Chest Pain – 1

CHEST PAIN  —  “It’s not my heart, is it?”  Start right off by ruling out myocardial infarction (MI) or ischemia (angina), i.e. coronary artery disease (CAD).  Not because it’s likely, but because it’s the unspoken “chief complaint.”  It’s all the patient cares about [& often all we care about too].

Clinically, the difference between Angina and an acute MI is whether the pain has been present and ongoing the last few days or not.

  • Chest pain in the exam room, or daily for the last week?  Could be an acute MI.
  • Transient chest pain a few days (weeks, months) ago?  May be angina, stable or unstable.
  • Persistent chest pain a month ago, 1-2 weeks’ duration?  Perhaps an old MI.
  • Ongoing daily chest pain the last 1-2 months?  Won’t have a thing to do with the heart.

As soon as the patient utters “chest pain,” I launch 3 sets of questions: 1) Symptom descriptors; 2) Associated symptoms; and 3) CAD risk factors.  I do this in order, right off the bat, every time.  It’s quick & easy, & reassures the patient that you’re serious.

1.  Symptom Descriptors of ischemic chest pain:

  • Heavy, dull, achy, squeezing, pressure-like, or something similar.  NOT sharp or stabbing.
  • NEVER “pleuritic,” i.e. hurts with each breath, cough, or movement of torso.
  • Location is usually sub-sternal or left chest, maybe only in, or radiate to, left shoulder, jaw, or upper arm, and even occasionally the right chest or epigastrium.  DON’T WORRY about numbness in the left arm, or pain below the elbow.
  • Duration 1-5 minutes.  Of course, a frank MI can last longer.  But a history of recurrent chest pains lasting 30-60 minutes won’t be ischemic.  Nor will pains that last seconds.

Actually, I once saw angina of 40 seconds duration.  A patient was hooked up to the machine, symptoms gone, the EKG normal, when he piped up, “Here it comes again.”  A repeat tracing showed classical diagnostic changes, & normalized in 40 seconds as the pain vanished.

Be aware that people are notoriously inaccurate at estimating time.  Three minutes of angina might feel like 30.  Conversely, if a patient seems melodramatic or histrionic, and says it lasted “5 minutes,” I might venture, “Let’s pretend the pain starts…Now!”  I clutch my chest, wait out 15 seconds of silence, then ask, “Is it still going on?”  I’ve had patients cut me off after 5 seconds, “Oh no, not that long.”

  • Exacerbated by exertion.  Classically-described chest pain occurring predictably at a given level of exertion (e.g. one flight, two blocks, three minutes of sex, etc.) is a give-away for angina.  But especially in the context of acute MI or unstable angina, maybe plaque disruption occurred when it wanted to, i.e. during rest & not exertion.

Still, pain of an acute MI occurring at rest should increase walking down a corridor.  A consistent history of recurrent pain worse after eating or lying in bed won’t be cardiac.  Today’s “severe pain” that didn’t exacerbate walking to the office probably isn’t either.

2.  Associated Symptoms:  I inquire about these rapid-fire, one after the other, so as not to forget:  “At the same time you have chest pain, do you also have…?”

  • Shortness of breath
  • Nausea or vomiting
  • Diaphoresis (“do cold, wet, drops of sweat break out on your forehead?”)
  • Lightheadedness or dizziness

The more of these symptoms that come and go together with the chest pain, the more I worry about angina.  These symptoms are also called “angina equivalents.”  We’ll discuss that more when we touch on the differentials of dyspnea, nausea, etc.

3.  Risk Factors for Coronary Artery Disease:  Concern yourself with Framingham hard risks:

  • Age: Men >40; Post-menopausal Women
  • Tobacco (any cigarettes in past month; regular smoking in past 1-2 years)
  • Hypertension
  • Diabetes
  • Hyperlipidemia

Other equally-hard risks include:

  • Strong Family History of CAD: within a few years of patient’s current age.  For women, a maternal family history of MI or CAD is particularly ominous.
  • Same-day cocaine or amphetamine use.
  • History of typical anginal exertional chest pain, even if that’s not the pain your patient is seeking care for today.

Don’t worry about soft risks such as obesity or sedentary life-style.

Physical Examination — not much of anything will help.  Check vital signs for hypertension.  Seek evidence for heart failure, such as jugular venous distention, bibasilar rales, S3 or S4 gallops, or pedal edema.  Auscultation won’t help unless there’s A. Fib, or an apical murmur of papillary muscle dysfunction [which I’ve never heard, & those patients are real ill].  Angina is a diagnosis made by history, but it’d be embarrassing not to do any exam.

There’s no magic formula to combine all this.  I’ve worked-up about patients with classic symptom complex but no risk factors, & conversely, also patients with vague non-descript symptoms but many risk factors.

What’s the work-up?

If the patient has suggestive symptoms right in the exam room, call 911 for transport to an ED.  If able, get an EKG on-site while waiting.  Administer oxygen, aspirin 325 mg, and maybe metoprolol if pulse & B/P aren’t low & there’s no recent asthma.

Do the same for patients with possible unstable ischemia.  Unstable means:

  • New onset of ischemic symptoms occurring with minimal exertion.
  • Accelerating symptoms with progressively less exertion within the last 48 hours (“crescendo angina,” particularly dangerous).
  • Symptoms at rest.
  • Symptoms recurring within 2 days of an M.I.  Ideally this patient would already be hospitalized, but you might get a compatible history of recent heavy chest pain, which resolved, but pain at rest has recurred.
  • First-ever episode of probable angina occurring that day.  The pain may well be gone, & the patient may look as healthy as anyone, but “first-ever” angina is by definition unstable.  Of course, most patients wait it out & present on another day, when stability has declared itself.

If symptoms and risk factors sound like angina, but aren’t present at the moment and don’t sound unstable, obtain an EKG.  It’ll probably be normal, or unchanged from prior tracings.  An abnormal EKG won’t make the diagnosis, but is essential to guide the work-up (see below).

And what if you’re convinced there’s no chance of coronary artery disease, such as in a young patient without risk factors, whose history doesn’t sound a bit like angina?  We sometimes obtain a “therapeutic EKG,” to be able to reassure, “it’s normal.”  That may be dishonest; after all, an EKG can be stone normal in the midst of a full-blown MI.  Though it’s equally phony to just auscultate & simply beam, “Your heart sounds perfect.”  Sure, many people will be reassured by a straight-forward explanation, but some are so nervous as to never sleep well without a “test”.

No matter what, NEVER EVER order cardiac enzymes in an out-of-hospital setting.  Imagine yourself under cross-examination on a witness stand, “And why did you order serum troponins?”  “To R/O MI” [duh].  And if you even had the least concern for MI, and didn’t call 911…!

For the patient currently asymptomatic, who generates enough suspicion for CAD as to warrant stress testing, there are various options:

  • If the baseline EKG is normal, order a basic exercise treadmill test (ETT).
  • If there are baseline S-T segment or T-wave abnormalities, exercise tracings won’t help.  You need to look at the myocardium real time.

Order a stress echocardiogram to see if focal areas don’t contract during exercise, i.e. wall motion abnormalities.  Or order an ETT with radionuclide scan (e.g. thallium) to see if any part of the myocardium lacks uptake (perfusion deficit).

For both tests, you need to compare the abnormality with a repeat study at rest.  If the deficit is identical, it diagnoses an old infarction, not current treatable ischemia.  If the exercise study is abnormal, but findings normalize at rest (termed “reversible”), that’s ischemia, potentially treatable by medicine, angioplasty, or bypass.

  • If the patient can’t exercise (e.g. bum knee, too frail, etc.), order a pharmacologic stress test using dobutamine, dipyridamole (Persantine), adenosine, etc.  These rev up the heart for the echo or the radionuclide scan.  Jargon: “dobutamine echo” “P-MIBI” (Persantine-SestaMIBI), etc.
  • Baseline left bundle branch block necessitates a pharmacologic stress radionuclide scan.

All of these tests have imperfect specificities and sensitivities.  If the stress test is positive, refer to cardiology.  If negative, but your suspicion for CAD is high, send the patient to cardiology anyway, for a possible cath.  Institute maximal medical therapy while consultation pending (aspirin, high dose statin for target LDL <70 mg/dL, maybe a beta-blocker).

Next postings cover other causes; see Chest Pain – 2 (“pleuritic” pain, in particular, lung conditions) and Chest Pain – 3 (non-pleuritic).

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