Hypothermia Flashcards
Hypothermia causes severe
Early and aggressive treatment can decrease morbidity and mortality in the critically ill patient.
____ is a common complication resulting from peripheral vasodilation when the periphery is warmed before the core
cardiovascular, respiratory, electrolyte, nervous system, acid-base, and coagulation abnormalities.
Rewarming shock
hypothermia <37 (98.6)- individual or combined effects of
excessive heat loss
decreased heat production
or a disruption of the normal thermoregulatory functions permit the core (vital organ) body temperature (CBT) to drop below species-specific physiologic parameters
Primary hypothermia, or “accidental” hypothermia
secondary hypothermia is a result of
subnormal temperature low environmental temperatures
disease, trauma, surgery, or drug-induced alteration in heat production and thermoregulation
Hypothermia traditionally has been classified as “mild,” “moderate,” or “severe” based purely on..
this classification is simple, it does not capture the functional changes that characterize the differing levels of symptoms not directly related to a specific CBT. Therefore some have proposed classifying the severity of hypothermia based on the clinical consequences at each stage, not strictly on the CBT
CBT
32°-37° C Mild Shivering, ataxia, vasoconstriction
28°-32° C Moderate Decreased level of consciousness, hypotension, ± shivering
<28° C Severe Loss of shivering, dysrhythmias, profound central nervous system deficits
severe hypothermia is marked by complete loss of the thermoregulatory system, an inability to _____ comatose states and susceptibility to ____
shiver (<28 - 82F) 32 = 89 +/- shiver
ventricular fibrillation
main thermostat of the body is the hypothalamus, with temperature changes sensed by the:
Secondary temperature sensors are located within the skin and
deep body tissues; namely, the:
preoptic and anterior hypothalamic nuclei
Temperature is sensed by the _____ family of ion channels, which are activated at distinct _____
peripheral input from the skin travels to the spinal cord or _____dorsal horn for passage to the _____ and thalamus
thermal information is then output to the ______
The behavioral and autonomic responses are linked to the ___ inputs in the brainstem
system is so precise that, in humans, changes in CBT of ____ degree Celsius result in ANS responses
transient receptor potential family of ion channels
temperature thresholds
trigeminal dorsal horn
midbrain
sensory cortex, producing the sensation of hot and cold
reticular
sweating to shivering within a span of 0.6° C
why is accurate CBT important
dramatic core/peripheral temperature gradients
Heat production is secondary to
most metabolically active systems:
depends on the metabolic rate of the body
As heat is produced, it distributes rapidly to core tissues but more slowly to the peripheral tissues via
chemical metabolism of energy substrates within cells.
brain, truncal organs, and active muscles
convective heat transfer through blood
conductive heat transfer through adjacent tissues
normal thermoregulatory response is to produce and retain heat, and thereby maintain the CBT. This is accomplished by
initial autonomic response causes specialized anastomoses, linking arterioles with veins, to open as the CBT nears 37° C, which prevents
Dogs have additional mechanism in their footpads, in which the veins are intimately associated with the arteries, so that
shivering, which is typically noted at a degree
behavioral -huddling and curling
physiologic - piloerection, peripheral vasoconstriction, and shivering
heat loss to the distal extremities
blood is heated before it is returned to the core
lower than the vasoconstrictive response
shivering, which is typically noted at a degree
important because it can be metabolically
inefficient and much of the heat can be lost to the environment
increase the metabolic rate by a factor of 4-10X
energy substrate for shivering is usually CHO
in glycogen-depleted patients, lipid and protein reserves need to be used.
.:.diminished in cachectic, old, and the very young
Convection
transfer of heat from the body surfaces to air
heat transfer is maximized when the air is circulated, as evidenced by the “wind chill factor” (perceived decrease in temperature with wind exposure).
Conduction
transfer of heat from body surfaces to objects that come into contact with the body, such as examination tables, and kennels.
Immersion hypothermia can cause a profound heat loss via this mechanism.
Radiation
loss of heat to surrounding structures that do not come into direct contact with the body, such as walls
via electromagnetic waves (photons) emitted from any object that has a temperature above absolute zero, and this energy transfers heat
This heat transfer occurs regardless of the temperature of the intermediary substance, such as air. Athletes commonly wear reflective blankets after extremely strenuous activities to limit this form of heat loss.
Evaporative
loss of heat from moisture on the body surfaces or through the respiratory tract to the environment
Although dogs and cats have minimal perspiration, this loss can be significant if the patient is wet, either incidentally or in preparation for surgery
primary detrimental cardiovascular changes found in hypothermia include:
initial response to hypothermia includes a mild
left shift in the oxygen-hemoglobin dissociation curve, may lead to peripheral tissue hypoxia or dysoxia
as the hypothermia progresses, vascular responsiveness to norepinephrine at the α1-receptor begins to:
bradycardia, hypotension, cardiac dysrhythmias, decreased cardiac output, and ultimately asystole
sinus tachycardia, vasoconstriction >CVP
decrease = loss of vasoconstriction and subsequent arterial vasodilation contributing to hypotension
bradycardia MoA:
atropine:
decrease in the rate of diastolic repolarization in the cells of the sinus node
makes the bradycardia nonresponsive to atropine administration
HR and contractility - temperature dependent changes:
should you elevate a bradycardic hypothermic patients HR
(a. non-reposive to atropine bc due to decreased rate of repolarization of SA node so stimulating will not increase it
b. mild-moderate low HR contractility is in fact increased)
Cardiac contractility is dependent on HR in hypothermic
if HR is allowed to remain low, the systolic function can actually increase, whereas the diastolic function decreases
when HR is artificially elevated, this protective benefit was lost
only applies to mild & moderate hypothermia
severe hypothermia = decreased myocardial contractility
dysarrhythmias
generally everything is just slower:
in humans, pathognomonic:
severe hypothermia initial dyarrhythmia:
As CBT approaches 23.5° C, 50% of dogs demonstrate ventricular fibrillation
cooling to 26° C profoundly increased the transmural dispersion of repolarization. This dispersion of repolarization is known to be a prerequisite for:
prolongation of the PR interval
widening of the QRS complex, and, in humans,
Osborn waves - J waves, are an acute ST-segment elevation at temperatures of 32° to 33° C
rarely been documented in small animals
atrial fibrillation, which can progress to vtach vfib
reentrant excitation and arrhythmogenesis and may be directly linked to ventricular fibrillation
respiratory:
decreased cellular metabolism = < CO2 =
at temperatures below 34° C, sensitivity to ppCO2 and carbon dioxide production decreases by 50% with an 8° C fall in body temperature
reduce the stimulus for respiration, < TV
- respiratory alkalosis may initially be present secondary to tachypnea, as the hypothermia progresses, the respiratory drive decreases and a respiratory acidosis occurs.
- The solubility of carbon dioxide is increased in cooled blood, which leads to further increases in blood carbon dioxide content.
loss of shivering, which in humans can occur at a wide range of temperatures:
(24° to 35° C) 75-95F
coagulation:
thrombocytopenia
platelet and coagulation factor activity dysfunction
disruption of fibrinolytic equilibrium
Primary hemostasis abnormalities MoA:
decreased platelet aggregation secondary to:
sequestration of plt - liver and spleen = quantitative platelet decrease
decreased production of thromboxane B2
decreased platelet granule secretion
attenuation of P selectin expression
diminished expression vWF receptor
Secondary coag.:
BIGGEST ISSUE WITH coag testing in hypothermic patients =
depressed enzymatic activity of activated clotting factors in hypothermia
kinetic coagulation tests are performed on warmed blood Therefore the standard clotting tests performed in the laboratory at 37° C will not reflect the effects of hypothermia on the patient’s clotting cascade
Thromboelastography (TEG) studies on hypothermic blood have resulted in mixed outcomes
coagulation testing should be performed with this in mind.
