and Alwyn Scott2
(1)
School of Computer Science, University of Manchester, Manchester, UK
(2)
Cardiology High Dependency Unit, Papworth Hospital NHS Foundation Trust, Cambridge, UK
Keywords
ACSSTEMINSTEMIAnginaST elevationST depressionMyocardial infarctionBiomarkersReciprocal changesBackground
Acute coronary syndromes are a group of conditions precipitated by a reduction or cessation of blood flow through the coronary arteries. An acute coronary syndrome (ACS) is a medical emergency requiring immediate intervention. ACS encompasses any narrowing or obstruction of the coronary arteries leading to acute symptoms. Acute coronary syndromes include:
ST elevation myocardial infarction (STEMI)
Non ST elevation myocardial infarction (NSTEMI)
Unstable angina
To better understand these syndromes it is necessary to gain an awareness of how the coronary arteries function and their anatomy. There a two principle coronary arteries, the left and right coronary arteries (Fig. 7.1). The left further subdivides into the left anterior descending and circumflex arteries that supply blood to the left side and front of the heart. The right coronary artery divides into the posterior descending and acute marginal arteries, supplying blood to the right atrium, right ventricle, SAN and AV node and some part of the left ventricle (Fig. 7.2).
Fig. 7.1
The coronary arteries
Fig. 7.2
Left and right coronary artery anatomy
The coronary arteries arise from the aorta and supply the heart muscle with blood and oxygen. The artery that supplies the posterior descending artery and one or more posterolateral branches is referred to as the dominant vessel. The right coronary artery is the dominant vessel in 80–85 % of cases, other people have a left dominant or codominant systems.
Any narrowing or blockage to these arteries can reduce or prevent blood flow reaching portions of the heart past the area of narrowing or blockage, leading in turn to an acute coronary syndrome. ACS often presents as chest pain, or tightness/discomfort of the chest. Pain may be accompanied by sweating and nausea. The pain may spread to other areas including the back, shoulders, neck, jaw and arms. The reason pain is felt in areas other than the chest, such as the arm and jaw is due to the brain’s inability to distinguish between visceral and somatic sensory distribution. Somatic pain originates in deep tissues and skin, whereas visceral pain derives from internal organs. This confusion originates from the fact that the visceral and somatic nerves from the heart and spinal nerves enter the spinal cord at the same point, causing the brain to interpret the pain as originating from the somatic regions. When a patient presents with chest pain it is important to rule out any other causes (Table 7.1) and ask appropriate questions to ascertain the type of pain the patient is experiencing (Table 7.2) and if it is cardiac in origin. Patients presenting with acute chest pain suspect of ACS should have the following assessments carried out:
Table 7.1
Chest pain differential diagnosis
Pericarditis/myocarditis |
Tamponade |
Angina |
Dissecting aortic aneurysm |
Oesophageal pain |
Musculoskeletal pain |
Pulmonary embolism |
Trauma |
Panic attack |
Arrhythmia |
Pleurisy |
Mastitis (seen in breastfeeding women) |
Table 7.2
Chest pain history questions
When did the pain start? |
Where did the pain start? |
What were doing at the time? |
Does the pain spread anywhere else? |
How would you describe the pain? |
Does the pain come and go or is it constant? |
Have you had pain like this in the past? |
Is there anything that makes the pain better or worse? |
On a scale of 0–10, 0 being no pain and 10 being the worst pain imaginable, what score would you give the pain at the moment? |
Do you feel short of breath? |
Have you had any nausea or vomiting? |
Do you have a history of heart attack and/or angina? |
12-lead ECG on admission followed by serial ECGs as required
Haemodynamic assessment
Complete medical history and history of presenting complaint
Blood test for cardiac biochemical markers
Suspected MI patients should have access to defibrillation, high flow oxygen and analgesia, usually an opiate given with an antiemetic. Cyclizine is not recommended due its potential hemodynamic effects. Antiplatelet aggregators, such as Aspirin are often given to impair platelet aggregation around the clot. Low molecular weight heparins are also often used in ACS patients to reduce coagulation of the blood. The authors do not include much information about specific drugs and their doses deliberately as this differs in certain countries and settings. Instead we recommend that the reader is familiar with their own local policies and procedures for the pharmacological management of patients.
Atherosclerosis
Is a process where arteries become hardened by plaques made up of fatty substances, such as cholesterol and triglycerides. The hardening and narrowing of the arteries can reduce the flow of blood and oxygen to the heart muscle causing coronary heart disease. In other arteries the process can cause stroke or peripheral arterial disease.
If a plaque ruptures (Fig. 7.3) it can lead to the formation of a blood clot, known as a thrombus. This clot can then block subsequent blood flow to portions of the heart supplied by the blocked artery (Fig. 7.4). An enzyme named thrombin causes fibrin to be formed from fibrinogen (Fig. 7.5). This mesh of fibrin traps blood cells and platelets. Platelet aggregation is triggered by the damage to the vessels endothelium caused by the rupture. The platelets attach to the exposed collagen by binding to von Willebrand’s factors.
Fig. 7.3
Atherosclerosis leading to coronary thrombus formation
Fig. 7.4
The occlusion in the right coronary artery can be clearly seen. This patient had a collateral vessel allowing blood to bypass the blockage naturally
Fig. 7.5
Thrombus formation leading to myocardial infarction
The risk factors for coronary heart disease can be split into modifiable and nonmodifiable risk factors (Table 7.3). Modifiable risk factors include things that can be changed or better managed by patients, usually by making certain lifestyle changes. Nonmodifiable risk however are beyond the control or influence of the patient, such as gender and genetic makeup.
Table 7.3
Modifiable and nonmodifiable coronary heart disease risk factors
Nonmodifiable | Modifiable |
|---|---|
Age | Smoking |
Race | High blood cholesterol |
Sex | High blood pressure |
Genetics | Obesity and inactivity |
Diabetes |
Angina
The extent of the arterial occlusion can cause symptoms of angina or other acute coronary syndromes. Nitrates, such as; glyceryl trinitrate (GTN), isosorbide mononitrate (ISMN) and isosorbide dinitrate (ISDN) are often used to relieve symptoms of angina. Nitrates work by dilating the coronary arteries and increasing blood/oxygen flow to the heart, whilst simultaneously reducing preload by dilating the systemic veins. Due to the mechanism of action and side effects of nitrates, patients can develop tachycardia, feel dizzy, have headaches and develop postural hypotension. There are several different types of angina, including:
Stable angina
Unstable angina
Prinzmetal’s/variant angina
Stable Angina
Stable angina pectoris (Fig. 7.6) is caused by atherosclerotic plaque(s) in one or more of the coronary arteries reducing blood flow to the heart. The reduced blood flow is not normally noticed during routine activities; but during situations requiring increased myocardial demand, angina symptoms become apparent. Pain is often felt in the chest, neck, jaw or arms and is essentially caused by demand for blood and oxygen being greater than supply. Exercise and emotional stress can trigger an angina attack.
Fig. 7.6
Stable angina pectoris
Unstable Angina
Unlike stable angina, symptoms can also occur during rest. There is significant narrowing of the arterial lumen substantially reducing coronary blood flow (Fig. 7.7).
Fig. 7.7
Unstable angina pectoris
Prinzmetal’s Angina
Also known as vasospastic or variant angina is a form of angina that is not caused by narrowing of the vessel due to plaques but instead by contraction of the smooth muscle tissue in the vessel termed vasospasm (Fig. 7.8). The narrowing of the artery due to contraction has the effect of reducing the amount of blood and oxygen to the heart leading to angina symptoms. The symptoms can occur at rest and usually at night. Prinzmetal’s angina is often seen as transient ST elevation on the ECG, sometimes with hyperacute T waves or T wave inversion. This can make it difficult to identify, as the ECG needs to be performed during an attack to see this effect.
Fig. 7.8
Prinzmetal’s angina
Clues to the presence of angina are seen as ischemic changes on the ECG. These signs of ischemia affect the T wave and ST segment causing either flattening or depression of the T wave/ST segment or the inversion of T waves (Table 7.4 and Fig. 7.9). In addition there are several different appearances to the presentation of ST depression, including upsloping, downsloping and horizontal (Fig. 7.10), which describe the position of the ST segment relative to the isoelectric baseline.
Table 7.4
Various signs of ischemia on the ECG
Fig. 7.9
Different presentation of ST depression (a) upsloping, (b) downsloping, (c) horizontal
Fig. 7.10
ST depression/T wave inversion seen in precordial leads
Digitalis Effect
Another situation which presents with widespread ST depression is digitalis/digoxin effect in which the morphology of the ST depression resembles a tick that is the wrong way around (reverse tick) or a gradual sloping (Figs. 7.11 and 7.12). Digitalis effect is caused by the drug digoxin. The presence of this effect does not imply digoxin toxicity. Further clues to this effect also include a shortened QT interval and possible PR interval prolongation and prominent U waves. A patient drug history is essential to confirm digitalis effect.
Fig. 7.11
The digoxin effect
Fig. 7.12
The digoxin effect showing clearly the ‘reversed tick’ ST depression
Myocardial Infarction
A myocardial infarction, commonly referred to as a heart attack is a term used to describe injury to the heart muscle caused by a lack of sufficient blood, oxygen and other nutrients (Fig. 7.13). There are two different classifications of myocardial infarction:
Fig. 7.13
Myocardial infarction
ST elevation myocardial infarction (STEMI)
Non ST elevation myocardial infarction (NSTEMI)
A myocardial infarction includes a variety of symptoms (Table 7.5) and can present in atypical ways. The most generally recognizable symptoms include a severe and persistent pain in the chest, often described as a crushing, squeezing or burning pain. The pain often spreads to the neck, arms and/or jaw. Nausea/vomiting, shortness of breath and a cold clammy appearance are also frequently observed. Sometimes patients can present with atypical signs and symptoms, this is more likely with the elderly and women. Angina pain is usually relieved by rest and angina medication. If the pain is different to the patients ‘normal’ angina pain and persists after rest/medication then myocardial infarction is highly likely.
Table 7.5
Signs and symptoms of myocardial infarction
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