Ideal IV anesthetics:
1-Drug compatibility (water solubility) and stability in solution.
2-lake pain on injection , veno irritation , and local tissue damage.
3-low potential to release histamine.
4-rabid and smooth onset of action without excitatory activity.
5-rabid metabolism to inactive metabolites.
6-a steep dose to minimize titratability and tissue accumulation.
7-lake of acute cardiovascular and respiratory depression.
8-decrease in cerebral metabolism and intracranial pressure.
9-rabid and smooth return to consciousness .
10-abcense of post operative nausea , vomiting, amnesia , psychoimetic
reaction , dizziness , headache , and prolonged sedation.
Anesthesia is produced by diffusion of drug from arterial
blood across the blood brain barrier in to the brain which
regulated by the following factors:
-protein binding: unbound drug is free to cross BBB.
-blood flow to the brain.
-extracellular PH and Pka of the drug: nonionized.
-solubility of the drug in lipid and water: high lipid
solubility enhances transfer in to the brain.
-speed of injection.
• Available as sodium salts (yellowish powder)
• Bitter taste + smell of garlic.
• Solution of thiobarbiturates are stable for 2 weeks.
• ph of solution of thiopental (2.5%) is 9.
• Does not cause pain on injection.
• Metabolized in liver to hydroxythiopental and carboxylic
• Produce anesthesia in less than 30 sec after iv injection.
• Induction dose: 3-5 mg/kg in adults
5-6 mg/kg in children
6-8 mg/kg in infants
recovery after 10 min
• Produce decrease in CPF there by lowering ICP.
• widely used to improve brain relaxation during
neurosurgery and to improve cerebral infusion pressure
after acute brain injury
-It cause dose dependent anticonvulsant activity.
-dose dependent respiratory depression.
-it cause decrease in cardiac output and ABP.
-early absence in eyelid reflex.
-tissue necrosis: median nerve damage may be occur
after extravenous injection in the antecubital fossa
if perivenous injection occurred the needle should be
left in place and injection of hyaloronidase.
-intra-arterial injection: pt usually complains of burning
pain & in this case:
-leave needle in artery.
-administrate papaverine 20 mg.
-heparin should be given iv and orally.
-stellate ganglion or brachial plexus block
may reduce arterial spasm.
-Pain on injection 32-67% of patients.
-t1/2 is 1-8 min (Barash 2009).
-Eimination half time 2-24 min.
-Metabolized in liver to sulfate and glucuronic acid which
are eliminated by kidney.
-Extra hepatic rout of elimination by lungs.
-Anesthesia is induced in 20-40 sec after iv administration.
-We can monitor the onset by loss of verbal contact.
-Induction dose 1.5 – 2.5 mg/kg.
-Children require bigger dose.
-Decrease CPF and ICP.
-Excitatory motor activity without EEG changes.
-Dose and concentration dependent cardiovascular depression.
-Dose dependent respiratory depression with apnea.
-Antiemetic effects (10-20 mg to treat nausea and emesis
in the early post operative period.
-Antidopamenergic which lead to euphoria.
-It decrease the pruritus produced by spinal opioids.
-Agent of choice in malignant hyperthermia suspictable pt.
-Propofol syndrome : after high dose infusion of propofol
for long time – myocardial failure – metabolic acidosis –
• no effect on bronchial muscle tone and
laryngospasm is particularly uncommon .
• regarded by most anesthetists as the drug of choice
for induction of anesthesia when LMA (Laryngeal
Mask Airway) is to be used.
-ph 6.9 , pain on injection , venoirritation.
-induction dose : 0.2-0.3 mg/kg.
-involuntary myoclonic movement are common at induction.
-metabolism in liver.
-it decrease CPF and ICP.
-inhibitory effect on adrenocortical synthetic function (5-8 h
after single use)
-inhibit platelet function.
-minimal cardiorespiratory depression .
-does not induce histamine release.
-high incidence of post op nausea and emesis .
-long term infusion in ICU (increase infection
-water soluble compound.
-potent anesthetics and analgesic properties +amnesia .
-metabolized by liver to norkitamine which excreted by
-elimination half life 2-4 h .
-dose dependent CNS depression + stimulation of limbic s.
-induction dose: 1-2 mg/kg IV.
-duration of action: 10-20min –full orientation require
more 60 – 90 min
-high incidence of psychomimetic reactions (namely ,
hallucination , nightmares , altered short term memory
, and cognition).
-ketamine increase CPF and ICP .
-bronchodilatory activity - minimal respiratory depression.
-increase oral secretion.
-cardiovascular stimulation + increase peripheral resistant.
-not recommended in severe coronary artery disease.
-increase pulmonary artery pressure (contraindicated
in poor right ventricular reserve.
-high risk pt: shocked patients.
-difficult locations: site of accidents.
-developing countries: where anesthetic
equipment and trained staff in short supply.
-medazolam , lorazepam , diazepam and antagonist
-metabolized in liver , excreted by kidney.
-short acting: midazolam - flumazenil.
-long acting: lorazepam.
-only midazolam can given by continuous infusion.
-all benzodiazepines produce: anxiolytic, anterograde
amnesia, sedative, hypnotic, anticonvulsant, and
spinally mediated muscle relaxant properties.
-dose dependent respiratory depression.
-it depress the swallowing reflex and depress upper
airway reflex activity.
-produce decrease in systemic vascular resistant and
blood pressure in large doses.
-specific antagonist :flumazenil
-alpha 2 adreno receptor agonist.
-approved by FDA for the short term less than 24 h
sedation of the mechanically ventilated pt in ICU.
-unique type of sedation-analgesia with less respiratory
depression + amnestic affect .
-it produce hypotension and bradycardia more than
-infusion rate 0.2-0.6 mcg/kg/h.
-improve post op pain control after major surgery.
-slower onset and offset than propofol , sedation
like midazolam. -high cost.