There are many causes of chest pain. Many non-cardiac conditions can mimic a myocardial infarction, and so the ECG can be extremely useful when making a diagnosis. However, the ECG is less important than the history and physical examination, because the ECG can be normal in the first few hours of a myocardial infarction.
Acute chest pain can be caused by:
• Myocardial infarction
• Pulmonary embolism
• Pneumothorax
• Pleurisy
• Pericarditis
• Aortic dissection
• Ruptured oesophagus
• Oesophagitis
• Collapsed vertebra
• Herpes zoster
Chronic or recurrent chest pain may be:
• Exertional angina
• Radiculopathy
• Muscular pain
• Oesophageal reflux
• Nonspecific pain
Acute Chest Pain
The typical pain of myocardial infarction is easy to recognize, the features being:
• central
• radiates to neck, jaw, teeth, arm(s) or back
• severe
• associated with nausea, vomiting and sweating.
Unfortunately not all patients have typical pain, and pain can even be absent. The diagnosis of a myocardial infarction depends on the history and examination, on the measurement of biochemical markers of cardiac muscle damage (especially the troponins) and on the ECG. A rise in troponin I or troponin T levels in patients with a history suggestive of a myocardial infarction is now taken to mean that infarction has occurred, but treatment still depends on the ECG.
The term ‘acute coronary syndrome’ is now used to include:
1) Myocardial infarction with ST-segment elevation on the ECG.
2) Myocardial infarction (as shown by a troponin rise) with only T-wave inversion or ST-segment depression.
3) Chest pain with ischaemic ST-segment depression but no troponin rise (what used to be called ‘unstable angina’).
4) Sudden death due to coronary disease.
Stable angina and ‘chest pain of unknown cause’ remain entirely proper diagnostic labels for those patients who are admitted to hospital with chest pain, but for whom the term ‘acute coronary syndrome’ is inappropriate.
The Development of ECG Changes in Myocardial Infarction
The sequence of features characteristic of ‘full thickness’, or ‘ST-segment elevation’, myocardial infarction is:
• Normal ECG
• Delayed intrinsicoid deflection
• Tall peaked T-waves (so called hyperacute T-waves)
• ST-segment elevation
• Development of Q-waves
• ST-segment returns to the baseline
• T-waves inversion
• Loss of R-wave voltage in anterior chest leads.
The ECG leads that show the changes typical of a myocardial infarction depend on the part of the heart affected.
Infarct
Accurate ECG interpretation in a patient with chest pain is critical. Basically, there can be three types of problems ⎯ ischaemia is a relative lack of blood supply (not yet an infarct), injury is acute damage occurring right now, and finally, infarct is an area of dead myocardium. It is important to realize that certain leads represent certain areas of the left ventricle; by noting which leads are involved, you can localize the process. The prognosis often varies depending on which area of the left ventricle is involved (i.e., anterior wall myocardial infarct generally has a worse prognosis than an inferior wall infarct).
Anterior and Lateral InfarctionAcute chest pain can be caused by:
• Myocardial infarction
• Pulmonary embolism
• Pneumothorax
• Pleurisy
• Pericarditis
• Aortic dissection
• Ruptured oesophagus
• Oesophagitis
• Collapsed vertebra
• Herpes zoster
Chronic or recurrent chest pain may be:
• Exertional angina
• Radiculopathy
• Muscular pain
• Oesophageal reflux
• Nonspecific pain
Acute Chest Pain
The typical pain of myocardial infarction is easy to recognize, the features being:
• central
• radiates to neck, jaw, teeth, arm(s) or back
• severe
• associated with nausea, vomiting and sweating.
Unfortunately not all patients have typical pain, and pain can even be absent. The diagnosis of a myocardial infarction depends on the history and examination, on the measurement of biochemical markers of cardiac muscle damage (especially the troponins) and on the ECG. A rise in troponin I or troponin T levels in patients with a history suggestive of a myocardial infarction is now taken to mean that infarction has occurred, but treatment still depends on the ECG.
The term ‘acute coronary syndrome’ is now used to include:
1) Myocardial infarction with ST-segment elevation on the ECG.
2) Myocardial infarction (as shown by a troponin rise) with only T-wave inversion or ST-segment depression.
3) Chest pain with ischaemic ST-segment depression but no troponin rise (what used to be called ‘unstable angina’).
4) Sudden death due to coronary disease.
Stable angina and ‘chest pain of unknown cause’ remain entirely proper diagnostic labels for those patients who are admitted to hospital with chest pain, but for whom the term ‘acute coronary syndrome’ is inappropriate.
The Development of ECG Changes in Myocardial Infarction
The sequence of features characteristic of ‘full thickness’, or ‘ST-segment elevation’, myocardial infarction is:
• Normal ECG
• Delayed intrinsicoid deflection
• Tall peaked T-waves (so called hyperacute T-waves)
• ST-segment elevation
• Development of Q-waves
• ST-segment returns to the baseline
• T-waves inversion
• Loss of R-wave voltage in anterior chest leads.
The ECG leads that show the changes typical of a myocardial infarction depend on the part of the heart affected.
Infarct
Accurate ECG interpretation in a patient with chest pain is critical. Basically, there can be three types of problems ⎯ ischaemia is a relative lack of blood supply (not yet an infarct), injury is acute damage occurring right now, and finally, infarct is an area of dead myocardium. It is important to realize that certain leads represent certain areas of the left ventricle; by noting which leads are involved, you can localize the process. The prognosis often varies depending on which area of the left ventricle is involved (i.e., anterior wall myocardial infarct generally has a worse prognosis than an inferior wall infarct).
The changes of anterior infarction are seen in leads V2–V5. Lead V1, which lies over the right ventricle, is seldom affected. The lateral wall of the left ventricle is often damaged at the same time as the anterior wall, and then leads I, VL and V6 show infarction changes. Persistent ST- segment elevation is quite common after an anterior infarction: it sometimes indicates the development of a left ventricular aneurysm, but it is not reliable evidence of this. The following ECG shows acute anterolateral infraction.
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| Acute anterolateral infraction |
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| Old anterior infraction |
One is that normally the R-wave gets larger as one moves from V1 to V6. If there is no R-wave “progression” from V1 to V6 this can also mean infarct. The second caveat is that, with a left bundle branch block, it is difficult to diagnoseMI. In a patient with chest pain and left bundle branch block, one must rely on cardiac enzymes (blood tests) and the history.
Posterior Infarction
It is possible to ‘look at’ the back of the heart by placing the V lead on the back of the left side of the chest, but this is not done routinely because it is inconvenient and the complexes recorded are often small. An infarction of the posterior wall of the left ventricle can, however, be detected in the ordinary 12-lead ECG because it causes a dominant R-wave in lead V1. The shape of the QRS complex recorded from lead V1 depends on the balance of electrical forces reaching the ECG electrode. Normally the right ventricle is being depolarized towards lead V1, so causing an upward movement (an R-wave) on the record; at the same time the posterior wall of the left ventricle is being depolarized, with the wave of excitation moving away from the electrode and so causing a downward movement (an S-wave) on the record. The left ventricle is more muscular than the right and therefore, exerts a greater influence on the ECG, so in lead V1 the QRS complex is normally predominantly downward, i.e. there is a small R-wave and a deep S-wave. In a posterior infarction, the rearward-moving electrical forces are lost so lead V1 ‘sees’ the unopposed forward moving depolarization of the right ventricle and records a predominantly upright QRS complex.
Inferior Infarction
There is ST elevation in lead II,III and aVF with reciprocal ST depression in V1-V3. There is also ST depression in lead I and aVL. The following two ECGs show acute and evolved inferior infarction.
Posterior Infarction
It is possible to ‘look at’ the back of the heart by placing the V lead on the back of the left side of the chest, but this is not done routinely because it is inconvenient and the complexes recorded are often small. An infarction of the posterior wall of the left ventricle can, however, be detected in the ordinary 12-lead ECG because it causes a dominant R-wave in lead V1. The shape of the QRS complex recorded from lead V1 depends on the balance of electrical forces reaching the ECG electrode. Normally the right ventricle is being depolarized towards lead V1, so causing an upward movement (an R-wave) on the record; at the same time the posterior wall of the left ventricle is being depolarized, with the wave of excitation moving away from the electrode and so causing a downward movement (an S-wave) on the record. The left ventricle is more muscular than the right and therefore, exerts a greater influence on the ECG, so in lead V1 the QRS complex is normally predominantly downward, i.e. there is a small R-wave and a deep S-wave. In a posterior infarction, the rearward-moving electrical forces are lost so lead V1 ‘sees’ the unopposed forward moving depolarization of the right ventricle and records a predominantly upright QRS complex.
Inferior Infarction
There is ST elevation in lead II,III and aVF with reciprocal ST depression in V1-V3. There is also ST depression in lead I and aVL. The following two ECGs show acute and evolved inferior infarction.
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| Acute and Evolve Inferior Infraction |
Right Ventricular Infarction
Inferior infarction is sometimes associated with infarction of the right ventricle. Clinically, this is suspected in a patient with an inferior infarction when the lungs are clear but the jugular venous pressure is elevated. The ECG will show a raised ST-segment in leads recorded from the right side of the heart. The positions of the leads correspond to those on the left side as follows: V1R is in the normal V2 position; V2R is in the normal V1 position; V3R etc. are on the right side, in positions corresponding to V3 etc. on the left side.
Inferior infarction is sometimes associated with infarction of the right ventricle. Clinically, this is suspected in a patient with an inferior infarction when the lungs are clear but the jugular venous pressure is elevated. The ECG will show a raised ST-segment in leads recorded from the right side of the heart. The positions of the leads correspond to those on the left side as follows: V1R is in the normal V2 position; V2R is in the normal V1 position; V3R etc. are on the right side, in positions corresponding to V3 etc. on the left side.
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