Sunday, August 05, 2012

Guidelines at a glance---chest pain

This is part of my ongoing attempt to alleviate guideline chaos for hospitalists, one guideline at a time. Here I will attempt a nuts-and-bolts summary of the ACCF/AHA 2007guidelines with the 2011 focused update incorporated. While the guideline title references NSTEMI/unstable angina it actually covers all patients presenting with chest pain including those who “rule out” and do not have ACS at all. Patients in the latter group are often attended by hospitalists.

This post will only address questions hospitalists are likely to encounter and will therefore encompass those patients who present as “chest pain-rule out” as well as the initial medical management of those with established or suspected ACS. Decisions usually deferred to cardiologists (invasive versus noninvasive strategy, antithrombotic therapies associated with PCI and revascularization strategies) will not be covered here even though they are included in the guideline document.

First a caveat. Before you go down the path of “R/O ACS” don't forget the life threatening alternative diagnoses: aortic dissection and pulmonary embolism. So apply the ADD and Wells scores to these patients early on when clinical judgment dictates.

Again the presentation the hospitalist most often encounters is “chest pain, rule out ACS.” That is, there are no initial objective diagnostic findings of ischemia and the presentation is not classic but “could be cardiac.” The essentials of the approach to this type of patient are conveyed in figure 2. Simply stated, if cardiac biomarkers and ECGs are normal over at least 12 hours (or the ECG is nondiagnostic) and the patient stabilizes (vitals stable and the pain does not recur or is grossly atypical) then stress imaging is the next step. If it is negative the patient may be discharged for outpatient follow up.

As to the choice of noninvasive imaging modalities a stress imaging test carries a class I recommendation while a CT coronary angio carries a class IIa (considered an alternative).

What about those patients who turn out to actually have ACS (that is they have initial positive objective findings, a classic or suspicious clinical presentation or ultimately “rule in”)?

  • IV nitro if persistent ischemia, heart failure or hypertension.
  • PO beta blocker in the first 24 hours absent decompensated heart failure, low output state, increased risk for cardiogenic shock or the usual contraindications.
  • a rate limiting calcium blocker if beta blocker contraindication, lack of evidence of systolic dysfunction or other contraindication.
  • an ACEI within 24 hours if EF .4 or less, systolic over 100, absent other contraindications
  • discontinuation of any non-ASA NSAIDs.

The above points assume ASA was given in the field, the ER or at home and carry a class I recommendation. Morphine, IV beta blockers, rate limiting calcium blockers for persistent/recurrent ischemia after optimal beta blocker, nitrate and ACEI use in patients with normal LV systolic function are considered reasonable and carry a class IIa recommendation.

What about initial antithrombotic therapies for patients with ACS?

  • ASA ASAP (assuming not already given) and indefinitely. Initial dose non-enteric coated.
  • Plavix load followed by maintenance for patients intolerant of ASA.
  • PPI if history of GI bleed with any antiplatelet.

The above recommendations are class I. If an initial noninvasive strategy is chosen a plavix load and maintenance is a class I recommendation, alongside ASA and anticoagulation.  The use of plavix and other antiplatelet drugs for patients who undergo an initial invasive strategy is not covered here.

For anticoagulation enoxaparin, fondaparinux or unfractionated heparin are given class I recommendations. However a class IIa recommendation favors the first two over the latter.

Bear in mind that this down-and-dirty summary of what hospitalists might need to refer to at the point of care is an oversimplification driven by some of my biases. For something more comprehensive and nuanced read the original document.

Update August 7 2012:

Another caveat. Don't forget that the STEMI/NSTEMI distinction is artificial. The true distinction is whether or not the patient has acute coronary occlusion! ST segment elevation is a surrogate for acute coronary occlusion but, as I have blogged here and here and as Dr. Smith has pointed out many times, not always a reliable one. Consequently a simplistic adherence to traditional “STEMI criteria” risks putting some patients with acute coronary occlusion in the wrong diagnostic category and depriving them of timely reperfusion. The savvy electrocardiographer will identify these patients; the performance driven approach will likely miss them.

Put another way, some patients meeting performance criteria for NSTEMI actually have acute coronary occlusion (with subtle electrocardiographic findings thereof) and should be considered STEMI equivalents.