Acute coronary syndrome: Clinical sciences

Acute coronary syndrome, or ACS, is one of the can’t-miss-diagnoses that must be ruled out when a patient presents with acute chest pain. ACS is caused by sudden decreased coronary blood flow, also known as cardiac ischemia. The three types are ST-elevation myocardial infarction or STEMI, non-ST-elevation myocardial infarction or NSTEMI, and unstable angina, where the latter two are collectively referred to as non-ST-elevation or NSTE-ACS. STEMI results from complete acute blockage of a coronary artery, leading to transmural infarct of the myocardial wall supplied by that artery. NSTEMI results from a supply and demand mismatch, leading to non-transmural subendocardial infarct. Lastly, unstable angina also results from a supply and demand mismatch, leading to myocardial ischemia, but hasn’t yet caused infarction.

The first step in approaching a patient with chest pain is to do an initial assessment with a focused history and physical examination, or H&P, along with a 12-lead ECG. Prompt ECG should be obtained within 10 minutes of hospital arrival and shouldn’t be delayed by H&P. When chest pain is due to cardiac ischemia, it usually worsens with exertion, is not relieved with rest, and doesn’t change with body positioning. Some patients may complain of chest discomfort, pressure, tightness, or burning-like sensation, as well as palpitations, dyspnea, diaphoresis, nausea and vomiting, dizziness, and syncope. Ischemic chest pain often radiates to other parts of the body, including the epigastrium, left shoulder and arm, neck, and lower jaw. Relevant medical history in patients with chest pain includes hypertension, dyslipidemia, diabetes, tobacco use, and a family history of myocardial infarctions.

Physical examination findings in patients with ACS can be variable, since proximal blockages in large vessels result in more myocardial damage than distal blockages in smaller branches. If a large myocardial area is affected, it can lead to decreased cardiac output. As a result, physical examination may show signs of cardiogenic shock, such as hypotension, tachycardia, diaphoresis, cool extremities, and pale skin. In addition, some patients may have evidence of acute heart failure, which is characterized by jugular venous distension, crackles on lung auscultation, new S3 gallop, new or worsening murmur, orthopnea and edema.

If there’s suspicion of ACS based on H&P, markers of myocardial injury like troponin should be obtained.

Some high yield facts to keep in mind! If a patient has a history of stable angina, changes in their presentation that may suggest ACS include chest pain at rest for more than 20 minutes at a time, new onset chest pain that greatly limits their physical activity, or a change from their baseline angina in terms of frequency, duration, or onset of chest pain with less exertion. Also, some patients, particularly both cis and trans females, older patients, and those with diabetes may present with dyspnea rather than chest pain.

While performing the initial assessment, establish IV access and attach cardiac and oxygen saturation monitors. Then, start MONA. M is for morphine, which is administered IV to manage pain. O stands for oxygen supplementation, which might be needed to maintain the patient’s O2 saturation above 90%. N is for nitrates, which can be administered sublingually or less commonly IV for vasodilation to improve blood flow to the myocardium. Lastly, A is for high-dose aspirin, which is 325 mg, and it’s given for its antiplatelet properties to prevent complete thrombosis. In addition to MONA, also give a high-intensity statin like high-dose atorvastatin to stabilize the plaque. Finally, give a beta blocker like metoprolol to decrease myocardial oxygen demand and decrease mortality.

Okay, now that you’ve done the initial assessments and acute management, it’s time to check the ECG results for STEMI. If ST segment elevation is seen in two contiguous leads, it confirms the diagnosis of STEMI. However, a left bundle branch block or LBBB can mask ST elevation, so the diagnosis can also be made if there’s a new LBBB with a presentation consistent with ACS. LBBB typically present as QRS longer than 120 ms, a dominant S wave in V1, broad notched R waves, and absent Q waves in the lateral leads like V6.

Once a STEMI diagnosis is made, get a cardiology consultation to help guide management steps. The primary goal of treatment should be to quickly reperfuse the ischemic tissue to limit myocardial necrosis. But first, additional medical therapy needs to be given as long as it does not delay starting reperfusion therapy. All patients should receive dual antiplatelet therapy or DAPT, which includes adding an oral antiplatelet medication on top of the aspirin they have already received. Similarly, they should also receive an anticoagulant to reduce the risk of thrombosis-related ischemic events.

Now, let’s look at the options for reperfusion therapy.