Chest Pain

Question 1

What is the presenting complaint

Answer 1

67 year old man with 2 hour history of severe chest pain

Question 2

What is a useful way to think of causes for chest pain

Answer 2

Visualise the anatomy of the region:
there could be pathology of the heart, aroma, lungs, pulmonary vessels, oesophagus, thoracic wall, thoracic muscles, thoracic nerves, or even upper areas of the stomach.

Question 3

What are some common causes of chest pain in patients who are over 60

Answer 3

Acute coronary syndrome 
Stable angina
 Pulmonary embolism (PE) 
Pleurisy (secondary to infection) 
Musculoskeletal 
† Oesophagitis hiatus hernia) (secondary to gastro-oesophageal reflux disease or Anxiety Oesophageal spasm
 Peptic ulcer disease 
Pneumothorax
 Myopericarditis Aortic dissection 
Aortic aneurysm 
Coronary spasm (e.g. secondary to cocaine) Boerhaave’s perforation of the oesophagus Cholecystitis

Question 4

Describe how we can categorise the differentials that may cause chest pain

Answer 4

Plumbing: Angina, Vasculitis

Pump; HF, Stenosis, HTN

Electrics; WPW, arryhtmias, fibrillation

Question 5

What symptoms may the patient display if there are plumbing issues

Answer 5

Heaviness, chest pain and SOB

Question 6

What symptoms may the patient display if there are pump issues

Answer 6

oedema, raised JVP, breathlessness

pattern of breathlessness important- may be Orthopnoea- leading to paroxysmal nocturnal dysponea- may need to sleep with multiple pillows.

Question 7

What symptoms may the patient display if there are electrical/conduction issues

Answer 7

Palpitations, SOB, syncope, pre-syncope

Question 8

What is pre-syncope

Answer 8

Presyncope occurs when a person almost but doesn’t actually lose consciousness, due to reduced flow of oxygenated blood to the brain.

Question 9

How would your differential change if the patient were a 20-year-old woman on the combined oral contraceptive pill?

Answer 9

A younger patient is less likely to be suffering from diseases of old age, such as: • Acute coronary syndrome • • • • Stable angina Myopericarditis (usually post-infarction) • Aortic dissection • • Aortic aneurysm

A younger female patient on the combined oral contraceptive pill is more likely to be suffering from: PE (the combined oral contraceptive pill is thrombogenic) Pneumothorax (especially if tall and thin) Cocaine-induced coronary spasm (still rare, but particularly unusual in the elderly!)

Question 10

When a patient arrives with chest pain, you need to be thinking about the conditions that present with chest pain that are potentially fatal and require immediate management.
Which diagnoses fall into this category? What features are going to alert you to these conditions?

Answer 10

The following diagnoses require immediate management and should be kept in mind:
• Acute coronary syndrome (unstable angina, or myocardial infarction (MI))
• Aortic dissection
• Pneumothorax
• PE
• Boerhaave’s perforation

Question 11

What is key in the history of acute coronary syndrome

Answer 11

History of sudden-onset, central crushing chest pain radiating to either/
both arms and neck, especially in someone with a previous history of angi- na on exertion or MI and/or cardiovascular risk factors (smoking, hyper- tension, hypercholesterolaemia, diabetes, family history).

Question 12

What are the key signs of acute coronary syndrome

Answer 12

Signs of hypercholesterolaemia: cholesterol deposits in small skin lumps on the tendons of the back of the hand or bony prominences like elbows (xanthomata), in creamy spots around the eyes (xanthelasma), or a creamy ring around the cornea (arcus). Note that arcus is a normal finding in the elderly.
− Signs of systemic atherosclerotic vascular disease: weak pulses, peripheral cyanosis, atrophic skin, ulcers, bruits on auscultation of carotids.
− Signs of anaemia. Anaemia can cause or exacerbate ischaemic heart dis- ease. You can look for the following signs of anaemia, and should do in an exam, but they are either unreliable or very rare in developed countries: conjunctival pallor (unreliable), glossitis, angular stomatitis, or koilonychia (all very rare).

Question 13

Describe signs of arrhythmia in acute coronary syndrome

Answer 13

− Signs of arrhythmia. If a patient has underlying ischaemic heart dis- ease and develops poor cardiac output due to an arrhythmia, it is likely that they will develop chest pain because their poorly perfused heart will become ischaemic. Thus, check for an irregularly irregular pulse (atrial fibrillation, atrial flutter with variable heart block, or frequent ectopics), a slow pulse (heart block), or a very fast pulse (atrial fibril- lation/flutter-induced tachycardia, re-entry tachycardias, ventricu- lar tachycardia). Also, atrial fibrillation is commonly due to previous ischaemic damage and therefore offers a clue as to what might be wrong with the patient.

Question 14

What are the key features of aortic dissection

Answer 14

− History of sudden-onset tearing chest pain radiating to the back.
− Absentpulseinonearm.
− Hypertension (in about 50% of cases) or hypotension (in about 25% of
cases).
− A difference in blood pressure between arms >20 mmHg (about a third of
cases).
− New-onset aortic regurgitation. This is caused by the new lumen tracking
down to the valve and making it incompetent.
− Pleural effusion, usually on the left. This is due to irritation of the pleura by
the dissecting aorta

Question 15

What is key in the history of pneumothorax

Answer 15

− History of sudden-onset pleuritic chest pain with breathlessness – but
beware, it may present as painless breathlessness.

Question 16

Describe the key signs of pneumothorax

Answer 16

A hyperinflated chest wall with impaired expansion. Normally the lack of
air in the pleural space creates a vacuum that holds the lungs to the chest wall. If air gets into the pleural space, unopposed elastic recoil of the chest wall will cause it to pop out, whilst at the same time the lungs will shrivel up. (Note this is different from lung collapse, in which a bronchus is obstructed and the air trapped distally in that segment is gradually absorbed into the blood.)
− Hyper-resonant percussion over the affected area.
− Absent breath sounds over the affected area. The crumpled up area of lung
will not have any air getting in or out.

Question 17

Describe a tension pneumothorax

Answer 17

Tracheal deviation. In tension pneumothorax, a flap of pleural membrane
acts as a valve so that the pleural space gets increasingly inflated with air. It eventually starts to deviate the mediastinum, and can compress the heart leading to cardiopulmonary arrest. Therefore, a trachea that deviates away from a suspected pneumothorax is an emergency requiring urgent inser- tion of a large-bore cannula in the mid-clavicular line just above the third rib to allow the air trapped in the pleural space to escape.

Question 18

What are the key features of PE

Answer 18

− Thisisadiagnosisofexclusionasitspresentationcanbeveryvariedandit
is therefore difficult to diagnose clinically.
− History of sudden-onset shortness of breath and/or haemoptysis and/or
pleuritic chest pain in someone with an inflamed limb and/or risk factors for blood clots (e.g. recent surgery, recent stasis, or hypercoagulable blood due to the oral contraceptive pill or malignancy).
162 Chest pain

                    − Signs of hypoxia. The patient may appear pale, have cold peripheries, feel lethargic and/or be drowsy or confused, depending on the degree of hypoxia. − Rightheartstrainevidencedbyaraisedjugularvenouspressure(JVP). − You should refer to the Wells’ criteria (see viva questions) for diagnosis of PE if you suspect this.

Question 19

What often causes PE

Answer 19

DVT

Question 20

What are the features of Boorhav’es perforation

Answer 20

Features of Boerhaave’s perforation: note that this is very rare, but it is asso- ciated with a high mortality and hence is included.
− History of sudden-onset severe chest pain immediately following an epi-
sode of vomiting. Shortness of breath and pleuritic pain may develop short-
ly afterwards due to subsequent pleurisy and effusion.
− Signs of a pleural effusion after some hours – dullness to percussion, absent
breath sounds, decreased vocal resonance.
− Subcutaneousemphysemaispresentinaminorityofcases.
− Abdominal rigidity, sweating, fever, tachycardia, and hypotension may be
present as the illness progresses but are non-specific.

Question 21

Bearing in mind the above, you take a history from Mr Shepherd. You find that he localizes the pain to his sternum. He says it came on 2 hours earlier in the afternoon as he was gardening and has been there since. He describes it as like ‘wearing a shirt two sizes too small’ and says it has not moved since it came on. The pain was not exacerbated by breathing, and was not position dependent. He does not have a cough but his pain improved minutes after he was given a glyceryl trinitrate (GTN) spray sublingually in the ambulance, going from 8/10 severity to 3/10 now.
He is a smoker with a 40-pack-year history, has hypertension that is managed with a calcium-channel blocker and hypercholesterolaemia for which he takes a statin. His father died of stroke in his 70s and his mother of ‘old age’ in her late 80s. He is not known to be diabetic.
On examination, Mr Shepherd appears relatively comfortable (on pain relief), with arcus but no other peripheral signs of cardiovascular disease. His pulse and blood pressure are taken in both arms and found to be equally regular, 84 bpm and 145/90 mmHg. His oxygen saturation is 98% on room air. Both heart sounds are audible with no added sounds and palpation of the chest does not bring on pain. Carotid bruits can be heard bilaterally on auscultation. His lungs have normal resonance to percussion, good air entry, and no abnormal sounds on auscultation. His trachea is central. His limbs show no signs of inflammation and he is not febrile.
In light of Mr Shepherd’s history, risk factors, and examination, a certain diagnosis for his chest pain appears increasingly likely.
What investigations would you like to request? Think particularly of how you can confirm your expected diagnosis and how you can rule out the ‘must exclude’ diagnoses listed above.

Answer 21

ECG
Blood tests (troponin, serum cholesterol, U&E, FBC, capillary glucose, inflammatory markers).
Erect chest radiograph
Second Line:
D-dimer levels

Question 22

Describe the ECG

Answer 22

Perform ECGs on anyone with suspected cardiac disease, either two ECGs 30 minutes apart or, if the patient has continuing chest pain, every 10–15 min- utes until the diagnosis is made. If the patient is admitted, ECGs should be performed daily for 3 days thereafter, as changes may take 24 hours or more to develop. In the context of chest pain, you are particularly looking for signs of ischaemia and arrhythmias (causing a drop in cardiac output and thus decreas- ing coronary perfusion). These signs are explained in detail in any guide to read- ing ECGs. Note that it is particularly important to look for signs of ST segment 9
elevation or new onset LBBB, as the management protocol for individuals with an ST elevation myocardial infarction (STEMI) differs from that for suspected non-ST elevation myocardial infarction (NSTEMI).

Question 23

Describe troponin

Answer 23

Troponin: this should be measured on admission and at 12 hours from the onset of pain. Troponin levels are extremely useful because of their high sensitivity and specificity for damage to cardiac muscle. The drawback is the minimum 8-hour delay in increased troponin levels. An alternative is CK-MB, an isotype of the enzyme creatinine kinase, which is released more rapidly following dam- age but which is less specific for cardiac damage. CK-MB levels fall back to normal within 2–3 days whereas troponin levels remain high for >7 days. Thus, CK-MB levels that are elevated >4 days after an MI suggest that there has been a re-infarction. Note: troponin levels are specific for cardiac damage but not 100% specific for acute coronary syndrome – you need to consider the context. Other conditions causing a raised troponin include: coronary artery spasm (e.g. from cocaine) or aortic dissection causing ischaemia, myopericarditis, severe heart failure, cardiac trauma from surgery or road traffic accident, and PE.

Question 24

Describe serum cholesterol

Answer 24

Serum cholesterol: hypercholesterolaemia is another risk factor for cardio- vascular disease that is often undiagnosed and that can be treated. It is worth noting that an MI will result in a decrease in total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) within about 24 hours of the infarct, and that levels will not return to normal (for that patient) for 2–3 months post-infarct. Thus, cholesterol levels should be measured as soon as possible if they are to guide future therapy.

Question 25

Describe FBC, U&Es, inflammatory markers and capillary glucose

Answer 25

Full blood count (FBC): anaemia from any cause is common and will exacer- bate any deficiency in cardiac perfusion, resulting in ischaemic heart disease. • Urea and electrolytes (U&Es): pay particular attention to the potassium, as this may be the cause of an arrhythmia. • Inflammatory markers: C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and the white cell count (WCC) from the FBC are all measures of inflammation. Accordingly these are elevated in inflammatory processes such as pericarditis and Bornholm’s disease (inflammation of intercostal muscles due to Coxsackie B virus infection), but will also be elevated following aortic dissection and MI, which cause inflammation of the affected tissues. • Capillary glucose: there is a significant increase in the risk of cardiovascular disease with diabetes mellitus, particularly if untreated. Type 2 diabetics typi- cally suffer from the complications of diabetes prior to becoming symptomatic for the diabetes itself, and as many as 50% may be undiagnosed. Critically, diabetics are more likely to present with ‘silent infarcts’ – that is, an MI in the absence of chest pain.

Question 26

Describe the erect chest radiograph

Answer 26

Erect chest radiograph: this should be done to help exclude a pneumothorax and aortic pathology (aneurysm or dissection, giving a wide mediastinum). Note that it is possible to have a normal chest radiograph in aortic dissection. If Boerhaave’s perfora- tion of the oesophagus is suspected, a chest radiograph will typically show air around the heart shadow (pneumomediastinum), a pleural effusion, and/or a pneumothorax.

Question 27

Describe D dimer levels

Answer 27

D-dimer levels: elevated D-dimers are simply symptomatic of breakdown of a fibrin clot due to any cause such as recent surgery or trauma, and are therefore not diag- nostic of DVT or PE specifically. However, low D-dimer levels can help rule out a DVT or PE as these are unlikely to occur without any fibrin breaking down. These are not done as standard in chest pain but to exclude PE.

Question 28

What does the ECG show

Answer 28

Mr Shepherd’s ECG shows ST depression and prominent R waves in V –V but 13 no signs of ST elevation.

Question 29

He begins to complain of pain once the analgesia wears off. His troponin is 6 ng/mL on admission, (normal range given by the lab <0.4 ng/mL). His chest radiograph is normal. In light of the history, examination, and investigations, what is the diagnosis? How else might this condition present?

Answer 29

Mr Shepherd is a 40-pack-year smoker with hypertension and hypercholestero- laemia who has presented with central crushing chest pain. This picture is typical for MI. He has elevation of cardiac troponin levels, suggesting MI. His ECG shows ST depression in leads V –V which would be consistent with an 13 anterior NSTEMI. Remember that transmural infarctions normally result in ST elevation on an ECG and are hence referred to as ST elevation myocardial infrac- tions (STEMIs). However, in the case of posterior wall transmural infarctions, the fact that the ECG chest leads are on the opposite side of the chest wall results in ST Thus, this could also represent a posterior infarct, which are treated like STEMIs despite the lack of ST elevation.

Question 30

Describe how MIs can often present differently

Answer 30

MIs present in many different ways and you should have a low threshold for suspect- ing it in anyone with cardiac risk factors. Ultimately, diagnosis depends on an elevated 12-hour troponin. Chest pain is not always a feature, particularly in the elderly and long-standing diabetics who frequently have neuropathy and dulled pain sensation. ECG readings are also non-diagnostic, as changes may not be present in infarction.

Question 31

What features of the history, clinical examination, and investigations helped you rule out your other ‘must exclude’ diagnoses?

Answer 31

* Aortic dissection? Mr Shepherd’s pain was not tearing and did not radiate to his back. His pulse and blood pressure were equal in both arms and chest radiography did not suggest a wide mediastinum. Ultimately, the way to rule out aortic dissection if you strongly suspect it is to do CT angiography of the chest or transoesophageal echo, looking for a false lumen. * Pneumothorax? Mr Shepherd did not have areas of the chest that were expanded and hyper-resonant, with decreased air entry. His trachea was not displaced and his chest radiograph is normal. * PE? Remember that this is a diagnosis of exclusion, so you have not strictly speaking ruled it out. However, the normal oxygen saturations (98% on room air), the ST depression on ECG, and the large rise in troponin make this unlikely (a small rise in troponin may be seen in PE). A D-dimer level was not requested but may in any case have been raised as a result of his infarction. * Boerhaave’s perforation of the oesophagus? Mr Shepherd did not give a his- tory of vomiting before the onset of his pain. A perforated oesophagus is a very rare diagnosis and even less likely without previous vomiting. Ultimately, the way to rule it out if you strongly suspect it is to perform a chest radiograph after swallowing a water-soluble contrast agent such as gastrograffin.

Question 32

How will the medical team manage Mr Shepherd acutely?

Answer 32

Having assessed the need for resuscitation (airways, breathing, and circulation, ABC), you should consider Mr Shepherd’s immediate management. Given that your differential includes life-threatening conditions, treatment should be started in tan- dem with your diagnostic screen. The longer-term management should consider secondary prevention of further cardiovascular events. Acutely, all patients with any acute coronary syndrome (STEMI, posterior inf- arcts, NSTEMI, unstable angina) are started on a cocktail of drugs that can be remembered by the mnemonic MONABASH: Morphine, for analgesia, and an anti-emetic such as metoclopramide (although there is some evidence that for patients with no gastrointestinal (GI) distur- bance there is no benefit in giving an anti-emetic) O xygen 166 Chest pain depression in leads V –V rather than ST elevation. Thus, this could also represent a 13 posterior infarct, which are treated like STEMIs despite the lack of ST elevation. What features of the history, clinical examination, and investigations helped you rule out your other ‘must exclude’ diagnoses? How will the medical team manage Mr Shepherd acutely? How does the management differ between full-thickness infarcts (STEMI and posterior infarcts) and partial-thickness infarcts (NSTEMI)? N itrates (e.g. GTN, isosorbide mononitrate infusion), for vasodilation Antiplatelets: aspirin, clopidogrel, and glycoprotein IIb/IIIa antagonists, to prevent further coronary thrombosis B eta-blockers, to reduce myocardial oxygen demand. These are contraindicated if the patient is in heart block, has asthma, or has any signs of acute heart failure ACE inhibitors, for multiple reasons including attenuation of post-infarct ventricular remodelling that can cause arrhythmias, reduction of angiotensin II-induced vasoconstriction improving cardiac blood flow and reducing after- load, and beneficial effects on endothelial function Statins, which in addition to reducing cholesterol levels are thought to improve endothelial function, modulate inflammatory responses (e.g. reduce CRP), maintain atherosclerotic plaque stability, and prevent thrombus formation; there is evidence to support their use in the acute setting Heparin (low-molecular weight heparin, LMWH), to prevent coronary thrombosis

Question 33

How does the management differ between full-thickness infarcts (STEMI and posterior infarcts) and partial-thickness infarcts (NSTEMI)?

Answer 33

``` STEMI patients (including posterior infarcts) should also receive either primary angioplasty or thrombolysis within 12 hours of the onset of pain, the sooner the better, and ideally within 2 hours of the onset of symptoms. Thrombolysis carries significant risks and therefore there are clear indications and contraindications with which you should familiarize yourself before referring a patient for thrombolysis. Angioplasty is superior to thrombolysis if both are equally available, but rapid treat- ment is even more important so you should not delay thrombolysis if angioplasty is not likely to be achieved within 2 hours of the onset of the symptoms. NSTEMI patients do not receive thrombolysis, as this does not appear to be effec- tive in them. However, NSTEMI patients are candidates for early angioplasty if their TIMI risk score is ≥3 (see Table 9.1): ```

Question 34

Describe the TIMI score for unstable angina

Answer 34

Table 9.1 TIMI score for NSTEMI unstable angina ≥3 risk factors for coronary artery disease Aspirin use in the last 7 days Raised cardiac markers (e.g. troponins) 1 point 1 point 1 point

Question 35

Mr Shepherd’s consultant decided that the prominent R waves on the ECG were more likely to represent a posterior infarct than an anterior NSTEMI. A right-sided ECG confirmed this and Mr Shepherd received primary angioplasty. What advice and medications should Mr Shepherd be discharged on?

Answer 35

Secondary prevention is important in patients with ischaemic heart disease. Mr Shepherd should be given the following advice and medication (lifelong): • Lifestyle changes: smoking cessation, low-salt diet, exercise, and weight loss. • Risk factor control with medications: − Blood pressure control: ACE inhibitors if the patient is <55 years and Caucasian, calcium-channel blockers or diuretic thiazides if the patient is >55 years or non-Caucasian. A mixture of these three classes of drug may be prescribed if the blood pressure cannot be controlled with one drug alone. − Cholesterol reduction: statins, or fibrates if statins are contraindicated. − Diabetic control: tight sugar control is important for cardiovascular risk, although far less important than blood pressure control in diabetics as shown by the United Kingdom Prospective Diabetes Study (UKPDS) trial. • Reduced thromboembolic risk: low-dose aspirin for life and clopidogrel for a period of 1 year. If there is severe left ventricular dysfunction, i.e. an ejection fraction <30% on echocardiogram, there is an increased risk of ventricular arrhythmias and death. Such patients are therefore candidates for implantable cardioversion devices (ICD), which detect the onset of ventricular arrhythmias and shock the heart to stop the arrhythmia.

Question 36

Mr Shepherd undergoes angioplasty to an occluded circumflex artery and is discharged. Four weeks later he presents again with chest pain. However, he says it is different from his previous pain. This time it radiates to his left shoulder, is worse on deep inspiration, and is aggravated by lying down. You note that he has a fever. What are the complications of an MI, and what has probably happened to Mr Shepherd? How should Mr Shepherd be managed on this admission?

Answer 36

Given the timing, fever, and pleuritic and positional aspects of the pain, Mr Shep- herd has most likely presented with Dressler’s syndrome. As in the management of any patient, you should first assess Mr Shepherd’s need for resuscitation (ABC), then confirm his diagnosis. A FBC will show leucocytosis and an ECG may show diffuse saddle-shaped ST elevation across a number of leads without reciprocal ST depression, and may also show PR depression. An echocar- diogram may show a pericardial effusion; this may also be visible on chest radio- graph. The ECG and chest radiograph will additionally help exclude a re-infarction or pulmonary pathology, respectively. Twelve-hour troponin levels should also be measured on this admission for the same reason. Having ordered the relevant investigations, Mr Shepherd should immediately be started on analgesia. Large doses of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) may be given and are usually sufficient. If there is a significant effu- sion, it can be aspirated (pericardiocentesis) to relieve pressure on the heart.

Question 37

What are the most common post-MI complications

Answer 37

The common complications of MI are covered in the mnemonic DARTH VADER: Death (probably not a complication to mention if asked!) Arrhythmia Rupture (either of the septum or the outer walls) Tamponade Heart failure Valve disease Aneurysm Dressler’s syndrome (autoimmune pericarditis 2–10 weeks after MI; note that simple post-MI pericarditis is more common than Dressler’s syndrome, pre- senting within 2–4 days) Embolism Re-infarction

Question 38

Mrs Thompson is a 62-year-old woman with known angina who has been referred by her GP following increasing frequency in her episodes of chest tightness. She says she usually suffers from angina two or three times a month, but that over the last 2 months her attacks have become more frequent. Some of these episodes are now occurring at rest, often following meals. They are partly alleviated by the GTN spray she has been using for her angina. She is a heavy smoker, blood pressure 163/94 mmHg, and cholesterol 6.5 mM. She had an angiogram 2 years earlier showing mild stenosis of the left circumflex artery. Her other medical history includes reflux disease, but no other conditions. Notably she has no history of gallstone disease and reports no change in stool or urine. On admission her examination and investigations are normal, including the ECG, 12-hour troponin levels, and temperature. The team has a high suspicion of a worsening of her angina and perform a repeat angiography, which is unchanged from her previous angiogram. What diagnoses should you be considering? Which investigations will help you determine the correct one?

Answer 38

Attacks of chest pain of increasing frequency and at rest should trigger alarm bells for the progression of her angina from stable to unstable. At the same time, the fact that her angiogram is unchanged should arouse your suspicion of another diagno- sis. The insidious course rules out acute conditions such as infarction or pericarditis. The important diagnoses to exclude are oesophageal spasm, cholecystitis, and acute pancreatitis. Both oesophageal spasm and cholecystitis are consistent with the his- tory of pain after meals, although a lack of known gallstone disease, unchanged urine and stool, and apyrexia argue against cholecystitis. Oesophageal spasm may be detected by barium swallow and oesophageal man- ometry, although a normal result does not exclude it. Ultimately the diagnosis may come down to a therapeutic trial. Mrs Thompson was prescribed a proton-pump inhibitor for presumptive oesophageal spasm secondary to reflux. She responded positively, confirming the diagnosis. If all else had been excluded, you may have considered a diagnosis of coronary artery spasm (sometimes called variant or Prinzmetal angina) or coronary syn- drome X. These are diagnoses of exclusion; they are extremely hard to demonstrate and are, in any case, rare in the absence of underlying coronary artery disease. It is best to avoid such ‘dustbin diagnoses’ until all other causes have been excluded.

Question 39

Mr Heyward is a 38-year-old man with increasingly severe chest pain that began during an evening in the pub. The pain has not radiated, and was not alleviated by GTN administered in the ambulance. He has a strong family history with both his father and brother suffering heart attacks in their fifties, and is a heavy smoker with a 50 pack year history. He is not known to have diabetes, hypertension, or high cholesterol. He has no other significant medical history, although you note that he had what sounds like a viral upper respiratory tract infection 3–4 days ago. On examination of his cardiovascular system you find no abnormalities. An ECG taken at the hospital is shown in Fig. 9.2. His other investigations were normal apart from mildly elevated inflammatory markers. What does the ECG show? What is the most likely diagnosis?

Answer 39

The ECG shows ST elevation in leads I, II, aVL, V –V , i.e. throughout most leads, 15 and slight PR segment depression. Acute coronary syndromes typically respond to vasodilators such as GTN. In addition, MI causes ECG changes which are reciprocal (i.e. ST elevation in some leads, ST depression in opposite anatomical leads). This is therefore unlikely to be an acute coronary syndrome, although troponin levels 12 hours after the onset of pain should be checked for confirmation. Pericarditis is the most likely diagnosis despite the atypical sounding pain and lack of a pericardial friction rub, which can be intermittent. A therapeutic trial of NSAIDs was prescribed which diminished the pain. The patient was treated with analgesia as an inpatient for a few days and was discharged once pain free. 9

Question 40

Mr Bromley is a 28-year-old, tall, thin man with a sudden onset of severe chest pain. He has recently been on a flight from Egypt and had knee surgery 1 month ago. Otherwise he says he has been fit and well, with no previous medical history. He is not known to have Marfan’s syndrome, although it has not been investigated, and there is no family history of note. He is a non-smoker with no risk factors for cardio- vascular disease. On examination he is pale, sweaty, and breathless. His pulse is weak and thready, but otherwise his examination is normal. What diagnoses are most likely? Which first-line investigations will help you determine the correct one?

Answer 40

In a tall, thin, young individual you should immediately be thinking of pneumo- thorax or Marfan’s syndrome predisposing to a dissected aortic aneurysm or aor- tic dissection. His recent air travel, although only a short trip, and surgery should alert you to the possibility of a PE. All of these conditions are associated with high mortality and so you must act fast. In your assessment of his ABC you should pay particular attention to his blood pressure – patients with an aortic aneurysm are often hypertensive but can become hypotensive if they dissect back into the peri- cardial space and develop cardiac tamponade (along with muffled heart sounds and distended neck veins). If they rupture into the chest cavity they tend to exsanguinate before they make it to hospital. An urgent chest radiograph will rule out a pneu- mothorax (although you should have detected this when palpating, percussing, and auscultating his chest) and will show a widened mediastinum in most cases of aortic dissection (~80%). PE is a diagnosis of exclusion, although CT pulmonary angiogra- phy (CTPA) can be helpful in making the diagnosis. Mr Bromley was hypotensive (80/46) but there was no difference in the blood pressure in each arm. His chest radiograph suggested a widened mediastinum. As he was not haemodynamically stable it was felt he should not undergo a CT and a transoesophageal echocardiogram was ordered at the bedside. This showed an aortic dissection near the aortic root and a pericardial effusion. Any dissection involving the ascending aorta, such as this one, is classed as a Stanford type A and is a surgical emergency. Dissections of the descending aorta, with no involvement of the ascending aorta, are called type B and are managed medically. However, surgery in type B is indicated if medical treatment fails and complications develop.

Question 41

Mr Perkins is a 32-year-old investment banker who presents with chest pain. It came on while he was at a party in a bar with friends. He has a family history of cardiovascular disease but no other cardiovas- cular risk factors. He is normally fit and well, although he says he has had a cold and fever for the past couple of days. His ECG shows >2 mm ST elevation in leads V –V and scheduled for angiogram- no coronary aftery occlusion What is the most likely diagnosis? Which question(s) in particular should you ask on the history?

Answer 41

Chest pain and fever suggest an acute inflammation due to, for example, myo- carditis/pericarditis but the ECG does not support this (it would classically show saddle-shaped ST elevation in a number of leads not conforming to the territory of a single coronary artery). Normal angiography ruled out coronary artery disease. The most likely diagnosis is coronary spasm due to cocaine usage. You should specifi- cally ask about recreational drugs in order to investigate this possibility.

Question 42

Mr Daniels is a 52-year-old man who presents to A&E with a 4-hour history of chest pain associated with nausea and vomiting. His cardiac risk factors include a 15-pack-year history of smoking, although he quit 10 years ago, and a father and brother who had heart attacks in their fifties. He has no other medi- cal history of note and reports no symptoms of reflux disease, but drinks 20 units of alcohol a week. On examination he appears uncomfortable and dyspnoeic. The rest of his examination is unremarkable except for mild consolidation at his left lung base. His ECG and troponin on admission are normal. A chest radiograph confirms a small effusion on the left. What are the most likely diagnoses? If his 12-hour troponin levels are normal, does this change your differential? What complications should you be particularly wary of?

Answer 42

Nausea and vomiting are commonly associated with inferior MIs. However, the small unilateral pleural effusion should alert you to the possibility of Boerhaave’s syndrome – a perforation in the oesophagus. This was indeed the case with this patient, whose 12-hour troponin levels proved to be normal. Note that the vomiting should precede the onset of pain in Boerhaave’s: contrast this with MI (pain pre- cedes vomiting), as it is the vomiting that causes the perforation (whereas in infarc- tion, it is the post-infarct inflammation that irritates the diaphragm). Not unusually, this patient was not a particularly good historian and could not recall which came first. Patients with Boerhaave’s are prone to develop a pleural effusion, pneumomedi- astinum and/or pneumothorax, perhaps followed by infection with gastrointestinal flora (mediastinitis and sepsis). Treatment consists of prompt antibiotic therapy and surgical repair of the oesophagus with mediastinal washout. Prognosis is grim, with a 30% mortality if surgical intervention is initiated within 24 hours, rising to 50–65% if surgery is delayed beyond 24 hours. Whilst it is a rare diagnosis it is important to be aware of it as early diagnosis is critical in increasing the chances of survival.

Question 43

Nausea and vomiting are commonly associated with inferior MIs. However, the small unilateral pleural effusion should alert you to the possibility of Boerhaave’s syndrome – a perforation in the oesophagus. This was indeed the case with this patient, whose 12-hour troponin levels proved to be normal. Note that the vomiting should precede the onset of pain in Boerhaave’s: contrast this with MI (pain pre- cedes vomiting), as it is the vomiting that causes the perforation (whereas in infarc- tion, it is the post-infarct inflammation that irritates the diaphragm). Not unusually, this patient was not a particularly good historian and could not recall which came first. Patients with Boerhaave’s are prone to develop a pleural effusion, pneumomedi- astinum and/or pneumothorax, perhaps followed by infection with gastrointestinal flora (mediastinitis and sepsis). Treatment consists of prompt antibiotic therapy and surgical repair of the oesophagus with mediastinal washout. Prognosis is grim, with a 30% mortality if surgical intervention is initiated within 24 hours, rising to 50–65% if surgery is delayed beyond 24 hours. Whilst it is a rare diagnosis it is important to be aware of it as early diagnosis is critical in increasing the chances of survival.

Answer 43

Mrs Peacock is presenting with an episode of chest pain and breathlessness, on a background of cardiovascular risk factors. Left heart failure secondary to myocar- dial ischaemia is a possibility, particularly given her risk factors (atrial fibrillation and recent stroke), with the breathlessness due to pulmonary oedema. However, if that were the case you would expect bibasal crackles on auscultation of her lungs. The chest radiograph, ECG, and troponin levels also fail to show signs of left heart failure or myocardial ischaemia. Her recent surgery and reduced mobility following her stroke are both risk factors for a PE, which would explain her breathlessness and reduced oxygen saturation. PE is a diagnosis of exclusion. However, the advent of CTPA has made it possible to see the embolus in a large number of cases. Mrs Peacock was indeed sent for CTPA and found to have multiple small clots in both lungs. She was started on low-molecular- weight heparin and made a good recovery. 9

Question 44

Why do some but not all patients with acute MIs get nausea and vomiting?

Answer 44

This is called the Betzhold–Jarisch reflex. Infarction of the inferior myocardium irritates the diaphragm, result- ing in vomiting. It is not uncommon for this to happen during angiography (and worth warning patients under- going angiography about!). Patients with infarcts in other territories will not irritate their diaphragm.

Question 45

How might occlusion of the different coronary vessels be distinguished on ECG?

Answer 45

Figure 9.3 Electrocardiogram (ECG) showing the coronary artery territories. The ‘Anterior/Septal leads’ correspond to the portion of the heart supplied by the left anterior descending artery. The ‘Right inferior leads’ correspond to the portion of the heart supplied by the right coronary artery. The ‘Left lateral leads’ correspond to the lateral wall of the left ventricle, supplied by both the left anterior descending and the circumflex arteries. • Anterior infarct: ST elevation in leads V2, V3, and V4 indicates infarction of the anterior surface of the left ventricle, supplied by the left anterior descending artery (LAD). • Right/inferior infarct: ST elevation in leads II, III, and aVF indicates infarction of the inferior surface, supplied by the right coronary artery (RCA). • Lateral infarct: ST elevation in leads V5 and V6 indicates infarction of the lateral surface of the left ventricle and may be involved in a circumflex (Cx) or LAD lesion. • Posterior infarct: ST depression in V –V with tall R waves is indicative of circumflex occlusion, i.e. a true 13 posterior infarct. This can be difficult to distinguish from LAD territory ischaemia: look particularly for a dominant R wave in V1 and inferior lead ST elevation in infarction.

Question 46

What are the earliest biochemical changes in MI? Why do we use troponin levels if they are only reliable after 8 hours?

Answer 46

Troponin levels are used because they have a very high specificity and sensitivity for cardiac damage. Other biochemical markers rise earlier, specifically myoglobin and CK-MB, one of the isomers of the enzyme creati- nine kinase. However, these are far less specific for cardiac damage.

Question 47

Compare the mechanism of action of aspirin, clopidogrel, and abciximab/tirofiban.

Answer 47

All of these are antiplatelet agents with different mechanisms of action: • Aspirin is an irreversible inhibitor of the enzyme cyclooxygenase (COX), which synthesizes inflamma- tory mediators including the platelet aggregator thromboxane A2. Platelets have no nuclei so cannot synthesize new COX enzymes to compensate for this irreversible inhibition. Aspirin’s action is reversed on synthesis of new platelets. • Clopidogrel irreversibly blocks the adenosine diphosphate (ADP) receptor on platelet cell membranes that prevents them binding to fibrinogen and hence inhibits platelet aggregation. • Abciximab and tirofiban reversibly block fibrinogen binding to the glycoprotein IIb/IIIa receptors on plate- let cell membranes that mediate platelet aggregation (abciximab is a monoclonal antibody, tirofiban a small molecule).

Question 48

A patient attends A&E with central crushing chest pain. Investigations reveal a normal ECG and normal troponins. All other investigations and examinations are normal, and a presumptive diagnosis of new-onset angina is made. What investigations should you request for a patient such as this presenting with new onset angina?

Answer 48

Exercise tolerance test. An exercise tolerance test may be performed to investigate the possibility of coronary artery disease and therefore the potential benefit to be derived from angioplasty. A patient’s ECG and blood pressure are monitored during increasing amounts of exercise (e.g. on a treadmill). ST depression of ≥2 mm, typical symptoms of exertional angina, or ST elevation ≥1 mm usually indicate stenosis of the coro- nary arteries. A fall in blood pressure during the test is a poor prognostic sign. It is worth noting that this test only has an 80% sensitivity and 70% specificity for detecting ischaemic heart disease (i.e. 30% of positive results will be false positives). Stress echocardiogram. Some patients cannot perform an exercise tolerance test, for example due to an inability to walk from severe arthritis, severe peripheral vascular disease, or COPD. In these cases a stress echocardiogram can be conducted. The patient is given dobutamine to simulate ‘stress’ while their cardiac function is assessed by echocardiogram. A normal heart shows increased motility when stressed, whereas ischaemic myocardium is hypokinetic. Myoview scan. This is an alternative to the tests above and provides a way of looking directly at blood flow within the heart muscle either during exercise (e.g. on an exercise bike) or under medically induced stress. Patients are injected with a radioactive contrast agent (thallium) and a picture taken with a gamma camera Pictures at rest and immediately after exercise/stress are compared. Areas of the myocardium with good perfusion appear as ‘warm’ spots on the scan. Angiography/angioplasty. If any of the tests above are positive, the patient is suitable for angiography to identify if there is stenosis of a coronary artery. If significant coronary artery disease were found, most centres would undertake coronary angioplasty.

Question 49

What ECG abnormalities would you expect in a patient who suffered a full thickness inferior MI 2 years previously? What is the basis for these changes?

Answer 49

Old infarcts are visible on ECGs as the infarcted tissue no longer conducts electrical impulses. If they are full thickness, they can be thought of as a window. Thus an electrode positioned next to an area of full- thickness infarct will look through the window of infarcted tissue and pick up the electrical impulses passing through the myocardium on the other side of the heart. This is evident in the ECG in the form of deep, so-called pathological, Q waves (>2 mm deep).

Question 50

Describe the progression of ECG changes you would expect to see over 7 days in a patient presenting with acute STEMI.

Answer 50

Classically you see the following changes: 1) Tented T waves in the affected leads within minutes of the occlusion (due to localized hyperkalaemia following myocyte ischaemia) 2) ST elevation in the affected leads with ST depression in the reciprocal leads, lasting 24–48 hours 3) T wave inversion, developing in 1–2 days and persisting for weeks or months 4) Q waves, developing within days and remaining permanently.