Blackboard Chest Pain EMQs Flashcards
A 73 year old banker complains of chest pressure which comes on predictably on exertion. It is relieved when he sits down and rests.
What is the diagnosis?
- Variant angina
- Unstable angina
- MI
- GORD
- Syndrome X
- Decubitus angina
- Pericarditis
- Aortic dissection
- PE
- Pneumothorax
- Herpes-Zoster virus
- Anxiety disorder
- Stable angina
- Stable angina
This patient has presented with stable angina. Resting ECG is often normal and the patient is asymptomatic. However during exercise stress ECG (most often the Bruce Protocol) there will be ST segment depression during exercise indicative of ischaemia and the patient will complain of chest pain. Those unable to exercise to an adequate level may need stress myocardial perfusion imaging or stress echocardiography. 1st line treatment involves lifestyle changes and antiplatelet therapy with aspirin. Anti-anginal theray will also be given, first line being beta-blockade. Statin therapy, blood sugar control in diabetics and BP control with antihypertensives may also be necessary. Those with LMS disease, 3 vessel disease or a reduced EF may benefit from CABG. Single vessel disease may benefit from PCI.
A 55 year old man is admitted to A&E with chest pain which is central in origin and came on while he was waiting for his bus. Troponin and CK-MB are not elevated.
What is the diagnosis?
- Variant angina
- Unstable angina
- MI
- GORD
- Syndrome X
- Decubitus angina
- Pericarditis
- Aortic dissection
- PE
- Pneumothorax
- Herpes-Zoster virus
- Anxiety disorder
- Stable angina
- Unstable angina
This is UA characterised by chest pain at rest. ECG will typically show ST depression and T wave inversion. Acute management includes antiplatelets and antithrombotics to reduce damage and complications. Long term management aims at reducing risk factors. Key risk factors include obesity, hypertension, smoking, hyperlipidaemia, FH, DM and positive FH. People with diabetes may again present with atypical symptoms. Cardiac biomarkers will not be elevated although in a patient who has had an acute MI days earlier, troponin may remain elevated (remains elevated up to 10-14 days after release). All patients with presumed cardiac chest pain should in the first instance get oxygen, morphine and GTN with antiplatelet therapy in the absence of contraindications.
A 59 year old woman complains of chest pain. ECG shows ST segment depression. However, a subsequent coronary angiogram is normal.
What is the diagnosis?
- Variant angina
- Unstable angina
- MI
- GORD
- Syndrome X
- Decubitus angina
- Pericarditis
- Aortic dissection
- PE
- Pneumothorax
- Herpes-Zoster virus
- Anxiety disorder
- Stable angina
- Syndrome X
This is cardiac syndrome X, not to be confused with the metabolic syndrome. Here, there is chest pain with usual ST segment changes associated with coronary artery disease but with normal coronary arteries. It is treated with calcium channel blockers such as nifedipine.
A 57 year old female complains of chest pain which occurs at rest. ECG performed on A&E admission shows ST elevation but a subsequent angiogram with a provocative agent shows an exaggerated spasm of the coronary arteries.
What is the diagnosis?
- Variant angina
- Unstable angina
- MI
- GORD
- Syndrome X
- Decubitus angina
- Pericarditis
- Aortic dissection
- PE
- Pneumothorax
- Herpes-Zoster virus
- Anxiety disorder
- Stable angina
- Variant angina
Variant angina (Prinzmetal) is angina caused by coronary artery vasospasm rather than atherosclerosis. It occurs at rest and in cycles. Many patients will also have some degree of atherosclerosis although not in proportion to the severity of the chest pain experienced. ECG changes are of ST elevation (rather than depression) when the patient is experiencing an attack and a stress ECG will be negative. Patients with Prinzmetal angina are often treated for ACS and indeed, cardiac biomarkers may be raised as vasospasm can cause damage to the myocardium. The gold standard investigation is with coronary angiography and the injection of agents to try to provoke a spasm.
A 44 year old female complains of a two week history of tight chest pain which occurs when he is lying down.
What is the diagnosis?
- Variant angina
- Unstable angina
- MI
- GORD
- Syndrome X
- Decubitus angina
- Pericarditis
- Aortic dissection
- PE
- Pneumothorax
- Herpes-Zoster virus
- Anxiety disorder
- Stable angina
- Decubitus angina
This patient has chest pain which occurs on lying down, which is decubitus angina by definition.
An overweight 63 year old male with a history of hypertension presents with cardiac sounding chest pain while watching TV. However, his cardiac biomarkers are not elevated. An ECG is ordered which shows ST depression and T wave inversion.
What is the diagnosis?
- Variant angina
- Unstable angina
- MI
- GORD
- Syndrome X
- Decubitus angina
- Pericarditis
- Aortic dissection
- PE
- Pneumothorax
- Herpes-Zoster virus
- Anxiety disorder
- Stable angina
- Unstable angina
This drug lowers heart rate, cardiac output and mean arterial blood pressure during exercise. It can also be used for migraine prophylaxis and glaucoma. This drug also causes a decrease in endogenous renin release.
Name the drug
- Alpha-1 agonist
- Alpha-2 agonist
- Beta-1 agonist
- Beta-2 agonist
- Adrenaline
- Beta blocker
- Calcium channel blocker
- ACEi
- Spironolactone
- GTN
- Loop diuretics
- Thiazide diuretics
- Beta blocker
Beta blockers lower heart rate, CO and MABP during exercise. They indeed also act to reduce renin release as well as the release of NA. Their use ranges from migraine prophylaxis, anxiety and hypertension to thyrotoxicosis, post-MI and chronic heart failure. They are also useful in arrhythmias where they act to increase the refractory period of the AVN.
This drug is a vasoconstrictor which can be used as a nasal decongestant. It is also mydriatic when used as an eye drop.
Name the drug
- Alpha-1 agonist
- Alpha-2 agonist
- Beta-1 agonist
- Beta-2 agonist
- Adrenaline
- Beta blocker
- Calcium channel blocker
- ACEi
- Spironolactone
- GTN
- Loop diuretics
- Thiazide diuretics
- Alpha-1 agonist
Alpha 1 agonists such as phenylephrine are vasoconstrictors and also have a use as a mydriatic. They are used as nasal decongestants as a result of their vasoconstrictor effect.
This drug leads to the release of NO to reduce venous return to the heart. Chronic use can lead to tolerance.
Name the drug
- Alpha-1 agonist
- Alpha-2 agonist
- Beta-1 agonist
- Beta-2 agonist
- Adrenaline
- Beta blocker
- Calcium channel blocker
- ACEi
- Spironolactone
- GTN
- Loop diuretics
- Thiazide diuretics
- GTN
GTN is glyceryl trinitrate, which leads to NO release. This causes vasodilation and a reduction in venous return to the heart, which decreases cardiac work load. This reduces preload (ventricular return) and afterload (peripheral vascular resistance). It is also weakly antiplatelet and has a weak direct action to vasodilate the coronary arteries. It is often also used sublingually for rapid relief of angina. Chronic use can indeed lead to tolerance and as such an eccentric regime is recommended.
This drug leads to arterial vasodilation by action on vascular smooth muscle cells. It can lead to unwanted ankle oedema, headache, hypotension and palpitations.
Name the drug
- Alpha-1 agonist
- Alpha-2 agonist
- Beta-1 agonist
- Beta-2 agonist
- Adrenaline
- Beta blocker
- Calcium channel blocker
- ACEi
- Spironolactone
- GTN
- Loop diuretics
- Thiazide diuretics
- Calcium channel blocker
This describes the action of a non-rate slowing dihydropyridine calcium channel blocker such as amlodipine. These act by inhibiting the opening of L-type calcium channels, inhibiting entry of calcium ions into VSMCs. This causes arterial vasodilation. These drugs are used for hypertension and angina and unwanted effects include those listed. The palpitations a patient may experience are due to reflex tachycardia from arterial vasodilation. Note also that rate-slowing calcium channel blockers also exist such as verapamil and diltiazem and uses for these also include arrhythmias such as paroxysmal SVT and AF.
A 72 year old male, in hospital post MI complains of dyspnoea and collapse four days later. He appears pale and his right leg is swollen compared to the left. Apex not displaced. No mumurs. Pulse 128 BP 100/55 temp37. JVP elevated. Bibasal crackles.
What is the diagnosis? A. DVT B. Ventricular tachycardia C. Pericarditis D. Papillary muscle rupture E. Unstable angina F. Tamponade G. Atrial Fibrillation H. Pulmonary oedema I. Pulmonary Embolus J. Angina
I. Pulmonary embolus
Patients with a high clinical suspicion of PE should be anticoagulated while waiting a definitive diagnosis unless contraindicated. The underlying pathophysiology is based on Virchow’s triad. SOB and chest pain are common symptoms and there may also be haemoptysis. Tachycardia is commonly seen. Raised JVP is a feature here which is elicited if cor pulmonale is present. This patient has DVT which is a strong PE risk factor. Recent acute MI is also a weak risk here. Other strong risk factors include obesity, surgery in the past 2 months, prolonged bed rest, malignancy, previous VTE, pregnancy and the thrombophilias such as factor V Leiden. ECG may be normal, or may show tachycardia, new RAD, new RBBB or the classical S wave in I, Q wave with T inversion in III. Various clinical probability scores exist for PE and D-dimer can be used to exclude PE as a diagnosis.
A 62 year old woman becomes unwell and dyspnoeic three days after an acute myocardial infarction. Apex 6th ICS mid axillary line, pansystolic murmur radiating to the axilla. Crackles bibasal to mid zones. JVP elevated, ankles swollen. Pulse 126, BP 105/65, RR 24
What is the diagnosis? A. DVT B. Ventricular tachycardia C. Pericarditis D. Papillary muscle rupture E. Unstable angina F. Tamponade G. Atrial Fibrillation H. Pulmonary oedema I. Pulmonary Embolus J. Angina
D. Papillary muscle rupture
Inferior MI can cause rupture of the posteromedial papillary muscle while anterolateral infarctions can cause rupture of the anterolateral papillary muscle. This has led to acute mitral regurgitation (RV papillary rupture is rare but can cause regurgitation of the tricuspid valve). Complete rupture of the papillary muscle is fatal and causes wide-open MR. Those with incomplete rupture need emergency cardiac surgery with inotropic support considered for transient stabilisation prior to this. The pansystolic murmur which radiates into the axilla is a sign of mitral regurgitation here. This has resulted in SOB and tachycardia.
A 50 year old male, has an anterior infarct but is thrombolysed within 3 hours. Three days later the patient developed sudden intermittent chest discomfort on mobilizing. Chest was clear. Heart sounds were normal. ECG shows ST elevation in leads II, III, aVF, AVL, and V1 to V6. pulse 90 , BP 125/90
What is the diagnosis? A. DVT B. Ventricular tachycardia C. Pericarditis D. Papillary muscle rupture E. Unstable angina F. Tamponade G. Atrial Fibrillation H. Pulmonary oedema I. Pulmonary Embolus J. Angina
C. Pericarditis
This patient has presented with pericarditis. Symptoms include a sharp and severe chest pain retrosternally which is worse on inspiration and when supine, relieved by sitting forwards. The classical finding on examination is a friction rub which is said to sound like ‘walking on snow’ (although this is not present most of the time). There may be diffuse ST elevations on ECG, an effusion on echocardiography and blood results suggesting inflammation. Complications include tamponade and constrictive pericarditis. The prior viral infection is a risk factor with the most common pericardial infection being viral. Bacterial purulent pericarditis also occurs. The inflammation is due either to direct viral attack or immune mediated damage. Other risk factors include male gender, post-MI (both ‘early’ and Dressler’s), post-pericardiotomy syndrome, neoplasm from local tumour invasion, uraemia and autoimmune conditions such as RA and SLE.
A 79 year old male with long standing angina presented to A and E with an anteroseptal MI. He became unrousable, HS were normal but pulse rate was 200 and regular BP 60/0 RR24
What is the diagnosis? A. DVT B. Ventricular tachycardia C. Pericarditis D. Papillary muscle rupture E. Unstable angina F. Tamponade G. Atrial Fibrillation H. Pulmonary oedema I. Pulmonary Embolus J. Angina
B. Ventricular tachycardia
VT and VF can occur during ischaemia and reperfusion and can be fatal. They can also occur at any stage after an MI due to re-entry circuits at the border between myocardial scar tissue and normal myocardium. They are commonly seen in patients who have a decreased ejection fraction. Appropriate treatment should be initiated with DC cardioversion and anti-arrhythmics. Electrolytes should also be optimised (especially potassium and magnesium levels) as electrolyte imbalances present an added risk of ventricular arrhythmias. Medical management afterwards is essential, especially with beta blockers which decrases incidence of ventricular events. Those with persistently low LV ejection fraction which is unresponsive should be considered for an implantable caridioverter defibrillator.
An 80 year old male with an anterior MI, initially improved, but then started deteriorating. Became very unwell, pale, no murmur, crackles at both lung bases, ankles swelling JVP increased, apex 6th ICS pulse 115 BP 125/88 RR 25
What is the diagnosis? A. DVT B. Ventricular tachycardia C. Pericarditis D. Papillary muscle rupture E. Unstable angina F. Tamponade G. Atrial Fibrillation H. Pulmonary oedema I. Pulmonary Embolus J. Angina
H. Pulmonary oedema
This patient has developed congestive heart failure as a complication of his MI. This is caused by decreased left ventricular function occuring after MI due to myocardial damage, infarct progression and remodelling of the LV tissue after the injury. Displaced apex beat is commonly found along with the other mentioned features in this history. Tests such as ECG, CXR, BNP (B-type natriuretic peptide) and echocardiogram will help confirm this diagnosis. CXR here is likely to confirm pulmonary congestion and may also show cardiomegaly. Initial symptomatic relief will involve diuretics and oxygen primarily, with the patient being sat upright. Treatment will also involve medication including beta blockers and ACE inhibitors.
A 55 year old obese female complains of an occasional burning pain behind the sternum. The pain is worse after large meals and when drinking hot liquids.
What is the diagnosis? A. Costochondritis B. Pulmonary Embolism C. Pericarditis D. Pneumothorax E. Angina F. Peptic ulcer disease G. GORD H. Aortic dissection I. Pneumonia J. MI K. Rib fracture
G. GORD
This patient has GORD characterised by heartburn and regurgitation of acid. It is more severe at night when the patient is lying flat and also when the patient is bending over. Risk factors include obesity and hiatus hernia. Diagnosis is generally clinical and can also be achieved by a diagnostic trial of a PPI. Normally an upper GI endoscopy is reserved for complications such as strictures, Barrett’s or cancer, or for atypical features. An OGD may show oesophagitis or Barrett’s (red velvety), however OGD may be normal. Manometry and pH monitoring may also be performed, but in this case, this patient will probably just have a therapeutic and diagnostic trial of a PPI instead of an OGD.
A 50 year old female presents with a sharp chest pain which is worse on inspiration. Her temperature is 38oC and she has a history of a recent viral infection. Her pulse is much weaker on inspiration and her JVP is raised.
What is the diagnosis? A. Costochondritis B. Pulmonary Embolism C. Pericarditis D. Pneumothorax E. Angina F. Peptic ulcer disease G. GORD H. Aortic dissection I. Pneumonia J. MI K. Rib fracture
C. Pericarditis
This patient has presented with pericarditis. Symptoms include a sharp and severe chest pain retrosternally which is worse on inspiration and when supine, relieved by sitting forwards. The classical finding on examination is a friction rub which is said to sound like ‘walking on snow’. There is pulsus paradoxus here too. There may be diffuse ST elevations on ECG, an effusion on echocardiography and blood results suggesting inflammation. Complications include tamponade and constrictive pericarditis. The prior viral infection is a risk factor with the most common pericardial infection being viral. Bacterial purulent pericarditis also occurs. The inflammation is due either to direct viral attack or immune mediated damage. Other risk factors include male gender, post-MI (both ‘early’ and Dressler’s), post-pericardiotomy syndrome, neoplasm from local tumour invasion, uraemia and autoimmune conditions such as RA and SLE.
A 26 year old racing driver is brought to A&E from an RTA. He is dyspnoeic, has a BP of 105/60 and pulse 95bpm. O/E the trachea is deviated to the Left and there is decreased expansion of the left side relative to the right.
What is the diagnosis? A. Costochondritis B. Pulmonary Embolism C. Pericarditis D. Pneumothorax E. Angina F. Peptic ulcer disease G. GORD H. Aortic dissection I. Pneumonia J. MI K. Rib fracture
D. Pneumothorax
This patient has developed a left sided tension pneumothorax and will need emergency intervention in the form of the insertion of a large bore cannula into the 2nd intercostal space in the MCL of the affected side. This will need to be followed by the insertion of a chest drain.
A 72 year old man with a history of hypertension, presents with sudden tearing chest pain radiating to the back. The peripheral pulses are absent and there is a widened mediastinum on CXR.
What is the diagnosis? A. Costochondritis B. Pulmonary Embolism C. Pericarditis D. Pneumothorax E. Angina F. Peptic ulcer disease G. GORD H. Aortic dissection I. Pneumonia J. MI K. Rib fracture
H. Aortic dissection
The tearing chest pain suggests aortic dissection. There may also be interscapular pain with dissection of the descending aorta. Dissecting aneurysms are either type A, which involves the ascending aorta, or type B. Type A dissections require urgent surgery whereas type B can be managed medically if it is not complicated by end organ ischaemia. BP differential between the 2 arms is a hallmark feature. Pulse differences may also be present in the lower limbs. There may also be the diastolic murmur of AR in proximal dissections. CXR may show a widened mediastinum like this case, and helps to rule out pulmonary causes of pain. A CT scan is indicated as soon as a diagnosis of aortic dissection is suspected and should be from the chest to the pelvis to see the full extent of the dissecting aneurysm. What you will see is the intimal flap. MRI is more sensitive and specific but is more difficult to obtain acutely.
A 66 year old male complains of a severe crushing pain in his chest. He is sweating, short of breath, says he feels sick and appears very drowsy. The pain is not relieved by the GTN spray he was given by his GP.
What is the diagnosis? A. Costochondritis B. Pulmonary Embolism C. Pericarditis D. Pneumothorax E. Angina F. Peptic ulcer disease G. GORD H. Aortic dissection I. Pneumonia J. MI K. Rib fracture
J. MI
This patient’s chest pain sounds like an MI. Chest pain is classically severe and heavy in nature (often described as crushing), located centrally with possible radiation to the left arm or jaw and lasts for >20 minutes. SOB due to pulmonary congestion and sweating due to high sympathetic output are also common symptoms. Risk factors incorporate the standard set of cardiovascular risks such as smoking, high BP, DM, obesity and dyslipidaemia. An ECG is indicated. STEMI, new LBBB or confirmed posterior MI is an indication for PCI/thrombolysis. It is worth noting that RV infarction is present in 40% of inferior infarcts so in this case, right sided ECG leads should also be obtained.
GTN is given in acute suspected MI (along with oxygen, aspirin and morphine). It acts to reduce myocardial oxygen demand and lessens ischaemia (and may rarely abort MI if there is coronary spasm). The fact it does not relieve the pain suggests this is not a typical episode of angina. Sublingual dosing should be given first and IV therapy is reserved for those with hypertension of heart failure. Morphine is essential to relieve pain and its related sympathetic response, which can add to myocardial oxygen demand.
Mrs E, a 26 year old American lady, arrives in A&E with severe central chest pain. She is shocked, pale and sweaty. You notice a complete set of LV luggage in her bay as you go over to examine her. An overwrought Mr E implores you to save the life of his wife and their unborn child.
What is the diagnosis? A. Pneumothorax B. Panic disorder C. Tietze's syndrome D. TIA E. Oesophageal reflux F. ACS G. Coctochondritits H. Herpes-Zoster I. Cyclical breast pain J. Ectopic pregnancy K. Pulmonary embolism L. Pleuritis M. Fibromyalgia
K. Pulmonary embolism
The underlying pathophysiology of PE is based on Virchow’s triad. SOB is a common symptom and there may also be pleuritic chest pain and haemoptysis. Most patients also describe a feeling of apprehension. Pregnancy is a strong risk and there has also presumably been long-haul air travel here. Other strong risk factors include recent surgery, DVT, obesity, prolonged bed rest, malignancy, previous VTE and the thrombophilias such as factor V Leiden. The oral contraceptive pill is also associated with an increased risk of VTE but is a weak risk factor. CXR may be normal or may have findings suggestive of PE such as band atelectasis, hemidiaphragm elevation, Fleischner’s sign, Westermark’s sign and Hampton hump. ECG may be normal, or may show tachycardia, new RAD, new RBBB or the classical S wave in I, Q wave with T inversion in III. Various clinical probability scores exist for PE and D-dimer can be used to exclude PE as a diagnosis.
Mr L, an investment banker, who is as wide as he is tall, has been brought in to A&E at 2am on Sunday after collapsing at the kebab shop in Shepard’s Bush Road. He is dressed in a schoolboy outfit, which only makes sense when a similarly dressed friend arrives and tells you that the office went clubbing at Po Na Na together. Apparently Mr L had been complaining of tight chest pain and anxiety earlier in the evening but a cigarette calmed him down.
What is the diagnosis? A. Pneumothorax B. Panic disorder C. Tietze's syndrome D. TIA E. Oesophageal reflux F. ACS G. Coctochondritits H. Herpes-Zoster I. Cyclical breast pain J. Ectopic pregnancy K. Pulmonary embolism L. Pleuritis M. Fibromyalgia
F. ACS
ACS refers to acute myocardial ischaemia caused by atherosclerotic disease and encompasses STEMI, NSTEMI and unstable angina. Once you are aware that this is what acute coronary syndrome encompasses then this diagnosis becomes obvious. This man is clearly overweight and is seen munching a kebab so there are clear cardiovascular risk factors here. The tight chest pain followed by collapse make this sound like a myocardial infarction. Those with identified STEMI should be considered for immediate reperfusion therapy by thrombolytics or percutaneous coronary intervention. Those with NSTEMI or unstable angina do not benefit from this. The pathophysiology underlying all three of these disease processes involves disruption of vulnerable or high risk plaques leading to platelet activation and thrombus formation. Blood flow is disrupted. Most complain of chest pain which is described as substernal pressure, heaviness, squeezing, burning or tightness. It may either localise or radiate to the arms, shoulders, back, neck or jaw and is usually reproduced by exertion, eating, exposure to cold or emotional stress. ECG and serum biomarkers like troponin will be useful in confirming the diagnosis.
Miss A, a 52 year old, attends Rapid Diagnostic Clinic for Breast Clinic at CX. She is concerned over an area of tenderness on her left breast. O/E you find that the lower medial quadrant of the right breast feels sore when you palpate deeply. There is no palpable lump and both mammography and ultrasound are normal.
What is the diagnosis? A. Pneumothorax B. Panic disorder C. Tietze's syndrome D. TIA E. Oesophageal reflux F. ACS G. Coctochondritits H. Herpes-Zoster I. Cyclical breast pain J. Ectopic pregnancy K. Pulmonary embolism L. Pleuritis M. Fibromyalgia
G. Costochondritis
This is costochondritis, or Tietze’s syndrome (which describes constochondritis accompanied by chest wall swelling), which presents with insidious onset of anterior chest wall pain which is made worse by certain movements of the chest and deep inspiration. The key sign here is that there is pain when palpating the costochondral joints, particularly the 2nd to the 5th and the diagnosis is clinical. Tests are done to exclude other diagnoses here such as breast pathology. First line treatment is with NSAIDs. Oral NSAIDs are preferred in a primary care setting and a beneficial response confirms the diagnosis. If NSAIDs or local corticosteroid injection (usually performed by a specialist) fail to make the symptoms better than you should seek further investigations and consider a wider differential diagnosis which include conditions like pleuritis, ACS, PE, rib fracture and GORD.
