Now that we talked all about the pathophysiology of ACS, let’s get into some basics of diagnosis (NOTE: I’m a clinical pharmacist therefore am by no means qualified to diagnose patients, but I do think a basic understanding of diagnoses is integral to understand the full picture…afterall how can I be recommending meds to treat my patients if I don’t even really know what’s going on with them?!).
Presentation
With the rupture of that lipid core, you better believe that most of your patients will be experiencing chest pain or angina. And unlike stable angina, this pain will not resolve upon rest because of that pesky little thrombus now completely or partially occluding blood flow.
It important to investigate what kind of chest pain your patient is presenting with. Remember, not all pain is equal (remember your PQRSTs of pain). The classic symptom is a heavy painful pressure that is constant – the classic “elephant sitting on my chest”.
But if the pain is changed during inspiration or expiration (with breathing) or is triggered by palpation, then you might want to investigate something else – like a trauma or something musculoskeletal.
ACS pain tends to be a substernal pressure that can also feel like indigestion and can also be radiating – specifically commonly seen to the left arm, up the neck, and to the jaw.
Common accompanying symptoms including diaphoresis (sweating), nausea and/or vomiting, and shortness of breath.
Side note: women are the most likely to present with atypical chest pain. They may present with extreme fatigue, symptoms of indigestion, fainting, pain in the lower abdomen, etc. Because of this, they are more likely to “shrug” of their symptoms and studies have actually shown that women wait much longer to call emergency services as compared to men.
Diagnosis
You need two main things to diagnosis an ACS event.
- Electrocardiogram (EKG) a lot of people in America will represent this ECG but I personally hate it and think it looks too much like EEG and it’s my blog, my rules so 🤷♀️
2. Cardiac Biomarkers
The EKG
Just some basics for the purposes of this discussion. An EKG is a test that measures the electrical activity of your heart. It’s noninvasive and involves the placement of electrodes placed on the skin.
Your heart is made up of a bunch of different types of cells but the two major cell types are the cardiomyocytes (muscle cells) and the cardiac pacemaker cells.
Believe it or not, your heart uses electricity to function. Pacemaker cells are actually super interesting. These specialized cells actually create rhythmic impulses of electricity that will then proceed down your cardiac conduction system to cause the heart to contract. They have natural automaticity, which means they can generate their own action potentials.
These pacemaker cells are found primarily in the sinoatrial (or SA node). The SA node is the collective term for a group of cells in the wall of the right atrium, near the entrance of the SVC.
Once they trigger an action potential, this electrical current is sent from the SA node to the Atrioventricular node (AV node) which, as the name suggests, is located within the base of the right atrium.
Another cool tidbit: your intrinsic rate at which your SA node fires is closer to 100 times per minute. But if you remember from our basic hemodynamics talk, 100 bpm is more at the upper end of the normal heart rate in humans.
This is where stimulation from the parasympathetic and sympathetic nervous system comes in. The native rate is constantly modified by input from these two systems to either speed up (sympathetic) or slow down (parasympathetic) your cardiac rate so that, at the end of the day, the average rate in adult humans is ~70 bpms.
Our body is incredibly resilient and natural has some “backup” systems or redunctancy in case our primary ones fail. In the case that the SA node fails or does not function properly, the AV node will take over the pacemaker responsibility as a secondary pacemaker. It’s not ideal, and will only fire about 40-60 bpms, but it will be enough to keep you alive until you can get some help from modern-day technology. (Note: the Purkinje fibers can also do this IF the AV node fails but at an even lower rate – more like 30-40 bpm.)
From the SA -> AV node the impulse next travels down to the bundle of His (consisting of left and right branches) and then down to the Purkinje fibers.
As the electrical impulse moves through each area of the conduction system of the heart, it will trigger depolarization and contraction of the cardiac myocytes.
Now, your AV node actually purposefully delays the conduction signal from the SA node – this is actually good – to ensure that the atria are empty of blood prior to the ventricles contracting.
By the way, this whole electrical business is the whole reason that being shocked at even a fairly low current of AC electricity can kill you. By disrupting these signals from the natural pacemaker of the heart, it can mess up the contraction process and lead to inappropriate or weak contractions causing little or no blood to leave the heart. No blood to the body, no life.
Luckily for us, some people way smarter than me figured out a long time that you can record this electrical activity to assess if the heart is functioning properly. Enter the EKG.
In a normal EKG, there is the P wave, the QRS wave, and the T wave.
In school, I memorized that the P wave showed atrial depolarization (contraction), the QRS wave showed ventricular depolarization (also atrial relaxation, but the electrical signal of the ventricles far outweighs the signal seen from the atria) and the T wave showed ventricular repolarization (relaxation).
What I didn’t really fully appreciate at the time, was that through these waves, the EKG also showed real-time tracking of the electrical signal traveling through each of these nodes.
The other thing I didn’t appreciate is that based on which leads in the EKG there are changes in, you can roughly pinpoint where in the heart issues are occuring.
When interpreting EKGs during an ACS event, special attention needs to be given to the S to T (ST) segment. Remember that this section of the EKG tells us about the function of ventricular contraction to relaxation. When enough blood coronary blood flow is blocked to the myocardium, the damage and necrosis (death) becomes transmural (in other words, involves the whole thickness of the myocardium). This is represented on the EKG as an ST elevation. And it looks exactly how you might think:
STEMIs (ST segment elevation myocardial infarctions) are bad. They are the worst and most severe of our heart attacks/ACS events and can represent full occlusion of the coronary artery.
Your patient may have some other EKG changes (i.e. ST segment depression, T-wave inversion, some Q wave changes) but if that ST segment is not elevated, they do not have a STEMI.
Cardiac Biomarkers
If you’re still with me here, now let’s talk about cardiac biomarkers.
Cardiac biomarkers are substances released into the blood when your heart is either damaged or stressed.
On a practical level, the one I see used the most often is troponin, though there are other cardiac biomarkers that can be used (i.e. creatine kinase (CK), creatine kinase myocardial band (CK-M), etc.).
Troponins are a group of proteins found in both skeletal and cardiac muscle fibers that regulate contraction.
Normally, when our heart is happy and healthy, troponin is only present in very small to undetectable quantities in our blood. However, when there is damage to the cardiac myocytes, troponin is released into the bloodstream.
The more damage to the heart, the more troponin released, the higher the troponin levels.
When your patient comes in with signs and symptoms of an MI (myocardial infarction), you better run a cardiac-specific troponin test.
Heads up: there are different types of troponin tests just like there are different types of troponin proteins. You got troponin C, troponin T, and troponin I. Their place in contraction are each different. Also, the forms of troponin C between cardiac (heart-specific) and skeletal (the muscle you have in a lot of other places) aren’t that different, so we tend to use troponin I and T tests instead.
One problem that you might run into with troponin (and other cardiac biomarker tests) is that they don’t rise in the blood *snaps* instantly. They take time to elevate in the blood (generally between 2-4 hours)
Because of this, it is very possible that you can have a patient with a STEMI present to the ED quickly and with low or undetectable troponin levels. Because of this, it’s super important to keep the patient for a while and trend their troponin levels to ensure they are not rising.
Thanks to recent advancements, many labs now offer high-sensitivity troponin testing which can detect positive levels sooner.
The other thing to know about troponin levels is that they may not normalize for days, sometimes for up to 10-14 days.
Putting it all Together
Now that you have officially sat through both my rants on EKGs and cardiac biomarker testing (pat yourself on the back for that), we can finally classify our three types of ACS events.
- ST segment elevation acute coronary syndrome / ST segment elevation myocardial infarction (STE-ACS / STEMI)
- Non-ST segment elevation myocardial infarction (NSTEMI)
- Unstable Angina (UA)
Because both NSTEMIs and UAs don’t involve any ST segment elevation, they are collectively known as Non-ST segment elevation acute coronary syndromes (NSTE-ACS).
The difference between them is that only STEMIs have ST segment elevations on the EKG (duh). STEMIs will also present with +troponins in bloodwork.
The thing that separates NSTEMIs from UA is the presence or absence of troponins in the blood. If you have +troponins, you have an NSTEMI. If your troponins are negative, you have UA.
That’s enough for today. Stay tuned for part 3 where we will talk about initial ED treatment as well as reperfusion strategies. Until then –
CARDS RX (explained) 