Lecture 2 - heatstroke (Walton) Flashcards
hallmark of heatstroke
severe CNS disturbance often associated with multiple organ dysfunction
heatstroke is a severe illness charaterized by core temperature over __ in dogs as well as CNS dysfunction
105.8F
not common in cats
exposure to high environmental temps is classified as __ vs strenuous exercise heat elevation is __
classical/non exertional heatstroke
exertional heatstroke
predisposing factors to heat stroke
obesity thick coat exercise laryngeal paralysis CV dz CNS dz prior heatstroke hypothyroidism
protective mechanisms from heat illness
thermoregulation
acclimatization
acute phase response
heat shock response protein production
heatstroke occurs when __ outweighs heat disspipation
heat generation
A rise in core temperature by __F sends stimulus to the hypothalamus causing peripheral vasodilation
1.8F
2 Response mechanisms for heat dissipation
sensible (conduction, conveciton, radiation)
insensible (evaporation)
70% of total body heat loss id due to __
radiation and convection (sensible response)
CS of insensible response to dissipate heat
panting
__ is part of the sensible response that allows unidirectional air flow through nose and out mouth increasing evaporative SA/heat loss
partial air system
factors that increase body temperature which in turn alerts the hypothalamus
metabolism
environment
muscular activity
how is heat lost via sensible response (radiation, conduction, convection)
hypothalamus increases sympathetic tone HR and CO increase splanchnic circulation decreases cutaneous vasodilation increased blood to muscle and skin = heat loss
EXAM: evaporative cooling failure is caused by
environmental temps greater than body temp
or
humidity above 80%
EXAM: Dehydration impairs thermoregulation by
decreasing evaporative heat loss as less water available for respiratory system
decreased heat dissipation through radiation and convection due to decreased blood flow to the periphery
__ is an adaptive physiologic response to environment and climatic change
acclimatization
can take dogs 20d to partially acclimatize and 60d to fully acclimatize
how do we acclimatize to compensate for increased temperatures
conserve salts; activate RAAS
conserve water to increase plasma volume; aldosterone and ADH
increase HR and CO
a systemic co-ordinated response that involves endothelial cells, leukocytes, and epithelial cells to protect tissue from injury and promote repair
acute phase response/proteins (APP)
Stimulants of APP
heatstroke bacterial/viral infection trauma neoplasia burns strenuous exercise IM dz
how do APP work?
modulate local and systemic acute inflamm response
stimulate hepatic produciton of anti-inflamm APP which inhibit production of reactive O2 spp and proteolytic enzymes
promotes wound healing and repair by stimulating endothelial cell adhesion, proliferation, and angiogenesis
APP inhibit production of __ and release of ___
reactive O2 spp
proteolytic enzymes
__ are regulatory molecular chaperones that protect cells from lethal stresses (protective proteins made when cells are stressed)
heatshock proteins
heatshock proteins can be stimulated by
heat
ischemia
endotoxemia
oxidative and nitrosative stresses
increased levels of heatshock proteins allows a transient state of __ to allow cell to survive lethal stage of heat stress
tolerance
causes of reduced HSP
aging
lack of acclimatization
genetic polymorphisms
HSP prevent protein __ and assist in __ protein to native configuration
breakdown
refolding denatured protein
HSP in the gut prevent loss of __ barriers and prevent __ leakage
epithelial
endotoxins
HSP interfer with oxidative stress and block the __ pathway
apoptosis
HSP prevent arterial hypotension to __
decrease cerebral ischemia and neural damage
HSP protect the CV by regulating
baroreceptor reflex response (abates hypotension and bradycardia)
pathophys of CV collapse 1
drop in BP and CO = shock
core BT increase vasodilation of blood vessels decrease splanchnic blood flow reactive nitrogen and oxygen produced splanchnic arterioles dilate
result decrease central venous pressure and CO = circulatory shock
pathophys of CV collapse 2
circulatory failure
splanchinic vessels constrict
panting
dehydration
plasma volume depletion and hypoperfusion
results in hypovolemia, circulatory failure and decreased heat dissipation
pathophys of CV collapse 3
arrythmias from hyperK+
indirect monocyte injury (hyperkalemia due to cell death) resulting in VPCs
causes of indirect myocyte injury
hyperthermia circulatory shock acidosis electrolyte abnorms thormboembolism
HS pathophys on the respiratory system
direct pulmonary epi injury
increased pulm vasculature resistance
causes: non-cardiogenic pulm edema, DIC, acute respiratory distress syndrome (ARDS)
may see alveolar pattern on rads
HS pathophys on the kindeys
direct and indirect thermal injury
hypoxia (shunts blood away = decr GFR)
microthrombi (DIC)
Rhabdomyolysis (nephrotoxic myoglobin) exacerbates AKI
the __ is intrinsically resistant to thermal injury
brain
indirect HS injury to the CNS results in
cerebral edema
hemorrhage and necrosis
infarcts
development of neurological derangement in HS is due to
ATP depletion
altered excitatory AA uptake by cells due to ATP depletion (uncontrolled excitation = seizures, death, coma)
___ is the first system to take the hit in HS
GI
what happens to the GI under HS
sepsis and endotoxemia
Hypovolemia - blood shunted - pooling and blood sludging in the splanchnic viscera lead to microthrombi = hypoxia and ischemia
GI integrity is lost (ulcers, sloughing) - bacteria translocate - sepsis and endotoxemia
decreased blood flow to the liver causes reduced __ and leads to
detoxification
centrilobular necrosis and cholestatic liver dz
direct damage to the capillary and venous endothelium by heat causes
DIC
- damage = inflammation
adherence of WBC and platelets - activates clotting cascade (Tissue factor) starting uncontrolled systemic coagulation
- coagulation factors/platelets depleted
- liver makes more coag factors
- consumed again = DIC
indirect cause of coagulation issues with HS
causes hemoconcentration
- dehydration (panting and GI loss)
- reduced viscosity of blood /sludge
- decreased O2 tension = hypoxemia and microthrombi
most common CS of HS
Panting
dry injected/hyperemic MM
tachycardia
temperature in patient with HS
Depends on chronicity, if going on long enough patient may become hypothermic (these p usually die)
CV CS of HS
Vaso collapse
weak pulses or pulse deficits
pale MM and incr CRT
arrythmias (v-tach, VPCs, afib)
GI CS of HS
Vomiting
bloody diarrhea
mucosal sloughing
smells bad
CNS CS of HS
coma obtunded (prostration) seizures ataxia blindness apnea tremors
Coagulopathy CS of HS
Petechae/ecchymoses
hemorrhage
3-5 days into HS may see
DIC
Renal failure
hepatic failure
GI damage
RBC hematology findings on blood smear
NRBC’s
heat damages BM causing premature release of NRBCs, increased # = increased severity = worse prognosis (DIC, AKI, death more likely)
why is there a thrombocytopenia on CBC in HS patient? how tx?
platelet consumption (vasculitis, GI bleed) hypertermia induced platelet aggregation
this is transient; do NOT tx w/ steroids like w/ IMT p but give plasma, no jug v. sticks, support
prolonged PT/PTT is correlated with grave prog
indicators on chm that there has been direct hepatocellular damage or hypoperfusion
increased ALP and ALT
*occurs w/in 24 hours of presentation
renal value on chem in HS p
azotemia; pre-renal and/or renal causes
HS causes muscle damage and decreased perfusion, you would expect to see what elevated values on serum chm
increased:
CK
ALT
Lactate
__ will decrease on chem in HS bc it is being utilized or being produced less
glucose (hypoglycemia)
causes: increased ATP demand, sepsis (using too much) and liver dysfunction (not producing enough)
mainstay tx of HS
Rapid cooling
O2
CV support (volume replacement)
manage secondary complications (shock, hypoglycemia, DIC, ARDS, renal failure)
negative prognositc indicators for HS patients
degree of temperature elevation
duration of exposure
requires immediate cooling to increase survival
recommendation for cooling HS patients
whole body wetting with tap water
muscle massage
blowing fan
RT or cooled IVF
why shouldn’t you use alcohol to cool HS patient
fire hazard if defirbillation required!
when to stop cooling?
d/c cooling at 103.5-104F to prevent rebound hypothermia
how should o2 be supplied to HS p?
O2 cages are contraindicated due to overheating
should place nasal cannula and/or intubate and give PPV (if not responsing to O2 therapy, hypoventilating, arrest)
for controlling initial hypotension with HS? if not responding to this tx?
IVF Crystalloids
synthetic colloids, positive inotropes/vasopressors (dopamine, epi)
want BP and pulse quality to increase, CRT and MM injection to decrease
myocardial damage and conduction disturbances from HS appear w/in __ hours
36
should have constant telemetry/ECG
most common arrhythmias seen with HS? when do you treat?
Vtach and VPCs
arrhythmia + hemodynamic compromise = treat with lidocaine
most idioventricular arrhythmia are not clinical/treated
why should you intubate HS patients
to protect the airway and administer oxygen
CNS compromise = decreased swallow/gag protection = risk aspiration
to prevent or reduce cerebral edema
O2 active cooling to decrease O2 req of brain mannitol elevate head avoid jug compression MAP over 80mmHg prevent hypercapnia (over 30mmHg)
over half of HS patients will have __ which needs to be treated
hypoglycemia, tx w/ dextrose bolus or CRI
renal system should be monitored closely; urine output should be __ and UA should be done to assess for urinary __ . If output is low then what can you do?
over 2mls/kg/hr
casts
keep BP above 80mmHg
furosemide, mannitol, dopamine PRN
__ may be given to effect to provide clotting factors
fresh frozen plasma (10ml/kg)
coagulation system should be monitored for
PT/PTT increase
FDP (fibrin degradation products) = DIC
the use of heparin to tx these patients is controversial
GI ulceration and support
H2 antagonist (famotidine)
PPI (omeprazole)
con: increase bacteria in stomach bc decrease pH
antiemetic (maropitant or metoclopramide) min risk of asp pneumonia
parenteral nutrition to promote healing!
+/- if bacteremia ab
monitoring required for HS patient
continuous! subjective and objective telemetry perfusion/shock/hydration vital signs PCV/TS coag PT/PTT/AT glucose lactate blood gas BP Urine output
HS CV CS
drop in BP and CO = CV shock
Circulatory failure
Arrythmias (hyperK+)
