inhalational agent

1. 1,1,1,-tri fluro-2-bromo-
2chlorethane

2.  Halothane was not chemically inert and
prolonged usage of this agent damage metal
rubber and some plastic component of the
anesthetic circuit
 Halothane is susceptible to spontaneous
oxidation and photochemical
decomposition
Requiring storage in tinted glass bottle (amber
glass bottle) containing 0.01% thymol ( it
renders its stability)

3.  Colorless liquid, relatively pleasant
smell, non irritant , decomposed by
light in to hydrochloric acid (HCL),
hydrobromic acid (Hbr), chloride (CL-),
bromide (Br-).
 Potent with a MAC of 0.75%.
 Carbon fluoride is responsible for non-
flammable and explosive nature.

4. Induction
 The potency and relative lack of irritation
favor the use of halothane for rapid smooth
inhalation induction of anesthesia especially
when it is administered together with 60-70%
N₂O.

5.  Halothane has a relatively low blood gas
solubility coefficient of 2.5 and thus
 Induction of anesthesia is relatively fast in
pediatrics
However it may take at least 30min for the
alveolar concentration to reach 50% of the
inspired conc.
This is slower than for Enflurane or Sevoflurane

6.  As with all volatile anesthetics it is
customary to use the techniques of
administration of a higher partial pressure of
anesthetic (PI) than the alveolar
concentration (PA) (over pressurization)
Induce halothane anesthesia with concentration
2-3× higher than the MAC value .
 The inspired value can be reduced when a
stable level of anesthesia has been achieved.

7.  For halothane MAC is almost
-1.1% in neonate.
-0.9% in infants.
-0.9% at 1-2 years.
-0.75% at 4-5 years.
-0.65% at 80 yrs.

8. • Recovery from halothane is slower
compared to newer drugs( induction is
also slower) because of its higher tissue
gas coefficient
 During awakening after halothane
anesthesia patient remain drowsy for
several hours.
Because of the reactive metabolite bromide
This is due to higher solubility in brain,

9.  The greater solubility of halothane in
those tissues increase the amount of
halothane that accumulate during
anesthesia
 Increase the time it takes to clear
halothane from those compartments
after administration is discontinued
Re-Distribution
Delayed awakening

10. Cardiovascular effects
 Potent direct myocardial depressant effect
 The most prominent circulatory effect of
halothane is dose dependent arterial
hypotension
 Decreased HR and coronary blood flow
 Slow conduction to AV node lead to
Bradycardia

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12.  During controlled ventilation halothane is
associated with dose dependent depression of
COP by decreasing myocardial contractility
(vasodilatation) thus there is reduction of
ABP.

13.  The hypotensive effect of halothane is
augmented by reduction in HR
Antagonism of bradycardia with atropine
usually leads to increased arterial BP
 The reduction in myocardial
contractility and low HR leads to
reduction in myocardial oxygen demand
and coronary blood flow
So halothane is advantageous in patients
with coronary artery disease.
Because of reduced oxygen demand
caused by low HR and decreased

14. • The depressant effect of halothane on
COP is aggravated in the presence of β-
blocker
• Inadequate anesthesia or exogenous
administration of CA’s increases
myocardial sensitization leading to
myocardial dysarrythmia and also cardiac
arrest
• During local infiltration with adrenaline
containing local anesthetic, caution
should be taken

15. -Over dosage of halothane causes
bradycardia and hypotension ,so
treat with atropine and
discontinue halothane.
Guidelines
Avoid hypoxemia and hypercapnia
Avoid concentration of adrenaline
greater than 1:100,000
Avoid a dosage in adults exceeding
10ml of 1:100,000 adrenaline in
10 min. or 30ml/hr.

16. Respiratory Effects
 Alveolar hypoventilation
(hypoxia) and arterial
hypercapnia occurs in a dose
dependent manner during
halothane anesthesia in a
spontaneously breathing patient
so patient breathing should be
assisted or controlled.

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18. • Non irritant, pleasant to breath during
induction of anesthesia
• The respiratory pattern associated with
halothane anesthesia is characterized by rapid
shallow respiration.

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20.  In awake individual hypercapnia
does not occur because even
small increase in arterial CO₂
stimulates the respiratory drive to
increase minute ventilation.
 Halothane and other volatile
anesthetics abolish physiologic
mechanism that protect against
hypercapnia

21.  Rapid loss of pharyngeal and laryngeal
reflexes might lead to risk of aspiration.
 Inhibition of salivary and bronchial secretion.

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23.  PaCO₂ increases as the depth of
anesthesia increases and patient
becomes hypoxic(PaCO2 increase
PaO₂ decrease)
 Decrease in mucociliary function
which may persist several hours
after halothane anesthesia.
This may contribute to post op.
hypoxia and atelectasis

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25. CNS
 Cerebral vasodilatation
 Increase CBF
 Increase ICP

26. Other systems
 Potentiate action of NDMR by
direct relaxation of skeletal
muscle.
 Trigger malignant hyperthermia.
 Post op. shivering is common in
old age (this increase O₂
requirement ⇒300% and result in
hypoxemia unless O₂ is

27.  GI motility is inhibited – paralytic illus
 PONV are seldom severe.
 Decrease HBF this is proportional to COP.
 Hepatic artery vasoconstriction

28. Biotransformation
 Major route of elimination is lung 80%
 10-20% is bio-transformed in the liver
 Small amount diffuse out through skin

29.  Hepatic biotransformation occurs
through the cytochrome P450
system resulting in the release of
bromide and chloride ion and the
formation of fluorine containing
compounds mostly trifluoroacetic
acid
 Many believe that the hepatic
complication of halothane results
from its biotransformation

30. Emergence
 Awakening is prompt but may take several
hours because of higher solubility of
halothane in brain, muscle, fat increase
accumulation
 Clearing time is increased after
discontinuation
 PONV

31. Halothane hepatitis
 Defined as the appearance of liver damage
within 28 days of halothane exposure in a
person in whom other known causes of liver
disease have been excluded.
 Approximately 20% of halothane is
metabolized in liver by the oxidative pathway,
the end product excreted in urine.

32.  The major metabolites are
bromine, chlorine, trifluoroacetic
acid and trifluoroacetyl-ethanol
amide.
 A small proportion of halothane
may undergo reductive
metabolism, particularly in the
presence of hypoxemia and when
the hepatic microsomal enzymes
has been stimulated by enzyme
inducing agents such as
phenobarbitone

33.  Reductive metabolism may result
in the formation of reactive
metabolite
 Chlorine when absorbed or contact
with dry soda lime and will get
broken down to BCDFE (2-bromo-2-
chloro-1,1-difluoroethene) which
has organ toxicity in animal models
Halothane hepatitis
 The product of reductive
metabolic pathway are more toxic
than those produced by oxidative
pathway.

34.  In mild cases halothane increase enzyme of
liver, but in several cases halothane hepatitis
and liver necrosis
 Incidence is 1:35,000

35.  This is supported by the fact that
the risk of post operative liver
dysfunction is increased in the
presence of
Obesity which increase hypoxia and
greater storage of halothane
Hypoxemia
A short interval b/n administrations
of
the drug
Enzyme induction produced by
drugs e.g.- phenobarbitone,
phenytoin

36. • The incidence of hepatic toxicity
is high in obese middle age
women but less in pediatric
(halothane is the drug of choice in
pediatrics)
• As a result of this concern the
committee on safety of medicine
has made the following
recommendations in respect
halothane.

37. 1. A careful anesthetic history
should be taken to determine
previous exposure and any
previous reaction to halothane.
2. Repeated exposure to halothane
with in a period of three months
should be avoided unless there
are over riding clinical conditions.
3. A history of jaundice or pyrexia
after previous exposure to
halothane is an absolute C/I to its
future use in that patient.

38. Precaution
• Space occupying lesion
• Pheochromocytoma
• MHT
• History of PPH,APH, hypovolaemic
• Unexplained liver dysfunction

39. Indication
• Induction of anesthesia in children
• Maintenance of anesthesia
• In air way obstructions

40. Advantage Disadvantage
-rapid and smooth
induction
-poor analgesia
-effective in low
conc.
-CA’s induced
arrhythmia
-Minimal stimulation
of salivary and
bronchial secretions
-post op. shivering
-bronchodilation -liver toxicity
-Muscle relaxation -slow recovery
-relative rapid
recovery, cheap
-Halothane hepatitis
-less stable

41. • Dose – induction-2-3% in adult
-1-2% child
- maintenance-0.8%-1.5%

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