hypothermia and anaesthesia implication
DESCRIPTION
reference from harrison , miller, pediatric anaesthetic book by dr.rabeca.....TRANSCRIPT
DR RIYAS A
hypothermia
Introduction
The balance b/w heat production and heat loss determines
Normally tightly regulated Speed of chemichal reaction varies Body enzyme sysytem has very narrow range
of temperature
Heat productio
n
•Basic metabolic process•Food intake•Muscular activity
Heat lost
•Radiation and conduction•Vaporization of sweat•Respiration•Urination and defication
hypothermia
Unintentional drop of body core temperature below 35°c or 95 °f
1° direct exposure of a previously healthy individual to cold
2°complication of severe disease
Risk factors
Extremes of age •elderly•neonates
enviornmental•Occupational,sports related•Inadequqate clothing•immersion
Insufficient food•Malnutrition•Marasmus•kwashiorkor
Risk factors
Endocrine related• DM• Hypoglycemia• Hypothyroidism• Adrenal
insufficiency• hypopitutarism
neurological• CVA• Hypothalamic
d/s• Parkinsons d/s• Spinal sord
injury
Multi system• trauma• Sepsis• Shock• Hepatic or renal
failure• Burns &
exfoliative dermatological lesions
• immobility
Pharmacological
EthanolBZDS
barbiturates
Phenothiazinescarcinamatosis
Anaestheticsantidepressants
thermoregulation
Heat loss occurs through five mechanisms
radiation conduction convection respiration evaporation
thermoregulation
It’s regulated through preoptic anterior hypothalamus
immediate
ANS+release of NE
↑ses muscle tone and shivering
↑ sesthermoge
nesis
↑ses BMR
thermoregulation
Delayed endocrine
Cutaneous cold thermoception direct redlex vasoconstriction
Prolonge dexposure thyroid axis increases MR
Thermoregulatory mechanism
Afferent
Center
efferent
thermoregulatory mechanism
Activated by cold
•Increase heat production•Shivering•Hunger•Increase voluntary activity•Increase scretion of NE,E
Activated by cold
•Decrease heat loss•Cutaneous vasoconstriction
Activate d by heat
•Incease heat loss•Cutanoeus vasodilatation•Sweating
•Increased respiration•Decrease heat production
Terms to remember
Threshold temperature •Central temperature that elicit a regulating effect
Interthreshold range •Temperature range over which no regulatory responses
gain •Intensity of regulatory response
Terms to remember
Mean body temperature •Physiologically weighted average temperature from various tissues
NST •Heat production not associated with muscle
ST •Through muscle activity
Terms to remember
Dietary thermogenesis
• Heat production by metabolism of nutrients
Over view
afferent
Cold - A deta
Warm unmyelinated C fiber
Now seems like TRP
Vanilloid menthol
TRPV 1-4--heat activated
TRPM8 and TRPA1cold
Threshold
Mechanism is unknown
0.5-1 degree celcius
Factors affecting threshold
Exercise NutrtionInfectionHypo & hyperthyroidismDrugs (alcohol,sedatives,nicttine)
Interthreshold range
Bounded by sweating threshold at its upper end
And vasoconstriction thgreshold at its lower end
0.2-0.4
efferent
Body responds to thermal perturbation via effector mechanism that increases mb heat production or alter enviornmental heat loss
Most commonly used one
behavioural
Cutaneous vaso constriction
• First one to develop 36.5-37°• Metabolic heat is lost by convection & radiation
Digital skin blood flow
capillary
nutrition
A – v shunt
Adrenergic nerve sympathetic nerve mediate constriction in A-V shunts
thermoregulator
y
Further decrease in temperature shivering commence
36.0-36.2°
Vasoconstriction & shivering characterised by
Threshold onset tempe at which effector activates
Gainrate of response to given decrease in core temperature
Max response intensity GA reduces the threshold by 2-3°c Gain & max response intensity are unaffected
NST
Increase in mb production not associated with muscular activity
Skeletal muscle and brown fatIntrascapular & perineal areasIn infants it’s the primary response
Clinical features
Mild 35° c – 32.2° c or 95 ° f – 90 °f
Moderate ˂32.2 ° c- 28° c or 90° F-82.4 ° f
Severe˂ 28 ° c or 82.4 ° F
mild
CNS
Linear depression of cerebral mbAmnesia , apathyMaladaptive behaviourDysarthriaImpaired judgement
CVS
RS
Tachyponea -- ↓se in MV↑sed O² cpnsumpationBronchorrhoea and spasm
mild
Neuro muscular
modearate
CNS• EEG abno• Progressive
depression of level of consiousness
• Pupillary dilatation• Paradoxical
dressing• hallucination
CVS• ↓se in PR & BP• ↑sed atrial and
ventriculaer arrhythmias
• J wave ECG changes
Respiratory• Hypoventialtion• 50 % ↓se in co₂
production• Absence of
protective airway reflex
moderate
Renal and endocrine• 50% ↓se in RBF• Renal autoregulation• Impaired insulin activity
Neuro mucular• hyporeflexia• Diminished shivering induced
thermogenensis• rigidity
Severe
CNSLoss of cerebrovascular
autoregulation
↓se in CBFCOMA
Loss of occular reflex
Progressive ↓se in EEG
severe
Renal and endo• ↓sed RBF,↓se in CO• Extrene oliguria• 80% in Mb
neuromuscular• No motion• ↓se nerve conduction velocity• Pheripheral areflexia• No corneal or occulo cephalic
reflex
Diagnosis & Stabilization
If ventricular fibrillation defibrillation with 2 J /kg not reverted rewarm 30° c (80 ° F) bfore next defibrillation
Supplemental O₂ is always warantedIf airway reflex are lost gentle intubationAtrial arrythmias should be waited
Diagnosis & stabilization
Pulmonary artery catheterization should be avoided
CVP in to the rt atrium should be avoidedIndwelling bladder catheter Dehydration correctionAcid base inbalance should be correct slowly
Rewarming
Active
passive
Passive
ROR0.5-2° cGood for previously healthy pt,who develop aut mild
primary hypothermiaPt should have sufficient glycogen to support endogenous
thermogenesis
active
Necessary in temp˂ 32°c or 90° fExtremes of ageCNS dysfunctionCardio vascular instabilityHormone insufficiencySuspicious secondary hypothermia
Active external rewarming
Forced air heating blankets
External heat exchange pads
Radiant heat sources
Hot packs
Electric blankets should be avoided
Active core rewarming
With heated humidified o₂ (40-45°c) via mask or ETT
Crystallods should be heated 40-42° c(can use in line heat exchanger)
i/v medications are with held below 30
MAP 60,if not maintaining dopamine 2-5mcg/kg/min
Options for rewarming
CPB•Full circulatory support with pump and oxygenator•Temp gardient –5 -10 ° c•Flow rate->2-7l/min…ROR up to 9.5° c/hr
hemodialysis•Single or dual vessel catheter•Exchange cycle volume—200-500ml/min•RORup to 2-3° c
Options for rewarming
CAVR•Percuta femoral cather 8.5 fr•Requires systolic BP >60•Flow rate225-375ml/min•ROR3-4°c
CVV•Central venous dual lumen or pheripheral•Flow rate 150-400ml/min•ROR2-3°c
Measuring core temperature
Pulmonary circulationTympanic memebraneNasopharynxOesophagusRectal and bladder are not accurate as they
are not well perfused
Thermal regulation during anaesthesia
GA1-3°cVasoconstriction and NST are the mechanisms
Development of hypothermia during GA
Results from combination of cold operating room enviornment as well as anaesthesia impaired regulation
Events that contribute
Interfere with hypothalamic thermostatAmbient temperature <21°cUnwarmed i/v fluidsDrug induced vasodilatationDecreased BMRBody cavities exposed to ambient temperatureHeat is recquired to humidify inhaled gases
Pattern of hypothermia
Phase 1:redistribution
Phase 2:linear phase
Phase 3:plateu phase
Redistribution
Laregest drop in core temp1-5°c with in 30-45minDue to vasodilatation and other effect of GAVasodilatation causes redistribution of heat from core to
pheriphery
Linear phase
1°c over 2-4 hrsGradual reductionThis is due to heat loss by
Radiation 40%
Convection30%
Evaporation15%
Conduction15%
Respiratory loss10%
Plateu phase
After 3-5 hrs Long casesCore temperature often stop decreasingIn this phase heat loss is matched by
metabolic heat production
Neuroaxial anaesthesia
Redistribution of body heat is the main stayInitial core hypothermia is not as pronounced
as in GAOther wise the first two phase are similarAll thermoregulatory responses are neurally
mediated and affects both pheripheral and central thermo regualtion
Consequences
Cardiac arrythmia & ischemiaIncreased PVRHb-0₂ dissociatio curve left shiftReversible coiagulopathyAltered mental status
consequences
Impaired renal functionDecresed drug mbPoor wound healingIncreased incidence of infectionPost operative protein catabolism and stress
response
Prevention and treatment of mild hypothermia
Minimal redistribution of heat
Cutaneous warming during anaesthesia
Internal warming
Minimal redistribution of heat
Pre operative warming of pheripheral tissue
Preoperative pharmacological vasodilatation (oral nifedepine)
Cutaneous warming
Passive insulationActive warmingInternal warmingAirway humidificationInvasive internal warming techniqueAmini acid infusion
In newborn
Has large skin surface area compared with their body mass and an increased thermal conductance
Evaporation of heat loss is due to ↓sed keratin content
Critical temperature ->this is the temperature below which an unclothed ,unanaesthetised individual cann’t maintain a normal core body temp
in adults 0° c in infants 22° c in pre term 28° c
In newborn
Neutral temperture:ambient temperture at which the o₂ demand is minimal & temperature regulation is achieved through non evaporative physical status
for adults 28°c neonates 32° c preterm 34° c
In newborn
Maintanance f core temperaturebin a cool enviornment result in an ↑sed O₂ consumption and mb acidosis
Particular concern is in view of thermoregulation in the newborn in head
Thin skull bone Sparse scalp hairin combination with close proximity of
well perfused brain further prefers heat loss from head
Thermoregulatory vasoconstriction and vasodilatation most likely establish during the first day of life and can occur in both premature and the full term infants
Deliberate intraoperative hypothermia
For protection against tissue ischemia(during cardiac and neuro surgery)
Drugs produces less protection than hypothermia does
Deep hypothermia remains routine for intentional circulatory arrest cases
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