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Hemodynamic Monitoring in Sepsis

Hemodynamic Monitoring in Sepsis. Shao-Hsuan Hsia, MD Pediatric Critical Care Medicine Chang Gung Children’s Hospital. Pathophysiology of septic shock Cardiac output monitoring Tissue perfusion monitoring Demand-supply balance. Definition of sepsis. Infection Bacteremia

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Hemodynamic Monitoring in Sepsis

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  1. Hemodynamic Monitoring in Sepsis Shao-Hsuan Hsia, MD Pediatric Critical Care Medicine Chang Gung Children’s Hospital

  2. Pathophysiology of septic shock • Cardiac output monitoring • Tissue perfusion monitoring • Demand-supply balance

  3. Definition of sepsis • Infection • Bacteremia • Systemic Inflammatory Response Syndrome (SIRS) • Sepsis: systemic response to infection • Severe sepsis: organ dysfunction, hypoperfusion or hypotension • Septic shock: hypotension • Multiple Organ Dysfunction Syndrome (MODS)

  4. Activation of Macrophages to Bacterial Invasion LBP - Lipopolysaccharide Binding Pro. LPS - Endotoxin NFkB- Nuclear Transcription Factor LBP LPS CD14 Mitogen Activating Protein Kinase Pathway Gene Activation NFkB Nucleus

  5. Molecular Basis of Shock NFB - nuclear transcription factor TNF TNF TNF R2 R1 Fas Acute Inflammatory Response Acute Inflammatory Response Apoptosis iNO Tissue Factor NFkB Complement Endonuclease Cytokines Adhesion Molecules

  6. NO (iNO) Stimulates Leukotriene, PAF, Cytokine and Oxygen Free Radical Release Vasodilation Decreases vascular permeability High concentrations are cytotoxic PAF Vasoconstriction/Vasodilation Hypotension & Cardiac Depression Vascular Leakage Leukotrienes Vasoconstriction Vascular Leakage IL-1 and TNF iNOS->NO (vasodilation, pulmonary artery pressure, cardiac output) PLA2-> PAF (hypotension) Activate coagulation (microcirculation) Myocardium depressors Damage endothelium Distrosion of myocardial O2 supply and consumption Cytokines and mediators

  7. Hypovolemic (loss of cardiac filling) Capillary leak (absolute hypovolemia) Venodilation (relative hypovolemia) Cardiogenic Decrease in contractility Obstructive Rise in pulmonary vascular resistance Distributive (hypoperfusion, despite normal/increased cardiac output) Macrovascular Decreased splanchnic blood flow Microvascular Shunting Cytotoxic Cellular inability to utilize oxygen, despite adequate supply Septic shock: a melting pot of shock etiologies

  8. Cardiovascular characteristics of sepsis (I) • Systemic vasodilation and hypotension (Psys < 90 mmHg) • Tachycardia (>100 beats/min) • Increased cardiacoutput (hyperdynamic), although contractility is depressed; hypodynamic in late shock • Ventricular dilation; decreased ejection fraction • Loss of sympathetic responsiveness

  9. Cardiovascular characteristics of sepsis (II) • Hypovolemia due to vascular leakage; central venous pressure may be decreased or increased depending upon fluid resuscitation • Compromised nutrient blood flow (microcirculation) to organs; decreased organ oxygen extraction

  10. Dellinger, Crit Care Med 2003 , 31(3): 946-55

  11. Dellinger, Crit Care Med 2003 , 31(3): 946-55

  12. Dellinger, Crit Care Med 2003 , 31(3): 946-55

  13. Morbidity and mortality of sepsis and septic shock • Leading cause of death in noncoronary ICU patients • 500,000 episodes sepsis/year in U.S. (35% crude mortality) • 200,000 cases septic shock (40% of sepsis cases) (40-70% mortality) • 40% hospital deaths after injury due to MODS

  14. The nature of septic shock • Shock • Abnormalities of microcirculation • Skeletal muscle: long arteriole contracted, short dilated • Intestine: redistribute from mucosa to muscle and serosa • Mesenteric:  in liver, pancrease, stomach, colon • Kidney: hypoperfusion, vasoconstriction • Coronary: vasodilation • Abnormalities of Oxygen delivery and uptake CO SVR MAP PCWP CVP Early    or    Late      or 

  15. Pathophysiology of septic shock • Cardiac output monitoring • Tissue perfusion monitoring • Demand-supply balance

  16. Cardiac output Monitoring • Gold Standards: Fick method: CO=O2 consumption/avDO2 • Alternatives: • indicator dilution methods • Dye dilution: Indocyanine green • Thermodilution: Swan Ganz, PiCCO • Echocardography • Doppler techniques • Bioimpedance

  17. Fick Method

  18. 非侵入性監測NICO

  19. Swan-Ganz catheterization

  20. Thermodilution and Cardiac Output

  21. PiCCO

  22. PiCCO: Gödje et al. Crit Care Med 2002 Vol. 30, No. 1

  23. Echocardiography • Left ventricular ejection fraction • SVC collapsibility • Left ventricle hypokinesia • Right ventricle dilatation • IVC enlargement • Pulmonary capillary wedge pressure

  24. Left ventricular ejection fraction Vieillard-Baron et al. Am J Respir Crit Care Med Vol 168. pp 1270–1276, 2003

  25. SVC collapsibility Vieillard-Baron et al. Am J Respir Crit Care Med Vol 168. pp 1270–1276, 2003

  26. Left ventricle hypokinesia Vieillard-Baron et al. Am J Respir Crit Care Med Vol 168. pp 1270–1276, 2003

  27. RV dilatation and IVC enlargement Vieillard-Baron et al. Am J Respir Crit Care Med Vol 168. pp 1270–1276, 2003

  28. Pulmonary capillary wedge pressure (PCWP) E=peak velocity of early mitral inflow, Vp=velocity of flow propagation of early mitral inflow, Ea=early diastolic velocity of mitral annular displacemen, Bouhemad et al. Anesthisiology 98(5): 1091-1100, 2003

  29. 非侵入性監測：Hemosonics

  30. 非侵入性監測：Hemosonics

  31. 非侵入性監測：Impedance Cardiography

  32. Disadvantages of invasive cardiovascular monitoring • Difficult to obtain access • Malposition: arterial puncture (2-16%). • Pneumothorax (incidence 2-4%) • Arrhythmias. • Knotting. • PA rupture with a mortality rate of 50%. • Infection • Thromboembolisms

  33. Pathophysiology of septic shock • Cardiac output monitoring • Tissue perfusion monitoring • Demand-supply balance

  34. Perfusion • The blood flow and oxygen delivered to the tissue bed. • Capillary refill time: weakly correlated • Lactate: lactic acidosis • Gastric intramural pH and pCO2 (tonometry) • Gastroduodenal mucosal oxygen saturation (ISO2) and hemoglobin concentration (IHB).

  35. Lactic acidosis and outcome of ECMO Cheung et al. CCM 2002; 30:2135-2139

  36. Gastric intramural pH (Tonometry)

  37. Gastric tonometry and septic shock Krafte-Jacobs et al. Chest 1995; 108:220-225

  38. Gastroduodenal mucosal oxygen saturation/hemoglobin concentration Spirt et al. Digestive Diseases and Sciences, 49 (6) pp. 906–913, 2004

  39. Pathophysiology of septic shock • Cardiac output monitoring • Tissue perfusion monitoring • Demand-supply balance

  40. Demand and supply balance • DO2 = C.O. × CaO2 = C.O. × (1.34 Hb × SaO2 ＋ 0.003 PaO2) • O2 Consumption = C.O. × (CaO2－CvO2) ≒ C.O. × (SaO2-SvO2) • For constant O2 consumption, cardiac output  SaO2-SvO2 • In sepsis, the relation between O2 demand and supply changes.

  41. Septic shock Oxygen uptake Normal O2 delivery ≈400 ≈ 700 ml/min/M2

  42. High cardiac output and O2 delivery must be maintained!!! Several notable studies showed that supranormal DO2 values DO NOT result in improved outcomes???

  43. Maldistribution Cell ischemia CO2 O2 Rich perfusion

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