in sepsis Septic shock Median 1.81 (IQR 1.49-2.02) Critically ill without septic shock Median 1.07 (IQR 0.95-1.14) Frequency 5 4 3 2 1 Frequency 12 10 8 6 4 2 0.8 1.1 1.3 1.6 1.8 2.1 2.4 2.6 2.9 3.1 3.4 0.5 0.9 1.3 1.7 2.1 2.5 2.9 3.3 3.7 4.1 Ea/Ees (sb) ratio Ea usually increases due to pharmacologic vasoconstriction Ea/Ees (sb) ratio Guarracino F. Crit Care 2014;18:R80
Levosimendan and myocardial depression in sepsis Levosimendan Dobutamine Baseline 24 h Baseline 24 h EDVI (ml/m 2 ) 75.8 ± 23.8 66.2 ± 24.6 ** 84.2 ± 25.1 82.9 ± 26.4 ESVI (ml/m 2 ) 46.7 ± 21.9 36.9 ± 19.4 ** 52.4 ± 25.8 50.5 ± 25.3 LVEF (%) 37.1 ± 3.0 45.4 ± 8.4 ** 37.3 ± 2.6 40.8 ± 11.3 42 37 31 26 20 Before After ** ** SVI LVSWI SVI LVSWI Levosimendan Dobutamine Morelli A. Intensive Care Med 2005;31:638-644
Ees (lev) Ees (base) Ea (lev) Ea (base)
Ventriculo-arterial coupling in aortic arch replacement Ees Ea Wegmann A. PLOS ONE 2014;9:e103588
Right ventricle Acute Pulmonary Hypertension Chronic Minutes C Heterometric adaption Homeometric adaption Hypertrophy homeometric Dilatation heterometric Decrease afterload Increase afterload
Pressure Ees Ees = (Pmax-mPAP)/Sv Ea = mpap/sv Ea ESP Ea/Ees = (ESP/SV) / (ESP/ESV) = ESV/SV Normal 0.5-0.7 ESV Volume EDV Increase in Ea/Ees ratio is invariably associated with EDV Vanderpool RR. Heart 2015
RV diastolic function Active relaxation Stiffness of the right ventricle
Right ventricular relaxation in PHT 150 P < 0.05 RV τ (ms) 100 50 33.5 40 0 Controle PHT 18.3 ± 3.2 mmhg 53.3 ± 32.4 mmhg N = 25 Murch SD. Pulm Circ 2015;5:370-375
RV τ correlates with RV DP 25 20 R = 0.93, P < 0.0001 Minimal RV DP (mmhg) 15 10 5 0 5 0 20 40 60 80 100 120 140 RV τ (ms) Murch SD. Pulm Circ 2015;5:370-375
Right ventricular pressure Diastolic stiffness correlates with RAP and SV Right ventricular volume Rain S. Circulation 2013;128:2016-2025
Mild PHT decreases LV relaxation 18 ** ** 14 LVEDP (mmhg) X LVEDV (ml) X Normal VCO E/E (lateral) Change in cardiac output after VCO (%) 9 5 0 12 9 6 3 0-3 -6-9 Control DD IPAH 11-10 -5-12 Control DD IPAH Kasner M. Am J Respir Crit Care Med 2012;186:181-189
Ea/Ees changes with different medications Drug Ea/Ees Dobutamine Decrease Levosimendan Decrease Milrinone Decrease Norepinephrine Decrease
Ea/Ees Isovolemic CP RVEF Ejection time RV dilatation Inhaled NO, PGI, milrinone RV pressure PDE-3/Levosimendan Dobutamine MVO2 Diuretics/CRRT T3 insufficiency Open FO RV output Hypoxemia RCA only perfused during diastole RV ischemia Vasopressin LV preload Cardiac output Organ failure Septal shift
Effect of fluid challenge on EA in sepsis N = 54 1.34-2.37 Normotensive Ea 1.81 Sepsis N = 81 N=9 N = 18 Preload responder Hypotensive N = 27 Ea 1.29 1.01-1.69 Preload nonresponder Pressure responders Ea 12 ± 7% Pressure nonresponders N=9 N=9 Explains why some septic patients increase CO without improving blood pressure after a FC Monge García MI. Intensive Care Med 2015;41:1247-1255
Hypotension - will a fluid challenge help? Increased SV not always results in a higher arterial pressure (dependent on arterial tone) Arterial elastance (Ea) is the best integrative parameter of overall arterial system behavior
LVESP Ees Ea LVEDP ESV EDV
ABP (mmhg) SVI (ml/m2) 180 160 140 120 100 80 60 40 20 0 2 4 6 8 10 12 14 16 18 Time (s) ABP SVI 30 25 Pressure (mmhg) 20 15 10 5 0 0 2 4 6 8 10 12 14 16 18 Time (s) CVP Ppc Paw Ppl
Dynamic arterial elastance Defined by ratio PPV/SVV during single MV breath N =25 - MAP responder 16, MAP non-responder 9 Responder# Non7responder# Responder" Non7responder" MAP$(mmHg)$ 100# 90# 80# 70# 60# 50# 40# Before# A0er# Cardiac'output'(l/min)' 9" 8" 7" 6" 5" 4" 3" 2" Before" A0er" Responder" Non4responder" Dynamic(arterial(elastance( 2" 1,5" 1" 0,5" 0" Before" A-er" García MIM. Crit Care 2011;15:R15
Dynamic arterial elastance Prediction of volume expansion on MAP AUC 95% CI Eadyn 0.986 ± 0.02 0.84-1.00 SVR 0.503 ± 0.12 0.3-0.71 MAP 0.604 ± 0.12 0.39-0.79 PP/SV 0.50 ± 0.12 0.3-0.7 García MIM. Crit Care 2011;15:R15
N = 53 80 VEs All fluid responders (increase CO 10%) Eadyn& 1,4" 1,2" 1" 0,8" 0,6" 0,4" 0,2" *** Ea#(mmHg/mL)# 3" 2,5" 2" 1,5" 1" 0,5" C"(mL/mmHg)" 2" 1,5" 1" 0,5" SVR$(dyn*s*cm-5)$ 2000" 1500" 1000" 500" 0" Responder" Non2Responder" 0" Responder" Non1Responder" 0" Responder" Non0Responder" 0" Responder" Non/Responder" MAP responders defined by increase MAP 10%) García MIM. Crit Care 2014;18:626
Predicting MAP after fluid challenge García MIM. Crit Care 2014;18:626
Eadyn also predicts MAP after NE N = 35 - Septic shock - decrease in NE 0.04 μg/kg/min (13 [37%] were NE responders - MAP > 15%) 2.0 1.8 AUC 95% CI 1.6 Eadyn 1.4 1.2 1.0 0.8 Eadyn 0.87 0.72-0.96 SVR 0.54 0.54-0.77 0.6 0.4 Compliance 0.61 0.43-0.77 Non-responders Responders < 0.90 gives 70% change of MAP Guinot PG. Crit Care 2015;19:14
Conclusions Estimation of the Ea/Ees ratio may provide another clue for a rational therapeutic choice Early right ventricular dysbalance in Ea/Ees ratio immediately results in increased EDV with septal shift and compromise of left ventricle In a FR patient with hypotension a Eadyn > 0.8 predicts an increase in MAP