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

4. SEPTIC SHOCK DEFINITIONS Bacteremia Septicemia
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 Severe Sepsis/SIRS
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. SEPTIC SHOCK CAUSATIVE MICROORGANISMS
Gram Negative
Most cases
E. COLI
Most likely
Klebsiella pneumoniae
Enterobacter aerogenes
Serratia marcescens
Gram Positive
Less common
Staphylococcus aureus
Viruses
Fungi
Rickettsiae
Protozoans

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

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

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

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

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

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

19. SEPTIC SHOCK PATHOGENESIS
Endotoxin is within the Gram Negative bacteria wall
Released into the blood during bacterial cell lysis
THE HOST REACTS TO THESE ENDOTOXINS AND EXOTOXINS BY RELEASING ENDOGENOUS MEADIATORS AND OTHER HUMORAL DEFENSE MECHANISMS INCLUDING COMPLEMENT, KININS AND OTHER COAGULATION FACTORS
CYTOKINES ARE: PEPTIDES THAT FUNCTION AS CELLULAR SIGNALS TO REGULATE THE AMPLITUDE AND DURATION OF THE HOST’S INFLAMMATORY RESPONSE
EG. TNF-TUMOR NECROSIS FACTOR
PROMOTES METABOLISM OF ARACIDONIC ACID
EG. IINTERLEUKIN 1
INDUCES HYPOTENSION
RECRUITS NEUTROPHILS:

20. PATHOGENESIS OF SEPTIC SHOCK
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
ENDOGENOUS MEDIATORS ATE: PROTEINS AND PHOSPHOLIPID MEDIATORS:
CYTOKINES (TNF AND INTERLEUKINS)
PLATELET ACTIVATING FACTOR
ARACHIDONIC ACID METABOLITES
MYOCARDIAL DEPRESSANT FACTOR
THREE PHASES:
1. CYTOKJINE SYNTHESIS
INTERACTION OF CERTAIN MICROBIAL MOLECULES WHICH, WHEN RECOGNIZED BY THE HOST RESULTS IN THE PRODUCTION OF MEDIATORS THAT AMPLIFY AND TRANSMIT THE MICROBIAL SIGNAL TO OTHER CELLS & TISSUES
2. CYTOKINE SYNTHESIS & SECRETION
INVOLVES RNA (MESSENGER) AND DNA
3. CASCADE PHASE:
ACTIVATION & RELEASE OF CENTRAL MEDIATOR (tnf,INTERLEUKIN AND SECONDARY MEDIATORS LIKE PROSTAGLANDINS & LEUKOTRIENES), ACTIVATION OF NEUTROPHILS, COMPLEMENT SYSTEM AND ONSET OF COAGULOPATHY))

21. PATHOGENESIS OF SEPTIC SHOCK
Endotoxins activates GRANULOCYTES
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
LEUKOTRIENES-CONSSTRICTIVE EFFECR ON BRONCHIAL SMOOTH MUSCLE; -INCREASED VASCULAR PERMEABILITY
ENHANCES THE EFFECT OF HISTAMINE
THEREFORE: WHEAL FLARE, ERYTHEMA,DECREASED PVR AND PERIPHERAL VOLUME, BRONCHOSPASMS
BRADYKININ-
STIMULATED PAIN RECEPTORS
INCREASED VASCULAR PERMEABILITY
INCREASED SECRETION FROM MUCOSU GLANDS
PLATELET ACTIVATING FACTOR (PAF)
INCREASED PLATELET AGGREGATION
I INCREASED VASCULAR PERMEABILKITY
INCREASED BRONCHIAL SMOOTH MUSCLE TONE
PROSTAGLANDINS
SMOOTH MUSCLE DILLATATION
BRONCHIOLE SMOOTH MUSCLE CONSTRICTION

23. PATHOGENESIS OF SEPTIC SHOCK
Thromboxane A2 and B2
Pulmonary vasoconstriction
Mediate broncho-onstriction
Potent platelet aggregator
Prostaglandin E and Prostacyclin
Potent vasodilator
May be responsible for hypotension
ENDOTOXINS ARE: COMPONENT OF GM NEG MICROBE’S CELL MEMBRANES AND ACTIVATE SEVERAL PROTEIN SYSTEMS:
A. OXYGEN RADICALS:
-ENDOTOXINS ACTIVATRE MACROPHAGES TO RELEASE SINGLE O2 MOLECULES. IN THE PRESENCE OF IRON, THESE O2 RADICALS CREASED DESTRUCTIVE HYROXYL RADICALS.
-ENDOTOXINS ALSO CAUSE MACROPHAGES TO RELEASE INTERLUEKIN -I AND TNF (TUMOR NECROSIS FACTOR0
INTERLUEKIN I - MOVES WBC’S TO INJURED CELLS
- STIMULATES RELEASE OF ARACHIDONIC ACID
- ACTIVATEZS PRODUCTION OF IRLUEKIN 2
-DECREASES LV EJECTION FRACTION, INCREASED CO, HR AND LVEDV
TNF:
-STIMULATES PLATELET ACTIVATING FACTORS AND PROSTAGLANDIN PRODUCTION

24. PATHOGENESIS OF SEPTIC SHOCK
Complement System Activated
Produce microemboli
Endothelial cell destruction
Histamine
Potent Vasodilator
Released by mast cells
Increases Capillary permeability (Fluid moves from vascular bed)
ARACHIDONIC ACID:
FATTY ACID PRECURSOR IS PRESENT IN MEMBRANE PHOSPHOLIPIDS AND IS LIBERATED BY ENDOTOXINS, CELLULAR AGITATION OR HYPOXIA.
METABOLIZES TO:
A.PROSTAGLANDINS OR B. LEUKOTRIENE
A. PROSTOGLANDIN:
MAY HAVE SYNTHESIS INHIBITED IN OVERWHELMING INFECTION
POTENT VASODILATORS
B. THROMBOXANE:
CHEMICAL MEDIATOR WHICH HAS POTENT VASOCONSTRICTING AND PLATELET AGGREGATING EFFECT CAUSING MALDISTRIBUTION OFOOD FLOW
ISSUE ISCHEMIA IS REULST
C. PROSTACYCLIN
RELEASED FROM VESSEL WALLS
POTENT VASODILATOR & ANTIAGGREGANT
I INITIAL DECREASE IN SVR

26. PATHOGENESIS OF SEPTIC SHOCK
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
LEUKOTRIENES:
OTHER PATHWAY IN ARACHIDONIC ACID CASCADE
SLOW REACTING SUBSTANCES OF ANAPHYLAXIS
MAY BE ASSOCIATED WITH INCREASED CAPILLARY PERMABILITY
BRONCHOCONSTRICTION AND CHEMICAL RESPONSE ACTIVATING MORE NEUTROPHILS
COMPLEMENT CASCADE SYSTEM
ACTIVATION OF A GROUP OF SERUM PROTEINS
DEFICIENCY INCREASES PTS. SUSCPETIBILITY TO INFECTION
‘ EFFECTS ARE CELL LYSIS, STIMULATION OF SMOOTH MUSCLE CONTRACTION, MAST CELL DEGRADATION, NEUTROPHIL CHEMOTAXIS AND ACTIVATION OF PHAGOCYTOSIS
CHAOTIC CELL LYSIS

27. PATHOGENESIS OF SEPTIC SHOCK
MYOCARDIAL DEPRESSANT FACTOR
MAY ENHANCE DEVELOPMENT OF MICRO EMBOLI
COAGULATION AND FIRBINOLYSSIS CASCADE:
INJURY TO VASCULAR ENDOTHELIUM INITIATES FORMATION OF FIBRIN
FIBRIN CLOT FORMATION ATTEMTPS TO STABILIZE THE SITE OF INJURY
DURING SEPSIS, CONSUMPTION OF VARIOUS FACTORS IN COAGULATION CASCADE AND FIRBIN CLOT FORMATION CAUSES MEDIATOR INDUCED DIC
BRADYKININ:
COAGULATION CASCADE AND COMPLEMENT ACTIVATION RELASES POTENT VASODILATOR, BRADYKININ
VOLUME DEPELTION CHARACHERTISTIC OF SPESIS IS CONSEQUENCE OF BRADYKININ;S ABILITY TO CREATE VASODILATION & CAPILLARY LEAK
MYOCARDIAL DEPRESSANT FACTOR
RELEASED BY ISCHEMIC PANCREATIC CELL
CAUSES DECREASE IN DEGREE AND VELOCITY OF MYOCARDIAL CELL CONTRATCION
INCREASES LACTATE PRODUCTION

28. HEMODYNAMIC ALTERATIONS OF SEPTIC SHOCK
Profound Vasodilation
Systemic vascular resistance is decreased
Blood Pressure falls
Veins dilate
Intravascular pooling in the venous capacitance system
PERIPERHAL VASODILATION:
RESULT OF ACTIVATION OF ARACHIDONIC ACID AND COMPLEMENT CASCADES WITH RELEASE OF VASOACTIVE SUBSTANCES
DILATION IN ARTERIAL AND VENOUS CIRCULATION INCREASES THE DIAMETER OF THE BLOOD VESSELS WHICH IN TURN DECREASES SVR AND PRELOAD

29. 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
RELEASE OF SYMPATHETCI CATECHOLAMINES, ANGIOTENSIN AND THROMBOXANE CREASTES PULMONARY, RENAL AND SPLANCHIC VASOCONSTRICTION
DIRECT EFFECT OF MICROBIALINVASION AND MEDIASTOR RELEASE DAMAGE THE VASCULAR ENDOTHELIUM.
MIGRATION AND AGGREGATION OF NEUTROPHILS AND PLATELETS TO THGE DAMAGED CELLS CREATE THROMBOSIS AND POTENTIAL EMBOLIC EVENTS
HISTAMINE AND BRADYKININ INCREASE CAPILLARY PERMEABILITY ALLOWING SERUM TO MIGRATE INTO INTERSTITIAL SPACE
THIS FLUID SHIFT DEPLETS CIRCULATING VOLUME AND INCREASES BLOOD VISCOSITY’
THEREFORE, IRREVERSIBLE CELLULAR DYSFUNCTION SECONDARY TO INADEQUATE TISSUE PERFUSION
DEMAND FOR OXYGEN EXCEEDS SUPPLY SO ANAEROBIC METABOLISM BEGINS. THEN CELL DEATH.

30. HEMODYNAMIC ALTERATIONS IN SEPTIC SHOCK
Decreased ejection fraction
Definition:
Percent of diastolic volume that is ejected during systole
COMBINATION OF VASODILATION AND THIRD SPACINF DURING SEPSIS PRODUCES A DRAMATIC DECREASE IN PRELOAND AFTERLOAD PRESSURES.

31. 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

32. 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

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

37. HYPERDYNAMIC PHASE CLINICAL MANIFESTATIONS
BP Falls
Decreased SVR
Decreased venous return
Decreased sympathetic tone
Diastolic pressure falls

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

42. HYPERDYNAMIC PHASE - CLINICAL MANIFESTATIONS
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

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

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

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

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

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

50. HYPODYNAMIC PHASE- CLINICAL MANIFESTATIONS
SNS Stimulation
Peripheral vasoconstriction
Narrowing pulse pressure
Cool, clammy skin
Increased afterload
Decreased contractility
PROFOUND HYPOTENSION

51. HEMODYNAMIC MANIFESTATIONS- HYPODYNAMIC PHASE
SVR increased
CO decreased
CI decreased
SEVERE MYOCARDIAL DEPRESSION
PA and PAWP pressures increased
Metabolic and respiratory acidosis with hypoxemia

52. CLINICAL MANAGEMENT Fluid Administration
To restore adequate ventricular preload
Maintain PAWP: 12 MM HG
Colloids vs. crystalloids
Colloids my cause movement of fluid into interstitial space because of the capillary permeability
If ineffective, may need Dopamine and Dobutamine
DOPAMINE:
LOW DOSES 2-4 MCG/KG/MIN: INCREASES RENAL BLOOD FLOW AND MODERATE PRESSOR EFFECT BY INCREASING CARDIAC PERFORMANCE
5-10 MCG/KG/MIN:
BETA-ADRENERGIC:
INCREASES HR AND CONTRACTILITY
>10 MCG/KG/MIN
ALPHA-ADRENERGIC- VASOCONSTRICTIVE
LEVOPHED:
POWERFUL ALPHA ADRENERGIC
PHENYLEPHRINE:
PURE ALPHA ADRENERGIC- DOES NOT DIRECTLY STIMULATE THE HEART

54. CLINICAL MANAGEMENT Mechanical Ventilation
Greater risk for acute lung injury and ARDS
Low tidal volume of 6 ml/kg
Maintain plateau pressures at 30 cm H2O or less
Reduction of mortality of 9%
DOPAMINE:
LOW DOSES 2-4 MCG/KG/MIN: INCREASES RENAL BLOOD FLOW AND MODERATE PRESSOR EFFECT BY INCREASING CARDIAC PERFORMANCE
5-10 MCG/KG/MIN:
BETA-ADRENERGIC:
INCREASES HR AND CONTRACTILITY
>10 MCG/KG/MIN
ALPHA-ADRENERGIC- VASOCONSTRICTIVE
LEVOPHED:
POWERFUL ALPHA ADRENERGIC
PHENYLEPHRINE:
PURE ALPHA ADRENERGIC- DOES NOT DIRECTLY STIMULATE THE HEART

56. CLINICAL MANAGEMENT 4. Glycemic Control Blood sugar 80-100 mg/dl
Mortality reduced by 3.4%
Blood glucose levels of mg/dl were associated with a worse outcome
DOPAMINE:
LOW DOSES 2-4 MCG/KG/MIN: INCREASES RENAL BLOOD FLOW AND MODERATE PRESSOR EFFECT BY INCREASING CARDIAC PERFORMANCE
5-10 MCG/KG/MIN:
BETA-ADRENERGIC:
INCREASES HR AND CONTRACTILITY
>10 MCG/KG/MIN
ALPHA-ADRENERGIC- VASOCONSTRICTIVE
LEVOPHED:
POWERFUL ALPHA ADRENERGIC
PHENYLEPHRINE:
PURE ALPHA ADRENERGIC- DOES NOT DIRECTLY STIMULATE THE HEART

57. CLINICAL MANAGEMENT 5. Prevention of Infection
Prevent ventilator associated pneumonia (VAP)
Maintain head of bed elevated at 30 degrees
Increase 23% infection in supine position
Oral Care – mouth is colonized within 24 hours
Deep oral suctioning above the ET cuff
DOPAMINE:
LOW DOSES 2-4 MCG/KG/MIN: INCREASES RENAL BLOOD FLOW AND MODERATE PRESSOR EFFECT BY INCREASING CARDIAC PERFORMANCE
5-10 MCG/KG/MIN:
BETA-ADRENERGIC:
INCREASES HR AND CONTRACTILITY
>10 MCG/KG/MIN
ALPHA-ADRENERGIC- VASOCONSTRICTIVE
LEVOPHED:
POWERFUL ALPHA ADRENERGIC
PHENYLEPHRINE:
PURE ALPHA ADRENERGIC- DOES NOT DIRECTLY STIMULATE THE HEART

59. CLINICAL MANAGEMENT
6. Xigris (Drotrecognifa-activated) aka Drotrecogin alfa (activated)
Approved by US Food and Drug in 2001
Recombinant form of human activated protein C
PROWESS Trial
DOPAMINE:
LOW DOSES 2-4 MCG/KG/MIN: INCREASES RENAL BLOOD FLOW AND MODERATE PRESSOR EFFECT BY INCREASING CARDIAC PERFORMANCE
5-10 MCG/KG/MIN:
BETA-ADRENERGIC:
INCREASES HR AND CONTRACTILITY
>10 MCG/KG/MIN
ALPHA-ADRENERGIC- VASOCONSTRICTIVE
LEVOPHED:
POWERFUL ALPHA ADRENERGIC
PHENYLEPHRINE:
PURE ALPHA ADRENERGIC- DOES NOT DIRECTLY STIMULATE THE HEART

60. CLINICAL MANAGEMENT Xigris Guidelines Known or suspected infection
2 or more signs of SIRS
At least 1 failing organ
High risk for death

61. CLINICAL MANAGEMENT Xigris Contraindications Active internal bleeding
Recent hemorrhagic stroke (3 mos)
Head traum (recent)
Epidural catheter
Intracranial mass

62. CLINICAL MANAGEMENT Xigris Cost - $6800/96 hour infusion Dosage:
24 mcg/kg/hour
Dedicated IV line
80% of the drug’s effects cleared within 30 minutes
Activity is reduced substantially in 15 minutes
DOPAMINE:
LOW DOSES 2-4 MCG/KG/MIN: INCREASES RENAL BLOOD FLOW AND MODERATE PRESSOR EFFECT BY INCREASING CARDIAC PERFORMANCE
5-10 MCG/KG/MIN:
BETA-ADRENERGIC:
INCREASES HR AND CONTRACTILITY
>10 MCG/KG/MIN
ALPHA-ADRENERGIC- VASOCONSTRICTIVE
LEVOPHED:
POWERFUL ALPHA ADRENERGIC
PHENYLEPHRINE:
PURE ALPHA ADRENERGIC- DOES NOT DIRECTLY STIMULATE THE HEART

63. CLINICAL MANAGEMENT 7. Antibiotic therapy
Instituted after the cultures are obtained
Third generation cephalosporins plus an aminoglycoside
THRID GENERATION CEPHALOSPORIN:
ANCEG
ROCEPHIN
AMINOGLYCOSDIE:
TOBRAMYCIN
GENTAMICIN
AMIKACIN
FOR SUSPECTED ANAEROBIC SOURCE LIKE: INTRAABDOMINA, BILIARY, OF FEMALE TRACT, ASPIRATION PNEUMONIA:
ADD CLINDAMYCIN OR METRO-NIDAZOLE
IF IMMUNOSUPPRESSED: CANCOMYCIN IN ADDITION TO ABOVE ANCEF AND GENT.

65. CLINICAL MANAGEMENT Possible anti-endotoxin drugs In research phase
Have been shown to decrease mortality significantly in patients with septic shock and gram negative bacteremia

66. COMPLICATIONS OF SHOCK
ARDS
ACUTE RENAL FAILURE
DIC
ACUTE RENAL FAILURE
MULTIPLE ORGAN DYSFUNCTION SYNDROME

67. SEVERE SEPSIS/SIRS Sepsis with acute organ dysfunction
750,000 cases /year
28%-50% mortality
Definition:

68. SIRS Systemic Inflammatory Response Syndrome 2 or more of:
Body Temperature > 38 degrees C or < 36 degrees F
Heart Rate >90/min
RR - >20/min; or PaCO2 <32 mm Hg
WBC - > 12,000 or > 10% bands

69. SEVERE SEPSIS/SIRS
Associated with organ dysfunction, hypoperfusion or hypotension
May include but are not limited to:
Lactic acidosis
Oliguria
Acute alteration in mental status

70. SEPSIS (SIRS)-INDUCED HYPOTENSION
Systolic BP of < 90 mm Hg or a reduction of > 40 mm Hg from baseline in the absence of other causes for hypotension

71. SEPTIC SHOCK / SIRS SHOCK
Subset of severe sepsis and defined as sepsis (SIRS)-induced hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include but not limited to:

72. SEPTIC SHOCK / SIRS SHOCK
Lactic acidosis
Oliguria
Acute alteration in mental status

73. MODS Multiple Organ Dysfunction Syndrome
Presence of altered organ dysfunction in an acutely ill patient such that homeostasis cannot be maintained without intervention

74. MODS Factors in the development Result of Bacterial factors
Inflammatory mediators
Endothelial injury
Disturbed hemostasis
Microcirculatory failure

75. MODS Factors Patients Primary Cellular Injury Advancing age
Pre-existing illness
Primary Cellular Injury
Underlying disease processes
Toxic effects of certain mediators

76. MODS Factors Microaggregates
Platelets, neutrophils, RBC’s and fibrin impair microcirculatory blood flow and produce tissue ischemia

77. MODS Factors Endothelial Cell Injury Proinflammatory cytokines
Alters vasomotor tone
Capillary leakage-pulmonary edema

78. MODS Factors Metabolic Derangement Mitochondrial dysfunction
Oxidants are produced during endotoxin induced shock

79. MODS Factors Humoral Mediators TNF- and IL-1
Attract leukocytes to site of infection
Excess levels cause general response

80. MODS Factors Therapy –induced dysfunction
Mechanical ventilation at higher volumes
Blood transfusions
Hyperglycemia
Activates tissue factor pathway for coagulation
Enhanced thrombin formation
Acute thrombosis

81. MODS

82. MODS

83. MODS

84. MODS

85. MODS

86. SIRS
Systemic Inflammatory Response Syndrome

87. SIRS
Systemic Inflammatory Response Syndrome

88. SIRS
Systemic Inflammatory Response Syndrome

89. SIRS
Systemic Inflammatory Response Syndrome

90. SIRS
Systemic Inflammatory Response Syndrome

91. SEVERE SEPSIS

92. SEVERE SEPSIS

93. SEVERE SEPSIS

94. SEVERE SEPSIS

95. SEVERE SEPSIS

96. SEVERE SEPSIS

97. IN SUMMARY......
SEPTIC SHOCK IS A MASSIVE INFECTION CAUSING VASODILATION AND INADEQUATE TISSUE PERFUSION
THERAPY IS AIMED AT IMPROVING DISTRIBUTION OF BLOOD FLOW AND TREATING INFECTION

98. THANK YOU