INDUCTION DRUGS Flashcards
Midazolam -Trade name -classification
-Versed
Benzodiazepine, hypnotic, sedative
Midazolam -Contradictions
Pregnancy
Lactation
CNS depression
Midazolam -Route -Dose
IV, IM, PO
(Adults)
IV: 1 - 2.5 mg
PO: 0.25 - 1 mg/kg,
IM: 0.02 - 0.08 mg/kg
(Children Pre-op) PO: 0.25 - 1mg/kg (20mg max)
Midazolam -MOA
(CNS depressant) Extensively bound to plasma proteins but MOA is unknown.
Midazolam -Onset, Peak, Duration
Onset IV:30 - 60 seconds
Peak IV: 5.6 minutes
Duration IV: 15 - 80 minutes
Midazolam -Elimination
Elimination Half-time (in the plasma) is 1.9 hours (9.5 hours later = 96.875% cleared)
Cleared primarily by the liver but kidneys as well (elimination half-time is not altered by renal failure). Metabolized by cytochrome p450 enzymes.
Midazolam -miscellaneous
benzodiazepine antagonist - flumazenil.
small doses (0.5-1 mg/kg) for paradoxical vocal cord motion and stridor post surgery.
Passes BBB
Cardiopulmonary bypass increases half-time dramatically.
Most common side effect is depression of ventilation caused by a decrease in hypoxic drive. Known for powerful amnestic effect
Sublimaze -Trade name -Classification
Fentanyl Opioid Agonist
Fentanyl -contradictions
- Reduce fentanyl doses in elderly or hypovolemic
- Crosses the placental barrier, may produce depression of respiration in the neonate.
- Prolonged respiratory depression after cessation of transdermal patch use.
Fentanyl -route -dose
Transdermal, IV, IM, Epidural/Spinal Analgesia:
IV: 1 - 2 mcg/kg
Induction: 30 mcg/kg; infusion: 0.2 mcg/kg/min
Epidural bolus:1 - 2 mcg/kg; infusion: 2 - 60 mcg/hr
Spinal bolus: 0.1 - 0.4 mcg/kg
Fentanyl -MOA
Mu-receptors, produce analgesia.
Fentanyl -onset, peak, duration
Onset
IV: within 30 seconds
IM: less than 8 minutes
Epidural/spinal: 4 - 10 minutes.
Peak IM: 20 - 30 min IV: 20 - 30 min
Duration IV: 30 - 60 minutes; IM: 1 - 2 hours Epidural/spinal: 4 - 8 hours.
Fentanyl -elimination
Renal Half time: 3.1 - 6.6 hours
Fentanyl -miscellaneous
Antidote: Narcan 0.2 - 0.4 mg IV
- Used as an induction agent to reduce the amount of other sedation medications
- Taken up 75% from lungs first pass pulmonary uptake
Lidocaine -trade name -classification (2)
(Xylocaine)
Class 1b antiarrhythmic agent (membrane stabilizing and mild NA channels effects) and a local anesthetic.
Lidocaine -contradictions
Do Not give this drug when PVCs occur with bradycardia or escape rhythm.
May cause Seizures, Restlessness, vertigo, tinnitus, and difficulty focusing.
Lidocaine -route -dose
Route: IV, IM, SQ, Topical, Epidural, Spinal.
Dose:
Caudal or epidural: 20 to 30 mL 1% solution (200- 300 mg); may also use 1.5 % and 2% solutions. With epinephrine for anesthesia other than spinal, max dose is 500 mg.
IV- 1 mg/kg bolus then 0.5 mg/kg/hr should not exceed 300 mg/hr. Use only preservative free forms for IV.
Anesthesia Induction dose: 20 mg IV Infiltration or PNB: 0.5 to 5 mg/kg
Transdermal: 3 patches within a 24 hr time frame Local:topical 0.6 to 3 mg/kg
Transtracehal: 80 to 120 mg, SLN 40 to 60 mg
Lidocaine -MOA
It is amide, binds to specific sites in voltage gated sodium channels blocking sodium current reducing excitability of neuronal, cardiac, CNS.
Lidocaine -onset, peak, duration
Onset:
IV 45 to 90 secs; infiltration 0.5 to 3 mins; epidural 5 to 25 mins
Peak:
IV 1 to 2 mins; infiltration and epidural less than 30 mins
Duration:
IV 10 to 30 mins; infiltration 0.5 to 1.5 hours, with epinephrine: 2 to 6 hours; epidural 1 to 3 hours, (prolonged with epinephrine)
Lidocaine -elimination
Hepatic
Lidocaine -miscellaneous
May be given in conjunction with epinephrine to help increase potency and decrease systemic effects.
Helps with laryngeal spasms.
Also blunts the gag reflex.
Adverse Effects: hypotension, bradycardia, heart block, respiratory depression or arrest, tinnitus, post-spinal block headache, loss of bladder and bowel control
propofol -trade name -classification
trade name: Diprivan
classification: Sedative/Hypnotic, anesthesia induction agent
propofol -contradictions
- Avoid in patients with known hypersensitivity to Propofol, its components or have a lipid metabolism disorder
- Do not use with patients who are sensitive to sodium metabisulfite
–may cause anaphylactic symptoms -Caution is advised in elderly, debilitated, and cardiac-compromised patients, pts with respiratory disease
-Controversy exists regarding whether Propofol should be avoided in patients who are allergic to eggs, soy, or peanuts.
propofol -route -dose
IV Dose:
Induction: 1.5 - 2.5 mg/kg
Anesthesia maintenance: 100 - 300 mcg/kg/min
Subhypnotic: 10 - 15 mg (used as antiemetic or to treat neuropathic pain)
propofol -MOA
Increases GABA affinity for GABAa receptor. This decreases the rate of disassociation of the inhibitory neurotransmitter, GABA from the receptor and increases the duration of the GABA-activated opening of the chloride channel which leads to hyperpolarization of cell membranes (inhibition of the cell)
propofol -onset, peak, duration
Onset: Dose Dependent, rapid onset, less than a minute
Peak 1 minute
Duration 15 - 45 minutes depending on dose
propofol -elimination
Hepatic P450 –water soluble metabolites excreted by the kidneys. Less than 0.3% is unchanged in urine
Half life 0.5 - 1.5 hours
propofol -miscellaneous
Can cause pain at injection site
Does NOT trigger malignant hyperthermia
· Strongly supports growth of E-cloi & Psudomonas aeruginosa.
· Prolonged infusions may result in excretion of green urine reflecting the presence of phenols. This does not alter renal function.
· Propolfol is associated with significant decreases in intraocular pressure that occur immediately after induction of anesthesia
· Can cause lactic acidosis in pediatric and adult patients with prolonged, high-dose infusions (Propofol infusion syndrome)
Rocuronium -trade name -classification
Zemuron, Esmeron (trade)
Classification Nondepolarizing Neuromuscular blocker (steroidal compound)
Rocuronium -contradictions
Bromide hypersensitivity
Precaution in liver patients
Rocuronium -route -dose
IV RSI dose: 0.6 - 1.2mg/kg
fasciculation dose:10% of full dose given before propofol dose when using succs.
maintenance dose adults: 0.1 - 0.2 mg/kg
children 0.08 - 0.12 mg/kg
Rocuronium -MOA
Binds to nicotinic acetylcholine receptors at the postsynaptic muscle membrane. Competes with acetylcholine for the active binding sites at the postsynaptic nicotinic acetylcholine receptor
Rocuronium -onset, peak, duration
Onset Intermediate-acting → 1 - 3 minutes
Peak 1.7 minutes
Duration 30 - 60 minutes *could be prolonged in pts with hepatic and renal disease*
Rocuronium -elimination
Half life 71 minutes
Billary
Rocuronium -miscellaneous
Reversal: Sugammedex Rocuronium
can be used in patients who are hemodynamically compromised due to the less or no histamines present in the drug
Use of inhalation agents, antibiotics, and magnesium may prolong the duration of action Drug of choice in RSI when succinylcholine is contraindicated
Etomidate -trade name -classification
Trade name- Amidate.
Classification- Central nervous system agent; nonbarbiturate hypnotic without analgesic activity
Etomidate -contradictions
Use cautiously in immunosuppressed patients.
Sepsis & Hemorrhage- as etomidate causes adrenocortical suppression by producing a dose-dependent inhibition of the cholesterol to cortisol conversion.
Patients with sepsis or hemorrhage need intact cortisol response.
Etomidate -route -dose
Dose-0.2-0.3 mg/kg over 30 to 60 seconds
Route IV
Etomidate -MOA
(Gaba- mimetic) A selective modulator of GABAA receptors as the site of action. Etomidate exerts its effects on GABAa receptors by binding directly to a specific site on the protein- enhancing the affinity of the inhibitory neurotrasmitter gaba for these receptors.
Etomidate -onset, peak, duration
Onset- 30seconds-60 seconds
Peak- within 1 minute
Duration- 3 to 10 mins
Etomidate -elimination
ester hydrolysis is the primary mode of metabolism in the liver and plasma
Etomidate -miscellaneous
Myoclonus (reduced by benzo premedication), tonic movements, HTN, hypotension, Tachycardia, bradycardia, PONV, hypo/hyperventilation, laryngospasm, hiccups, snoring.
Succinylcholine -trade name -classification
Anectine, Quelicin (trade)
Classification Depolarizing skeletal muscle relaxant
Succinylcholine -contradictions
- Succinylcholine should not be used for routine intubation in children younger the age of 12 because of reports of sudden cardiac arrest in children with undiagnosed duchenne muscular dystrophy and with muscle disorders.
- Malignant hyperthermia, genetic variants of plasma cholinesterase or cholinesterase deficiencies, myopathies associated with elevated creatinine phosphokinase values, muscle disorders or muscular dystrophies, acute narrow-angle glaucoma, severe muscle trauma or muscle wasting, neurologic injury (i.e., paraplegia, quadriplegia, spinal cord injury, or cerebrovascular accident),
- hyperkalemia, severe sepsis, electrolyte imbalances, or third-degree burns over more than 25% total body surface due to potentially life threatening hyperkalemia.
- Repeated doses at short intervals (less than 5 minutes) are associated with bradycardia.
Succinylcholine -route -dose
Dose Adults:
intravenous: 1 - 1.5 mg/kg Children: intravenous: 1 - 2 mg/kg; intramuscular: 2 - 4 mg.kg
Dosage forms: injection: 20 mg/mL; powder for infusion: 500 mg (mix in 500 mL for 1 mg/mL solution.
Route IV, IM
Succinylcholine -MOA
Partial agonist against the nicotinic acetylcholine receptor (nAChR) and depolarizes (opens) the ion channels.
Binds to two alpha subunits
-This opening requires the binding of only one molecule of SCh to the α subunit. The other α subunit can be occupied by either acetylcholine or SCh. -Because SCh is not hydrolyzed by acetylcholinesterase, the channel remains open for a longer period of time than would be produced by acetylcholine, resulting in a depolarizing block (sustained depolarization prevents propagation of an action potential)
Succinylcholine -onset, peak, duration
Onset 30 - 60 secs
Peak 2 minutes
Duration 5 - 10 minutes
The short duration of action of succinylcholine is due to its rapid hydrolysis by butyrylcholinesterase (plasma cholinesterase) to succinylmonocholine and choline, such that only 10% of the administered drug reaches the neuromuscular junction.
Succinylcholine -elimination
Cleared from the area of the NMJ and is exposed to hydrolysis by plasma cholinesterase 90% metabolized by cholinesterase in plasma. 10% excreted unchanged by the kidneys
Half life 47 seconds
Succinylcholine -miscellaneous
Pretreat with atropine because of the incidence of bradycardia
S/S: Sinus bradycardia, junctional rhythm, and even sinus arrest.
Hyperkalemia: Associated with approximately 0.5 mEq/dL increase in the plasma potassium concentration from the skeletal muscles in healthy individuals, which is well tolerated and generally does not cause dysrhythmias.
Increased intraocular pressure: The intraocular pressure peaks at 2 to 4 minutes after administration and returns to normal by 6 minutes,
Increased intracranial pressure, Myoglobinuria, Myalgias, Masseter spasm
Cardiac dysrhythmias are most likely to occur when a second dose of succinylcholine is administered approximately 5 minutes after the first dose.
These cardiac effects reflect the actions of succinylcholine at cardiac muscarinic cholinergic receptors where the drug mimics the physiologic effects of acetylcholine.
