What’s going on, guys. My name is Brad and welcome to nursing.com. And in today’s video, what we’re going to be doing is we’re going to discuss angina. We’re going to talk about some of the different types of angina that you may come across, as well as, some signs and symptoms that a patient may experience, and some treatment modalities that we may be giving patients as a result.  Without further ado, let’s dive in. 

So angina is specifically chest pain that starts at the heart. It’s important to remember that.  Patients can have chest pain for all sorts of different kinds of reasons, right? Patient could sustain a pneumothorax, a collapsed lung.  Or a tumor in the lungs could also cause chest pain in a patient. All sorts of different reasons why a patient could have chest pain, but angina is specifically chest pain that starts at the heart for one reason or another, those coronary arteries, the vessels on the heart themselves, are blocked and blood flow to those tissues is impeded. And so whenever we’re talking about angina, we’re primarily talking about two different types. There’s stable angina as well as unstable angina. Now, whenever we’re discussing stable angina, this is a situation where a patient has some degree of coronary artery disease, some degree of blockages within those vessels of the heart.  But it’s not enough to threaten their life. This usually is brought on by strenuous exercise or activity. That’s when chest pain presents in these patients and it usually subsides with rest.  But in unstable angina, it’s a very different story. This is the kind of angina where a patient has a significant degree of blockages within those coronary arteries, to the point that they’re not getting adequate blood flow or oxygen to those tissues of the heart, and this brings on chest pain.  And in these situations, rest does not cure this chest pain. 

And so whenever I think about angina, I really like to think about a car engine and the oil in the car. I think that this is always something that is very applicable, you know. It’s very comparable to a heart and the vessels in our body. You think about the engine being the heart, right? It’s the heart of the car. And the oil is the blood of the car. The engine, all of these pipes in this vehicle, in this body, need oil in order to continue to survive. So think about all of these little, small, intricate, tiny pipes coming off of this engine and what would happen if you didn’t change your oil filter for a very long time. Crud is going to slowly build up in these pipes. And these tiny little pipes, crud is going to build up because that gunk is just backing up and it’s not properly being filtered out. So what happens then, if a piece of this gunk were to break off and completely occlude and prevent oil from getting back to the engine? Same kind of concept. There’s some sort of occlusion, there’s some sort of degree of blockage, preventing blood from actually perfusing the heart itself. 

Some of the key assessment findings that you’re going to find with angina, of course, number one is chest pain. There are all sorts of different descriptors that a patient may give for chest pain. It could be stabbing, or crushing, burning. A lot of times we hear patients describe it like an elephant is sitting on the chest, a pressure. And of course this pain can radiate, and radiate down the arm to the jaw, through the sternum and through the back.  A lot of different descriptors that a patient could give for chest pain. Shortness of breath. Diaphoresis – patients becoming excessively sweaty. Of course, you could think if a patient is experiencing angina, the body is in a fight or flight situation, activation of that sympathetic nervous system. So, you know, shortness of breath, diaphoresis, dizziness.  Palpitations are also a big one that you could see. Remember, that electrical conduction system of the heart actually resides within the heart muscle itself. And so if the heart muscle itself is not getting the blood and oxygen it needs, you can think, neither is that conduction system. So palpitations and electrical abnormalities are not uncommon. Some of the vital sign derangements that we could see with patients, one is tachycardia. You know, the heart not getting blood and nutrients is basically, the brain interprets that as “why is the heart not getting blood and nutrients?” We need to get more blood to that heart. And so to compensate, tachycardia. The heart just starts pumping harder. We need to get blood, blood, where the heart is starving. We need to give blood to the heart. Hypotension is another one. And the way that I like to think about this is, remember, the heart is a muscle, right? And so the way I think about this is, have you ever fallen asleep on your arm? I think we all have. And you wake up and it’s super numb. Sometimes you can’t even move it. That’s a muscle, right. And why did your arm fall asleep and did you lose all that strength? It’s because when you fell asleep on it, you blocked off blood flow to that arm. Same kind of concept. As that heart muscle goes longer and longer and longer goes without oxygen and blood, the weaker and weaker it gets.  The less effective it pumps and therefore blood pressure drops. 

And now some of the labs and diagnostic tests that we look at whenever we’re talking about angina as well, two primary ones, we really look at EKG. This is the  ST wave, particularly. We look for ST elevation or ST depression.  You’ll recall, maybe go reference our EKG lesson here on nursing.com, but you will recall the ST wave – ST elevation or ST depression is one of the primary things that we look at on EKG, which can be reflective of cardiac ischemia or actual infarction, a heart attack. And then we also trend something called troponin. It’s a cardiac enzyme. It’s an actual laboratory value that we looked at, it is the gold standard, and is directly reflective of cardiac injury. 

Now, what medications might we see prescribed for a patient who’s experiencing angina? Well, you’ve got to remember, the overall idea here is that we have a heart that is starving for blood. So the aim, the overall idea of our treatment modalities, is to increase heart flow, right? We want to increase blood flow through those coronary arteries. And we do so through the use of several different types of medications, one, our vasodilatory agents. Kind of like this image here on the right.  The idea is, the more narrow a pipe that you have that fluid is flowing through, the less fluid that can flow through it. But if we’re able to widen that intra arterial lumen, if we’re able to widen the pipe, then we’re able to deliver more fluid to the heart tissues. And so, some of the vasodilatory agents that we see given are nitroglycerin. We see it all the time in the CVICU.  You may have also heard patients being educated, if you’re at home and you have chest pain, put a nitroglycerin tablet under your tongue. The entire aim of that medication is to dilate those coronary arteries and increase blood flow to the heart. Another medication, that is along the same lines that you may see given, is morphine. Now, of course we know morphine is used to treat pain, but it has very similar effects like nitro does. It dilates those vessels of the heart. We could also see anti-platelets such as aspirin given to prevent further platelet aggregation to whatever that is that is occluding that heart vessel, could be a clot. We want to prevent platelets from aggregating further. Then we could also see anticoagulant medications such as IV heparin. Same similar idea. We want to prevent any kind of clot from getting larger, but we also want to thin that blood in an attempt to sort of lubricate that vessel and keep that vessel patent. And of course, patients are short of breath. There is an increased myocardial oxygen demand. The heart is working harder and harder because of that blocked artery so patients are going to need supplemental O2. 

So what are we going to educate our patient on? It’s very important that we educate our patient on the importance of smoking cessation. Smoking is one of the leading causes of coronary artery disease in patients. Smoking directly leads to vasoconstriction of those coronary arteries. And as we’ve already previously discussed, the more narrow the inside of that vessel is, the less fluid that can actually flow through to the heart. We’re also going to want to educate our patients on the importance of diet and exercise. Also, as we saw on a previous slide, the deposition of those fatty atherosclerotic plaque into the vessels, it’s directly tied and linked to poor diet. We want to make sure we educate on the importance of limiting fatty, fried foods. We also want to make sure we educate on the importance of limiting salt intake as well because salt can lead to high blood pressure and blood pressure control is the next thing that we want to make sure we educate our patients on. Again, same concept, right? Hypertension, high blood pressure, more narrow arteries, less blood flow to the heart. And of course, diabetes control is something else that we want to make sure that we’re educating patients on as well. Remember, what is diabetes, lack of insulin, high blood glucose. And you can imagine the more sugar that you have in your blood, same concept of pouring sugar into a glass of water. If you were pouring a glass of sweet tea and the more sugar you dumped into that glass of sweet tea, the thicker and thicker your blood is going to get, same concept with high blood glucose levels. The more sugar you have in your blood, theoretically, the more thick your blood is and the more difficult it is for that thicker blood to perfuse those coronary arteries and the tissues of the heart. 

And so to summarize some of the key points, let’s remember that angina is chest pain that starts at the heart. Remember there are all different types of reasons that a patient could be experiencing chest pain, but this is always cardiac in origin. Remember that there’s a stable versus an unstable angina, stable being associated with strenuous activity, but subsides with rest and unstable being the type that is more life-threatening and can lead to hemodynamic instability. Talking about assessment findings, chest pain, chest pain, chest pain, along with all the different descriptors that a patient may provide for that chest pain. Palpitations, because that electrical conduction system resides within that poorly perfused heart muscle. Tachycardia, the brain saying, Hey, we’re not getting enough blood to the heart, let’s increase the heart rate. And of course, EKGs, checking for ST wave elevation depression, as well as troponin, which is that lab value, the cardiac enzyme that’s directly reflective of cardiac injury or insult. Also remembering that all of our medical interventions that we’re going to provide for a patient are directly geared at increasing blood flow to that heart: nitroglycerin, morphine, those vasodilatory agents, along with antiplatelets and anticoagulants all need to get blood flow to that heart. And patient education, which we just discussed. 

I hope that you guys found the video helpful. Be sure to check out some of our other angina related cheat sheets down below. Have a great day. Go out there and be your best selves. And as always, happy nursing.