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SAM Exam 1 > Lecture 2 - heatstroke (Walton) > Flashcards

Lecture 2 - heatstroke (Walton) Flashcards

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1
Q

hallmark of heatstroke

A

severe CNS disturbance often associated with multiple organ dysfunction

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2
Q

heatstroke is a severe illness charaterized by core temperature over __ in dogs as well as CNS dysfunction

A

105.8F

not common in cats

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3
Q

exposure to high environmental temps is classified as __ vs strenuous exercise heat elevation is __

A

classical/non exertional heatstroke

exertional heatstroke

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4
Q

predisposing factors to heat stroke

A 
obesity 
thick coat 
exercise 
laryngeal paralysis 
CV dz 
CNS dz 
prior heatstroke 
hypothyroidism
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5
Q

protective mechanisms from heat illness

A

thermoregulation
acclimatization
acute phase response
heat shock response protein production

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6
Q

heatstroke occurs when __ outweighs heat disspipation

A

heat generation

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7
Q

A rise in core temperature by __F sends stimulus to the hypothalamus causing peripheral vasodilation

A

1.8F

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8
Q

2 Response mechanisms for heat dissipation

A

sensible (conduction, conveciton, radiation)

insensible (evaporation)

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9
Q

70% of total body heat loss id due to __

A

radiation and convection (sensible response)

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10
Q

CS of insensible response to dissipate heat

A

panting

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11
Q

__ is part of the sensible response that allows unidirectional air flow through nose and out mouth increasing evaporative SA/heat loss

A

partial air system

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12
Q

factors that increase body temperature which in turn alerts the hypothalamus

A

metabolism
environment
muscular activity

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13
Q

how is heat lost via sensible response (radiation, conduction, convection)

A 
hypothalamus increases sympathetic tone 
HR and CO increase 
splanchnic circulation decreases 
cutaneous vasodilation 
increased blood to muscle and skin = heat loss
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14
Q

EXAM: evaporative cooling failure is caused by

A

environmental temps greater than body temp
or
humidity above 80%

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15
Q

EXAM: Dehydration impairs thermoregulation by

A

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

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16
Q

__ is an adaptive physiologic response to environment and climatic change

A

acclimatization

can take dogs 20d to partially acclimatize and 60d to fully acclimatize

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17
Q

how do we acclimatize to compensate for increased temperatures

A

conserve salts; activate RAAS
conserve water to increase plasma volume; aldosterone and ADH
increase HR and CO

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18
Q

a systemic co-ordinated response that involves endothelial cells, leukocytes, and epithelial cells to protect tissue from injury and promote repair

A

acute phase response/proteins (APP)

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19
Q

Stimulants of APP

A 
heatstroke 
bacterial/viral infection
trauma 
neoplasia 
burns 
strenuous exercise 
IM dz
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20
Q

how do APP work?

A

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

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21
Q

APP inhibit production of __ and release of ___

A

reactive O2 spp

proteolytic enzymes

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22
Q

__ are regulatory molecular chaperones that protect cells from lethal stresses (protective proteins made when cells are stressed)

A

heatshock proteins

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23
Q

heatshock proteins can be stimulated by

A

heat
ischemia
endotoxemia
oxidative and nitrosative stresses

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24
Q

increased levels of heatshock proteins allows a transient state of __ to allow cell to survive lethal stage of heat stress

A

tolerance

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25
causes of reduced HSP
aging lack of acclimatization genetic polymorphisms
26
HSP prevent protein __ and assist in __ protein to native configuration
breakdown | refolding denatured protein
27
HSP in the gut prevent loss of __ barriers and prevent __ leakage
epithelial | endotoxins
28
HSP interfer with oxidative stress and block the __ pathway
apoptosis
29
HSP prevent arterial hypotension to __
decrease cerebral ischemia and neural damage
30
HSP protect the CV by regulating
baroreceptor reflex response (abates hypotension and bradycardia)
31
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
32
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
33
pathophys of CV collapse 3
arrythmias from hyperK+ indirect monocyte injury (hyperkalemia due to cell death) resulting in VPCs
34
causes of indirect myocyte injury
``` hyperthermia circulatory shock acidosis electrolyte abnorms thormboembolism ```
35
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
36
HS pathophys on the kindeys
direct and indirect thermal injury hypoxia (shunts blood away = decr GFR) microthrombi (DIC) Rhabdomyolysis (nephrotoxic myoglobin) exacerbates AKI
37
the __ is intrinsically resistant to thermal injury
brain
38
indirect HS injury to the CNS results in
cerebral edema hemorrhage and necrosis infarcts
39
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)
40
___ is the first system to take the hit in HS
GI
41
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
42
decreased blood flow to the liver causes reduced __ and leads to
detoxification | centrilobular necrosis and cholestatic liver dz
43
direct damage to the capillary and venous endothelium by heat causes
DIC 1. damage = inflammation adherence of WBC and platelets 2. activates clotting cascade (Tissue factor) starting uncontrolled systemic coagulation 3. coagulation factors/platelets depleted 4. liver makes more coag factors 5. consumed again = DIC
44
indirect cause of coagulation issues with HS
causes hemoconcentration 1. dehydration (panting and GI loss) 2. reduced viscosity of blood /sludge 3. decreased O2 tension = hypoxemia and microthrombi
45
most common CS of HS
Panting dry injected/hyperemic MM tachycardia
46
temperature in patient with HS
Depends on chronicity, if going on long enough patient may become hypothermic (these p usually die)
47
CV CS of HS
Vaso collapse weak pulses or pulse deficits pale MM and incr CRT arrythmias (v-tach, VPCs, afib)
48
GI CS of HS
Vomiting bloody diarrhea mucosal sloughing smells bad
49
CNS CS of HS
``` coma obtunded (prostration) seizures ataxia blindness apnea tremors ```
50
Coagulopathy CS of HS
Petechae/ecchymoses | hemorrhage
51
3-5 days into HS may see
DIC Renal failure hepatic failure GI damage
52
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)
53
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
54
indicators on chm that there has been direct hepatocellular damage or hypoperfusion
increased ALP and ALT | *occurs w/in 24 hours of presentation
55
renal value on chem in HS p
azotemia; pre-renal and/or renal causes
56
HS causes muscle damage and decreased perfusion, you would expect to see what elevated values on serum chm
increased: CK ALT Lactate
57
__ 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)
58
mainstay tx of HS
Rapid cooling O2 CV support (volume replacement) manage secondary complications (shock, hypoglycemia, DIC, ARDS, renal failure)
59
negative prognositc indicators for HS patients
degree of temperature elevation duration of exposure requires immediate cooling to increase survival
60
recommendation for cooling HS patients
whole body wetting with tap water muscle massage blowing fan RT or cooled IVF
61
why shouldn't you use alcohol to cool HS patient
fire hazard if defirbillation required!
62
when to stop cooling?
d/c cooling at 103.5-104F to prevent rebound hypothermia
63
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)
64
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
65
myocardial damage and conduction disturbances from HS appear w/in __ hours
36 should have constant telemetry/ECG
66
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
67
why should you intubate HS patients
to protect the airway and administer oxygen CNS compromise = decreased swallow/gag protection = risk aspiration
68
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) ```
69
over half of HS patients will have __ which needs to be treated
hypoglycemia, tx w/ dextrose bolus or CRI
70
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
71
__ may be given to effect to provide clotting factors
fresh frozen plasma (10ml/kg)
72
coagulation system should be monitored for
PT/PTT increase FDP (fibrin degradation products) = DIC the use of heparin to tx these patients is controversial
73
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
74
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 ```
75
HS CV CS
drop in BP and CO = CV shock Circulatory failure Arrythmias (hyperK+)

SAM Exam 1 (15 decks)

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