Autonomic ANTAGONISTS Flashcards
List the parasympathetic and sympathetic antagonists
- para: atropine, scopalamine
- SNS: prazosin, carvedilol, atenolol, metoprolol, propanolol
Atropine mechanism of action
-competitive antagonist for the muscarinic R’s ACh binding site
Clinical uses of atropine
- interrupt or prevent vagal rxn
- restore AV conduction in disorders causing prolonged AV nodal refractoriness: inferior wall MI, digitalis intox
Circulatory system effects of atropine
-increase HR, decrease AV nodal refractoriness, decrease parasympathetic mediated systemic vasodilation
CV effects of adrenergic antagonists
- decrease HR, decrease conduction (inc refractoriness), decrease inotropy and metabolic rate
- inhibit renin release
- arteriolar vasodilation, venodilation
Prototypical a adrenergic antagonists, actions, and uses
- 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
Side effects of a adrenergic antagonists
-postural hypotension may occur
4 beta adrenergic antagonists
- propanolol
- metoprolol
- atenolol
- carvedilol
4 classification schemes for B-antagonists
- B1 selectivity
- Intrinsic sympathomimetic activity: partial agonists
- lipid solubility
- duration of action
Who do we worry about prescribing nonselective B blockers to?
-those with COPD, asthma, etc bc blocks B2 which is needed fro bronchdilation
Lipid solubility and B blockers
- 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
Nonselective vs selective B blockers
Propanolol and Carvedilol are nonselective B blockers and carvedilol is also a a1 blocker
-Metoprolol and atenolol are B1 selective
Clinical uses of B blockers
- HF (do not use in class 4!)
- MI/angina
- arrhthmias
- HTN
B blockers adverse effects
- 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
B blockers withdrawal phenomenon
-prolonged block upregulated B1 receptors, so when block is stop tachycardia, arrhythmia, and angina can happen
Are B blockers a good idea in acute cardiogenic shock?
- NO! need to keep whatever CO the heart can give!
- give once he is stable to prevent the neurohormonal activation that leads to CHF
4 conditions to not give B blockers
- decompensated CHF
- stage 4 CHF
- cardiogenic shock
- complete heart block, but can be used after stable from an MI
What is the role of B blockers in stable coronary disease?
-decrease metabolic demand of the heart
Ischemia is a mismatch between what?
-O2 supply and demand
Major determinants of mycardial O2 supply
- blood oxygen level: impaired in hypoxia (poor ventilation, anemia)
- coronary perfusion at rest and flow reserve: impaired in atherosclerosis, thrombosis, vasospasm
Endocardial perfusion occurs during ________. The higher ventricular diastolic P and shorten diastolic duration, the less effect endocardial perfusion. When is this impaired?
- diastole
- HTN, tachycardia
5 major determinants of myocardial O2 demand
-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
2 major benefits of B blockade in the rx of ischemia
- improve myocardial O2 supply: dec HR to prolong diastole, improve subendocardial perfusion
- decrease myocardial O2 demand: cardiac depressants suppress HR and contractility, blocks sympathetic reflex, reduces double product, helps reduce BP
7 ideal candidates for B blocker use
- prominent relationship of physical activity to angina attacks
- coexistent HTN
- history of supraventricular or ventricular arrhthmias
- previous MI
- LV systolic dysfunction
- mild to moderate HF sxs (class 2 or 3)
- prominent anxiety state
Poor candidates for B blockers
- 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
