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

Lecture 2 - heatstroke (Walton) Flashcards

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
Q

causes of reduced HSP

A

aging
lack of acclimatization
genetic polymorphisms

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26
Q

HSP prevent protein __ and assist in __ protein to native configuration

A

breakdown

refolding denatured protein

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27
Q

HSP in the gut prevent loss of __ barriers and prevent __ leakage

A

epithelial

endotoxins

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28
Q

HSP interfer with oxidative stress and block the __ pathway

A

apoptosis

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29
Q

HSP prevent arterial hypotension to __

A

decrease cerebral ischemia and neural damage

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30
Q

HSP protect the CV by regulating

A

baroreceptor reflex response (abates hypotension and bradycardia)

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31
Q

pathophys of CV collapse 1

A

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
Q

pathophys of CV collapse 2

A

circulatory failure

splanchinic vessels constrict
panting
dehydration
plasma volume depletion and hypoperfusion

results in hypovolemia, circulatory failure and decreased heat dissipation

33
Q

pathophys of CV collapse 3

A

arrythmias from hyperK+

indirect monocyte injury (hyperkalemia due to cell death) resulting in VPCs

34
Q

causes of indirect myocyte injury

A 
hyperthermia 
circulatory shock
acidosis
electrolyte abnorms 
thormboembolism
35
Q

HS pathophys on the respiratory system

A

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
Q

HS pathophys on the kindeys

A

direct and indirect thermal injury
hypoxia (shunts blood away = decr GFR)
microthrombi (DIC)
Rhabdomyolysis (nephrotoxic myoglobin) exacerbates AKI

37
Q

the __ is intrinsically resistant to thermal injury

A

brain

38
Q

indirect HS injury to the CNS results in

A

cerebral edema
hemorrhage and necrosis
infarcts

39
Q

development of neurological derangement in HS is due to

A

ATP depletion

altered excitatory AA uptake by cells due to ATP depletion (uncontrolled excitation = seizures, death, coma)

40
Q

___ is the first system to take the hit in HS

A

GI

41
Q

what happens to the GI under HS

A

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
Q

decreased blood flow to the liver causes reduced __ and leads to

A

detoxification

centrilobular necrosis and cholestatic liver dz

43
Q

direct damage to the capillary and venous endothelium by heat causes

A

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
Q

indirect cause of coagulation issues with HS

A

causes hemoconcentration

  1. dehydration (panting and GI loss)
  2. reduced viscosity of blood /sludge
  3. decreased O2 tension = hypoxemia and microthrombi
45
Q

most common CS of HS

A

Panting
dry injected/hyperemic MM
tachycardia

46
Q

temperature in patient with HS

A

Depends on chronicity, if going on long enough patient may become hypothermic (these p usually die)

47
Q

CV CS of HS

A

Vaso collapse
weak pulses or pulse deficits
pale MM and incr CRT
arrythmias (v-tach, VPCs, afib)

48
Q

GI CS of HS

A

Vomiting
bloody diarrhea
mucosal sloughing
smells bad

49
Q

CNS CS of HS

A 
coma 
obtunded (prostration) 
seizures 
ataxia 
blindness 
apnea 
tremors
50
Q

Coagulopathy CS of HS

A

Petechae/ecchymoses

hemorrhage

51
Q

3-5 days into HS may see

A

DIC
Renal failure
hepatic failure
GI damage

52
Q

RBC hematology findings on blood smear

A

NRBC’s

heat damages BM causing premature release of NRBCs, increased # = increased severity = worse prognosis (DIC, AKI, death more likely)

53
Q

why is there a thrombocytopenia on CBC in HS patient? how tx?

A 
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
Q

indicators on chm that there has been direct hepatocellular damage or hypoperfusion

A

increased ALP and ALT

*occurs w/in 24 hours of presentation

55
Q

renal value on chem in HS p

A

azotemia; pre-renal and/or renal causes

56
Q

HS causes muscle damage and decreased perfusion, you would expect to see what elevated values on serum chm

A

increased:
CK
ALT
Lactate

57
Q

__ will decrease on chem in HS bc it is being utilized or being produced less

A

glucose (hypoglycemia)

causes: increased ATP demand, sepsis (using too much) and liver dysfunction (not producing enough)

58
Q

mainstay tx of HS

A

Rapid cooling
O2
CV support (volume replacement)
manage secondary complications (shock, hypoglycemia, DIC, ARDS, renal failure)

59
Q

negative prognositc indicators for HS patients

A

degree of temperature elevation
duration of exposure

requires immediate cooling to increase survival

60
Q

recommendation for cooling HS patients

A

whole body wetting with tap water
muscle massage
blowing fan
RT or cooled IVF

61
Q

why shouldn’t you use alcohol to cool HS patient

A

fire hazard if defirbillation required!

62
Q

when to stop cooling?

A

d/c cooling at 103.5-104F to prevent rebound hypothermia

63
Q

how should o2 be supplied to HS p?

A

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
Q

for controlling initial hypotension with HS? if not responding to this tx?

A

IVF Crystalloids

synthetic colloids, positive inotropes/vasopressors (dopamine, epi)

want BP and pulse quality to increase, CRT and MM injection to decrease

65
Q

myocardial damage and conduction disturbances from HS appear w/in __ hours

A

36

should have constant telemetry/ECG

66
Q

most common arrhythmias seen with HS? when do you treat?

A

Vtach and VPCs

arrhythmia + hemodynamic compromise = treat with lidocaine

most idioventricular arrhythmia are not clinical/treated

67
Q

why should you intubate HS patients

A

to protect the airway and administer oxygen

CNS compromise = decreased swallow/gag protection = risk aspiration

68
Q

to prevent or reduce cerebral edema

A 
O2
active cooling to decrease O2 req of brain
mannitol 
elevate head 
avoid jug compression
MAP over 80mmHg 
prevent hypercapnia (over 30mmHg)
69
Q

over half of HS patients will have __ which needs to be treated

A

hypoglycemia, tx w/ dextrose bolus or CRI

70
Q

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?

A

over 2mls/kg/hr
casts
keep BP above 80mmHg
furosemide, mannitol, dopamine PRN

71
Q

__ may be given to effect to provide clotting factors

A

fresh frozen plasma (10ml/kg)

72
Q

coagulation system should be monitored for

A

PT/PTT increase
FDP (fibrin degradation products) = DIC

the use of heparin to tx these patients is controversial

73
Q

GI ulceration and support

A

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
Q

monitoring required for HS patient

A 
continuous! subjective and objective 
telemetry 
perfusion/shock/hydration
vital signs 
PCV/TS 
coag PT/PTT/AT
glucose 
lactate 
blood gas 
BP 
Urine output
75
Q

HS CV CS

A

drop in BP and CO = CV shock
Circulatory failure
Arrythmias (hyperK+)

SAM Exam 1 (15 decks)

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