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General Anesthetics

GENERAL ANESTHETICS Anesthetic Potency of Inhaled General Anesthetic:


Anesthesia – denotes a lose of sensibility -is defined quantitatively as the minimum alveolar concentration. (MAC)
which is the concentration of anesthetic gas needed to eliminate movement
Surgical Anesthesia – is a controlled degree of CNS among 50% of patients challenge to a noxious stimulus. The more potent
depression with the following component an anesthetic, the lower its value for MAC.
Properties of Modern inhalational Anesthetics
• Analgesia – lack of pain
• Amnesia – lack of memory MAC % atm Blood/gas solubility coefficient
• Inhibition from reflexes such as bradycardia and
A. GAS 0.43 – 0.47
laryngospasm 110 or 105
Nitrous Oxide
• Skeletal muscle relaxation
• (altered state consciousness) state of unconsciousness. B. Halogenated gases (volatile)
Depth of Surgical Anesthesia – can be divided into a series
of four sequential stages: 1. Halothane 2.3 – 2.4
Depth of Surgical Anesthesia – can be divided into a series 0.75 – 0.77
Stage I: Analgesia of four sequential stages: 1.68 1.9
Loss of pain sensation results from interference. With sensory transmission 2. Enflurane
Stage
in the I:spinothalamic
Analgesia tract. The patient is conscious and conversational. A 1.15 1.4
Loss of pain sensation results from interference. With sensory transmission
reduced awareness of pain occurs as stage II is approached. 3. Isoflurane
in the spinothalamic tract. The patient is conscious and conversational. A
0.16 12
reduced awareness of pain occurs as stage II is approached. 4. Methoxyflurane
Stage II: Excitement
The patient experience delirium and violent combative behaviour. There is a Comparison of the different Pharmacologic effects of Inhaled
Stage II: Excitement
rise and
The irregularity
patient in blood
experience pressure.
delirium Thecombative
and violent respiratorybehaviour.
rate may be increase
There is a General Anesthetics
rise and irregularity in blood pressure. The respiratory rate may be increase General Cardiac Sensitization
Stage III: Surgical anesthesia Anesthetic Effects of Myocardium to BP Respiration
Regular
Stage III:respiration and relaxation of the skeletal muscle occur in this stage.
Surgical anesthesia Actions of
Eye reflexes
Regular decreases
respiration progressively,
and relaxation of the until themuscle
skeletal eye movements cease
occur in this stage.and Epinephrine
the pupil
Eye is fixed.
reflexes Surgery
decreases may proceeduntil
progressively, during
the this
eye stage.
movements cease and
1. Halothane slows heart Increases  B.P Rapid/shallow
the pupilIV:
Stage is Medullary
fixed. Surgery may proceed during this stage.
paralysis rate due to sensitization of Dose resp ventilatory
Severe
Stage
Two IV: depression
Medullary
Kinds of Anesthetics
the resp. center & vasomotor center. Death can
paralysis
General reduction of myocardium esp dependent depression
rapidly ensure.
Severe depression of the resp. center & vasomotor center. Death can cardiac to adrenergic
Sympathetic agonist, cardiac
TwoA.Kinds
Inhalational
rapidly ensure.
of General Anesthetics activity dis, hypoxia and
B. Intravenous
A. Inhalational B. Intravenous cardiac electrolyte
output is  imbalance –may
Inhalational Gen Anesthetics Induce ventricular
arrhythmias
1. N2O (Nitrous oxide) – laughing gas Comparison of the different Pharmacologic effects of Inhaled
2. Halothane 2. Enflurane
No Brady Lower incidence  B.P Dose-dependent
General Anesthetics
cardia, No  of arrhythmias resp depression
3. Enflurane
General in C.O
Cardiac and less
Sensitization Causes
4. Isoflurane sensitization to to bronchodilatation
Anesthetic Effects of Myocardium BP Respiration
5. Methyoxyflurane the myocardium
Actions of
6. Diethyl ether toEpinephrine
catecholamines
Newer Inhalational General Anesthetics
Never Inhalational Gen Anesthetics
1. Desflurane 2. Seroflurane 3. Isoflurane Causes direct does not cause  B.P - Significant
Mechanism of Action of Inhalational General Anesthetics coronary sensitization of resp
1. Desflurane
MechanismTheseofagents
Action of Inhalational
decrease General
the firing Anesthetics
rate of nerve cells by vascular myocardium rarely Depression
2. Seroflurane
Thesethe
agents decrease the potential.
firing rate of nerve cells the
by redistribution. causes Arrhythmias  C.O - due to the
decreasing rise of the action They inhibit
decreasing theinrise of the action potential. Theyion.
inhibit the Capable of hypercapnia
rapid increase membrane premeability to sodium worsening
rapid increase in membrane premeability to sodium ion. ischemia

No receptors have been found to interact with the anesthetic 4. Nitrous Minimal C.O Little effect but  BP and Minimal effect
No
andreceptors have been found
no neurotransmitters to interact
are involve in theirwith the anesthetic
action. oxide combination with a total
and no neurotransmitters are involve in their action. more potent Peripheral
KINETICS OF ANESTHESIA anesthetic leads to resistance
Kinetics of Anesthesia
1. Induction 2. Maintenance 3. Recovery  sympathetic when in
Kinetics of Anesthesia stimulation Combination
of more
A Induction and Recovery
Three from
stages of Anesthesia
Anesthesia Potent
Induction – is theThree stages
period of Anesthesia
of time from onset of administration of the anesthetic
anesthetic to the development of effective surgical anesthesia in the
1. Induction
patient. 2.fast
It depends on how Maintenance 3. Recovery
the anesthetic reaches the brain. Comparison of the different Pharmacologic effects of Inhaled
1. Induction
Recovery – is the time 2. Maintenance
form discontinuation of adm.3.ofRecovery
anesthetic until General Anesthetics
consciousness is regained .It depends on how fast the anesthetic is
removed from the brain. Other Differences
drugs administered by inhalation; the rate of onset & recovery are Potency/induction Muscle relaxation Organ toxicity and other
influenced by the following factors: recovery onset – Analgesia adverse effect
1. Solubility of anesthetic – this is expressed as the blood / gas concentration
of gas in the blood, relative to the gas equilibrium phase. The greater the Halothane Potent Good muscle Extensively metabolize and
relaxation but Biotransformation
blood / gas partition coefficient the more soluble is the anesthetic agent in
lacks significant intermediates may result to
the blood. Analgesia hepatotoxic metabolites – “
a. If a drug has a low solubility (low-blood / gas partition coefficient) little Halothane Hepatitis”
-malignant hyperthermia
of the drug is dissolve in the blood. Therefore the equilibrium between
Comparison
Enflurane of thethan
Less potent different
Good Pharmacologic
muscle 2% is effects of Inhaled
me tabolized to fluoride
inhaled anesthetic and arterial blood is rapidly achieve, and only a few
additional molecules of the anesthetic is required to raise the arterial halothane but itGeneral Anesthetics
relaxation relaxes ion which is excreted by the
produces more the uterus kidney
tension. This results to rapid induction and short recovery. Other Differences
rapid induction -contraindicated in pnts with
Example – Nitrous Oxide (NaO) = 0.47 B/G coefficient and recovery
Potency/induction Muscle relaxation OrganRenal Failure.
toxicity EEC pattern –
and other
recovery onset – Analgesia char. ofeffect
adverse seizure activity – may
lead to Frank Seizure
b. If the anesthetic has high solubility – it is more dissolve
completely in the blood – so greater amounts of the Isoflurane More potent than Good muscle Low biotransformation low
Enflurane relaxation organ toxicity
anesthetic and longer periods of time are required to raise
arterial tension. This results in increase times of induction Nitrous Not very potent Poor surgical May diffuse into body cavities
Oxide when use alone anesthetic if use –  the pressure or expand
and recovery also slower to changes in the cone of the
but produce the alone but good the volume of gas in air
inhaled drug. Ex. Halothane – 2.3 B/G coefficient fastest induction Analgesic pockets may lead to:
2. Rate of ventilation – an increase rate of delivery of anesthetic gas and recovery a. Distention of the bowel
to the lungs results in most anesthetic being delivered to the b. Expansion or rupture of a
alveoli. This increases the rate at which the arterial blood pulmonary cyst
c. Rupture of the tympanic
approaches equilibrium. The effect of - ventilation is most
membrane in an occluded
pronounced for anesthetics with high solubility in blood. middle ear
3. Increase alveolar blood flow – high blood flow causes more of the d. Pneumoce phalus
anesthetic agent to be removed from the alveoli hastening -when it is dissolve in the blood
anesthesia. may enlarge the volume
of air emboli
B. Maintenance of Anesthesia – maintenance is the time during which
the patient is surgically anesthetized, anesthesia is usually
maintained by the administration of gases or volatile anesthetics
since these agents offer good minute to minute control over the depth
of anesthesia.
Properties of Halogenated Inhalation Anesthetics
Summary of Therapeutic Advantages and Disadvantages
of Anesthetic Agents
Inhalation Advantages Disadvantages
Halothane Enflurane Isoflurane Sevoflurane Desflurane Anesthetics

Induction speed 2.3 1.8 1.4 0.7 0.4 1. Nitrous - good analgesia -Diffusion hypoxia and
( λ) Oxide - rapid onset/recovery other complications
-safe non-irritating - Incomplete anesthesia
Irritation of Low Low Moderate Low Moderate -no muscle relaxation
respiratory tract -must be use with other
Muscle Low Moderate Moderate Moderate Moderate anesthesia for surgical anesthesia
relaxation
Myocardial High Moderate Low High Low -best agent in -reduces hepatic and
depression 2. Halothane Pediatric pnts renal flow
Sensitization of High Moderate Low Low Low -prod. Bronchodilatation -hepatotoxic, malignant
myocardium Summary ofgood
Therapeutic
for AsthmaticsAdvantages and Disadvantages
hyperthermia

% Metabolized 20 2 0.2 3 0.02 of Anesthetic- B.P


Agents
-dysarrhythmias (vent.
Fibrillation)
Inhalation Advantages Disadvantages
 Diffusion hypoxia – can occur at the termination of nitrous oxide anesthesia Anesthetics
if a patient abruptly breaths room air. (There is a rapid outward diffusion of
3. Enflurane Good muscle relaxation -Frank seizure
nitrous oxide from tissues into the bloodstream and then into the alveoli
-prod. Bronchodilation rapid -potential renal toxicity
where it decreases the alveolar tension – lowers arterial oxygen levels). induction/recovery

 Treatment or Remedy – administration of 100% O2 for a short time at the 4. Isoflurane -good muscle relaxation -significant resp depression.
termination of Nitrous Oxide Anesthesia. -rapid recovery
-stability of cardiac output
 N2O is also associated with high incidence of post-operative nausea & -does not raise intracranial
vomiting. pressure

 N2O – can cause leucopenia & Megaloblastic anemia due to in activation 5.Thiopental -rapid onset -no analgesia
of Vit. B12 -little muscle relaxation
-laryngospasm
 Methoxyflurane – fruity odor – most potent (MAC 0.16) but high blood – gas
coeff about 12 results to prolonged induction and recovery. High renal toxicity – 6. Ketamine -potent analgesia -disorientation hallucination
(High output Renal Failure) due to liberation of significant amount of Fluoride ion changes in perception
as Biotransformation product.
 Diethyl ether – highly flammable & explosive;  sympathetic activity,
bronchodilatation but may cause laryngospasm. It is a myocardial depressant –
but C.O and B.P is  due to the  sympathetic activity.

Intravenous General Anesthetics : are often use for the rapid


induction of anesthesia

A.Barbiturates – Ultra-short Acting:


1. Thiopental
2. Thiamylal
3. Methohexital
 Acts less than one (1) minute,  B.P due to myocardial depression.
Depresses the resp center in a dose dependent manner may cause
laryngospasm – not an analgesic.
B. Ketamine (Ketalar) – Dissociative anesthesia – a short – acting non
barbiturate – induces a dissociative state in which the patient appears to be
awake consist of Amnesia. Analgesia and often catatonia (rigidity). There is
disorientation, hallucinations and changes in perception.

Combination Anesthetics – lighter stage of anesthesia is


produce using 2 or more drugs.

A.Balanced Anesthesia : Full loss of consciousness and pain – induced


reflexes with muscle relaxation using:

a. Ultra – short acting barbiturate


b. Opioid analgesic (Meperidine, Morphine, Fentanyl or
Sufentamil)
c. Muscle relaxation
d. Nitrous Oxide + Oxygen

B. Neuroleptanesthesia – is induced by the combined actions of a narcotic


analgesic (Fentanyl) and a neuroleptic agent (Droperidol), together with
N2O & Oxygen. Consciousness is not lost, there is tranquility and reduce
motor activity. Useful in pnt wherein cooperation is needed (diagnostic
procedures) but may cause resp. depression.

Pre-Anesthetic Medications :

- Administered prior to anesthesia to reduce pain, relieve


anxiety decrease excess salivation and to combat nausea.

A. Anxiolytic drugs – provides sedation, relieve anxiety-


Benzodiazepam - diazepam, Lorazepam and Midazolam
B. Narcotic Analgesic - reduces pain – Morphine Fentanyl
C. Neuroleptics - promethazine, trimeprazine or
chlorpromazine; use to sedate and for its anti-emetic
properties.
D. Anticholinergic - Atropine and Scopolamine
decreases bronchial and salivary secretions, and promote
bronchodilatation.