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Thiopentone

Introduction:
Thiopentone is ultrashort acting barbiturate which is the Sulphur
analogue of sodium pentobarbital. Sulphur increases the lipid
solubility of STP. It was discovered by Waters and Lundy in 1934.

Principal actions:
Hypnosis and anticonvulsant action

Mode of action
Basically enhances the inhibitory neurotransmitter GABA and
decreases the release of excitatory NT Ach.

Presentation of drug:
STP is available as hygroscopic yellow powder in 20 ml vial,
containing thiopentone sodium and 6% sodium carbonate stored
under atmosphere of nitrogen in vial.
It is available in 0.5 gm and 1 gm vials.
The drug is reconstituted in sterile water prior to its use to yield a
2.5% solution.
pH of the solution is 10.8 and it is stable for 24 to 48 hours at room
temperature.

Route of administration:
STP is administered IV only.

Pharmacokinetics:
It produces unconsciousness in one arm brain circulation i.e around
15 seconds.
Induction is very smooth and rapid
Rapid induction is due to high lipid solubility and high degree of non-
ionization (STP is 60% nonionized at pH 7.4).
Elimination half life of STP is around 3.4 to 22 hours, average being
10.4 hours but patient regain consciousness after 15-20 minutes
because of rapid redistribution of drug to fatty tissues and muscles.
In blood about 80-90% is bound to protein, mainly albumin.
Metabolism of this drug occurs mainly in liver by oxidation to form
pentobarbitone and urea.
Metabolites are excreted mainly by kidneys.

Pharmacodynamics:
CVS:
Negative inotropic effect
Decreases BP due to decrease in CO and decrease in SVR
Maintains the integrity of baroreceptor reflex, such that there is
increase in HR.

Respiratory:
Potent respiratory depressant
Transient apnea occur after induction dose.
At higher doses, it can decrease ventilator response to hypercapnia.
Laryngospasm and bronchospasm can occur if painful stimulus is
given at inadequate depth of anesthesia.

CNS:
Produces rapid and smooth induction.
Maximum depth of unconsciousness is produced in 60 seconds.
Has excellent anticonvulsant properties.
It has antanalgesic effect.
It decreases intracranial tension, cerebral oxygen consumption and
cerebral metabolic rate, drug is choice for cerebral protection.

GI
Decreases intestinal activity

Eye
Decreases IOP

Thyroid
Has antithyroid properties

Pregnancy
It crosses placenta and reaches equilibrium within 3-5 minutes and
achive high concentration in fetus brain

Uses:
For induction of anesthesia: 2-7 mg/kg avg. 5 mg/kg
Management of status epilepticus: 5 mg/kg/hr

Contraindications:
Absoule:
Porphyria
Previous h/o anaphylaxis to STP

Relative
Hypotension/shock
Patient with fixed CO lesion
Asthmatics
Uncontrolled HTN
Renal disease

Intraarterial injection

Succinylcholine

Presentation:
Succinylcholine is a white, odorless, slightly bitter powder and very
soluble in water. For clinical use it is available both in powder form
or already prepared form (50 mg/ml) like this vial.
Methylparaben 0.1% is added as a preservative.
Vials should be stored at controlled temperature of 4-8 deg C.
The multidose vials are stable for upto 14 days at room temperature
without significant loss of potency.

Introduction:
Sux is an ultra-short acting depolarizing MR. It is quaternary amine
ester and chemically a dicholine ester of succinic acid. It is commonly
used as bromide or chloride salt.

Principal action
Blockade of brief duration of skeletal muscle relaxation via Ach
receptor.

MOA

Pharmacokinetics:
After IV administration it causes brief but rapid onset of skeletal
muscle relaxation.
Brief duration of action of drug is due to an initial rapid redistribution
phase.
Onset of action is in 30-90 seconds and duration of action 5-10
minutes.
The drug is hydrolyzed by plasma cholinesterase to
succinylmonocholine and choline. Succinylcholine is further
hydrolyzed by pseudocholinesterase to succinic acid and choline.
About 2-110% of drug is excreted unchanged in urine.

Pharmacodynamics:
CVS
Respi
Muscle
GI
Eye
CNS
Metabolic

Uses:
To facilitate the tracheal intubation 1.5-2 mg/kg
To treat laryngospasm 10 to 15 mg or 0.1 mg/kg IV
During anesthesia for ECT
For brief muscle relaxation required during reduction of joint
dislocation
S/E
Massive hyperkalemia: in conditions like upper motor neuron disease,
stroke, burns, brain and spinal cord lesions, severe metabolic acidosis,
crush injuries, prolonged immobility, etc.
Cardiac dysrhythmia: sinus bradycardia, junctional rhythms, and
ventricular arrhythmias
Post-op myalgia: prevented by self taming of fasciculation, de-
fasciculation dose of NDMR
Rhabdomyolysis
Prolonged apnea: atypical pseudocholinesterase
Phase II block with repeated, large dose or infusion
Increase: IOP, IGT, ICT
Trismus

C/I
Hyperkalemia
Acute or chronic renal failure
Increase ICT
Upper motor neuron disease
Burns
Hx of malignant hyperthermia

Midazolam

Presentation:
Midazolam is available as clear, colorless solution containing
Midazolam hydrochloride in strength of 1 mg/ml in 5 and 10 ml vials
and 5 mg/ml in 1 ml ampoules. Vials and ampoules of midazolam
contain 0.01% disodium edetate with 1% benzyl alcohol as a
preservative. Preservative free is also available.

Introduction
Midazolam is a short acting water soluble BZD. It contains imidazole
ring in its structure which accounts for stability of midazolam in
aqueous solution and its rapid metabolism. It is 2-3 times more potent
than diazepam.
At pH less than 4, the imidazole ring remains open rendering it water
soluble and pH above 4, the imidazole ring closes, making it highly
lipid soluble.

Principal actions
It has the following principal actions:
- Hypnosis
- Sedation
- Anxiolysis
- Anterograde amnesia
- Anticonvulsant
- Muscle relaxant

Route of administration:
IV, IM, Oral, Intrathecally and epidurally

Pharmacokinetics:
Bioavailability after oral route is 45% and by IM route is 80-100%.
Highly protein bound- 96%
Midazolam is completely metabolized in liver to hydroxylated
derivatives by hepatic oxidative mechanism- these water soluble
metabolites are then excreted in urine as glucuronide conjugate.
Metabolits are physiologically active compounds and excreted in
urine.
The elimination half life of drug is 1.5 to 3.5 hours.

Uses:
Premedication prior to anesthesia- 0.5 mg/kg orally 30 minutes before
induction; IM for premedication 0.05-0.1 mg/kg
Sedation: 0.07 0.1 mg/kg IV and titrated
Induction of anesthesia: 0.1 -0.4 mg/kg IV over 20-30 seconds
ICU sedation: 0.03 0.2 mg/kg/hr
Onset of sedation : after IM doses: 15 minutes, after IV doses: 1-1.5
minutes. Duration of action: 2-6 hours.
Atropine

Presentation:
Atropine is available as clear, colorless, isotonic solution for IV or IM
injection containing Atropine sulphate monohydrate in strength of 0.6
mg/ml in 1 ml ampoules. Also available in 0.5% and 1% eye drops.
Atropine should be stored away from light and should never be
frozen.

Pharmacokinetics:
50% bound to plasma proteins: mainly to A1AG.
Metabolized in liver by enzymatic hydrolysis and 94% is excreted in
urine as metabolites and rest is unchanged.

Atropine fever:
Therapeutic doses of atropine dilates cutaneous blood vessels
(atropine flush) and may cause rise in body temperature (atropine
fever) due to suppression of sweat gland activity especially in infants
and small children.

Uses of atropine
- To counteract bradycardia due to vagal stimulation
- To alleviate muscarinic side effects of anticholinesterase drugs
used for reversal of NM blockade
- Premedication before GA to dry up secretions
- As cycloplegic
- Treatment of OP poisoning
- For treatment of rapid type of mushroom poisoning as it acts as
antidote to alkaloid muscarine.
- Reduce the incidence and treatment of OCR

Onset of action 1 minute and duration of action 30-60 minutes after


IV dose.

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