Evaluation of Chest Pain with Dr. Prashanth Thakker

1. Initial Evaluation: How do you define Angina?
   1. What does it mean to say “Typical Angina” vs. “Atypical Angina”? What do these terms mean to you when evaluating a patient?

So the terminology has changed. The updated chest pain guidelines recommend using the terminology of “cardiac” and “non-cardiac” chest pain. “cardiac chest pain” or “angina”, is the pain associated with cardiac ischemia. But, when you approach a patient with chest pain, I think the initial thing you want to do as a student or resident is to recognize if the cause of the chest pain is life threatening. There are certain characteristics of chest pain that are more consistent with those life-threatening causes. For example, “tearing” chest pain radiating to the back should make you think of an aortic dissection, or substernal chest “pressure” that typically comes on with exertion but is now occurring at rest, might be more consistent with an MI. Once you have ruled out an emergent problem, you can start to consider a differential diagnosis for chest pain where common causes typically have an associated symptom profile. I think determining the quality of the pain is very helpful in sorting out the underlying cause. For “cardiac chest pain”, this typically presents as a “pressure” that usually comes on for minutes at a time, is made worse with exertion, and is relieved by rest or nitroglycerin. Cardiac chest pain can classically radiate to the arm or jaw, and can be associated with nausea, vomiting, and diaphoresis. Although, when patients do not present with these classic symptoms, this does not mean you can necessarily rule out cardiac chest pain. You always need to consider cardiac risk factors and understand that certain demographics can have a different quality of chest pain that is caused by cardiac ischemia. Something that can be very helpful is understanding a patient’s clinical history. If a patient has had a cardiac event before, you will want to ask them if their current chest pain is similar to when they had a prior event. If it is, that should definitely raise your suspicion for cardiac chest pain. Ultimately, taking a thorough history and physical is critically important to help determine the underlying source of a patients pain and what the next best step may be.  

• What questions do you typically ask patients presenting with chest pain to help differentiate the etiology of their symptoms?

Firstly, I would say that a detailed history and physical should be largely guided by your clinical suspicion. So, my line of questioning might change as I am trying to “rule in” or “rule out” certain diagnoses based on the information I am receiving from the patient and what objective evidence I have. However, there a few questions I will ask most patients with chest pain.

The first thing I ask patients is when did it start? Obviously, if a patient says they have been having this pain for 20 years then that might change your perspective of on how you approach that patient. Then I will typically ask the patient to describe their symptoms. Listening to the patient answer this question is very important, and occasionally requires additional prompting to help with their description. Are they describing having “an elephant on my chest”? Do they have chest tightness? Squeezing? Sharp pain? When does it usually happen? What brings it on? How long does it last? What makes it better? What makes it worse? Are there any other symptoms they have when the chest pain comes on? If the patient has been having these symptoms for a while, why are they just now coming in? Using the OPQRST model of questioning here can be very helpful, but this is a skill that requires experience and practice just like any other.

• Do you have a mental model of how you approach integrating the recent history and potential atherosclerotic risk factors?

So in addition to obtaining a detailed history regarding the nature of a patient’s chest pain, it’s also important to understand this patient within the context of their medical history. Obviously, there are traditional coronary artery disease risk factors that you will want to know as these may raise your suspicion for cardiac chest pain. For example, Diabetes, Obesity, Hypertension, and Hyperlipidemia can all increase one’s risk of coronary artery disease. It is also very important to take a good social and family history. We know that smoking is also a modifiable risk factor for CAD, and that cocaine use has been associated with coronary vasospasm, which can cause chest pain. But what I find to be increasingly important is to take a good family history of cardiac events, because we are finding that the genetic and epigenetic factors of coronary disease are increasingly important. Adding some of these traditionally associated factors to the patient’s subjective history can really help raise or lower my clinical suspicion.

It is also important to know that there are certain population that are more prone to premature coronary artery disease than others, so you know when to deviate from these common illness scripts. For example, I recently took care of a 34 year old male of Southeast Asian decent without some of these traditional risk factors who had borderline ST elevations on his EKG. As he didn’t fit the classic picture, his care was unfortunately delayed because the primary team was trying to find alternative causes of his pain. When the patient finally made it to the cath lab, he was found to have critical coronary disease and needed stents placed. Some other patient populations that come to mind are patients with HIV, chronic inflammatory conditions, connective tissue disorders or congenital heart disease. Examples such as these are great reminders not to anchor or mentally shut off diagnosis when you are thinking of integrating potential atherosclerotic risk factors in patients with chest pain.

• When evaluating patients with chest pain in general, are there any “can’t miss” diagnoses that should always be considered? What is a good way to ensure one does not miss these diagnoses?

The first thing that comes to mind is an aortic dissection, like I briefly mentioned earlier. One simple thing that a house officer or student can do for every patient to presents with chest pain and hypertension is to obtain a bilateral blood pressure. This simple step can help you determine if you need urgent imaging or can help you rule out this diagnosis. Another important MI mimicker is a pulmonary embolism. Sometimes an EKG can show an inferior MI pattern, but the patient could be having a PE rather than a true MI. Looking for hypoxia and being mindful of other PE associated symptoms can help you determine when working up a PE may be necessary. Furthermore, there a few rarer MI mimickers such as coronary vasopasm or spontaneous coronary dissection that can be very severe and present as a classical MI. Other things to consider would be myocarditis/pericarditis, or an esophageal pathology such as an esophageal rupture. I often try to think of the different anatomical structures in the chest cavity and run through potential life-threatening causes, which may inform my questioning and diagnostics. However, I think the most important thing you can do is to keep an open mind and not anchor on certain diagnosis when evaluating patients.

• Taking a step back: Let’s say you have just been called by the ED to evaluate a patient with chest pain. Can you walk us through how you would chart review this patient to help inform the way you think about them? (prior ischemic evaluations, medications, co-morbities, etc)

So when I am opening the medical record to evaluate a patient, there a few things I think are important. Firstly, I think the vitals are vital. I want to make sure the patient has some degree of hemodynamic stability to help me triage my thinking and determine if I need to expedite my workflow. The next thing I typically do is look through the clinical history to look for those traditional risk factors that I mentioned earlier. Then I will see if the patient has known coronary disease and try to define it. Have they been admitted for chest pain before? What happened that time? Did they get any invasive or non-invasive testing that tells me about their coronary anatomy? The next thing I will do is look through the medications. Is this patient on any medications for heart disease? Are they prescribed nitroglycerin or other coronary vasodilators? This may help you determine if this is a new or ongoing problem for the patient. Once I have looked through that, I will look over the labs and imaging tests if they have been obtained thus far. Is there anything concerning on these tests? These are the questions I am asking myself as I look through the chart.

Something I think is important to recognize, is that using the EMR in this way is like working in reverse because we start to form ideas before we actually see the patient. The problem with this is that it can make it harder to truly find out what is going on with the patient because we have a preformed notion from our chart reviewing, or from what we were told by the triage or ED physicians. So I would just use this as another reminder to stay away from anchoring and to try and use your chart reviewing as a way to connect the dots with the data you are gathering from the patient.

After I am done reviewing, I will go see the patient. The first thing I am trying to determine is if the patient is stable or not? Is the patient relaxing in bed with the cell phone or are they holding their chest and short of breath when talking to you? This is critically important in determining the acuity of management and will help guide which questions you ask as we discussed earlier. In terms of the physical exam, it’s very important. I want to know if the patient is warm and well perfused, or are they showing signs of shock? Does this patient have a murmur? Aortic stenosis, for example, can sometimes look like an MI and is something you can pick up on exam. Does the patient have pain when I press on their chest? That would make me think of a musculoskeletal pathology. So you can see a physical exam is still an important piece of the puzzle.

• Defining terms: What exactly are “Acute Coronary Syndromes?”
  • When can you say a patient is having an “Acute Coronary Syndrome?” What does the term ACS encompass?

When I think of acute coronary syndrome, I think of someone who is having an unstable coronary event. The different components of the ACS Spectrum would be Unstable Angina, NSTEMI, and STEMI. What these terms basically represent is a range of processes that can cause poor perfusion to the myocardium in a certain coronary artery territory. You may or may not see EKG changes or biomarker elevation (Troponins) which can help you determine the what process is going on and is how we decide which term to use. There are patients who have intermittent exertional chest pain with the appropriate risk factors that we say have “unstable angina” if they don’t have EKG or troponin changes. Although, ACS really focuses more on NSTEMI and STEMI and obviously the EKG would be what delineates those two terms. I think more important than using the exact terminology, however, would be trying to determine the mechanism by which myocardial ischemia is being caused. Is a patient having troponin elevation because of an acute plaque rupture or do they have poor myocardial perfusion because they are really hypotensive from sepsis? Understanding the patient as a whole will help you determine what is happening in their coronary arteries.

• The ECG + Troponins are typically the most helpful diagnostic tests in the evaluation of chest pain– In basic terms, how do you think about these tests and what are you looking for?

Absolutely, these are essential components of a patients work up. For troponins, I think it is important to consider if they are positive and what is the trend. If the troponins are negative, then the likelihood of a true ACS event is very unlikely. If the troponins show a rise and fall, this is more of what you see in ACS. Understanding the degree of rise and troponin peak should also clue you in to the severity of an ACS event and help you determine what underlying mechanism of injury may be. The ECG is also critically important. The most important thing you can do when evaluating an EKG is to compare it to a prior one. Does this patient have dynamic changes? If the patient has ST changes, q waves, or T wave inversions, I want to know if they are new. Are these dynamic changes occurring when the patient is having symptoms? This can clue you in to if the patient is having ongoing ischemia. I think it is also important to consider the timing of these tests. Some patients may come in with a classic story and arteriosclerotic risk factors but have negative troponins. This could just be that you caught the patient early in their disease process and the troponins have not had time to become positive yet. Use your clinical suspicion when interpreting these tests and know when to repeat them. Sometimes our pre-test probability is so high for coronary ischemia based on the clinical history alone, that we may treat a patient for ACS without positive troponins or EKG changes. So, these tests are important, but not everything.

             TTE is often used in the early in the evaluation of ACS – What are you looking for?

Of course. Sometimes a team will call the cardiology service because a patient has mild ST changes and it isn’t clear if the patient is having an acute coronary event. We can use the echocardiogram to obtain different views of the left ventricle that correlate with a particular wall of the ventricle. Each wall of the left ventricle is classically supplied by certain coronary anatomy, similar to how we associate coronary territories on EKG. If we see ST changes in the anterior distribution on the EKG, and you see the anterior wall is squeezing okay on the TTE, then you feel more reassured that the patient likely isn’t having a transmural infarct (and vice versa). Other things an echo can tell you if a patient is presenting late in their course, is if they are having mechanical complications of an MI such as a papillary muscle rupture or ventricular aneurysm. You can also see if there is a large pericardial effusion if there is some concern for pericarditis as the source of chest pain. So this can be a very useful test when evaluating these patients.

Often we are trying to determine if patients are having a Type 1 or Type 2 pattern of myocardial infarction – Can you briefly explain the difference between these two ,how the diagnostic tests we mentioned earlier help you determine which is which, and why this distinction is important for us to make?

I think this is a really good question. What you are essentially trying to decide is what is actually driving the process of myocardial ischemia. A Type 1 NSTEMI is caused by an acute plaque rupture causing limited coronary flow and subsequent ischemia. A Type 2 NSTEMI is when there is limited supply of blood flow due to fixed coronary stenosis in the setting of greater myocardial demand. Often times when patients are very sick, they have an increased “demand” for myocardial blood flow that the fixed stenosis cannot accommodate. These patients can have elevated troponins, but we think and treat them differently than patients who have an acute plaque rupture. This forces you to think about the patient in context. If the patient was previously at their baseline, but starting having sudden onset chest pain with troponin elevation, I would think more of a Type 1 process. But when it is a patient who is hypotensive from sepsis or bleeding, or has significant tachycardia or hypertension, these patients should be thought about differently. That is why we refer to Type 2 NSTEMI as a “supply and demand mismatch” and can be caused by many number of causes. Sometimes, it is not clear if a patient is having Type 1 or Type 2 pattern of injury. Sometimes in those situations, we may get more testing like an echocardiogram to look for wall motion abnormality or a drop in the EF. We can also use a risk stratification tool like the GRACE or TIMI scores to help determine best next steps or how time sensitive an invasive evaluation may be.

• Initial Management:
  • What does “medical therapy” look like in the context of ACS? Does medical therapy change based on the pattern of myocardial infarction?

All patients that come in with acute coronary syndrome, whether you are worried about a STEMI or an NSTEMI, you should be thinking about using anticoagulation as long as there is no contraindication. The ACC guidelines say that you can use heparin or lovenox to accomplish this, however, we typically use heparin at our institution due to it’s rapid onset and offset of action. Furthermore, all patients with ACS should be loaded with high dose Aspirin (325mg). In regards to P2Y-12 inhibitors, it’s actually very interesting to think about. Currently there is competing data on whether loading patients up front with medicines like clopidogrel or prasugrel really provides benefit to the patient. This has caused some heterogeneity in practice and has become more institution based. If a patient is coming in a with a clear STEMI, then they should definitely be loaded with one of these medicines because we will hopefully be able to fix the culprit coronary lesion. When it comes to NSTEMI, it is a little more complicated. If there is some concern for multi-vessel coronary disease then it may be reasonable to hold off on loading this medicine because of the surgical implications. Some examples that come to mind are patients with an ST elevation in AVR, or an indication of some degree on multivessel disease on EKG, CT, or stress test. These patients likely should have their anatomy defined before we load them. Other medicines that we think of in these situations would be beta blockers and statins. Beta blockers should be used in most patients with ACS, especially if they are presenting with hypertension as they can help offset some of that myocardial demand. Statins also are used in the acute setting to help stabilize any plaques before patients can get definitive therapy.

• Are there situations where we should be hesitant to start medicines like beta blockers in the context of ACS?

Yes, I think the biggest thing I would worry about is starting a beta blocker in patients who show signs and symptoms of shock. This is why doing a thorough physical exam can be so important. One of the first things I will do when examining a patient is feel for the temperature of their hands and feet. If the patient feels cold, then I start to worry they are very peripherally “clamped down” to compensate for poor cardiac output and are not adequately perfusing their extremities. These patients may need additional medicines like inotropes to support their cardiac output and a beta blocker could make them worse. Cardiogenic shock is a real complication of an acute MI, so it something to always consider in this patient group. Some other signs and symptoms you may see associated with this would be other signs of inadequate tissue perfusion, like an elevated lactate or liver function tests. Other things to consider regarding medical management of ACS would be GI bleeding or recent strokes, as these could be contraindications to starting anticoagulation or anti-platelet agent agents.  

• In my experience, management of an NSTEMI is less straight forward as it represents a broader spectrum of patients – what information helps you decide on if we should pursue early invasive management or an ischemic-driven approach? (Risk stratification, urgent LHC vs. outpatient stress, etc.)

I think patients presenting with a true NSTEMI who are having active chest pain should have their anatomy defined. We are more aggressive in terms of defining anatomy with cardiac catheterization in these patients because we know that their risk of mortality at 30 days is higher. Risk stratification tools (GRACE, TIMI) can be helpful for this kind of patient as well to help determine higher or lower risk and decide how urgent an evaluation may be. I think there are patients, for example, that may have metastatic cancer or are very frail, that may not tolerate a procedure. Some patients have extensive peripheral vascular disease and have poor access sites for a cardiac cath. These are things that should be taken into consideration as well when deciding on the next best test. One of the ways we think about this is in terms of pre-test probability. As in, “how likely is it that this patient has critical coronary artery disease?”. If your pre-test probability is high, then you should proceed with the best test which is a cardiac cath. If your pre-test probability is moderate, then other tests such as a Coronary CTA or a stress test would be reasonable. I think when deciding on which stress test to utilize (as there are several different types), you have to think about the type and quality of data you are going to get back with each test. For example, if you are worried about concomitant valve disease, then getting a stress echo may be a better option for that patient than a nuclear stress because it will give you that structural data. But if a patient already has a known wall motion abnormality or has a known bundle branch block, this could reduce the sensitivity of a stress echo. It’s important to understand the limitations of each test as well. Additionally, a stress test will only tell you if a patient has fixed stenosis causing ischemia or not. It will not tell you if a patient has only 20-30% stenosis which may be a patient that needs to have their CAD risk factors managed more aggressively. So you have to take each patient individually and decide which test will give you the highest quality and relevant data.

• Do you have any clinical pearls for medicine residents/medical students for evaluating chest pain that we have not yet discussed?

No, I think that’s it. I think getting a really good history, not putting your blinders on, and not anchoring are really important. I would also remember to stay humble because you’re going to have presentations that are that are going to be atypical. You don’t know what you don’t know, that’s the advice I always give folks.