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Forgot account? Not Now. Related Pages. Medical e-books for free download Book. The initial treatment is carotid sinus massage, and if this proves ineffective, intravenous adenosine. What is the problem? What to do The catch here is that the dominant R wave in lead V1 may be mistakenly thought to be due to right ventricular hypertrophy. In a young woman who complains of breathlessness after a pregnancy, pulmonary embolism is obviously a possibility, and this might well cause ECG evidence of right ventricular hypertrophy — but in the presence of the WPW syndrome this would be very difficult to diagnose from the ECG.
The only thing that might help the diagnosis would be the appearance of right axis deviation, which is not part of the WPW syndrome, and is not present here. So, look for another cause of breathlessness, such as anaemia. What is the rhythm, and what would you do immediately, and in the long term? The key to the diagnosis lies in the ECG when the heart is in sinus rhythm, but this is not always available.
Patients with a broad complex tachycardia in the context of an acute myocardial infarction must be assumed to have a ventricular tachycardia, but that does not apply here. In this record the QRS complexes are not very broad, the axis is to the right, and there is no concordance of the QRS complexes — all pointing to a supraventricular origin. In favour of a ventricular tachycardia is the fact that the height of the primary R wave in lead V1 is greater than that of the secondary R wave.
However, taking these features together with the clinical picture, the rhythm is probably supraventricular. What to do Carotid sinus pressure is the first move. If there is severe haemodynamic compromise the patient may need urgent electrical cardioversion, but intravenous flecainide would be a reasonable first choice. In fact, in this case the arrhythmia terminated spontaneously, revealing a short PR interval and a QRS complex with a delta wave.
So this patient had the WPW syndrome, and needed an electrophysiological study with a view to ablation of the accessory tract. Despite having been treated with angiotensin-converting enzyme inhibitors and diuretics, there was evidence of severe heart failure. Having seen the ECG and chest X-ray, what more do you want to know? Clinical interpretation The absence of atrial activity and the peaked T waves are consistent with hyper- kalaemia. The right axis deviation and deep S waves in lead V6 could indicate right ventricular hypertrophy and could result from chronic lung disease.
This woman had been treated with a combination of captopril 25 mg, three times daily which tends to raise the serum potassium level and three co-amilofruse tablets per 24 h furosemide 40 mg plus amiloride 5 mg in each tablet. The com- bination of captopril and amiloride causes marked potassium retention, and in this case the serum potassium level was 7. When the hyperkalaemia was corrected, sinus rhythm with clear P waves was restored and the peaked T waves became normal.
The right axis deviation, clockwise rotation and inverted T waves in the inferior leads persisted. What does this ECG show? Does anything about it surprise you? Patients who are in pain with an acute myocardial infarction usually have a sinus tachycardia, but here vagal overactivity is causing a bradycardia. What to do First degree block is not important in itself, but with evidence of vagal overactivity, atropine should be given. Otherwise this patient can be treated in the usual way with pain relief, aspirin, and percutaneous coronary intervention PCI or thrombolytics.
The slurred upstroke to the QRS complex suggests the Wolff—Parkinson—White WPW syndrome, so this is a re-entry tachycardia, with depolarization spreading down the accessory pathway. What to do Carotid sinus pressure is always the first thing to try in patients with a supravent- ricular tachycardia.
In most such patients, adenosine is the first drug to use, but in cases of the WPW syndrome it must be used with caution. It can block the atrio- ventricular node and increase conduction through the accessory pathway, and if atrial fibrillation is present this can lead to ventricular fibrillation.
Digoxin, verap- amil and lidocaine can have the same effect. The safe drugs in this situation are the beta-blockers, flecainide and amiodarone. The pain is sometimes caused by excitement. He has never had any pain without some precipitating cause. The upper ECG shows a recording made at rest, and the lower record comes from his exercise test, after 5 min of the Bruce protocol.
What do the ECGs show? In this case, the ST segment elevation cleared immediately on resting — elevation like this is an occasional mani- festation of ischaemia rather than infarction. He needs long-term management with aspirin, and probably a statin and an angiotensin-converting enzyme inhibitor, and risk factors must be addressed.
Since the exercise test was See p. He had no pain. What is the rhythm, and how would you treat him? However, the lack of concordance i. What to do If the patient has pulmonary oedema, preparations for DC cardioversion should be made immediately. While waiting for this he should be treated with diamorphine, intravenous diuretics and lidocaine or intravenous amiodarone.
This ECG was recorded after cardioversion, when he was well. His serum troponin level remained normal following admission, so he had not had a myocardial infarction. How would you report on this ECG, and what do you think the underlying disease is? The broad complex tachycardia was therefore almost certainly ventricular in origin. He now has evidence of conduction tissue disease, with first degree block and LBBB.
Since chest pain has not been a feature of his illness, it seems likely that he has a dilated cardiomyopathy. What to do If after treatment with an angiotensin-converting enzyme inhibitor and amiodarone the patient has another episode of ventricular tachycardia, an implanted defibrillator may be needed. His ECG had been normal 6 months ago. What does this record show and what would you do? LBBB masks any changes there might be as the result of a myocardial infarction.
What to do The LBBB has evidently developed in the last 6 months, and the history suggests a myocardial infarction. Provided there are no contraindications, percutaneous coro- nary intervention PCI or a thrombolytic agent is indicated. The ventricular extra- systoles should not be treated. What to do The immediate risk is low and there is no evidence for the likelihood of benefit from thrombolysis.
Although the patient is now asymptomatic he should remain in hos- pital for observation and the plasma troponin level should be checked 12 h after the onset of pain. The risk of reinfarction in the next 3 months is relatively high compared with the risk following an ST segment elevation myocardial infarction, and coronary angiography is needed.
Is any action necessary? It is seldom of any clinical significance. What to do In the absence of symptoms or abnormal signs, no action is necessary. What to do The patient should be given diamorphine and aspirin immediately, and percutaneous coronary intervention PCI or thrombolysis as soon as possible.
The extrasystoles should not be treated. Can this man be allowed to hold a commercial driving licence? They represent septal depolarization, not an old lateral infarction. What to do The ECG is normal, and if the man has no other evidence of heart disease he can hold a commercial driving licence. If in doubt, an exercise test should be performed. She did not survive. She had some chest pain on both sides, which sounded pleuritic. Does her ECG help with her diagnosis and treatment?
A pulmonary angiogram was performed as part of a series of investigations. The right mid-zone is perfused, but the rest of the lung fields have poor or no perfusion due to multiple pulmonary emboli.
Note how the T wave inversion is at a maximum in lead V1 and becomes pro- gressively less marked from lead V2 to V4. What to do In the context of a delivery 3 months previously, this ECG pattern of right ventri- cular hypertrophy almost certainly indicates multiple pulmonary emboli causing pulmonary hypertension. The pulmonary angiogram confirms this diagnosis. Anti- coagulants, and possibly thrombolysis, are needed urgently.
What does it show and what would you recommend? Atrioventricular conduction occurs via the posterior fascicle of the left bundle branch. What to do Progression to complete block can occur but is relatively rare. In the absence of symptoms, standard UK practice would be not to insert a permanent pacemaker; however, any symptoms suggestive of a bradycardia should be investigated immediately.
There were no abnormal physical findings. The ECGs of athletes can show ST segment and T wave changes due to left ventricular hypertrophy, but anteroseptal T wave inversion of this degree in a healthy young man almost certainly represents hypertrophic cardiomyopathy. What to do Echocardiography will confirm the diagnosis. Ambulatory ECG recording will show whether the patient is having ventricular arrhythmias. He must not play competitive sports, and his close relatives should be screened.
What is the rhythm, and what would you do? It is, however, an accelerated idioventricular rhythm. What to do This rhythm is quite commonly seen in patients with an acute myocardial infarction, and indeed is not uncommon in ambulatory ECG records from normal people. In a hypertensive patient, beta-blocker treatment is a possible explanation. Voltage criteria for left ventricular hypertrophy are extremely unreliable when there is no other evidence of this. The peaked T waves could be due to hyperkalaemia but are more often a normal variant.
What to do All these possible abnormalities are seen in normal athletes, and the likelihood is that they are of no significance. In a patient with hypertension, beta-blocker treat- ment could be the cause of the bradycardia.
He is now breathless. What does this ECG show and what treatment is needed? The breathlessness suggests that he may have developed left ventricular failure, and he must be admit- ted to hospital and treated with diuretics and if necessary intravenous nitrates to induce vasodilation.
The patient will need long-term treatment with an angiotensin- converting enzyme inhibitor: the best time to begin treatment is a matter for debate but it should be within 2 or 3 days of the onset of the infarction. He will also need long-term treatment with aspirin, as a prophylactic against further infarction. This is her ECG. She recovered spontaneously. What is this rhythm, and what would you do?
We have no ECG from this patient recorded in sinus rhythm, which is always the most helpful thing in deciding between these possibilities. The complexes are not very wide, which would be consistent with a supraventricular origin with aberrant conduction, but the left axis deviation and probable concordance point to ventricular tachycardia.
The key is the two narrow complexes near the beginning of the record: these are slightly early and are probably capture beats. They indicate that with an early supraventricular beat the conducting system can function normally; by implication, the broad complexes must be due to ventricular tachycardia. What to do An elderly patient with heart failure is more likely to have ischaemic disease than anything else, but all the possible causes of heart failure must be considered.
The sudden onset of an arrhythmia could be due to a myocardial infarction. Pulmonary emboli can cause sudden arrhythmias, though these are more often supraventricular than ventricular.
It is important to consider whether this rhythm change is related to treatment, in which case it could be due to an electrolyte imbalance or to the pro-arrhythmic effect of a drug the patient is taking. There were no abnormalities on examination other than a slow and irregular pulse. What is the diagnosis and how can his problem be treated? The record shows sinus rhythm with a junctional escape beat, in which the atrium is activated retrogradely.
Even though his bradycardia is asymptomatic, he will need a permanent pacemaker because antiarrhythmic agents given for the tachycardia may make his bradycardia worse. What are the implications for surgery? What to do In large groups of patients, ventricular extrasystoles are correlated with heart disease of all types. In individuals, however, extrasystoles may well occur in a perfectly normal heart — indeed, virtually everyone has extrasystoles at times.
Ventricular extrasystoles become more common with increasing age, and this patient is 80 years old. They should not be treated. He had had several episodes of pain that appeared to be due to ischaemia, but they had no clear relationship with exertion. What does this record show, and what would you do? Ischaemic ST segment depression, accounting for his pain. He should be taught the methods of inducing vagal activity, but prophylactic drug therapy will be needed: a beta-blocker or verapamil should be tried first.
Electrophysiological investigation, with a view to ablating an abnormal pathway, may be needed. There are two possible explanations for the abnormality it shows, though only one of these would explain his history.
What is the likely diagnosis? The changes are therefore probably due to a posterior myocardial infarction, which would fit the history of chest pain 3 weeks previously. What to do It is important not to miss a diagnosis of pulmonary embolism. The patient should be re-examined to ensure that there is no clinical evidence of right ventricular hypertrophy. A chest X-ray examination should be carried out, and an echocardio- gram may be helpful. Is the ECG normal? What would you tell the licensing authority?
If lead III is recorded with the patient taking a deep breath in, the changes will often normalize as shown below. How would you have managed her? What to do In this patient the diagnosis of an acute infarction was excluded when the plasma troponin levels were found to be normal.
An exercise test was performed, but was limited by breathlessness without further ECG change. A coronary angiogram was completely normal.
The chest pain was therefore thought to be musculoskeletal in origin, and the T wave changes were presumably due to her ethnicity. He was cold and clammy. His heart rate was rapid and his blood pressure was unrecordable.
There were signs of left ventricular failure. What do they show and what would you do? What to do The cardiovascular collapse results from the rapid heart rate, with a loss of diastolic filling.
Carotid sinus pressure may temporarily increase the degree of block and establish the diagnosis, but it is unlikely to convert atrial flutter to sinus rhythm. Intravenous adenosine is likely to have the same effect as carotid sinus pressure. A patient who is haemodynamically compromised by a tachycardia should be treated with immediate DC cardioversion.
Ventricular extrasystoles are in themselves usually not important, but in a patient complaining of attacks of dizziness, ventricular extrasystoles that are frequent and multifocal may be causing haemodynamic impairment. What to do It would be worth recording an ambulatory ECG to see if the patient is having runs of ventricular tachycardia, but the extrasystoles probably do need suppressing.
A beta-blocker would be the first drug to try, and then amiodarone. What physical signs would you look for, and what is the next stage in her management? There is nothing other than the voltage criteria which are unreliable to suggest left ventricular hypertrophy, so mitral stenosis must be considered — although significant mitral stenosis usually causes right ventricular hypertrophy. The palpitations could be due to atrial fibril- lation if the patient has mitral stenosis.
What to do Look for the tapping apex beat, the loud first sound, the opening snap and the mid-diastolic murmur that are characteristic of mitral stenosis. Echocardiography will be helpful in distinguishing between valve disease and left ventricular hypertro- phy as a cause of left atrial hypertrophy. Ambulatory ECG recording may be neces- sary to identify the cause of the palpitations. Treatments to be considered if she has mitral valve disease and atrial fibrillation are digoxin or a beta-blocker, anticoagu- lants, and mitral valve surgery.
If the breathlessness turns out to be due to poor left ventricular function, an angiotensin-converting enzyme inhibitor is needed. He is untreated — how would you manage him? What to do This patient has had no chest pain, but has developed a very large heart with atrial fibrillation; the ECG shows LBBB, which prevents any further interpretation. Isch- aemia seems unlikely, and the diagnosis is almost certainly dilated cardiomyopathy of unknown cause. An echocardiogram may show some mitral regurgitation due to left ventricular dilatation, but the valves will probably be structurally normal.
There will probably be globally reduced left ventricular function with a low ejection frac- tion. It is unlikely that a primary cause will be found, though alcoholism is the important one to exclude. Treatment would be the usual combination of diuretics, an angiotensin-converting enzyme inhibitor, digoxin, anticoagulants and ultimately cardiac transplantation. What abnormalities does his ECG show, and what treatment is needed? The key is to identify the rhythm first, from the lead II rhythm strip at the bottom.
The results of an ambulatory ECG recording and an exercise test would be interesting, but the patient needs immediate treatment, and amiodarone would probably be the drug of choice. A coronary angiogram should be considered because there may be one or more critical stenoses amenable to percutaneous coro- nary intervention PCI , and this might abolish the ventricular tachycardia.
She was a non-smoker and had no risk factors for coronary artery disease. What do you think is going on? The other raised ST segments, which are widespread, could well be due to pericarditis. What to do The patient should be examined lying flat, because this gives the best chance of hearing a pericardial friction rub — and this is what was found here.
The pericarditis could, of course, be due to an infarction, but repeated ECGs showed no develop- ment of an infarction pattern, and the raised ST segments persisted for several days.
An echocardiogram showed a pericardial effusion. The pericarditis, and presumably the associated atrial fibrillation, were due to the rheumatoid arthritis. During attacks she does not feel dizzy or breathless, and the palpitations stop suddenly after a few seconds.
Physical examination is normal, and this is her ECG. What is the diagnosis and what advice would you give? Unlike the Wolff—Parkinson— White WPW syndrome, in which there is an accessory pathway separate from the atrioventricular node and His bundle, in the LGL syndrome there is a bypass close to the atrioventricular node, connecting the left atrium and the His bundle.
What to do Ambulatory ECG recording may confirm the diagnosis if attacks are frequent enough. An electrophysiological study and ablation of the abnormal tract may be necessary. The ventricular extrasystoles are not impor- tant, but she should be advised not to smoke, and to avoid alcohol and caffeine.
The anaesthetist asks for comments. However, when as large as this — and particularly when the patient is asymptomatic — peaked T waves are nearly always perfectly normal. What to do Ensure that the patient has no cardiac symptoms, and check his electrolyte levels preoperatively. He was breathless and his blood pressure was unrecordable. What does the ECG show and how should he be treated?
In this case, features against the rhythm being ventricular tachycardia are the right axis deviation and the lack of concordance in the QRS complexes i. The combination of right axis deviation and an LBBB pattern in a broad complex tachycardia suggests that the origin is in the right ventricular outflow tract.
What to do Any patient with an arrhythmia and evidence of haemodynamic compromise in this case, breathlessness and a very low blood pressure needs immediate cardiover- sion. While preparations are being made, it would be reasonable to try intravenous lidocaine or amiodarone. Once the arrhythmia has been corrected, an electrophysi- ological study is needed, because right ventricular outflow tract tachycardia is the one variety of ventricular tachycardia that should be amenable to ablation therapy.
He did not complain of chest pain. There are three main abnormalities. How should he be treated? The lateral T wave changes are presumably due to ischaemia. What to do Ventricular extrasystoles should not be treated, and left anterior hemiblock is not an indication for pacing.
In the absence of pain, the anterior infarction cannot be assumed to be new, so percutaneous coronary intervention PCI or thrombolysis should not be given. He needs an angiotensin-converting enzyme inhibitor and a diuretic. The clinical history is not helpful, nor is the fact that the patient is haemodynamically stable. The combination of right axis deviation, RBBB and the R1 peak being higher than the R peak in lead V1 make it likely that this is a supraventricular tachycardia with RBBB rather than ventricular tachycardia.
What to do Carotid sinus massage. If this has no effect, try intravenous adenosine, and if this is ineffective, try intravenous lidocaine. He was unconscious and had a stiff neck and bilateral extensor plantar responses. His heart was clinically normal. What to do It is possible that this patient had a myocardial infarction which caused a cerebro- vascular accident because of an arrhythmia or a cerebral embolus, and that the cerebrovascular accident caused the seizure. The unconsciousness and the bilateral extensor plantar responses could simply be post-ictal.
However, such a sequence would not explain the stiff neck, which would seem to point to either a subarach- noid haemorrhage or meningitis. Changes like those in this ECG are common in subarachnoid haemorrhage, probably because of intense coronary vasospasm result- ing from catecholamine release. Measurements of the blood troponin level are unlikely to help to differentiate between a primarily cardiac and a primarily neuro- logical event.
This patient did indeed have a subarachnoid haemorrhage, and the ECG eventually returned to normal. He has a raised jugular venous pressure, a tender and distended liver, and marked peripheral oedema. Does this ECG help with the diagnosis and what might you need to do? What does the chest X-ray show? Clinical interpretation Small QRS complexes are seen with a pericardial effusion, and sometimes in patients with chronic lung disease.
The widespread T wave changes would be consistent with pericardial disease. There is nothing in this record to suggest pulmonary disease. What to do The physical findings, the ECG and the chest X-ray would fit with a pericardial effusion associated with malignancy.
You should look carefully at the jugular venous pressure to see if it rises with inspiration, indicating pericardial tamponade. Echo- cardiography is essential, and if there is evidence of right ventricular collapse in diastole, a pericardial drain should be inserted.
The patient had a malignant peri- cardial effusion. Unfortunately the chemical pathology laboratory burned down last night. The flat T waves with obvious U waves suggest hypokalaemia. The downward- sloping ST segments suggest digoxin effect. What to do The clinical picture fits hypokalaemia and digoxin toxicity. Since the electrolyte and digoxin levels cannot be measured, stop the digoxin and any potassium-losing diuretics.
Give the patient potassium orally. Monitoring the T and U waves is a crude but effective way of judging the serum potassium level. Superficially, leads I, VL and V5—V6 might mistakenly be interpreted as suggesting left bundle branch block, but it is important to look at all the leads because the diagnosis here is best seen in lead V2.
In this case there is no dominant R wave in lead V1, so the accessory conducting bundle is on the right side, and this is the WPW syndrome type B. What to do The WPW syndrome is associated with paroxysmal tachyarrhythmia, which may cause collapse.
Asymptomatic WPW syndrome should be left untreated, but it is important in this case to establish — perhaps by ambulatory ECG recording and exercise testing — whether the patient was having paroxysmal tachycardia or not. If there is reason to suppose that an arrhythmia caused his collapse and head injury he needs electrophysiological ablation of the abnormal conducting pathway.
What is the diagnosis, and what would you do? Clinical interpretation This is marked left ventricular hypertrophy. It can be difficult to distinguish between T wave inversion due to ischaemia and the T wave inversion of left ventricular hypertrophy, and when the T wave is inverted in the septal leads V3—V4 , ischaemia has to be considered. Angina, dizziness and left ventricular hypertrophy in an year-old may be due to tight aortic stenosis, though hypertension is a possibility.
In this patient the aortic valve gradient was 20 mmHg, indicating trivial stenosis of the valve, so the left ventricular hypertrophy must be due to the long-standing hypertension. The angina may well improve with adequate blood pressure control and the usual anti-anginal medication, but if it does not, then 85 years is not too old for coronary angiography with a view to percutaneous coronary intervention PCI or bypass surgery.
What are the possible diagnoses? This ECG does not show the pattern of left ventricular hypertrophy, so aortic stenosis is unlikely. Anterior T wave inversion is characteristic of hypertrophic cardiomyopathy, but this does not nor- mally cause a prolonged QT interval.
What to do Initial treatment is with a beta-blocker, but an ICD implantable cardioverter defib- rillator must be considered. What to do There is enough evidence here from leads III and VF to justify percutaneous coro- nary intervention PCI or thrombolysis — which should, of course, be combined with pain relief and aspirin. In the absence of contra- indications, the patient should be given aspirin immediately, and then thrombolysis or percutaneous coronary intervention angioplasty as soon as possible.
In a patient with heart failure and a heart murmur the likely diagnosis is severe aortic valve disease. What to do The heart failure must be treated with diuretics, but it is essential to establish the cause of the left ventricular hypertrophy before selecting long-term treatment. It could be due to aortic stenosis or regurgitation, to mitral regurgitation or to hyper- tension.
While an angiotensin-converting enzyme inhibitor would be appropriate treatment for a patient with hypertension or mitral regurgitation, it would be poten- tially dangerous in a patient with aortic stenosis. An echocardiogram is the essential next step. This patient had severe aortic stenosis, and needed an aortic valve replacement.
Between attacks he was well, there were no physical abnormalities, and his ECG was normal. Eventually this ECG was recorded during one of his attacks.
What is the arrhythmia and what would you do? The ST segment depression in sinus rhythm is mild and not sufficient to make a confident diagnosis of ischaemia, but because the depression is horizontal, ischaemia seems likely.
What to do Patients who have only occasional episodes of an arrhythmia, and who are other- wise well, are always difficult to manage. This patient should certainly have an echocardiogram to exclude a cardiomyopathy, and an exercise test to investi- gate the possibility of ischaemia and exercise-induced arrhythmias.
At the age of 60 years, coronary angiography is probably indicated. Electrophysiological studies can be carried out to determine which antiarrhythmic agent to use in individual cases; however, in practice, amiodarone is just as effective as the agent selected by means of these studies. If the episodes were causing syncope, an implanted defibril- lator could be considered. What is the rhythm, and what is the underlying problem?
What to do A combination of the WPW syndrome and atrial fibrillation is very dangerous, because it can degenerate into ventricular fibrillation. The arrhythmia needs treating as an emergency, whatever the clinical state of the patient. It is important not to use drugs that may block the atrioventricular node and increase conduction through the accessory pathway, because this will increase the risk of ventricular fibrillation. Therefore, adenosine, digoxin, verapamil and lidocaine are contraindicated.
The drugs that slow conduction in the accessory pathway, and are therefore safe, are the beta-blockers, flecainide and amiodarone. Thereafter, an electrophysiological study to identify and ablate the accessory pathway is essential. What physical signs would you look for? However, there are no other features of left ventricular hypertrophy on this trace, which is fairly characteristic of hypertrophic cardiomyopathy. Myocardial infarction is uncommon in people of this age.
Hypertrophic cardiomyopathy is best diagnosed by echocardiography, which will show asymmetric septal hypertrophy, systolic anterior movement of the mitral valve apparatus, and sometimes early closure of the aortic valve. What to do This ECG should alert you to check the serum potassium level immediately: in this patient it was found to be 7. It settled rapidly with treatment of the diabetes. How would you proceed? This is quite common following a myocardial infarction, but in a healthy subject it is prob- ably of no significance.
What to do If the individual has no symptoms and the physical examination is normal, no further action is needed.
Accelerated idioventricular rhythm should not be treated. The history of anorexia and weight loss suggests digoxin toxicity, and the weakness could be due to hypokalaemia. The ECG supports this. Lead V6 shows digoxin effect, and coupled ventricular extrasystoles are a feature of digoxin toxicity. The flat T waves and prominent U waves suggest hypokalaemia. What to do Remember that hypokalaemia potentiates the effect of digoxin.
Therefore, stop the digoxin, check the electrolytes, and give oral potassium supplements. Do not give antiarrhythmic agents. Treat the heart failure with vasodilators. This woman improved dramatically when her digoxin dose was reduced and she was given oral potassium. Then she was prescribed an angiotensin-converting enzyme inhibitor and a reduced dose of diuretics. What is the probable cause of his angina, and what would you do? The lateral T wave inversion could indicate left ventricular hypertrophy or ischaemia, and this patient could have aortic stenosis or coronary disease.
In the absence of tall R waves, lateral ischaemia seems more likely than left ventricular hypertrophy, but it is often difficult to distinguish between these on the ECG. What to do Echocardiography will show whether the patient has significant aortic valve disease. Remember that anaemia can cause systolic murmurs and angina, though probably not this degree of T wave inversion.
The patient had coronary disease. What had happened? An alternative explanation, given the widespread changes, would be pericarditis. The second ECG is normal.
It occurs at rest, and the characteristic raised ST segments seen in the ECG are not reproduced by exertion. It has been shown by angiography during pain to be due to spasm of one or more coronary arteries. Relatively few patients with this type of angina have totally normal arteries, and spasm may occur at the site of atheromatous plaques. Coronary angiography is indicated. Nifedipine and nitrates may be helpful, but the condition is difficult to treat. What does his ECG show, and how would you treat him?
In favour of the former are the relatively wide QRS complexes and the fact that the R peak is greater than the R1 peak in lead V1 i. Against ventricular tachycardia are the right axis deviation and the differ- ent directions of the QRS complexes in the chest leads. What to do The problem is to decide whether the patient had a myocardial infarction compli- cated by ventricular tachycardia, or whether the arrhythmia is causing the anginal pain.
Detailed answers concentrate on the clinical interpretation of the results and give advice on what to do. The book can be used as a standalone method of practising ECG interpretation, and even with the most difficult ECGs a beginner will be able to make an accurate description of the trace and will be guided towards the key aspects of the interpretation.
Several of the cases incorporate chest X-rays and coronary angiograms illustrating the appearances that are associated with various cardiac conditions. We are always looking for ways to improve customer experience on Elsevier. We would like to ask you for a moment of your time to fill in a short questionnaire, at the end of your visit.