Acute coronary syndrome: Clinical sciences

Acute coronary syndrome, or ACS, is a critical diagnosis to consider in all individuals presenting with acute chest pain. It’s caused by a sudden reduction in coronary blood flow, known as cardiac ischemia. In most cases, this sudden reduction results from the rupture or erosion of an atherosclerotic plaque, which triggers thrombosis. There are three types of ACS, including ST-elevation myocardial infarction, or STEMI; non-ST-elevation myocardial infarction, or NSTEMI; and unstable angina.

Now, if your patient presents with a chief concern suggesting acute coronary syndrome, first, perform an ABCDE assessment to determine if they’re unstable or stable.

If unstable, stabilize their airway, breathing, and circulation, which might require endotracheal intubation and mechanical ventilation. Next, obtain IV access and start continuous vital sign monitoring and cardiac telemetry. Finally, ensure that a defibrillator is available, and the defibrillator pads are in place.

Okay, now that we’ve covered the approach to unstable patients, let’s return to the ABCDE assessment and focus on stable individuals.

If your patient is stable, obtain a focused history and physical examination.

Patients often describe chest pain, along with chest discomfort, pressure, or tightness, like something heavy is sitting on their chest.

Often, this feeling doesn’t stay in one place; it can radiate down the left arm, up into the neck, or even to the jaw.
When the pain is due to acute cardiac ischemia, it tends to get worse with exertion, doesn’t go away with rest, and doesn’t change with movement or position. Along with chest pain, individuals might report non-specific symptoms, such as shortness of breath, sweating, epigastric pain, or nausea.

When taking a history, be sure to look for risk factors for heart conditions, such as hypertension, diabetes mellitus, hyperlipidemia, obesity, tobacco use, and a family history of coronary artery disease.

Individuals with ACS might have a completely normal physical exam, but they can also present with dyspnea, tachycardia, and diaphoresis. Findings can also vary based on the location and extent of heart damage.

For example, the involvement of the papillary muscle can cause mitral regurgitation and a new systolic murmur.

On the flip side, extensive damage to the heart muscle can lead to heart failure and signs like jugular venous distention, hepatomegaly, lung crackles, and lower extremity edema.

At this point, you should suspect ACS, so act fast. Immediately order a 12-lead ECG and check cardiac troponin, which is a serum marker of myocardial injury. Make sure to obtain the ECG within 10 minutes of the patient’s arrival. Do not delay it for history taking or physical examination. Time is critical!

As you're doing this, begin initial management, since assessment and treatment should happen simultaneously. Start by obtaining IV access and setting up continuous vital sign monitoring with cardiac telemetry. If needed, provide supplemental oxygen to maintain saturation above 90%.

Initial management also includes several key medications. Have the patient chew a high-dose aspirin to inhibit platelet aggregation and give sublingual nitroglycerin to improve coronary blood flow and relieve chest pain. To help stabilize the plaque impairing blood flow, administer a high-intensity statin.
Finally, if there are no contraindications such as acute heart failure or heart block, give a beta-blocker to reduce myocardial oxygen demand. If the chest pain persists despite nitroglycerin, think of IV morphine for additional relief.

As soon as you receive ECG results, you need to assess the type of ACS. First, let’s focus on STEMI.

STEMI occurs due to complete, acute blockage of a coronary artery, leading to infarction. If there is elevation of the ST segment of 1 mm or greater in two or more contiguous leads, it confirms the diagnosis of STEMI.
However, a left bundle branch block can mask ST elevation, so the diagnosis can also be made if there’s a new left bundle branch block along with a presentation strongly suggestive of MI.

In this case, look for a wide QRS complex greater than 120 milliseconds, a dominant S-wave in V1, and broad, notched R-waves with absent Q-waves in the lateral leads like V5 and V6.

Cardiac troponin levels will be elevated in STEMI, but these results may not be available right away. The key point is not to wait for the troponin level before making the diagnosis. ECG findings alone are enough to diagnose STEMI.

Once you diagnose STEMI, the primary goal of treatment is to achieve rapid reperfusion and minimize myocardial damage.

However, while preparing for reperfusion, you should also initiate additional medical therapy. All individuals should receive dual antiplatelet therapy, known as DAPT, which means adding an oral P2Y12 inhibitor, such as clopidogrel or ticagrelor, to aspirin. Additionally, administer a parenteral anticoagulant to reduce the risk of further thrombosis. Administer these medications promptly, but never at the cost of delaying reperfusion therapy, which includes percutaneous coronary intervention, or PCI for short, and fibrinolytic therapy. PCI is the preferred strategy over fibrinolytic therapy for reperfusion in patients with STEMI; however, PCI cannot be used in all patients.

Then assess the time of symptom onset to presentation because is a key factor that determines which treatment can be used safely and effectively.

If it has been less than 12 hours since symptom onset, the next step is to assess if PCI is available within 120 minutes of the patient’s first medical contact, either at the patient’s current location or by transfer to a PCI-capable medical center.

If PCI is available within 120 minutes, proceed with emergent coronary angiography and PCI. During PCI, an interventional cardiologist inserts a catheter, usually through the radial or femoral artery. Using imaging guidance, they thread it up to the coronary arteries. Once the blockage is identified, they advance a balloon-tipped catheter across it, inflate the balloon to open the artery, and place a stent to keep the vessel open and restore blood flow.

If PCI is not available within 120 minutes, administer fibrinolytic therapy within 30 minutes of arrival at the hospital. Fibrinolytic therapy involves medications that dissolve blood clots, such as alteplase and streptokinase.

However, keep in mind that these medications are contraindicated in some individuals, such as those with active bleeding, recent stroke, or significant head trauma. Finally, after giving fibrinolytic therapy, arrange immediate transfer to a PCI-capable center.