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SEPTIC SHOCK

SEPTIC SHOCK. By Marian D. Williams RN BN CEN CFRN CCRN. SEPTIC SHOCK. Most common cause of death in non-cardiac ICU’s in the US Most cases are nosocomial Increased incidence due to advanced invasive technology Elderly are at greatest risk Mortality:40%-85%. SEPTIC SHOCK.

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SEPTIC SHOCK

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  1. SEPTIC SHOCK By Marian D. Williams RN BN CEN CFRN CCRN

  2. SEPTIC SHOCK • Most common cause of death in non-cardiac ICU’s in the US • Most cases are nosocomial • Increased incidence due to advanced invasive technology • Elderly are at greatest risk • Mortality:40%-85%

  3. SEPTIC SHOCK • 10th leading cause of death in the United States • 139% increase from 1979 - 1987

  4. SEPTIC SHOCK • DEFINITIONS • Bacteremia • Presence of BACTERIA in the blood • Body’s defense systems effectively destroy bacteria • Septicemia • Presence of MICROBES in the blood associated with systemic infection

  5. SEPTIC SHOCK • Sepsis • Systemic inflammatory response to infection. • Severe Sepsis/SIRS • Sepsis associated with evidence of one or more acute organ dysfunctions

  6. SEPTIC SHOCK RISK FACTORS • Patient related • < 1 year of age • > 65 years of age • Debilitated • Malnourished • Chronic health problems

  7. SEPTIC SHOCK RISK FACTORS • Treatment Related • Invasive lines and procedures • Surgical procedures • Treatment for burns or traumatic wounds • Immuno-suppression

  8. Gram Negative Most cases E. COLI Most likely Klebsiella pneumoniae Enterobacter aerogenes Serratia marcescens Gram Positive Less common Staphylococcus aureus Viruses Fungi Rickettsiae Protozoans SEPTIC SHOCK CAUSATIVE MICROORGANISMS

  9. SEPTIC SHOCK CAUSATIVE MICROORGANISMS • Gram Negative • Responsible for the majority of the cases

  10. ENTRY SITES FOR SEPTIC SHOCK • Most common - GU Tract • GI Tract • Respiratory Tract • Skin

  11. SEPTIC SHOCK PATHOGENESIS • Proinflammatory and procoagulation responses dominate and lead to uncontrolled inflammation and advanced coagulopathy

  12. SEPTIC SHOCK PATHOGENESIS • Three known problems • Excess Coagulation • Exaggerated or malignant inflammation • Impaired fibrinolysis

  13. SEPTIC SHOCK PATHOGENESIS • Balance of coagulation and fibrinolysis shifts toward increased coagulation via the extrinsic pathway

  14. SEPTIC SHOCK PATHOGENESIS • In mice, microthrombi developed in the hepatic circulation within 5 minutes of injection of endotoxin

  15. SEPTIC SHOCK PATHOGENESIS • Endotoxin is within the Gram Negative bacteria wall • Released into the blood during bacterial cell lysis

  16. Macrophages Phagocytic cells found in the lung interstitium and alveoli, liver, sinuses etc. Activated by endotoxin to release cytokines Cytokines Tumor necrosis factor Major endogenous toxin * Interleukin-1 Interleukin-2 PATHOGENESIS OF SEPTIC SHOCK

  17. Endotoxins activatesGRANULOCYTES Releases toxic mediators e.g. platelet activating factor, Oxygen derived free radicals Proteolytic enzymes Endotoxins activate arachidonic acid cascade Results in prostaglandin, leukotrienes, thromboxane A etc effecting smooth muscle PATHOGENESIS OF SEPTIC SHOCK

  18. Thromboxane A2 and B2 Pulmonary vasoconstriction Mediate broncho-onstriction Potent platelet aggregator Prostaglandin E and Prostacyclin Potent vasodilator May be responsible for hypotension PATHOGENESIS OF SEPTIC SHOCK

  19. Complement System Activated Produce microemboli Endothelial cell destruction Histamine Potent Vasodilator Released by mast cells Increases Capillary permeability (Fluid moves from vascular bed) PATHOGENESIS OF SEPTIC SHOCK

  20. Myocardial Depressant factor (MDF) Released from pancreas Decreases contractility of the heart Coagulation system is activated Kinin System activated Bradykinin is released Vasodilation Increased capillary permeability PATHOGENESIS OF SEPTIC SHOCK

  21. PATHOGENESIS OF SEPTIC SHOCK • MYOCARDIAL DEPRESSANT FACTOR • MAY ENHANCE DEVELOPMENT OF MICRO EMBOLI

  22. HEMODYNAMIC ALTERATIONS OF SEPTIC SHOCK • Profound Vasodilation • Systemic vascular resistance is decreased • Blood Pressure falls • Veins dilate • Intravascular pooling in the venous capacitance system

  23. HEMODYNAMIC ALTERATIONS OF SEPTIC SHOCK • Mal-distribution of blood flow • Some tissues under-perfused and some tissues are over-perfused • Excessive flow rates to areas of low metabolic demand limits O2 extraction • Therefore, difference in arterial and venous O2 content

  24. HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK • Decreased ejection fraction • Definition: • Percent of diastolic volume that is ejected during systole

  25. HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK • Decreased Ejection Fraction • Depressed myocardial contractility despite increased cardiac output • Right ventricular dysfunction is common – usually as a result of pulmonary hypertension and myocardial depression

  26. HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK • Increased capillary permeability • Fluid movement out of the vascular beds and into the interstitial space • Generalized soft tissue edema results • Edema can interfere with tissue oxygenation and organ function

  27. HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK • Microembolization • Results in sluggish blood flow • Decreased oxygen utilization therefore increased risk of D. I. C.

  28. HYPERDYNAMIC PHASECLINICAL MANIFESTATIONS • BP Falls • Decreased SVR • Decreased venous return • Decreased sympathetic tone • Diastolic pressure falls

  29. HYPERDYNAMIC PHASE -CLINICAL MANIFESTATIONS • Increased sympathetic tone • Widened pulse pressure • Heart rate increases in attempt to increase CO to compensate for decreased blood pressure

  30. Impaired gas exchange Pulmonary blood congestion Pulmonary blood flow decreases Respiratory rate and depth increase Early respiratory alkalosis Crackles may be audible Interstitial pulmonary edema HYPERDYNAMIC PHASE -CLINICAL MANIFESTATIONS

  31. HYPERDYNAMIC PHASE - CLINICAL MANIFESTATIONS • Impaired Gas Exchange • Pulmonary vascular resistance increases • Pulmonary congestion results

  32. Febrile Possible associated chills Skin pink and warm Peripheral vasodilation LOC may be altered Cerebral ischemia HYPERDYNAMIC PHASE-CLINICAL MANIFESTATIONS

  33. Decreased SVR Cardiac output high Cardiac Index high Decreased venous return Pulmonary artery pressures below normal PCWP below normal HEMODYNAMIC MANIFESTATIONS-HYPERDYNAMIC PHASE

  34. HEMODYNAMIC MANIFESTATIONS-HYPERDYNAMIC PHASE • Maldistribution of blood flow • Oxygen consumption is decreased • SVO2 levels are above normal

  35. HYPODYNAMIC PHASE-CLINICAL MANIFESTATIONS • Decreased cardiac output • Rapid, shallow respirations • Crackles and wheezes • Pulmonary congestion • Decreased Urinary output • Renal hypoperfusion • Lethargic

  36. HYPODYNAMIC PHASE- CLINICAL MANIFESTATIONS • SNS Stimulation • Peripheral vasoconstriction • Narrowing pulse pressure • Cool, clammy skin • Increased afterload • Decreased contractility • PROFOUNDHYPOTENSION

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