Module 6 Flashcards
Normal UOP
0.5-1 ml/kg/hr
or 800-2000 mL/daily
Oliguria
<500 mL/day
or <0.5ml/kg/hr for six hours
Infection
invasion of sterile tissue by microbes
prompts inflammatory/immune response
Septicemia
presence of microbes in circulating blood
SIRS
systemic inflammatory response syndrome
uncontrolled inflammation not d/t infection resulting in impaired organ function and altered hemodynamics
SIRS criteria
T >38 or <36
HR >90
RR >20 or PaCO2 <32
Altered mental status
WBC >12 or <4 or >10% immature band formsS
Sepsis
SIRS + infection
clinical manifestations similar to SIRS
dysregulated host response to infection resulting in widespread inflammation + organ dysfunction
MODS
multiorgan dysfunction syndrome
altered organ function in acutely ill patients where homeostasis cannot be maintained without intervention
Levels of immunity
first = physical barriers
second = innate immunity (neutrophils, macrophages, histamine)
third = acquired immunity (T-cells, B-cells)
Causes of elevated lactate
hypoperfusion (sepsis)
impaired hepatic clearance (cirrhosis)
medications (b2 agonist, metformin)
hypoxia
Disseminated Intravascular Coagulation (DIC)
release of cytokines + procoagulant agents cause excessive clotting
results in micro-thrombi that become lodged in smaller blood vessels/capillaries
activates fibrinolysis which inhibits platelet aggregation
cause ischemia –> necrosis of tissue or organ dysfunction
consumptive coagulopathy –> increased r/o bleeding d/t decreased number of circulating platelets, fibrin, clotting factors
Sepsis + GI
altered gastric mucosa
r/o peptic ulcers, bleeding
ileus
mucosal ischemia = increased permeability of gut bacteria = bacterial translocation
Sepsis + GU
r/o AKI
fluid + electrolyte imbalances
Sepsis + CV
decreased cardiac output (low preload, impaired cardiac contractility)
micro-emboli decrease perfusion to peripheral tissue + cause organ dysfunction/necrosis
r/o bleeding d/t consumption of platelets, fibrin, clotting factors
Sepsis + ARDS
acidosis –> hyperventilation
can lead to ARDS
need for mechanical intubation
Sepsis 1 hour bundle
1) lactate (remeasure if >2)
2) obtain blood cultures BEFORE abx (do not delay more than 1 hour)
3) broad-spectrum abx
4) crystalloid fluids 30 mL/kg (for hypotension or elevated lactate)
5) vasopressors if fluids don’t work
Vasopressors for Sepsis
TARGET MAP 65
norepinephrine
vasopressin
epinephrine
dobutamine
steroids can be added if ongoing vasopressor treatment indicated
How long can vasopressors be administered through a PIV
6 hours
Causes of SIRS
pancreatitis
burns
multiple trauma
aspiration
ischemia
hemorrhagic shock
Stages of ARDS
early = exudative
intermediate = proliferative
late = fibrotic
Exudative phase of ARDS
ACUTE INFLAMMATION
massive inflammation –> nonhydrostatic pulmonary edema
alveoli fill with fluid = decreased compliance, impaired gas exchange, V/Q mismatch
inflammation promotes coagulation = formation of hyaline membrane impermeable to gas exchange
hypoxemia refractory to supplemental O2, tachycardia, tachypnea, SOB, bilateral opacities on CXR, hypercapnia
Proliferative phase of ARDS
TISSUE REPAIR
residual debris cleared by phagocytes
restoration of alveoli epithelium
restoration of alveolar surface area + reabsorption of pulmonary fluid
improved oxygenation
Fibrotic phase of ARDS
SCARRING + LONGTERM ISSUES
fibrosis of alveoli–> pulmonary HTN + pulmonary fibrosis
longterm impaired gas exchange
r/o RHF
impaired function depression, anxiety, PTSD, chronic respiratory dysfunction
Causes of hypovolemia in SIRS
insensible losses s/t increased metabolism, fever, tachypnea
vascular permeability –> third spacing
decreased oral intake
Definition of AKI
increase in creatinine by 26.5 umol or 1.5x of baseline within 24 hours
oliguria for 6 hours
**GFR cannot be used to diagnose AKI
Prerenal causes of AKI
hypovolemia
NSAIDs (target afferent arteriole
low cardiac output (heart failure)
Intrarenal causes of AKI
ischemia –> acute tubular necrosis
certain drugs (chemotherapy)
CT contrast
infection
Postrenal AKI
obstruction (kidney stone)
BPH
neurogenic bladder
S/S AKI
fluid overload (pulmonary edema)
hyponatremia (impaired reabsorption/excretion)
hyperkalemia
metabolic acidosis
increased creatinine/BUN/decreased GFR
oliguria or anuria
hypocalcemia/hyperphosphatemia (inverse relationship)
anemia (kidneys release EPO)
platelet abnormality/bleeding (urea impairs clotting)
neuro: fatigue, seizures, coma
Diuretic phase of AKI
kidneys lose ability to concentrate urine
low urine specific gravity
polyuria
r/o hypovolemia, hypotension, hyponatremia/hypokalemia
Conditions causing hyperkalemia
tissue trauma (rls of intracellular content)
bleeding
blood transfusion
metabolic acidosis
Hyperkalemia EKG
peaked T waves
prolonged PRI
wide QRS
PVCTr
Treatment for hyperkalemia
insulin + dextrose
kayexalate
calcium gluconate (stabilize cardiac membrane)
loop diuretics
dialysis
B2 agonist
sodium bicarbonate (increase pH, cause cells to shift hydrogen outward and potassium inward)
S/S of acidosis
Kussmaul resps
flushed, warm skin (vasodilation)
hypotension
headache
tachycardia
N/V
bradycardia
altered LOC
Nutrition + kidney disease
important to maintain adequate nutrition to prevent proteolysis
when glucose low, body breaks down fat/protein to convert into glucose
protein metabolism –> ammonia –> urea
kidney unable to excrete urea –> uremia –> encephalopathy
CXR
ID infection (pneumonia common cause of sepsis)
pulmonary complications (edema, ARDS)
assess cardiac silhouette
12-Lead ECG
sepsis can cause cardiac dysfunction + development of arrhythmias
obtain baseline info on pt cardiac rhythm
ID if heart site of infection
ABG
evaluate end-organ perfusion (lactate)
assess acid-base imbalances
oxygenation/hypercapnia
VBG
similar information as an ABG but easier to obtain
uses different parameters
