shocky Flashcards
hypotension
bradycardia
warm, dry skin
classic signs of
neurogenic shock
clinical hallmark of neurogenic shock
very ↓ SVR + signs of excessive PS activity (ex: bradycardia)
every shock needs
- find and treat cause
- maximize O2 support
- fluid resuscitation (except cardiogenic - diurese to decrease preload first)
- glucose control = good outcomes
why epinephrine for anaphylaxis?
decreases basophil and mast cell degranulation
vasoconstricts
reverses airway constriction
anaphylaxis: volume results x3
vasodilation
peripheral pooling
relative hypovolemia
(d/t increase capillary permeability)
four systems activated with septic shock
complement, coagulation, kinin systems, cellular immunity
hypovolemic shock class I
0-15% loss
minimal tachycardia (usually no Δ in BP, RR, pulse pressure) delayed cap refill (loss of 10%)
hypovolemic shock class II
15-30% loss
tachycardia, tachypnea, pulse pressure
cool/clammy, delayed cap refill
slight anxiety
hypovolemic shock class III
30-40% loss
significant tachycardia, tachypnea, SBP
oliguria
confusion or agitation
hypovolemic shock class IV
greater than 40% loss
significant tachycardia, tachypnea, BP, pulse pressure (or no DBP)
oliguria/anuria
LOC
cold & pale
these patients may not have tachycardia in response to hypovolemia
BB, CCB, or pacemakers
plasma cascades activated in MODS
complement, kallikrein‐kinin, coagulation, fibrinolytic
reperfusion injury
organ damage occurring after reestablishment of blood flow post-ischemia
O2 radicals attack already damaged tissues
seen in MODS
myocardial depression in MODS d/t
caused by: myocardial depressant factor (MDF), TNF, IL‐1 → cardiac contractility
alterations: α‐adrenergic receptors (heart)
myocardial hypoxia
primary MODS
initial organ insult (usually d/t ischemia, impaired perfusion) results in inflammatory response / ex: shock, trauma, thermal injury, soft tissue necrosis, invasive infection
hypoperfusion both local (in organs) & generalized (gen not always seen)
stress response initiated, not usually as exaggerated as secondary - neutrophils primed can lead to secondary
secondary MODS
results from another insult (often mild), NOT primary MODS, but after latent period since primary - organs different from primary site
primed neutrophils go bananas disproportional to insult = inflammation self-perpetuates
primed macrophages release mediators to further damage endothelium
MODS monitoring consideration
primary hard to monitor, secondary has an established pattern
secondary MODS phase: approximately 24 hours post-event
low‐grade fever, tachycardia, tachypnea, dyspnea, altered mental status, general hyperdynamic and hypermetabolic state
secondary MODS phase: 24 to 72 hours
lung failure begins; ARDS possible
secondary MODS phase: 7 - 10 days
intensification of hypermetabolic/hyperdynamic state; bacteremia w enteric organisms common; development of hepatic, intestinal, and renal failure
secondary MODS phase: 14 - 21 days
↑ severity of renal & liver failure; encephalopathy w AMS (confusion - deep coma); hematologic & myocardial failure = late manifestations; death
secondary MODS phases x4
24ish - fever, tachy, AMS, general hyperdynamic/hypermetabolic
24-72 lung failure begins, possible ARDS
7-10 worsened hyper state, gut bacteremia common, development of hepatic, intestinal, renal failure
14-21 worsened renal/liver failure (liver develops early but not detectable until late), encephalopathy = AMS (coma possible), heme & myocardial failure = late manifestation, death
late manifestation of secondary MODS
hematologic & myocardial failure
major burn injury when and what it involves
burn greater than 20% BSA in adults
associated with massive evaporative H2O losses & flux of large amounts of fluid/electrolytes in tissues
manifestations: generalized edema & circulatory hypovolemia