High Acuity Final Exam- Fall 2015
SIRS and MODS (pg. 875-887; pg. 14-20; pg. 22-25)
SIRS (pg. 879)
Proinflammatory response precipitated by a nonspecific insult, abnormal response to
injury-
o Unregulated Inflammation and Endothelial response
o Excessive vasodilatation
o Exaggerated cellular activation
o Accelerated coagulation
o Microcirculation disrupted
Decreased oxygen extraction
Sepsis syndrome is the most common cause of SIRS
Risk Factors of SIRS:
o Older age
o Baseline organ dysfunction
o Malnutrition
o Immunosuppression
o GI hypoperfusion
o Smoking
o Increased BMI
Clinical Manifestations (two or more of the following):
o Core temp. greater than 100.9 *F or less than 96.8*F
o Tachycardia greater than 90 BPM
o Respiratory rate (mean): greater than 20 breaths/min., or PaCO2 less than 32
mm Hg
o WBC: greater than 12,000; less than 4,000; or greater than 10% band formation
SIRS Take Away
o Respiratory Rate – most sensitive indicator
o Calcium or Beta Blockers may not elevate heart rate
Therefore no or limited tachycardia
o Extreme age may not have symptoms
o Hypotension – important indicator, may not be evident
o in SIRS unless dehydrated
o Procalcitonin: PCT level differentiate between infectious and noninfectious SIRS
o Lactate levels correlate with mortality
MODS (pg. 880-885)
Courtney Cox
, A progressive failure of two (2) or more organ systems resulting from malignant
intravascular inflammation and resultant tissue hypoxia
Primary MODS Pathway
o Develops within the first 72 hours of admission as a direct consequence of injury,
hemorrhage, or hypoxia
o Shock
o Sepsis= Infection + SIRS
Secondary MODS Pathway
o The hosts response to toxins that occurs within the context of SIRS rather than a
direct response to the initiating insult
o Deregulated apoptosis
o Age
Pathophysiologic Changes in MODS
o Misdistribution of Circulating Volume
Excessive persistent inflammatory response
Actual/relative volume loss
Decreased cardiac output
Low cardiac output myocardial depressant factor may lead
to pancreatitis
Hemorrhage
Opportunistic infections- CMV, Herpes Virus-6 (increased cytokines)
o Microvascular Coagulopathy
Release of endotoxins/cellular mediators
Protein C
o Imbalance of Oxygen Supply/Demand
Decreased supply
Decreased utilization (deranged microcirculation)
Increased demand
o Metabolic Derangements
Failure of microcirculation to remove end products
Increase lymphocytes in GI, Liver, Kidney, Heart
Decreased neutrophils- b/c they have been amped up for so long
o Uncontrolled Systemic Inflammation
Immune cells activated, then down regulated (creating immune
deficiency state )
Increase capillary permeability (organ edema- ARDS, Brain)
Vasodilation (Nitrogen Oxide)
Oxygen Free Radicals (tissue damage)
o Unregulated Apoptosis
Apoptosis= regulated normal cell death
Courtney Cox
SIRS and MODS (pg. 875-887; pg. 14-20; pg. 22-25)
SIRS (pg. 879)
Proinflammatory response precipitated by a nonspecific insult, abnormal response to
injury-
o Unregulated Inflammation and Endothelial response
o Excessive vasodilatation
o Exaggerated cellular activation
o Accelerated coagulation
o Microcirculation disrupted
Decreased oxygen extraction
Sepsis syndrome is the most common cause of SIRS
Risk Factors of SIRS:
o Older age
o Baseline organ dysfunction
o Malnutrition
o Immunosuppression
o GI hypoperfusion
o Smoking
o Increased BMI
Clinical Manifestations (two or more of the following):
o Core temp. greater than 100.9 *F or less than 96.8*F
o Tachycardia greater than 90 BPM
o Respiratory rate (mean): greater than 20 breaths/min., or PaCO2 less than 32
mm Hg
o WBC: greater than 12,000; less than 4,000; or greater than 10% band formation
SIRS Take Away
o Respiratory Rate – most sensitive indicator
o Calcium or Beta Blockers may not elevate heart rate
Therefore no or limited tachycardia
o Extreme age may not have symptoms
o Hypotension – important indicator, may not be evident
o in SIRS unless dehydrated
o Procalcitonin: PCT level differentiate between infectious and noninfectious SIRS
o Lactate levels correlate with mortality
MODS (pg. 880-885)
Courtney Cox
, A progressive failure of two (2) or more organ systems resulting from malignant
intravascular inflammation and resultant tissue hypoxia
Primary MODS Pathway
o Develops within the first 72 hours of admission as a direct consequence of injury,
hemorrhage, or hypoxia
o Shock
o Sepsis= Infection + SIRS
Secondary MODS Pathway
o The hosts response to toxins that occurs within the context of SIRS rather than a
direct response to the initiating insult
o Deregulated apoptosis
o Age
Pathophysiologic Changes in MODS
o Misdistribution of Circulating Volume
Excessive persistent inflammatory response
Actual/relative volume loss
Decreased cardiac output
Low cardiac output myocardial depressant factor may lead
to pancreatitis
Hemorrhage
Opportunistic infections- CMV, Herpes Virus-6 (increased cytokines)
o Microvascular Coagulopathy
Release of endotoxins/cellular mediators
Protein C
o Imbalance of Oxygen Supply/Demand
Decreased supply
Decreased utilization (deranged microcirculation)
Increased demand
o Metabolic Derangements
Failure of microcirculation to remove end products
Increase lymphocytes in GI, Liver, Kidney, Heart
Decreased neutrophils- b/c they have been amped up for so long
o Uncontrolled Systemic Inflammation
Immune cells activated, then down regulated (creating immune
deficiency state )
Increase capillary permeability (organ edema- ARDS, Brain)
Vasodilation (Nitrogen Oxide)
Oxygen Free Radicals (tissue damage)
o Unregulated Apoptosis
Apoptosis= regulated normal cell death
Courtney Cox
