Hypothermia and anaesthesia implication

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reference from harrison , miller, pediatric anaesthetic book by dr.rabeca.....

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Hypothermia and anaesthesia implication

  1. 1. D R R I Y A S A hypothermia
  2. 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. 3. • Basic metabolic process • Food intake • Muscular activity Heat production • Radiation and conduction • Vaporization of sweat • Respiration • Urination and defication Heat lost
  4. 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. 5. Risk factors Extremes of age • elderly • neonates enviornmental • Occupational,sports related • Inadequqate clothing • immersion Insufficient food • Malnutrition • Marasmus • kwashiorkor
  6. 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
  7. 7. Pharmacological Ethanol BZDS barbiturates Phenothiazines carcinamatosis Anaesthetics antidepressants
  8. 8. thermoregulation  Heat loss occurs through five mechanisms   radiation  conduction  convection  respiration  evaporation
  9. 9. thermoregulation  It’s regulated through preoptic anterior hypothalamus
  10. 10. immediate ANS+release of NE ↑ses muscle tone and shivering ↑ ses thermogenesis ↑ses BMR
  11. 11. thermoregulation  Delayed  endocrine  Cutaneous cold thermoception direct redlex vasoconstriction  Prolonge dexposure thyroid axis increases MR
  12. 12. Thermoregulatory mechanism  Afferent  Center  efferent
  13. 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. 14. • Incease heat loss • Cutanoeus vasodilatation • Sweating Activate d by heat • Increased respiration • Decrease heat production
  15. 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. 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. 17. Terms to remember Dietary thermogenesis •Heat production by metabolism of nutrients
  18. 18. Over view Effernt responses Preoptic nuclei of anterior hypothalamus heat cold Thermal receptors Cold warm
  19. 19. afferent  Cold - A deta  Warm unmyelinated C fiber
  20. 20.  Now seems like TRP  Vanilloid  menthol
  21. 21.  TRPV 1-4--heat activated  TRPM8 and TRPA1cold
  22. 22. Threshold  Mechanism is unknown  0.5-1 degree celcius
  23. 23. Factors affecting threshold  Exercise  Nutrtion  Infection  Hypo & hyperthyroidism  Drugs (alcohol,sedatives,nicttine)
  24. 24. Interthreshold range  Bounded by sweating threshold at its upper end  And vasoconstriction thgreshold at its lower end  0.2-0.4
  25. 25. efferent  Body responds to thermal perturbation via effector mechanism that increases mb heat production or alter enviornmental heat loss
  26. 26. Most commonly used one behavioural
  27. 27. Cutaneous vaso constriction • First one to develop 36.5-37° • Metabolic heat is lost by convection & radiation
  28. 28. Digital skin blood flow capillary nutrition A – v shunt Adrenergic nerve sympathetic nerve mediate constriction in A- V shunts thermoregulatory
  29. 29.  Further decrease in temperature shivering commence  36.0-36.2°
  30. 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. 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. 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. 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. 34. mild Renal and endocrine Neuro muscular • Diuresis • ↑sed hormonal levels • ↑se in mb and shivering • ↑sed muscle shivering and tone • fatigue
  35. 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. 36. moderate Renal and endocrine • 50% ↓se in RBF • Renal autoregulation • Impaired insulin activity Neuro mucular • hyporeflexia • Diminished shivering induced thermogenensis • rigidity
  37. 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. 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. 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. 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
  41. 41. Rewarming  Active  passive
  42. 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. 43. active  Necessary in temp˂ 32°c or 90° f  Extremes of age  CNS dysfunction  Cardio vascular instability  Hormone insufficiency  Suspicious secondary hypothermia
  44. 44. Active external rewarming  Forced air heating blankets  External heat exchange pads  Radiant heat sources  Hot packs  Electric blankets should be avoided
  45. 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. 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. 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. 48. Measuring core temperature  Pulmonary circulation  Tympanic memebrane  Nasopharynx  Oesophagus  Rectal and bladder are not accurate as they are not well perfused
  49. 49. Thermal regulation during anaesthesia  GA1-3°c  Vasoconstriction and NST are the mechanisms
  50. 50. Development of hypothermia during GA  Results from combination of cold operating room enviornment as well as anaesthesia impaired regulation
  51. 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. 52. Pattern of hypothermia Phase 1:redistribution Phase 2:linear phase Phase 3:plateu phase
  53. 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. 54. Linear phase  1°c over 2-4 hrs  Gradual reduction  This is due to heat loss by
  55. 55. Radiation 40% Convection 30% Evaporation 15% Conduction 15% Respiratory loss 10%
  56. 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. 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. 58. Consequences  Cardiac arrythmia & ischemia  Increased PVR  Hb-0₂ dissociatio curve left shift  Reversible coiagulopathy  Altered mental status
  59. 59. consequences  Impaired renal function  Decresed drug mb  Poor wound healing  Increased incidence of infection  Post operative protein catabolism and stress response
  60. 60. Prevention and treatment of mild hypothermia  Minimal redistribution of heat  Cutaneous warming during anaesthesia  Internal warming
  61. 61. Minimal redistribution of heat  Pre operative warming of pheripheral tissue  Preoperative pharmacological vasodilatation (oral nifedepine)
  62. 62. Cutaneous warming  Passive insulation  Active warming  Internal warming  Airway humidification  Invasive internal warming technique  Amini acid infusion
  63. 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. 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. 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. 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. 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

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