Action of Beta Blockers?

I know that beta blockers block the epi/nor epi sites as well as decrease the afterload and contractility. I am having difficultly making the connection as to how this leads to a decreased HR and pulse. I was under the impression that EPI makes you vasoconstrict. But doesn't your BP decrease when you vasodilate?


...Confused
If you block the action of epi you get less of what epi does. Beta receptors are more prevelent in the heart than in the blood vessels. Beta blockers reduce the workload of the heart by blunting the mechanism that makes the heart beat faster and harder. BP does go down when you dilate, this also lowers the workload on the heart. You only give this to a patient who has normal or high BP and HR. Anyone bradycardic or hypotensive wouldn't receive a beta blocker (nursing would know to withhold). I think you understand but don't know that you understand. Hope that helps.

You need to understand that epinephrine acts on several types of "adrenergic" receptors to include alpha and beta. Your alpha 1 receptors are commonly associated with vasoconstriction, while beta one receptors are associated with cardiac excitation. I think your question relates to beta 1 receptors?Have you studied the physiology of said receptors? Basically, the activation of a beta 1 receptor results in a change in the receptor confirmation. Some simplify this to a "lock and key" action. This in turn causes the release and activation of special types of G proteins. These lead to the activation of a membrane bound enzyme called adenyl cyclase. Adenyl cyclase, then catalyses the conversion of ATP to cAMP. cAMP in turn causes a cascade of events that lead to increased contractility of the heart and increased heart rate.Hopefully, you can appreciate that by blocking the action of epinephrine at a beta 1 receptor, we inhibit a process that causes the heart rate to increase and increased myocardial contractility.

Beta blockers as you know decrease the workload of the heart. They also as you say decrease afterload. This is going to be your best friend. CO = HR x SV. Cardiac output = Heart rate x Stroke Volume. Cardiac output = volume of blood pumped by heart per minute (liter/min). Stroke volume = volume of blood pumped from one ventricle per minute (usually left ventricle). Remember that stroke volume consists of preload, afterload, and contractility. If any of these three things are affected, it affects stroke volume....thus affecting heart rate and cardiac output. When one goes up, the other usually goes down. If stroke volume goes down, HR goes up. If beta blockers decrease afterload (resistance heart must work against to pump blood into periphery) and contractility, the blood pressure will decrease b/c you're vasodilating. Heart rate goes down, stroke volume (compensatory mechanism) goes up.However, the easiest way to think of it is that you know that beta-blockers affect the sympathetic nervous system which causes you to vasoconstrict and increase heart rate. If it's working against the SNS, it'll have the opposite effect..lower BP and lower HR. However, that formula I gave you is still good to know especially for the cardiac section of your med-surg class. Good luck.

This is what we've learned in Pharm:Beta 1 receptor sites deal with:Heart--increased heart contraction-->increased HRKidneys--increased renin secretion-->increased angiotensin-->increased BPBeta 2 receptor sites deal with:Smooth Muscle (GI tract)--decreased GI tone and motilityLungs--inducing bronchodilationUterus--relaxation of the uterine smooth muscleLiver--activation of glycogenolysis-->increased blood sugarNow, all you have to do is realize that you're focused on the action of BLOCKERS, so just do the opposite action.

Also note; some beta blockers are nonspecific, while others are beta 1 specific and still others have both alpha and beta blocking properties.

Quote from sj73201This is what we've learned in Pharm:Beta 1 receptor sites deal with:Heart--increased heart contraction-->increased HRKidneys--increased renin secretion-->increased angiotensin-->increased BPBeta 2 receptor sites deal with:Smooth Muscle (GI tract)--decreased GI tone and motilityLungs--inducing bronchodilationUterus--relaxation of the uterine smooth muscleLiver--activation of glycogenolysis-->increased blood sugarNow, all you have to do is realize that you're focused on the action of BLOCKERS, so just do the opposite action.

Actually, asthma is not an absolute contraindication. With B1 selective agents and a patient with mild to moderate asthma that is reasonably well controlled, I would have no problem. The literature also supports this stance.

You are right, I should have worded that differently and said "be careful if someone has asthma". Thanks!

Quote from SillyInScrubsYou are right, I should have worded that differently and said "be careful if someone has asthma". Thanks!