Ask the Clinical Instructor:A Q&A column for those new to the cath lab

Beta-blockers are used for a variety of different situations. You will see them used for heart rate control, blood pressure management, long-term angina treatment and cardiomyopathy, just to name a few. This topic can generally be a 2- to 3-hour lecture just to cover the basics. I will try to address the important points in a few paragraphs. To understand how beta-blockers work, we must first revisit some basic physiology and pharmacokinetics. If we recall a visit to our basic terminology, we should know that any medication that has an effect on the heart rate is considered a chronotropic agent (chrono = time) and any medication that affects the force of contraction is an inotropic agent. These are the principle properties affected by beta-blockers. Beta properties are a branch of the sympathetic nervous system, which is the cornerstone for many medications you will see given in the cath lab. The other branch that we deal with are the ‘alpha’ properties, which we will only discuss briefly. What are the alpha and beta properties? In the heart, lungs and arteries, there are specific receptor sites to achieve certain actions. We are concerned with alpha and beta properties. You can see what effects these two agents have on the specific target areas in Table 1. In the heart, there are only beta receptors (beta1, to be specific). Only beta medications can increase the heart rate through this stimulation. That’s why if we give Isuprel, the heart rate increases (+ chronotropy) and the automaticity of heart increases. Unfortunately, unwanted vasodilation can also occur in the periphery. There are not any alpha receptors in the heart, so any hemodynamic changes due to alpha stimulation are not a cause of stimulation to the heart (more to follow on this). In the lungs, bronchoconstriction is bad. We treat bronchoconstriction with beta medications (specifically, beta2) to achieve bronchodilation, such as Albuterol, Isoetharine and Terbutaline. In the peripheral arteries, there are both alpha and beta receptors that are integral to our management of specific conditions. Beta medications will cause vasodilation, which is sometimes unwanted because it will decrease the blood pressure. In cases where we want help with the blood pressure by constricting the arterial vasculature, we can use neosynephrine (phenylephrine), which is a potent alpha stimulant. It has very little effect on the heart, so the resultant vasoconstriction can help create a higher blood pressure. Unfortunately, this can also increase the workload of the heart due to the increased afterload effects. Another question that I routinely get is, Why do we give epinephrine if it is going to vasodilate the vasculature? Many medications have the properties of BOTH alpha and beta (see Table 2). Epinephrine is one of those medications. It is PREDOMINATELY beta (to increase heart rate, force of contractions and automaticity), but also has slight alpha properties (to vasoconstrict). This is why it is a medication of choice in a cardiac arrest situation, because pure beta property, as in Isuprel, would adversely create vasodilation. This is also one reason why you do not see Isuprel in ACLS algorithms anymore. A closer look at beta-blockers Now, with beta-blockers, we are looking to ‘stop’ the results of the beta stimulation. As we saw, beta stimulation in the body results in increased heart rate, force of contractions, bronchodilation and vasodilation. When beta-blockers are administered, the beta receptor sites are not very specific, and can not differentiate between an actual agent and a blocker agent. The blocker agent takes up the receptor sites, preventing the beta stimulation actions from occurring. From what we discussed before, we know that the administration of beta-blockers would PREVENT chronotropic effects, it would PREVENT inotropic effects, it would PREVENT bronchodilation and PREVENT vasodilation. Understanding that beta-blockers have slight effects on the lungs and the vasculature, we can see how it can affect heart rate and blood pressure. If the beta receptors are ˜blocked’ to prevent stimulation, then the heart rate will not increase, and will likely even slow down a little because of the lack of ‘accelerant’ stimulation. If we remember that: CARDIAC OUTPUT (blood pressure) = STROKE VOLUME x HEART RATE then by changing the inotropic (force of contraction > stroke volume) and chronotropic (heart rate) effects, we can also manage the blood pressure. Ultimately, to answer your question, the blood pressure is lowered because we controlled the chrontropic and inotropic effects of that stimulation. The blocking of these actions also decrease the excitability of the heart (automaticity), decrease the cardiac workload (preload and afterload), and decrease myocardial oxygen consumption. These are the main reasons that patients with an active acute myocardial infarction (AMI) will receive beta-blocker agents early in their treatment. It allows the heart to have a reduced workload. Considerations prior to agent administration Some important considerations before administration would be to detect the presence of any form of AV block. We would not want to administer an agent that could lower the heart rate to a patient already susceptible to an abnormally low heart rate. We would also not want to administer it to someone who is in an already hypotensive or hypovolemic state. We would also not want to administer it to someone with active bronchospams or a history of uncontrolled COPD, for the risk of bronchoconstriction would be present, and possibly worsened by, beta-blocker administration. One of the problems with patients on large doses of beta-blockers is that when they encounter a medical condition that would require an increase in heart rate (i.e., hypoxia, hypovolemia, etc.) the body can have a delay in achieving this heart rate increase. This delay is because of the beta blockade that will keep their heart rate and stroke volume lower and keep the body’s response to those conditions in check. When to use alpha agents We will most commonly use alpha-stimulating medications when there is poor blood pressure because of unwanted vasodilation of the vasculature. This can also be considered in hypotensive states where we do not wish to over-stimulate the heart with beta agents. The alpha agents provide marked constriction of the vasculature, effectively increasing blood pressure. One last tip As your cardiologist is running off his list of medications to administer during a case, how do you know what medications are beta-blockers? Simple. Any medication ending in -lol is a beta-blocker. Some examples of commonly administered beta-blockers are listed in Table 3. As you care for your AMI, hypertensive and angina patients, you can now see why beta-blocker administration can be important to control both their heart rate and blood pressure. Next month, we will answer a question about activated clotting time (ACT) checks in the cath lab. Email your question to: tginapp@rcisreview.com

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