VALLEY Review FINAL Flashcards
(182 cards)
1
Q
• What is LD50/ED50?
A
The ratio is the therapeu,c index (TI). Defined by the dose that is lethal in 50% of subjects (LD50) divided by the dose that produces the desired effect (ED50). The larger the TI , the greater the margin of safety
2
Q
What is the elimination half life (T1/2) of a drug? What two factors determine T1/2?
A
Elimination half life is time it takes for the plasma concentration to fall by one half. T1/2 is directly related to volume of distribution and inversely related to clearance. T1/2=Vd/Cl
3
Q
Explain first order and zero order kinetics?
A
With first order a percentage of drug in eliminated per unit of time. With zero order kinetics a fixed amount of drug is eliminated per unit of time
4
Q
What is the equation for Volume of distribution? How is is calculated?
A
Vd=Q/Cpp, where Vd is the volume of distribution, Q is the dose of drug injected and Cp is the plasma concentration of drug after distribution.
5
Q
Diffusion of a drug across a membrane is propor,onal on the concentration gradient. Diffusion is also dependent on what 3 other factors?
A
Lipid solubility,
thickness of the membrane,
molecular weight of the substance.
6
Q
The degree of protein binding is dependant on what primary factor?
A
The amount of protein in the blood
7
Q
What is the most important determinant of build up of an an intravenous anesthetic in a given tissue?What other factors will effect drug concentration in tissues?
A
Blood flow to the tissue
Lipid solubility, ionization
8
Q
Drugs absorbed from GI tract must first pass through what organ?
A
Liver first pass effect
9
Q
What agents used in anesthesia are weak bases? •
A
Weak bases include; all opioids, benzodiazepines, etomidate, propofol, and ketamine.
10
Q
What is an acid? Define weak acid?
A
Hydrogen ion or proton donor.• A weak acid is not ionized 100% in solution
11
Q
What agents used in anesthesia are weak acids?
A
Barbiturates
12
Q
What happens to the concentration of weak acid in nonionized form as pH falls?
A
Concentration increases (Rule: acid + acid=more non-ionized)
13
Q
A weak acid with a pH of 7.8 will be more than 50% or less than 50% non-ionized at pH of 7.4 ?
A
More than 50% non-ionized
14
Q
Do drugs that are weak acids form salts with posi,ve ions such as sodium or nega,ve ions such as Sulfate or Chloride?
A
Positive ions
15
Q
A new drug, Z sulfate, has a pKa of 8.0. Will this drug be more than 50% ionized or les than 50% ionized at normal body pH?
A
The drug is a weak base therefore more than 50% ionized.
16
Q
• What are six central nervous system action of benzodiazepines?
A
• Antianxiety, sedative, hypnotic,
anticonvulsant, amnestic, muscle relaxant
17
Q
• How do benzodiazepines modify GABAergic transmission?
A
Benzodiazepines attach to the receptor adjacent to the GABA-A receptor and enhance the actions of GABA
18
Q
At what anatomical site do benzodiazepines
work?
A
Reticular activating system (RAS)
19
Q
Can withdrawal of benzodiazepines occur?
A
Withdrawal symptoms (agitation, insomnia, tremulousness) can occur.
20
Q
What is the extent of protein binding of diazepine, midazolam and lorazepam in a healthy adult?
A
• Benzodiazepines are extensively protein bound. Diazepam and lorazepam are 98%, midazolam is 94%
21
Q
• Are Diazepam and lorazepam freely water soluble?
A
• No
22
Q
• What is the elimination half time of midazolam
A
• 1.7-2.6 hours
23
Q
When is midazolam soluble in water? Midazolam
comes in solu#on with what pH?
A
Midazolam is water soluble when pH is < 4.0. Midazolam is available in solution with pH of 3.5.
24
Q
• How are benzodiazepines metabolized?
A
Midazolam, diazepam are oxidized in the liver, lorazepam is conjugated in the liver
25
Clinical effects of benzodiazepines • Can small doses of benzodiazepines affect respiration?
Premedication normally have little effect on respiration and PaCo². Small doses can depress ventilation in geriatric patients.
26
• What pharmacological agents are used to
| treat withdrawal from alcohol?
• Benzopiazepines (chlordiazepoxide, lorazepam).
27
• Why are benzodiazepines good premedications for a patient receiving a regional anesthetic?
The powerful antianxiety and amnesia actions of benzodiazepines
28
List three drugs that may be used to antagonize the central nervous sytem depression produced by benzodiazepines? • Which of these agents is specific?
• Flumazenil is a competitive antagonist for benzodiazepines. Physostigmine (Antilirium®) and aminophylline are nonspecific antagonist for benzodiazepines
29
• What is the half life of Flumazenil?
Approximately 60 minutes
30
• When is Flumazenil indicated?
Flumazenil is indicated for benzodiazepine overdose, or for reversal of sedative effects produced by benzodiazepines during general anesthesia, or during surgical procedures
31
• How should Flumazenil be used?
A series of small doses over 1-3 minutes up to 1mg usually reverses the therapeutic effects. Repetitive small doses up to 5mg over 2-10 min for benzodiazepine overdoses.
32
Which IV agents will decrease ICP?
Barbiturates, opioids, benzodiazepines, etomidate, and propofol. •
33
Name two non opioid induc&on agents that are associated with excitatory phenomena during induc&on? •
Methohexital and etomidate •
34
What agent is related chemically to Phencyclidine “angel dust”
Ketamine
35
• How does ketamine produce dissociative anesthesia?
• Ketamine produces dissociation between the
| thalamocortical system and the limbic system
36
The CNS actions of ketamine appear to be primarily related to its action on what receptor?
• NMDA (N-methyl-D-aspartate)
37
• What other receptors does ketamine work on? •
Non NMDA glutamate receptors,
nicotinic receptors,
muscarinic receptors, and opioid receptors.
38
Barbiturates, benzodiazepines, propofol and etomidate produce their CNS actions by working on what receptor?
GABA
39
• What is responsible for the short elimination half life of ketamine?
Extensive hepatic metabolism
40
How is propofol eliminated?
Hepatic metabolism
41
The dysphoria (emergence delirium) associated with ketamine is caused by what? ••
due to depression of auditory and visual relay nuclei leading to misperception and/or misinterpretation of auditory and visual stimuli. Loss of skin and musculoskeletal sensations produces a sensation of bodily detachment or floating
42
What receptor does ketamine interact with to produce dysphoria?
Kappa, antagonism of muscarinic receptor, and possibly the sigma receptor
43
What drug would you give to a patient that becomes agitated and hallucinogenic during emergence from ketamine anesthesia?
A benzo such as midazolam
44
In what group of patents is ketamine contraindicated in?
Pts with Increased ICP
45
Does ketamine produce bronchodilation or bonchoconstriction?
Bronchodilation
46
Which nonopioid induction agent is associated with increase airway secretion?
Ketamine
47
Co-administration of what drug may be helpful to prevent excessive secretions with ketamine?
Glycopyrrolate
48
Which non-opioid induction agent is associated with increases in BP, HR and myocardial contractility?
Ketamine
49
Does ketamine depress pharyngeal and laryngeal reflexes?
No, these reflexes remain intact •
50
Venous thrombosis and phlebitis are most likely with what non-opioid anesthetics? Why?
Diazepam, lorazepam, and etomidate. Because these agents are dissolved in propyleneglycol
51
Which induction agent directly depresses the adrenal cortex
Etomidate
52
What are four potential complications during recovery from etomidate?
1) Suppression of adrenocortical response to stress
2) Nausea and vomiting
3) low plasma cortisol concentrations
4) depressed immune response.
53
What are five measurable cardiovascular effects of ketamine?
Increases in: mean aortic pressure, pulmonary artery pressure, CVP, HR, and cardiac index.
54
How does ketamine produce these CV effects?
SNS stimulation
55
What effect does etomidate have on cerebral blood flow, ICP and cerebral oxygen consumption? •
Etomidate, a potent vasoconstrictor decreases cerebral blood flow, ICP and cerebral oxygen consumption
56
What nonopioid induction agent best maintains cardiovascular stability?
Etomidate
57
How does the BP response to an induction dose of propofol differ from that of thiopental? What causes this effect?
The decrease in BP produced by propofol is greater than that produced by thiopental The effect is caused by a Decrease in SVR
58
How does propofol decrease BP and cardiac output?
Arterial vasodilation, and a decrease in myocardial contractility.
59
What is the most important advantage of propofol over other IV induction agents?
Faster and more complete awakening
60
What other actions of propofol enhance this drugs usefulness?
Antiemetic and pruritic effects
61
What is the IV induction dose of ketamine?
1-2mg/kg IV
62
What is the IM induction dose of ketamine?
5-10mg/kg IM
63
What drugs cannot be mixed with ketamine?
Any alkaline solutions such as barbiturates and diazepam
64
Which nonopioid induction agent depresses ventilation the least?
Ketamine
65
Which nonopioid induction agent produces profound analgesia?
Ketamine
66
• What are possible disadvantages of propofol use?
Allergic reactions to phenol nucleus and diisopropyl side chain.
Prolonged myoclonus has been reported caution in patients with uncontrolled epilepsy.
Potential for bacterial contamination. propofol strongly supports the growth of e-coli and pseudomonas aeruginosa
Propofol pain at injection site
67
What is the major inhibitory neurotransmitter of the CNS?
GABA • •
68
What ion channel is opened by this neurotransmitter?
Chloride
69
How do barbiturates modify GABAergic transmission?
By attaching to receptors nearby the GABA receptors and prolonging the attachment of GABA to its receptor.
70
Where do barbiturates work?
Reticular activating system (RAS)
71
What happens to onset, duration of action, and elimination of thiopental in the patient with acidosis? why
Thiopental is weak acid, and is therefore un-ionized in the presence of acidosis. Onset of action is faster, duration of action is shorter, and elimination will be slower (due to increase in Vd)
72
Thiopental will have a pronounced effect in a patient with liver disease and associated hypoalbuminemia? Why?
72-86% of thiopental is bound to albumin. In liver disease and hypoalbuminemia these is an increase in “free” frac5on of drug leading to pronounced effects
73
How are the actions of general IV anesthetics terminated?
Redistribution
74
What is the pH of a barbiturate containing solution?
pH of solutions containing barbiturates is > 9.0
75
Barbiturates should not be mixed with what types of solutions? Why
Acidic solution such as LR. Precipitation will occur
76
How long does it take for thiopental to reach the brain?
LOC in 10-15 seconds
77
What is the elimination half life of thiopental?
11.6 hours
78
What are the cardiovascular effects of induction doses of thiopental?
In normovolemic patients there is a mild and transient fall in BP due to peripheral vasodilation
79
What is the primary rationale for barbiturate therapy in head injury patients?
Barbiturates can quickly lower ICP
80
What induction agents are appropriate for pa5ents with increased ICP?
Thiopental, etomidate, propofol, midazolam
81
Does an induction dose of thiopental ordinarily obtund the laryngeal reflexes?
No
82
Does an induction dose of thiopental produce good analgesia?
No. barbiturates including thiopental may cause hyperalgesia with subanesthetic doses.
83
What are the disadvantages of the barbiturates as induction agents?
Lack specificity of effect in the CNS
Have a lower therapeutic index than benzodiazepines
Result in tolerance more easily than benzodiazepines Have a greater liability for abuse
High affinity for drug interactions
Paradoxical excitation especially in the elderly
Decrease in pain threshold with small doses
“Hangover effect”
84
What is some of the unique properties of methohexital compared to thiopental?
• The principle disadvantage of methohexital is increased incidence of excitatory phenomena such as involuntary skeletal muscle movements (myoclonus), and hiccough.. High doses of methohexital is associated with seizures in approximately 1/3 of patients.
85
List the barbiturates from highest to least potent?
Relaive potency of barbiturates used for IV induction, assuming thiopental is 1, thiamylal is 1.1, and methohexital is 2.5.
86
What is the mechanism of apnea after thiopental administration?
Thiopental is a potent respiratory depressant. It reduces the sensitivity of the central respiratory center for CO2
87
List three signs and symptoms of intra-arterial thiopental injection?
1) Arterial spasm with intense pain down the arm
2) blanching of skin with disappearance of pulses distally
3) eventual cyanosis and possible gangrene
88
Which class of drugs can used to treat inadvertent intra-arterial injection of thiopental?
Nonselective alpha blockers phenoxybenzamine, phentolamine.
89
Do induction doses of barbiturates cause hepatic enzyme induction?
No
90
The use of barbiturates is absolutely contraindicated in which two disease states?
Status asthmaticus; porphyria
91
What barbiturates release histamine?
Thiopental, thiamylal.
92
How are the opioid receptors classified?
Mu, kappa, delta
93
What receptor is responsible for the analgesic effects of the opioids?
Mu-1
94
What opioid receptor is responsible for the adverse effects of opioids?
Mu-2
95
Stimulation of what opioid receptor will decrease shivering?
Kappa
96
What opioids can be used to decrease post-operative shivering?
The opioid agonist meperidine, or the agonist antagonist butorphanol-Stadol®
97
• What is the mechanism of action of intrathecally or epidurally (Neuraxial) administered opioids?
inhibit substance P release
98
Explain the differences in onset and duration of action of the different opioids when given via intrathecal route? •
What drug characteritic is responsible for these differences?
• What is the clinical significance of these differences
• Hydrophillic opioids such as morphine cross lipid membranes slowly. After intrathecal placement, morphine diffuses out of the intrathecal space slowly, (Onset of action is slow and duration of action is prolonged). With lipophilic opioids such as fentanyl, diffusion out of CSF is rapid, resulting in rapid onset of ac
99
Late respiratory depression associated with
morphine
100
NO late respiratory depression
Fentanyl
101
Early respiratory depression
Fentanyl
102
What are potential side effects of neuraxial opioids?
Pruritis, nausea, urinary retention
103
Does stimulation of mu-1 have high or low abuse potential?
low
104
Does stimulation of mu-2 have high or low abuse potential?
High
105
Physical dependence with this opioid receptor
mu2
106
List four common side effects of intrathecal (spinal) opioid administration?
Pruritis, most common (60%)
Urinary retention (50%)
Nausea and vomiting (20-30%),
Respiratory depression (5-7%)
107
At what anatomical locations do opioids work to produce spinal analgesia?
Substantia gelatinosa of the spinal cord,
108
What opioid receptors promote respiratory depression?
Mu-2 •
109
What opioid depresses myocardial contractility and increases heart rate?
Meperidine
110
What is the major clinical implications of the opioid-induced decrease in gastrointestinal tone and motility?
Delays gastric emptying and increases risk of aspiration
111
How do opioids (except meperidine) produce bradycardia?
With the exception of meperidine, opioids stimulate the vagal nuleus in the medulla, which increases vagal impulses to the heart.
112
Does opioid-induced spasm of sphincter of Oddi cause pain?
yes
113
What agents can be used to reverse this effect?
Glucagon, Naloxone, NTG
114
• The incidence and severity of opioid-induced skeletal muscle rigidity may be increased by what inhalation agent?
NITROUS
115
What are the two most common side effect of fentanyl (IV)? •
• Severe respiratory depression, Nausea and vomiting •
116
How do opioids cause nausea and vomiting?
By stimulating the chemoreceptor trigger zone.
117
What narcotic should be avoided in patients on MAO inhibitors?
MEPERIDINE
118
• What opioid agonist cause histamine release?
Morphine and Meperidine
119
Why might blood pressure decrease after administration of sufentanil?
• Sufentanil may produce a dose dependent decrease in heart rate , probably by stimulation of the vagal nucleus in the medulla
120
Metabolism of alfentanyl
Remifentanil is metabolized to inactive metabolites by blood and tissue nonspecific esterases. Remifentanil has T½ 10-30 min.
121
What are the clinical significance of these metabolites?
Morphine-6-glucoronide is an active metabolite which can accumulate in patients with renal impairment leading to respiratory depression. Normeperidine is an active metabolite that can also accumulate in patents with renal impairment and lead to CNS excitation.
122
List the metabolites of morphine, meperidine, and fentanyl?
Morphine’s principle metabolites are morphine-3- glucuronide and 5-10% of metabolites is morphine-6- glucruronide.
Meperidine’s hepatic metabolism is extensive with 90% of drug metabolized to normeperidine and meperidinic acid.
Fentanil is metabolized in the liver to norfentanil
123
List the opioid agonist from fastest onset of action to slowest?
RASFM
1) Remifentanil,
2) Alfentanil, 3) Sufentanil,
4) Fentanyl,
5) Morphine, Meperidine
124
• List the opioids agonist from shortest to longest duration of action?
1) Remifentanil (shortest)
2) Alfentanil 3) Morphine
4) Sufentanil
5) Meperidine 6) Fentanyl (longest)
125
List the opioids agonist from highest to lowest potency?
1) Sufentanil (2000-4000x morphine),
2) Remifentanil 470x morphine,
3) Fentanyl 50-100 x morphine,
4) Alfentanil 10 x morphine,
5) Morphine,
6) Meperidine 0.1 x morphine
126
List the opioids agonist from highest to lowest lipid solubility?
Sufentanyl, remi
127
Most potent opioid
Sufentanyl
128
Highest lipid soluble opiods
Sufentanyl
129
Naloxone has affinity for what opioid receptors?
Mu (strongest)
130
What is the duration of action of naloxone?
60 minutes
131
• What four adverse cardiopulmonary changes may develop if large doses of naloxone are given?
Hypertension, cardiac dysrhythmias (V-fib), pulmonary edema, and tachycardia.
132
Succinylcholine interacts with what receptor at the neuromuscular junc3on? •
Nicotinic
133
What could cause HR/BP to increase in response to succinylcholine?
Succinylcholine stimulates nicotinic receptors at the autonomic ganglia.
134
How are the actions of succinylcholine and acetylcholine terminated?
Succinylcholine is hydrolyzed by plasmacholinesterases. Acetylcholine is hydrolyzed by true tissue cholinesterases at the NMJ
135
What are 2 other names for plasma cholinesterases
Pseudocholiesterases, plasma cholinesterases, butyrocholinesterases.
136
Describe the two phases of succinylcholine
| metabolism?
• Step 1 : succinylcholine is metabolized by plasma cholinesterases to succinylmonocholine + choline.
Step 2: succinylmonocholine is metabolized by by plasma cholinesterases to succinic acid + choline.
137
What are 11 possible complications associated with succinylcholine administration?
1. Hyperkalemia
2. Bradycadria
3. Increase heart rate/BP
4. Skeletal muscle myalgia
5. Allergic reac3ons
6. Triggering Malignant hyperthermia
7. Masseter Spasms
8. Myoglobinuria
9. Increase intraocular pressure
10. Increase intragastric pressure
11. Increase ICP
138
Why is succinylcholine contraindicated in pa3ents with nerve damage?
When motor nerves to skeletal muscles are damaged, nicotinic receptors of the skeletal muscle cell up regulate. These extrajunctional nicotinic receptors are exceptionally responsive to succinylcholine. Potassium leaves the cells in excessive quantities when succinylcholine triggers these channels to open leading to hyperkalemia
139
How should you treat the bradycardia caused by succinylcholine?
Prior administration of atropine
140
After succinylcholine administration to a normal patient, how much can serum K be elevated?
• 0.5-1 mEq/l
141
List 5 conditions that may accentuate succinylcholine-induced hyperkalemia?
Unhealed 3rd degree burns 2. Denervation os skeletal muscle (praplegia, hemiplegia) 3. Severe skeletal muscle trauma 4. Upper motor neuron injury (head injury, Parkinson’s, CVA) 5. Muscular dystophy
142
• What chemical group do all muscle relaxants have in common? • What is the significance of this?
• Quaternary ammonium group • This means that all muscle relaxants are completely ionized, highly water soluble
143
• Muscle relaxants distribute primarily to what body compartment?
Extracellular fluid compartment
144
• By what mechanism does pancuronium increase heart rate? • Pancuronium increase HR by what percentage?
Pancuronium competitively inhibits acetylcholine from attaching to muscarinic receptors of the SA node (atropine-like effect) • 10-15%
145
What is the priming principle for nondepolarizing muscle relaxants
• A subtherapeutic dose of a non-depolarizing agent (10% of the ED95) is given, followed in 3-5 minutes by the remainder of the dose. It is speculated that the primary dose will occupy 50-70% of the receptors and the large subsequent dose rapidly blocks the remaining receptors causing a prompt onset of action
146
Hoffman elimination is dependant on what two factors? •
Temperature and pH. The rate of Hoffman elimination is slowed by acidosis or decreases in body temperature
147
What is the metabolite of ester hydrolysis of atracurium that although unlikely can cause CNS stimulation?
• Laudanosine
148
List 4 muscle relaxants that least us the kidneys as a route of elimination?
Succinylcholine, atracurium, cisatracurium, and mivacurium
149
Does fade occur with non-depolarizing NMB?
Yes
150
Does fade occur with phase I block with succinylcholine?
No
151
Does post-tetanic potentation occur with non-depolarizing NMB?
yes
152
Does post-tetanic potentation occur with phase I block from succinylcholine
no
153
What drugs can increase the effects of nondepolarizing NMB agents? •
```
Volatile anesthetics
Aminoglycoside
Antibiotics
Cardiac an3dysrythmics
Local anesthe3cs
Diure3cs
Magnesium
Lithium •
Ganglionic Blockers
Cyclosporins
```
154
What agent can lead to resistance to nondepolarizing NMB agents?
• Patients chronically treated with phenytoin are resistant to the effects of NMB. Higher doses may be needed.
155
• What lab test assesses plasma pseudocholinesterase?
Dibucaine
156
What are the four anticholinesterase drugs that have NMB reversal effects? • • •
• Edrophonium, neostigmine, pyridostigmine, physostigmine
157
Which of these are tertiary amines? anticholinesterase
Physostigmine
158
Which of these are quarternary amines? •
• Edrophonium, neostigmine, pyridostigmine
159
Explain how these agents work?
They competively inhibits acetylcholine from attaching to sites on the acetcholinesterase molecule. Acetylcholine concentrations are therefore substantially increased.
160
How does neos#gmine and pyridos#mine bind to acetycholinesterase?
Covalentlly
161
• How does edrophonium bind to acetylcholinesterase?
Electrostatic binding
162
Which agents appear to work presynaptically?
Neogstimine
163
Cholinesterase agents work at what receptor?
These agents indirectly stimulate muscarinic and nicotinic receptors by increasing the concentration of acetylcholine at the receptor sites.
164
• What are five effects of the muscarinic
receptor stimulating properties of
anticholinesterase drugs?
1. Bradycardia
2. Increase salivary and bronchial secre#ons
3. Bronchoconstriction
4. Hyperperistalsis of GI tract
5. Miosis
165
• What is the treatment for cholinergic crisis?
• Atopine, pralidoxime (2-Pam)
166
Identify 3 anticholinergic drugs used to
| inhibit muscarinic receptors?
Atropine, glycopyrrolate, scopolamine
167
Antimuscarinics suppress which division of the autonomic nervous system?
Parasympathetic division of the autonomic nervous system. They antagonize the effects of acetylcholine on tissues innervated by postganglionic parasympathetic nerves at the muscarinic receptor.
168
How does atropine and other antimuscarinics increase heart rate?
• By competitively antagonizing acetylcholine
released from the vagus nerve at muscarinic
receptors of the SA node.
169
What are the clinical uses of antimuscarinics agents?
| Clinical Uses
1. Antisialagogue
2. Sedation and amnesia
3. Increase heart rate
4. Bronchodilation
5. Reversal of cholinergic crisis
170
Which antimuscarinic has the greatest and
| which has the least antisialagogue effect?
• Greatest=scopolamine, least=atropine
171
Which antimuscarinic has the greatest and
| which has the least sedative effects?
Greatest=scopalamine, least=glycopyrrolate
172
Which antimuscarinic has the greatest and
| which has the least effect on heart rate?
Greatest=atropine, least=scopolamine
173
Do antimuscarinics relax smooth muscle?
Yes, Ipatropium (Atrovent is given as MDI)
174
Do antimuscarinics interfere with sweating?
Yes. Large doses of atropine may increase
| body temperature
175
How does atropine promote gastroesophageal
| reflux
By decreasing the tone of lower esophageal sphincter.
176
• The action of what antimuscarinic parallels the more
| rapid onset of edrophonium?
• Atropine
177
What is the concern of giving scopolamine to the
| elderly (>76yrs) or young (<13yrs)?
Scopolamine may cause restlessness and confusion
178
Which antimuscarinic can trigger the central anticholinergic syndrome?
Scopolamine, and to a lesser extent atropine
179
What are CNS symptoms of central anticholinergic
| syndrome?
Confusion, restlessness, agitation, delirium and
| hallucinations, somnolence and coma.
180
What are peripheral symptoms of anticholinergic
| crisis?
Dry mouth, blurred vision, tachycardia, dry and
flushed skin, rash and fever (especially in
children)
181
What group of patients are susceptible to
| anticholinergic syndrome?
Small children and infants, and the elderly
182
How is anticholinergic syndrome treated?
IV physostigmine (Antilirium®)
