Tuesday, 29 May 2012

MCQ Clinical Year Part6/10 CVS


Choose only ONE answer
51. A young man comes to the A & E Department complaining of feeling unwell and palpitations. Supraventricular tachycardia is confirmed on ECG and he responds to carotid sinus massage. Subsequently, the ECG shows a PR interval of 0.09 sec, widened QRS complex in all leads with a slurred upstroke, dominant R wave in V1 and left axis deviation.
    What is the most likely diagnosis?
    Rheumatic fever
    Wolff–Parkinson–White syndrome
    Atrial fibrillation
    ASD
    Right bundle-branch block

    The ECG features are typical of Wolff-Parkinson-White (WPW) syndrome. This condition is classically associated with a short PR interval (< 0.12 s). Slurring of the QRS complex is due to an extra wave called a delta wave. As the AV node and bypass tract have different conduction speeds and refractory periods, a re-entry circuit can develop, causing paroxysms of tachycardia. Carotid sinus massage or intravenous adenosine will often terminate an episode of this form of tachycardia. One of the features of myocarditis due to rheumatic fever is a prolonged PR interval. This occurs due to a first- or second-degree block. In atrial fibrillation, the ECG shows normal but irregular QRS complexes; there are no P waves but the baseline may show irregular fibrillation waves. A right bundle-branch block presents with wide QRS complexes, dominant R in lead V1, inverted T waves in V1 – V4 and a deep wide S wave in lead V6. Atrial septal defects are usually associated with a right bundle-branch block. This leads to an rSR pattern 

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    52. An obese 50-year-old woman suddenly develops dyspnoea and hypotension 3.5 days after undergoing a total abdominal hysterectomy. There is mild jugular venous distension with prominent A waves. The lung fields are clear. ECG shows tachycardia with a right bundle-branch block and minor ST-segment changes.
    What is the most likely diagnosis?
    Acute myocardial infarction
    Pulmonary embolism
    Aspiration pneumonia
    Aortic dissection
    Pneumothorax

    Pulmonary embolism presents with a raised jugular venous pressure (JVP) and right bundle-branch block due to acute right heart failure. Hypotension in an acute MI would cause gross ST-segment abnormalities on ECG. Clear lung fields on auscultation preclude a diagnosis of pneumonia. Aortic dissection would cause an MI or aortic regurgitation before causing respiratory distress.

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    53. A patient presents with congestive heart failure.
    Which drug may be effective in reducing mortality?
    Enalapril
    Aspirin
    Digoxin
    Frusemide
    Lidocaine

    Standard drugs like digitalis and diuretics have not been shown to improve survival rates. A number of studies have conclusively demonstrated that reduction in left ventricular afterload prolongs survival rates in congestive heart failure. Vasodilators such as angiotensin-converting enzyme (ACE) inhibitors are thus effective by inhibiting the formation of angiotensin II and thus affecting coronary artery tone and arterial wall hyperplasia. Lidocaine and other antiarrhythmic agents are useful only when there is arrhythmia associated with heart failure. Aspirin is indicated only in cases of coronary occlusion or myocardial infarction.

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    54. A 20-week pregnant woman with a history of asthma is noted to have consistent blood pressure readings over 170/95 mmHg.
    Which of the following antihypertensives would you initiate for this patient?
    Nifedipine
    Diltiazem
    Bendrofluazide
    Enalapril
    Losartan

    Dihydropyridines (eg nifedipine) are safe and effective in pregnancy, whereas the role of diltiazem is less clear. Bendrofluazide is relatively contraindicated, while ACE inhibitors and angiotensin receptor blockers are absolutely contraindicated.

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    55. A 63-year-old man with known chronic heart failure is admitted with symptoms at rest. Examination reveals pitting oedema to his knees, elevated jugular venous pressure and basal crepitations. He is in sinus rhythm at a rate of 80 bpm and his blood pressure is 100/60 mmHg. Current medication includes bisoprolol 10 mg once daily, frusemide 80 mg once daily and ramipril 2.5 mg twice daily. Blood tests reveal a sodium concentration of 133 mmol/l, potassium 4.9 mmol/l and creatinine of 169 mmol/l. The admitting doctor commences him on iv frusemide 80 mg twice daily and increases his ramipril to 5 mg twice daily.
    When you review him the following day what other drug would be most appropriate to add in?
    Amiloride 5 mg od
    Bendrofluazide 2.5 mg od
    Bumetanide 2 mg bd
    Metolazone 5 mg od
    Spironolactone 25 mg od

    This man has decompensated CHF with symptoms at rest (New York Heart Association class IV). Examination has revealed significant fluid retention. The initial management plan of changing to iv frusemide is sensible since coexistent gut wall oedema is likely to impinge on oral absorption. Increasing the vasodilators in the form of ramipril is again a sensible approach. The addition of a thiazide (inhibiting sodium reabsorption in distal tubule) may work in synergy with a loop diuretic; the same is true for metolazone. Spironolactone, an aldosterone antagonist, has been shown to improve the mortality rate and symptoms and reduce hospitalisation in patients with severe CHF already on conventional treatment. Benefits are in addition to its diuretic effect since aldosterone itself has adverse effects on myocardial structure and function. Clearly, careful monitoring of renal function and biochemistry is important in such patients.

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    56. A 65-year-old man presents to casualty with severe chest pain. ECG shows anterior ST-segment elevation and he receives prompt thrombolysis with reteplase with good resolution of changes. He is commenced on aspirin, a b-blocker, an ACE inhibitor and a statin. His initial progress is complicated by further pain, worse with inspiration and movement and relieved by non-steroidal drugs. You are called to see him on day 5 postinfarct when he complains of shortness of breath on walking to the bathroom. He looks unwell with a cool periphery and resting tachycardia. Blood pressure is reduced at 90/50 mmHg. Jugular venous pressure is elevated to around 8 cm and rises with inspiration. His ECG shows preserved anterior R waves and anterolateral T-wave inversion together with sinus tachycardia. Chest X-ray shows an increase in the cardiothoracic ratio but clear lung fields.
    What is the most likely complication to have developed to account for this deterioration?
    Cardiogenic shock
    Mitral regurgitation
    Pericardial tamponade
    Pulmonary embolism
    Ventricular septal defect

    Devastating complications still do occur following acute myocardial infarction. Cardiogenic shock tends to occur early following a large infarct (or in the presence of already impaired left ventricular function), typically in the first 24–48 hours. The development of acute mitral regurgitation or VSD is associated with severe pulmonary oedema. While they would give rise to an elevation of jugular venous pressure, Kussmaul’s sign would not be present (increase in JVP with inspiration). Although pericarditis is common following an MI, and in particular anterior MI, tamponade occurs relatively infrequently. Chest X-ray shows a large heart with normal pulmonary vasculature. Echocardiography is vital to assist in the management of such a patient and permits easy differentiation of the possible causes of haemodynamic collapse.

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    57. A 65-year-old man is admitted via A&E with acute shortness of breath. His past medical history includes an anterior MI 5 years ago. He is usually short of breath after walking around 400 m (0.25 mile), but is not on regular treatment. Clinically he is distressed: respiratory rate 30/min, basal crepitations to mid-zones, saturations 90%, pulse rate 110 sinus, blood pressure 180/100 mm Hg. The casualty officer has already given iv diamorphine 5 mg, iv metoclopramide and iv frusemide 40 mg (twice) but the patient remains short of breath, although saturations have increased to 94% with high-flow oxygen. CXR confirms pulmonary oedema.
    What further intravenous therapy would you commence?
    Atenolol iv
     Dobutamine iv
    Dopamine iv
    GTN iv
    Milrinone iv

    This patient has severe pulmonary oedema. Initial treatment includes sitting the patient up and administering high-flow oxygen. High catecholamine levels and activation of the renin–angiotensin–aldosterone systems drive the peripheral vasoconstriction, which increases myocardial oxygen demand. Traditionally, treatment has been with diuretics, but the benefits probably relate to their vasodilatatory actions. Early use of more powerful vasodilators represents a more attractive strategy and includes iv diamorphine and iv GTN (short half-life). Early administration of an oral ACE inhibitor would also be recommended. Inotropic agents should be considered in the context of cardiogenic shock (low blood pressure with impaired tissue perfusion).

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    58. A 50-year-old woman is referred to out-patients for a previously asymptomatic atrial septal defect (ASD). She is new to the area and was last seen around 6 years ago in her previous local hospital. She is a smoker but without other significant medical history. She now complains of shortness of breath on exertion, together with peripheral oedema. Clinical examination reveals her to be clubbed and cyanosed. Her pulse rate is 90 bpm and blood pressure 98/60 mmHg. Echo demonstrates a dilated right heart with an estimated right ventricular pressure of 90 mmHg and significant tricuspid and pulmonary regurgitation.
    What is the likely diagnosis?
    Cor pulmonale
    Eisenmenger’s syndrome
    Infective endocarditis
    Primary pulmonary hypertension
    Pulmonary emboli disease

    This woman has developed massive irreversible pulmonary hypertension as a consequence of a previous left to right shunt. Pulmonary pressures have now reached systemic level. The reversal of a left to right shunt as a consequence of pulmonary hypertension is known as Eisenmenger’s syndrome, and is generally the result of a previously undiagnosed ASD, ventricular septal defect (VSD) or patent ductus arteriosus. It may also result from an incompletely corrected Fallot’s tetralogy or Ebstein’s anomaly. Prognosis is poor, although a few patients may be candidates for heart–lung transplantation. Symptomatic treatment is directed towards right heart failure. Complications include polycythaemia, bleeding disorders and cerebral embolism or abscess. Since there is a particularly high risk in those of childbearing age, patients should be given appropriate advice and information to avoid pregnancy.

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    59. A 40-year-old man is referred by his GP for advice with regard to primary prevention of cardiovascular disease. He is a smoker with a strong family history of premature death from ischaemic heart disease. Following a period of lifestyle modification, his fasting cholesterol concentration is 7.2 mmol/l. On consultation of the local guidelines you find that his estimated 10-year risk of a coronary heart disease event is > 30%.
    What would you advise?
    Cholestyramine
    Dietician advice
    Fibrate
    Nicotinic acid
    Statin

    The National Service Framework for Coronary Heart Disease (2000) and the Joint British Society Guidelines recommend targeting individuals with a 10-year risk of a coronary heart disease event of > 30%. Individuals should be offered interventions to address all modifiable risk factors, including dietary advice, smoking cessation advice and support, moderation of alcohol consumption and weight reduction where appropriate. In respect of lipid management, non-pharmacological and pharmacological interventions should be utilised to achieve a total cholesterol concentration < 5.0 mmol/l and an LDL cholesterol concentration of < 3.0 mmol/l. The results of several important trials support the use of statins in primary prevention, these include: WOSCOPS (pravastatin) AFCAPS/TEXCAPS (LEVASTATIN).

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    60. Left bundle branch block is associated with which one of the following conditions?
    Ischaemic heart disease
    Mitral stenosis
    Pericarditis
    Pulmonary embolism
    Tricuspid stenosis

    Mitral stenosis, tricuspid stenosis and secondary pulmonary hypertension due to pulmonary embolism are associated with right ventricular strain and hypertrophy with partial or complete right bundle branch block. Pericarditis is not associated with bundle branch block.

    Prepared by:
    Kevin Wong
    Anthony Chan

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