INHALATIONAL ANAESTHETICS

BY
DR. EZE EZINNE
 LEARNING OBJECTIVES
• To know the different inhalational anesthetic
agents
• Know their mechanism of action
• Know their mode of delivery
• Know their organ system effects
• Know their adverse effects
• Know some select conditions where use is
contraindicated or preferred
 INTRODUCTION
Anaesthesia is a state of controlled, temporary and reversible loss
of sensation +/- awareness (consciousness) that can be
induced for medical purposes.
In general anaesthesia means loss of sensation.
5 neurophysiologic effects are sought after with the induction of
anaesthesia:
• Unconsciousness
• Amnesia
• Analgesia
• Inhibition of autonomic reflexes
• Skeletal muscle relaxation
No one currently available anaesthetic drug can achieve all 5
desired effects well, hence the practice of balanced
anaesthesia.
This is the practice of combining intravenous and inhaled
anaesthetic drugs to take full advantage of the favorable
properties of each while minimizing their adverse effects.
The ideal anaesthetic drug
• Induce rapid smooth loss of consciousness
• Be rapidly reversible
• Possess wide margin of safety
There are volatile liquids and gaseous anaethetics, all of which are
administered by inhalation.
Volatile anaesthetics include – halothane
enflurane
isoflurane
desflurane
sevoflurane
They are liquids at room temperature because they have high boiling
point and low vapor pressure.
Gaseous anaesthetic agents are nitrous oxide and xenon.
They have high vapor pressure and low boiling point hence they are
gases at room temperature.
 MECHANISM OF ACTION
In general anaethetics affect neurons at various cellular
locations.
They act by either strengthening inhibition or diminishing
excitation
Chloride ion, glycine and potassium ion channels are the major
inhibitory ion channels while serotonin, glutamate and
acetylcholine are the major excitatory channels
 PHARMACOKINETICS
Inhaled anaesthetics are taken through gaseous exchange in alveoli of
the lungs.
Alveoli - blood – effector sites in CNS
To achieve anaesthesia the concentration of drugs in the CNS needs to
change rapidly, there are however factors that affect CNS
concentration changes.
These include uptake and distribution factors such as
• inspired concentration and alveolar ventilation
• Solubility of the agent
• Cardiac output
• Alveolar-venous partial pressure difference
• metabolism
• Hyperventilation increases the speed of induction of
anaesthesia with inhaled anaesthetics
• Increase in inspired partial pressure/ concentration
accelerates induction.
• Those that are relatively insoluble in blood and brain are
eliminated faster and recovery quicker
• Increased cardiac output increases blood uptake of
anaesthetic agents with resultant increase in
redistribution and decrease rate of induction of
anaethesia.
Though metabolism doesn’t play a significant role in elimination
of these drugs, however hepatic metabolism may contribute
to elimination and in turn recovery from some of them
especially halothane
Halothane undergoes significant metabolism(40%) during an
average anaesthetic procedure.
Nitrous oxide is not metabolized by human tissue.
 PHARMACODYNAMICS
CNS
Inhaled anaesthetics decrease metabolic activity of the brain
They cause cerebral vasodilation .
Stages of CNS depression
I – analgesia: initially analgesia without amnesia
later both
II – excitement: patient appears delirious, may vocalize,
completely amnesic,
↑ respiratory rate(RR), heart rate (HR) and blood pressure (BP)
this is the light stage and is shortened by rapidly increasing
concentration of the agent.
III – Surgical anaesthesia : slowing of RR and HR
complete cessation of spontaneous
respiration (apnea)
There are four planes of stage III based on ocular movements, eye
reflexes and pupil size which correlate with depth f anaesthesia.
IV – medullary depression: this is the deep stage of anaesthesia
severe CNS depression
depression of medullary vasomotor
& brainstem respiratory centers
Without circulatory and respiratory support death would occur.
CVS
Halothane, isoflurane, desflurane and enflurane (HIDE) depress
normal cardiac contractility.
Sevoflurane, isoflurane and desflurane (SID) produce greater
vasodilation with minimal effect on cardiac output.
These are preferred for patients with impaired myocardial
function.
Nitrous oxide also depresses myocardial function in a
concentration-dependent manner
Inhaled anaesthetics reduce myocardial oxygen consumption
They decrease arterial blood pressure
They increase coronary flow (oxygen supply to the heart is
improved)

RESPIRATORY EFFECTS
All volatile anaesthetics cause varying degrees of
bronchodilation, this makes them suitable for asthmatic
patients and those with active wheezing,
However pungency of some like isoflurane and desflurane cause
airway irritation which may provoke coughing and breath-
holding.
This property makes them unsuitable for use in patients with
bronchospasms.
Halothane and sevoflurane are considered non pungent hence
making them the anaesthetic agents of choice for patients
with airway problems.
Nitrous oxide as well is nonpungent and can be used in patients
with bronchospasms.
Inhalational anaesthetics depress mucocilliary function in the
airway.
With prolonged exposure - mucus pooling and plugging –
atelectasis – post op complications – hypoxaemia – infections.
UTERINE SMOOTH MUSCLE
Nitrous oxide has little effect on the uterine muscles.
Halogenated anaesthetics are potent uterine muscle relaxants.
This makes them suitable for use
- intrauterine fetal manipulation
- manual extraction of retained placenta during delivery.
Can also cause increased uterine bleeding.
 ADVERSE EFFECTS
ACUTE TOXICITY
Nephrotoxicity
Haematotoxicity
Malignant hyperthermia
Hepatotoxicity (halothane hepatitis)

CHRONIC TOXICITY
Teratogenicity
carcinogenicity
 The End

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