Common Anesthesia Medications Flashcards
Discuss determinants of cardiac status and ways to affect it
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
Discuss general principles for vasoactive and vasodepressive medications
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
Discuss the mechanism of action of each of the vasoactive agents
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
Discuss the mechanism of action of vasodepressive agents
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
Discuss the mechanism, indication and contraindications for benzodiazepines
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
Discuss the risk factors for post-operative nausea and vomiting
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
Discuss the mechanism and dose of ondansetron
- 4-8mg IV Q6H after surgery
Mechanism - antagonist to 5HT3 receptor in chemoreceptor trigger zone and GI tract
Discuss the mechanism and dose of dexamethasone for PONV
- 8-10mg IV before induction
- unknown mechanism
Discuss mechanism and dose for haloperidol and prochlorperazine
- 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
Discuss mechanism and dose of diphenhydramine
- 25-50mg PO/IV Q6H
Mechanism - H1 receptor antagonist at vomiting centre and vestibular system
Discuss when to give anti-emetic prophylaxis
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
Discuss the indications and contraindications for muscle relaxants
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
Discuss the two types of muscle relaxants
- Competitive non-depolarizing muscle relaxant that can be antagonized
- Mivacurium, Rocuronium
- Non-competitive depolarizing muscle relaxant that cannot be antagonized
- Succinylcholine
Discuss the mechanism, dose and reversal of rocuronium
- 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
Discuss the mechanism and dose for succinylcholine
- 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
Discuss the ascending sensory nociceptive pathway
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
Discuss the descending modulating pathway
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
Differentiate between acute and chronic pain
- Acute pain serves a purpose
- Chronic pain when lasts longer than 3-6 months or persisting beyond resonable amount of time of tissue healing
Discuss analgesia at each of the ascending and descending pain pathways
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
Discuss the mechanism of action of acetaminophen
- inhibit central COX enzyme and spinal serotonergic pathway as well as decrease inflammation
Discuss the mechanism of action of NSAID
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
Discuss the mechanism of action for opioids
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
