Atropine - Anticholinergic, Antimuscarinic Flashcards
What is the typical intravenous dose range for Atropine?
A) 0.1-0.2 mg
B) 0.2-0.4 mg
C) 0.4-0.6 mg
D) 0.6-0.8 mg
C) 0.4-0.6 mg
What is the concentration of Atropine in a standard solution where 1 mL contains 0.1 mg of Atropine?
A) 0.01 mg/mL
B) 0.1 mg/mL
C) 1 mg/mL
D) 10 mg/mL
B) 0.1 mg/mL
(0.1 mg/mL)
What is the typical onset time for intravenous Atropine administration?
A) 15-30 seconds
B) 30-45 seconds
C) 45-60 seconds
D) 60-90 seconds
C) 45-60 seconds
How long does it generally take for Atropine to reach peak effect when administered intravenously?
A) 1-2 minutes
B) 2-4 minutes
C) 5-10 minutes
D) 10-15 minutes
B) 2-4 minutes
(IM=30mins)
What is the typical duration of action for intravenous Atropine?
A) 30 minutes
B) 1 hour
C) 1-2 hours
D) 2-4 hours
C) 1-2 hours
What is the primary mechanism of action of Atropine?
A) Agonizes beta-adrenergic receptors
B) Antagonizes muscarinic receptors
C) Inhibits alpha-adrenergic receptors
D) Activates dopamine receptors
Answer: B) Antagonizes muscarinic receptors o increase heart rate.
What is a notable central nervous system effect of Atropine due to its ability to cross the blood-brain barrier (BBB)?
A) Sedation
B) Emergence delirium
C) Increased intracranial pressure
D) Muscle rigidity
B) Emergence delirium
Crosses BBB (tertiary amine) → emergence delirium
How does Propofol interact with the effects of Atropine on heart rate?
A) Enhances Atropine’s ability to increase heart rate
B) Attenuates Atropine’s response, and larger doses of Atropine do not overcome this effect
C) Has no effect on Atropine’s response
D) Potentiates the bradycardic effects of Atropine
B) Attenuates Atropine’s response, and larger doses of Atropine do not overcome this effect
Propofol attenuates Atropine’s response that cannot be overcome by larger doses (aka larger Atropine doses wont ↑HR when Propofol is on board)
What can occur with subclinical doses of Atropine due to its effect on the M1 receptor?
A) Tachycardia
B) No change in heart rate
C) Paradoxical bradycardia
D) Hypertension
C) Paradoxical bradycardia
Subclinical doses → paradoxical bradycardia d/t presynaptic M1 inhibition. This receptor’s job is to ↓Ach release via negative FB. Blockade of M1 “turns off” this feedback loop and allows for continued release of Ach → bradycardia
What is the role of the M1 receptor in the regulation of acetylcholine release?
A) Increases acetylcholine release
B) Decreases acetylcholine release through negative feedback
C) Directly stimulates heart rate increase
D) Modulates dopamine release
Answer: B) Decreases acetylcholine release through negative feedback
How does blockade of the M1 receptor contribute to paradoxical bradycardia with subclinical doses of Atropine?
A) Increases acetylcholine release through enhanced feedback
B) Decreases acetylcholine release due to reduced feedback inhibition
C) Inhibits acetylcholine release by activating sympathetic pathways
D) Enhances feedback inhibition of acetylcholine release
Answer: B) Decreases acetylcholine release due to reduced feedback inhibition
Subclinical doses → paradoxical bradycardia d/t presynaptic M1 inhibition. This receptor’s job is to ↓Ach release via negative FB. Blockade of M1 “turns off” this feedback loop and allows for continued release of Ach → bradycardia
Why is Atropine ineffective in increasing heart rate in transplanted hearts?
A) It does not cross the blood-brain barrier
B) It is an indirect-acting agent and cannot affect the transplanted heart’s neural control
C) It is a direct-acting agent and works only on transplanted hearts
D) It directly stimulates the heart’s pacemaker cells
Answer: B) It is an indirect-acting agent and cannot affect the transplanted heart’s neural control
Indirect acting = ineffective on transplanted hearts
