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D R R I Y A S 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
• Basic metabolic process
• Food intake
• Muscular activity
Heat
production
• Radiation and conduction
• Vaporization of sweat
• Respiration
• Urination and defication
Heat lost
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
Ethanol
BZDS
barbiturates
Phenothiazines
carcinamatosis
Anaesthetics
antidepressants
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
↑ ses
thermogenesis
↑ses BMR
thermoregulation
 Delayed  endocrine
 Cutaneous cold thermoception direct redlex
vasoconstriction
 Prolonge dexposure thyroid axis increases MR
Thermoregulatory mechanism
 Afferent
 Center
 efferent
thermoregulatory mechanism
• Increase heat production
• Shivering
• Hunger
• Increase voluntary activity
• Increase scretion of NE,E
Activated
by cold
• Decrease heat loss
• Cutaneous vasoconstrictionActivated
by cold
• Incease heat loss
• Cutanoeus vasodilatation
• Sweating
Activate
d by heat
• 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
Effernt responses
Preoptic nuclei of anterior hypothalamus
heat cold
Thermal receptors
Cold warm
afferent
 Cold - A deta
 Warm unmyelinated C fiber
 Now seems like TRP
 Vanilloid
 menthol
 TRPV 1-4--heat activated
 TRPM8 and TRPA1cold
Threshold
 Mechanism is unknown
 0.5-1 degree celcius
Factors affecting threshold
 Exercise
 Nutrtion
 Infection
 Hypo & hyperthyroidism
 Drugs (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
thermoregulatory
 Further decrease in temperature shivering
commence
 36.0-36.2°
Vasoconstriction & shivering characterised by
 Threshold onset  tempe at which effector activates
 Gainrate 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 fat
 Intrascapular & perineal areas
 In 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
CVS
RS
• Linear depression of cerebral mb
• Amnesia , apathy
• Maladaptive behaviour
• Dysarthria
• Impaired judgement
• Tachycardia then brady
• Cardiac cycle prolongation
• Vasoconstriction
• Increased CO & BP
• Tachyponea -- ↓se in MV
•↑sed O² cpnsumpation
• Bronchorrhoea and spasm
mild
Renal and
endocrine
Neuro
muscular
• Diuresis
• ↑sed hormonal
levels
• ↑se in mb and
shivering
• ↑sed muscle
shivering and tone
• fatigue
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
CNS
Loss of
cerebrovascular
autoregulation
↓se in CBF
COMA
Loss of occular reflex
Progressive ↓se in
EEG
CVS
↓se BP
HR
CO
Pre entrant cardia
arrhythmias
Max risk of
ventricular
fibrillation
asystole
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 waranted
 If airway reflex are lost gentle intubation
 Atrial arrythmias should be waited
Diagnosis & stabilization
 Pulmonary artery catheterization should be avoided
 CVP in to the rt atrium should be avoided
 Indwelling bladder catheter
 Dehydration correction
 Acid base inbalance should be correct slowly
Rewarming
 Active
 passive
Passive
 ROR0.5-2° c
 Good for previously healthy pt,who develop aut mild
primary hypothermia
 Pt should have sufficient glycogen to support endogenous
thermogenesis
active
 Necessary in temp˂ 32°c or 90° f
 Extremes of age
 CNS dysfunction
 Cardio vascular instability
 Hormone insufficiency
 Suspicious 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
• RORup to 2-3° c
Options for rewarming
CAVR
• Percuta femoral cather 8.5 fr
• Requires systolic BP >60
• Flow rate225-375ml/min
• ROR3-4°c
CVV
• Central venous dual lumen or pheripheral
• Flow rate 150-400ml/min
• ROR2-3°c
Measuring core temperature
 Pulmonary circulation
 Tympanic memebrane
 Nasopharynx
 Oesophagus
 Rectal and bladder are not accurate as they are not
well perfused
Thermal regulation during anaesthesia
 GA1-3°c
 Vasoconstriction 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 thermostat
 Ambient temperature <21°c
 Unwarmed i/v fluids
 Drug induced vasodilatation
 Decreased BMR
 Body cavities exposed to ambient temperature
 Heat 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 temp
 1-5°c with in 30-45min
 Due to vasodilatation and other effect of GA
 Vasodilatation causes redistribution of heat from core to
pheriphery
Linear phase
 1°c over 2-4 hrs
 Gradual reduction
 This is due to heat loss by
Radiation
40%
Convection
30%
Evaporation
15%
Conduction
15%
Respiratory
loss
10%
Plateu phase
 After 3-5 hrs
 Long cases
 Core temperature often stop decreasing
 In this phase heat loss is matched by metabolic heat
production
Neuroaxial anaesthesia
 Redistribution of body heat is the main stay
 Initial core hypothermia is not as pronounced as in
GA
 Other wise the first two phase are similar
 All thermoregulatory responses are neurally
mediated and affects both pheripheral and central
thermo regualtion
Consequences
 Cardiac arrythmia & ischemia
 Increased PVR
 Hb-0₂ dissociatio curve left shift
 Reversible coiagulopathy
 Altered mental status
consequences
 Impaired renal function
 Decresed drug mb
 Poor wound healing
 Increased incidence of infection
 Post 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 insulation
 Active warming
 Internal warming
 Airway humidification
 Invasive internal warming technique
 Amini 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
Hypothermia and anaesthesia implication

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Hypothermia and anaesthesia implication

  • 1. D R R I Y A S A hypothermia
  • 2. 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
  • 3. • Basic metabolic process • Food intake • Muscular activity Heat production • Radiation and conduction • Vaporization of sweat • Respiration • Urination and defication Heat lost
  • 4. 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
  • 5. Risk factors Extremes of age • elderly • neonates enviornmental • Occupational,sports related • Inadequqate clothing • immersion Insufficient food • Malnutrition • Marasmus • kwashiorkor
  • 6. 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
  • 8. thermoregulation  Heat loss occurs through five mechanisms   radiation  conduction  convection  respiration  evaporation
  • 9. thermoregulation  It’s regulated through preoptic anterior hypothalamus
  • 10. immediate ANS+release of NE ↑ses muscle tone and shivering ↑ ses thermogenesis ↑ses BMR
  • 11. thermoregulation  Delayed  endocrine  Cutaneous cold thermoception direct redlex vasoconstriction  Prolonge dexposure thyroid axis increases MR
  • 13. thermoregulatory mechanism • Increase heat production • Shivering • Hunger • Increase voluntary activity • Increase scretion of NE,E Activated by cold • Decrease heat loss • Cutaneous vasoconstrictionActivated by cold
  • 14. • Incease heat loss • Cutanoeus vasodilatation • Sweating Activate d by heat • Increased respiration • Decrease heat production
  • 15. 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
  • 16. Terms to remember Mean body temperature • Physiologically weighted average temperature from various tissues NST • Heat production not associated with muscle ST • Through muscle activity
  • 17. Terms to remember Dietary thermogenesis •Heat production by metabolism of nutrients
  • 18. Over view Effernt responses Preoptic nuclei of anterior hypothalamus heat cold Thermal receptors Cold warm
  • 19. afferent  Cold - A deta  Warm unmyelinated C fiber
  • 20.  Now seems like TRP  Vanilloid  menthol
  • 21.  TRPV 1-4--heat activated  TRPM8 and TRPA1cold
  • 22. Threshold  Mechanism is unknown  0.5-1 degree celcius
  • 23. Factors affecting threshold  Exercise  Nutrtion  Infection  Hypo & hyperthyroidism  Drugs (alcohol,sedatives,nicttine)
  • 24. Interthreshold range  Bounded by sweating threshold at its upper end  And vasoconstriction thgreshold at its lower end  0.2-0.4
  • 25. efferent  Body responds to thermal perturbation via effector mechanism that increases mb heat production or alter enviornmental heat loss
  • 27. Cutaneous vaso constriction • First one to develop 36.5-37° • Metabolic heat is lost by convection & radiation
  • 28. Digital skin blood flow capillary nutrition A – v shunt Adrenergic nerve sympathetic nerve mediate constriction in A- V shunts thermoregulatory
  • 29.  Further decrease in temperature shivering commence  36.0-36.2°
  • 30. Vasoconstriction & shivering characterised by  Threshold onset  tempe at which effector activates  Gainrate 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
  • 31. NST  Increase in mb production not associated with muscular activity  Skeletal muscle and brown fat  Intrascapular & perineal areas  In infants it’s the primary response
  • 32. 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
  • 33. mild CNS CVS RS • Linear depression of cerebral mb • Amnesia , apathy • Maladaptive behaviour • Dysarthria • Impaired judgement • Tachycardia then brady • Cardiac cycle prolongation • Vasoconstriction • Increased CO & BP • Tachyponea -- ↓se in MV •↑sed O² cpnsumpation • Bronchorrhoea and spasm
  • 34. mild Renal and endocrine Neuro muscular • Diuresis • ↑sed hormonal levels • ↑se in mb and shivering • ↑sed muscle shivering and tone • fatigue
  • 35. 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
  • 36. moderate Renal and endocrine • 50% ↓se in RBF • Renal autoregulation • Impaired insulin activity Neuro mucular • hyporeflexia • Diminished shivering induced thermogenensis • rigidity
  • 37. Severe CNS Loss of cerebrovascular autoregulation ↓se in CBF COMA Loss of occular reflex Progressive ↓se in EEG CVS ↓se BP HR CO Pre entrant cardia arrhythmias Max risk of ventricular fibrillation asystole
  • 38. 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
  • 39. Diagnosis & Stabilization  If ventricular fibrillation  defibrillation with 2 J /kg not reverted rewarm 30° c (80 ° F) bfore next defibrillation  Supplemental O₂ is always waranted  If airway reflex are lost gentle intubation  Atrial arrythmias should be waited
  • 40. Diagnosis & stabilization  Pulmonary artery catheterization should be avoided  CVP in to the rt atrium should be avoided  Indwelling bladder catheter  Dehydration correction  Acid base inbalance should be correct slowly
  • 42. Passive  ROR0.5-2° c  Good for previously healthy pt,who develop aut mild primary hypothermia  Pt should have sufficient glycogen to support endogenous thermogenesis
  • 43. active  Necessary in temp˂ 32°c or 90° f  Extremes of age  CNS dysfunction  Cardio vascular instability  Hormone insufficiency  Suspicious secondary hypothermia
  • 44. Active external rewarming  Forced air heating blankets  External heat exchange pads  Radiant heat sources  Hot packs  Electric blankets should be avoided
  • 45. 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
  • 46. 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 • RORup to 2-3° c
  • 47. Options for rewarming CAVR • Percuta femoral cather 8.5 fr • Requires systolic BP >60 • Flow rate225-375ml/min • ROR3-4°c CVV • Central venous dual lumen or pheripheral • Flow rate 150-400ml/min • ROR2-3°c
  • 48. Measuring core temperature  Pulmonary circulation  Tympanic memebrane  Nasopharynx  Oesophagus  Rectal and bladder are not accurate as they are not well perfused
  • 49. Thermal regulation during anaesthesia  GA1-3°c  Vasoconstriction and NST are the mechanisms
  • 50. Development of hypothermia during GA  Results from combination of cold operating room enviornment as well as anaesthesia impaired regulation
  • 51. Events that contribute  Interfere with hypothalamic thermostat  Ambient temperature <21°c  Unwarmed i/v fluids  Drug induced vasodilatation  Decreased BMR  Body cavities exposed to ambient temperature  Heat is recquired to humidify inhaled gases
  • 52. Pattern of hypothermia Phase 1:redistribution Phase 2:linear phase Phase 3:plateu phase
  • 53. Redistribution  Laregest drop in core temp  1-5°c with in 30-45min  Due to vasodilatation and other effect of GA  Vasodilatation causes redistribution of heat from core to pheriphery
  • 54. Linear phase  1°c over 2-4 hrs  Gradual reduction  This is due to heat loss by
  • 56. Plateu phase  After 3-5 hrs  Long cases  Core temperature often stop decreasing  In this phase heat loss is matched by metabolic heat production
  • 57. Neuroaxial anaesthesia  Redistribution of body heat is the main stay  Initial core hypothermia is not as pronounced as in GA  Other wise the first two phase are similar  All thermoregulatory responses are neurally mediated and affects both pheripheral and central thermo regualtion
  • 58. Consequences  Cardiac arrythmia & ischemia  Increased PVR  Hb-0₂ dissociatio curve left shift  Reversible coiagulopathy  Altered mental status
  • 59. consequences  Impaired renal function  Decresed drug mb  Poor wound healing  Increased incidence of infection  Post operative protein catabolism and stress response
  • 60. Prevention and treatment of mild hypothermia  Minimal redistribution of heat  Cutaneous warming during anaesthesia  Internal warming
  • 61. Minimal redistribution of heat  Pre operative warming of pheripheral tissue  Preoperative pharmacological vasodilatation (oral nifedepine)
  • 62. Cutaneous warming  Passive insulation  Active warming  Internal warming  Airway humidification  Invasive internal warming technique  Amini acid infusion
  • 63. 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
  • 64. 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
  • 65. 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
  • 66.  Thermoregulatory vasoconstriction and vasodilatation most likely establish during the first day of life and can occur in both premature and the full term infants
  • 67. 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