Intraoperative Hypothermia

Intraoperative Hypothermia

2. Hypothermia is a core temperature of less than
36°C. (applies regardless of the patient’s initial
temperature).
Mild : 35-32 C
Moderate : <32 –28 C
Severe : <28 C
Circulatory arrest –no flow in the
blood vessels
DHCA –no blood flow during deep
hypothermia

3. Risk Factors
Hypoglycemia and Wernicke'sdisease may lead to
hypothermia secondary to hypothalamic dysfunction.
Other endocrine disorders such as hypothyroidism
and hypoadrenalismpredispose to hypothermia
because of decreased metabolic rate.
Severe burns and other dermal diseasesmay impair
the ability of the skin to thermoregulate or prevent
vasoconstriction.
Patients at the extremes of ageare more vulnerable
to hypothermia.
The use of any drug, including alcohol,that causes
altered sensorium places a patient at higher risk for
hypothermia.

4. Mortality & Prognosis
Despite immediate treatment,
improved prehospital survival and
rewarming techniques in hospital,
accidental hypothermia is associated
with a high mortality ranging from 30-
80%.
Walpoth, 1990, 11 pts –35% mortality
Kornberg, 1996, 24 pts –87% mortality
Hauty, 1987, 82% mortality, no survivors with temps <20 C.

5. Mortality & Prognosis
Farstad, 2001, 26 pts –79% mortality
Gilbert, 2000, successful resus of pt
with central temp of 13.7 C.
K levels >10, pH<6.5 & low PaO2 are
poor prognostic indicators.
Prognosis worsens in pts with
asphyxia

7. Cardiovascular system
Initial tachycardia, then bradycardia.
Pulse decreases by 50% at 28 C.
Bradycardia is due to decreased
spontaneous depolarization of
pacemaker cells (refractory to
Atropine).
Cardiac index and MAP decreased
J waves (Tomaszewkski, 1938)

8. Cardiovascular system
J waves are potentially diagnostic but
not prognostic.
Appear at temps below 32 C.
Size of J wave does increase with temp
decrease.
Normally upright in aVL, aVF and L
praecordial leads.
May be result of hypothermic ion flux
alterations, with delayed depol or
repol of LV wall.

10. Cardiovascular system
All atrial and ventricular dysrrhythmias
are common.
As hypothermia worsens, first the PR
interval, then QRS interval and finally
the QT interval becomes prolonged.
Sinus rhythm and junctional rhythms
are common.
AF often occurs at temps below 32 C.
This usually converts spontaneously
during rewarmingbut mesenteric
emboli are a hazard.

11. Cardiovascular system
Asystole and VF occur spontaneously
at core temps below 25 C.
Decrease in transmembrane RP occurs
which decreases the ventricular
dysrrhythmia threshold.
A cold heart has a large dispersion of
repolarization which facilitates the
development of a conduction delay.
The AP is also prolonged.

12. The CNS
Cerebral depression
6-7% decrease in metabolism for each
1 C decline in temperature.

13. Renal System
Cold diuresisregardless of state of
hydration.
Temps of 27-30 C: only 50% renal blood
flow.
Cold diuresis is GF which doesn’t clear
nitrogenous waste products.
Initial relative central hypervolaemia due
to peripheral vasoconstriction,cold
diuresis helps to decrease the
vasoconstriction-induced capacitance
vessel overload.
Oxidative tubular activity depressed–
decreased Na and water resorption.
Can render pt hypovolaemic.

14. Respiratory System
Initial stimulation of respiration.
Progressive decrease in resp. minute volume
which is proportional to the drop in
metabolism.
CO2 production decreases.
Also CO2 retention and respiratory acidosis
can occur.
Viscous brochorrhea, decreased ciliary
motility, noncardiogenic pulmonary oedema.
Oxy-Hbcurve shifted to left.

15. Haematological Changes
Coagulation cascade impaired.
Plasma fibrinolytic activity is enhanced.
Induces thrombocytopenia
–Hepatic and splenic
sequestration
–Increased bleeding time
Reversed by rewarming
Abnormal platelet aggregation
–Surface molecule expression
reduced
Volume depletion –haemoconcentration –increased
blood viscosity –thrombosis.
Hessell EA, et al. J Surg Res 1980;
28:23-4

16. Acid-Base Balance
Lactic acidosisdue to decreased
peripheral perfusion with
compensatory respiratory alkalosis.
Respiratory depression–respiratory
acidosis.
Reduced enzyme kinetics

17. Endocrine System
Initial hyperglycaemia(inhibition of
insulin release and decreased use of
insulin peripherally).
ACTH and TSH increased.
Elevated catecholamines and cortisol.

18. Drug metabolism
Mild hypothermia decreases the
metabolism of most drugs
Propofol---during constant infusion,
plasma conc. is 30 percent greater than
normal
Atracurium--a 3 ℃reduction in core
temp. increase the duration of muscle
relaxation by 60 percent
Significantly prolongs the postoperative
recovery period

19. Thermal comfort
Patients feel coldin postoperative
period, sometimes rating it worse than
surgical pain
Shivering occurs in ~40 percent of
unwarmed patients who are recovery
from GA

20. Septicaemia and
Hypothermia
Host defences are compromisedand
there is a predisposition to infection.
Usual signs of infection including fever
are absent.
Decreased BM release and circulation
of neutrophils. Impaired neutrophil
migration and bacterial phagocytosis.
Role of antibiotic prophylaxis in adults
is not clear.
Elderly patients with thermoregulatory
failure have a high mortality and
should be considered to be septic.

21. Severe hypothermia
Hypothermia to < 30
o
C cuse many serious SE
It decreases perfusion and oxygenation by:
Impairingmyocardial contractility; reducing
CO; and dysrhythmia (Steen PA, 1980/Bjornstad
H, 1993)
Peripheral vasoconstriction;
Increasing blood viscosity (Poulos ND, 1991)
Shifting the O2 dissociation curve to the left.
(This can lead to renal failure, pulmonary
oedema, metabolic acidosis and inadequate
cerebral blood flow)

22. Severe hypothermia
Impairs clotting (Rohrer MJ, 1992)
Depresses the immune system,
(van Rijen EA, 1997)
Disrupts serum potassium
homeostasis, (Sprung J, 1991)
Alters acid base balance, (Alfaro V,
1996)
Hypoglycaemia (Tashima CK , 1973)

23. Potential Adverse Effects of
Hypothermia in Neonates
Hypertension
Cardiac arrhythmia
Persistent acidosis
Increased oxygen consumption
Increased blood viscosity
Reduction in platelet count
Pulmonary hemorrhage
Sepsis
Necrotizing enterocolitis

24. Hypothermia in the Elderly
Body temperature must decrease to a lower
levelin the elderly before vasoconstriction or
shivering is triggered.
Lasts longerthan it does in young patients.
Recoveryfrom even mild hypothermia is
prolonged in the elderly because their lower
metabolic rate produces less heat

25. Hypothermia in the
Elderly
May exacerbate the decreased
clearance of drugsin the elderly,
accompanied by a decreased MAC in
the elderly
Associated with an increased risk of
perioperative myocardial infarction.

26. Investigations
FBC, U&E, Glucose, ABG, B/Cs and
consider TFTs.
The Hct is high due to decreased
plasma volume.
Normal WCC doesn’t exclude infection.
Hypothermia enhances the cardiac
toxicity and obscures ECG changes of
hyperkalaemia.
Hypokalaemia is most common with
chronic hypothermia.

27. Investigations
Serum enzymes are elevated –
rhabdomyolysis is commonly
associated with cold exposure.
Leucopaenia and thrombocytopaenia
usually reverse with rewarming.
ECG
X-rays and other investigations
according to clinical scenario.

28. Epidemiology
40-60% after volatile anesthetics
33% during epidural anesthesia
Young male adult, rare in elder (age impairs
thermoregulatory control)
Length of anesthesiaor surgery
Peri-op rewarmingprocedure: if not
Mild hypothermia
–The more serioushypothermia, the higher
the probability
Anesthetic used
–Less common with propofol; more with
halogenated agent, pentothal

29. Prevention
Limit internal redistribution (Skin surface
rewarming with forced-air warmerfor 30
minutes )
Increase heat content by generating
endogenous production
Limit radiation and convection on skin
Room temperature > 23
o
C if the op field is
large
IV solution rewarming
Respiratory path
Active heat transfer

30. Rewarming
Passive vs. Active
Active : external or internal

31. Passive External Warming
No added heat, non invasive
Treatment of choice for mild
hypothermia.
Keep ambient temp >25 C.
Keep head covered –30% of body heat
can be lost via the head.
Rewarming rates vary between 0.5-2.0
C/hr.

32. Indications for Active
Rewarming
CVS instability
Moderate or severe hypothermia (<32
C).
Inadequate rate or failure to rewarm.
Endocrine insufficiency
Traumatic or toxological peripheral
vasodilation.
Secondary hypothermia impairing
thermoregulation.

33. Active Internal
Rewarming
1.Humidified, heated oxygen
Via face mask or ETT, not exceed 40 C.
2. Warmed IV fluids
3. Peritoneal Lavage
Infuse 1L of warmed balanced salt, solution for one min and then
drain.
Fluid rates of 10-12L/hr are possible. Exacerbates hypokalaemia.
4. Pleural Lavage
Preferably left side, Infuse 1L warmed N/S for 1 min and then drain, Can
use one tube anteriorly in 2
nd
or
3
rd
ICS MCL and second tube in PALat 5
th
to 6
th
ICS.

34. 5-Diathermy
Restores body heat by ultrasonic waves, microwaves or
shortwaves.
Involves the conversion of energy waves into heat.
Noninvasive way to deliver heat to core tissues.
6-Extracorporeal Blood Warming
CPB: major advantage is preservation of flow if mechanical
cardiac activity is lost during rewarming.
VVR: blood removed from CVP, heated to 40 C and returned via
second CVP or large peripheral venous catheter.
Haemodialysis: portable and efficient. Consider in electrolyte
abns, RF or intoxication with a dialysable substance.

35. Intravenous fluids
1L of IV fluids at ambient
temperature or 1 unit of
refrigerated blood decreases the
mean body temperature 0.25 ℃
Heating fluids to near 37 ℃helps
prevent hypothermia and is
appropriate if large volumes are
being given

36. The intensity of shivering
(grades)
Crossley et al:
0=no shivering,
1= piloerection or peripheral vasoconstriction
but no visible shivering,
2 =muscular activity in only one muscle
group,
3=muscular activity in more than one muscle
groupbut not generalized shivering,
4=shivering involving the whole body. Only
patients who developed (Grade 3 or 4
shivering in recovery room for at least 3 min
were be treated).
Anaesthesia 1994; 49: 205–7.

37. Management
Mainstay of
treatment of
postoperative
shivering is
pharmacological

38. Meperidine
Wrench et al, suggested that the minimal
effective dose of meperidine for treating PS
is approximately 0.35 mg/kg.
Anaesthesia 1997; 52:32–6.
The anti-shivering effect is minimally
impaired by small-dose naloxone, which
blocks most mu-receptors, and is diminished
by large-dose naloxone, which blocks both
mu-and k-receptors . Suggest that k-opioid
receptors may play a more important role .
Anesthesiology 1993; 79:1193-1201.
 Decrease shivering threshold twice as
vasoconstriction threshold
 Monoamine reuptake inhibition
 NMDA receptor antagonist
 Stimulation of ą2 adrenoceptors

39. Meperidine( Demoral)
Sweating
Vasoconstriction
Shivering threshold
The side effects of sedation
and respiratory depression,
which may be induced with
previously administered
opioids or anesthetics.

40. Morphine, Fentanyl,
Sufentanil and Alfentanil.
Meperidine is more effective
in treating shivering than
equianalgesic doses of mu-
receptor agonists, such as
morphine, fentanyl,
sufentanil and alfentanil .
Anesthesiology 1998; 89: 43–8.
Br J Anaesth 1997; 79: 541–2
Acta Anaesthesiol Scand 1984; 28:138–43.

41. Nalbuphine
Both nalbuphine and meperidine
provide a similar rapid and potent anti-
shivering effect. Nalbuphine may be
an alternative to meperidine for
treating postanesthetic shivering.
Anesth Analg. 1999 Mar;88(3):686-9.

42. Tramadol
Chan et al,IV tramadol (0.25 mg/kg) effectively
controlled shivering during cesarean delivery under
regional anesthesia with minimal side effects, however,
he reported that, increasing the tramadol dose to 0.5
mg/kg did not increase its therapeutic effect.
Can J Anaesth 1999; 46: 253–8.
Trekova et al,showed that tramadol at 1-2 mg/kg
arrested completely the postoperative trembling or cut
significantly its intensity in 98% patients and reported
no valuable changes in arterial pressure or cardiac beat
rate.
Anesteziol Reanimatol. 2004 Sep-Oct ;( 5):86-9.
De Witte et al,who assessed the effects of different
doses of tramadol on shivering after general
anesthesia, reported that Tramadol 1 mg.kg-1 or more
abolished shivering completely 5 min after treatment in
all patients.
Acta Anaesthesiol Scand 1997; 41: 506–10.

43. α2-Adrenergic Agonists
Clonidine 1.5 0r 3µg/kg, bolus injection, stop
shivering within 5 mins.
Clonidine 75μg
–lower the threshold of cutaneous vasoconstriction
and shivering by 0.5
o
C
–Bolus & perfusion:
–At the end of op: 1.5 or 3μg/kg
–Cardiac surgery: 200 to 300μg
As premedication :with clonidine 200-300 µg;
with dexmedetomidine 2.5 µg/kg ,reduced
postop shivering

44. α2-Adrenergic Agonists
Delaunay et al,showed that clonidine
reduced the thermoregulatory
thresholds for both vasoconstriction
and shivering. This suggests that it
acts by impairing central
thermoregulatory control. However,
clonidine is associated with side
effects such as bradycardia,
hypotension, and sedation.
Anesthesiology 1993; 79: 470–4.

45. Dexmedetomidine
Intraoperative intravenously
administration of dexmedetomidine 1
microg kg-1 reduces postanaesthetic
shivering as does meperidine 0.5 mg
kg -1 in patients after major surgery.
Eur J Anaesthesiol. 2006 Feb;23(2):149-53.

46. ketamine
Dal et al,ketamine can be an alternative
prophylaxis against postoperative
shivering in patients with bradycardia,
hypotension, respiratory depression,
nausea, vomiting and allergic reactions
to pethidine.
British Journal of Anaesthesia 2005
95(2):189-192

47. ketamine
Competitive NMDA receptor antagonist, also
inhibits postoperative shivering. It is likely
that NMDA receptor antagonists modulate
thermoregulation at a number of levels.
Opioid agonist, blocking amine uptake in the
descending inhibitory monoaminergic pain
pathways, having a local anaesthetic action
and interacting with muscarinic receptors.
Therefore it probably controls shivering by
non-shivering thermogenesis either by action
on the hypothalamus or by the ß-adrenergic
effect of norepinephrine.Anesthesiology2002; 96:
467–84

48. Ondansetron
Powell et al,ondansetron 8 mg given
before the induction of anesthesia,
reduces the incidence of PAS in adults.
Lack of hemodynamic side effects .
Anesth Analg 2000;90:1423-1427

49. Ondansetron
Specific inhibition of the 5-HT3 system,
therefore, produced a dose-dependent
reduction in shivering, being statistically
significant at the larger dose. Perhaps 5-HT3
inhibition has a specific antishivering effect .
The PAS effect of ondansetron is independent
of intraoperative core hypothermia,
suggesting that it inhibits thermoregulatory
responses by a central mechanism.
Guyton AC, ed. Textbook of medical physiology. 6th ed.
Philadelphia:WB Saunders, 1991:886–98.

50. Intrathecal fentanyl for prevention
of shivering in cesarean section.
The addition of 20 microg fentanyl
intrathecally can reduce the incidence
and severity of intraoperative and
postoperative shivering after spinal
anesthesia for patients who were
receiving cesarean section without
increasing other side effects.
J Med Assoc Thai. 2005 Sep;88(9):1214-21.

51. Intrathecal meperidine decreases
shivering during cesarean delivery under
spinal anesthesia.
intrathecal meperidine (0.2 mg/kg)
decreases the incidence and intensity
of shivering after spinal anesthesia for
cesarean delivery.
Anesth Analg. 2004 Jan;98(1):230-4

52. Other drugs
NMDA receptor antagonist:
Ketamine
Magnesium sulfate 30mg/kg
Methylphenidate 20mg
Analeptic agent, block reuptake of 5-HT
Physostigmine 0.04mg/kg
Central acting cholinesterase inhibitorAnesthesiology 1998;88:108–13.[
Doxapram 100mg or 1.5mg/kg
Respiratory stimulant, central action on pons
Anaesthesia 1991;46:460–1
–Recovery of the descending inhibitor control of the
supraspinal effecting centers

53. Dexamethasone decreases the incidence of
shivering after cardiac surgery: a randomized,
double-blind, placebo-controlled study.
Dexamethasone is effective in decreasing
the incidence of shivering. The effectiveness
of dexamethasone is independent of
temperature and duration of
cardiopulmonary bypass. Shivering after
cardiac surgery may be part of the febrile
response that occurs after release of
cytokines during cardiopulmonary bypass.
Anesth Analg. 1998 Oct;87(4):795-9

54. Dexmedetomidine for the
treatment of postanesthesia
shivering in children.
This study demonstrates the efficacy
of dexmedetomidine in the treatment
of postanesthesia shivering.
Paediatr Anaesth. 2007 Apr;17(4):341-6

56. Neuroprotection Defined
“Protection implies improved
outcome as evidenced by
electrophysiologic, metabolic, or
histologic indexes of recovery or,
ultimately, by improved clinicalrecovery.”
Cucchiara, Black, Michenfelder. Clinical Neuroanesthesia,
2nd Ed. Churchill Livingstone, 1998; p 200.

57. Potential Mechanisms of Action
of Hypothermia (Cerebral
Protection)
Reduces cerebral metabolism
Preserves ATP levels
Decreases energy utilization
Suppresses Excitotoxic AA accumulation
Reduces NO synthase activity (Thoresen M, 1997)
Suppresses free radical activity
Inhibits apoptosis
Prolongs therapeutic window.
Less mitochondrial dysfunction.
Increased concentration of brain-derived neurotropic
factor.
Less DNA injury

58. I
s
c
h
e
m
i
c
C
a
s
c
a
d
e
Clinical Neuroanesthesia, 2nd Ed. Churchill Livingstone, 1998; p 184.

59. Cerebral Protection
Animal Data
Hypothermia is neuroprotectivein
models of stroke, traumatic brain injury,
global brain ischemia
–Primate, dog, cat, rodent
–Also protective in tissue culture model,
suggesting direct protective effect
Protective in various models of perinatal
asphyxia

60. Cerebral Protection
Animal Data
In 7day old rat
,
hypothermia for a period as
short as 3hours after hypoxia-ischaemiahad
some neuroprotective effect, and histological
differencesbetween treatment and control
brains could still be detected 6weeks later.
Thoresen M. Posthypoxic cooling of neonatal rats provides
protection against brain injury. Arch Dis Child 1996
In newborn piglets, 3hours ofcooling exerted
only a modest neuroprotective effect and there
was no protection at all in more severely
injured animals
Haaland K . Posthypoxic hypothermia in newborn piglets.
Pediatr Res 1997

61. Animal Data –What does
it tell us?
Hypothermia (32 –34
o
C) is sufficient
–28 –32
o
C used in cardiac surgery, but increases
complications
Early initiation (within 6 hours) post brain
injury is critical
Short duration (<12 hours) appears to delay
rather than prevent injury
–48 hours better in some models; complications
increase if go beyond 72 hours
Active rewarming reduces effectiveness

62. Therapeutic Hypothermia
(Human)
1
st
reported use of therapeutic
hypothermia in TBI in 1943.
1
st
reported use as a protective
adjunct to neurosurgery in 1955.

63. Therapeutic Hypothermia
(Human)
Abandoned from common practice in
70’s-80’s d/t associated complications.
Revived interest in 90’s after multiple
animal studies showed neuroprotective
benefit w/ even mild hypothermia.

64. Cerebral Protection
(Human)
Neurological deficit and mortality is
reducedwhen mild to moderate
hypothermia is induce within 6 to 24
hours following head injury, cardiac
arrest, and stroke, and maintained for
24 to 48 hours.
The detrimental effect of hyperthermia
in patients with cerebral ischemia has
been well documented,and should be
treated aggressively.

65. Modest Hypothermia as a
Neuroprotective Strategy
Two multicenter randomized studiesevaluating
hypothermia as a neuroprotective strategy have
been conducted
1) The first utilizing selective hypothermia has
been completed *.
No difference between hypothermia and controls
for all patients were observed.
2) For infant with moderate encephalopathy
(aEEG determined) more cooled versus control
infants i.e. 52% versus 34% (p=0.02) had a
favorable outcome. In addition the cooled versus
control infants were less likely to be severely
affected i.e. 11% versus 28% (p=0.03) respectively
Gluckman et al Pediatr Res 2004

66. Stroke?
Schwab S, et al. Moderate Hypothermia
in the Treatment of Patients with
Severe Middle Cerebral Artery
Infarction.Stroke 1998;29:2461-6.
Krieger DW, et al.Cooling for Acute
Ischemic Brain Damage (COOL AID) An
Open Pilot Study of Induced
Hypothermia in Acute Ischemic Stroke.
Stroke 2001;32:1847-1854.

67. Effect of Mild Hypothermia on
Uncontrollable Intracranial Hypertension
after Severe Head Injury
Mild hypothermia is a safe & effective
method to control traumatic
intracranial hypertension
to improve M&M rates.
Osaka, Japan
J Neurosurg 79:363-368, 1993.

68. Treatment of Traumatic Brain
Injury with Moderate Hypothermia
Treatment with moderate hypothermia
for 24 hours in patients with severe
traumatic brain injury and coma scores
of 5 to 7 on admission
hastened neurologic recovery
and may have improved the
outcome.
N Engl J Med 1997;336:540-6

69. A Multicenter Prospective Randomized
Controlled Trial of the Efficacy of Mild
Hypothermia for Severely Head Injured
Patients with Low Intracranial Pressure
Mild hypothermia should not be used
for the treatment of severely head
injured Pts with low ICPbecause this
therapy conveys no advantageover
normothermia in such patients.
J Neurosurg 94:50-54,2001

70. Lack of Effect of Induction of
Hypothermia after Acute Brain
Injury
Treatment with hypothermia, with the
body temperature reaching 33 C
within eight hours after injury, is not
effective in improving outcomes in
patients with severe brain injury.
N Engl J Med 2001;344:556-63.

71. Hypothermia in Trauma
Meta-analysis of 12 clinical trials found
nosignificant benefitand increased risk
of pneumonia(Cochrane Database Syst Rev 2004;
(4):CD001408)
Reanalysis of multi-institutional trial
noted significant benefit in patients
<45yowho were hypothermic on
admission(NNT 4).(Cochrane Database Syst Rev
2004; (4):CD001408)

72. Mild Intraoperative Hypothermia during
Surgery for Intracranial Aneurysm
Intraoperative hypothermia did not
improve the neurologic outcomeafter
craniotomy among good-grade
patients with aneurysmal subarachnoid
hemorrhage.
N Engl J Med 2005;352: 135-45.

73. Hypothermia in neonate
Current evidence is inadequateto
assess either safety or efficacy of
therapeutic hypothermia in newborn
infants with HIE, this should be further
evaluated in well designed RCT.

74. Evidence Summary

75. Evidence Summary
May have a role in neuroprotection in cases of
refractory elevated ICP or cardiac arrest.
Likely result in an increase in complications.
Not necessary for
neuroprotection in CABG
or aneurysmal SAH surgery.
May have a neuroprotective role in certain Pts
after head trauma, however methods of
therapy remain unclear.

76. Future Directions
Regional hypothermia: local brain
cooling.
Utilize neuroprotective benefits &
limits systemic complications.
Focal cooling probes (neurosurgery) &
helmets (stroke & head injury).

77. Myocardial Protection
The primary advantage of cold cardioplegia is
to lower myocardial oxygen demands and the
rate and development of ischemic damage
when blood supply must be interrupted to
provide the technical advantages of a quiet dry
operative field, or becomes maldistributed due
to coronary obstruction or retrograde routes of
administration (right ventricular ischemia).

78. MYOCARDIAL
PROTECTION GENERAL
Hypothermiaisthefirsttriedmethodformyocardial
protection.Hufnagelusedicedslushin1961.
Primaryeffectsofhypothermia
1)Heartratefalls.
2)Vascularresistanceincreases.
3)Bloodpressurefalls
4)Oxygenconsumptionfalls.
5)Bloodpropertieschange
-Increasedviscosity,Hb-O2affinity,gassolubility
6)Changesinpatternsofsubstratemetabolism
7)Reducedrateofphysicalbiochemicalreaction
8)Decreasedmembranefluidity
9)Waterbecomesviscous,lessionized,andundergoes
conformationalchange

79. Secondary effects of
hypothermia
 1)Impairedperfusion
 2)Metabolicacidosis
 3)Tissuehypoperfusionandhypoxia
 4)Shiftinacidbasebalance
 5)Alteredmetabolism
 6)Depressedmetabolism
 7)ReductionofenergyO2demand
 8)Decreasedenergyproduction
 9)Decreasedfunctionofmembraneboundenzymes
 10)Failureofionichomeostasis
 11)Cellswelling
 12)Improvedmembraneprotection
 13)Depressedmetabolism
 14)Alkalineshiftinneutrality
 15)Iceformation

80. Common pitfalls of cooling technique
1)Insufficientcoldcardioplegicsolutiondeliveredtothe
myocardium
2)Cardioplegicsolutionnotcoldenough
3)Excessiveentryofwarmbloodintothecoldheart
4)Excessiveheartgainfromtheenvironment
5)Airembolismduringreinfusionofcardioplegicsolution
6)Ineffectivetopicalcoolingbecausetheirrigatingfluid
is
 notcoldenough,the flowratetoolowor
distribution
 overtheheartuneven
7)Myocardialtemperaturenotmonitored
8)Coldinjuryduetoice-slush
9)Arterialpressuretoolowduringreperfusion

81. Prospective Randomized Trial of Normothermic
v. Hypothermic Cardiopulmonary Bypass on
Cognitive Function after CABG Surgery
Hypothermic CPB does not provide
additional central nervous system
protection in adult cardiac surgical
patients who were maintained
at either 30 or 35°C during CPB.
Anesthesiology 2001; 95:1110–9.

82. Induced Hypothermia
Post resuscitation measure for RoSC
after cardiac arrest
Cooling to 32-34 deg C x 12-24 hrs
Pts that remain unconscious
Out of hospital VF
Improved survival and neurologic
outcomes
More studies needed for broader
applications

83. Treatment of Comatose Survivors
of out-of-Hospital Cardiac Arrest
with Induced Hypothermia
Outcome Hypothermia Normothermia
(n=43) (n=34)
Normal 15 7*
Moderate Disability 6 2
Severe Disability 0 2
Death 22 23
P=.04 Unadjusted odds ratio for good outcome 2.65( CI,1.02
to 6.88)

84. Figure 1. Cooling Device Used in the Hypothermia after Cardiac Arrest Study,
W hich Operates by Circulating Cool Air over the Patient.

85. Case report
Case report from dept of Cardiothoracic
surgery, University Hospital Ostrava, Czech
Republic –successful resus of 26yr old
male, found 15 hours after a suicide
attempt (carbamazepine OD) in deep
hypothermia of 19 Cwith circulatory
arrest. ECC was used to rewarm pt –
pt showed no neurological deficit at
time of discharge from hospital.

86. CPR in hypothermic
patient
CPR –chest wall elasticity and pulmonary
compliance are decreased with cold so more
force is needed to depress the chest wall.
Concern that in the severely hypothermic pt,
cardioactive medications can accumulate to
toxic levels in peripheral circulation if given
repeatedly.Withhold IV drugs if core temp
<30 C. If temp >30 C administer IV meds
with increased intervals between doses.

87. Mild Therapeutic Hypothermia to
Improve the Neurologic Outcome after
Cardiac Arrest
In patients who have been
successfully resuscitated after cardiac
arrest due to ventricular fibrillation,
therapeutic mild hypothermia
increased the rate of a favorable
neurologic outcome and reduced
mortality.
N Engl J Med 2002;346:549-56. 2002 –
Vienna, Austria

88. Mild Therapeutic Hypothermia to Improve
Neurologic Outcome after Cardiac Arrest
Outcome a HypothermiaNormothermi
Good Outcome
Death
75/136(55%)
56/137(41%)
54/137(39%)
76/138(55%)
NEJM 2002;346:549

89. Hypothermia Questions
Cool how quickly?
–ASAP, but at least within 6 hours of event
–Longer the delay, the longer hypothermia must be
continued to provide protection
How cold?
–At least 35
o
C core temperature but not lower than
32
o
C
How to cool? Use NSAID?
–Blanket cooling not effective in adults;
intravascular cooling with bolus of iced RL or NS is
promising
–Selective head cooling may benefit neonates

90. Hypothermia Questions
How long to cool?
–At least 12 hours; 24 hours probably better
How to rewarm?
–Worse outcome if rewarm rapidly
–Management of shivering/stress response?
Which patients should be cooled?
–Lack clear outcome predictors in children (eg, aEEG)
–Only comatose children after ROSC who are
“hemodynamically stable”
–Should cooling start in the field or at the referring hospital?

91. Hypothermia Questions
How to monitor cooling?
–Bladder, rectal or blood temperature? Brain
temperature?
How should we manage shivering?
–If use NMB, need to monitor EEG
–Electroencephalographic seizures may be more
common than clinically recognized –should we load
with anticonvulsants?
How to adjust medications in HT patient
Are there useful biomarkers?

92. Conclusion
Hypothermia remains the most common
cause of postoperative shivering
Hypothermia is associated with
shivering and many complications,
patient should be kept normothermia
Prevention of hypothermia consists of
limiting heat loss and active rewarming
system

93. Conclusions
Skin surface rewarming is less efficient then
medical treatment.
All antishivering drugs except ketanserin have
some analgesic properties in humans,
suggested that pain and thermoregulation are
tightly connected
No single structure or pathway is responsible
for the shivering response

94. References
Jan De Witte,M.D.,Eaniel l. Sessler,M.D.:
Periooperative Shivering -physiology and
pharmacology.Anesthesiology 2002;96:467 -84
D.J.Buggy and A.W.A.
Crossley:Thermoregulation,mild perioperative
hypothermia and post-anaesthetic shivering.
British Journal of Anaesthesia 2000;84(5):615-
28
Pascal Alfonsi:Postanaesthetic Shivering
Epidemiology,Pathophysiology,and
Approaches to Prevention and
Management.Drugs 2001;61(15):2193 -2205
Peter MD; Sessler, Daniel I. MD: Non-
thermoregulatory Shivering in Patients
Recovering from Isoflurane or Desflurane
Anesthesia. Anesthesiology 1998; 89(4): 878-
886

95. Thanks for your attention
Questions??