Lecture 4 - IV Anesthetics Flashcards
Name the IV Anesthetics
what are the three goals of a balanced anesthetic technique?
Propofol
Ketamine
Etomidate
Dexmedetomidine
Benzodiazepines
Barbituates
Balanced technique: Amnesia, Analgesia, Muscle Relaxation. Not acheived By IV anesthetics alone; must use combination of drugs
Propofol
- mechanisms
- considerations upon administration of the drug
mechanism: Potentiation of chloride current mediated through the GABA Type A receptor complex; increases this conductance therefore further inhibiting the post synaptic cell and inhibiting AP
Considerations: have to use with sterile technique; Must use within 6 hours after opening; Do not give to persons with egg allergies
Propofol
- pharmacokinetics (lipid solubility, metabolism, excretion, redistribution)
Highly lipid soluble Rapid onset Rapidly metabolized by the liver Excreted by the Kidneys Redistribution -- wake up 8-10 minutes after induction bolus
Propofol -- CNS effects CVD effects Respiratory effects GI
CNS – AMNESIA with NO ANALGESIA properties.
deceased CNS blood flow and metabolic rate
Decreases ICP
Anticonvulsant
Neuro protective
CVD – Vasodilation; Decreased systemic blood pressure
Respiratory – Depressant; suppresses upper airway reflexes
Anti-emetic
propofol Side effects;
what is propofol Infusion syndrome?
Pain on injection;
Propofol Infusion Syndrome: —
lactic acidosis via an unclear mechanism
Reversible in early stages
propofol Clinical uses:
- Induction of anesthesia — but NOT ANALGESIA
- Maintenance of anesthesia — As an infusion , in combination with volatile anesthetics and opioids (balanced anesthesia regimen) or with opioids and benzodiazepines (total intravenous anesthesia technique)
- Sedation – Repeated boluses and/or intravenous infusion for procedure like endoscopy, MRI, dental extractions etc
Ketamine –
mechanism –
Pharmacokinetics (solubility, onset, duration, metabolism, excretion)
Mechanism: Antagonist of the NMDA Receptor (+some direct mu related activity). inhibits the effects of glycine and glutamine; inhibiting the Action potential
lipid soluble, low protein binding Rapid onset, relatively short duration Metabolized in the liver to Nor ketamine ( less potent) Excreted in the urine Wake up is due to redistribution
Ketamine effects:
CNS
CVD
Resp
CNS Effects – Dissociative Anesthesia, + ANALGESIA, increased Cerebral blood flow and metabolitic rate, can produce seizure like activity (Not used for neurosurgery)
CVD - Sympathetic stimulation; Increased BP, HR, C.
Resp – No effect on rate; (apnea with rapid infusion); bronchodilator (good for asthmatics); Can increasd salivary and bronchail secretions (therefore given with glycopyrolate)
Ketamine –
Primary side effect:
how can this be managed?
Emergency Delerium; Nightmares hallucinations (decreased with benzos)
Clinical Uses of ketamine
how is it administered
• Induction of anesthesia:
IV or IM
Maintenance:
Sedation:
Post op pain
Etomidate
Mechanism
Pharmacokinetics (BBB penetrance; peak onset; protein binding; metabolism; excretion)
Mechanism of action: (similar to propofol) – potentiates GABA receptor conductance
Pharamacokinetics – rapid BBB penetrance; peak onset of 1 minute; 76% bound to albumin; Metabolism by ester hydrolysis; excreted in urine and bile
Etomidate effects
- CVD
- resp
- CNS
- endocrine
CVD – minmial changes in BP, HR; good for patients who are cardiovascularly unstable
Resp – Minimal depressant effect
CNS - cerebral vasoconstriction; decreased blood flow and metabolic rate
Endo – Adrenocortical suppression due to 11 beta hydroxylase inhibition
Etomidate
best clinical use
- Clinical Uses:
* Induction of anesthesia — mostly for patients with cardiovascular issues
Dexmedetomidine -
Mechanism
Pharmacokinetics
Mechanism: Agonist of Alpha2 receptors in the pons; decreases NE secretion
Pharmacokintics: Water soluble; short term sedation?
Dexmedetomidine effects
CNS
CVD
RESP
CNS – Analgesia, Sedation; no effect on cerebral metabolic rate
CVD – Depression; brady cardia, hypotension
Resp System – Minimal depressant effect
Dexmedetomidine
clinical use
§ Sedation:
• Short-term sedation of intubated and ventilated patients in the ICU
• Radiological procedures, MRI and interventional radiology
general – loading dose followed by infusion
Benzodiazepines name them; Mechanism Pharmacokinetics (differences in metabolism)
Midazolam, Diazepam, Lorazepam (Ativan)
Mechanism of action -
Enhance affinity of the GABA receptor for GABA
HOWEVER There is a specific binding site
Pharmacokinetics
§ Highly protein bound to albumin
§ Highly lipid soluble
§ Hepatic metabolism:
Midazolam – metabolite is inactive
Diazepam – 2 metabolites are both active; patients have a “hangover” – not a preferred drug
Benzodiazepines
effects
CNS
RESP
CVD
a negative side effect
CNS: Sedation, hypnosis, anterograde amnesia
Anticonvulsant
RESP: minmal resp depression
CVD – slight decrease in systemic vascular resistsnace and BP
Pain with injeciton with Diazepam (like propofol) —
Benzodiazepines
how is it adminstered
best clinical use ?
Pre-operative Medication –
• Midazolam – can be given IV, PO, Rectally, Intranasal
• Diezepam – PO
Barbituates
name a few
Mechanism
Pharmacokinetics –
Thiopental, Methohexital
Mechanism: GABA receptor potentiation
Pharmacokinetics – Metabolized in the liver, excreted in the urine; enhanced effects with alcohol
Barbituates
CNS effects - (general effects; which one can activate epileptic foci)
CVD
RESP
CNS effects: Sedation, anesthesia NO ANALGESIA ↓CBF, ↓ICP, ↓CMRO2 ; Methohexital activates epileptic foci
Cardiovascular system:
• Peripheral vasodilatation with modest ↓ in BP
Respiratory system:
Respiratory depressant effect: ↓minute ventilation, tidal volume and respiratory rate
↓ventilatory responses to hypercapnia and hypoxia
Barbituates
- consideration take when giving bolus through a line? (why?)
a primary side effect
exacerbation of what disease?
Precipitation when mixed with acidic drugs in an IV line, due to its Alkaline pH
* Pain, intense vasoconstriction and gangrene on intra-arterial injection * Exacerbation of acute intermittent porphyria;
Barbituates
clinical uses?
(BUT NOT USED ANYMORE)
Induction of anesthesia:
Neuroprotection:
Treatment of raised intracranial pressure
Treatment of focal cerebral ischemia
