Is Volume-Responsiveness the Same as Preload? Michael R. Pinsky, MD, Dr hc Department of Critical Care Medicine University of Pittsburgh No Not Now Not Ever Is cardiac output responsive to intravascular fluid loading? • Assumes that venous return and LV preload are the primary determinants of cardiac output (Starling’s Law of the Heart) • Assumes low LV end-diastolic volume (EDV) equals preload-responsiveness • Attempts to assess EDV through surrogate measures – CVP, Ppao, LV end-diastolic area, RV EDV, intrathoracic blood volume CVP before volume expansion in Responders (R) and Non-Responders (NR) * 12 Pra (mm Hg) 10 * 8 6 4 2 0 Calvin 1981 Schneider 1988 Reuse Wagner Michard 1990 1998 2000 Michard & Teboul. Chest 121: 2000-8, 2002 Changes in stroke volume (%) CVP does not predict volume responsiveness r = 0.45 Baseline PRA (mm Hg) Wagner et al. Chest 1998 Ppao (mm Hg) before volume expansion in Responders (R) and Non-responders (NR) R Calvin (Surgery 81) Schneider (Am Heart J 88) Reuse (Chest 90) Diebel (J Trauma 94) Tavernier (Anesthesiology 98) Michard (AJRCCM 00) 2 Wagner (Chest 98) Tousignant (Anesth Analg 00) 8±1 10 ± 2 10 ± 4 16 ± 6 10 ± 4 10 ± 3 NR 7±2 10 ± 2 10 ± 3 15 ± 5 12 ± 3 11 ± p < 0.05 10 ± 3 12 ± 3 14 ± 4 16 ± 3 p < 0.05 Michard & Teboul. Chest 121: 2000-8, 2002 Ppao does not predict preload-responsiveness Non-responders Ppao (mm Hg) Responders $ $ Pre Post * Pre Post Tousignant et al. Anesth Analg 90:351-5, 2000 Neither DCVP or DPpao Mirror DSV Lichtwarck-Aschoff et al. Intensive Care Med 18: 142-7, 1992 Changes in global EDV predict DSV But individual subjects have markedly different relations Lichtwarck-Aschoff et al. Intensive Care Med 1992; 18: 142-7 RVEDV (mL/m2) before volume expansion in Responders (R) and Non-responders (NR) * 150 120 * 90 60 30 0 Calvin 1981 Schneider 1988 Reuse 1990 Diebel 1992 Diebel 1994 Wagner 1998 Michard & Teboul. Chest 121: 2000-8, 2002 Echocardiographic LVEDA (cm2/m2) R Feissel (Chest 01) 10 ± 4 NR 10 ± 2 Tavernier (Anesthesiology 98) 9 ± 3 12 ± 4 * Tousignant (Anesth Analg 00) 15 ± 5 20 ± 5 * (cm2) * p < 0.05 LV EDV in Responders and Non-responders of fluid resuscitation 16 LVEDA 14 before fluid infusion 12 _ 10 (cm2/m2) 8 6 _ 4 responders non responders Feissel et al. Chest 119:867-73, 2001 End-diastolic Area (EDA) to Predict Preload-Responsiveness Non-responders Responders EDA cm2 * Pre Post ** Pre Post Tousignant et al. Anesth Analg 90:351-5, 2000 End-expiration: The pressure which is important to a distensible structure is the transmural pressure Inside pressure minus outside pressure Transmural pressures determine Starling’s forces across capillaries Ventricular preload 5 10 5 5 15 10 0 10 Transmural Pressure is the Amount Above the Surface Pra, Ppao, RVEDV and LVEDA are not always accurate indicators of preload 1- Pra and Ppao are rarely expressed as transmural pressures 2- Even transmural Ppao depends on LV compliance 3- RVEDV measures are influenced by tricuspid regurgitation 4- LVED Area may not reflect LVED Volume 5- All these parameters are supposed to give information on the preload of one ventricle but not on the global cardiac preload Or…… Neither CVP or Ppao reflect Ventricular Volumes or Tract Preload-Responsiveness Preload Preload Responsiveness Kumar et al. Crit Care Med 32:691-9, 2004 Starling’s Law of the Heart Lives! Kumar et al. Crit Care Med 32:691-9, 2004 Hemodynamic Truths • • • • • Tachycardia is never a good thing Hypotension is always pathological There is no normal cardiac output CVP is only elevated in disease Peripheral edema is of cosmetic concern Hemodynamic Effects of Changes in Intrathoracic Pressure Venous Return Thorax LV Ejection Spontaneous Ventilation Positive-Pressure Ventilation SVrv (ml/kg) Time (sec) Pratm (mm Hg) Ppl (mm Hg) CVP (mm Hg) Pinsky. J Appl Physiol 56:1237-45, 1984 Effect of IPPV on LV Pressure and Volume IPPV 20 ml/kg IPPV 20 ml/kg 190 170 150 Stroke Volume Variation LV pressure (mm Hg) 130 110 90 70 Cardiac Compression 50 30 10 -10 15 20 25 30 LV volume (ml) 35 40 PPV and SVV Predict Preload-Responsiveness 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. Jardin et al. Circulation 83: 266-27, 1983 IPPV Perel et al. Anesthesiology 67: 498-502, 1987 SPV-IPPV Tavernier et al. Anesthesiology 89: 1313-1321, 1998 SPV-IPPV Ornstein et al. J Clin Anesth 10:137-140, 1998 SPV-IPPV Michard et al. Am J Respir Crit Care Med 159:935-939, 1999 Dalibon et al. Brit J Anaesth 82:97-103, 1999 Michard et al. Am J Respir Crit Care Med 162: 134-138, 2000 Michard & Teboul JL Crit Care 4: 282-289, 2000 Feissel et al. Chest 119: 867-873, 2001 Berkenstadt et al. Anesth Analg 92: 984-989, 2001 SPV-IPPV Reuter et al. Intensive Care Med 28: 392-398, 2002 Boulain et al. Chest 121:1245-52, 2002 Reuter et al. British J Anaesth 88: 124-126, 2002 Slama et al. Am J Physiol 283:H1729-33, 2002 Reuter et al. Crit Care Med 31: 1399-1404, 2003 Vieillard-Baron et al. American J Resp Crit Care Med 168:671-676, 2003 Marx et al. European J Anaesth 21: 132-138, 2004 Systolic pressure variations correlate with stroke volume variations measured by the pulse contour technique In general: SPV under estimates SVV by 5% Reuter et al. Brit J Anaesth 88:124-6, 2002. Practical Limitations of PPV • Requires fixed HR – Atrial fibrillation, frequent PVCs • Requires no spontaneous ventilatory efforts – Can not use during CPAP, PSV • Magnitude of PPV or SVV will change with changing tidal volume • Heart failure may give false positive response! Spontaneous Ventilation Alters LV Filling by Ventricular Interdependence Taylor et al. Am J Physiol 213:706-10, 1967 Effect of ventilation on RV and LV Output Spontaneous inspiration Ventricular Interdependence Minimal Ventricular Interdependence Positive-pressure Inspiration Pinsky et al. J Appl Physiol 58:1189-98, 1985 Effect of Positive-Pressure Ventilation on Dynamic LV Volumes and Pressure ECG (m v) 0 .8 0 .6 0 .4 0 .2 Pa (m m H g) 140 120 Protocol: 100 80 40 Ppa 30 (m m H g) 20 Measured LV areas using echocardiographic imaging IPPV during closed and open chest Pre and post CPB 10 20 P ra 15 (m m H g) 10 8 6 L V A rea (cm ²) 4 2 P aw (cm H 2 O ) 20 10 0 0 2 4 T im e (se co n d s) 6 8 Denault et al. Chest 116:176-86, 1999 C h a n g e s in S 1 0 -1 Changes in SAP can not be explained by changes in LV Volumes -1 -2 -2 -3 -3 -4 -2 0 2 4 6 8 10 -4 -1 2 -1 0 2 2 1 1 0 0 -1 -1 -2 -2 -3 -3 -4 -4 C h a n g e s in E S A (cm ²) Neither end-diastolic volume or end-systolic volume changes parallel SPV C h a n g e s in E D A (cm ²) -4 -2 0 2 4 6 8 10 12 -4 -1 2 -1 0 1 1 0 0 -1 -1 -2 -2 -3 -4 -2 0 2 4 6 8 % C h a n g e in S A P 10 12 -3 -1 2 -1 0 -8 -6 -4 -2 0 2 -8 -6 -4 -2 0 2 -8 -6 -4 -2 0 2 % F a ll in S A P Denault et al. Chest 1999; 116:176-86 There is no relation between pulse pressure variation and initial LV enddiastolic area (EDA) in patients during CABG surgery EDA (cm2) 20 15 Preload Preload Responsiveness 10 n=9 r2 = 0.11 5 0 0% 2% 4% 6% 8% 10% 12% 14% 16% PPV (%) Gunn et al. Crit Care & Shock 5: 170-6, 2002 T IM E S S E R IE S FREQUENCY A rte ria l P re s s u re Fourier Analysis: 1 .0 0 500 0 .7 5 400 0 .5 0 300 0 .2 5 200 0 .0 0 The changes in SAP poorly reflect airway pressure induced changes in LV volumes, but reflect very well changes in airway pressure 100 -0 .2 5 -0 .5 0 0 0 500 1000 1500 2000 0 1 2 3 4 5 A irw a y P re s s u re 1 .0 500 0 .8 400 0 .6 0 .4 300 Primary harmonic 0 .2 200 0 .0 -0 .2 100 -0 .4 0 0 500 1000 1500 2000 0 1 2 3 4 5 4 5 E c h o c a rd io g ra p h ic L V A re a 1 .0 500 400 0 .5 300 0 .0 200 -0 .5 100 -1 .0 0 0 500 1000 1500 2000 0 1 2 3 Denault et al. Chest 1999; 116:176-86 Asynchronous High Frequency Jet Ventilation in Acute Ventricular Failure SVrv SVlv PAo Platm Ppatm Pratm Paw Ppl Pinsky et al. J Appl Physiol 58:1189-98, 1985 Asynchronous High Frequency Jet Ventilation in Acute Ventricular Failure Pinsky et al. J Appl Physiol 58:1189-98, 1985 Cardiac cycle-specific increases in ITP during Acute Ventricular Failure SVlv ml/kg QAo PAo mm Hg early systolic late systolic early systolic late systolic Pinsky et al. J Appl Physiol 60:604-12, 1986 Pressure-Volume Loops During Positive Pressure Ventilation End systole Transmural Pressure Airway Pressure Left Ventricular Volume Denault et al . J Appl Physiol 91:298-308, 2001 Positive-Pressure Ventilation Alters Both Preload and Afterload Denault et al. J Appl Physiol 91:298-308, 2001 CPAP 5 mm Hg 160 160 140 140 120 120 LV Pressure (mm Hg) LV Pressure (mm Hg) IVC occlusion 100 80 60 40 100 80 60 40 20 20 0 0 -20 -20 15 20 25 30 35 40 15 20 LV Volume (ml) 140 140 LV Pressure (mm Hg) LV Pressure (mm Hg) 160 120 100 80 60 40 100 80 60 40 20 0 0 -20 -20 25 30 40 120 20 LV Volume (ml) 35 CPAP 15 mm Hg 160 20 30 LV Volume (ml) CPAP 10 mm Hg 15 25 35 40 15 20 25 30 35 40 LV Volume (ml) Kim et al. Proc Am Thorac Soc 3:A297, 2006 Effect of Tidal Volume on LV Pressure and Volume 190 190 170 170 5 ml/kg 150 15 ml/kg 150 130 130 110 110 90 90 70 70 50 50 30 30 10 10 -10 -10 15 20 25 30 35 15 40 20 25 30 35 40 190 190 170 170 10 ml/kg 20 ml/kg 150 150 130 130 110 110 90 90 70 70 50 50 30 30 10 10 -10 15 20 25 30 35 40 -10 15 20 25 30 35 40 Kim et al. Proc Am Thorac Soc 3:A297, 2006 PPV and SVV during IPPV • Reflect complex interactions between preload and afterload • Potential false positive PPV with inspiration – Severe CHF-Reverse Bernheim Effect – Cor pulmonale- Minimize ventricular interdependence • Potential false positive SVP with inspiration – Stiff chest wall + large tidal volume: Valsalva Maneuver – Whenever ITP increases rapidly • These limitations dissolve with passive leg raising Limits of Preload-Responsiveness • Preload Preload-responsiveness • Preload-responsiveness Need for fluids • The means of altering preload matters – Size of Vt, passive leg raising, spontaneous breaths • Different measures of pressure or flow variation will have different calibrations • Pinsky Intensive Care Med 30: 1008-10, 2004 Thank You