Acute Coronary Syndrome (ACS) refers to a trio of diagnoses:
Non-ST elevation myocardial infarction (NSTEMI)
ST-elevation myocardial infarction (STEMI)
All three can result from a ruptured or erodedcoronaryarteryplaque. You can think of them as lying along a disease spectrum with unstable angina as a milder form of the disease and STEMI as the most severe.
Myocardialinfarction (MI) can be classified as either type 1 or type 2. Type 1 MIs are caused by plaque rupture while type 2 MI refers to myocardial infarction secondary to decreased supply (i.e. anemia, hypoxemia, hypotension) or increased demand (i.e. arrhythmias such as atrial fibrillation with rapid ventricular response).
ACS is life-threatening and must be recognised and treated in a timely manner. Remember: time is myocardium!
This guide has been created to assist students in preparing for emergencysimulation sessions as part of their training. It is not intended to be relied upon for patient care.
Clinical features of ACS
Cardiac risk factors
The list of differentials for chest pain is long. However, a focused history covering cardiac risk factors can help you to determine which patients are more likely to be suffering from ACS.
Cardiac risk factors can be categorised as non-modifiable or modifiable
Family history of ischaemic heart disease
Congenital heart disease
When a patient presents with chest pain, it is impossible to arrive at a diagnosis without further examination and investigation. A comprehensive history of the chest pain using a SOCRATES method (see our chest pain history taking guide) can help to narrow the differential diagnosis considerably. However, you will still require further investigations such as ECG and serum troponin levels to be confident of the diagnosis.
Common symptoms in ACS
Chest pain – the result of ischaemia to the cardiac muscle
Referred pain– chest pain can radiate to the epigastrium, arm, neck and jaw (referred pain occurs because the nerves that supply these non-cardiac areas originate from the same spinal segment as the nerves to the heart)
Shortness of breath
Nausea and vomiting
Syncope – the result of hypoperfusion of the brain secondary to reduced cardiac output
SilentMIs do not present with these classical symptoms. Females, the elderly and diabetics are at increased risk of suffering ACS with minimal symptoms. Often the only symptom may be shortness of breath.
You need to both requestinvestigations and reviewresults as they become available
You don’t have to memorise everything off by heart, ask for guidelines and algorithms that are relevant (i.e. ACS guidelines)
If you would like medications or fluids, these will need to be prescribed
Don’t forget to document everything you have found and done in the patient notes!
You are likely to be called to see this patient either:
On the ward or
As a new presentation to ED with chest pain
Perform a quick general inspection of the patient to get a sense of how unwell they are:
If the patient is unconscious, check for a pulse and check that the patient is breathing.
If the patient is unconscious or unresponsive and not breathing start the basic life support (BLS) algorithm as per resuscitation guidelines. Call 2222 for help! (see our BLS guide here)
Perform AVPU and assess their consciousness level
How do they look?
What is their breathing like?
Are there any clues from around the bedside? (look for drug charts, medication, IV lines, monitoring equipment etc)
Introduce yourself to the patient
If the patient is able to answer questions, ask how they are feeling
Ensure you have everything that is available to you
Drug charts including diabetes charts!
Assess the patient’s ability to speak, listen to the patient’s breathing for added sounds and inspect the mouth.
If you think your patient has a compromisedairwayyouneedhelp! Put out a crashcallimmediately as you require urgentanaestheticinput to securetheairway. You can perform some simple airway manoeuvers in the meantime.
Maintaining the airway whilst awaiting senior support
1. Perform a head tilt, chin lift manoeuvre.
2. If noisy breathing persists, try a jaw thrust.
3. If this is still not enough to open up the airway you can consider the use of an airway adjunct:
If your patient is still semi-conscious then consider using a nasopharyngeal (NP) airway.
If your patient is able to tolerate an oropharyngeal (OP, or Guedel) airway then you can use one of these. However, this indicates that your patient is seriously unwell as they no longer have a gag reflex.
Reassess after any intervention
If your patient starts to improve throughout your assessment, they may no longer be able to tolerate the OP airway and you should remove it as soon as possible to prevent gagging/aspiration.
Oxygen saturation: aim for 94-98%.
Tachypnoea is the body’s response to hypoxia and as the myocardium becomes more hypoxic the respiratory rate will rise.
Impaired consciousness may lead to a reduced respiratory rate (bradypnoea).
Auscultate both lungs:
Reduced air entry bilaterally suggests significant airway compromise and the need for critical care input.
Crackles or crepitations on auscultation may represent pulmonary oedema due to impaired cardiac function.
Palpate and percuss to assess chest expansion and resonance/dullness.
Arterial blood gas
An arterial blood gas may be useful to quantify the degree of hypoxia if your patient has very low oxygen saturations.
An ABG should not delay ACS management.
A chest x-ray is not immediately indicated if all your examination findings are normal.
If your examination findings are in keeping with pulmonary oedema you should treat accordingly and avoid delaying treatment whilst waiting for a CXR.
Administer oxygen as soon as possible if oxygen saturations are below 94%.
High-flow oxygen (15 litres) through a non-rebreathe mask.
If the patient is conscious, sit them upright.
Maintain oxygen saturations between 94-98%
If your patient is unconscious and their respiratory rate is inadequate (too slow or irregular with big pauses), you can provide assisted ventilation through a bag-valve-mask (BVM).
Ventilate at a rate of 12-15 breaths per minute (roughly one every 4 seconds)
Where indicated, treat pulmonary oedema due to heart failure with Furosemide.
If the patient is hypotensive, diuretics are contraindicated and critical care input should be sought urgently.
Reassess after any intervention.
Your patient will be may be tachycardic or bradycardic
Pain may lead to hypertension
Hypotension is a late sign and represents cardiac failure (remember type 2 MIs are caused by hypoperfusion of the cardiac tissues due to hypovolaemia).
Your patient may appear clammy/pale/grey.
Capillary refill time may be normal or sluggish due to hypovolaemia.
Take blood samples
Try if possible to collect blood samples duringcannulation
Troponin I or Troponin T: The cardiac enzymes are released from damaged cardiac cells and are a key part of diagnosing myocardial infarction.
Full Blood Count: For a haemoglobin and platelet measurement. You can also look for markers of infection.
CRP: For markers of infection/inflammation.
Urea and Electrolytes: To assess renal function
Liver Function TestsandClotting
Record an ECG
You want to get an ECG as soon as possible so you can know what you are dealing with:
STEMI: The ECG will show ST elevation or a new Left Bundle Branch Block (LBBB)
NSTEMI: T wave inversion or ST depression
Unstable angina: No specific ECG changes
Secure intravenous access
The gold standard is to insert 2 large bore cannulas for acutely unwell patients.
Patients who are having a STEMI will require emergency percutaneous coronary intervention (PCI). You must speak to the cardiology team ASAP.
ACStreatment is often remembered by the mnemonic MONA which stands for morphine, oxygen, nitrates and aspirin. We have already covered oxygen in breathing.
Morphine has a dual purpose in ACS treatment, both as a coronary artery vasodilator which results in improved cardiac tissue perfusion and as an analgaesic.
Nitrates also cause coronary artery vasodilation, which improves cardiac perfusion and therefore reduces chest pain as a secondary effect.
Glyceryl trinitrate (GTN) spray is commonly used
If the patient is hypotensive, nitrates are contraindicated due to their vasodilatory effects (see urgent critical care input)
Aspirin is an anti-platelet medication.
The underlying pathophysiology in MI is often a plaque rupture and secondary platelet aggregation, ultimately result in clot formation within the coronary vessel.
A high dose of aspirin (300mg rather than the usual daily dose of 75mg) is given to try and improve blood flow through the coronary vessels by inhibiting platelet aggregation.
Further blood thinning agents
Most people with ACS will be offered an addition form type of antithrombotic medication.
This can be Fondaparinux or alternatively Heparin if the patient is about to undergo PCI for a STEMI.
Check your medical school/hospital’s local guidelines for ACS treatment.
Administer IV fluids
Titrate your fluids to the patient’s level of haemodynamic instability
Typically NaCl 0.9% or Hartmann’s solution is used for fluid resuscitation
Be aware of the risk of pulmonary oedema if ventricular function is impaired
Reassess after any intervention
Blood glucose level
Check the patient’s blood glucose level, particularly if they are a known diabetic
What size are they?
Are they equal?
Are they reactive to light?
Assess level of consciousness – AVPU/GCS
The above Airway, Breathing and Circulation problems can all alter the patient’s neurological status because of decreased cerebral perfusion, causing the patient to be confused or drowsy.
A formal record of your patient’s consciousness level will be really useful for tracking progress and changes throughout treatment.
Reassess after any intervention
We routinely expose unwell patients to make sure that we aren’t missing anything.
Patients with ACS can develop a fever as part of the catecholamine response.
Urine output will likely need monitoring if administering fluids, to ensure an accurate fluid balance is recorded.
Re-assess after any intervention
It is essential to continually reassess ABCDE and treat issues as you encounter them. This allows continual reassessment of the response to treatment and early recognition of deterioration.
Well done! You have successfully implemented the immediate treatment for your patient. You are now waiting for your patient with a STEMI to go for PCI or you have started appropriate treatment for an NSTEMI. There are just a few more things to do…
Take a history
If possible, it is important to revisit history taking to clarify risk factors for ACS and other relevant medical information. If the patient is confused you might be able to get a collateral history from staff or family members as appropriate. Check out the history taking guides here.
Additionally, make sure to check the medications you have just prescribed and what the patient normally takes. This helps reduce prescribing errors and allows you to consider any possible drug interactions.
It is really important that you document your initial ABCDE findings, any interventions you made and the response the patient had to those interventions. Also make sure document salient points from the history.
You need to discuss the patient with the medicalteam. If your patient requires PrimaryCoronaryIntervention you will need to speak to Cardiology directly.
As a junior doctor it would be appropriate to give an SBARR handover outlining your assessment and actions, and to discuss the following:
Does the patient further treatment?
Are there any further assessments, investigations or interventions required?
Does the patient need a referral to HDU/ICU?
Should they be referred for a review by a specialist doctor?
Should any changes be made to the management of their underlying conditions?