What drug is the main muscarinic antagonist used in cardiology?
there’s also scopolamine, but that has more CNS effect
What bad thing happens when there’s too much parasympathetic discharge?
“Vaso-vagal reaction” - bradycardia /heart CO reduced + peripheral vasodilation leads to reduced BP and syncope.
Clinical uses of atropine?
Interrupt/prevent vaso-vagal reactions -can be caused by catheterization).
Reduce AV nodal refractoriness -in partial AV block due to inf. wall MI or digoxin toxicity.
(also, unrelatedly, as antidote to cholinesterase inhibitor poisoning, such as Sarin gas)
Review: What does agonism of alpha-1 do?
Constricts vascular smooth muscle.
Constricts GU smooth muscle.
Review: What does agonism of alpha-2 do?
Constricts vascular smooth muscle.
Promotes platelet aggregation (minor role).
Review: What does agonism of beta-1 do?
Increased heart inotropy and chonotropy.
Increased kidney renin secretion.
Review: What does agonism of beta-2 do?
Dilation of vascular smooth muscle.
Dilation of airway smooth muscle.
What are prototypical alpha adrenergic antagonists?
What are they used for?
Prazosin (alpha-1»_space; alpha-2)
Doxazosin, terazosin (pure alpha-1 antagonism)
These are “third line” drugs for hypertension.
They can also be used to help people pee when there’s outlet obstruction.
(“-zosin” = alpha antagonist)
What does it mean for a beta-blocker to have Instrinsic Sympathomimetic Activity (ISA)?
Drug is a partial agonist that produces blockade by shielding receptors from more potent agonists.
(none of the 4 main beta blocker discussed have ISA)
How does lipid solubility relate do to absorption, metabolism, and half life? (Which drugs are notably lipid soluble/hydrophilic?)
More lipid soluble: more absorption, hepatic metabolism, shorter half life. (propanolol, metoprolol)
More hydrophilic: Less absorption, renal metabolism, longer half life. (atenolol)
Side effects of too much beta-1 antagonism?
Bradycardia, AV block, reduced LV contractility (in severe HF)
Side effects of too much beta-2 antagonism?
Bronchoconstriction (especially a problem in pts with asthma).
Unopposed alpha agonism -> Raynauld’s, sexual dysfunction, limb ischemia, etc.
Is there beta-blocker withdrawal?
Yes. Beta 1 receptors seem to be upregulated with chronic beta blocker use.
Effect of beta blockers on lipids?
Increased triglycerides, decreased HDL.
Should beta blockers be used for cardiogenic shock?
No! Such a patient needs inotropic support.
Once a patient has recovered from cardiogenic shock, but has CHF, are beta blockers useful?
Yes, probably. They’ll reduce the metabolic demand of the heart, and counteract the increased pressures / RAAS activation that lead to remodeling.
A patient has a STEMI with complete AV block, but is perfusing well. Should a beta blocker be used?
No. Complete heart block is a contraindication for beta blockers.
But, they can be started as soon as such a patient is revascularized.
Should a beta blocker be used for chronic stable angina? Why or why not?
Yes, as they reduce the metabolic demand of the heart. Also, longer diastole = more coronary perfusion.
7 relative contraindications for beta blockers?
more important to understand these than to memorize, probably
Asthma / COPD.
Severe LV dysfunction (NYHA class IV).
History of severe depression (interesting).
Symptomatic peripheral vascular disease.
Severe bradycardia or heart block.
“Brittle diabetes” (big swings in blood glucose, from hypo to hyper etc., usu. T1D).