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Boards: Environmental > Hypothermia and targeted temperature management. JVECC. 2017 > Flashcards

Hypothermia and targeted temperature management. JVECC. 2017 Flashcards

1
Q

How much cooler than the trunk (core temperature) are the extremities (peripheral temperature)?

A

2-4 degrees C lower

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2
Q

Explain heat dissipation by radiation

A

heat loss to objects in the environment, not in direct contact with the body

any object with temperature > absolute zero (e.g., body) emit electromagnetic radiation –> infrared thermal radiation heat transfer

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3
Q

How does the mechanism of primary heat loss differ between humans and animals?

A

animal - primary heat loss convection and conduction
humans - primary heat loss radiation (65%)

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4
Q

How does fat keep an animal warm?

A

insulates because it has only 1/3 the conductivity of other tissues - less heat can dissipate into the periphery to be lost

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5
Q

Where are thermoreceptors located?

A
  • hypothalamus
  • skin
  • spinal cord
  • abdominal viscera
  • great veins
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6
Q

Define primary and secondary hypothermia - why is it clinically important to differentiate them?

A

Primary hypothermia
- animal is exposued to a cold environment but has normal heat production

Secondary hypothermia
- altered heat production and thermoregulatory ability of an animal due to illness, injury, or drug therapy

pathophysiologic adverse effects occur at higher temperature in secondary hypothermia!

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7
Q

For every 1 degree C drop in core temperature there is a xxxxxxx decline in cerebral blood flow

A

6-7%

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8
Q

Describe the cerebral changes in hypothermia

A
  • decline in cerebral blood flow
  • <92F (33C)&raquo_space; changes to the cerebral electrical acitvity and temp-dependent enzymes cease to function
  • <85F (29C)&raquo_space; hypothalamus stops working&raquo_space; worsens hypothermia (no thermoregulation)
  • moderate to severe hypothermia&raquo_space; cerebral edema from decreased blood flow and ischemia
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9
Q

Why does the hypothermic brain withstand ischemia longer?

A

due to the decreased metabolic demands from suppression of brain activity

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10
Q

List the cardiovascular effects of moderate to severe hypothermia

A
  • decreased spontaneous depolarization of pacemaker cells –> bradycardia that’s unresponsive to atropine
  • reduced alpha-1 receptor affinity –> vasodilation –> hypotension
  • slowed myocardial conduction –> arrhythmias
  • cold diuresis –> hypovolemia
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11
Q

List ECG abnormalities and arrhythmias seen in hypothermia in veterinary patients

A
  • prolonged action potential duration
  • legnthened PR and QT intervals
  • widened QRS complexes
  • atrial fibrillation (dogs)
  • ventricular tachycardia (dogs)
  • isorhythmic AV dissociation (cat)

most common in people: atrial fibrillation

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12
Q

Why do hypothermic patients have a slower RR?

A

hypothermia –> decreased metabolism –> decreased CO2 production –> decreased respiratory drive

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13
Q

How does hypothermia affect the oxygen-hemoglobin dissociation curve?

A

left-shift (at 30C/86F) clinically applicable??

other causes: alkalosis, decreased 2,3-DPG, decreased CO2

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14
Q

at what temperature does GI dysmotility in hypothermia occur?

A

< 34C/93.2F

generalized ileus at < 28C/82F

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15
Q

Why do hypothermic patients develop GI ulceration?

A
  • decreased local perfusion
  • increased gastric acid production
  • decreased duodenal bicarbonate production
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16
Q

Explain why hypothermic patients may develop hyperglycemia

A

poor perfusion + microcirculatory thrombosis –> pancreatitis –> decreased insulin production

+ increaesed sympathetic tone (increased glucose production and release by liver)

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17
Q

Explain why hypothermic patients develop hypovolemia

A

“cold diuresis”
mild hypothermia –> sympathetic tone increased –> peripheral vasoconstriction –> increased central blood flow —> increased renal blood flow

progressive hypothermia –> reduced ADH concentration

(moderate/severe hypothermia –> decreased CO –> decreased renal blood flow –> AKI)

18
Q

In a hypocoagulable hypothermic patient, what clotting time abnormalities would you expect?

A

coagulopathy is from the cold directly inhibiting clotting cascades, but there are normal concentration of clotting factors

PT/aPTT –> machine warms sample –> doesn’t reflect coagulopathy in hypothermia –> normal results

19
Q

Why is plasma therapy in patients with coagulopathy of hypothermia not indicated?

A

clotting factors are present at normal concentrations –> hypothermia inhibits enzymatic processes of clotting

20
Q

How are PLTs affected in hypothermia

A

Thrombocytopenia
* sequestered in the spleen and liver (reversible with rewarming)

Decreased PLT aggregation
* decreased TXA2
* decreased PLT granule secretion
* decreased vWF receptor expression

21
Q

Why would hypothermic patients be immuno-compromised?

A

Leukopenia
* decreased circlulating leukocytes
* impaired leukocyte release from bone marrow
* compromised neutrophil and monocyte tissue migration

In people —> increased infection rate and poor wound healing

22
Q

What are the most common electrolyte disorders in hypothermia and how do they develop?

A

hyperkalemia and hyponatremia

decreased NaKATPase pump activity

23
Q

What is the recommended temperature for fluids used for active core rewarming

A

IV fluids - 104-107.6F
peritoneal/pleural lavage - 104-109.4F

24
Q

At what temperature should active rewarming be discontinued?

A

98.6F –> change to passive rewarming only

25
Q

What is the “afterdrop” phenomenon when warming hypothermic patients?

A

rewarming –> improved perfusion and circulation of cold peripheral blood to the core –> cooling

26
Q

Name methods of active core rewarming

A
  • warmed IV fluids
  • warmed humidified inhaled air
  • warm water enema
  • warm infusion of urinary bladder, peritoneal, pleural space - lavage
  • extracorporeal rewarming
27
Q

List methods of fluid warming for core rewarming methods

A
  • microwaving - must be < 80 seconds
  • in-line warmer
  • immersion of IV tubing in warm water
  • convection oven
28
Q

List concerns with microwave fluid warming

A
  • uneven heat distribution
  • risk of overheating
  • potential instability of the non-polyvinyl chloride components of the bags
  • bag warming often insufficient because fluid will cool down in the IV line
29
Q

What is “rescue collapse”?

A

cardiac arrest in severely hypothermic human patients (not reported in vet med)
- associated with rescue and transport
- cardiac arrhythmias triggered by interventions (e.g., IVC) and inadvertent further cooling

30
Q

What is the reasoning behind prophylactic Abx therapy in hypothermiic patinets?

A

hypothermia causes decreased neutrophil function and leukocyte sequestration

31
Q

How should arrhythmias from hypothermia be treated?

A

rewarming + standard treatment

  • most therapies (e.g., defibrillation and pacing) may not work
  • don’t consider any treatments ineffective until it failed in a normothermic patinet
32
Q
A
33
Q

What is the “afterdrop” phenomenom when rewarming a patient

A

body temp drops during rewarming
- from cold peripheral blood circulating to the core and warm core blood to the periphery

34
Q

What is “rewarming shock” and what is recommended to prevent this?

A

When external rewarming is applied without core warming (particularly when only extremities are rewarmed)
- peripheral vasodilation –> hypotension –> distributive shock

recommended to administer warmed IV fluids at the same time as external warming

35
Q

What is the main cause of MODS in hypothermic patients?

A

Ischemia-Reperfusion Injury after rewarming

36
Q

List the proposed benefits of targeted temperature management (TTM) after CPA

A
  • reduce BBB permeability
  • modulate inflammatory response
  • reduce cerebral and other organ metabolic demand
  • reduce mitochondiral injury and dysfunction
  • atttenuate excitatory neurotransmitter response
  • attenuate Ca-dependent neuro signaling
  • reduce ROS production
  • reduce cell death from necrosis and apoptosis
37
Q

What is the the American Heart Association’s recommendation on targeted temperature management following CPA

A

in comatose adults with ROSC after CPA - selected and steadily maintained temperature at 32-36 C for at least 24 hours

38
Q

What are the phases of targeted temperature management and what are each phase’s complications?

A

Induction
* hypovolemia
* electrolyte disturbances
* hyperglycemia
* shivering (treat with sedation and counterwarming of hands, face, feet)
Maintenance
* typical signs of prolonged sedation, e.g., pressure sores, pneumonia, other infections
Rewarming
* electrolyte and hemodynamic disturbances

39
Q

List adverse effects of targeted temperature management

A
  • arrhythmias
  • pneumonia
  • metabolic and electrolyte disturbances
  • seizures
  • cardiovascular changes
  • insulin resistance
  • decreaed drug clearance (reduced hepatic metabolism)
  • leukopenia
  • thrombocytopenia
40
Q

What is the current RECOVER guideline recommendation of targeted temperature management after CPA?

A

mild therapeutic hypothermia (91.4 +/- 1.8 F) for 24-48 hours in dogs and cats that remain comatose after successful resuscitation

only if MV, intensive nursing care, and CC available

Do not rewarm following cardiac arrest

Boards: Environmental (5 decks)

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