hemodynamic management of septic shock

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hemodynamic management of septic shock

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HEMODYNAMIC HEMODYNAMIC MANAGEMENT OF SEPTIC MANAGEMENT OF SEPTIC SHOCK SHOCK Christian Popa, MD CPT, MC, USA Walter Reed Army Medical Center Clinical Spectrum of Infection Clinical Spectrum of Infection Infection Sepsis Severe Sepsis Septic Shock Bacteremia ACCP / SCCM Consensus Definitions of ACCP / SCCM Consensus Definitions of SIRS and Allied Disorders SIRS and Allied Disorders SIRS The systemic inflammatory response to a variety of severe clinical insults. Manifested by 2 or more of the following conditions: Temperature >38 deg C or <36 deg C HR >90 beats/min Respiratory Rate >20 breaths/min or PaCO2 <32 torr (<4.3 kPa) WBC >12,000 or <4,000 cells/mm3 or >10% bands SEPSIS The systemic response to infection. Manifested by the same criteria as SIRS. (Critial Care Med 1992 (20):864-874) ACCP / SCCM Consensus Definitions of ACCP / SCCM Consensus Definitions of SIRS and Allied Disorders SIRS and Allied Disorders (Critial Care Med 1992 (20):864-874) SEVERE SEPSIS Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Perfusion abnormalities include but are not limited to: lactic acidosis oliguria mental status SEPTIC SHOCK Sepsis with hypotension (SBP<90), despite adequate fluid resuscitation and perfusion abnormalities as listed for severe sepsis. Patients on inotropic/ vasopressor agents may not be hypotensive. Incidence / Magnitude of Problem Incidence / Magnitude of Problem • 300,000 to 500,000 cases of bacteremia each year in the US with associated 20-30% mortality. • 200,000 bouts of septic shock. • Sepsis is the leading cause of death in noncoronary intensive care units. • Mortality has changed little over the last 20 years. • Incidence of sepsis appears to be increasing. Reasons Underlying Rising Incidence Reasons Underlying Rising Incidence of Sepsis and Continued High of Sepsis and Continued High Mortality Mortality ● Increased patient age ● Increased use of cytotoxic/immunosuppresive drug therapy ● Increased incidence of concomittent medical illness ● Increased use of invasive devices for diagnosis and therapy ● Rising incidence of infections due to organisms other than Gram negative bacteria (Gram + bacteria, fungi, and possibly viruses) ● Perhabs, the emergence of antibiotic resistant organisms (Chest 1991 (99): 1000-09). Individual Host Risk Factors Individual Host Risk Factors ● Extremes of age ● Chronic disease ● Substance abuse ● Immunosuppressive therapy ● Vascular catheterization ● Prosthetic devices and urinary catheters ● Tracheal intubation Bone, RC. The Pathogenesis of Sepsis. Ann Int Med 1991(115): 457-69. Brun-Bruisson et al. prospectively studied 11,828 consecutive admissions to 170 adult ICU’s in France over a 2 month period in 1993. Of these , 64% were medical admissions, while 18%, 14%, and 4% were scheduled surgery, unscheduled surgery, or nonoperative trauma respectively. They found a 9% incidence of clinically suspected and confirmed sepsis with a 28 day mortality of 56% in patients with severe sepsis. Only 3 of 4 patients presenting with clinically suspected severe sepsis had documented infection. The mortality of the culture negative sepsis subgroup was statistically similar to the overall group. JAMA. 1995 ;274: 968-974 Risk Factors for both early (<3days) and secondary (3-28 days) death Simplified Acute Physiology Score (SAPS) II # of acute organ system failures Risk Factors for early death low arterial pH (<7.33) (P<.001) & shock (P= .03) Risk Factors for secondary (>3d) death admission category (unscheduled surgery >> medical > scheduled surgery > nonoperative trauma (P<.001) rapidly or ultimately fatal underlying disease (P<.001) preexisting liver (P=.01) or cardiovascular (P=.02) insufficiency hypothermia (P=.02) thrombocytopenia (P=.01) multiple sources of infection (P=.02) Brun-Bruisson et al. JAMA, 1995, 274; 12: 968-974 Hemodynamic Abnormalities in Septic Hemodynamic Abnormalities in Septic Shock Shock ● Prototypic example of distributive shock. ◆ Severe in SVR and generalized blood flow maldistribution develop in almost all affected patients. ◆ After aggresive volume loading (adequate preload), C.O. normal in 80% of patients with septic shock. ◆ This is in contrast to cardiogenic, extracardiac obstructive, and hypovolemic forms of shock which C.O. ◆ Initial in LVEF occuring within 24 hours of onset with associated increase in both end-systolic and end-diastolic indices. ◆ This pattern of LVEF and LVEDV is characteristic of survivors and is reversible. Ventricular function/size normalize 7-10 days following onset. ◆ This pattern of dysfunction was extended to the R ventricle in 1990 by Parker et al. Chest 1990; 97:126-31. [...]... *Maldistribution of flow Differential Diagnosis of Septic Shock q Other Nonseptic Causes of Hyperdynamic Shock x x x x x x x x x overdosage of drugs with vasodilator properties Toxic Shock Syndrome primary/secondary adrenal insufficiency anaphylactic reactions severe anemia severe liver disease AV fistulas thyroid storm severe thiamine deficiency Differential Diagnosis of Septic Shock q The forms of shock generally... endotoxin, IL-1, Il-2 produced no depression of myocyte contraction Endotoxin and IL-2 have produced hemodynamic alterations similar to septic shock in some human studies TNF, based on animal models & in vitro myocyte preparation studies appears to be one of the major mediators of cardiovascular insufficiency in septic shock Chest 1991; 99: 1000-09 Role of TNF-a in Septic Shock (Clinical Infectious Diseases... vascular permeability of the gut Immunologic x Induction of hepatic acute phase synthesis x Fever x Promotion of IL-1, IL-2, PAF, IL-6, and eicosanoid production x Stimulation of B & T lymphocyte proliferation Pathogenesis of Septic Shock Journal of Infection 1995; 30: 201-206 MONOCYTE CD 14 Bacteria LPS LPS TNF-A ENDOTHELIAL CELL LBP LPS soluble CD 14 LBP LPS Pathogenesis of Sepsis Mediated Hemodynamic Dysfunction... Evidence for Maintenance of Supranormal Levels of DO2 in the Critically Ill q q q q q Acute endotoxemia and acute bacteremia animal models of sepsis induce a pathologic dependence of VO2 on DO2 Numerous clinical studies of ARDS, sepsis syndrome, septic shock, and critical illness claim to show pathologic dependence of VO2 on DO2 Several clinical studies have found that survivors of critical illness have... 125 ml Hemodynamic Patterns with Prognostic Value q A lower heart rate at the onset of disease is predictive of survival q Normalization within 24 hours of either tachycardia or elevated cardiac index is associated with survival Persistence of hyperdynamic state increases likelihood of death Parker et al Serial Cardiovascular Variables in Survivors and Nonsurvivors; HR as an Early Predictor of Prognosis... dilatation are also associated with survival This perhabs reflects Frank-Starling compensation of sepsis induced myocardial depression Parrilo, JE Pathogenetic Mechanisms of Septic Shock, NEJM 1993; 328(20): 1471-77 Jardin et al (University of Vienna) prospectively studied 27 surgical ICU patients in early septic shock MAP normal Blood volume 500 ml > normal if PCWP < 20 mm Hg DO2 > 600 ml/min/m2 VO2 > 170 ml/min/m2 q For septic patients . HEMODYNAMIC HEMODYNAMIC MANAGEMENT OF SEPTIC MANAGEMENT OF SEPTIC SHOCK SHOCK Christian Popa, MD CPT, MC, USA Walter Reed Army Medical Center Clinical Spectrum of Infection Clinical. studies appears to be one of the major mediators of cardiovascular insufficiency in septic shock. Chest 1991; 99: 1000-09. Role of TNF-a in Septic Shock Role of TNF-a in Septic Shock ● TNF-a has been. sources of infection (P=.02) Brun-Bruisson et al. JAMA, 1995, 274; 12: 968-974 Hemodynamic Abnormalities in Septic Hemodynamic Abnormalities in Septic Shock Shock ● Prototypic example of distributive

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Mục lục

  • HEMODYNAMIC MANAGEMENT OF SEPTIC SHOCK

  • Clinical Spectrum of Infection

  • ACCP / SCCM Consensus Definitions of SIRS and Allied Disorders

  • Slide 4

  • Incidence / Magnitude of Problem

  • Reasons Underlying Rising Incidence of Sepsis and Continued High Mortality

  • Individual Host Risk Factors

  • PowerPoint Presentation

  • Slide 9

  • Hemodynamic Abnormalities in Septic Shock

  • Changes in Cardiac Performance During Acute & Recovery Phases of Septic Shock

  • Hemodynamic Patterns with Prognostic Value

  • Slide 13

  • Why Is Ventricular Function Impaired ?

  • Slide 15

  • Myocardial Depressant Substance

  • Role of TNF-a in Septic Shock

  • Biologic Actions of TNF-a (Cachectin)

  • Pathogenesis of Septic Shock

  • Pathogenesis of Sepsis Mediated Hemodynamic Dysfunction

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