Cardiovascular Effects of Autonomic Antagonists Flashcards Preview

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Flashcards in Cardiovascular Effects of Autonomic Antagonists Deck (29)
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1
Q

What are the roles of muscarinic receptors in the heart?

A
  1. reduce automaticity in SA node
  2. reduce inotropy in atrial myocardium
  3. increase refractoriness in AV node

minimal ventricular and his involvement

2
Q

What are the roles of muscarinic receptors in the vasculature?

A

vasodilation of systemic arterioles

minimal venous involvement

3
Q

Consequences of parasympathetic discharge on cardiac tissue?

A
  1. reduced heart rate, reduced AV nodal conduction = profound bradycardia
  2. reduced systemic arteriolar resistance via vasodilation leading to reduction in systemic arterial pressure
4
Q

_____ is the prototypical competitive antagonist for the muscarinic receptor’s ACh binding site.

A

atropine

5
Q

Why don’t we use scopolamine in cardiology?

A

scopolomine is a muscarinic antagonist but has strong central effect so it’s used in motion sickness vs in cardiac tx

6
Q

Effects of atropine

A

increase heart rate, reduce AV nodal refractoriness, reduce vasodilation

7
Q

Uses of atropine

A

prevent vagal reaction, restore AV conduction in disorders w/impaired AV nodal refractoriness like digitalis toxicity and inferior wall MI

8
Q

Do beta blockers tend to work via beta1 or beta2 receptors?

A

beta 1 –> decrease heart rate, increase refractoriness/reduce impulse conduction, reduce inotropy/metabolic rate, inhibit renin release

9
Q

What are the effects of alpha blockers?

A
  1. arteriolar vasodilation via alpha1, alpha2
  2. venodilation via alpha1
  3. improve voiding function in pts with urinary bladder outlet obstruction (prazosin)
10
Q

Prototypical alpha1, alpha2 antagonist

A

prazosin –> alpha1 > alpha2

11
Q

Prototypical pure alpha1 blocker

A

doxazosin, terazosin

12
Q

Clinical uses of alpha blockers

A
  1. to decrease peripheral vascular ressitance

2. third line tx of htn

13
Q

What limits the use of alpha blockers in the elderly?

A

adverse reaction of postural hypotension

14
Q

What the pharmacokinetic differences between pure alpha 1 blockers and dual blockers?

A

pure alpha1 blockers have slower onset and longer duration

15
Q

Why do we prefer beta1 selective blockers?

A

beta 2 blockers will cause bronchoconstriction

16
Q

What is ISA?

A

intrinsic sympathomimetic activity –> partial agonists that produce blockade by shielding receptors from more potent agonists

17
Q

Which beta blockers are lipophilic and what does this do?

A

propranolol, metoprolol –> readily absorbed by GI tract, metabolized by liver –> short half life

18
Q

Which beta blockers are hydrophilic and what does this do?

A

atenolol –> longer half life b/c longer absorption/metabolism –> kidney metabolism –> gotta be careful in people with kidney disease

19
Q

Which beta blockers have ISA?

A

acebutolol, pindolol at low doses –> act as beta blockers at higher doses

20
Q

Which is non selective? propranolol, metoprolol, atenolol, carvedilol

A

propranolol, carvedilol (alpha 1 blockade)

21
Q

Which is lipophilic? propranolol, metoprolol, atenolol, carvedilol

A

propranolol> metopropolol, carvedilol > atenolol

22
Q

Which is renal clearance? propranolol, metoprolol, atenolol, carvedilol

A

atenolol

23
Q

4 general cardiac conditions in which beta blockers are useful

A
  1. heart failure
  2. mi/angina
  3. arrhythmias
  4. htn
24
Q

Adverse effects of beta blockers

A
  1. sinus bradycardia, sinus arrest, AV block
  2. reduce LV contractility in symptomatic heart failure
  3. bronchoconstriction
  4. fatigue, mental deprex, nightmares, sexual dysfunction
  5. limb ischemia in those with PVD, raynauds
  6. withdrawal
  7. increased TG, reduced HDL
25
Q

Why does sudden beta blocker removal cause withdrawal symptoms in patients with chronic beta blockade?

A

b/c you upregulate beta receptors when on beta blockers so sudden removal of the drug leads to overstimulation of beta receptors –> increased heart rate, etc.

26
Q

What is the treatment option of choice in patients with CHF?

A

carvedilol –> not just a beta blocker (reduces myocyte injury, hypertrophy, and activation of RAAS), but also alpha blocker ( reduces vasoconstriction, reduces sodium retention even more)

27
Q

What is the Bezold-Jarisch reflex?

A

The Bezold–Jarisch reflex is responsible for the sinus bradycardia that commonly occurs within the first 60 minutes following an acute myocardial infarction, and explains the occurrence of AV node block in the context of acute posterior or inferior myocardial infarction –> vagal nerve stimulation due to ischemia

28
Q

Beta blocker or no? MI with complete heart block

A

no –> contraindication (complete heart block) overrides indication (acute MI)

29
Q

How do beta blockers improve myocardial O2 supply?

A

reduce heart rate –> increase diastole –> improve subendocardial perfusion

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