Anesthesia

1. Presentation by
Mohamed Arsath Buhari Saleem
DA (nbe) - C.S.I Kalyani GH
IV INDUCTION AGENTS

2. A drug or combination of drugs, which will induce anesthesia, safe and
reversible, when injected in sufficient doses and which could also be given
intermittently or by infusion for maintenance
Classification:
 Inhalation Agents
 IV Induction Agents
INDUCTION AGENTS

3. IV INDUCTION AGENT
Barbiturates Non-Barbiturates
• Thiopentone
• Thiamylal
• Methohexital
• Phenobarbitone
• Secobarbital
• Pentobarbital
• Benzodiazepines: Diazepam,
Midazolam, Lorazepam
• Phenol Derivatives: Propofol
• Ketamine
• Neurolept anaesthesia:
Droperidol+Fentanyl
• Imidazole derivative:
Etomidate
• Eugenols: Propanidid

4. It can also be classified into:
 Rapid acting
 Slower acting
Rapid acting:
• Barbiturate: Thiopental, Methohexital,
• Propofol
• Etomidate
• Steroid: Althesin, Pregnonolone
• Propanidid
Slower acting:
• Ketamine,
• Benzodiazepines: Midazolam, Diazepam
• Droperidol + Fentanyl
IV INDUCTION AGENT

5.  Structural activity of barbiturates:
• Substitution of the hydrogen at the carbon atom position 5 with alkyl or aryl group is
essential for hypnotic and sedative activity.
• A phenyl group on C5 or on one of the N2 of the barbituric acid ring is essential for
anti convulsion activity.
• Increase in the length of one or both of the alkyl side chain at C5 increases hypnotic
potency, but if the side chains are increased more than 5 or 6 carbon hypnotic activity
is reduced and anticonvulsant property results.
BARBITURATES

6. BARBITURATES

7.  History:
Thiopental Sodium was first used in 1934 by Lundy and Waters
 Basic pharmacology:
• Thiopental is sulphur analogue of pentobarbital
• Ultra Short acting barbiturate.
• Yellowish-white hygroscopic power, with a bitter taste and faint smell
of garlic.
• Highly alkaline drug, PH of 10-11 and Pka of 7.6. It is diluted to
2.5% solution.
• Elimination half-life is 9Hrs.
THIOPENTONE SODIUM

8. THIOPENTONE SODIUM
• Thiopentone Vial contains N2 gas, which
prevents thiopental powder coming in contact
with CO2.
• The buffering action of the sodium carbonate
in the presence of atmospheric CO2
maintains the moderate alkalinity.
• Decrease in the alkalinity of barbiturates
solutions can result in their precipitation as
free acid.
• Hence therefore, they should not be
reconstituted with Ringerʼs lactate solution,
and also should not be mixed with acidic
solution.

9.  Mechanism of action:
• Thioepntone acts on the GABA
receptor which is a Ligand –
gated chloride channels.
• Activation of GABA receptor
increases chloride conductivity
through the ion channel causing
hyperpolarisation and thereby
reducing the excitability of the
postsynaptic neuron.
THIOPENTONE SODIUM

10.  Dose:
Adults - 3 to 5 mg/kg
Children - 5 to 6 mg/kg
Infants - 7 to 8 mg/kg
• Injection of thiopentone given over a period of 15 seconds, the injection is
continued until the desired level of narcosis is reached.
• Respirations must be assisted if unduly depressed.
• Slow injection rates are associated with reduced incidents of apnea and
hypotension.
THIOPENTONE SODIUM

11.  End point for induction
• Loss of eyelash reflex (excellent sign of adequate
induction).
• Loss of palpebral reflex.
• Loss of verbal contact.
• Dysarthria.
• Loss of gagging or coughing in response to LMA
insertion.
• Loss of response to surgical stimuli.
THIOPENTONE SODIUM

12. PHARMACOLOGICAL ACTIONS
 Central Nervous System:
When given I.V effect is seen within 30 seconds and rapidly crosses blood brain barrier.
The cerebral cortex and the ascending reticular – activating system are depressed before
the medullary center.
• Hypnotic action.
• Retrograde Amnesia
• Reverse steal or Robin Hood effect.
• Decreases cerebral blood flow,
• Decreases intra cranial pressure.
• Decreases cerebral metabolism and oxygen consumptions (CMRO2) and hence is
cerebral protective.
THIOPENTONE SODIUM

13. Mechanism of Neuroprotection:
• It inhibits the action of nitric oxide or inactivate nitric oxide in vascular
smooth muscle and attenuation of N-methyl-D-aspartate (NMDA) and
AMP- mediated glutamate excitation
 Respiratory System:
• Causes central respiratory depression, treated with gentle IPPV.
• Does not affect larynx directly, but increases sensitivity to stimuli (Saliva,
blood mucus, for which laryngeal spasm may occur).
THIOPENTONE SODIUM

14.  Cardiovascular System:
• Decrease cardiac output
• Hypotension
• It has direct depressant action on the Myocardium and hence decreases the
Myocardial Contractility (Interference with calcium transport across
myocardial cells)
• Increases myocardial oxygen consumption
• Decreases Coronary blood flow
• Arrhythmias (rare as long as hypercarbia and hypoxia are avoided)
THIOPENTONE SODIUM

15.  Alimentary tract:
• Decreases intestinal motility
 Liver and Kidneys:
• It is a powerful stimulator ADH [Antidiuretic hormone]. Urine output is
decreased because renal blood flows and renal artery construction.
 Reproductive System:
• It rapidly crosses the placental barrier, and enters the fetal circulation.
• Neonatal respiration can be depressed by thiopentone and the degree of
depression depends upon the dose of the drug given to the mother and the
duration of time that elapses between induction of anesthesia and delivery of the
baby.
THIOPENTONE SODIUM

16.  Metabolic effects:
• Heat loss results because of vasodilatation of cutaneous and skeletal muscle vessels,
which may contribute to post-Op shivering.
Lower induction dose of thiopentone will be required:
• Pre medicated patients.
• Severe anemia or burns.
• Malnourished
• Uremia and liver failure.
• Hypovolemia
THIOPENTONE SODIUM

17. Drug
Effect
1 Adrenergic drug Increased risk of arrhythmias.
2 Probenicid and
Slulphafurazole
Potentiates the effect of thiopentone.
3 Propofol Synergistic anaesthetic effect.
4. Volatile agent Halothane reduces the apparent volume
of distribution of thiopental, synergistic
effect of anaesthesia.
THIOPENTONE SODIUM
Drug Interaction that affects the Dynamic of Thiopental.

18.  Clinical Uses:
• Induction agent (Drug of choice in Neurosurgical Operations )
• Anticonvulsant agent.
• To produce simple sedation.
• Infusion of 2 to 3 mg/kg/hr has been used to treat refractory aminophylline seizures.
• To control the hyper dynamic state after coronary by-pass surgery.
• Thiopental is the DOC in hyperthyroidism because of its thiourea structure leads
antithyroid activity of the drug
• ECT
THIOPENTONE SODIUM

19.  Contraindication
Absolute:
• Porphyria:
Barbiturates can precipitate acute or even fatal
attacks of porphyria owing to the induction of
Delta ALA –synthetase which catalyses the rate
limiting step in biosynthesis of porphyrins.
• Cardiovascular collapses or shock.
THIOPENTONE SODIUM

20. Relative Contraindications:
• Cardiovascular disease: Ischemic heart disease, Hypertension, Valvular
Heat diseases
• Respiratory obstruction or inadequate airway before induction or where
maintenance of airway is difficult.
• Status Asthmatics
• Hypothyroid
• Hypovolemia, Hemorrhage, Burns, fluid depletion and dehydration.
• Uremia
• Acute Adrenocortical insufficiency
• Sever septicemia
THIOPENTONE SODIUM

21.  Complication/Side effects/adverse effects:
(i) Local Complications:
• Pain, Redness, Swelling hematoma due to high
alkalinity of the solution. It might lead to median
nerve injury, if injected into antecubital fossa.
• Hence the antecubital fossa is considered the
Graveyard of thiopentone.
THIOPENTONE SODIUM

22. (ii) Accidental intra-arterial
injection:
• Pain during injection.
• A white hand with cyanosed
fingers due to arterial spasm,
which may be due to arterial
thrombosis.
• Patches of skin discoloration
in the limb.
THIOPENTONE SODIUM

23.  Pathogenesis:
The change in PH of thiopental which occurs when it is mixed with blood in an artery results in
precipitation or Rombid crystals, as these crystals remain in the small vessels (they cut the intima)
their irritation property causes a local release of nor-adrenaline with subsequent vascular spasm and
causes arterial thrombosis and endothelial damage may occur.
 Treatment:
Leave cannula in the artery. Dilution of injected thiopentone with heparin (1000 U) and saline.
Papaverine 40-80 mg in 10-20 ml of saline is injected.
Prostacycline infusion 1 micro g/ml.
Dexamethasone 8 mg. injection to reduce edema.
Tolazoline 5ml of 1% solution is given ( nor-adrenaline antagonist)
Perform Stellate ganglion/Brachial plexus block to remove vasoconstriction and pain.
Vascular surgery if required.
THIOPENTONE SODIUM

24.  Excretion
• Barbiturates are principakky biotransformed via hepatic oxidation to in active water
soluble metabolites which is eliminated via kidneys
• Methohexital is eliminated via feces
THIOPENTONE SODIUM

25.  History:
It is the most recent intravenous anesthetic agent.
It was introduced in 1977 by kay and Rolly.
 Basic Pharmacology:
• Group: alkyl phenols.
• Insoluble in water, hence clinically available as
1% emuslion contaning 10% Soya bean oil,
2.25% Glycerol, 1.2% Purified egg
phosphatides. Earlier it was prepared with
cremophor EL.
• PH of 7, Pka in water is 11.
• It is available as 1% solution in 20ml clear glass
ampoules (or) vials, 50 and 100 ml vials, and in
50ml pre filled syringes.
• Highly lipid soluble.
PROPOFOL

26.  Mechanism of Action:
• Selective GABA receptor agonist and allosterically increases the binding
affinity of GABA.
• When GABA receptor is activated trans membrane chloride conductance
increases, resulting in hyperpolarization of the postsynaptic cell membrane
and functional inhibition of the postsynaptic neurons.
• Hyperpolarization of cell membrane decreases the rate of dissociation of
GABA from its receptor, thereby increasing the duration of the GABA-
activated opening of the chloride channel.
PROPOFOL

27.  Effect on organ system:
(i) CNS
• Decreases cerebral metabolic rate for oxygen (CMRO2).
• Decreases cerebral blood flow.
• Decreases intracranial pressure.
• Tolerance does not develop, and is an uncommon agent of physical
dependence or addiction
PROPOFOL

28. (ii) CVS
• Decreases systematic blood pressure.
• Negative inotropic effect (due to decrease in intracellular calcium
availability secondary to inhibition of trans-sarcolemma calcium influx.)
• Decrease in Heart rate and sometimes Asystole
• An infusion of propofol resulting is a significant reduction in both
myocardial blood flow and myocardial oxygen consumption. Finding
suggests that the global myocardial oxygen supply ratio is preserved.
PROPOFOL

29.  Respiration system:
• Propofol produces does-dependent depression of ventilation with apnea
occurring is 25% to 35% patients after induction.
• Maintenance infusion of propofol decreases tidal volume and frequency
of breathing.
• It produces bronchodilation and decreases the incidence of intra-
operative wheezing in patients with asthma.
PROPOFOL

30.  Hepatic and Renal Function:
• It does not affect hepatic and renal function.
• Prolonged infusion of propofol may result in excretion of green colored urine, which
reflects, the presence of phenols in the urine.
 Eye:
• Decreases the intraocular pressure occur immediately after induction
PROPOFOL

31.  Dose of propofol:
• Induction of general Anesthesia: 1 to 2.5 mg/kg I.V
• Maintenance of general anesthesia: 50 to 200 micro g/kg/min I.V
• Sedation: 25 to 100 micro g/kg/min I.V.
 Metabolism:
• Propofol is rapidly metabolized is the liver, conjugation to glucuronide and sulphate to
produce water-soluble compounds, which are excreted by the kidneys.
• Metabolites of propofol are inactive.
• Propofol itself results in a concentration dependent inhibition of Cytochrome P-450
and then may alter the metabolism of drug dependent enzyme system.
PROPOFOL

32.  Clinical use:
• GA: induction drug of choice for many forms of anesthesia, especially
when rapid and complete awakening is considered essential. Commonly
used for producing I.V conscious sedation or as a part of balanced (or)
total I.V anaesthesia
• Preferred induction agent for Day care surgery
• Antiemetic effect: (10 to 15 mg i.v)
 Mechanism:
Propofol uniformly depress CNS structures, including sub cortical centers to
inhibit nausea and vomiting or produces direct depressant effect on the
vomiting center. It is also believed that antiemetic effect of propofol based on
inhibition the dopaminergic system.
PROPOFOL

33. • Antipruritic Effect:
Propofol 10mg I.V is effective is the treatment of pruritus associated with Neuraxial
opioid or cholestasis.
• Anti-convulsion activity:
Due to GABA mediated pre-synaptic and post-synaptic inhibition
A dose of more than 1mg/kg I.V decreases seizure duration.
PROPOFOL

34.  Side effect:
• Allergic Reactions:
Allergic components of propofol are phenyl and diisopropyl side chain.
• Pain on Injection:
It is the most common side effect associated with Propofol. Using large veins and avoiding veins in
the dorsum of the hand and adding Lidocaine to the propofol solution can reduce this.
• Hypotension:
The most significant side effect on induction is the decrease in systemic blood pressure.
• Bacterial Growth:
Propofol strongly supports growth of Escherichia coli and pseudomonas Aeruginosa
PROPOFOL

35. • Miscellaneous effects:
Temporally abolition of tremors in patients with Parkinsonʼs disease may
occur after the administrating of propofol. For this reason propofol may
not be ideally suited for patients undergoing stereotactic neurosurgery
such as pallidotomy.
PROPOFOL

36. • Propofol infusion syndrome is a rare syndrome which affects patients
undergoing long-term treatment with high doses of propofol. (>4
mg/kg/hr for more than 24 hours)
• Risk Factors: carbohydrate depletion, severe illness, and concomitant
administration of catecholamines and glucocorticosteroids
• The pathophysiology is impairment of mitochondrial beta-oxidation of
fatty acids, disruption of the electron transport chain, and blockage of
beta-adrenoreceptors and cardiac calcium channels
PROPOFOL INFUSION SYNDROME

37. • It can lead to cardiac failure, rhabdomyolysis, metabolic
acidosis and renal failure and is often fatal.
• Hyperkalemia, hypertriglyceridemia, and hepatomegaly are also
key features.
• It occurs more commonly in children, and critically ill patients
receiving catecholamine and glucocorticoids are at high risk.
• Treatment is Supportive. Early recognition of the syndrome
and discontinuation of the propofol infusion reduces
morbidity and mortality.

38.  History:
Ketamine was synthesized in 1962 by Stevens and was first used in humans in 1965 by
Corrsen and Domino.
 Basic Pharmacology:
• Ketamine belongs to Phencyclidines group.
• Molecular weight 238 KD.
• White partially water-soluble and forms a white crystalline powder supplied as a colourless
solution in concentration of 10% 50% and 100%.
• It contains Benzethonium as a preservative.
• PH varies between 3.5 to 5.5 PKA is 7.5
KETAMINE

39. • Highly lipid soluble.
• Of the non volatile agents, Ketamine comes closest to being a “complete”
anesthetic as it induces analgesia, anesthesia and unonsciuosness.
• The commercial preparations being mixture of both isomers S and R in equal
amounts.
• The S(+) isomer producers:
More intense analgesia
More rapid metabolism and thus recovery.
Lower incidence of the Emergence of reactions than the R (-) isomer.
KETAMINE

40.  Mechanism of Actions:
Ketamine interacts with
• N-methyl-D- aspartate (NMDA) receptors,
• opioid receptors
• monoaminergic receptors,
• muscarinic receptors and
• voltage sensitive calcium channels receptors.
KETAMINE

41. • N-Methyl-D- Aspartate Receptors Antagonism:
The NMDA receptors, a member of the glutamate receptor family.
Ketamine is a non-competitive antagonist of the NMDA receptor calcium
pore.
Ketamine interacts with the Phencyclidine-Binding receptor site, leading to
inhibition of NMDA receptor activity.
KETAMINE

42. • Opioid Receptors:
Ketamine interacts with mu, delta, kappa receptors.
It an antagonist at mu receptors and an agonist at kappa receptors.
• Monoaminergic Receptors:
The antinociceptive actins of ketamine may involve inhibiting descending
monoaminergic pain pathways.
• Muscarinic Receptors:
Antagonist effect of ketamine at muscarinic receptors is more likely than an
agonist effect and hence produces anticholinergic symptoms (Emergence delirium,
bronchodilation, sympathomimetic action)
KETAMINE

43.  Pharmacology:
Effect on the organ system:
 CNS
It produces an anesthetized state, which has been termed as “Dissociative Anaesthesia”
which is characterized by dissociation between the thalamo-cortical and limbic systems.
Dissociative anesthesia resembles a cataleptic state in which the
• eyes remain open with
• a slow nystagmic gaze,
• have profound analgesia, and
• maintain corneal, cough and swallow reflexes, which is assumed to be not protective.
KETAMINE

44. Emergence reactions:
• When patient is coming out of Ketamine anesthesia the experience is termed as
“Emergence Reactions”. The common manifestations of these reactions, which
vary in severity, include dreaming, extra corporeal experiences (Sense of floating
out of body), and illusions (misinterpretation of a real external sensory
experience).
• These are often associated with excitement, confusion, euphoria and fear.
• Dreams and hallucinations can occur up to 24 hrs after administration to
Ketamine. The dreams frequently have a morbid content and are often
experienced in vivid colours. Usually disappear within few hours
• Cortical blindness may be transiently present.
• Can be decreased by using BZD and Thiopentone
KETAMINE

45. • Ketamine increases cerebral metabolism,
• Increases cerebral blood flow
• Increases intracranial pressure.
• Increases CMRO2.
All these characteristics preclude its use in patients with sapce occupying
intracranial lesions and in head trauma
KETAMINE

46.  Respiratory System:
• Transient apnea is followed and decreased in respiratory rate and tidal volume.
• The pharyngeal and laryngeal reflexes remain active.
• Protection is not absolute and that silent aspiration can still occur (especially in
children).
• It causes a marked increase pharyngeal secretion and hence anticholinergic
agent should be administered prior to Ketamine.
• It is a bronchial. Smooth muscle relaxant and hence can be used in patients
with reactive airway disease, bronchospasm pulmonary compliance is
improved.
• It is safe to use in status Asthmatics.
KETAMINE

47.  Eye sign of Ketamine:
• Pupils dilated
• Lacrimation
• Raised IOP
• Nystagmus
• Eyes open
• Diplopia
• Loss of light reflex.
KETAMINE

48.  CVS:
• Increase in Blood Pressure of around 15-25%.
• Increase in Heart rate, cardiac output and pulmonary artery pressure.
Mechanism:
• Increase in circulating norepinephrine (noradrenaline) after ketamine.
• These changes are caused by Central Nervous System stimulation with an
increase in sympathetic flow.
• It blocks the re-uptake mechanism.
• Releases noradrenaline from the sympathetic ganglia.
• It increases myocardial oxygen consumption and direct myocardial
depressant, hence contraindicated in patients within Ischemic heart
disease.
KETAMINE

49.  DOSES OF KETAMINE:
Induction of general Anaesthesia:
0.5 to 2 mg/kg I.V
4 to 6 mg/kg I.M
 Maintenance of General Anaesthesia:
0.5 to 1 mg/kg I.V with N20 50% in 02
15-45 mg/kg/min I.V with N2O 20-70% in O2
30-90 mg/kg/min I.V without N2O. Sedations and Analgesia:
0.2 to 0.8 mg/kg/I.V
2-4 mg/kg/.min I.M
KETAMINE

50. Metabolism:
• Ketamine is metabolized extensively by hepatic microsomal enzymes.
• Norketamine is the active metabolite may contribute to prolonged effects of
Ketamine.
• Norketamine is eventually hydoxylated and then conjugated to form more water
soluble and inactive glucuronide metabolites that are excreted by the Kidneys.
KETAMINE

51.  Other effects:
Raises intraocular pressure and may cause postoperative nausea and vomiting.
Increases muscle tone and causes sudden jerky movements, which may
interfere with surgery and require sedation with Diazepam (reduces the
incidence of involuntary muscle movements.)
 Clinical uses:
• As sole anaesthetic agent for minor surgery.
• As induction agent.
• State of acute shock (Hypovolemic patients).
• Dressing burns patient, Debridementʼs and skin grafting.
KETAMINE

52. • Neuraxial analgesia.
Ketamine ampules (without preservative) can be used for spinal anaesthesia.
Labor analgesia is achieved without associated depression to the fetus.
Epidural use for postoperative pains.
• For induction of anesthesia in small children
• Where airway control is difficult.
• Certain neurological, radio diagnostic and therapeutic procedures.
• For intubation as an alternative to topical awake intubation in presence of full stomach.
• For patients with acute intermittent porphyria.
• For prevention and management of priapism.
• In muscular dystrophy and myopathic disorder (to avoid thiopentone use).
KETAMINE

53.  Drug interactions
• When administered in presence of halothane may result in hypotension. It interacts
with synergistically with volatile anesthetics.
• Its acts as an addition with propofol, BZD and GABA receptor mediated agents.
• Diazepam and midazolam attenuates cardiostimulatorty effetcs of ketamine
• Alpha and Beta adrenergic antagonist unmask direct myocardial depressant effects of
ketamine, which is normally overwhelmed by sympathetic stimulation.
KETAMINE

54.  Contraindications:
• Psychiatric disturbances (Schizophrenia).
• Patients on thyroid medication.
• In hypertensive patients.
• IHD patients (severe myocardial disease, coronary insufficiency).
• Patients with increased intra cranial pressure and with intracranial mass lesion.
• In open eye injury (or) other ophthalmologic disorders Nystagmus).
• In patients with vascular aneurysms (sudden change in arterial pressure).
KETAMINE

55.  History:
Etomidate was synthesized in 1964. It was introduced into clinical practice in 1972.
 Basic Pharmacology:
• It is a carboxylated imidazole derivative
• It is presently formulated in 0.2% solution with 35% propylene glycol.
• PH of 6.9 and Pka of 4.2
 Doses of Etomidate:
• Induction of GA: 0.2 to 0.6 mg/kg I.V
• Maintenance of GA: 10 micro gm/kg/min with N2O
• Sedation and Analgesia: 5 to 8 micro gm/kg/min I.V (only for short periods of sedation because
of inhibition of corticosteroid synthesis.
ETOMIDATE

56. Pharmacological action of Etomidate:
 Central Nervous System:
The primary action of Etomidate is hypnosis, which is achieved in one arm-brain
circulation.
Mechanism:
• Depresses reticular activating system and mimics inhibitory effects of GABA
• It reduces cerebral blood flow, CMRO2, without altering mean arterial pressure and
Cerebral Perfusion Pressure is maintained.
• It decreases the intracranial pressure in previously increased ICP.
• It also decreases the intra ocular pressure
ETOMIDATE

57.  Respiratory System:
• It has minimal effect on Ventilation.
• Do not include histamine release. But still produces only light anesthesia
for laryngoscpy even in large doses.
• Ventilator response to carbon dioxide is depressed.
• On induction it produces brief period of hyperventilation.
• Hiccups (or) coughing may be seen during induction.
ETOMIDATE

58.  Cardiovascular System:
• An induction dose of 0.3 mg/kg results in almost no change in heart rate,
mean arterial pressure, stroke value (or) systemic vascular resistance and
cardiac output.
• Patients with valvular heart disease may exhibit a 20% fall in systemic
blood pressure hence administration to acutely hypovolemic patients
results in sudden hypotension.
• It decreases 50% myocardial blood flow and oxygen consumption and a
20% to 30% increase in coronary sinus blood oxygen saturation.The
myocardial oxygen supply / demand ratio is thus well maintained.
• The hemodynamic stability seen with Etomidate may be due to lack of
effect both on the sympathetic nervous system and baroreceptor function.
ETOMIDATE

59.  Endocrine effect:
• Inhibits conversion of cholesterol to cortisol and inhibiting enzymes
involved in aldosterone synthesis
• Patients experiencing sepsis (or) hemorrhage, who might require an intact
cortisol response, would be at disadvantage.
• Vitamin-C supplementation can restores cortisol levels to normal.
 Metabolism:
Etomidate is rapidly metabolized by hydrolysis of the ethyl ester side chain to its
carboxylic acid ester, resulting in water soluble and inactive compounds.
Metabolized by M-dealkylisation.
ETOMIDATE

60.  Uses:
• Cardiovascular disease (coronary artery bypass, valve
surgery)
• Reactive airway disease (do not release histamine)
• Intra cranial hypertension
• For cardio version (rapid onset and quick recovery)
ETOMIDATE

61.  Adverse Effects:
• Pain on intravenous injections (phlebitis, thrombosis and thrombophlebitis)
• Abnormal muscular movements of a myoclonic nature. (Myoclonus, dystonia
and tremor)
• Adrenocortical Suppression:
• Nausea and Vomiting
• Laryngospasm and unexpected Apnea.
ETOMIDATE

62. Sources:
Morgon and Mikhail’s Clinical anesthesiology 5th Edition
www.ncbi.nlm.nih.gov
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