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PHARM INDUCTION DRUGS > INDUCTION DRUGS > Flashcards

INDUCTION DRUGS Flashcards

1
Q

Midazolam -Trade name -classification

A

-Versed

Benzodiazepine, hypnotic, sedative

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2
Q

Midazolam -Contradictions

A

Pregnancy

Lactation

CNS depression

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3
Q

Midazolam -Route -Dose

A

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)

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4
Q

Midazolam -MOA

A

(CNS depressant) Extensively bound to plasma proteins but MOA is unknown.

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5
Q

Midazolam -Onset, Peak, Duration

A

Onset IV:30 - 60 seconds

Peak IV: 5.6 minutes

Duration IV: 15 - 80 minutes

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6
Q

Midazolam -Elimination

A

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.

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7
Q

Midazolam -miscellaneous

A

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

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8
Q

Sublimaze -Trade name -Classification

A

Fentanyl Opioid Agonist

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9
Q

Fentanyl -contradictions

A
  • 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.
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10
Q

Fentanyl -route -dose

A

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

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11
Q

Fentanyl -MOA

A

Mu-receptors, produce analgesia.

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12
Q

Fentanyl -onset, peak, duration

A

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.

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13
Q

Fentanyl -elimination

A

Renal Half time: 3.1 - 6.6 hours

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14
Q

Fentanyl -miscellaneous

A

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
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15
Q

Lidocaine -trade name -classification (2)

A

(Xylocaine)

Class 1b antiarrhythmic agent (membrane stabilizing and mild NA channels effects) and a local anesthetic.

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16
Q

Lidocaine -contradictions

A

Do Not give this drug when PVCs occur with bradycardia or escape rhythm.

May cause Seizures, Restlessness, vertigo, tinnitus, and difficulty focusing.

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17
Q

Lidocaine -route -dose

A

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

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18
Q

Lidocaine -MOA

A

It is amide, binds to specific sites in voltage gated sodium channels blocking sodium current reducing excitability of neuronal, cardiac, CNS.

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19
Q

Lidocaine -onset, peak, duration

A

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)

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20
Q

Lidocaine -elimination

A

Hepatic

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21
Q

Lidocaine -miscellaneous

A

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

22
Q

propofol -trade name -classification

A

trade name: Diprivan

classification: Sedative/Hypnotic, anesthesia induction agent

23
Q

propofol -contradictions

A
  • 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.

24
Q

propofol -route -dose

A

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)

25
Q

propofol -MOA

A

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)

26
Q

propofol -onset, peak, duration

A

Onset: Dose Dependent, rapid onset, less than a minute

Peak 1 minute

Duration 15 - 45 minutes depending on dose

27
Q

propofol -elimination

A

Hepatic P450 –water soluble metabolites excreted by the kidneys. Less than 0.3% is unchanged in urine

Half life 0.5 - 1.5 hours

28
Q

propofol -miscellaneous

A

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)

29
Q

Rocuronium -trade name -classification

A

Zemuron, Esmeron (trade)

Classification Nondepolarizing Neuromuscular blocker (steroidal compound)

30
Q

Rocuronium -contradictions

A

Bromide hypersensitivity

Precaution in liver patients

31
Q

Rocuronium -route -dose

A

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

32
Q

Rocuronium -MOA

A

Binds to nicotinic acetylcholine receptors at the postsynaptic muscle membrane. Competes with acetylcholine for the active binding sites at the postsynaptic nicotinic acetylcholine receptor

33
Q

Rocuronium -onset, peak, duration

A

Onset Intermediate-acting → 1 - 3 minutes

Peak 1.7 minutes

Duration 30 - 60 minutes *could be prolonged in pts with hepatic and renal disease*

34
Q

Rocuronium -elimination

A

Half life 71 minutes

Billary

35
Q

Rocuronium -miscellaneous

A

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

36
Q

Etomidate -trade name -classification

A

Trade name- Amidate.

Classification- Central nervous system agent; nonbarbiturate hypnotic without analgesic activity

37
Q

Etomidate -contradictions

A

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.

38
Q

Etomidate -route -dose

A

Dose-0.2-0.3 mg/kg over 30 to 60 seconds

Route IV

39
Q

Etomidate -MOA

A

(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.

40
Q

Etomidate -onset, peak, duration

A

Onset- 30seconds-60 seconds

Peak- within 1 minute

Duration- 3 to 10 mins

41
Q

Etomidate -elimination

A

ester hydrolysis is the primary mode of metabolism in the liver and plasma

42
Q

Etomidate -miscellaneous

A

Myoclonus (reduced by benzo premedication), tonic movements, HTN, hypotension, Tachycardia, bradycardia, PONV, hypo/hyperventilation, laryngospasm, hiccups, snoring.

43
Q

Succinylcholine -trade name -classification

A

Anectine, Quelicin (trade)

Classification Depolarizing skeletal muscle relaxant

44
Q

Succinylcholine -contradictions

A
  • 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.
45
Q

Succinylcholine -route -dose

A

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

46
Q

Succinylcholine -MOA

A

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)

47
Q

Succinylcholine -onset, peak, duration

A

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.

48
Q

Succinylcholine -elimination

A

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

49
Q

Succinylcholine -miscellaneous

A

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.

50
Q
A

PHARM INDUCTION DRUGS (1 decks)

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