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Part 1 60 Cardiology SBAs, EMQs & MCQs

CARDIOLOGY EMQ 1 Question: Choose which clinical diagnosis is most likely to be associated with the pulse features described a. Atrial fibrillation b. Aortic stenosis c. Aortic incompetence d. Mitral stenosis e. Supraventricular tachycardia f. Complete heart block g. Benign ventricular ectopics h. Anxiety Q1: A 52-year-old man, previously fit and well, has become increasingly short of breath on exertion and has been admitted following a dizzy spell. Amongst other clinical signs you notice that his pulse is 60 beats per minute, sinus rhythm. It is slow rising. A1: B. Aortic Stenosis (AS). In AS the pulse is typically slow and/or has a sustained upstroke of the arterial pulse, and the pulse may be of low volume. This is because the left ventricle is working hard to drive blood out thorough the narrowed aortic valve. There may also be a noticeable delay between the first heart sound (on auscultation) and the corresponding pulse in the carotid artery (so-called 'apical-carotid delay'). Similarly, there may be a delay between the appearance of each pulse in the brachial artery (in the arm) and the radial artery (in the wrist). Q2: A 46-year-old man attends for outpatient assessment following referred by his GP. He complains of an episodic sudden onset of very a fast pulse rate, and a fluttering sensation within his chest. He takes his pulse at the time and states the rate can be greater than 200 beats per minute. Each episode lasts typically for few minutes and then reverts spontaneously. His GP had requested a 24 hour tape recording, but this was normal. A2: E. Supraventricular Tachycardia (SVT). This is the classical history associated with SVT. It often presents in younger patients, although it can be seen in older patients. The arrhythmia typically arises from the atria and therefore the rate is often greater than 200 beats per minute. Episodes are often self-terminating, but if treatment is required adenosine is usually the first line drug. Beta-blockers are also useful. If haemodynamically unstable cardioversion should be performed as it is safe and effective.

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Q3: A 46-year-old Asian gentleman attends the outpatient department referred by his GP. He complains of increasing shortness of breath and a reduced exercise tolerance at the gym. He has been fit and well all his life. Amongst other clinical signs the pulse has a tall upstroke and then seems to ‘fall away’. Blood pressure is 140/50. A3: C-Aortic incompetence. A collapsing pulse and wide pulse pressure are almost always diagnostic of some degree of aortic incompetence. It is associated with a congenital bicuspid aortic valve and symptoms may begin on in the 3rd or 4th decade of life. SOB is usually the predominant symptom. Echocardiography is the most useful investigation, helping to quantify the degree of incompetence and plan treatment. If there is evidence of left ventricular dilatation then ACE inhibitors will be prescribed. Q4: An 84 year old farmer is admitted to the acute medical receiving unit with dizzy spells. His pulse is very slow and irregular. His blood pressure is 120/80 mmHg. There are intermittent irregular visible pulsations noted on inspection of his venous pressure A4: F. Complete Heart Block. Patients with complete AV block typically experience bradycardia (as low as 28 beats per minute during sleep), hypotension, and at times, hemodynamic instability. In some cases, exercising may be difficult, as the heart cannot react quickly enough to sudden changes in demand or sustain the higher heart rates required for sustained activity. They often present with dizzy spells. In this case treatment will be referral for a permanent pacemaker, however a temporary wire is not required as he is haemodynamically stable. Q5: A 46 year old consultant endocrinologist at your hospital has been complaining of irregular episodes of palpitations for a few years. They are worse following ingestion of alcohol and coffee and also tend to be worse at night. On examination heart sounds are normal. The pulse is irregular at times. Echocardiography is entirely normal. A5: G. Benign Ventricular Ectopics. This is a benign condition caused by ventricular extra-systoles and tends to have a benign course. A typical history is feeling an extra-beat followed by a slight pause and then the heart beat returns to normal. Usually patients have a structurally normal heart and 24 hr tape simply reveals ectopic beats.

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CARDIOLOGY EMQ 2 Question: Choose which clinical diagnosis is most likely to be associated with the murmurs described a. Ventricular septal defect b. Aortic stenosis c. Aortic incompetence d. Mitral stenosis e. Pulmonary stenosis f. Mitral incompetence g. Tetralogy of fallot h. Tricuspid incompetence Q1: A 26-year-old patient with Noonan Syndrome. On auscultation you hear a soft ejection systolic murmur at the left upper sternal border, louder with inspiration. A1: E. Pulmonary Stenosis. The classical murmur is heard at the left upper sternal border and is louder with taking a deep breath (which increases venous return). Pulmonary stenosis is associated with Noonan syndrome, a relatively common genetic condition, and a type of dwarfism. It affects males and females equally and about half have pulmonary stenosis. Q2: A 46-year-old Asian gentleman with blood pressure 140/50 mmHg. You hear an early diastolic murmur over the upper sternal border louder with expiration. A2: C. Aortic Incompetence. Early diastolic murmurs often point to outflow tract valvular regurgitation. The fact that it is louder with breathing out suggests a murmur on the left side of the heart Q3: A 22-year-old patient with Downs’ syndrome. There is evidence of finger clubbing and resting oxygen saturations are 87%. On auscultation you hear a loud 4/6 pan-systolic murmur at the lower sternal border. A3: A. VSD with subsequent development of Eisenmenger syndrome. The diagnosis is ventricular septal defect (VSD). The patient has trisomy 21 which has a clear association with cardiac malformations including VSD. Eisenmenger syndrome develops whenever there is a persistent uncorrected left to right cardiac shunt, which over time leads to chronically elevated right sided pressures and ultimately pulmonary hypertension. Patients become cyanotic and prognosis is poor. Q4: A 64 year old gentleman 4 days following primary PCI for an LAD infarct. He becomes short of breath and hypotensive. On examination there is a loud pansystolic murmur at the lower sternal border and apex. Echocardiogram reveals turbulent flow in the region of the septum on para-sternal long-axis view.

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A4: A. VSD. This is an acquired VSD, which may be a consequence of a large infarct. It is rare, but may happen and clinicians should be aware of the possibility as prompt treatment is required. Usually a discussion with the cardiac surgeons will be needed. Q5: A 67-year-old lady has become progressively short of breath. You hear a loud ejection systolic murmur which radiates to both carotids. A5: B. Aortic Stenosis. Aortic stenosis is a common problem. Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85 have the disorder. Treatment is usually by conventional surgery and the cut-off is either a gradient greater than 60mmHg, or the development of symptoms. In those not fit for surgery there is increasing use of newer percutaneous methods.

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CARDIOLOGY EMQ 3 Question: Which of the following JVP appearances is most likely to be seen in the clinical pictures described? a. Raised JVP, normal waveform b. JVP rising with inspiration c. Large ‘a’ wave d. Absent ‘a’ wave e. Large ‘v’ wave f. Cannon ‘a’ wave g. Elevated JVP but no waveform, or change with breathing h. Slow ‘y’ descent Q1: An 84-year-old lady with moderate impairment of left ventricular ejection fraction. She has recently undergone hip replacement and has a positive 4 litre fluid balance in the last 2 days. A1: A. Raised JVP, normal waveform. This is most likely simple fluid overload and in the presence of reasonable renal function will respond to appropriate therapy with IV diuretics. The JVP will be elevated as the right side of the heart fails to clear the backload of fluid returning form the venous system. Q2: An 84 year old farmer is admitted to the acute medical receiving unit with collapse. His pulse is very slow and irregular. His blood pressure is 62 mmHg systolic and he is sweaty. There are intermittent irregular visible pulsations noted on inspection of his venous pressure. A2: F. Cannon ‘a’ wave. Patients with complete AV block typically experience bradycardia (as low as 28 beats per minute during sleep), hypotension, and as in this case, hemodynamic instability. In this case the cannon ’a’ wave is caused by the lack of synchronization between the atria and the ventricles. The ventricles occasionally contract against a closed AV valve, giving rise to the JVP appearance. A temporary wire is required as he is haemodynamically unstable. Q3: A 45-year-old lady is an inpatient in the oncology department with metastatic melanoma. She has received a recent course of chemotherapy, but has developed acute shortness of breath and is hypotensive. Bedside echocardiogram reveals a 2.5cm circumferential pericardial effusion. A3: B. JVP rising with inspiration. This is called Kassmaul’s sign, or “paradoxical” rise in the JVP with inspiration. Normally the venous pressure (and the JVP) falls with a deep breath as intrathoracic venous return rises (this is why murmurs on the right side of the heart are louder with inspiration). If the JVP rises with inspiration it is ‘paradoxical’ and signifies that an extrinsic force, in this case, an effusion, compresses the ventricle. Treatment is peri-cardiocentesis. Effusions are very common in malignant disorders, but easily treatable.

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Q4: A 65-year-old gentleman has recently undergone radiotherapy treatment for lung carcinoma. He is progressively short of breath and CT scan of the chest demonstrates mediastinal lymphadenopathy and dilated neck veins. A diagnosis of SVC obstruction is made. A4: G. Elevated JVP, but no waveform, or change with breathing. Patients with SVC obstruction have a persistently elevated JVP. It is usually associated with tumor invasion although may also result from the use of vascular devices and procedures e.g. neck lines. Treatment is usually in the form of steroids if it is caused by malignancy, or diuretics. Q5: A 54 year old lady has recently undergone pacemaker lead extraction for endocarditis. It was a difficult procedure and the ventricular lead was tethered to the tricuspid valve. Echo now confirms severe tricuspid incompetence. A5: F. Large ‘v’ wave. A large ‘v’ wave typically suggests tricuspid incompetence. In this case the tricuspid valve has been damaged during the lead extraction and is regurgitant. The JVP will demonstrate large ‘v’ waves during ventricular systole. The liver may be enlarged and is often pulsatile (the latter finding being virtually diagnostic of tricuspid insufficiency). Peripheral edema is often found. In severe cases, there may be ascites.

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CARDIOLOGY EMQ 4 Question: what is the most likely diagnosis from the ECG description provided? a. Acute inferior myocardial infarction b. Atrial fibrillation c. Pericarditis d. Anterior myocardial infarction e. Complete AV block f. Right Ventricular Hypertrophy g. Ventricular Tachycardia h. Supraventricular Tachycardia Q1: A 54-year-old man with a history of smoking presents with sudden onset of cheat pain and ST elevation across leads V1-V4. A1: D. Anterior myocardial infarction. This is an acute anterior (probably LAD) infarct and the patient should receive primary PCI if available. If PCI is not available, and there are no contraindications, he should receive thrombolytic therapy. The most likely vessel to be occluded is the left anterior descending artery. The aim of treatment is to re-establish flow in the vessel. Q2: A 26-year-old gentleman complains of chest pain for two days. He had a cold last week and the pain is worse when he takes a deep breath. The ECG demonstrates global saddle-shaped ST elevation. A2: C. Pericarditis. Pericarditis typically causes ST elevation across all leads on the ECG. It is also described as ‘saddle’ shaped. It tends to resolve with anti-inflammatory therapy and an echocardiogram should be performed to rule out any effusion. It is often preceded by an influenza type illness. Q3: A 33-year-old lady with Tetalogy of Fallot (TOF) attends for annual review. She had corrective surgery as a young child, with closure of the VSD and placement of a pulmonary homograft. She keeps well. On inspection of her ECG there are tall R waves in leads V1-V4 and a deep s wave in lead I. A3: F. Right Ventricular Hypertrophy. Patients with TOF almost always have RVH (Tetralogy of Fallot corresponds to 1. VSD; 2. Over-riding aorta; 3. Pulmonary stenosis; and 4. RVH). Q4: A 13-year-old girl attends for outpatient assessment referred by GP. She complains of episodic sudden, immediate onset of very fast pulse rate, and a fluttering sensation within her chest. Her mother takes her pulse at the time and states the rate can be greater than 200 beats per minute. The 24 hour tape has been performed and demonstrates 2 episodes of fast heart rate. It looks regular. The rate is 190 per minute and the QRS duration is 90ms.

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A4: H. Supraventricular Tachycardia. SVT arises from the atria. If there is aberrant conduction it may mimic a wide-complex tachycardia. Symptoms can come on suddenly and may go away without treatment. They can last a few minutes or as long as 1 or 2 days, sometimes continuing until treated. The rapid beating of the heart during SVT can make the heart a less effective pump so that the cardiac output is decreased and the blood pressure drops. If a patient is hypotensive they should undergo electrical cardioversion which is safe and effective Q5: A 64 year old lady with a history of rheumatic heart disease attends out-patients. She is thin, has a malar flush and has had a St Judes mitral valve replacement 3 years previously. She is now very short of breath when before this wasn’t a problem. ECG does not show any discernable p wave and the tracing has a ‘saw-tooth’ appearance. The QRS complex duration is 160ms. There is a negative deflection in lead V1. A5: B. Atrial fibrillation. Almost all patients with rheumatic mitral valvular disease develop AF at some point. The saw tooth nature of this ECG would suggest flutter although it is hard to be definitive until you see the ECG. The negative deflection in lead V1 also suggests left bundle branch block, which is very common following surgery. Chris Lockhart

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CARDIOLOGY EMQ 5 Question: for each of the scenarios involving cardiac chest pain, what is the best treatment strategy? a. Dual anti-platelet therapy b. Dual anti-platelet therapy, low molecular heparin c. Warfarin d. Thrombolytic therapy e. Long acting nitrate preparation f. Non-steroidal anti-inflammatory preparations g. Primary percutaneous coronary intervention h. GTN spray Q1: A 56-year-old gentleman presents to the emergency room in a large teaching hospital with central crushing chest pain and ST elevation in leads II, III, and aVF. A1: G. Primary percutaneous coronary intervention. There is now convincing evidence that the best treatment for acute STEMI is primary PCI. Of course the patients will have been loaded with aspirin and plavix first, and will receive unfractionated heparin during the procedure. However, the best outcomes are seen in those who get immediate access to percutaneous revascularisation and stenting. Q2: A 26-year-old gentleman complains of chest pain for two days. He had a cold last week and the pain is worse when he takes a deep breath. The ECG demonstrates global saddle-shaped ST elevation. A2: F. Non-steroidal anti-inflammatory preparations. The diagnosis is pericarditis and treatment is usually conservative with NSAIDs. Troponin rises are often seen and in the presence of ST elevation , doctors are often tempted to treat as acute coronary event. However, with careful clinical examination and scrutiny of the ECG the diagnosis can usually be made correctly. Q3: A 72-year-old lady underwent CABG 4 years ago. She has now started complaining of chest discomfort typically in the morning when she goes out to walk her dog. It is worse when going up hills. She is already on aspirin, a statin and a beta blocker. A3: E. Long acting nitrate. This is stable angina. The options here are e. or h. GTN spray may be considered, but probably will often have a very temporary effect and probably a better option is a longer acting preparation with sustained release throughout the day. Q4: A 64-year-old man has just been discharged following percutaneous coronary intervention. He was treated with drug-eluting stents. What combination of drugs must he remain on for at least a year?

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A4: A. Aspirin and plavix (dual anti-platelet therapy). Following the use of drug-eluting stents there is now clear evidence from a number of trials that patients should remain on both aspirin and plavix for one year, and then to switch to aspirin alone. This is because of the risk of sub acute stent thrombosis. Typically there is a 1% risk of acute stent thrombosis in the first 6 weeks. There is about a 10% risk of instent re-stenosis over the next one year. Q5: A 24 year old lady has just been discharged following successful percutaneous closure of an ASD with an amplatzer device. She complains of palpitations and ECG confirms AF. Subsequent 24 hour tape confirms two very short-lived episodes of AF. A5: A. Aspirin and plavix. The AF is short-lived and tends to happen after a device is placed in the atrial septum. In this case aspirin and plavix are used for 6 moths until the device has endothelialised and then stopped. If the AF was permanent then warfarin and DCC should be considered.

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CARDIOLOGY EMQ 6 Question: For each of the arrythmias described what would be your first line treatment strategy? a. Lignocaine b. Cardioversion c. Adenosine d. Amiodarone e. Digoxin f. Metoprolol g. Warfarin h. Magnesium sulphate Q1: A 56-year-old gentleman has recently recovered from a large anterolateral infarct. He presents to A&E with heaviness in his chest and is clod and clammy. ECG demonstrates a wide-complex tachycardia. There is concordance across all leads. The rate is 170 bpm. Blood pressure is maintained at 120/80 mmHg. A1: A. Lignocaine. This is Ventricular Tachycardia (VT). Because the blood pressure is maintained lignocaine is a good first line agent. It is a membrane stabiliser and is used effectively for VT. If the patient were to become haemodynamically unstable he should be cardioverted. Q2: A 72-year-old lady has just undergone a laparoscopy for acute cholecystitis. She is pyrexic, although white cell count and CRP is normal. She has developed atrial fibrillation. A2: D. Amiodarone. This is post-operative AF and chemical cardioversion with amiodarone is a reasonable option. She almost certainly is on IV antibiotics, as infection may be the precipitating factor causing the AF, as opposed to any underlying cardiac abnormality. Q3: A 17-year-old girl attends assessment referred by GP. She complains of episodic sudden, immediate onset of very fast pulse rate, and a fluttering sensation within her chest. You take her pulse and it is greater than 200 beats per minute. A3: C. Adenosine. Adenosine causes transient complete AV block, causing asystole and therefore breaking the cycle of re-entrant tachycardia. It is therefore useful in the treatment of SVT, but is associated with chest discomfort and patients often feel very unwell. It is, however, very short-acting and thus its effects do not last for long. Q4: A 46-year-old man attends for assessment referred by his GP. He complains of episodic sudden, immediate onset of very fast pulse rate, and a fluttering sensation within his chest. The pulse rate is greater than 200 bpm. ECG demonstrates a wide-complex tachycardia and the blood pressure is 60mmHg systolic

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A4: B. Cardioversion. It is hard to speculate as to the exact rhythm although it is probably VT. It may also be SVT with aberrant conduction. In any case given the haemodynamic compromise this patient should be sedated, and cardioverted without delay. This is the safest option in this case. Q5: A 22-year-old lady has just undergone a laparotomy for acute bowel perforation. She is pyrexic with raised white cell count and CRP. She has developed atrial fibrillation with fast ventricular response. You note she has a history of rheumatoid arthritis with lung involvement and PFTS suggest a restrictive pattern A5: E. Digoxin. This is post-operative AF but in this case amiodarone should be avoided. She is relatively young and has evidence of pulmonary fibrosis. Therefore amiodarone would be contraindicated. Rate control with digoxin is a good option and infection should be treated with IV antibiotics.

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CARDIOLOGY EMQ 7 Question: For each of the clinical scenarios and corresponding congenital cardiac anatomical defects described below, what is the correct term? a. Tetralogy of fallot b. Congenital correction of transposition of the great arteries c. Atrioventricular septal defect d. Ebsteins anomaly of the tricuspid valve e. Pulmonary stenosis f. Ventircular septal defect g. Atrial Septal defect h. Patent Foramen Ovale Q1: A 56-year-old university lecturer has been complaining of migraine for two years. He is referred to the medical outpatient dept with an episode of left arm weakness that spontaneously resolved. CT brain and echocardiogram are normal. A bubble contrast echo, however clearly demonstrated bubbles passing from the right atrium into the left atrium, increased following the valsalva manoeuvre. What is the diagnosis? A1: H-Patent foramen ovale. PFO is very common (25% of the population). It has been causally linked with migraine; the mechanism thought to be small emboli passing from the defect to the left sided systemic circulation and thus causing micro-infarcts. When it is associated with larger emboli, say from a DVT, and giving rise to TIA or indeed CVA, the term cryptogenic stroke is used. Common convention is to close the PFO with an occluder device from the venous system if there have been neurogical sequelae. However, clinical trials are still awaited and other clinicians feel warfarin is better for prevention of events. Q2: A 21-year-old girl with trisomy 21 and arterial saturations of 81% at rest. Echocardiogram shows bidirectional flow at the upper end of the septum involving the mitral valve, which is also leaking. What is the diagnosis? A2: C-Atrioventricular septal defect. The anatomy described is AVSD, which is commonly seen in T21. This girl unfortunately has not had this defect repaired and thus has developed Eisenmenger complex. This arises when there is sustained left to right flow for many years which leads to chronically high right sided pressures. Q3: A 41-year-old man with O2 saturations of 78% on room air and is increasingly SOB. There is a loud pan-systolic murmur and a pulmonary ejection systolic murmur. Echocardiogram demonstrates the left ventricle is anterior and supplies the pulmonary circulation. There is also a VSD. What is the diagnosis? A3: B-Congenital correction of transposition of the great arteries (CCTGA). Transposition of the great vessels means the aorta arises from the RV and the pulmonary arteries arise from the LV. It is not

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compatible with life unless there is a co-existent septal defect to allow blood to mix. In CCTGA the ventricles are anatomically switched. There is an anterior LV which gives rise to the pulmonary circulation and the RV is the systemic ventricle. It is often associated with pulmonary stenosis and VSD. Q4: A 2 week old neonate with failure to thrive. Echo reveals a VSD, over-riding aorta, pulmonary stenosis and a RV impairment. What is the diagnosis? A4: A-Tetralogy of Fallot. This combination is tetralogy of fallot. Children usually do well with corrective surgery but will often require a pulmonary valve replacement (homograft) later in life. Q5: A 6-year-old child with Noonan syndrome is seen at the developmental clinic. There is a harsh ejection systolic murmur louder on deep inspiration. Echo shows turbulent flow in the right ventricular outflow tract. A5: E-Pulmonary Stenosis. Noonan syndrome is associated with pulmonary stenosis. Right sided murmurs are louder on inspiration as a deep breath increases systemic venous return ie to the right side of the heart and thus the murmur intensity is increased.

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CARDIOLOGY EMQ 8 Question: For each clinical scenario described what is the lost likely cause of the hypertension. a. Cushings syndrome b. Acromegaly c. Renal artery stenosis d. Phaeochromcytoma e. Coarctation of aorta f. Type 1 diabetes g. Essential hypertension h. Sub-dural haematoma Q1: A 76-year-old gentleman is admitted with increasing subtle confusion. Clinical examination is normal, with no lateralising neurological signs. You notice however that his BP is 182/90 mmHg, and his pulse is 42/min. Blood pressure has always been normal beforehand according to the GP. There is a remote history of a fall 5 weeks ago. What is the diagnosis and most likely cause of hypertension? A1: H. Sub-dural haematoma. This is the most likely diagnosis here given the clinical details. Cushing’s reflex denotes that in order to maintain cerebral perfusion in the setting of raised intracranial pressure, blood pressure rises and heart rate often falls. Q2: A 46-year-old lady with increasing obesity, and a new diagnosis of osteoporosis and type 2 diabetes. Blood pressure is 156/90 mmHg. What is the unifying diagnosis? A2: A-Cushing’s syndrome. This is the most likely diagnosis. It may arise secondary to steroid use, pituitary disease or secondary to exogenous ACTH or cortisol production. It can be diagnosed through an overnight dexamethasone suppression test. Q3: A 35-year-old man with intermittent flushing and palpitations. 24-hour blood pressure monitor reveals average daytime pressure of 178/96mmHg. What is the most likely diagnosis? A3: D-Phaeochromocytoma. Although a rare condition, given the symptoms, phaeochromocytoma needs to be excluded, as it is readily treatable. Q4: A 60-year-old lady presents with acute shortness of breath. Her oxygen level (PaO2) is low at 6.1. CXR reveals unilateral pulmonary oedema and there is left bundle branch block on the ECG. Coronary angiography had been performed 2 months previously and was known to be normal. BP is 210/110 mmHg. What is the most likely diagnosis? A4: C-Renal artery stenosis. This is a rare cause of hypertension and can rarely give rise to unilateral pulmonary oedema. The exact mechanism for this is not known. Diagnosis is by ultrasound or magnetic resonance imaging of the renal vessels.

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Q5: A 26 year old girl presents 18 weeks pregnant. She has been increasingly SOB. It emerges she was told she had a heart murmur as a child. You examine her and note a systolic murmur radiating through to the back and the femoral pulses are very difficult to feel. What is the diagnosis? A5: E. Coarctation of aorta- mild coarctation may often be asymptomatic. However, the weak distal pulses suggest this as a diagnosis. She will need an echocardiogram and will require surgical correction following delivery. CARDIOLOGY EMQ 9 The haemodynamically unstable patient a. Pulmonary embolism b. Inferior myocardial infarction c. Cardiac tamponade d. Left ventricular failure e. Aortic dissection f. Severe mitral regurgitation g. Severe aortic stenosis h. Right ventricular infarction i. Hypertrophic cardiomyopathy j. Coarctation of the aorta 1. A 66 year old man presents with a 2 day history of back/interscapular pain which is sharp and tearing in nature. He is a known hypertensive, but BP on admission is 85/40. His 12 lead ECG shows evidence of ST elevation in leads II,III and aVF. On examination he has evidence of severe aortic regurgitation, not previously documented, with high volume pulses. e) This patient gives a suitable history and features for acute aortic dissection, although on oaccasions the history may be more of acute onset (minutes/hours) of intrascapular/chest pain. If the dissection flaps extends to include the ascending aorta/aortic root then the right coronary artery can become compromised resulting in an inferior myocardial infarction. However, this patient should not be thrombolysed until a dissection has been excluded with a contrast enhanced CT of the thorax. Involvement of the aortic root can also compromise the aortic valve resulting in aortic regurgitation 2. A 72 year-old man becomes hypotensive 2 hours after apparently successful thrombolysis for an inferior myocardial infarction. A right praecordial lead ECG shows normal ST segments in V4R to V6R. On examination there is a new systolic murmur and the LV apex is thrusting. There is florid pulmonary oedema. f). Mechanical complications of myocardial infarction include papillary muscle infarction (resulting in severe mitral regurgitation) and VSD which can both cause hypotension. The findings of a normal RV

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lead ECG, a systolic murmur and volume overloaded apex make acute MR the most likely diagnosis although an echocardiogram would need to be performed to exclude the formation of a VSD which tends to occur with anterior myocardial infarctions. Acute MR results in severe pulmonary oedema. 3. A 63 year old lady is diagnosed as having a posterior myocardial infarction, for which she is thrombolysed. She becomes progressively more hypotensive, and is observed to have an elevated JVP. Her lung fields are clear and auscultation is normal. h) Right ventricular infarction is the most commonly associated with an inferior MI, but can also be a complication of a posterior circulation infarct, particularly in patients who have a dominant circumflex system. In patients suffering a posterior MI who become hypotensive, a right precordial lead ECG should be performed. 4. A 33 year old lady presents with a syncopal episode 1 week after ankle surgery. Her BP is 75/34, her heart rate is 160 bpm in atrial fibrillation and her PaO2 is 10.5 kPa on 60% FiO2. Her chest x-ray is clear. a) A pulmonary embolus should be suspected in any patient who is hypoxic and tachycardic, particularly if there is evidence of new atrial fibrillation/flutter. The marked hypotension in this case is a worrying sign and suggests the patient may be suffering a massive PE, with the embolus obstructing both pulmonary arteries at the bifurcation of the main pulmonary artery (saddle embolus) and she requires an urgent CT pulmonary angiogram and consideration for thrombolysis. 5. An 86 year-old man presents with a 2 week history of worsening dyspnoea and syncope. He has a weak pulse and his BP is 110/85. On auscultation there is a soft cresendo-decresendo systolic murmur. The first heart sound is present, but S2 is absent. There are crackles throughout both lungs and CXR confirms pulmonary oedema. g). This patient has features of severe aortic stenosis, such as low volume pulse, narrow pulse pressure, an ejection systolic murmur and absent S2. A soft or inaudible S2 suggests that the aortic valve is severely calcified and has lost its pliability, resulting in a loss of the closing sound of aortic valve closure. Severe aortic stenosis manifests with chest pain (angina), dyspnoea (increased left atrial pressure) and syncope (overstimulation of mechanoreceptors in the left ventricle triggering a reflex bradycardia/vasodilatory response)

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CARDIOLOGY SBA 1 A 32-year-old gentleman presents to the emergency department with pleuritic chest pain, mild SOB and pyrexia. The SHO in A & E is concerned about the ECG appearance and contacts you. It demonstrates saddle shaped ST elevation across all leads. What is the appropriate therapeutic option in the first instance pending further investigation?

A. Beta Bocker B. Aspirin C. NSAID D. Reteplase E. Low molecular weight heparin

c. NSAID The clinical history suggests pericarditis and this is certainly the most likely diagnosis given the initial ECG. If symptoms improve following NSAID use then this also points towards the potential diagnosis. He should also have an echocardiogram and possibly a CTPA is clinically merited. CARDIOLOGY SBA 2 A 64-year-old gentleman presents with markedly increased SOB on exertion and feeling generally fatigued all the time. This has occurred gradually over the last few months. He also complains of a fast pulse that is irregular. ECG confirms atrial fibrillation with a fast ventricular response; furthermore he is hypotensive. Echocardiogram is normal. You elect for rate control with DCC as an inpatient. Which investigation is mandatory before cardioversion ?

A. CXR B. INR C. CT pulmonary angiogram D. Coagulation screen E. Trans-oesophageal echocardiogram (TOE)

e. TOE As you have elected for cardioversion and his symptoms have lasted greater than 24 hours then there is a theoretical risk of LA appendage thrombus. This is a contraindication to electrical cardioversion and therefore TOE needs to be performed in this case to rule this out. CARDIOLOGY SBA 3 A patient presents with heart failure following a number of myocardial infarcts. Their symptoms are difficult to control and you prescribe carvedilol, furosemide, perindopril, spironolactne and metolozone. They are also on warfarin therapy as the ejection fraction is less than 20% on echo. Following discharge they present with profound hypokalaemia. Which drug would you withdraw first?

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A. carvedilol B. furosemide C. perindopril D. spironolactone E. metolozone

e. metolozone. Metolozone is a potent thiazide diuretic and thus can cause profound hypokalaemia. Furosemide can also cause low potassium but is not as strong. Carvedilol, perindopril and spironolactone all have a tendency to raise serum potassium and should be continued. CARDIOLOGY SBA 4 A 47-year-old lady with a background history of scleroderma presents with progressive shortness of breath. Her lungs are clear but there is a pan-systolic murmur at the lower left sternal border. CXR and CT chest are normal. Echocardiogram reveals severe tricuspid incompetence and an estimated pulmonary artery pressure of 89mmHg. Which therapeutic modality would be the first line agent of choice in this case?

A. sildenafil B. carvedilol C. salbutamol D. bosentan E. inhaled prostacyclin

a. sildenafil. This is primary pulmonary hypertension, a progressive and serious condition which often requires treatment. It is related to autoimmune rheumatological disorders. In this case first line treament would be sildenafil which promotes pulmonary vasodilatation and thus reduces PA pressure. If this fails then bosentan (an endothelin receptor antagonist) and prostacyclin may be of benefit. CARDIOLOGY SBA 5 A 65-year-old gentleman with a history of myocardial infarction presents feeling unwell and dizzy. He is cold, clammy and his pulse is racing. There is no chest pain. ECG shows a wide-complex tachycardia, rate 200/minute, with concordance across all leads. Blood pressure is 72mmHg systolic. What is the optimal treament?

A. IV metoprolol B. IV amioderone C. DC cardioversion (DCC) D. IV lignocaine E. Verapamil

c. DCC

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This is VT until proven otherwise and should be treated as such. In the presence of hypotension the safest option is DCC, with sedation beforehand. If there is no hypotension then lignocaine is a good option. CARDIOLOGY SBA 6 A 54-year-old woman has just returned to the ward following successful ablation for a supraventricular tachycardia. She begins to feel unwell and is found to be SOB, tachycardic and hypotensive, with pulsus paradoxus of 20mmHg. She remains in sinus rhythm, but her JVP is raised and does not fall with inspiration. What initial treatment is indicated?

A. Repeat ablation B. Coronary angiography C. CPAP D. Pericardiocentesis E. IV beta blocker

d. Pericardiocentesis Cardiac Tamponade is a complication of ablation occurring in about 1% of cases. It is readily treatable by pericardiocentesis if performed promptly. It is confirmed by echocardiography and it only takes 100mls of blood to cause tamponade if it collects rapidly. CARDIOLOGY SBA 7 A 62-year-old gentleman with a history of surgical correction of a aortic coarctation in childhood, presents at the clinic progressively SOB. There is an ejection systolic murmur heard best over the aortic area. You diagnose aortic stenosis. What is the most likely aetiology of the aortic stenosis?

A. Aortic sclerosis B. Age degeneration C. Post surgery to correct coarctation D. Bicuspid aortic valve E. Post infective endocarditis

D. Bicuspid aortic valve Bicuspid aortic valve is often associated with coarctation and often leads to aortic stenosis requiring surgery later in life.

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CARDIOLOGY SBA 8 An 84-year-old farmer is admitted to the acute medical receiving unit with dizzy spells. His pulse is very slow and irregular. His blood pressure is 120/80 mmHg. There are intermittent irregular visible pulsations noted on inspection of his venous pressure. ECG confirms rate of 35/min. What is the most likely diagnosis?

A. Slow AF B. Aortic stenosis C. Complete Heart Block D. Sinus Bradycardia E. Postural hypotension

c. Complete Heart Block The history is very suggestive of CHB. Whilst haemodynamocally stable the pulse and JVP features strongly suggest complete AV dissociation. CARDIOLOGY SBA 9 A 46-year-old man attends for outpatient assessment referred by GP. He complains of episodic sudden, immediate onset of very fast pulse rate, and a fluttering sensation within his chest. He takes his pulse at the time and states the rate can be greater than 200 beats per minute. Each episode lasts typically for few minutes and then reverts spontaneously. His GP had requested a 24 hour tape recording, but this was normal. ECG demonstrates a delta upstroke and tall R waves in leads V1-V3 indicative of pre-excitation. What is the most likely diagnosis?

A. Ventricular Tacyhcardia B. Sinus Tachycardia C. Anxiety Disorder D. Wolf Parkinson White E. Phaeochromocytoma

d. Wolf Parkinson White This is the classical history associated with SVT. Wolf Parkinson White is a form of SVT denoted by evidence of pre-excitation on the ECG. It can often present in younger patients, although also seen in older patients. The arrhythmia typically arises from the atria and therefore the rate is often greater than 200 beats per minute. Episodes are often self-terminating, but if treatment is required adenosine is usually the first line drug. Beta-blockers are also useful. You should not use digoxin or verapamil as it can promote excitation through the accessory pathway. If haemodynamically unstable cardioversion should be performed as it is safe and effective. CARDIOLOGY SBA 10 A 56-year-old university lecturer has been complaining of migraine for two years. He is referred to the medical outpatient department with an episode of left arm weakness that spontaneously resolved. CT brain and echocardiogram are normal. A bubble contrast echo, however clearly demonstrated bubbles passing from the right atrium into the left atrium, increased following the valsalva manoeuvre.

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What is the diagnosis? A. Patent Foramen Ovale B. Atrial septal Defect C. Atrioventricular Septal defect D. VSD E. Normal physiology

a. Patent Foramen Ovale. PFO is very common (25% of the population). It has been causally linked with migraine; the mechanism thought to be small emboli passing from the defect to the left sided systemic circulation and thus causing micro-infarcts. When it is associated with larger emboli, say from a DVT, and giving rise to TIA or indeed CVA, the term cryptogenic stroke is used. Common convention is to close the PFO with an occluder device from the venous system if there have been neurogical sequelae. However clinical trials are still awaited and other clinicians feel warfarin is better for prevention of events. Cardiology SBA 11 In the investigation of infective endocarditis, which of the following statements are correct? a) According to the Duke criteria, auscultation of a new murmur fulfils a minor criterion for the diagnosis of infective endocarditis b) The presence of haematuria is a common finding in endocarditis c) The presence of a vegetation can usually be detected with transthoracic echocardiography d) Elevated levels of CRP and erythrocyte sedimentation rate (ESR) fulfil 1 minor criterion of the Duke criteria for diagnosing infective endocarditis. e) A normal transoesophageal echocardiogram rules out the diagnosis of infective endocarditis b). The presence of haematuria is a common finding in endocarditis The clinical diagnosis of infective endocarditis is made using the criteria developed by a group from Duke University by meeting either; 2 major, 1 major and 3 minor, or 5 minor criteria. The presence of a new murmur fulfils a major criterion. Haematuria and proteinuria are extremely common findings in endocarditis and are usually caused by an immune glomerulonephritis mediated by the circulating immunoglobulins stimulated by the infection. This may be present even when the urea and creatinine are normal. Urinalysis should be part of the routine assessment of patients with endocarditis and is a simple non-invasive test for monitoring progress. Persistent or recurrent haematuria may indicate failure of medical treatment. The C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are not part of the Duke criteria for the diagnosis of endocarditis. However, they are nearly always raised in endocarditis and they are useful for monitoring response to treatment A normal transoesophageal echo has a negative predictive value of over 90% in excluding endocarditis in clinically suspected cases with a high index of suspicion. However, a single

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transoesophageal echo, cannot exclude endocarditis. Repeating the transoesophageal echo after a few days provides further reassurance and is probably the most effective way of excluding endocarditis (negative predictive value of over 95%). Cardiology SBA 12 A 48-year old patient gives a 5 day history of dyspnoea. He is found to be in atrial fibrillation. Which is the most appropriate management plan? a) Chemical cardioversion with IV amiodarone b) Chemical cardioversion with IV flecainide c) Anticoagulation with warfarin and rate control d) Transthoracic echocardiogram to exclude thrombus followed by DC cardioversion e) Anticoagulation with warfarin then initiation of oral amiodarone (loading) c). Anticoagulation with warfarin and rate control Neither chemical or DC cardioversion should be attempted in a patient with AF that is presumed to be >48 hours in duration without prior adequate anticoagulation. Adequate anticoagulation is considered to have been achieved when a target INR of 2-3 has been reached for a minimum of 4 weeks. Cardioversion can be safely performed if a left atrial thrombus has been excluded on transoesophageal echocardiography. However, transthoracic echocardiography is unable to visualize the left atrial appendage satisfactorily and cannot exclude left atrial thrombus. Both amiodarone and flecainide are anti-arrhythmic agents and should not be commenced until the patient is formally anticoagulated in this setting. Even chemical cardioversion can disrupt a thrombus sitting in the left atrial appendage leading to stroke . Cardiology SBA 13 A patient becomes hypotensive following thrombolysis for an inferior myocardial infarction. Right ventricular infarction is suspected. What is the most appropriate initial treatment? a) IV nitrates b) IV dobutamine c) IV noradrenaline d) IV fluids e) Insertion of a temporary pacemaker wire d). IV fluids The aim of treatment in patients with haemodynamically significant right ventricular infarction is to increase the right-sided stroke volume. If there is no evidence of associated left ventricular dysfunction, patients should be given several litres of IV normal saline rapidly. Drugs that reduce the pre-load, such as nitrates, opiates and diuretics, should be avoided. If volume loading does not improve the blood pressure, then inotropes can be considered. In patients with left ventricular dysfunction, reducing the afterload will help forward flow from the right ventricle, therefore,

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vasoconstrictors such as noradrenaline should be avoided where possible. Dobutamine can augment forward flow and the cardiac output through its inotropic and chronotropic effects upon the left ventricle. An infarcted, poorly functioning right ventricle can have its stroke volume significantly compromised by concurrent bradyarrhythmias in which case temporary pacing is indicated. Cardiology SBA 14 In a patient with left ventricular heart failure and classified in New York Heart Association (NYHA) functional class II, which of the following medications is of prognostic benefit? a) Carvedilol b) Digoxin c) Frusemide d) Spironolactone e) Isosorbide mononitrate a). Carvedilol Cardio-selective beta blockers (bisoprolol, carvedilol, metoprolol) have been shown to improve morbidity (reduce admissions with LVF) and mortality in NYHA class I-IV patients. NYHA class I refers to patients without any symptoms of dyspnoea at rest or even on exertion. NYHA classes II, III and IV refer to patients with dyspnoea on moderate exertion, minimal activity and at rest respectively. Beta blockers reduce the activation of the renon-angiotensin-aldosterone axis which has a deleterious effect upon left ventricular (LV) remodeling by causing dilatation. Digoxin, nitrates and frusemide are helpful in alleviating symptoms of LV failure, but have not been shown to offer a prognostic benefit. Spironolactone, an aldosterone antagonist, has been shown to reduce mortality in patients with class III-IV failure only. Cardiology SBA 15 Which of the following investigations is the most important in evaluating a patient with confirmed left ventricular failure and recurrent syncope? a) Echocardiogram b) Exercise stress test c) Stress echocardiogram d) Holter monitoring e) Serum brain natriuretic peptide (BNP) d). Holter monitoring Patients with impaired left ventricular (LV) ejection fraction are at a much greater risk of developing malignant ventricular arrhythmias and should be suspected in any heart failure patient who presents with syncope. If this is confirmed on monitoring then the patient would be eligible for an implantable cardiovertor defibrillator (ICD). None of the other tests would provide useful

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information in the syncopal patient with LV failure, unless their symptoms were manifesting on exertion, in which case an exercise stress test could be considered. Patients with heart failure are also liable to postural hypotension due to excessive diuretic therapy.

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CARDIOLOGY MCQ 1. Features of severe mitral regurgitation include:

A. Cardiomegaly B. S4 C. Loud S1 D. Diastolic rumble E. Systolic thrill over apex

A,E Mitral regurgitation may lead to cardiomegaly as there is progressive volume overload. There may be an S3 due to rapid ventricular filling but not usually an S4 (caused by contraction of stiff ventricle). A loud S1 is more typically associated with mitral stenosis. There may be a systolic thrill. 2. Features of severe aortic stenosis include:

A. Collapsing pulse B. S4 C. LBBB D. Plateau pulse E. Displaced apex beat

B,C,D Severe aortic stenosis is associated with a plateau, slow rising pulse. The stiff ventricle contracting may cause S4 to be heard. LBBB can arise due to conduction disease. The apex is usually heaving and undisplaced. 3. Signs of cardiac tamponade include:

A. Tachycardia B. Hypotension C. Raised JVP that falls with deep breath D. Pulsus paradoxus E. Decreased urinary output

A,B,D,E Tamponade is associated with a raised JVP that (paradoxically) does not fall with inspiration (Kausmaul’s sign). The rest are associated with clinical tamponade. Chris Lockhart 4. Possible causes of atrial fibrillation include:

A. Mitral stenosis B. Thyrotoxicosis C. Pneumonia

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D. Pregnancy E. Dilated cardiomyopathy

A,B,C,D,E These are all causes of AF, which if treated promptly and appropriately, can prevent recurrence of the arrythmia. 5. Associations of VSD include:

A. Harsh systolic murmur B. RBBB C. Trisomy 21 D. Aortic coarctation E. Pulmonary stenosis

A,B,C,D,E All of the above are associated with a VSD 6. Features of aortic coarctation include:

A. diastolic murmur B. diastolic tail on echocardiogram of the descending aorta C. radio-femoral delay D. rib-notching E. kyphoscoliosis

B,C,D It is typically a systolic murmur that is heard best at the back in the inter-scapular space. Rib-notching is because of the formation of collateral vessels. Kyphoscoliosis is more likely associated with Marfan’s syndrome. 7. Associations with constrictive pericarditis include:

A. tachycardia B. raised JVP C. previous radiotherapy to chest wall D. 5-fluorouracil E. tesicular tumors

A,B,C

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Pericarditis is associated with tachycardia and raised JVP due to increased atrial pressures. It may be a complication of previous radiotherapy. 5-fluorouracil is associated with coronary vasospasm. Testicular tumors are associated with supraventricular tachycarrythmias 8. Possible causes of Ventricular tachycardia include:

A. Ischaemic cardiomyopathy B. Ebsteins anomaly of the tricuspid valve C. Arrythmogenic right ventricle D. Low potassium E. erythromycin

A,B,C,D,E Ebstein’s anomaly of the tricuspid valve (TV) is a condition where the TV annulus is much lower into the ventricle (ie ventricular atrialisation) and patients are at risk of sudden death. Profound electrolyte disturbance can cause VT. Any drug that prolongs the QT interval can cause VT.