INTRAVENOUS ANAESTHETIC AGENTS Flashcards by Iseoluwa Ojo

What are IV Anaesthetic Agents / Induction drugs?

These are drugs that, when given intravenously in an appropriate dose, cause a __________________________.

Often described as occurring within “________________________________ time”

rapid loss of consciousness

one arm-brain circulation

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One-arm brain circulation time

that is simply the time taken for ____________________________________________ , where they have their effect; normally ___________

the drug to travel from the site of injection (usually antecubital) to the brain

10 -20 secs

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Properties of an ideal IV induction drug

Physical / Chemical properties
• _________-soluble & _________ in solution
•(Cheap or Expensive?)
• Stable on exposure to ______
• ________ shelf-life
• No ________ on intravenous injection
• Not painful when injected into _________
• _________ when injected subcutaneously
• Low incidence of _________

• Water ; stable

Cheap; light

Long; No pain; an artery

Non-irritant ; thrombophlebitis

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Properties of an ideal IV induction drug  Pharmacokinetic properties

•_____________ in one arm-brain circulation time
•_________________ to vessel rich tissue

• Rapid __________ and ————-

• No _____________

Rapid onset

Rapid redistribution

clearance and metabolism

active metabolites

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Properties of an ideal IV induction drug

Pharmacodynamic properties
• _______________ ratio (ratio of ________:____________ dose)

• Minimal ___________ and ————- effects

• No _________________/___________ reactions

High therapeutic

toxic dose : minimally effective

cardiovascular and respiratory

histamine release; hypersensitivity

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Properties of an ideal IV induction drug

Pharmacodynamic properties
• No _________ effects
• No _____________ movements
• No emergence __________
• No ________ effect
• No ___________ ____________
• Safe to use in ________

emetic; involuntary

nightmares; hang over

adrenocortical suppression

porphyria

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List 2 ideal Intravenous Anaesthetic agents

There is however No ideal Intravenous Anaesthetic agent.

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Intravenous anaesthetic agents

Advantages
• rapid and smooth ________ of anaesthesia
• little ________ requirement (syringes, needles, catheters)
•easy _____________ of drugs

induction

equipment

administration

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Intravenous anaesthetic agents

DisAdvantages

•difficult ________________ once administered
• less control of _________________ of anaesthesia
•lack of ____________ support
•poor tolerability in ________,___________, or ____________ individuals.

retrieval of drug

depth and duration

ventilatory

debilitated, dehydrated or toxic

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Classification
A. Rapidly Acting (1o) Induction agents
__________

__________

__________ Compounds

__________

Barbiturates
Alkyl phenols
Imidazole Compounds
Eugenols

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Classification
A. Rapidly Acting (1o) Induction agents
Barbiturates -3
Alkyl phenols-1
Imidazole Compounds-1
Eugenols -1

Methohexital
Thiopental Thiamylal

Propofol

Etomidate

Propanidid

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__________ rapidly acting (1•) induction agent has been withdrawn from market

Propanidid- withdrawn from market

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Slower Acting (___________) agents

__________ derivatives
__________
__________

basal narcotic

Phencyclidine

Benzodiazepines

Opioids

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Slower Acting (basal narcotic) agents

Phencyclidine derivatives
___________

Benzodiazepines
_________ , _________

Opioids
_________, _________, _________, _________

Ketamine

Diazepam Midazolam.

Fentanyl Alfentanil Sufentanil morphine

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General uses of IV anaesthesia agents

As __________ agents

__________________ (TIVA)
________ Sedation
________ to ________ Anaesthesia ________
________ protection
________ therapy

Induction

Total IntraVenous Anaesthesia
ICU Sedation
Supplement ; Regional Anaesthesia Anticonvulsant
Brain protection
Electroconvulsive therapy

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TIVA- both ________/_________ of anaesthesia

ICU Sedation: _________,_________

Anticonvulsant: _____,__________

Brain protection: ___________ ( causes reduced ________ )

Electroconvulsive therapy esp. _________ preferred to __________

Induction/Maintenance

Propofol,Midazolam

STP, midazolam

Propofol; CMRO2

methohexithal; propofol

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Most commonly used iv induction agent is ????

Thiopentone

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A thiopentone

thio____________

Physical properties:
_______ powder, (soluble or insoluble?) in water with PH of ____, PKa of 7.6 Solution not stable for > ______ after reconstitution in _____ to a 2.5%
Best prepared fresh

barbiturate

Yellow ; soluble

10.8 ; 24 hrs

water

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A thiopentone

Mode of Action

Act primary at synapses by depressing _____________ to _____________ and inhibit ____________________

post-synaptic sensitivity to neurotransmitters

pre-synaptic neurotransmitter release

A thiopentone

Administration-

Dose:____ route ____mg/kg
Onset time; _________________ time
DOA: _____________,
Repeated doses effect is ___________
Other route- ________, onset time is within _________

iv; 3-7

one arm-brain circulation

5-15 mins

cumulative; rectally; 15 mins

Thiopentone

Systemic Effects

CVS- ______ (By ____%), _______ leading to _________tension

Resp. Sys – __________ resp centre, ± ________
Reduces resp centre’s response to _______.

Histamine release may lead to ___________

CNS- _________→ __________ .

Anticonvulsant, ↓_____,_____,______

Skin- ___________ around neck
and chest occasionally

↓CO; 20; ↓PVR; hypotension

Depresses; apnoea; CO2

bronchospasm

depressed; hypnosis

CBF, ICP, IOP

erythematous rash

Thiopentone

Metabolism
________- main site, @ rate of ______% per hr.

_______% remain in body after 24 hrs.

(Active or Inactive?) metabolites excreted mainly in the ________ , 0.5% excreted unchanged

Liver; 10-15

30; Inactive

urine

Thiopentone

Contra-indications

Severe __________ or __________
Previous __________
Acute __________ __________
Acute __________ __________

Severe hypotension or shock
Previous anaphylaxis
Acute intermittent porphyria
Acute bronchial asthma

Thiopentone

Extravascular injection → _________

Inadvertent intra-arterial injection → arterial ______, __________ → __________ of e.g. the hand

Mgt:___________ in the artery, Flush with ________, Inj . _________ to relieve spasm, Keep the hand ______, _______ it, ± anticoagulant therapy

severe pain

spasm; thrombosis; gangrene

leave needle; saline

procaine; warm; elevate

Ketamine A ___________ derivative • Widely used as ________ in developing countries Enjoys wider use in _______ because of less post- anaesth effects Available as ________________- 1%, 5% soln.

phencyclidine; TIVA children colorless solution

Ketamine Main action- __________ anaesthesia (combination of ___________ with ______________ i.e. _____________). ________,__________ reflexes are preserved

Dissociative profound analgesia with superficial sleep light hypnosis Gag, eyelash

Ketamine Administration- Iv dose-____ mg/Kg, onset time within _____, DOA of ________ im dose-______ mg/Kg, onset time within __________, DOA of ____________ Other routes- ______,_______,_________,__________

1-2; 1 min; 5-10 mins 5-10; 5 mins; 10-20 mins orally, intrathecally, rectally, nasally

Ketamine Systemic Effects • – CVS- ____SBP,DBP, ——-PR,→____CO Resp system- ______ stimulation, with ————- of airway reflexes but _______ still possible. Broncho__________. CNS- _____ CBF, CMR, IOP. _____ ,______ . State of ________ Anaesthesia. GIT- _____mucous secretions including salivation, _____ Post-op. nausea and vomiting. Others- ______ uterine tone.↑ Adr, and Noradr, circ. Levels

↑; ↑; ↑ mild; preservation; aspiration; dilatation ↑; Amnesia, Analgesia; Dissociative ↑; ↑; ↑

Ketamine Metabolism- occurs in ______; excreted in ________

Liver Urine

Ketamine Clinical importance- Good _________ and ________ Potent _________ effect Can be used as _____ anaesthetic agent, ______ for many surgeries Anaesthesia in ________,_____________ , LMIC

CVS and RS stability Analgesic; sole; TIVA war zones ,burn dressing

KETAMINE Disadvantages •Slower ———— time •Slower _________ •Poor ___________ •Unpleasant __________,________

induction; recovery muscle relaxation dreams, hallucinations,

emergence delirium from ketamine can be reduced by premedication with _______,_________,__________

diazepam, midazolam, lorazepam

Ketamine Contra-indication •_______tension •___________ disturbance

Hyper Psychiatric

Propofol. A ________ derivative: 2,6-diisopropylphenol Presented as _________-in-water emulsion containing 1% (10 mg/ml, common) or 2% propofol in soybean, purified egg phosphatide, and sodium hydroxide. No preservative, good culture medium for bacteria

phenol white oil

Propofol The onset of its action begins after ______ After a single dose patient recovers after ________ with a _______ head and _____ hangover.

30 s. 5 min Clear; no hangover

Administration of Propofol •For induction: iv bolus _________ mg/Kg, with onset time of ______, DOA ________ after a single dose •For maintenance: infusion of _______ mg/Kg/hr For Children: ↑doses above by _____% for induction, and by _______% for maintenance

1.5-2.5 30 secs; 10 mins 4-12 ; 50; 25- 50

Propofol Effects CVS: ____ BP, ___ SVR→____ CO by ____ %, without ____________ . Attenuates haemodynamic response to laryngoscopy Rapid bolus injection may cause _________ and __________ RS: ________ with rapid bolus, suppression of ________, depresses ventilatory response to _________,____________ . Broncho_________.

↓; ↓; ↓; 20; reflex increase in HR bradycardia and asystole apnoea; laryngeal reflexes hypercarbia and hypoxia dilatation

PROPOFOL CNS: ______,______ induction with _______ and ————- recovery. -_____ ICP, CPP, CMRO2, beneficial in __________. GIT: intrinsic __________ properties Others- free radical scavenger, Long term infusion (>48hrs) may lead to _______________ , and ↑ mortality esp. in __________ Causes ——— on injection, may be reduced by Addition of ________, _______ the drug, or use of ____________

smooth, rapid rapid and clear-headed ; ↓; neurosurgery anti-emetic ; hypertriglyceridaemia children in ICU; pain; Lidocaine; cooling; large veins

Propofol Metabolism- mainly in ______ to (active or inactive?) __________ + other extra hepatic clearance. Metabolites, and small unchanged form excreted in urine Renal and Hepatic disease have NO clinically significant effect on metabolism

Liver; inactive glucoronide

Propofol Contraindications- ______, untreated __________, ______tension pts

Shock hypovolaemia hypo

Ketofol (mixture of ________ and _________ ) Different concentrations(____,____,____,_____) Some studies have been done to show efficacy of the combination in procedural sedation.

ketamine and propofol 1:1, 1:2, 1:3, 1:4

Midazolam A water (soluble or insoluble?) ________-________ (Mildly or Highly?) protein bound, ______% Presentation- ________, ________ solution

soluble ; Imidazo-benzodiazepine Highly ; 97% clear, colorless

Midazolam Main actions Hypnosis- iv ________ __________ ___________ __________ amnesia Anticonvulsant ___________

induction; Sedation Anxiolysis; Anterograde Muscular relaxation

Midazolam Administration _____________/sedation: im/iv dose :_____ mg/kg _______ pre-induction Induction dose: iv- ________ mg/kg onset time within ______, DOA _________ Other routes- intrathecal, epidural, oral ( ________/__________)

Premedication 0.05-0.1; 30mins 0.2-0.3; 2-3 mins 10-15 mins sweetened/ flavored

Midazolam Effects CVS: ____BP,____ SVR, but _______ PR lesser than propofol, thiopentone, hence produces _____________ haemodynamics RS: impairs respiratory response to ________, respiratory _________, ______ may occur CNS: ____ CBF, ____ CMRO2→ ____ ICP- brain protection against ischaemia

↓; ↓; reflex ; reflex ↑ relatively stable hypercapnoea; depression; apnoea ↓; ↓; ↓

Midazolam Metabolism- occur in _____, excreted in _______. -termination of action of single dose is due to _____________ from _______ to ___________

Liver; urine re-distribution brain ; peripheral tissues