By Dr. Thomas Burnell and Dr. Bethany Turner
Next Lesson - Haemodynamic Shock
Core
Acute coronary syndrome is a group of conditions caused by a sudden fall in blood flow to the heart. Most often the cause is an atherosclerotic plaque in a coronary artery. Atherosclerotic plaques can partially block (occlude) coronary arteries. This may cause ischaemia (restriction of blood supply to tissue, reducing perfusion). If a plaque ruptures (splits open), a thrombus (blood clot) forms on it and can block the artery completely. This causes infarction and necrosis of myocardial tissue. Acute coronary syndrome is part of ischaemic heart disease.
Acute coronary syndromes include:
- Unstable angina
- Non-ST-Elevation Myocardial Infarction (NSTEMI)
- ST-Elevation Myocardial Infarction (STEMI)
Risk factors for acute coronary syndrome can be split into two categories:
- Modifiable risk factors include: smoking, hypertension, dyslipidaemia (abnormal blood fats such as cholesterol), diabetes, obesity, sedentary behaviour (too little physical activity).
- Non-modifiable risk factors include: male sex, advanced age, family history.
Myocardial infarctions (MI, colloquially known as a heart attack) occur when a coronary artery is suddenly blocked (occluded), either completely or partly. This causes infarction (tissue death due to lack of perfusion) of the cardiac tissue that the artery supplies.
Patients commonly present with central chest pain that may feel crushing, squeezing or tight. It may come on at rest and last longer than 15 minutes. The pain may radiate to the left arm, the neck and jaw. The sympathetic nervous system may be activated in response to the fall in cardiac output, resulting in nausea, generalised pallor (pale skin) and sweating. The patient may also be breathless (dyspnoea). Not everyone has central chest pain as the main symptom, and some infarctions are "silent" and go unnoticed.
There are two main types of myocardial infarction:
- STEMI - there is complete coronary artery occlusion causing a transmural (full-thickness) injury to a region of the myocardium. The main changes on an ECG are:
- ST elevation.
- Over time the patient may develop a pathological Q wave (an abnormal downward dip at the start of the main spike, or QRS complex) on the ECG, which often persists after recovery.
Diagram - The changes seen in the ECG of a STEMI patient over time. ST elevation is only present acutely post-MI, before disappearing. A "pathological Q wave" often develops and may remain after a STEMI
SimpleMed original by Dr. Bethany Turner
- NSTEMI - there is usually partial occlusion of a coronary artery (about a quarter of people with NSTEMI have a completely blocked artery) causing a sub-endocardial injury (partial-thickness - the inner layer of the heart wall is affected, while the outer layers are not fully involved). The main changes in an ECG are:
- ST segment depression and/or T-wave inversion. The ECG can also be normal.
Diagram - The features of an NSTEMI on an ECG
SimpleMed Original by Dr. Bethany Turner
In an MI, the dead muscle tissue does not produce an action potential (an electrical signal). The ECG therefore ‘sees through’ the infarcted area and picks up the signal from the opposite side of the heart. This signal is directed away from the electrode and so causes a pathological Q wave. A pathological Q wave therefore usually means that muscle necrosis has occurred, although other conditions that change the QRS complex can also cause one.
By the classical definition, a Q wave is pathological if it is seen in two contiguous leads (neighbouring leads that look at the same area of the heart) and meets either or both of these criteria:
- It lasts at least 40 ms (0.04 seconds), which is one small square wide on a standard ECG
- It is at least 25% (a quarter) of the height of the R wave in the same lead
Some ECG teaching resources (for example Life in the Fast Lane) also list a depth of more than 2 mm (two small squares) as a criterion.
The first drugs given for a suspected MI can be remembered by the mnemonic MONA. It is only a memory aid and does not cover all treatment (for example, oxygen is no longer given to everyone):
- Morphine - to ease the patient's pain.
- Oxygen - not given routinely. It is offered only if the oxygen saturation is below 94% (hypoxaemia, meaning low blood oxygen), aiming for a saturation of 94% to 98%. People with COPD (chronic obstructive pulmonary disease) who are at risk of a high blood carbon dioxide level aim for 88% to 92% until blood gas results are available.
- Nitrates, usually glyceryl trinitrate (GTN) given under the tongue (sublingual) or in the cheek (buccal) - to relieve pain. They cause vasodilation of veins to reduce venous return (the blood returning to the heart) and ease strain on the heart, and they increase the blood flow through the coronary arteries.
- Aspirin - anti-platelet.
Myocardial ischaemia is when the blood supply to the heart muscle does not meet its metabolic demands (its need for oxygen). The pain this causes is called angina. The usual cause is a narrowing of the lumen of the coronary arteries, typically by atherosclerosis. The plaque is much more stable than in a STEMI or NSTEMI. The narrowing reduces blood flow to the myocardium. There are two main forms of myocardial ischaemia:
- Stable angina - myocardial ischaemia only occurs when the metabolic demands of the heart are increased e.g. during exercise. The pain is relieved by rest when the metabolic demand of the heart reduces again. Symptoms and signs include:
- Dull, central chest pain on exertion that is relieved by rest.
- Pain may radiate to the shoulder, jaw or left arm.
- The resting ECG can be normal. During an attack (for example on exercise), an ECG may show ST depression in the leads corresponding to the affected area of the heart, due to the ischaemia of the heart muscle.
- Unstable angina - angina that is new, or suddenly worse than before, and that often occurs at rest or on minimal exertion. The pain is usually more intense and lasts longer than in stable angina.
- The patient has dull, central pain that often occurs at rest or on minimal exertion, and the pain is getting worse.
- An ECG may show ST depression and/or T wave inversion in the leads corresponding to the affected area of myocardium, but it can also be normal.
- Unstable angina is different to NSTEMI as there is no necrosis of myocardium, therefore the troponin is not raised, as the heart muscle tissue is intact.
Angina can be brought on by a number of causes which all result in an increased workload (and so metabolic demand) of the heart:
- Exercise - increased heart rate to meet metabolic demand.
- Stress, emotion and cold weather - all stimulate the sympathetic nervous system which leads to an increased heart rate.
- Eating - eating leads to vasodilation in the arteries to the gastrointestinal tract to aid digestion. This can lower blood pressure, which activates baroreceptors (pressure sensors in the walls of blood vessels), leading to an increased heart rate to restore blood pressure. The extra work raises the oxygen demand of the heart. The exact cause of angina after meals is still debated.
GTN can be given to relieve stable angina and may also help relieve chest pain in unstable angina, although it does not treat the underlying plaque instability. GTN causes vasodilation of veins, reducing venous return (the blood returning to the heart) and therefore the workload of the heart. It can lower blood pressure, so it is not given to patients with hypotension (low blood pressure). Relief of pain by GTN does not show whether the pain is cardiac, so it must not be used to make a diagnosis.
Investigations into Acute Coronary Syndromes
The type of acute coronary syndrome a patient presents with (unstable angina, NSTEMI or STEMI) needs to be determined in order to treat the patient appropriately.
To differentiate between myocardial ischaemia and infarction, a troponin assay can be carried out. When myocytes die in infarction, they release troponin I and troponin T into the blood stream which can be detected using a blood test. Troponin can usually be detected within a few hours of an MI and can remain elevated for over two weeks. Troponin will not be present in the blood in patients with unstable angina as there is no myocyte death in this condition, only ischaemia.
To differentiate between a STEMI and NSTEMI, an ECG can be done. As explained above, the main difference between the two on an ECG is that a STEMI has ST elevation. An NSTEMI does not, and may show ST depression, T wave inversion, or both. The ECG can also be normal, so a normal ECG does not rule out an acute coronary syndrome.
An invasive coronary angiogram can be done to identify the affected coronary artery and see if it has been occluded or not. Dye is injected through a thin tube (catheter) so that the arteries show up on X-ray. A stent (a small tube that holds the artery open) can be placed during the same procedure, which is called percutaneous coronary intervention (PCI). In a STEMI that presents within 12 hours of the start of symptoms, angiography followed by PCI is the preferred way to reopen the artery if PCI can be delivered within 120 minutes of the time when fibrinolysis (clot-dissolving drugs) could have been given. In NSTEMI or unstable angina, angiography is offered at once if the patient is unstable, and considered within 72 hours if their risk score is intermediate or higher.
Other investigations can be done to assess the patient’s condition:
- Chest X-Ray - is there any pulmonary oedema?
- Urea and electrolytes - to assess kidney function, which affects the choice and dose of some drugs. Cardiogenic shock (the heart cannot pump enough blood to supply the organs) is recognised by examining the patient, not by this test alone.
- Bedside cardiac monitoring (continuous ECG monitoring) - to help spot if the patient goes into ventricular tachycardia (a dangerously fast rhythm starting in the ventricles, the lower chambers of the heart) or ventricular fibrillation (a chaotic rhythm in which the heart cannot pump blood).
- Echocardiogram (an ultrasound scan of the heart) - shows whether the heart has been damaged, for example areas of muscle that no longer move normally, and detects valve damage. It will also detect left ventricular impairment (weak pumping of the main pumping chamber), which may lead to heart failure.
A patient can experience chest pain for multiple reasons. If the chest pain is cardiac, generally the pain will be dull, poorly localised and worse on exertion. If the chest pain is pleuritic (related to the pleura of the lungs), generally the pain will be sharp, well localised and worse on inspiration.
Some causes of chest pain include (categorised into systems):
- Cardiac:
- Myocardial infarction - STEMI, NSTEMI.
- Myocardial ischaemia - stable or unstable angina.
- Pericarditis - inflammation of the pericardium often due to a viral illness. It causes retrosternal, sharp and localised chest pain, and a pericardial rub may be heard on auscultation of the chest. Saddle-shaped ST elevations may be present on an ECG.
- Aortic dissection - when the inner wall of the aorta tears. It causes sudden, severe chest pain that may radiate from the front to the back, and can be associated with collapse.
- Respiratory:
- Pneumonia - infection and inflammation can irritate the pleura.
- Pleurisy - inflamed pleural layers rub against each other causing pain.
- Pulmonary embolism - blockage of an artery in the lungs (the pulmonary circulation), usually by a blood clot. It causes sudden breathlessness and chest pain that is often sharp and worse on breathing in.
- Musculoskeletal:
- Rib fracture - pain worse on inspiration.
- Costochondritis - inflammation of the costal cartilage (the cartilage joining the ribs to the breastbone). Pain is localised and is worse when the area is pressed.
- Upper gastrointestinal:
- Acid reflux.
- Peptic ulcer disease.
Edited by: Dr. Ben Appleby
Reviewed by: Dr. Marcus Judge
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