UPMC Critical Care.

Transcription

1 UPMC Critical Care

2 Functional Hemodynamic Monitoring Michael R. Pinsky, MD, Dr hc Department of Critical Care Medicine University of Pittsburgh

3 Important Conflicts of Interest

4 Unimportant Conflicts of Interest Michael R. Pinsky, MD is the inventor of a US patent Use of aortic pulse pressure and flow in bedside hemodynamic management owned by the University of Pittsburgh, plus 2 other complexity patents. Michael R. Pinsky, MD is a co-founder and stockholder of Intelomed Michael R. Pinsky, MD is or was* a medical advisor for: Abbott Corporation* Applied Physiology Ltd.* Arrow International* Cheetah Medical* Edwards Lifesciences Hutchinson Medical* LiDCO Ltd Massimo* väsamed* Michael R. Pinsky, MD is or was* receiving research funding from: Deltex Ltd* Pulsion Ltd* Edwards LifeSciences Michael R. Pinsky, MD is receiving research funding as Principal Investigator from the NHLBI and (co-i) DoD T32 HL07820, R01 NR and W81XWH

5 Monitoring Truth No monitoring device, no matter how accurate or insightful its data will improve outcome, Unless coupled to a treatment, which itself improves outcome Pinsky & Payen. Functional Hemodynamic Monitoring, pp 1-4, 2004 Pinsky & Payen. Crit Care 9: Pinsky. Chest 132:2020-9, 2007

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7 Why Measure Cardiac Output? Cardiac output varies with metabolic rate Threshold levels define low output disease states But does knowing cardiac output improve diagnosis, treatment or outcome from critical illness?

8 Survivorship Relative to TO Survivors (%) Oxygen Transport (ml/min/m 2 ) Bland et al. Crit Care Med 13:85-92, 1985

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10 Resuscitation Protocols Based on Invasive Hemodynamic Monitoring Improve Survival Early goal-directed therapy for severe sepsis Rivers et al. New Engl J Med 345: , 2001 Intra-operative goal-directed therapy Gan et al. Anesthesiology 97:820-6, 2002 Post-operative resuscitation in high risk patients McKendry et al. Br Med J 329:258-65, 2004 Pearse et al. Crit Care 9: R687-93, 2005

11 Preoptimization Pre- and intra-operative goal-directed therapy in high risk surgical patients Resuscitation to relatively higher levels of DO 2 Sinclair et al. BMJ 315:909-12, 1997 Venn et al. Br J Anaesth 88: 65-71, 2002 Prevent occult tissue hypoperfusion Mythen & Webb. Arch Surg 130: 423-9, 1995 Reduces vasopressor requirements during cardiac surgery Goepfert et al. Intensive Care Med 33: , 2007

12 Preoptimization

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14 Pre-optimization Improves Outcome Kern & Shoemaker. Crit Care Med 30: , 2002

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16 Goal-directed Therapy: 15-year follow up Median increase in survival 1107 days (> 3 years) Hazard ratio 1.8 (95% CI 1.2 to 2.8) Rhodes et al. Intensive Care Med 36: , 2010

17 15 years survival Any Complication Rhodes et al. Intensive Care Med 36: , 2010

18 Goal-directed Therapy: 15-year follow up Any Cardiac Lung Renal Rhodes et al. Intensive Care Med 36: , 2010

19 Goal-directed Therapy: 15-year follow up Control Group Protocol Group Rhodes et al. Intensive Care Med 36: , 2010

20 Three Primary Clinical Problems How to identify patients who are becoming hemodynamically unstable before they progress too far? How to determine the most appropriate therapy to reverse the primary cause for impending circulatory shock? How to you implement the most appropriate therapy with when individual responses of patients and skill level of care givers vary?

21 Three Primary Clinical Problems How to identify patients who are becoming hemodynamically unstable before they progress too far? How to determine the most appropriate therapy to reverse the primary cause for impending circulatory shock? How to you implement the most appropriate therapy with when individual responses of patients and skill level of care givers vary?

22 Identifying Cardiovascular Reserve: StO 2 during an vascular occlusion test Vascular occlusion test 100 T0 T1 T2 StO StO 2 (%) 40 reoxygenation 20 Occlusion Release Time (sec) Torres et al. J Surg Res 130:279, 2006 Gomez et al. Intensive Care Med 34:1600-7, 2008

23 Non-Invasive Assessment of Cardiovascular Reserve: StO 2 StO 2 Curve During Vascular Occlusion and Release Normal Trauma post-initial resuscitation Torres et al. J Surg Res 130:279, 2006 StO2 (%) 0:00:00 0:01:00 0:02:00 0:03:00 0:04:00 0:05:00 0:06:00 0:07:00 0:08:00 0:09:00 0:00:00 0:01:00 0:02:00 0:03:00 0:04:00 0:05:00 0:06:00 0:07:00 0:08:00 0:09:00 Occlusion Release StO2 (%) Occlusion Release 10 0

24 StO 2 Recovery in Health and Disease P< 0.01 Torres et al. J Surg Res 130:279, 2006 Gomez et al. Intensive Care Med 34:1600-9, 2008

25 StO 2 Deoxygenation and Recovery in Disease StO 2 (%) Occlusion Day 0 Early in Resuscitation 20 Day 1 Sepsis Syndrome & Organ Dysfunction Day 2 Resolution and Recovery Time (min) Gomez et al. Intensive Care Med 34:1600-7, 2008

26 StO 2 Deoxygenation Rate Predicts Change in SOFA Score in Septic Patients n =17 n =16 Mesquida et al. Intensive Care Med 38:592-7, 2012

27 Predicting the Need for Life-Saving Interventions (LSI) Stat Evac Trauma Patients All Patients LSI No LSI n=194 n=61 n=133 p Age (yrs) 43 (27-58) 47 (34-68) 39 (27-39) 0.01 Sex (male), n (%) 119 (61) 42 (69) 77 (58) 0.15 Localization of injury, n(%) Head & Neck 84 (43) 37 (61) 47 (35) Face 39 (20) 15 (25) 24 (18) 0.3 Chest 44 (23) 24 (39) 20 (15) Abdomen 33 (17) 21 (34) 12 (9) Extremity 69 (36) 26 (43) 43 (32) 0.2 Prehospital Physiology Highest heart rate, bpm 98± ±19 97± Lowest systolic arterial blood pressure, mm Hg 120±13 119±17 121± Highest respiratory rate, cpm 17±2 18±3 17± Glasgow Coma Score <15, n(%) 52 (27) 25 (41) 27 (20) Tissue oximetric saturation Deoxygenation slope, %/sec 0.15 ( ) 0.13 ( ) 0.17 ( ) Reoxygenation slope, %/sec 2.1 ( ) 1.9 ( ) 2.3 ( ) 0.13 Baseline, % 80 (74-86) 80 (74-84) 80 (86-74) 0.9 Prehospital serum lactate, mmol/l 2 ( ) 2.2 ( ) 1.8 ( ) 0.02 Guyette et al. J Trauma 72:930-5, 2012

28 StO 2 VOT DeOx Predicts need for Life- Saving Interventions in Trauma Patients DeO 2 ReO 2 Lowest Systolic BP Sensitivity ROC Specificity Area under ROC curve = Lowest Systolic BP Guyette et al. J Trauma 72:930-5, 2012

29 Three Primary Clinical Problems How to identify patients who are becoming hemodynamically unstable before they progress too far? How to determine the most appropriate therapy to reverse the primary cause for impending circulatory shock? How to you implement the most appropriate therapy with when individual responses of patients and skill level of care givers vary?

30 Why Not Give Volume to All Hemodynamically Unstable Patients? Signs of cardiovascular insufficiency are impressive but not specific Hypotension must decrease blood flow to the heart and brain Most forms of circulatory shock have a pathological component of decreased effective circulatory blood volume

31 Fluid Challenge as a Clinical Trail If one wishes to know if a patient will increase their cardiac output in response to intravascular volume loading, then a time-honored way to determine if the patient is to give a bolus of fluid (~5-10 ml/kg) over < 30 minutes and note if there is an increase in flow

32 Why Not Give Volume to Every Unstable Patient as Primary Resuscitation Therapy? Predicting Fluid Responsiveness in ICU Patients Responders / Non-Responders % Responders Calvin (Surgery 81) 20 / 8 71 % Schneider (Am Heart J 88) 13 / 5 72 % Reuse (Chest 90) 26 / % Magder (J Crit Care 92) 17 / % Diebel (Arch Surgery 92) 13 / 9 59 % Diebel (J Trauma 94) 26 / % Wagner (Chest 98) 20 / % Tavernier (Anesthesiology 98) 21 / % Magder (J Crit Care 99) 13 / % Tousignant (A Analg 00) 16 / % Michard (AJRCCM 00) 16 / % Feissel (Chest 01) 10 / 9 53 % Mean 211 / % Michard & Teboul. Chest 121:2000-8, 2002

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34 Is Cardiac Output Adequate? Is blood flow adequate to meet metabolic demands? Will increasing intravascular volume increase cardiac output? Will decreasing the driving pressure for venous return decrease cardiac output? Preload Responsiveness

35 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

36 CVP before volume expansion in Responders (R) and Non-Responders (NR) 12 R NR 10 * * CVP (mm Hg) Calvin Schneider Reuse Wagner Michard Michard & Teboul. Chest 121: , 2002

37 Changes in stroke volume (%) CVP does not predict volume responsiveness r = 0.45 Baseline CVP (mmhg) Wagner & Leatherman. Chest 113: ,1998

38 Ppao (mm Hg) before volume expansion in Responders (R) and Non-responders (NR) R NR Calvin (Surgery 81) Schneider (Am Heart J 88) Reuse (Chest 90) Diebel (J Trauma 94) Tavernier (Anesthesiolgy 98) Michard (AJRCCM 00) Wagner (Chest 98) Tousignant (Anesth Analg 00) p < 0.05 p < 0.05 Michard & Teboul. Chest 121: , 2002

39 Ppao does not predict preload-responsiveness Responders Non-responders Ppao (mm Hg) $ * $ Pre Post Pre Post Tousignant et al. Anesth Analg 90:351-5, 2000

40 Neither CVP or Ppao Mirror SV Lichtwarck-Aschoff et al. Intensive Care Med 18: 142-7, 1992

41 Echocardiographic LVEDA (cm 2 /m 2 ) R NR Feissel (Chest 01) Tavernier (Anesthesiology 98) * Tousignant (Anesth Analg 00) * cm 2 * p < 0.05

42 LV EDA in Responders and Non-responders of fluid resuscitation 16 LVEDA before fluid infusion (cm 2 /m 2 ) responders non responders Feissel et al. Chest 119:867-73, 2001

43 The use of transesophageal echocardiography for preload assessment in critically ill patients responders non-responders EDA cm 2 * ** Pre Post Pre Post Tousignant et al. Anesth Analg 90:351-5, 2000

44 Neither CVP or Ppao reflect Ventricular Volumes or Tract Preload-Responsiveness Preload Preload Responsiveness Kumar et al. Crit Care Med 32:691-9, 2004

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46 Starling s Law of the Heart Lives! Kumar et al. Crit Care Med 32:691-9, 2004

47 Hemodynamic Effects of Changes in Intrathoracic Pressure Venous Return Thorax LV Ejection

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49 Spontaneous Ventilation Positive-Pressure Ventilation SVrv (ml/kg) Time (sec) Pra tm (mm Hg) Ppl (mm Hg) CVP (mm Hg) Pinsky. J Appl Physiol 56: , 1984

50 Effect of Positive-Pressure Ventilation on LV Volumes and Pressure ECG (mv) Intact Anesthetized Human Pa (mm Hg) Ppa (mm Hg) Pra (mm Hg) LV Area (cm²) 4 2 Paw (cm H 2 O) Time (seconds) Denault et al. Chest 1999; 116:176-86

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52 LV Pressure-Volume Loop LV Pressure (mm Hg) End-systole Ejection (stroke volume) Isometric Relaxation Aortic Valve Opening Isometric Contraction Mitral Valve Opening Diastolic filling End-diastole LV Volume (ml) Patterson & Starling. J Physiol (Lon) 48: ,1914

53 Pressure-Volume Loops During Positive Pressure Ventilation End systole Transmural Pressure Airway Pressure Denault et al. J Appl Physiol 91: , 2001 Left Ventricular Volume

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55 Effect of IPPV on LV Pressure and Volume IPPV 20 ml/kg IPPV 20 ml/kg LV pressure (mm Hg) Stroke Volume Variation Decreased Preload LV volume (ml) Kim et al. Crit Care Med 36: , 2008

56 Preload-Responsiveness is Dependent on Initial Volume Status and Cardiac Contractility LV Stroke Volume LV End-Diastolic Volume

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58 150 Effect of IVC Occlusion on Flow Measures in Man Arterial Pressure Arterial Pressure (mm Hg) Cineflo Aortic Flow Probe Aortic Flow (L/min) Time (1 s) Marquez et al. Crit Care Med 36:3001-7, 2008

59 Relation Between Stroke Volume and Pulse Pressure During IVC Occlusion in Man 40 Stroke Volume Arterial Pulse Pressure Marquez et al. Crit Care Med 36:3001-7, 2008

60 Effect of Mechanical Ventilation on PP and SV Baseline (Vt 10 ml/kg) PP (mm Hg); SV (ml) PP SV 5 0 Insp Insp Insp Heartbeat (n) Mesquida et al. Intensive Care Med 37:1672-9, 2011

61 Definitions: Pulse Pressure & Systolic Pressure 45 Airway Pressure (cm H 2 O) Arterial Pressure (mm Hg) PPmax SP max PPmin SP min Systolic Pressure (SP) = SP max -SP min Pulse Pressure (PP) = PPmax-PPmin PPV = PP/mean PP 40 2 seconds Michard et al. Am J Respir Crit Care Med 159:935-9, 1999

62 Baseline PPV Predicts Volume Responsiveness y = 0.95x r 2 = Changes in Cardiac Index (%) Baseline PPV (%) Michard et al. Am J Respir Crit Care Med 162:134-8, 2000

63 Receiver Operator Characteristic (ROC) Curve for >15% increase in cardiac output to a 500 ml volume challenge in patients in septic shock 100 PP Sensitivity (%) SPV Pra Ppao PPV >13% SPV > 13% Pra > 8 mm Hg Ppao > 12 mm Hg Specificity (%) Michard et al. Am J Respir Crit Care Med 162:134-8, 2000

64 Effect of IVC Occlusion on Flow Measures in Man Arterial Pressure (mm Hg) Aortic Flow (L/min) Arterial Pressure Cineflo Aortic Flow Probe Esophageal Doppler Flow (L/min) Hemosonic Esophageal Doppler Calculated Flow Pulse Oximetry Density Pulse Oximetery Plethysmograph Time (1 s) Marquez et al. Crit Care Med 36:3001-7, 2008

65 13 % Am J Respir Crit Care Med 2000; 162: % 11 % Chest 2004, 126: % 17 % Chest 2005;128; % Crit Care Med 2005;33: PPV 16 % 10 % 12 % 15 % 12 % 12.5 % 12 % M. Cannesson, J. Slieker, O. Desebbe, F. Fahdi,O. Bastien, JJ. Lehot

66 Positive-Pressure Ventilation-Induced Changes in LV Output Mechanical insufflation RV filling * pulmonary transit time RV output at inspiration LV filling 2-3 heart beats later ** if RV with preload reserve * ** if LV with preload reserve LV output at expiration from Jean-Louis Teboul

67 Goal-Directed Therapy Using PPV in High-Risk Surgery Patients Pulse Pressure Minimization Lopes et al. Crit Care 11:R100-7, 2007

68 Goal-Directed Therapy Using PPV in High-Risk Surgery Patients Fluid resuscitation to keep PPV or SVV <10% 16 pt in Intervention Group v. 17 in Control Group Both groups were comparable in terms of demographic data, ASA score, type, and duration of surgery. Intervention Group (n=16) Control Group (n=17) Intra-op fluids 4,618 ± 1,557 1,694 ± 705 ml (P < ) ΔPP decrease 22 ± 75 to 9 ± 1% (P < 0.05) no change Median post-op LOS 7 17 days (P < 0.01) # post-op comp/pt 1.4 ± ± 2.8 (P < 0.05) Median mech vent 1 5 days (P < 0.05) ICU stay 3 9 days (P < 0.01) Lopes et al. Crit Care 11:R100-7, 2007

69 Goal-Directed Therapy Using PPV in High-Risk Surgery Patients Lopes et al. Crit Care 11:R100-7, 2007

70 PPV v. GEDV Targets as Guides to Resuscitation Porcine hemorrhagic shock model (MAP 40 mmhg x 60 m) Resuscitation with HES as needed to targeted minimal PPV or PAC-derived GEDVI All static and dynamic markers to tissue oxygenation and hemodynamic stability similar in both groups following resuscitation Volume and time to resuscitation higher with GEDV target than PPV minimization (<10%) target 1,305 ± 331 v. 965±245 ml (p<0.05) 24.8±4.7 v. 8.8±1.3 min (p<0.05) DeOliveira et al. J Trauma 67: , 2009

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72 Technical Limitations of PPV and SVV for Assessment of Preload-Responsiveness Requires fixed HR Atrial fibrillation, frequent PVCs Requires positive-pressure ventilation Requires no spontaneous ventilatory efforts Can not use during CPAP, PSV, A/C Cor Pulmonale and ventricular interdependence Magnitude of PPV or SVV will change if tidal volume changes Changes in vasomotor tone will alter the PPV/SVV relation

73 Dynamic shifts in Intrathoracic Blood Volume during IPPV 10 Inspiration Expiration SV RV - SV LV (ml) Vt 5mL/kg Vt 10mL/kg Vt 15mL/kg Vt 25mL/kg Heartbeat (n) Mesquida et al. Intensive Care Med 2011 doi: /s

74 190 Effect of Tidal Volume on LV Pressure and Volume ml/kg ml/kg ml/kg ml/kg Kim et al. Crit Care Med 36: , 2008

75 Spontaneous Ventilation Alters LV Filling by Ventricular Interdependence Taylor et al. Am J Physiol 213:706-10, 1967

76 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: , 1985

77 Prediction of Fluid Responsiveness Spontaneous breathing and arrhythmias ABF PLR Volume Loading The PLR effects occur over a epoch of time encompassing several cardiac and respiratory cycles Monnet et al. Crit Care Med 34:1402-7, 2006

78 Change in Mean Aortic Flow during PLR 80 Mean aortic flow (%) * * Non responders Responders *P < 0.05 base 1 legs up base 2 post VE Monnet et al. Intensive Care Med 31: , 2005

79 How to assess preloadresponsiveness in spontaneously breathing patients? Volume challenge Passive leg raising DeBacker & Pinsky. Intensive Care Med 33:1111-3, 2007

80 Can FHM be used in Spontaneous Ventilating Patients in Septic Shock? Lanspa et al. Shock 39:155-60, 2013

81 Can FHM be used in Spontaneous Ventilating Patients in Septic Shock? Lanspa et al. Shock 39:155-60, 2013

82 Can FHM be used in Spontaneous Ventilating Patients in Septic Shock? Lanspa et al. Shock 39:155-60, 2013

83 Can FHM be used in Spontaneous Ventilating Patients in Septic Shock? SVV >17% VCCI >15% AoVV no Lanspa et al. Shock 39:155-60, 2013

84 Is arterial tone normal? Normal baroreceptor reflex mechanisms vary vasomotor tone to maintain arterial pressure constant despite changes in cardiac output, thus. Hypotension is always pathological Normotension does not mean hemodynamic stability

85 Arterial Tone Assessed by Ventriculo-Arterial Coupling Stroke Volume Defines Arterial Pulse Pressure 100 E a Arterial Pulse Pressure Arterial Elastance (E a ) Stroke Volume

86 Comparing PPV to SVV as Dynamic Arterial Elastance Arterial Pulse Pressure 100 Increased Dynamic Arterial Elastance Dynamic E a Decreased dynamic Arterial Elastance 0 0 Stroke Volume 50

87 Ventriculo-Arterial Coupling Vasopressor Therapy - Hemorrhage Acute Heart Failure Tamponade + Volume Loading Exercise Increase catecholamines + Sepsis Vasodilator Therapy Stroke Volume - Pulse Pressure

88 Changes in Vasomotor Tone alter LiDCO-derived PPV/SVV Normal PPV/SVV Pre: PPV/SVV.13/.09 = 1.44 Post: PPV/SVV.17/.15 = 1.13 Increase vasodilation Increase vasodilation PPV (%) 20 17(6) SVV (%) (10) (6) 10 9 (6) Pre Post Pre Post Vasodilator therapy increased PPV 13% to 17% and SVV from 9% to 15% (P<0.001). Hadian et al. J Crit Care 26: 328.el-e8, 2011

89 Comparing PPV to SVV as Dynamic Arterial Elastance PPV/SVV Monge et al. Crit Care 15:R15, 2011

90 Dynamic Arterial Elastance >0.89 Predicts a >15% increase in MAP Ea dyn > % sensitivity 100% specificity Monge et al. Crit Care 15:R15, 2011

91 Limits of Preload-Responsiveness Approaches in Practice Preload Preload-responsiveness Preload-responsiveness Need for fluids The means of altering preload matters Size of Vt, passive leg raising, spontaneous breaths The PPV/SVV will vary with vasomotor tone Szold et al. Intensive Care Med 15:368-71, 1989 Wiesenack et al. Anesth Analg 96: , 2003 Pinsky. Anesth Analg 96: , 2003 Reuter et al. Intensive Care Med 29: , 2003 Pinsky Intensive Care Med 30: , 2004 Hadian et al. J Crit Care 2010 (doi:10/ /j.jcrc )

92 Flow and Pulse Pressure Variation SV, PP & PLR CO > 10-15% accurately identify subjects whose cardiac output will increase during a fluid challenge and by how much SV, PP & PLR CO can be used to monitoring the change in cardiac output in response to therapy If SV, PP or PLR CO are not present, then fluid loading will not increase cardiac output

93 Continuous Monitoring of Preload Responsiveness Arterial Pressure Non-invasive BMEye, Fenapres Invasive Arterial catheterization Arterial flow Esophageal Doppler Deltex CardiaQ Echocardiogram, htee Combined Pressure and Flow Pulse Contour Technology PiCCO, LiDCO, FloTrac BMEye PPV > 13% SVV > 10% CO > 10% PPV 20% SVV 10%

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95 Clinical Implications We can identify critically ill patients by their changing arterial pressures and flow We can identify the presence or absence of volume responsiveness and assess easily arterial tone at the bedside Using these dynamic measures and defined resuscitation algorithms, we can effectively resuscitate high risk surgery patients reducing post-operative complications and length of stay The short term benefits of Pre-optimization protocols appear to be sustained over time

96 Clinical Implications Pre-optimization in high-risk patients is cost-effective Reduces post-operative complications Improves long-term survival Target audience: Anesthesiologists Location: Peri- and Intra-operative Care Post-operative preload-optimization of cardiac surgery patients is cost-effective but unclear if confirming a survival advantage Target audience: ICU physicians and nurses

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98 Hemodynamic Monitoring Protocol Is the patient hemodynamically stable? Do Nothing Yes No Is the patient preload-responsive? Yes No Does the patient hypotensive and have reduced vasomotor tone? Yes No Yes No Volume bolus Add Vasopressor Volume bolus Add Vasopressor Add Inotrope Reassess the patient Pinsky. Protocolized care, in: Pinsky & Payen. Functional Hemodynamic Monitoring, pp , 2004

99 Applications of Functional Hemodynamic Monitoring Define resuscitation options in circulatory shock UPMC Pre-optimization trial in high risk surgery (Whitehurst & Pinsky) Spanish Multi-center Trail Resuscitation from Shock: Muras Closed loops control during in-flight resuscitation (Guyette) Define fluid requirements in ARDS Better rationale than Pra or Ppao used in the ARDSNet Fluids and catheters treatment trial (FACTT) Monitoring fluid removal during hemodialysis (Pinsky) Cadaveric support prior to organ harvesting (Kellum)

100 Thank You