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Beta Blockers – Selective vs Non-Selective Beta Blockers | Uses | Beta Blocker Side Effects

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Find out what are beta blockers used for, the difference between selective and non selective beta blockers, the side effects of beta blockers AND how beta blockers work (mechanism of action). Also includes why are beta blockers contraindicated in asthma and an overview on adrenergic receptors, how do beta blockers work in heart failure and how do beta blockers work in hypertension.

Reeta blockers are one of the most common classes of drugs mentioned in medicine as the name suggests their mechanism of action is by blocking or antagonizing the beta adrenergic receptors in the body so let’s quickly recap what the different adrenergic receptors are responsible for an under new acree scepter itself is a receptor that is bound by catecholamines such

As epinephrine and norepinephrine we have alpha 1 alpha 2 beta 1 2 and even b 2 3 adrenergic receptors that are usually g-protein coupled receptors that ultimately lead to an increase in cyclic a mp leading to downstream effects alpha 1 receptors are present in the vascular beds both arterial and venous beds an activation of these receptors leads to vasoconstriction

Meaning that we have an increase in the mean arterial pressure and also increased venous return other effects include mydriasis meaning pupil dilation remember d4 dilation as well as contraction of the you ethyl sphincter and the prostate alpha 2 receptors are receptors that decrease the sympathetic tone in various tissues these tissues include the pancreatic islet

Cells and adipose cells where they decrease insulin release and decrease lipolysis respectively they also cause less aqueous humor to be produced from the ciliary body of the eye beta 1 receptors are found on the cardiac myocytes as well as on the sinoatrial and atrioventricular nodes their activation leads to an increase in contractility turned a positive ionotropic

Effect and also an increase in the conduction through the sa and the av nodes termed a positive crona tropic effect these receptors are also actually present in the juxtaglomerular apparatus which when activated lead to an increase in the production of renin for beta 2 the receptors ultimately lead to smooth muscle relaxation therefore we have bronchodilation

And razor dilation because these receptors are present in the airways and in the vessels interestingly they’re also present in the uterus and so by causing smooth muscle relaxation they actually prevent premature labor beta-2 receptors are also present in other tissues such as in adipose cells pancreatic islet cells and the ciliary body however compared to alpha

2 receptors the effects are basically the opposite for example we have an increase in lipolysis and increase in insulin release and an increase in aqueous humor production now for the classification beta blockers are divided into several different classes based on which receptors they block non-selective beta blockers don’t discriminate between beta 1 or beta

2 receptors and examples of which include propanolol and timolol beats a1 selective as you can imagine only block the beta 1 receptors and these include metropole bisoprolol and atenolol thirdly we have beta blockers that also have some alpha blocking properties such as labetalol finally some beta blockers have some intrinsic sympathomimetic activity meaning

They can also even act as agonists on the beta receptors as well as acting as antagonists this is in a competitive way examples include a sebou talal and pinda law now let’s look at when you would give them and the uses of beta blockers first off we have the decrease in myocardial contractility and a decrease in the heart rate meaning they decrease the oxygen

Consumption from the contractility and due to the slower heart rate we have a longer perfusion time during diastole therefore this is why we use beta 1 selective agents in chronic heart failure unstable angina acute coronary syndromes and hypertrophic obstructive cardiomyopathy secondly beta blockers are also often used as anti hypertensive medications but they

Are not usually the first line the first line is usually ace inhibitors diuretics or calcium channel blockers beta blockers are often used when the patients have high perd alongside something else such as chronic heart failure patients that are hypertensive so how do they drop the blood pressure so we know blood pressure is given by the cardiac output multiplied by

The systemic vascular resistance and the kanak output itself is given by the heart rate multiplied by the stroke volume we know that the drop comes from the decreased cardiac output coming from a decreased heart rate and the lower contractility and so if we use a beta blocker with some alpha antagonizing properties like labetalol we also see a drop in the systemic

Vascular resistance due to the vasodilation and that also contributes to the decrease in blood pressure labetalol itself is often used in hypertensive emergencies due to the fact that it acts quickly and is safe to use in pregnancy we then have things like migraine prophylaxis examples of beta blockers used as migraine prophylaxis include metroprolol or similar

The catecholamine crisis that is seen in a thyroid storm may also be treated by beta blockers specifically propanolol is used alongside prednisone and proprio thea uracil and this combination of therapy is known as the three p’s then beta blockers can be used as a treatment for essential tremors and finally they can be used as antiarrhythmic agents specifically

Their class to antiarrhythmics which are often used post myocardial infarction where there is a high risk of an arrhythmia now let’s take a look at some of the side effects of beta blockers first of all due to the negative crona tropic effect we can of course get bradycardia and even hard block this is why they are often contraindicated in people with heart block

Secondly due to the decrease in contractility as well as the decrease in heart rate they can actually cause the cardiac output to drop so much that circulation backs up into the lungs causing pulmonary edema for this reason beta blockers need to be used slowly and carefully and it’s also why it’s so crucial to look for signs of pulmonary edema in these patients

Next we have the effect of blocking the beta-2 receptors in the airways we know that activation of these receptors normally gives us bronchodilation but if we block them we end up with bronchoconstriction and therefore we can end up exacerbating the symptoms of asthma or copd so often in patients with asthma or copd it’s better to give the cardio selective beta

Blockers erectile dysfunction is another potential side effect of beta blocker therapy finally we have the treatment for when beta blockers are not appropriate and we end up with a patient who has beta blocker toxicity the antidote is glucagon because it has been shown to improve nodal conduction and therefore increases the heart rate as well as increasing myocardial contractility

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Beta Blockers – Selective vs Non-Selective Beta Blockers | Uses | Beta Blocker Side Effects By Rhesus Medicine