The ECG in Patients with Chest Pain

5


The ECG in Patients with Chest Pain




HISTORY AND EXAMINATION


There are many causes of chest pain. All the 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 (to a lesser extent) the physical examination, because the ECG can be normal in the first few hours of a myocardial infarction.


Some causes of chest pain are listed in Box 5.1.



Box 5.1   Causes of chest pain


Acute chest pain



Chronic or recurrent chest pain



The ECG in Figure 5.1 was recorded in an A & E department from a 44-year-old man with rather vague chest pain. He was thought to have a viral illness and his ECG was considered to be within normal limits. He was allowed home, and died later that day. The post-mortem examination showed a myocardial infarction which was probably a few hours old, and corresponded with his A & E attendance.




ACUTE CHEST PAIN


The features of acute chest pain associated with different causes are summarized in Box 5.2.



Box 5.2   Features of acute chest pain


Myocardial infarction



Pulmonary embolism



Other lung disease, e.g. infection or pneumothora



Pericardial pain



Aortic dissection



Oesophageal rupture



Spinal pain



Shingles (herpes zoster)



The physical examination of a patient with chest pain may reveal nothing other than the signs associated with the pain itself (anxiety, sinus tachycardia, restlessness or a cold and sweaty skin), but some specific signs are worth looking for:




CHRONIC CHEST PAIN


The main differential diagnosis of chronic chest pain is between angina and the chest pain that is common in middle-aged men, but for which no clear diagnosis is usually made. This pain is sometimes called ‘atypical chest pain’, but this is a dangerous diagnostic label because it implies that there is a diagnosis (by implication, cardiac ischaemia) but that the symptoms are ‘atypical’. Some of these pains are musculoskeletal, Tietze’s syndrome of pain from the costochondral junctions being the most obvious, but in most cases the best diagnostic label is ‘chest pain of unknown cause’. This indicates a possible need for later re-evaluation.


The important features in the history that point to a diagnosis of angina are that the pain:



The physical signs to look for are:





THE ECG IN PATIENTS WITH MYOCARDIAL ISCHAEMIA


Myocardial infarction is, properly, a term describing myocardial cell death due to ischaemia. The histological changes – and ECG changes – can take several hours to appear, and the entire process leading to a healed infarction can take 5 or 6 weeks. Myocardial injury causes release into the blood of biomarkers such as troponin T or I and the MB fraction of creatine kinase, CK-MB. Therefore the release of these biomarkers can reflect the necrosis of myocardial cells, but it also occurs in situations other than coronary artery occlusion ( Box 5.3). Thus, although a rise in the blood levels of biomarkers supports the diagnosis of myocardial infarction it is not sufficient, and the most commonly used parts of the ‘universal definition’ of myocardial infarction, require both clinical evidence of myocardial ischaemia and a rise and/or fall of blood troponin levels. Box 5.4 shows the types of infarction listed in the universal definition, drawn up by the ESC/ACCF/AHA/WHF Task Force (Jaffe, A.S., Simoons, M.L., Chaitman, B.R. and White, H.D., on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction. European Heart Journal (2012) 33, 2551–2567). Box 5.5 lists the diagnostic criteria for each type of infarction.



Box 5.3   Causes of plasma troponin elevation other than myocardial infarction





Box 5.4   Types of myocardial infarction





Box 5.5   Criteria for myocardial infarction


Acute myocardial infarction



• Detection of rise and/or fall of cardiac biomarkers (preferably troponin) together with evidence of myocardial ischaemia and at least one of the following:



• Sudden unexpected cardiac death, often with symptoms and ECG changes of ischaemia; or evidence of fresh coronary thrombus at post mortem, before blood samples are taken or before a rise in cardiac biomarkers could be expected


• Myocardial infarction related to PCI (percutaneous coronary intervention) – a rise of troponin to five times the upper limit of normal, plus new ischaemic symptoms or new ECG changes or imaging evidence of loss of viable myocardium


• Myocardial infarction related to CABG (coronary artery bypass grafting) – elevation of troponin level to ten times the upper limit of normal, plus either new ECG changes, evidence of loss of viable myocardium, or angiographically demonstrated graft occlusion


• Pathological findings of an acute infarction


Prior myocardial infarction


Any one of:



The universal definition does not use the term ‘acute coronary syndrome’ at all, although this is a term in widespread clinical use, albeit with variations in what should be included. The term is most commonly used to describe patients with a clinical ‘coronary event’ of various types, including:



and sometimes



‘Stable angina’ is an entirely proper diagnostic label for a patient with intermittent chest pain associated with transient ECG changes, and ‘chest pain of unknown cause’ is the best label if no diagnosis has been made.



ECG CHANGES IN ST SEGMENT ELEVATION MYOCARDIAL INFARCTION (STEMI)


The sequence of features characteristic of STEMI is:



The universal definition of STEMI requires new ST segment elevation at the J point (the junction of the S wave and the ST segment) in two contiguous leads, with the cut-off points in leads V2-V3 at > 0.3 mV in men or > 0.15 mV in women, and in other leads at > 0.1 mV. The ECG leads that show the changes typical of a myocardial infarction depend on the part of the heart affected.



INFERIOR INFARCTION


Figures 5.2, 5.3 and 5.4 show traces taken from a patient with a typical history of myocardial infarction: on admission to hospital, 3 h later, and 2 days later. The main changes are in the inferior leads: II, III and VF. Here the ST segments are initially raised, but then Q waves appear and the T waves become inverted. Figure 5.2 includes coronary angiograms showing the effects of an occluded right coronary artery in an inferior STEMI.






ANTERIOR AND LATERAL INFARCTION


The changes of anterior infarction are seen in leads V2-V5. Lead V1 which lies over the right ventricle, is seldom affected (see Fig. 5.5, which includes corresponding coronary angiograms).



When the lateral wall of the left ventricle is damaged by occlusion of the left circumflex coronary artery, leads I, VL and V6 will show infarction changes. Figure 5.6 shows the record of a patient with an acute lateral STEMI, with the corresponding coronary angiograms. Figure 5.7 shows a record taken 3 days after a lateral infarction, with Q waves and inverted T waves in leads I, VL and V6.




The ECG in Figure 5.8 shows an acute STEMI affecting both the anerior and lateral parts of the left ventricle.



The ECG in Figure 5.9 was recorded several weeks after an anterolateral myocardial infarction. Although the changes in leads I and VL appear ‘old’, having an isoelectric ST segment, there is still ST segment elevation in leads V3-V5. If the patient had just been admitted to hospital with chest pain these changes would be taken to indicate an acute infarction, but this patient had had pain more than a month previously. 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.



An old anterior infarction often causes only what is called ‘poor R wave progression’. Figure 5.10 shows the record from a patient who had had an anterior infarction some years previously. A normal ECG would show a progressive increase in the size of the R wave from lead V1 to V5 or V6. In this case the R wave remains very small in leads V3 and V4, but becomes normal-sized in V5. This loss of ‘progression’ indicates the old infarction.



The time taken for the various ECG changes of infarction to occur is extremely variable, and the ECG is an unreliable way of deciding when an infarction occurred. Serial records showing progressive changes are the only way of timing the infarction from the ECG.



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 from the ordinary 12-lead ECG because it causes a dominant R wave in lead V1. Normally the left ventricle, being more muscular than the right, exerts a greater influence on the ECG, so in lead V1 the QRS complex is predominantly downward. With 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.


Figure 5.11 shows the first record from a patient with acute chest pain. There is a dominant R wave in lead V1 and ischaemic ST segment depression (see p. 231) in leads V2-V4. The chest electrodes were then moved to the V7-V9 positions: all in the same horizontal plane as V5, with V7 on the posterior axillary line, V9 at the edge of the spine, and V8 halfway between, on the midscapular line. The ECG record then showed raised ST segments, with Q waves typical of an acute infarction.




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 raised ST segments 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 Vi position; V3R etc. are on the right side, in positions corresponding to V3 etc. on the left side. Figure 5.12 is from a patient with an acute right ventricular infarct.




MULTIPLE INFARCTIONS


Infarction of more than one part of the left ventricle causes changes in several different ECG territories. This usually implies disease in more than one of the main coronary arteries. The ECG in Figure 5.13 shows an acute inferior myocardial infarction and marked anterior ST segment depression. Later, coronary angiography showed that this patient had a significant stenosis of the left main coronary artery.



Fig. 5.14 is the record from a patient with an acute inferior myocardial infarction. Poor R wave progression in leads V2-V4 indicates an old anterior infarction as well.


Figure 5.15 is an ECG showing an acute inferior STEMI and anterior T wave inversion due to an NSTEMI of uncertain age.

Related posts:

  1. Conclusions: Four Steps to Making The Most of the ECG
  2. The ECG in Patients with Breathlessness
  3. The ECG When the Patient has a Tachycardia
  4. The ECG in Healthy People

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 26, 2016 | Posted by in CARDIOLOGY | Comments Off on The ECG in Patients with Chest Pain

Full access? Get Clinical Tree
Get Clinical Tree app for offline access