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Cardiology > Autonomic ANTAGONISTS > Flashcards

Autonomic ANTAGONISTS Flashcards

1
Q

List the parasympathetic and sympathetic antagonists

A
  • para: atropine, scopalamine

- SNS: prazosin, carvedilol, atenolol, metoprolol, propanolol

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2
Q

Atropine mechanism of action

A

-competitive antagonist for the muscarinic R’s ACh binding site

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3
Q

Clinical uses of atropine

A
  • interrupt or prevent vagal rxn

- restore AV conduction in disorders causing prolonged AV nodal refractoriness: inferior wall MI, digitalis intox

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4
Q

Circulatory system effects of atropine

A

-increase HR, decrease AV nodal refractoriness, decrease parasympathetic mediated systemic vasodilation

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5
Q

CV effects of adrenergic antagonists

A
  • decrease HR, decrease conduction (inc refractoriness), decrease inotropy and metabolic rate
  • inhibit renin release
  • arteriolar vasodilation, venodilation
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6
Q

Prototypical a adrenergic antagonists, actions, and uses

A
  • prazosin: a1>a2
  • doxazosin, terazosin: pure a1 blocker; slower onset, longer duration than prazosin
  • actions: arteriolar and venodilation= decreased PVR
  • 3rd line rx of HTN, improve voiding function in pts with urinary bladder outlet obstruction
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7
Q

Side effects of a adrenergic antagonists

A

-postural hypotension may occur

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8
Q

4 beta adrenergic antagonists

A
  • propanolol
  • metoprolol
  • atenolol
  • carvedilol
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9
Q

4 classification schemes for B-antagonists

A
  • B1 selectivity
  • Intrinsic sympathomimetic activity: partial agonists
  • lipid solubility
  • duration of action
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10
Q

Who do we worry about prescribing nonselective B blockers to?

A

-those with COPD, asthma, etc bc blocks B2 which is needed fro bronchdilation

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11
Q

Lipid solubility and B blockers

A
  • lipophilic: readily absorbed in GI, metabolized in liver, short half life, greater CNS effect= propanolol, metoprolol
  • hydrophilic: atenolol= longer half life, often metabolized by kidneys, not as readily absorbed; avoid in kidney disease pts
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12
Q

Nonselective vs selective B blockers

A

Propanolol and Carvedilol are nonselective B blockers and carvedilol is also a a1 blocker
-Metoprolol and atenolol are B1 selective

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13
Q

Clinical uses of B blockers

A
  • HF (do not use in class 4!)
  • MI/angina
  • arrhthmias
  • HTN
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14
Q

B blockers adverse effects

A
  • severe sinus bradycardia, sinus arrest, AV block
  • reduced LV contractility in severe symptomatic heart failure!!!
  • bronchoconstriction if nonselective
  • fatigue, mental depression, nightmares!!!
  • sexual dysfunction
  • may precipitate Raynaud’s in pts with the dz, may worse limb ischemia in pts with severe PVD
  • WITHDRAWAL PHENOMENON
  • increase TG, decrease HDL
  • can mask sxs of low glucose in DM
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15
Q

B blockers withdrawal phenomenon

A

-prolonged block upregulated B1 receptors, so when block is stop tachycardia, arrhythmia, and angina can happen

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16
Q

Are B blockers a good idea in acute cardiogenic shock?

A
  • NO! need to keep whatever CO the heart can give!

- give once he is stable to prevent the neurohormonal activation that leads to CHF

17
Q

4 conditions to not give B blockers

A
  • decompensated CHF
  • stage 4 CHF
  • cardiogenic shock
  • complete heart block, but can be used after stable from an MI
18
Q

What is the role of B blockers in stable coronary disease?

A

-decrease metabolic demand of the heart

19
Q

Ischemia is a mismatch between what?

A

-O2 supply and demand

20
Q

Major determinants of mycardial O2 supply

A
  • blood oxygen level: impaired in hypoxia (poor ventilation, anemia)
  • coronary perfusion at rest and flow reserve: impaired in atherosclerosis, thrombosis, vasospasm
21
Q

Endocardial perfusion occurs during ________. The higher ventricular diastolic P and shorten diastolic duration, the less effect endocardial perfusion. When is this impaired?

A
  • diastole

- HTN, tachycardia

22
Q

5 major determinants of myocardial O2 demand

A

-HR
-heart contractility
-double product: HR x systolic P
-preload: elevated BV and venous tone increase diastolic filling pressure, ventricular V and stress
-afterload: increased PVR increases systolic myocardial wall tension
=HTN, exertion, tachycardia, sympathetic activation elevate O2 demand

23
Q

2 major benefits of B blockade in the rx of ischemia

A
  1. improve myocardial O2 supply: dec HR to prolong diastole, improve subendocardial perfusion
  2. decrease myocardial O2 demand: cardiac depressants suppress HR and contractility, blocks sympathetic reflex, reduces double product, helps reduce BP
24
Q

7 ideal candidates for B blocker use

A
  1. prominent relationship of physical activity to angina attacks
  2. coexistent HTN
  3. history of supraventricular or ventricular arrhthmias
  4. previous MI
  5. LV systolic dysfunction
  6. mild to moderate HF sxs (class 2 or 3)
  7. prominent anxiety state
25
Q

Poor candidates for B blockers

A
  • asthma or reversible airway component in CLD pts
  • severe LV dysfunction with severe HF sxs (class 4)
  • history of severe depression
  • raynaud phenomenon
  • symptomatic peripheral vascular disease
  • severe bradycardia or heart block
  • brittle diabetes

Cardiology (27 decks)

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