Common Anesthesia Medications Flashcards

1
Q

Discuss determinants of cardiac status and ways to affect it

A

Preload
- Decrease with venous vasodilators (nitroglycerine, nitroprusside) or diuretics (furosemide)
- increase with IV fluids
Heart Rate
- decrease with beta blockers (metoprolol, esmolol) or calcium channel blockers (diltiazem, verapmil)
- increase with anticholinergics (atropine), beta agonist (ephedrine, epinephrine) or pacemaker
Contractility
- decrease with general anesthetic or beta blocker (labetalol) or CCB
- increase with beta agonist (ephedrine, epinephrine, dobutamine) or aortic balloon pump
Afterload
- decrease with arterial vasodilators (nitroprusside, hydralazine) or ACE inhibitor
- increase with alpha agonist (phenylephrine, norepinephrine) or IV fluids

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2
Q

Discuss general principles for vasoactive and vasodepressive medications

A

Vasoactive
- bradycardia without hypotension: atropine
- hypotension and bradycardia: ephedrine
- hypotension without bradycardia: phenylephrine
- hypotensive shock: phenylephrine or norepinephrine
- cardiac arrest: epinephrine
Vasodepressive
- hypertension and tachycardia in response to surgery: opioid or increase inhaled analgesia
- hypertensive crisis: labetalol

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3
Q

Discuss the mechanism of action of each of the vasoactive agents

A

Ephedrine
- indirect stimulation of adrenergic receptors (alpha 1, beta 1&2) leading to vasoconstriction (alpha 1), increased HR and contractility (beta 1)
Phenylephrine
- selective alpha-1 adrenergic receptor agonist leading to vasoconstriction
Epinephrine
- non-selective agonist of all adrenergic receptors (alpha 1&2, beta 1&2&3) leading to vasoconstriction, increased HR and contractility
Norepinephrine
- mostly alpha 1 and 2 adrenergic receptor agonist
Atropine
- anticholinergic by competitive antagonism of muscarinic receptor which increase HR
Vasopressin
- ADH bind to ADH receptor leading to vasoconstriction

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4
Q

Discuss the mechanism of action of vasodepressive agents

A

Hydralazine
- alpha 1 antagonist leading to peripheral vasodilation and decrease BP
Labetalol
- alpha 1 and beta 1&2 antagonist resulting in vasodilation, decrease HR and decrease contractility

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5
Q

Discuss the mechanism, indication and contraindications for benzodiazepines

A
Mechanism
- Inhibit GABA
Indication
- anxiolytic
- hypnotic
- alcohol withdrawal
- anticonvulsant
- general anesthesia
Contraindication
- Hx of substance disorder
- fall risk
- cognitive disorder
- narrow angle, glaucoma, OSA, myasthenia gravis, liver disease
- pregnancy
- use of CNS depressant
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6
Q

Discuss the risk factors for post-operative nausea and vomiting

A
Patient
- young
- female
- prior hx
- motion sickness
- non-smoker
Surgical
- longer surgery
- gynecological, urology, breast or middle ear surgery
Anesthetic
- general anesthesia
- peri- or post-op opioids
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7
Q

Discuss the mechanism and dose of ondansetron

A
  • 4-8mg IV Q6H after surgery
    Mechanism
  • antagonist to 5HT3 receptor in chemoreceptor trigger zone and GI tract
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8
Q

Discuss the mechanism and dose of dexamethasone for PONV

A
  • 8-10mg IV before induction

- unknown mechanism

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9
Q

Discuss mechanism and dose for haloperidol and prochlorperazine

A
  • haloperidol 0.5-4mg IV at end of surgery
  • prochlorperazine 5-10mg IV at end of surgery
  • metoclopramide option post-operative
    Mechanism
  • D2 receptor antagonist in chemoreceptor trigger zone
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10
Q

Discuss mechanism and dose of diphenhydramine

A
  • 25-50mg PO/IV Q6H
    Mechanism
  • H1 receptor antagonist at vomiting centre and vestibular system
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11
Q

Discuss when to give anti-emetic prophylaxis

A
Low Risk
- Hx of PONV or 2 risk factors
- single antiemetic
Moderate Risk
- Hx of PONV and 1 risk factor or 3 risk factors
- 2 agents with one being ondansetron
High Risk
- Hx of PONV on more than 1 occasion plus 1 risk factor
- all anti-emetics
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12
Q

Discuss the indications and contraindications for muscle relaxants

A
Indications
- induction
- mechanical ventilation
- during surgery
- prior to ECT
- emergency treatment for laryngospasm
Contraindications
- Inability to maintain airway
- lack of resuscitation equipment
- known hypersensitivity
- positive history of malignant hyperthermia
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13
Q

Discuss the two types of muscle relaxants

A
  • Competitive non-depolarizing muscle relaxant that can be antagonized
    • Mivacurium, Rocuronium
  • Non-competitive depolarizing muscle relaxant that cannot be antagonized
    • Succinylcholine
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14
Q

Discuss the mechanism, dose and reversal of rocuronium

A
  • 4-16mcg/kg/min
    Mechanism
  • competitive antagonist to cholinergic nicotinic receptor
  • onset in 60sec but last 40 minute
    Reversal
  • Atropine 0.01mg/kg with Edrophonium 0.5-1mg/kg
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15
Q

Discuss the mechanism and dose for succinylcholine

A
  • 1mg/kg
  • infusion of 50-150mcg/kg/min
    Mechanism
  • binds nicotinic receptor and depolarizes motor plate so that post-synaptic membrane remains depolarized and unresponsive to ACh
  • onset of 60 sec and lasts 5-10 minutes
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16
Q

Discuss the ascending sensory nociceptive pathway

A

Transduction
- noxious stimuli activate nociceptor on free nerve endings
Transmission
- primary afferent sensory neuron transmit signal from periphery to spinal cord
- Delta fiber are myelinated mechanoreceptor and thermoreceptors so have fast somatotopically organized pain
- sharp/pricking pain
- C-fiber have polymodal receptor and are unmyelinated and less somatopically organized
Transmission
- primary afferent neuron synapse with secondary afferent neuron in substantio gelitanosa within dorsal horn
- secondary afferent cross spinal cord and travel in contra-lateral lateral spinothalamic tract to thalamus
- thalamus intergrate and sort according to region
- in ventral posterior lateral nucleus of thalamus synapse on tertiary neuron which goes to parietal lobe
Perception
- interpretation of pain

17
Q

Discuss the descending modulating pathway

A

Origin in Brainstem
- peri-aqueductal grey matter and locus ceruleus
- can be controlled by higher cerebral areas
Descending
- Descending nerve fibers travel in spinal cord to synapse on primary and secondary afferent neuron
- descending fiber secrete enkephalin, serotonin and norepinephrine to inhibit primary and secondary afferent neuron

18
Q

Differentiate between acute and chronic pain

A
  • Acute pain serves a purpose

- Chronic pain when lasts longer than 3-6 months or persisting beyond resonable amount of time of tissue healing

19
Q

Discuss analgesia at each of the ascending and descending pain pathways

A

Ascending Nociceptive Pathway
- Foundational analgesia block nociception, transduction or transmission by decreasing inflammation
- local anesthetic block Na channel to prevent transmission
Descending Anti-Nociceptive Pathway
- pro-antinociceptive which activate descending pathway
- opioid activate endogenous receptors
- tramadol activate endogenous opioid receptors, alpha 2- adrenergic and serotonin
Descending Pro-Nociceptive Modulation
- inhibit descending pro-nociceptive signal
- NMDA antagonist (ketamine)
- anti-convulsants block voltage gated Ca channel

20
Q

Discuss the mechanism of action of acetaminophen

A
  • inhibit central COX enzyme and spinal serotonergic pathway as well as decrease inflammation
21
Q

Discuss the mechanism of action of NSAID

A

Reversible COX-1 and COX-2 inhibitors
- inhibit COX-1 leading to increased gastric secretion and disruption of platelet homeostasis
- inhibit COX-2 to inhibit inflammation and acute pain
COXib is irreversible inhibitor of COX-2 Only
- decreased risk of PUD
- preserved platelet homeostasis which improves tissue healing
- COX-2 inhibition only
- has increased risk of cardiovascular disease
- contraindicated in those with sulfa allergy

22
Q

Discuss the mechanism of action for opioids

A

Mechanism
- activate mu receptor resulting in analgesia, sedation and respiratory depression
- activate kappa receptor resulting in weak analgesia, sedation and psychomimetric side effect
- activate delta receptor resulting in weak analgesia and respiratory depression
Work at 4 Levels
- suppression of limbic and cerebral cortex so not aware of pain
- activation of peri-aqueductal grey in brainstem to activate anti-nociceptive pathway
- inhibit neurotransmission at synapse between primary and secondary afferent neuron
- activate peripheral opioid receptors to decrease pro-inflammatory neuropeptides