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182 Cards in this Set
- Front
- Back
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What are the 2 opioid receptors that cause ventilatory depression and physical dependence?
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Mu2 and Delta
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Which opioid has the longest elimination half time?
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Fentanyl (3.1-6.6)
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Which opioid has the shortest elimination half time?
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Remifentanil (0.17-0.33)
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Which opioid has the largest lipid solubility coeffeicient?
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Sufentanil 1778
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Which opioid has the smallest lipid solubility coeffeficient?
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Morphine (1.4)
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What affect do opioids have on cardiovascular system?
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generally minimal
Meperidine and Morphine can cause histamine release and decrease BP and CVR Fentanyl family can cause vagus mediated bradycardia |
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What effect do opioid have on Respiratory system?
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Decrease response to hypercarbia
Decrease hypoxic drive Muscle rigidity can occur |
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What affect do opioid have on CNS
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Decrease CBF, ICP, and CMRO2 (less than benzos and barbs do)
stimulate the chemoreceptor trigger zone (N/V) |
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What affect do opioids have on GI system?
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increase gastric emptying time
decrease peristalsis biliary spasm |
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What affect do opioid have on Endocrine system?
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block stress hormone release
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what is Meperidine metabolized to?
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normeperidine: can cause seizures
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How is morphine metabolized?
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conjugated with glucuronic acid to active metabolite
Morphine-3-glucuronide (inactive) Morphine- 6-glucuronide (active metabolite with potency and duration greater than that of morphine) |
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How is Remifentanyl metabolized and what does this do to elimination half time?
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Metabolized by Ester Hydrolysis, so doesn't go through Phase I and II and has a much faster half time than other opioids (10 minutes)
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List the Risk factors for PONV
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age: Pedi> adult
Gender: Femals> males (4X increase with menstrual cycle) Body weight: obesity Nonsmoker Hx of N/V or motion sickness Anxiety Presence or absence of food Gastroparesis Type of surgery Longer surgery Anesthetic agents: nitrous and opioids |
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What types of surgery can increase risk for PONV?
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abdominal
females having laparoscopic T& A Strabismus repair Orchiopexy middle ear long surgery |
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What muscle twitch is looked at with ulnar nerve stimulation (TOF)?
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adductor pollicis
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What muscle twitch is looked at with facial nerve (CN VII)stimulation (TOF)?
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orbicularis oculi
corrugator supercilli |
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What is the mechanism of action of the barbiturates?
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Depression of the reticular activating system in brainstem
GABA mediated |
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What are the 2 ways that barbiturates stimulate the GABA receptors?
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1. Enhance the action of GABA: prevent dissociation of GABA from receptors and prolong the effects of GABA
2. Mimic the action of GABA: directly activate the receptor |
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What does GABA receptor stimulation do?
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causes increase conduction of chloride ions into the cell
this results in hyperpolarization of the postsynaptic membrane so it cannot respond and generate an action potential |
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What are the 4 classification of Barbiturates?
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Thiobabiturates
(thiopental and thiamyl) Methylbarbiturates Oxybarbiturates methylthiobarbiturates (not used clinically) |
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Are barbiturates mostly nonionized or ionized at physiologic pH?
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Nonionized
Ex: thiopental has pka= 7.6, so is 60% nonionized |
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Are babiturates acids or bases?
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acids
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Are barbiturates highly lipid soluble or poorly lipid soluble?
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Highly lipid soluble
fat:blood coefficient is high Fat acts as an inactive reservior |
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Are barbiturates highly protein bound?
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yes
Thiopental= 80% methohexital 85% |
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what are 2 contraindications for barbiturate use?
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status asthmaticus
porphyria |
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What are the indications for use of barbiturates in anesthesia?
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Induction
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When a barbiturate is infitlrated, what is the treatment?
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Phentolamine
a dilute solution of papaverien or procaine to inhibit smooth muscle contraction |
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What affect do barbiturates have on HR and BP?
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decraese BP secondary to vasodilation
Increased HR (somewhat) Pt with poorly controlled HTN is prone to BP swings on induction |
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How are barbiturates metabolized?
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Oxidation in the liver to inactive, water-soluble metabolites
*thiopental does have an active metabolite |
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What is the volume of distribution of thipental and methohexital?
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thiopental - 2.5
methohexital- 2.2 |
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What is the clearance of thiopental and methohexital?
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thiopental - 3.4
methohexital - 10.9 |
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is the elimination half time the same for thiopental and methohexital?
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NO
thiopental-11.6 methohexital - 3.9 (has shorter half time b/c has faster clearance) |
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Are benzodiazepines acids or basic drugs?
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basic drugs
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What is the mechanism of action of benzos?
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facilitate binding of GABA to receptor, so don't activate the receptor themselves but modulate response to GABA by enhancing the affinity of receptor for the neurotransmitter
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Why do benzos have a ceiling effect?
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B/c there is a built in limitation of GABAergic transmission
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When would you use thiopental vs. propofol?
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pt has no history of post op N/V
pt staying overnight in hospital |
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What is the chemical structure of benzos?
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7 member diazepine ring
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What happens to the benzene ring of midazolam when it is exposed to physiologic pH?
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it closes and midazolam is converted to a lipid-soluble drug
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what is the pka of midazolam?
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6.15
at physiologic pH, non-protonated, nonionized form predominates (b/c it is a basic drug) |
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does midazolam have active metabolites?
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NO
Diazepam (valium) is metabolized to active metabolites in phase I |
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What is the reversal agent for Benzos?
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Flumazenil
Benzo competitive agonist |
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Succinylcholine is contraindicated in what populations and why?
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Children and Adolescents d/t risk of hyperkalemia, rhabdomyolysis and cardiac arrest in children with undiagnosed myopathies
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Depolarizing mm agents act as
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acetylcholine receptor agonist
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Non depolarizing function as
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competitive anatagonist
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depolarizing agents are metabolized by
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they diffuse away from the neuromuscular junction and are hydrolyzed by the liver and plasma by pseudocholinesterase
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Succ raises serum K by
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0.5 Meq/L
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the more potent the non depolarizing agent
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the longer its speed of on set
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Succ causes what kind of block
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Phase I
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the goal of muscle relaxants is to
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"maximize nicotinic transmission while minimizing muscarinic s/effects"
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Name the 3 locations of cholinergic receptors
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1. post junctional nicotinic cholinergic receptor
2. extra junctional cholinergic receptors-occur post injuries 3. prejunctional nicotinic receptors-interfers with the release |
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NDA-non depolarizing agents cause what kind of block and act as Ach receptors
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Phase II
Competitive antagonist |
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what is up regulation ? and what cautions must we anticipate?
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extra junctional receptors denervation injuries causes chronic decreased Ach release and compensatory increase in ACh receptors= up regulation....
1. Exaggerated response to depolarizers with increased K released 2. Resistance to NDA |
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Tetany
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50 or 100Hz a sustained contraction for 5 sec indicates adequate reversal
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Phase I is characterized by
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decreased contraction, decreased response, decreased amplitude and NO/absent posttetanic potentiation
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When giving succs, when can a Phase II block be present?
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Very high doses of Succ are given or repeated doses
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Ideal conditions for intubation are present when
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fade is seen in the adductor pollicis. Note the A. pollicis is not a centrally located muscle so it takes longer and does not show the ideal conditions of the larnynx for intubation
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what muscles are more releable for extubation conditions
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adductor pollicis
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muscle for monitoring intubation conditions
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facial nerve stimulation of the orbicularis oculi
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side effects of succ
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CV decreased HR
fasciculation hyperkalemia myoglobinuria myalgias MH intragastric pressure intraocular pressure intracranial pressure |
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What does pre-treatment refer to and what are the advantages
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It attenuates muscle fasciculation, giving a dose of NDA prior to succ
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what does a dibucaine number reflect
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quality not quantity ie. the dibucaine number is proportional to pseducholinestrase function and independent of the amount of the enzyme
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why is the onset of succs rapid
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low lipid solubility
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intubating dose for succ
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1-1.5mg/kg IV may be higher if pretreated (4mg/kg IM dose)
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what is down regulation
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condition with fewer Ach receptors eg M. gravis
1. resistance to Depolarizers 2. increased sensitivity to NDA |
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nAcHr UP REGULATION
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sc injury
CVA burns prolonged immobilty prolonged exposure to NMB MS GB |
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Down regulation
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M.gravis
Ach OD organophosphate poisoining |
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Dissapearance of 4th, 3rd, 2nd twitch indicates what % of blockade respectively?
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75%, 80% and 90%
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other clinical indicators of recovery from NMB
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head lift
NIF -25cm Forceful hand grip |
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succ drug interactions
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cholinestrase inhibitors
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atacurium is metabolized by
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ester hydrolysis and hoffman elimination
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metabolite for atacurium is
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laudanosine~ occuras at high levels if pt has liver d'se
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pancuronium s/e include
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vagal blockade and catecholamine release
VEA |
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dosing of neostigimine and glyco ratio, for example 4mg of neo X of glyco
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0.8 mg
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how many twitches must be present inorder to give reversal agent
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1 twitch in TOF
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MAximum dose of neostgime that can be given
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5mg
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What are the 2 Barbiturates in anesthetic practice?
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Thiobarbiturates:
Thiopental= sodium pentothal Thiamyl Methylbarbiturates: Metrhohexital (brevital) |
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What are the effects of Benzos?
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Anxiolysis
Sedation anterograde Amnesia Spinal cord mediated muscle relaxation (GABA-mediated) |
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Dosing for Thiopental and Thiamyl
Induction Onset Peak Duration |
Induction: 3-5 mg/kg
Onset: 10-20 seconds Peak: 30-40 seconds Duration: 5-15 minutes (not duration of drug in body; just to awakening) |
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Midazolam
Vd Protein Binding Clearance |
Vd= 1.0-1.5 (L/kg)
Protein Binding = 96-98% Clearance= 6-8 (ml/kg/min) |
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What are the major kinetic differences b/t Midazolam and Diazepam that make Midaz a better drug?
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Clearance for midaz is much higher, so it has a faster elimination half time (1-4 hrs) where Diazepam's is 21-37 hrs.
Midaz is metabolized to inactive metabolites and Diazepam has active metabolites in phase I |
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With what patients should Midazolam be used with caution?
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Elderly
COPD, Hypovolemia when using other respiratory depressants (ie fentanyl) |
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what are the cardiovascular effects of Benzos?
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Minimal effect
dose dependent decrease in BP, CO, SVR Dose dependent increase in HR |
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Midazolam
Dosing for Premedication/sedation Induction Onset Peak Duration |
Premedication: 0.5- 1.0 mg IV
Induction: 50-350 mcg/kg (3.5 mg - 24.5 mg) Onset: 30 second - 1 minute Peak: 3-5 minutes Duration: 15-80 minutes |
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What is the mechanism of action of Propofol?
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GABA- Mediated
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what is the only sedative hypnotic that produces anxyolysis?
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Midazolam
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What is the only sedative hypnotic that produces Analgesia?
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Ketamine
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Propofol
Vd Clearance Elimination half time |
Vd = 3.5-4.5 (liters/kg)
Cl = 30- 60 (ml/kg/min) Elimination half time = 0.5-1.5 hours |
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How is Propofol metabolized?
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hepatic metabolism is rapid to inactive metabolites
(there is some extrahepatic mechanism of metabolism b/c clearance exceeds hepatic blood flow) |
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what is propofol clearance in comparison to Thiopental
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Propofol has unusually high clearance: 10X thiopental (3.9 ml/kg/min)
Propofol: 30-60 (ml/kg/min) |
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What are Propofol's effects on CV?
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Decrease BP, SVR, PReload, myocardial contractility
Impairs normal baroreflexx (small and transient changes in HR and CO) 1.4:100,000 cases--Parasympathetic system predominance (decreased HR) |
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What are Propofol's effect on Respiratory system?
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Dose dependent depression
-Decreased RR and Tidal Volume -decreased upper airway reflexes (increased risk of aspiration; "full stomach") |
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What are Propofol's effect on Central Nervous system?
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Decreased cereberal O2 consumption
decreased CBF, ICP *Anti-Emetic properties Excitatory activites on induction (secondary to subcortical glycine antagonism), may see involuntary muscle contractions Anti-pruritic Anti-Convulsant |
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What is the Dosing for propofol
Induction Infusion Sdation Bolus Sedation infusion Peak Durations |
Induction: 2-2.5 mg/kg
Infusion: 50-200 mcg/kg/min Sedation Bolus: 25-50 mg (0.5-1 mg/kg) Sedation infusion: 25-100 mcg/kg/min |
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Propofol
Onset Peak Duration |
Onset: 40 seconds
Peak: 1 minute Duration: 5-10 minutes (to awakening not full metabolism) |
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Is Ketamine a basic or acid drug?
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Basic
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What is the pka of Ketamine?
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7.5
7.4< 7.5 BH+---- B + H+ The reaction go toward the protonated ionized form |
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How is ketamine metabolized?
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metabolized to norketamine (1/3 to 1/5 as potent as ketamine)
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Mechanism of action of Ketamine
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NMDA receptor noncompetitive antagonist
opioid receptor interaction |
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What type of anesthesia does Ketamine produce?
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Dissociative anesthesia
-resembles cataleptic state Eyes open with slow nystamic gaze Hypertonus and purposeful movement Sedation, immobility, amnesia, marked analgesia and dissociation from the environment Emergence delirium |
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What are Ketamine's effects on the organ systems?
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CV: Increased HR, BP, and CO
respiratory: Increased secretions, bronchodilation CNS: increased CBF, ICP, Cerebral O2 consumption |
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Why would you use Ketamine vs the other sedative hypnotics?
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1. If patient is hemodynamically unstabe
2. Don't have an IV; can give IM |
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What is the mechanism of action of Etomidate?
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1. Depresses the RAS (Reticular Activating System)
2. Mimics the effects of GABA 3. Increases the affinity of receptors for GABA |
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Which sedative hypnotic can cause adrenocortical suppression?
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Etomidate
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What are the contraindications for Etomidate?
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Porphyria and adrenal suppression
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What are the effects of Etomidate on CV and Respiratory system?
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CV: minimal
Resp.: less depression than with barbiturates, benzos or propofol |
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what are the 2 major problems with Etomidate?
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causes PONV
adrenocortical suppression |
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How is Etomidate metabolized?
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Hydrolysis of ethyl ester side chain results in inactive metabolite
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What is Propofol's context sensitive half time for infusions up to 8hours long?
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< 40 minutes
* Big advantage |
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Why is Thiopental's context sensitive half time high?
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B/c is has high blood:fat coefficient, so tissue stores get saturated and also is metabolized to active metabolites that will prolong sedation
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What does Propofol do to baroreflexes?
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impairs normal function, so won't compensate for low BP
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Which 2 sedative hypnotics can cause involuntary muscle moevements (myoclonus) on induction?
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Propofol and Methohexital (brevital)
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pKa of Etomidate
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pka = 4.2,
it is a basic drug, so at phhysiologic pH, the nonionized, nonprotonated form predominates |
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morphine analgesic dose
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2.5-15mg/kg
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Kinetics for morphine in regard to solubility, protein binding and what it means
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poorly lipid soluble-slow onset and highly protein binding-long duration
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meperidine causes a less biliary effect d/t
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anti-spasmodic effect similar to atropine
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meperidine is metabolism by demethylation and hydrolysis to
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Normeperidine which produces CNS effects which can cause seizures
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meperedine is contraindicated in what psych patients
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those receiving MAOI
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dosages for demerol
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25-100mg
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Active metabolites for dilaudid are
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dihydromoprphine
dihydroisomorphine |
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VD for dilaudid is...and what does it mean
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high 4l/kg
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inactive metabolite for dilaudid is
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hydromorphone-3-glucoronide
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dosage for hydromorphone
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0.5-2mg
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kinetics for fentanyl
1. faster onset why? 2. shorter duration why? 3. longer elimination, why? |
more lipid soluble
re-distributes to other tissues larger VD |
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Fentanyl is metabolized to
|
norfentanyl~similar to normeperidine
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What are the advantages of using Fentanyl in terms of S/E
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no release of histamine
no myocardial depression supression of stress response |
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side effects of fentanyl
|
carotid sinus reflex of the heart is depressed causing decreased HR
chest wall rigidity |
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fentanyl dosages
|
25-100mcg
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Kinetics for sufentanil
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highly protein bound, higly lipid soluble
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what is the difference btn fentanyl and sufentanil
|
sufentanil is rapid onset and more potency!!!!
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sufentanil dosages
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2-10mcg/kg
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alfentanil pka is
|
6.8 means
90% nonionized at physiologic pH This is different from most other opioids |
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Definition of Opioids?
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all exogenous substance both natural and synthetic binding to opioid receptors producing "morphine-like" effects
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location of opioid receptors
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CNS, mostly brainstem & spinal cord
Periphery |
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mechanism of action of opioids
|
G-Protein-coupled receptors
cause Hyperpolarization and inhibition of neurotransmission increased potassium from iinside to outside, so inside is more negative |
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does morphine have high or low lipid solubility?
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Low lipid solubility
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Which of morphine's metabolites is active?
|
morphine 6- glucuronide
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Which drugs can cause muscle rigidity?
|
Opioids
Centrally mediated hypertonus of striated muscle Mostly ass. with Fentanyl family can be a significant problem when trying to ventilate patient |
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Which Opioid is structurally similiar to Atropine and how does this change its effects?
|
Meperidine (Demerol)
has a mild atropine-like anti-spasmodic effect so causes less biliary spams than other opioids |
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What is the major use for Meperidine (Demerol) in anesthesia?
|
Post-op shivering
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When is the use of Meperidine (Demerol) contraindicated?
|
when patient on MAOIs
(Libby Zyon Case NY) |
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How much of initial fentanyl dose undergoes first pass pulmonary uptake?
|
estimated 75%
|
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what causes Fentanly to have increased duration of action and increased context senstitive half time?
|
High lipid solubility-- saturation of inactve tissues
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Why does Fentanyl have a longer elimination half time than morphine (even though has shorter duratin of action)?
|
because has larger Vd
so has longer elimination half time, but shorter analgesia effect time than morphine |
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What are the advantages of Fentanyl compared to other Opioids?
|
stable hemodynamics
no histamine release cause suppression of stress hormone |
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What are the major side effects of Fentanyl?
|
Carotid sinus reflex control of heart is depressed (decreased HR)
Chest wall rigidity |
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Is Sufentanil the same in terms of potency as Fentanyl?
|
NO
Sufentanil is 10X more potent |
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Is Alfentanil more or less potent than Fentanyl
|
Less (1/4 to 1/10th less potent)
|
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How does Alfentanil differ from most other opioids?
|
Pka is 6.5 (less than pH) and most other opiods have pKa> pH
so alfentanil has 90% nonionized form available |
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Why does alfentanil have more rapid onset and shorter duration of action than Fentanyl even though it is less lipid soluble?
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b/c has high nonionzed fraction at physiologic pH (pKa is 6.5) and smaller Vd (highly protein bound)
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When does Alfentanil have peak brain effects?
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less than 1 minute
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What can happen if give alfentanil at a dose of 150-175 mg/kg?
|
Chest wall rigidity in 90-100% of patients
|
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Can Remifentanyl be used for induction?
|
NO
not suitable alone for induction intrea-op infusion ofr analgesia: 0.3-1 mcg/kg/min |
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How do 5-HT3-Receptor antagonists work?
|
work on receptors in GI tract and CTZ in brain that mediate vomiting and cause anti-emetic effects
|
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What does reglan (Metoclopramide) do?
|
GI prokinetic
increases lower esophageal sphinceter tone stimulate upper GI motility No effect on gastric acidity |
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Where are the storage vesicle found in the neuromuscular junction?
|
in the presynaptic nerve terminal
|
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Where is the motor end plate in the neuromuscular junction
|
on the post synaptic side
|
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How big is the synaptic cleft?
|
15-20 nm
|
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Where are the Cholinergic Nicotinic receptors located?
|
Skeletal muscle
|
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Where are the Cholinergic Muscarinic receptors located?
|
Glands
Smooth muscle (bronchial, GI, Bladder, Bl vessels) Heart (SA node, AV node) |
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What happens when an action potential on the neuron depolarizes its terminal?
|
The Na ions will rapidly enter the cell and then Ca ions go into the cytoplasm and permits the storage vesicle to mobilize and fuse with the presynaptic membrane and release Ach
|
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What makes the storage vesicles mobilize and fuse with the presynaptic membrane?
|
Ca ions going into the cytoplasm
|
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What happens when Ach binds to the nicotinic cholinergic receptors?
|
a conformational change occurs and open the Na channel
then the action potential continues along the muscle membrane and the Ttubule system-- this opens Ca channels and causes actin and myosin to contract |
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Where are the nicotinic cholinergic receptors located with in the neuromuscular junction?
|
Motor end plate
|
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Where is acetylcholinesterase found
|
on the motor end plate
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What the mechanism of action of Succinylcholine?
|
Ach receptor partial agonist
Attaches to 1 or more of the alpha subunits mimicking Ach Neuromuscular blockade results b/c the depolarized postjunctional membrane can't respond to subsequent release of Ach |
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What cholinergic receptor does Sccinycholine act on?
|
Postjunctional nicotinic cholinergic receptors
|
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when Ach is Hydrolized by Acetycholinesterase, what is the result?
|
Choline and Acetate
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Who should not get Depolarizers (succs) b/c of Ach Up-Regulation?
|
these patients will have an exaggerated response to Succs:
Spinal cord injury CVA Thermal injury Prolonged immobility Prolonged exposure to neuromuscular blockade multiple sclerosis Guillian-Barre |
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What is the TOF
|
4 successive 0.2 msec stimuli in 2 seconds
Amplitude of the 4th twitch over the first given as % |
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Characteristics of Phase II block
|
will be fade with TOF
Will be post Tetanic Facilitation Will not be any Facciculations |
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Char. of Phase I block
|
Decreased contraction in response to single twitch
Decreased amplitude, but sustained response to continous stimulation no post tetanic facilitation Onset is accopanied by skeletal muscl facciculations |
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How do Antibiotics affect Non-depolarizer and succs?
|
Potentiate the effects of both
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How do antidysrhythmics affect NDA and Succs
|
Potentiate both
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How do anticonvulsants (esp Phenytoin) affect NDA and Succs
|
Succs: unknown
NDA: Resistance |
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List some drugs that potentiate the effects of NonDepolarizers
|
Abx
Antidysrhythmics Lasix Inhaled anesthetics Mag sulfate Ketamine Local anesthetics Anti-HTN Dantrolene (used in tx of MH) |
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How does Hypothermia affect Neuromuscular blockers?
|
Prolongs duration of action
|
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Are nondepolarizers ionized or nonionized at physiologic pH
|
they are highly ionized and water soluble at phys pH
b/c of quaternary ammonium groups |
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Are the nondepolarizers highly lipid soluble?
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No
Have limited lipid solubility |
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What is the volume of Distribution of nondepolarizers?
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200 ml/kg = 4 L = ECF
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List some variable that will effect Nondepolarizers
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Temperature: Hypothermia prolongs block
Acid/base: acidosis potentiates block and antagonizes reversal Electrolyte abnormalties: Hypokalemia, Hypocalcemia, Hypermanesemia potentiated Age: neonates have increased sensitivity, but also have increased Vd, so dose is not decreased Drugs Concurrent diseases |
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what is the time for onset of action of most Nondepolarizers
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2-7 minutes
Much longer than succs (Depolarizer) |
