Week 15: Impaired Immunity Flashcards
(77 cards)
Systemic inflammatory response syndrome (SIRS), triggers, criteria needed, what does it advance to?
*Generalized inflammation in organs remote from initial insult
*Consider fairly reversible. Problem is that it advances to MONS
Criteria (2 or more needed):
- Fever greater than 38.0 or less than 36
- hr greater than 90
- RR greater than 20
- WBC above 12,000, less than 4,000
- Bands greater than 10%
Triggers
- Mechanical tissue trauma: burns, crush injuries, surgical procedures
- Abscess formation: intra-abdominal, extremities
- Ischemic or necrotic tissue: pancreatitis, vascular disease, MI
- Microbial invasion: Bacteria, viruses, fungi
- Endotoxin release: Gram-negative bacteria
- Global perfusion deficits: Post–cardiac resuscitation, shock states
- Regional perfusion deficits: Distal perfusion deficits
Multiple organ dysfunction syndrome (MODS)
- failure of two or more organ systems
- Homeostasis cannot be maintained without intervention-Results from SIRS
- SIRS and MODS represent ends of a continuum
- Transition from SIRS to MODS DOES NOT occur in a clear-cut manner
Consequences of inflammatory response
- Low BF
- Release of mediators
- Direct damage to endothelium
- Hypermetabolism
- Vasodilation leading to dec SVR
- Inc in vascular permeability
- Activation of coagulation cascade
- Inflammation can travel to other organs and cause the same response in other organs
SIRS and MODS patho and stages
- Organ and metabolic dysfunction
- Hypotension
- Decreased perfusion
- Formation of microemboli
- Redistribution or shunting of blood
Stage 1:
local cytokine relase
Stage 2:
release of cytokines into systemic system
stage 3:
Humoral cascade (clotting cascade being released systemically in multiple organs)
SIRS/MODS in respiratory system
- Alveolar edema
- Decrease in surfactant
- Increase in shunt
- V/Q mismatch
- End result: ARDS
- 70% will go into MODS, so the VAP protocols are essential
Cardiovascular system SIRS/MODS patho
- Myocardial depression and massive vasodilation
- decreased CO, decreased preload, increased afterload leading to ischemia to the heart
- Depressed cardiac muscle function
Renal system SIRS/MODS patho
Acute renal failure
- Hypoperfusion leading to ischemia
- Release of mediators
- Activation of renin–angiotensin– aldosterone system to compensate (which causes vasoconstriction, furthering ischemia)
- Nephrotoxic drugs, especially antibiotics further the insult. Quinolines, Sulfas, Vancomycins
GI system SIRS/MODS patho
- Motility decreased: Abdominal distention and paralytic ileus
- Decreased perfusion: Risk for ulceration and GI bleeding
- Potential for bacterial translocation
Hypermetabolic state
- Hyperglycemia–hypoglycemia
- Insulin resistance
- Catabolic state
- Liver dysfunction
- Lactic acidosis
Hematologic system SIRS/MODS patho
- DIC
- Electrolyte imbalances
- Metabolic acidosis
SIRS/MODS collaborative care prevention
- Prognosis for MODS poor
- Goal: Prevent progression of SIRS to MODS
- Vigilant assessment-ongoing monitoring to detect early signs of deterioration or organ dysfunction-critical
- Prevention and treatment of infection
- Aggressive infection control strategies to dec risk for nosocomial infections
- Once an infection suspected, institute interventions to control source !~
SIRS/MODS collaborative care oxygenation
Maintain tissue oxygenation
- Dec O2 demand
- Sedation
- Mechanical ventilation (on volume control)
- Paralysis
- Analgesia
- Optimize O2 delivery
- Maintain normal hemoglobin level
- Maintain normal PaO2
- Individualize tidal volumes with PEEP ( don’t want too much volume, can cause barotrauma)
Maintenance of tissue oxygenation with SIRS/MODS
Maintenance of tissue oxygenation
Enhance CO
- Increase preload or myocardial contractility: dopamine and dobutamine
- Reduce afterload: Nipride or nitro drip,
- Give levofed to cause vasoconstriction: cuts circulation into the periphery increasing SVR and preload
SIRS/MODS collaborative care with nutrition
- Nutritional and metabolic needs
- Goal of nutritional support: Preserve organ function-total energy expenditure-often inc 1.5 to 2.0 times: need HIGH PROTEIN feed.
- Nutritional and metabolic needs
- Use of enteral route preferred to parenteral nutrition
- Monitor plasma transferrin & prealbumin levels to assess hepatic protein synthesis
SIRS/MODS failiing organs
Support of failing organs
- ARDS: Aggressive O2 therapy and mechanical ventilation
- DIC: Appropriate blood products
- Renal failure: Continuous renal replacement therapy or dialysis
Shock, classifications
- Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
- Imbalance in supply/demand for O2 and nutrients
-
Classification of shock
Cardiogenic:
Hypovolemic:
Distributive:
Obstructive:
cardiogenic shock
Definition
- Systolic or diastolic dysfunction
- Compromised cardiac output (CO)
Precipitating causes
- Myocardial infarction
- Cardiomyopathy
- Blunt cardiac injury
- Severe systemic or pulmonary hypertension
- Cardiac tamponade
- Myocardial depression from metabolic problems
patho of cardiiogenic shock
decrease in filling that leads to a decrease in stroke volume. Up to 85% die
CO lesss than 4 or cardiac input of less than 2.5
Manifestations of Cardiogenic shock
Early manifestations
- Tachycardia; Hypotension
- Narrowed pulse pressure
- ↑ myocardial O2 consumption
Physical examination
- Tachypnea, pulmonary congestion
- Pallor; cool, clammy skin
- Dec capillary refill time
- Anxiety, confusion, agitation
- ↑ in pulmonary artery wedge pressure
- Dec renal perfusion and UO
Absolute hypovolemia
loss of intravascular fluid volume
- Hemorrhage; GI loss (e.g., vomiting, diarrhea)
- Fistula drainage; Diabetes insipidus
- Hyperglycemia; Diuresis
relative hypovolemia
- Results when fluid volume moves out of vascular space into extravascular space (e.g., interstitial or intracavitary space)
- Termed third spacing
patho of hypocolemic shcok
- greater than 40% volume loss is irreversible and there will be permanent damage. Body tries to autoregulate, but can’t past this 40%, causing ischemia and damage to all organs
- Look at H&H, (see an increase with diabetes insipidous or third spacing, otherwise it will go down), look at electrolytes (increase in K+), ABGS, CV o2 sat, watching UO hourly (have to be cathed)
clinical manifestations of hypovolemic shock
- Anxiety
- Tachypnea
- Inc in CO, heart rate
- Dec in stroke volume, PAWP, urinary output
- If loss is >30%, blood volume is replaced.
Distributive shock/neurogenic shock and clinical manifestations
- Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks
- Can occur in response to spinal anesthesia
- Results in massive vasodilation > lead to pooling of blood in vessels
Clinical manifestations
- Hypotension
- Bradycardia
- Temperature dysregulation (resulting in heat loss) (warm skin from vasodilation, then it cools and get hypothermia)
- Dry skin
- Poikilothermia (taking on the temperature of the environment)
distributive shock/anaphylactic shock, manifestations, treatment
Acute, life-threatening hypersensitivity reaction
- Massive vasodilation; Release of mediators
- ↑ capillary permeability
Clinical manifestations
- Anxiety, confusion, dizziness
- Sense of impending doom; Chest pain
- Incontinence
- Swelling of the lips and tongue, angioedema
- Wheezing, stridor; Flushing, pruritus, urticaria
- Respiratory distress and circulatory failure
Treatment
- A (establish this quick) BCDE
- If you don’t have an epi pen, have them in a position to help with vasodilation, so you want their feet elevated
- Epi (adrenaline) lasts only 20 minutes, then it needs to be repeated (give every 3-5 minutes in hospital until you get a response)
- High flow oxygen is appropriate for these patients (veni mask, face mask)
- IV fluids: Adults 500-1,000, children crisiloid 20ml/kg
- Give steroids and medications to help with allergic reactions (hydrocortisone, chloriphenamine



