Final Flashcards
Tertiary amine that crosses BBB that has been linked with postop delirium?
atropine and scopolamine
What are CV side effects of succs?
bradycardia (especailly peds)
What electrolyte imbalance can succs cause?
transient hyperkalemia (0.5 mEq/L) in normal physiology
Which populations are at increased risk for hyperkalemia with succs?
burns, trauma, paralysis, CVA, GBS, prolonged immobilization, polyneuropathy, head injury, myopathies, Duchenne’s MD
When does the risk of hyperK peak for succs?
7-10 days
What is a common side effect of succs in women and outpatient procedures?
myalgia- can use defasciculating dose and NSAIDs to decrease
What is a transient effect of succs that lasts 5-10 minutes?
increased IOP (increases by 5-15 mmHg for 2-4 min after admin)
Besides increased IOP, what can succs also increase?
intragastric pressure and ICP
How is succs metabolized?
rapidly metabolized by pseudocholinesterase to succinylmonocholine and succinic acid
How is the action of succs terminated naturally?
diffusion away from NMJ
Which NMB is associated with a vagolytic effect?
pancuronium
What is a byproduct of Hoffman elimination with atracurium and what can it cause?
laudanosine- seizures
The indirect actions of NMBs on cardiac are due to ? and are associated with which two NMBs the most?
histamine release; atracurium and mivacurium
The aminosteroids are all affected by ? due to liver metabolism and biliary excretion. In liver failure, ? is preferred.
liver function; cisatracurium
Which aminosteroid is affected most by renal function?
pancuronium
How do nondepolarizing NMBs affect the elderly?
onset is slower due to slower circulation times, and aminosteroids have an increased DoA
How do nondepolarizing NMBs affect the obese?
require quick onset, DoA is increased with aminos
How do nondepolarizing NMBs affect pediatric pts?
NMJ is immature and sensitivity changes through life (need dose change)
Which NMBs are the most common causes of allergic reactions?
roc and succs
anticholinergic drugs interfere with normal inhibition on the release of ?, which is why their effects are called ? or ?
norepinephrine; parasympatholytic or sympathomimetic
Anticholinergic drugs are selective for which receptors?
muscarinic cholinergic- competes against ACh
Where are M1 receptors?
CNS and stomach
Where are M2 receptors?
heart and lung
Where are M3 receptors?
CNS, smooth muscles of airway, glandular tissues
Where are M4 and M5 receptors?
CNS
What are the symptoms of organophosphate poisoning/overdose?
narrowed pupils, agitation, excessive secretions, arrhythmias, cardiovascular/respiratory collapse, coma
What are the desired effects of dexmedetomidine?
sedative, analgesic, sympatholytic properties; reduces anesthetic requirements- does NOT cause significant resp depression, may reduce postop shivering
What are some SE of dexmedetomidine?
bradycardia, systemic hypotension
What is considered small doses of dopamine and what are its effects?
<2 mcg/kg/min- minimal adrenergic effects- open dopaminergic receptors
What is considered moderate doses of dopamine and what are its effects?
2-10 mcg/kg/min- beta 1 stimulation
What is considered higher doses of dopamine and what are its effects?
10-20 mcg/kg/min- alpha 1 stimulation
What is malignant hyperthermia?
RYR1 gene mutation- allows massive release of Ca from SR
What are the signs and symptoms of MH?
tachycardia, hypercarbia, hyperthermia, masseter spasm, tachypnea, arrhythmias, metabolic acidosis, muscle rigity, myoglobinemia, hyperkalemia
What are some triggers for MH?
succs, volatile anesthetics (isoflurane, desflurane, sevoflurane, halothane, enflurane)
How is esmolol metabolized?
rapid redistribution and hydrolysis by RBC esterases
Hoffman elimination is dependent on?
temp and pH
What do you use when there is no response to TOF? Describe what it is and what it’s used to assess.
post-tetanic facilitation; 50 Hz stimulus for 5 seconds, then apply 1 Hz stimulus and count responses- assesses for deep blockade
Dopamine is an endogenous catecholamine that is an immediate precursor to?
norepinephrine
What is a direct precursor of dopamine?
L-dopa
Beta 1 selective blockers should have less inhibitory effect on beta 2 receptors and are preferred for? What is an example of a beta 1 selective antagonist?
those with COPD and PVD; metoprolol
List some opioid agonists
morphine, meperidine, fentanyl (and others in fentanil family), codeine, dilaudid, oxy, hydrocodone, methadone, heroin
List some opioid agonist-antagonists
pentazocine, butorphanol, nalbuphine, buprenorphine, nalorphine, bremazocine, dezocine, meptazinol
List the opioid antagonists
naloxone, naltrexone, nalmefene
What is metoprolol?
cardioselective (B1) antagonist
What is milrinone and how does it work?
phosphodiesterase inhibitor; positive inotrope with vasodilation by blocking cAMP breakdown
What are some adverse effects of beta blockers?
heart block, heart failure, AV block, sinus arrest, hypotension, bronchospasm in asthma patients
What is the MoA of propofol?
GABA agonist (potentiates inhibitory transmission)
Who should you avoid propofol in?
allergy to egg yolk (soy lecithin)
When should you discard propofol?
6 hours if in syringe, 12 hours if in tubing
How quickly does propofol work and when do pt start to wake up due to redistribution?
30 seconds; 2-8 minutes
How is propofol metabolized?
extrahepatic clearance (pulmonary uptake and first pass elimination), conjugation in liver to inactive metabolites
What are s/s of propofol infusion syndrome?
metabolic lactic acidosis, hypertriglyeridemia, hypotension, arrhythmia, rhabdo, acute renal failure, hepatomegaly
What are the desired effects of propofol?
antiemetic, antipruritic, anticonvulsant, amnesia, sedation
What are the CV effects of propofol?
tachycardia on induction, decreased contractility and preload, hypotension
What are the respiratory effects of propofol?
apnea on induction
What are the cerebral effects of propofol?
decreased CBF and ICP- sometimes can have excitatory phenomena like m. twitching, opisthotonus
What is the MoA of etomidate?
depresses RAS and mimics inhibitory effects of GABA
What can long infusions of etomidate cause?
adrenal corticoid suppression
Where is etomidate metabolized and where is it excreted?
liver; urine and bile
What is a common side effect of etomidate?
myoclonus
Does a standard induction dose of etomidate inhibit ventilation?
no
Why is etomidate the desired induction drug for hemodynamically unstable patients?
it has minimal effects on the CV system- contratility and CO usually unchanged
What are cerebral effects of etomidate?
decreased CMR, CBF and ICP
What is the relationship between fentanyl and etomidate?
fentanyl decreases myoclonus but also increases plasma levels and prolongs elimination
What is the MoA of barbiturates?
depress RAS, enhance transmission of GABA, suppress excitatory ACh
How are barbiturates biotransformed?
hepatic oxidation to inactive water soluble metabolites
What are the CV effects of barbiturates?
decreased BP and increased HR- peripheral pooling of blood due to vasodilation (ensure adequate volume status and baseline autonomic tone)
What are the respiratory effects of barbiturates?
depress medullary ventilation, decreases response to hypercapnia and hypoxia
What are the cerebral effects of barbiturates?
decreased CBF, ICP, but decrease in CPP
What are the renal and hepatic effects of barbiturates?
decreased RBF and GFR; decreased HBF and can trigger porphyria
What is the MoA of ketamine?
NMDA antagonist (blocks glutamate and glycine)- dissociates thalamus from limbic cortex
What is the metabolite of ketamine?
norketamine- ACTIVE
What are the CV effects of ketamine?
increased BP, HR, CO, increased PAP and myocardial work
Who should you avoid ketamine in?
patients with CAD, uncontrolled HTN, CHF
What are the respiratory effects of ketamine?
potent bronchodilator, increased salivation- minimal effect on ventilatory drive
What are the cerebral effects of ketamine?
increased CMRO2, CBF, ICP
What are some common undesired effects of ketamine?
emergence delirium and nausea at high doses
Glycopyrrolate is the recommended anticholinergic for which cholinesterase inhibitors?
neostigmine and pyridostigmine
What is glycopyrrolate used to offset?
bradycardia and increased salivation
Prolonged duration of action of succinylcholine can occur in:
high doses and those with decreased psuedocholinesterase activity
What are some meds and conditions that can decrease pseudocholinesterase activity?
hypothermia, pregnancy, carcinoma, hepatic disease, Reglan, neostigmine, esmolol, atypical enzyme
What are some conditions that can increase pseudocholinesterase activity?
obesity, alcoholism, psoriasis, ECT therapy
Pseudocholinesterase is synthesized by?
liver
What are some contraindications to succs?
pseudocholinesterase deficiency, those sensitive to hyperkalemia (burns, digitalis, GBS), glaucoma
What is the RSI dose of roc?
1.2 mg/kg
What is the dose of propofol?
1-2 mg/kg
What is the dose of etomidate?
0.2-0.3 mg/kg
What is the dose of ketamine?
2-4 mg/kg
Which non depolarizers are short acting and what is that time frame?
mivacurium, <30 minutes
Which non depolarizers are intermediate acting and what is that time frame?
atracurium, cisatracurium, vecuronium, rocuronium 30-60 minutes
Which non depolarizers are long acting and what is that time frame?
pancuronium, >60 minutes
What is the site of action for neuromuscular blocking agents?
ACh receptors (alpha subunit)
What is the dose of succinylcholine in mg/kg?
1-1.5 mg/kg
What paralytics are best for those with renal failure?
atracurium and cisatracurium
How are labetolol and esmolol different?
labetolol is beta/alpha 7/1 whereas esmolol is selective beta
The most indirect adrenergic agonist with mixed alpha and beta effects that does not decrease uteroplacental blood flow
ephedrine
List some anticholinergic medications
atropine, glycopyrrolate, scopolamine
What are the intubating and maintenance doses of cisatracurium?
intubation 0.1 mg/kg
maintenance 0.02 mg/kg
What is the typical final concentration of phenylephrine?
100 mcg/ml
