Acute Coronary Syndrome (ACS)


Acute Coronary Syndrome (ACS)

Medical Principles


Insufficient supply of blood to the heart, usually due to a blocked artery, causing cell and tissue death.

Goal of Care

Transport to hospital where the artery can be opened or kept open.

Myocardial Infarction (MI) is usually caused by a clot in the coronary arteries that completely blocks blood flow beyond its location.  It is triggered by a rupture of plaque in the walls of a coronary artery and is defined as death of myocardial cells due to ischemia. MI can show up in two ways. Acute, significant damage shows up on ECG with elevation of the ST segments, called an “ST-Elevation MI” or “STEMI”. When there is only small amounts of damage, the ECG can be normal but cardiac enzymes, proteins that are necessary for proper heart function and released into the blood stream when heart damage is occurring, will rise over 3-6 hrs.

Unstable Angina is temporary insufficient blood supply without permanent damage. The pain of MI and UA are similar and both require urgent care. The goal of care in myocardial infarction is to open the artery and the goal in unstable angina is to keep it from closing.

Chest pain is the most common symptom but only about 30% of patients with ACS have the classic chest heaviness with radiation to arms or jaw, shortness of breath and sweating. In fact, atypical pain (just about anything else) is more common than typical pain! Diabetics and women have “atypical” pain complaints – or minimal complaints – even more commonly.

The diagnosis requires an ECG, cardiac serum markers that signify damaged and leaking cells, and sometimes imaging (including angiograms). In some cases a firm diagnosis even with these tests is difficult.

Guiding Principles

Patients with myocardial infarction on the electrocardiogram are losing muscle with each minute of delay to definitive treatment.

Chest pain can also be the presentation of other life threatening conditions such as thoracic aortic dissection, pulmonary embolus, pericarditis, ruptured esophagus or other perforated viscus.

The treatment of choice for STEMI is angioplasty or thrombolysis. Follow the policy and guidelines for your region regarding destination decision rules for STEMI.

Patients with chest pain but not STEMI do not require emergency angioplasty. They can be taken to the closest facility for diagnosis, decision making, and initial treatment. A secondary transfer can be arranged, usually routine for both the transfer and the cath lab, if angioplasty is ultimately indicated.

Beware patients who are hypo-perfusing or are developing congestive heart failure or both. These patients are developing cardiogenic shock and require immediate urgent intervention

A 12 lead ECG should be acquired early to rule out or rule in ST-Segment Myocardial Infarction (STEMI). Early notification to activate the hospital response to receiving a STEMI has saved lives.

If IV access is required, the left arm is preferred. Keep the middle and distal third of right forearm clear to facilitate potential radial artery access for percutaneous coronary artery intervention

Oxygen should be titrated based on pulse oximetery aiming for an O2 Saturation of 95% if the patient is not SOB or in shock. Patients who are SOB or in shock require high flow O2. If there is difficulty with the probe acquisition due to patient condition, oxygen should be applied liberally. Patients with COPD, especially if on home oxygen, should have their saturation titrated to around 92-95%

ASA helps to prevent re-occlusion but will not open the artery. It has been shown to reduce mortality and is one of the most important early treatments the patient can receive.

Nitroglycerin has not been proven to improve outcomes. Nitroglycerin may relieve the pain of angina but will not relieve the pain of M.I. and may well worsen outcomes if it causes hypotension. It is absolutely contraindicated in hypo-perfusing patients with right sided infarcts on ECG as it can cause significant hypotension.

ENTONOX has been used for chest pain but has some cautions. ENTONOX can cause rebound hypoxemia due to displacement of oxygen in the alveoli as the nitrous diffuses out of the blood stream. It is vital to supplement any patient during and after nitrous use with high flow oxygen by simple face mask in order to avoid hypoxia and increasing the myocardial injury.

Patients who are stable and without acute ischemia on 12 lead ECG can be transported by a BLS crew although it must be recognized that these patients are still potentially very ill.

Back to Top