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5 DISEASES OF THE CARDIOVASCULAR SYSTEM 1. The pain of myocardial ischaernia a is typically induced by exercise and relieved by rest b radiates to the neck and jaw but not the teeth c rarely lasts longer than 10 secondsafter resting d is easily distinguished from oesophageal pain e invariably worsens as exercise continues 2. Syncope a followed by facial flushing suggests a tachyarrhythmia b without warning suggests a vaso-vagal episode c on exercise is a typical feature of mitral regurgitation d is the commonest cause of falls amongs~ elderly patients e is a recognised presenting feature of pulmonary embolism P - - - - 3. Recognised features of severe cardiac failure include a tiredness b weight loss c epigastric pain d nocturia e nocturnal cough 26 4. In the normal human heart a the atrio-ventricular node is usually supplied by the left circumflex coronary artery b beta-1 adrenoceptors mediate chronotropic responses c pulmonary artery systolic pressure normally varies between 90 and 140 mmHg d the annulus fibrosus aids conduction of impulses from the atria to the ventricles, e cardiac output is the product of heart rate and ventricular end-diastolic volume 5.

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5 DISEASES OF THECARDIOVASCULAR SYSTEM1.The pain of myocardial ischaerniaa is typically induced by exercise and relieved by restb radiates to the neck and jaw but not the teethc rarely lasts longer than 10 secondsafter restingd is easily distinguished from oesophageal paine invariably worsens as exercise continues

2.Syncopea followed by facial flushing suggests a tachyarrhythmiab without warning suggests a vaso-vagal episodec on exercise is a typical feature of mitral regurgitationd is the commonest cause of falls amongs~ elderly patientse is a recognised presenting feature of pulmonary embolism P - - - -

3.Recognised features of severe cardiac failure includea tirednessb weight lossc epigastric paind nocturiae nocturnal cough

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4.In the normal human hearta the atrio-ventricular node is usually supplied by the left circumflex coronary arteryb beta-1 adrenoceptors mediate chronotropic responsesc pulmonary artery systolic pressure normally varies between 90 and 140 mmHgd the annulus fibrosus aids conduction of impulses from the atria to the ventricles,e cardiac output is the product of heart rate and ventricular end-diastolic volume

5.

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In the normal electrocardiograma the PR interval is measured from the end of the P wave to the beginning of the R waveb each small square represents 40 milliseconds at a standard paper speed of 25 mm/secc the heart rate is 75 per minute if the R-R interval measures 4 cmd R waves become progressively larger from leads V1 to V6e the P wave represents sinoatrial node depolarisation

6.The following pulse characteristics are typical features of the disorders listedbelowA pulsus bisferiens - combined mitral stenosis and regurgitationB pulsus paradoxus - aortic regurgitationc collapsing pulse - severe anaemiad pulsus alternans - extrasystoles every alternate beate slow rising pulse - mitral stenosis

7.The following statements about the jugular venous pressure (JVP) are truea The external jugular vein is a reliable guide to right atrial pressureb The JVP is conventionally measured fro the suprasternal notchc The normal JVP, unlike the blood pressure, does not rise with aii-x_ietyd The normal JVP does not rise on abdominal compressione The normal JVP falls during inspiration

8.These abnormalities of the jugular venous pulse are associated with thedisorders listed belowa cannon waves pulmonary hypertensionb giant 'a' waves tricuspid stenosisc 'v'waves = tricuspid regurgitationd inspiratory rise in jugular venous pressure = pericardial tamponadee absent'a'waves = atrio-ventricular dissociation

9.Abnormalities on palpation of the praecordium are associated with thefollowing disordersa 'tapping' apex beat = right ventricular hypertrophy b left parasternal heave = right ventricular hypertrophyc lower left parasternal systolic thrill = mitral regurgitation

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d impalpable apex beat = emphysemae double apical impulse = left ventricular aneurysm

10.The following auscultatory findings are associated with the phenomena shown belowa third heart sound = opening of mitral valveb varying intensity of first heart sound = AV dissociationc soft first heart sound = mitral stenosisd reversed splitting of second heart sound - left bundle branch block - /'e fourth heart sound = atrial fibrillation

11.A third heart sound (S3) is a typical finding in a mitral stenosisb healthy young athletesc constrictive pericarditis d left ventricular failure e lone atrial fibrillation

12.The following statements about cardiac murmurs are truea diastolic murmurs are a recognised feature of normal pregnancyb ventricular septal defects produce pansystolic murmursc an early high-pitched diastolic murmur suggests mitral stenosisd late-systolic murmurs suggest mitral valve prolapsee mitral diastolic murmurs are best heard at the left sternal edge with the patient leaning forwards

13.Features that suggest a ventricular tachycardia rather than supraventriculartachycardia includea a ventricular rate > 160/minuteb termination of the arrhythmia with carotid sinus pressurec variable intensity of the first heart soundd the presence of cardiac failuree QRS complexes < 0.14 sec in duration on ECG

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14.In the investigation of patients with suspected heart diseasea the normal upper limit for the cardiothoracic ratio on chest X-ray is 0.75b a negative exercise ECG excludes the diagnosis of ischaernic heart disease" c 'step-up' in oxygen saturation at cardiac catheterisation suggests an intracardiac shuntd doppler echocardiography reliably assesses pressure gradients between cardiac chambers e radionuclide blood pool scanning accurately quantifies left ventricular function

15.The following statements about cardiac rhythms are truea Cardiac rate falls with inspiration in autonomic neuropathyb Re-entry tachyarrhythmias arise from anomalous AV conductionc Sinus bradycardia < 60/min is a normal occurrence during sleepd Sinus arrest is defined on ECG by P waves which do not elicit QRS complexese Episodes of both bradycardias and tachycardias suggest the sick sinus syndrome

16.In a patient with a recurrent AV nodal reentry tachycardiaA adenosine is the prophylactic therapy of first choiceb the cardiac rate is often 160-220 beats per minutec polyuria after a prolonged episode is characteristicd symptoms are invariably present during episodese transient bundle branch block on ECG indicate's coexistent myocardial ischaernia

17.Typical feature-of Wolff-Parkinson- syndrome includea tachyarrhythmias resulting from re-entry phenomenonab ventricular pre-excitation via an accessory AV pathwayc atrial fibrillation with a ventricular response of > 160/mind ECG between bouts showing prolonged PR interval with narrow QRS complexese useful therapeutic response to verapamil or digoxin

18.

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Atrial tachycardia with AV block is typically associated witha an irregularly irregular pulseb slowing of the atrial rate on carotid sinus massagec presence of P waves identical to those found during sinus rhythm'd digoxin toxicity and intracellular potassium depletione bizarre broad QRS complexes on ECG

19.Atrial fibrillation isA present in 10% of the elderly population over the age of 75 yearsb usually readily converted to permanent sinus rhythm using DC cardioversionc associated with an annual stroke risk of 5% if structural heart disease is presentd a common presenting feature of the sick sinus syndromee usually associated with a ventricular rate< 100 /min even before therapy is introduced

20. In patients with atrial fibrillation

a aspirin therapy alone does not reduce the risk of strokeb the radial pulse is typically irregularly irregularc the response in cardiac output to exercise is reduced due to the absenceof atrial systoled elective DC cardioversion is contraindicated during anticoagulant therapye alcohol abuse should be considered as a likely cause

21.Ventricular ectopic beatsa produce a clinically detectable reduction in stroke volumeb which are symptomatic usually indicate underlying heart diseasec secondary to cardiac disease typically disappear on exercised are likely to be escape beats when there is underlying bradycardiae following acute myocardial infarction indicate the need for antiarrhythmictreatment

22.In ventricular tachycardiaa underlying cardiac disease is usually presentb amiodarone is useful in the prevention of recurrent episodesc a shortened QT interval on ECG predisposes to recurrent episodesd carotid sinus massage usually slows the cardiac rate transiently

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e complicated by acute cardiac failure, cardioversion should be avoided

In ventricular fibrillationa the radial pulse is extremely rapid and threadyb unresponsive to treatment, profound hypokalaemia should be suspectedc ECG confirmation is vital before DC shock is administeredd cardioversion should be synchronised with the R wave on ECGe immediate lignocaine therapy avoids the need for cardioversion

24.In cardiopulmonary resuscitationa a sharp blow to the praecordium helps restore sinus rhythmb asystole is the commonest finding on ECGc a normal ECG suggests profound hypovolaemiad if cardioversion fails intracardiac adrenaline should be givene the compression to ventilation ratio should be 5 : 1

25.In the management of cardiac arrhythmiasA moderation of alcohol consumption should be advisedb symptoms are a reliable guide to the efficacy of drug treatmentc endocardial pacing should be considered for refractory paroxysmal tachycardiasd combination drug therapy is often better than monotherapye treatment of the causative disease is of no proven benefit

26.Digoxina shortens the refractory period of conducting tissueb usually converts atrial flutter to sinus rhythmc acts primarily on cell membrane ionic pumpsd effects are potentiated by hyperkalaern iae is a recognised cause of ventricular arrhythmias

27.The cardiac drugs listed below are associated with the following adverseeffectsa digoxin - acute confusional stateb verapamil - constipation c amiodarone - photosensitivity d propafenone -corneal microdeposits;e lignocaine - convulsions

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28.In the classification of antiarrhythmic drugs, the following statements are truea class I agents inhibit the fast sodium channelb class 11 agents are beta-adrenoceptor antagonistsc class I I I agents prolong the action potentiald class IV agents inhibit the slow calcium channele many antiarrhythmic agents have actions in more than one class

29.The following class 11 antiarrhythmic drugs selectively block the beta 1 adrenoceptorA sotalolb atenololc acebutolold metoprolole timolol

30.Amlodarone therapya prolongs the plateau phase of the action potentialb potentiates the effect of warfarinc is useful in the prevention of VT but not SVTd should be withdrawn if corneal deposits occure has a significant negative inotropic action

31.The following statements about atrioventricular block are truea first degree block produces a soft first heart soundb the PR interval is fixed in Mobitz type I second degree blockc decreasing PR intervals suggests Wenckebach's phenomenond irregular cannon waves in the JVP suggest complete heart blocke the QRS complex in complete heart block is always broad and bizarre

32.Absolute indications for permanent endocardial pacing includea asymptornatic congenital complete heart blockb asymptomatic Mobitz type I second degree heart blockc Adams-Stokes attacks in the elderlyd complete heart block due to rheumatic mitral valve disease

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e symptomatic second degree heart block following acute inferior myocardialinfarction

33.The following statements about bundle branch block (BBB) are trueA Right BBB is most often the result of left ventricular hypertrophyB Right BBB produces right axis deviation with a QRS > 0. 12 sec on ECGc Right BIBB produces fixed splitting of the second heart soundd Left BBB produces reversed splitting of the second heart sounde Left posterior herniblock produces left axis deviation on ECG

34.

Typical clinical features of acute circulatory failure due to anaphylacticshock includea elevated jugular venous pressureb warm dry skinc stridord confusione polyuria

35.Acute circulatory failure with an elevated central venous pressure are typicalfindings ina acute pancreatitisb massive pulmonary embolismc ruptured ectopic pregnancyd acute right ventricular infarctione pericardial tamponade

36.In a patient with cardlogenic shock due to acute myocardial infarctiona the absence of pulmonary oedema suggests right ventricular infarctionb the central venous pressure is the best index of left ventricular filling pressurec dopamine in low dose increases renal blood flowd high flow, high concentration oxygen is indicatede colloid infusion is indicated if oliguria and pulmonary oedema develop

37.In the treatment of cardiac failure associated with acute pulmonary oedema

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a controlled oxygen therapy should be restricted to 28% oxygen in patients who smokeb morphine reduces angor animi and dyspnoeac frusemide therapy given intravenously reduces preload and afterloadd nitrates should be avoided it the systolic blood pressure < 140 mmHge ACE inhibitors decrease the afterload but increase the preload

38.Right ventricular hypertrophy is a recognised finding in the followingcardiac disordersa tricuspid stenosisb constrictive pericarditisc cor pulmonaled atrial septal defecte mitral stenosis

39.Left ventricular hypertrophy is a typical finding in the following cardiac disordersa mitral stenosisb aortic stenosisc Addison's diseased left atrial myxomae hypertrophic cardiomyopathy

40.In chronic biventricular cardiac failureA angiotensin II contributes to renal salt and water retentionb excess ADH is the major cause of oedemac hyponatraemia usually indicates total body sodium depletiond cardiac sympathetic neural activity is markedly diminishede atrial natriuretic peptide is released

41.In the management of chronic heart failurea ACE inhibitor therapy reduces subsequent hospitalisation ratesb coagulation is impaired and thromboembolic risk therefore declinesc drug suppression of ventricular arrhythmia improves prognosisd the value of diuretic therapy is principally attributable to sodium depletione digoxin is only of benefit if atrial fibrillation coexists

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42. The diagnosis of rheumatic fever in a patient with an elevated ASO titre is

confirmed bya fever with an elevated erythrocyte sedimentation rateb arthralgia and a previous history of rheumatic feverc chorea and a prolonged PR interval on ECGd erythema nodosum and arthritise rheumatic nodules and pancarditis

43.In patients with significant mitral stenosisa the mitral valve orifice is reduced from 5 CM2 to about 1 CM2b a history of rheumatic fever or chorea is elicited in over 90%c left atrial enlargement cannot be detected on the chest X-rayd the risk of systemic emboli is trivial in sinus rhythme mitral balloon valvuloplasty is not advisable if there is also significant mitralregurgitation

44.Expected findings in a patient with significant mitral stenosis includea a soft early diastolic murmurb a quiet first sound and absence of an opening snapc left parasternal heave suggesting pulmonary hypertensiond a displaced apex beate the opening snap occurring just before the second heart sound

45.Recognised features of chronic mitral regurgitation includea soft first heart sound and loud third heart soundb presentation with signs of right ventricular failurec the severity of regurgitation is increased by afterload reductiond a pansystolic murmur and hyperdynamic displaced apex beate atrial fibrillation requiring anticoagulation

46.Disorders typically producing the sudden onset of symptomatic mitral regurgitation include a Marfan's syndrome b acute myocardial infarction c acute rheumatic fever

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d infective endocarditis e diphtheria

47.Clinical features suggesting severe aortic stenosis includea late-systolic ejection clickb pulsus bisferiensc heaving, displaced apex beatd syncope associated with anginae loud second heart sound

48.Disorders associated with aortic regurgitation include a ankylosing spondylitis b Marfan's syndrome c syphilitic aortitis d persistent ductus arteriosus e Takayasu's disease

49.In a patient with aortic regurgitation in normal sinus rhythma a mid-diastolic murmur is usually due to concomitant mitral stenosisb a systolic murmur is often due to coexistent aortic stenosisc a left parasternal heave and displaced apex beat are expected findingsd systemic diastolic arterial pressure is usually lowe a short early diastolic murmur suggests mild regurgitation

50.The following statements about tricuspid valve disease are truea murmurs are best heard in mid-sternum at the end of expirationb ascites occur with tricuspid regurgitation but not stenosisc tricuspid stenosis produces cannon waves in the JVPd both stenosis and regurgitation produce systolic hepatic pulsatione endocarditis suggests the possibility of intravenous drug abuse

51.The typical features of congenital pulmonary stenosis includea breathlessness and central cyanosisb giant'a'waves in the JVPc loud second heart sound preceded by an ejection systolic clickd left parasternal heave and systolic thrille enlargement of the pulmonary artery visible on chest X-ray

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52.In infective endocarditisa streptococci and staphylococci account for over 80% of casesb left heart valves are more frequently involved than right heart valvesc normal cardiac valves are not affectedd glomerulonephritis usually occurs due to immune complex diseasee a normal echocardiogram excludes the diagnosis

53.In the management of infective endocarditisA blood cultures are best obtained when the fever peaksb antibiotic therapy should be delayed pending bacteriological confirmationc parenteral antibiotic therapy should be continued for 6 weeksd persistent fever suggests the possibility of antibiotic allergye cardiac surgery should be considered if the vegetations are very large

54.The risks of developing clinical evidence of coronary artery disease areA increased by exogenous oestrogen use in postmenopausal femalesb diminished by stopping smokingc reduced by the moderate consumption of alcohold increased in hyperfibrinogenaerniae increased by hypercholesterolaemia but not hypertriglyceridaernia

55.In the investigation of suspected angina pectorisa the resting ECG is usually abnormalb exercise-induced elevation in blood pressure indicates significant ischaemiac a normal ECG during exercise excludes angina pectorisd coronary angiography is only indicated if an exercise test is abnormale physical examination is of no clinical value

56.In the treatment of patients with angina pectorisa aspirin reduces the frequency of anginal attacksb glyceryl trinitrate is equally effective when swallowed as when taken sublingually

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c calcium antagonists are more effective for coronary artery spasm than beta-blockersd tissue levels of nitrates must be consistently high for maximum therapeuticeffecte beta blockers are more effective than other anti-anginal agents

57.In the management of angina pectorisa coronary angioplasty improves symptoms and subsequent mortalityb coronary angioplasty should not be performed on stenotic arterial graftsc 90% of patients undergoing coronary artery grafting are pain free 5 years postoperationd coronary artery grafts improve prognosis in patients with stenosis of the left main coronary arterye the natural history of coronary artery disease is of progressively severe pain

58.Unstable angina isA invariably preceded by a history of effort anginab associated with progression to myocardial infarction in 15%c due to plaque rupture, thrombosis or coronary artery spasmd an indication for immediate exercise testing to assess prognosise best managed by emergency coronary artery bypass surgery

34.The clinical features of acute myocardial infarction includea nausea and vomitingb breathlessness and angor animic hypotension and peripheral cyanosisd sinus tachycardia or sinus bradycardiae absence of any symptoms or physical signs

60.Findings consistent with anterior myocardial infarction occurring within theprevious 6 hours includea hypertension and raised JVPb pericardial friction rubc ST elevation > 2 mm in leads 11, 111 and AVF on ECGd gallop rhythm and soft first heart sounde serum lactate clehydrogenase activity >3000 i.u./L

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61.The following drug therapies improve the long-term prognosis after acute myocardial infarction a aspirin b nitrates c calcium antagonists d ACE inhibitors e beta blockers

62.Coronary artery thrombolysis with streptokinase therapy isa of no proven benefit to patients over the age of 75 yearsb more beneficial in patients with ST depression than ST elevationc relatively contrainclicated in patients with uncontrolled hypertensiond best avoided in patients with chest pain without elevation of serum creatine kinase activitye more likely to cause anaphylactic shock than therapy with tissue plasminogenactivator

63.In the treatment of acute myocardial infarctiona aspirin given within 6 hours of onset reduces the mortalityb streptokinase therapy reduces infarct size and mortality by > 25%c diamorphine is better given intravenously than by any other routed immediate calcium channel blocker therapy reduces the early mortality ratee mobilisation should be deferred until cardiac enzymes normalise

64.In the treatment of arrhythmias following acute myocardial infarctiona atropine should be given for all sinus bradycardiasb frequent ventricular ectopics usually require lignocaine therapyc complete heart block in inferior infarcts; usually requires endocardial pacingd lignocaine therapy should be given before cardioversion for ventricular fibrillatione cardioversion is indicated for all tachyarrhythmias inducing acute circulatory collapse

65.

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The following statements about the prognosis of acute myocardial infarction are truea 75% of all deaths occur within the first 24 hoursb Survivors of early VF have a worse prognosisc Stress and social isolation adversely affect the prognosisd 5 year survival is 75% for those who leave hospitale Late mortality is determined by the extent of myocardial damage

66.The following statements about systemic hypertension are truea Casual blood pressure recordings correlate poorly with life expectancyb Systolic hypertension alone is of little prognostic valuec Most patients have a normal plasma renin concentrationd 15% of the adult UK population have essential hypertensione 15% of hypertensives have hypertension secondary to other disorders

67.Recognised causes of secondary hypertension includea persistent ductus arteriosusb primary hyperaldosteronismc acromegalyd oestrogen-containing oral contraceptivese thyrotoxicosis

68.In a patient with systemic hypertension, the following findings suggest thediagnoses showna symmetrical small joint polyarthritis: hyperparathyroidismb radio-femoral delay in the pulses: renovascular diseasec left ventricular failure:phaeochromocytomad epigastric bruit: coarctation of the aortae palpably enlarged kidneys: renovascular disease

69.Complications of systemic hypertension includeA retinal microaneurysmsb dissecting aneurysm of the ascending aortac renal artery stenosisd lacunar strokes of the internal capsulee subdural haemorrhage

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70.In the investigation of systemic hypertensionA hyperkalaernic metabolic acidosis indicates hyperaldosteronismb excretion urography is useful in the diagnosis of renal artery stenosisc normal urinary 5-1-11AA excretion excludes phaeochromocytomad urine analysis for blood, protein and glucose is essentiale the commonest cause of electrolyte abnormalities is diuretic treatment

71.Accelerated phase or malignant hypertension is suggested byhypertension anda a loud second heart soundb a heaving apex beatc headached retinal soft exudates or haemorrhagese renal or cardiac failure

72.In the emergency treatment of accelerated hypertensiona the aim is to lower the systolic blood pressure to normal within 60 minutesb intravenous sodium nitroprusside is usually necessary to control the severe hypertensionc parenteral therapy is preferable to oral therapyd vasodilator therapy to reduce the afterload should be usede ACE inhibitors are indicated if renal artery stenosis is suspected

73.In the treatment of mild to moderate systemic hypertensiona treatment has more effect on the risk of stroke than the risk of coronary heart diseaseb weight reduction is more important to prognosis than stopping smokingc treatment is less likely to be of benefit if cardiac or renal disease are presentd there are no proven benefits of therapy in patients aged over 70 yearse moderation of alcohol consumption is likely to improve blood pressure control

74.Important explanations for hypertension refractory to medical therapy include

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a poor compliance with drug therapy b inadequate drug therapy c phaeochromocytorna d primary hyperaldosteronism e renal artery stenosis

75.Recognised causes of pulmonary arterial hypertension include a mitral stenosis b atrial septal defect c chronic obstructive pulmonary disease d pulmonary thromboembolism e persistent ductus arteriosus

76.Typical clinical features of primary pulmonary hypertension includeA male preponderanceB exertional syncopeC systemic arterial emboliD giant 'a' waves in the JVP and right parasternal heaveE loud second heart sound and early diastolic murmur

77.

Clinical features characteristic of massive pulmonary embolism includea central and peripheral cyanosisb pleuritic chest pain and haernoptysisc breathlessness and syncoped tachycardia and elevated JVPe Q waves in leads 1, 11 and AVL on ECG

78.Recognised features of pulmonary infarction includea peripheral blood leucocytosis and feverb pleuro-pericardial friction rubc blood-stained pleural effusiond development of a lung abscesse ipsilateral elevation of the hemidiaphragm

79.In the treatment of acute pulmonary thromboembolisma streptokinase therapy should be given immediatelyb 24% oxygen therapy should correct hypoxaemia

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c diamorphine therapy should be avoided if the patient is severely hypoxicd heparin infusion should be given until warfarin therapy has become effectivee warfarin therapy should be continued for 4 weeks

80.Dilated (congestive) cardiornyopathy isa usually idiopathicb associated with pathognomonic ECG changesc a recognised complication of cytotoxic chemotherapyd associated with chronic alcohol abusee caused by coxsackie A infection

81.The clinical features of restrictive(obliterative) cardiornyopathy includea a presentation which mimics that of constrictive pericarditisb primarily characterised by impaired diastolic functionc association with primary or secondary amyloidosisd complication of conditions inducing a marked peripheral blood eosinophiliae gross cardiornegaly on chest X-ray

82.Clinical features compatible with idiopathic dilated cardlornyopathyincludea absence of a previous history of angina or myocardial infarctionb deep Q waves in anterior ECG leadsc biventricular dilatation with an ejection fraction < 20%d dyskinetic segment of left ventricle on echocardiographye functional mitral regurgitation

83.Clinical features compatible with hypertrophic cardiornyopathy includea family history of sudden deathb angina pectoris and exertional syncopec jerky pulse and heaving apex beatd murmurs suggesting both aortic stenosis and mitral regurgitatione soft or absent second heart sound

84.Typical features of acute pericarditis includea chest pain resembling that of myocardial infarction

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b a friction rub that is best heard in the axilla in mid-expirationc ST elevation on the ECG that is concave upwardsd elevation of the serum creatine kinasee ECG changes that are only seen in the chest leads

85.In a 20-year-old woman with acute pericarditis, the following disordersshould be excludeda Hodgkin's diseaseb systemic lupus erythematosusc coxsackie A virus infectiond acute rheumatic fevere rubella virus infection

86.The typical features of constrictive pericarditis includea severe breathlessnessb a normal chest X-rayc a previous history of tuberculosisd tachycardia and a loud third heart sounde marked elevation of the JVP with a steep Y and 'y' descent

87.Central cyanosis in infancy is an expected finding in the followingcongenital heart diseasesa persistent ductus arteriosusb transposition of the great arteriesc coarctation of the aortad Fallot's tetralogye atrial septal defect

88.The following statements about persistent ductus arterlosus are trueA Blood usually passes from the pulmonary artery to the aortab The onset of heart failure usually occurs in early infancyc A systolic murmur around the scapulae is typicald Shunt reversal is indicated by cyanosis of the lower limbse Prophylactic antibiotic therapy to prevent endocarditis is indicated

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89.Typical clinical features of coarctation of the aorta includea an association with a bicuspid aortic valveb cardiac failure developing in male adolescentsc palpable collateral arteries around the scapulaed rib notching on chest X-ray associated with weak femoral pulsese ECG showing right ventricular hypertrophy

90.In atrial septal defecta the lesion is usually of secundum typeb the initial shunt is right to leftc splitting of the second heart sound increases in expirationd the ECG typically shows right bundle branch blocke surgery should be deferred until shunt reversal occurs

91.In small ventricular septal defectsa the murmur is confined to late systoleb the heart is usually enlargedc there is a risk of infective endocarditisd surgical repair before adolesence is usually indicatede most patients are asymptomatic

92.In right-to-left shunt reversals of congenital heart disease

(Eisenmenger'ssyndrome)a pulmonary arterial hypertension is usually presentb closure of the underlying lesion produces symptomatic reliefc the chest X-ray is typically normald central cyanosis and finger clubbing are often presente physical signs of the underlying lesion persist unchanged

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93.In Fallot's tetralogya pulmonary and aortic stenosis are combined with a VSDb finger clubbing and central cyanosis are present from birthc the second heart sound is loud and widely split on inspirationd the chest X-ray and ECG are typically normale cyanotic spells occur due to episodes of dysrhythmia

94.Cardiovascular changes in normal pregnancy includea an increase in cardiac output by 150% by 12 weeksb tachycardia, elevated JVP and third heart soundc reduction in systemic diastolic pressured pulmonary systolic murmure increased blood coagulability

95.Recognised causes of deep vein thrombosis includea pregnancyb polycythaemiac prolonged travellingd cardiac failuree carcinomatosis

96.Clinical features of deep venous thrombosis includea cold, painful, blue limb with altered sensationb the absence of any abnormal physical signc warm, painless, oedematous, white limbd calf tenderness and fevere syncopal episode during defecation

97.In intermittent claudication due to atherosclerosisA pain is typically relieved by rest and elevation of the legb secondary ischaernic ulcers are usually painlessc pedal pulses are often still palpabled exercise which causes pain should be avoidede the risk of progression is lessened by warfarin

98.Recognised causes of Raynaud's phenomenon includeA beta-blocker therapy

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B cryoglobulinaemiaC progressive systemic sclerosisd vibration traumae giant cell arteritis

99.Arterial embolism is a recognisedcomplication ofA left atrial myxomab atrial septal defectc myocardial infarctiond infective endocarditise persistent ductus arteriosus

100.Clinical presentations of acute systemic arterial embolism includea a warm, painful, swollen legb left pleuritic chest painc a painful, cold leg with altered sensationd hypogastric pain with watery diarrhoeae expressive dysphasia after myocardial infarction

101.The risk of dissecting aortic aneurysm is increased ina Marfan's syndromeb coarctation of the aortac pregnancyd calcific aortic stenosise syphilitic aortitis

102.Characteristic features of dissecting aortic aneurysm include ahaernopericardium b acute paraparesis c interscapular back pain d early diastolic murmur e pleural effusion

103.In the New York Heart Association grading of dyspnoea or anginaa Grade 0 = asymptomaticb Grade 1 = symptoms on moderate

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exertion with minor restriction of activityc Grade 2 = symptoms on mild exertion with major restriction of activityd Grade 3 = symptoms on moderate exertion with major restriction of activitye Grade 4 = symptoms occur even at rest

104.Components of the jugular venous pulse are explained on the basis of the following eventsa 'c' wave = closure of the tricuspid valveb 'a'wave = atrial systolec 'v'wave = onset of ventricular systoled 'x'descent = atrial relaxatione 'y'descent = opening of tricuspid valve and onset of ventricular diastole

105.The following statements about the measurement of the blood pressure are truea An arm cuff smaller than recommended lowers BP recordingsb Appearance of the first Korotkov sound denotes systolic pressurec Muffling of the sound denotes phase V diastolic pressured Inter-observer variation is less with phaseIV than phase Ve Resting BP should be recorded, as random BP recordings do not correlate with morbidity

106.In the normal ECGa depolarisation proceeds from epicardium to endocardiumb depolarisation away from the positive electrode produces a positive deflectionc depolarisation of the interventricular septum is recorded by the wave in V5 + V6d the AVR lead = right arm positive with respect to the other limb leadse voltage amplitudes vary with the thickness of cardiac muscle