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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