Shock and MODS Flashcards
definition of shock
state of cellular ad tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilization, or a combination of these processes
oxygen delivery (DO2)
total amount of oxygen delivered to the tissues per minutes
factors that affect oxygen delivery
hemoglobin
cardiac output
arterial oxygen saturation
oxygen consumption (VO2)
total amount of oxygen removed from the blood due to aerobic metabolism
factors that affect how oxygen is consumed
fever
inflammation
hyperthyroidism
adrenergic drugs
increased muscular activity
seizures
pain
vent weaning
shivering
oxygen extraction
how cells extract oxygen from blood
based upon energy needs
the amount of oxygen uploaded into tissues
oxygen extraction ratio (O2ER)
ratio of O2 consumption
(VO2)/(DO2)
cardiac O2ER
> 60%
hepatic O2ER
45-55%
renal O2ER
<15%
venous oxygen saturation (SVO2)
measures the amount of oxygen returned to the right side of the heart after the organs/tissues have extracted O2
measured from the pulmonary artery
what does low SVO2 indicate
the supply of O2 is not meeting tissue or cellular demands
increased oxygen consumption
what does high SVO2 indicate
inadequate oxygen extraction from the tissues
SVO2 of a healthy body
70%
contributors to low SVO2
low hemoglobin
low cardiac output
heart failure
pulmonary emboli
increased oxygen demand
contributors to high SVO2
sepsis (high CO, low extraction)
acidosis
hypothermia
excessive use of vasoactive drugs
central venous oxygen saturation (ScvO2)
measures blood return from the upper body (head and upper extremities)
from the jugular or subclavian vein
values slightly lower than mixed SVO2
normal range of ScvO2
65-75%
activities that increase VO2 consumption
nursing assessment
positioning
dressing change
bed bath
restlessness and agitation
weighing patient on sling bed scale
visitors
causes of abnormally high O2ER
decreased oxygen delivery or increased consumption
hypoxia
anemia
shock states
shivering
MODS
what does a low O2ER suggest
increased oxygen delivery but decreased oxygen consumption
malnutrition
hyperventilation
hypometabolism
sedation
hypothyroidism
paralysis
objective parameters of shock
arterial pH (7.35-7.45)
serum lactate (>2 mmol/L)
base deficit: the amount of base required to titrate 1 liter of arterial blood back to normal
procalcitonin for septic shock and MODS
4 shock classifications
cardiogenic
hypovolemic
obstructive
distributive: septic, neurogenic, anaphylactic
4 shock phases
initial
compensatory
progressive
refractory
initial phase of shock
decreased cardiac output
decreased perfusion
decreased oxygenation = anaerobic metabolism -> lactic acidosis
compensatory phase of shock
neuroendocrine begins to augment cardiac output and blood flow to restore blood volume
glucocorticoids: increased glucose
catecholamines: increased HR, RR, BP
vasopressin: increased fluid retention
progressive phase of shock
compensatory changes not working, hyporesponsive to catecholamines
poor perfusion
low blood flow
metabolic waste
MODS
persistent hypotension
imbalanced oxygen delivery and consumption
increasing lactic acid levels
hypoxia
cellular death
refractory phase of shock
cellular destruction and ischemia
not responsive to vasopressors
hypoxemic despite oxygen therapy
circulatory failure
impending death
significant vascular volume loss
tissue death
oxygen delivery and consumption not corrected with interventions
multiple organ failure (MOF)
DIC
4 categories of shock management
optimize oxygen delivery to hypoxic tissue
fluid resuscitation
perfusion and pressure support
perfusion and oxygenationi
shock management: interventions to optimize oxygen delivery to hypoxic tissue
patient may require intubation
close assessment of arterial blood gases
optimize gas exchange
assess for hyperoxemia
shock management: interventions for fluid resuscitation
restore preload and cardiac output
start with crystalloids (NS or LR) 20-30mL/kg IV rapid infusion
RBCs
restore interstitial and intravascular volume: colloids, albumin, starches, dextrans
shock management: interventions for perfusion and pressure support
vasopressors
epinephrine, dopamine, phenylephrine, vasopressin, norepinephrine
shock management: interventions for perfusion and oxygenation
ECMO: extracorporeal membrane oxygenation
shock priorities
CAB: circulation (stop bleeding), airway, breathing
D: disability (neuro, alert and oriented, PERRLA)
E: environment (temp control)
E: expose patient (look for bleeding or injury)
F: five adjuncts/focused assessment (Xray, ABD, NG/OG, labs, monitor, family)
G: give comfort
H: history
I: inspect (head to toe)
components to assess what kind of shock it is
patient history
physical exam
diagnostics
components of patient history
recent illness
fever
chest pain
traumatic injury
toxins/ingestions
recent hospitalization
environmental exposure
components of physical exam
vital signs
neuro
skin: color, temp, rashes, moisture, sores
cardiovascular: JVD, heart sounds
respiratory: lung sounds, skin, cap refill, ABG
GI: abd pain, rigidity, guarding, rebound
renal: urine output
components of diagnostic exams for shock
physical exam
EKG
CXR
CT
infectious source?
labs:
CBC
blood culture
UA, UDS, urine HCG
CMP
lactate and procal
coagulation
ABG
lumbar puncture
compensatory mechanisms of shock
increased heart rate (except in neurogenic)
increased respiratory rate
increased glycolysis
decreased urine output
decreased flow to internal organs
decreased peristalsis (ischemic bowel)
cool skin
diaphoresis
hypovolemic shock
profound dehydration
plasma loss related to increased capillary permeability as in the case of burn injury
blood loss: traumatic injury, GI bleed, intracranial hemorrhage
clinical manifestations of hypovolemic shock
tachycardia
narrowed pulse pressure
hypotension
increased respiratory rate
decreased urine output
pale, cool, clammy skin
delayed cap refill
pathophysiology of hypovolemic shock
decreased circulating volume
decreased venous return
decreased stroke volume
decreased cardiac output
decreased cellular oxygen supply
impaired tissue perfusion
impaired cellular metabolism
neurogenic shock
disruption of autonomic nervous system
neurogenic shock etiology
spinal cord injury
spinal anesthesia
anoxic brain injury
depressive drugs
clinical manifestations of neurogenic shock
decreased blood pressure
bradycardia, no reflexive tachycardia
increased respirations
warm dry skin
decreased cardiac output
poikilothermia: inability to regulate core body temperature, takes on temp of room
anaphylactic shock
allergic response
anaphylactic shock clinical manifestations
tachycardia
wheezing/stridor
rash/hives/swelling
vomiting
decreased cardiac output
hypotension
confusion, headache, loss of consciousness
wheezing, cough, or difficulty getting air
swollen eyes, lips, tounge
fast heart rate
hives
abdominal pain or vomiting
anaphylactic treatment
airway and breathing
epinephrine, IM, IV
vasopressors (possibly)
diphenhydramine
H2 blocker, famotidine
solumedrol or dexamethasone
IV NS or LR bolus
continuous monitoring for rebound
septic shock
elevated temp, HR, RR, WBCs
severe sepsis progresses into septic shock
hypoperfusion
hypotension
lactic acidosis
oliguria
fluid shifting from vascular space (relative hypovolemia/endotoxins)
septic shock clinical manifestations
tachycardia and hypotension
high cardiac output with low systemic vascular resistance
wide pulse pressures
bounding pulses
fever or hypothermia
increased SVO2
decreased CVP (decreased preload)
sepsis related organ failure
lungs, heart, kidneys, liver, and coagulation factors
obstructive shock etiology
tension pneumothorax: compresses the heart, needs emergent chest tube
cardiac
cardiogenic shock etiology
pump failure
acute MI
cardiomyopathy
myocardial contusion
myocarditis
cardiogenic shock clinical manifestations
tachycardic, dysrhythmias
decreased cardiac output
tachypnea
crackles
weak and thready pulses
diminished heart sounds
decreased urine output
etiology of MODS
injury or infection
MODS results in…
hypoxia
anaerobic metabolism
lactic acidosis
unregulated apoptosis due to inflammation
disrupted blood flow -> microvascular coagulopathy
MODS
control infection
enhance perfusion
consider steroids
consider RBCs
mechanical ventilation
sedation
glucose control and enteral feeds
initiate renal replacement therapy
heparin
educate family
prognosis 40-80% mortality
MODS clinical manifestations
abnormals in all system assessments
Becks triad
hypotension
increased CVP (JVD)
muffled heart tones
