Flashcards in Lecture 26: CV effects of Autonomic ANTAGONIST drugs Deck (42):
What are the parasympathetic agonists? Antagonists?
What is the MoA for Atropine?
Competitive antagonist for the muscarinic receptor’s acetylcholine binding site
What is the difference between atropine and scopolamine?
Both are competitive antagonists for muscarinic receptors
However, scopolamine acts on CNS
Atropine cannot act on CNS
What are the circulatory effects of atropine?
Increases heart rate by withdrawal of vagal influence
i. Decreases AV nodal refractoriness
ii. increases SA node conduction
Decreases parasympathetic systemic arteriolar vasodilation (in areas such as the skin and GI tract)
What are the clinical uses for atropine?
1. Prevention of vagal reaction
2. Restore AV conduction in conditions with prolonged AV nodal refractoriness such as inferior wall MI and digitalis intoxication
What are the side effects for atropine?
1. Dry mouth/skin
What are the sympathetic antagonists?
What are the alpha adrenergic antagonists?
1. Prazosin (prazocin)a
What is the MoA of Prazosin?
Alpha 1 receptor antagonist >> alpha 2 antagonist
Results in decreased SVR and decreased blood pressure
Inhibition of vasoconstriction
What are the indications for use of Prazosin/Prazocin?
Hypertension (to decrease peripheral vascular resistance by vasodilation)
Urinary bladder obstruction
What are the side effects of Prazocin?
What are the characteristics of doxazosin and terazosin?
Similar to prazosin but are pure alpha1 blockers and have no alpha2 activity
What are the Beta adrenergic antagnoists?
What are the classification schemes for beta adrenergic antagonists?
1. Beta1 selectivity
-B2 blockers can cause bronchoconsriction
2. Intrinsic sympathomimetic activity (ISA)
-B-blockers with ISA are partial agonists that may produce blocked by shielding receptors from more potent agonists
3. lipid solubility
4. duration of activity
What beta blockers are lipid soluble? Significance?
Readily absorbed by GI tract
Metabolized by liver
Short half life
What beta blockers are water soluble? Significance?
Not as readily absorbed or metabolized
Longer halflifes and metabolized in kidney
What are the effects of beta blockers?
1. Decrease HR, impulse conduction and contractility
2. Decreases myocardial demand
3. used to treat heart failure, MI/angina, arrhythmias, HTN
What are the adverse effects of beta blockers?
1. Sinus bradycardia, sinus arrest, AV block
2. Reduced LV contractility
4. sexual dysfunction
5. mental depression, nightmares
6. May precipitate Raynaud’s phenomenon
What is the MoA of Propranolol?
Non-selective B1 and B2 antagonist
Lipophilic, decreases HR and contractility
That means this motherfucker can lead to bronchoconstriction
What are the indications for propranolol?
2. Ventricular arrhythmias
CHEAP AS FUCK
What is the MoA of metoprolol?
Beta1 Selective antagonist
Lipophilic, decreases HR and contractility
Does not lead to bronchoconstriction
When is metoprolol indicated?
1. stable CHF
What is the MoA of atenolol?
Beta 1 selective
Decreases HR and contractility
What are the indications for atenolol?
4. stable CHF
What are the characteristics of Esmolol?
Decreases heart rate and does nothing to contractility
Applicable to patients with pulmonary disease
VERY fucking expensive
Used for tachy, atrial fib, and tachycardia
What are the characteristics of Carvedilol?
Nonselective beta1 and beta2 antagonist
Also blocks alpha1 receptors
Decreases HR and conractility
Used for heart failure and hypertension
Which beta blockers are beta1 selective?
Which beta blockers are non-selective?
For a patient in cardiogenic shock, would you use beta-blockers?
No, patient needs inotropic support
Therefore, give this patient dobutamine
Once patient with cardiogenic shock stabilizes, would it be a good time to give beta-blockers?
Yes, in order to counteract the negative effect of NE on remodeling
Increased filling time and decreased demand
What are the effects of muscarinic activation in the heart?
Decrease automaticity of SA node
Decreased inotropy in the atrial myocardium
Increase refractoriness in the AV node
What are the effects of muscarinic activation in the vasculature?
Increase in vasodilation in the systemic arterioles
What is the CV response to a generalized parasympathetic discharge (vagal reaction or faint)?
Why is beta1 receptor indicated for congestive heart failure?
Decreases renin production from kidney
Decreases myocyte hypertrophy/myocyte injury due to inappropriate downregulation of beta1 receptors
Improves supply and decreases demand
What would you use to treat a patient with complete heart block and acute inferior MI (as shown by ST eleations)?
No, you never want to give betablockers to someone in complete heart block!
Give Atropine instead (in order to improve CO)
When the patient is stabilized (no more heart block), would you then give beta blockers?
Betablockers are indicated for MI as it decreases the size of the infarcted tissue
This is because it decreases demand of the heart and increases supply (by allowing greater diastolic filling)
What would you use to treat a patient with chronic stable angina?
Beta-blockers are indicated because it reduces ischemic damage
What does ischemia result from? Significance?
Mismatch between O2 supply and demand
Can be corrected by beta-blockers
What are the major determinants of myocardial?
Double product (HR x systolic pressure)
What are the benefits of beta-blockade in the treatment of ischemia?
1. Improve myocardial O2 supply
-decreasing HR will prolong diastole and improve subendocardial perfusion
2. Decrease myocardial O2 demand
-suppresses both HR and contractility as well as sympathetic reflex
-leads to less O2 demand
-blocks sympathetic reflex
What are beta-blockers ideal therapies for?
1. Prominent relationship of physical activity to attacks of angina
2. Coexistent hypertension
3. History of supraventricular or ventricular arrhythmias
4. Previous myocardial infarction (STANDARD OF CARE)
5. Left ventricular systolic dysfunction
6. Mild to moderate heart failure symptoms
7. Prominent anxiety state