cardiology for mrcp part 1

1. CARDIOLOGY For MRCP part 1 Dr Simon Thackray Specialist Registrar & Honorary Lecturer in Cardiology Dr Justin Ghosh Lecturer in Clinical Cardiology

2. Anatomy

3. Right coronary artery

4. Left coronary artery

5. Question 1: Which of the following regarding the coronary collateral circulation is true? Collaterals are often demonstrated by angiography in coronary arteries with 80% stenoses Collaterals usually take several days to manifest angiographically after acute MI Collaterals represent the formation of new vessels as opposed to the utilization of existing blood vessels Coronary collaterals can dilate in response to nitrates and beta-adrenergic agonists and constrict in response to serotonin None of the above

6. The correct answer is d Collaterals tend to manifest in arteries with 90% or greater stenoses They are formed from very small, but pre-existing blood vessels normally present. Occur within a few hours in up to 50% of MI patients They have in-tact / functioning endothelium so will respond like normal coronary vasculature

7. Venous anatomy

8. Venous anatomy / anomaly

9. Q2: Which of these statements regarding the jugular venous pulse is correct?

10. The correct answer is B Upper limit of normal is 4cms H20 (=9cms or 90mm H2O in total / 28 (the relative atomic mass of mercury) = 4mmHg In health, the JVP drops during inspiration, but the amplitude (i.e. the magnitude of excursion from trough to peak) increases. A waves are still occasionally seen in atrial fibrillation, as there can be some organised atrial systolic activity. Canon a wave sin CHB Often with a pulsatile liver, but not in SVCO.

11. Phases of the JVP. A wave – atrial systole (and ‘venous milking’) C bump - (c for carotid, due to the proximate carotid impulse) followed by the X descent - (designed purely to confuse trainees), as the atrium fills, and also the base of the heart moves downwards. V wave – As the name suggests, the tricuspid valve is snapped shut (or not) Y down slope – tricuspid valve is open, passive filling

12. Types of JVP (not exhaustive list!) Peaked a wave – when the right atrium has to push: RVH, tricuspid stenosis, RV or Bi-V constriction. Canon waves – A-V dissociation, as the atria push against a shut tricuspid valve. TR – marked V wave and sharp CV descent Unilateral or asymmetrical JVP’s IJ thrombosis – when associated with oropharyngeal infection – lemmieres syndrome. Congenital Mediastinal nodes

13. Arterial waveforms

14. Anacrotic - AS

15. Bisferiens Bisferiens – When stroke volume is large, two systolic peaks. AR (with AS also) and HOCM. Remember both in systole

16. Dicrotic Pulse (rare as rocking horse , not to be confused with bisferiens), this is an exaggeration of the dicrotic notch (therefore occurring in diastole), seen in hypotensive patients with reduced PVR.

17. Pulsus alternans Alternating pulse volume (not respiratory variation) seen with poor LV function. (see also electrical alternans)

18. Pulsus bigeminus Seen in bigeminy due to altering R-R interval, very difficult to separate clinically from alternans.

19. Pulsus Paradoxus (a beloved MRCP topic) May be reversed (due to mechanical ventilation – a sensitive sign of hypovolaemia) Tamponade, asthma, constrictive pericarditis

20. Q 3: Which of the following is most likely to cause of a loud first heart sound? a) Severe rheumatic mitral stenosis b) Bradycardia c) WPW d) Hypovolaemia e) Right bundle branch block

21. A is the obvious answer, but C is the correct answer.

22. Splitting of the second heart sound

23. Opening snap The snap is caused by sudden flexing of the AMVL, pushed towards the LV cavity by high left atrial pressure (and low LV pressure). The shorter time to the snap, the higher the pressure. This relationship will be affected if LV pressure tends to be increased i.e. AR or LVH. No opening snap in AF

24. S3 & S4

25. Q4: Which of the following situations would have the most pressing requirement for warfarin anti-coagulation a) Established atrial fibrillation with severe mitral valvular disease b) A bioprosthetic aortic valve replacement. c) A Patch repair of an atrial septal defect d) A mechanical prosthesis in the mitral postion e) A Mechanical prosthesis in the aortic position.

26. The answer is d Biorostheses do not require warfarin Neither do patch repairs (usually aspirin for 6 months) Mitral valves (low flow velocities) are more thrombogenic

28. Embryology

32. Atrial septal formation. Aaaggghhh!!!

33. ASD’s Commonest type : secundum up to 1% of population 25% of people have a ‘probe patent’ foramen ovale – 10% on echo (PFO) – predisposes to embolic events No SBE prophylaxis required

34. Q7: The commonest pathological sequelea in ASD is a: Systemic Thrombo-embolism b: Pulmonary hypertension c: Heart failure d: Infective endocarditis e: Nitrogen bubble formation and embolisation ‘the bends’

35. The correct answer is a the commonest haemodynamic sequelea of ASD is atrial stretch and subsequent atrial arrhythmias, and this in turn leads to clot formation. 20PH is recognised (increased in females), but is less common. Heart failure is an unusual complication, as is I.E. The bends are a well recognised complication of ASD in SCUBA divers, and the combination of the two will not allow someone to dive again.

36. Ventricular Septal formation

37. Types of VSD Acquired – post infarct (bad news) Congenital Complete (AV canal defect – also bad news) Membranous Muscular Apical The larger the hole, the larger the shunt.

39. ECG’s & Electrophysiology Atrial repolarisation His bundle activation Sino-atrial node recovery time Inter-atrial conduction velocity Trans ventricular septal depolarisation

40. The correct answer is b

41. Autorhythmic cells Those capable of spontaneous discharge Other tissues are: strands of fibres towards the AV node, the AV node, Maheim fibres (near the AV node) His-Purkinje system in the R & L bundle and fascicles).

43. In Contractile cells: Depolarization is very rapid & is due to the inward diffusion of sodium (0). Repolarisation begins with a slow outward diffusion of potassium, but that is largely offset by the slow inward diffusion of calcium. So, repolarisation begins with a plateau phase. Then, potassium diffuses out much more rapidly as the calcium channels close, and the membrane potential quickly reaches the 'resting' potential.

44. Q9: Typical features of the Wenckebach phenomena include a) Progressive shortening of the PR interval b) Progressive shortening of the R-R interval c) Progressive broadening of the QRS duration d) Alternating non-conducted p waves e) Invariably present in VT

45. The correct answer is b

46. Q10: Atrio-ventricular nodal refractoriness is mainly dependent on a) Left ventricular loading characteristics b) Serum potassium levels c) AV nodal conduction velocities d) The preceding R-R interval. e) Sinus node rate

47. The correct answer is D

48. P wave amplitude Conduction velocity – electrolytes, autonomic state, metabolic state etc.. The distances involved from right to left atria The bulkiness of both atria (p pulmonale / p mitrale) None of these really affect the PR interval to a profound extent, the AV node is much more critical to that.

49. Myocardial Contraction ATP dependent (obviously). Relaxation is also an ‘active’ energy dependent process End diastolic fibre length dependent (starling) Macroscopically – contraction of the LV is longitudinal, transverse and rotational

50. Cardiomyocytes Have several nuclei Contraction is utterly Ca++ dependent, most calcium never leaves the cell, just washes in an out of the sarcoplasmic reticulum. Calcium passes through voltage-gated channels on the SR – sometimes known as ryanodine receptor. The uptake receptor is called the SERCA pump. Stored in calsequestrin.

51. Contractile proteins Myosin = thick filaments Actin = thin filaments, these contain tropomysin and troponin C,T and I

52. Beta 1 adrenergic effects are via cyclic AMP causing increased free calcium Cholinergic receptors increase cyclic GMP

53. ECG’s RBBB Commonly seen in the general population. The RB is quite ‘fragile’. QRS > 120 (100 – 120 = partial RBBB) RSR pattern – right praecordial leads. Often inverted T waves here Deep S waves (longer in duration that the preceding R wave) laterally. No axis shift (if there is think LAHB) ** if there is also persistent ST elevation in the right praecordial leads think Brugada Associated with RBBB: Acute PE, ASD, RV strain.

54. Left anterior Hemi-block Right axis deviation QRS <120 RSR pattern in II, III and AVF Can be a variation of normal

55. Left Posterior Hemi-block Rare Almost always pathological

56. Left Bundle Branch block Usually pathological; Poor prognostic marker in heart failure QRS>120 (essential, between 100 and 120 = partial LBBB) Notched R waves laterally (M) Small or absent r wave in right praecordial leads Prolonged intrinsicoid deflection (60msecs)

57. Axis deviation causes of a Northwest axis (no man's land) emphysema hyperkalaemia lead transposition artificial cardiac pacing ventricular tachycardia

58. causes of right axis deviation normal finding in children and tall thin adults right ventricular hypertrophy chronic lung disease even without pulmonary hypertension anterolateral myocardial infarction left posterior hemiblock pulmonary embolus Wolff-Parkinson-White syndrome - left sided accessory pathway atrial septal defect ventricular septal defect

59. causes of left axis deviation left anterior hemiblock Q waves of inferior myocardial infarction artificial cardiac pacing emphysema hyperkalaemia Wolff-Parkinson-White syndrome - right sided accessory pathway tricuspid atresia ostium primum ASD injection of contrast into left coronary artery

60. Antiarrhythmics (I) Vaughan – Williams is an oversimplification, but a reasonable starting point Class I drugs mainly act on the fast Na channel (and to some extent K channels)

61. Mechanisms of Arrhythmia Enhanced automaticity (e.g. inappropriate sinus tachycardia, some VT’s) 20% Triggered activity (ventricular ectopics) 5% Re-entry mechanisms (commonest) 75% Two routes of attack, via conduction velocity or via refractoriness

62. Class 1a Slow the rate of rise of the action potential, so delay depolarisation Quinidine, procainamide and disopyramide Quinidine: vasodilates; hypotensive. Not negatively inotropic. Chinconism, auto-immune type reactions. – not used often (at all really) – risk of torsade.

63. Procainamide (1a) AF and VT – rarely used though Multiple side effects – SLE type syndrome

64. Disopyramide (1a) Used increasingly in VT patients unable to take amiodarone. Also used to treat some bradycardias (neurocardiogenic syncope) Prolongs APD and ERP Muscarinic blocker therefore anticholinergic (vagolytic) Negatively inotropic. Side effects relate to

65. Class 1BLignocaine, mexelitine, phenytoin Reduce action potential duration (in ventricular myocytes not atrial) Only really active on re-entrant circuits, giving bi-directional block Short half life (so infusion needed) Only –ve inotropic at very high doses Side-effects are CNS, rarely malignant hyperthermia Mex is the oral version of Lig (more or less), used to treat VTsometimes

66. Class 1cFlecainide, Propafenone, Moricizine Flecainide Acts on rapid Na+ channel, slows onset of AP, and also reduces conduction velocity Can be pro-arrhythmic (especially in ischaemic tissue, and during exercise) Negatively inotropic Renally excreted Avoid in CAD and CHF and caution in heart block Excellent in AVRT (accessory pathways) PR / QRS / ST / QT intervals all increase

67. Propafenone Blocks fast sodium channels Depresses LV function, but less than Flec’ The +ve enantiomer is also beta-blocking Used in SVT’s Use is retsricted in heart failure and CAD (similar to Flec’), but it may be different due to its beta-blocking action

69. Class II – The beta-blockers Effect is usually due to the –ve levorotatory stereo-isomer Also local anaesthetic (at high doses) No effect on action potential, but block the effect of catecholamines on APD and ERP Sotalol is also Class III, and will prolong ERP by slowing repolarisation

70. Class IIIAmiodarone, Sotalol, Bretylium, ibutilide, dofetilide Amiodarone Heavy liver metabolism, Desmethylamiodarone also active (binding to fast sodium channels) Prolongs APD and refractoriness Slows sinus rate and prolongs QT interval (Actually has class I, II and III effects)

71. Amio Cont Excreted in bile Amio & Desmeth bind avidly to tissues hence long half life (myocardial concentration 50x that of plasma) Steady state takes 256 days (4.5 HL’s) Improved survival compared to placebo post cardiac arrest (AVID)

72. Amio 1/3 Need to sop drug at 5 years due to S/E Pulmonary fibrosis (cough/SOB/even pyrexia) Uncommon at <300 mg/day Hyper or hypo thyroidism. Due to I load, and inhibition of peripheral T4 to T3 conversion Corneal microdeposits Skin hypersensitivity and discolouration

73. Class IV – Ca++ Channel blockers Dilt and verapamil block slow calcium channels Prolongs APD (in purkinje fibres) Verapamil negatively inotropic – dilt much less so SVT’s and RVOTT (LBBB morphology VT)

74. Adenosine Nucleoside Interacts with A1 receptors on cardiac cells activating K+ channels (Acetylcholine) Increased GMP activity in AV node and decreased CAMP activity Half life is 1-6 seconds Caffeine and theophylline antagonise

75. 1)A 60 year old man is readmitted 7 days after an inferior myocardial infarction, with acute pulmonary oedema. He was not thromolysed on his initial admission. On examination he has a systolic murmur and BP 180/110. The most helpful investigation would be : Echocardiogram Troponin assay Angiography Holter monitoring Swan Ganz catheterisation & Pa02 measurements

76. The likely diagnosis for this man is: a)Ischaemic LVF b)Reocclusion of the right coronary artery. c)Ventricular tachycardia. d)Ventricular septal defect. e)Acute MR due to papillary muscle rupture.

77. ) The correct answers are 1(a) and 2(e). The presentation is classical for both acute VSD and acute MR, and echocardiography would be quickly diagnostic. If patients with an inferior infarct, acute MR is more probable. If the infarct had been antero-septal, VSD would have been more likely.

78. A 75year old man is admitted following a collapse while walking has dog. He has an ejection systolic murmur, and echocardiography shows aortic stenosis with a gradient of 108mmHg. The most useful test is: a)Holter monitoring b)Exercise tolerance testing. c)Transoesophageal echocardiography. d)Coronary angiography. e)Tilt testing.

79. The answer is (d). Syncope on exertion with the echo findings confirm the diagnosis of haemodynamically significant AS. With the diagnosis made, the remaining question is : does this man need CABG while having his aortic valve replaced.

80. You need to design a clinical trial to assess the effectiveness of a new beta blocker (X) in heart failure patients. The trial design should be: a) A double blind crossover study with 3 months bisoprolol and 3 months X. b) A Single blind placebo controlled trial. c)A double blind placebo controlled study. d)A double blind parallel group study comparing X with carvediolol. e)A multicentre, double blinded, randomised, placebo controlled study.

81. The correct answer is (d). Cross over studies are good for assessing small numbers of patients, for symptoms and other softer endpoints. The treatments being compared would need fairly clear onset and offset timings, as a period of `washout` between treatment periods may be needed. For a treatment where mortality needs assessing parallel groups would be much better. Double blinding is better than single!!! It would be un-ethical to assign a heart failure patient to a treatment allocation of no beta blocker(placebo).

82. A 60year old patient is admitted with a collapse. The ECG shows sinus bradycardia with occasional episodes of AV block upto 3.1 seconds. The QRS duration is 178ms. The recommended treatment should be: a)Implantation of a VVIR pacemaker b)Implantation of a DDD(R) pacemaker c)Implantation of a AAIR pacemaker. d)Implantation of a Bi-Ventricular pacemaker. e)A period of observation and 24hour holters.

83. The correct answer is (b). If the patient had pauses and AF then (a) would be correct. Implanting an Atrial pacemaker is not helpful if the site of block is futher downstream (AV)!!!! A Bi-pacemaker is a bit of a red herring. Irrespective of the QRS duration, if there is not moderate to severe heart failure, there would be no benefit. Observation would be risky, as the next time he collapses he could be standing at the top of a very tall flight of stairs. Are you brave enough to observe him?

84. Nomenclature of Pacemakers * They are named with a 5 letter code (but you should make sure you know at least the first 3), in which the first letter indicates the chamber that receive pacing impulse, the second letter tells the chamber in which R wave (or P wave) sensing is occurring. The third letter describes the mode of action

85. Patients with symptomatic systolic heart failure should receive (unless otherwise contraindicated) : a)ACE inhibitors and beta blockers b)Diuretics and beta blockers c)Spironolactone, ACE inhibitors and Digoxin. d)ACE inhibitors, beta blockers, diuretics and Angiotensin receptor blockers. e)None of the 1-4

86. The correct answer is (d). This is a bit contentious, but looking at recent evidence: If the patient has symptomatic heart failure they should be on a diuretic! ACE inhibitors and beta blockers have good mortality evidence, and all should receive them. Recent result have also shown additional benefits with the A2RA candesartan for heart failure patients. ValHeft also showed benefit for Valsartan.

87. For hypertension which of the following is true: a)It is acceptable to use diltiazem in the presence of heart failure. b)All antihypertensives are effectively the same. c)Single agents should be maximally uptitrated before considering an additional agent. d)Diuretics are a good choice for Afro-Caribbean patients e)B.P. has not been shown to be linked with mortality.

88. The correct answer is (d). It is better to avoid all Ca antagonists in CHF. The NSF marks Amlodipine as the only approved Ca antagonist. The most negatively inotropic is Verapamil. The guidelines from the Joint British Societies indicate that multiple agents will often be required, and high doses of single agents is associated with side effects. Afro-Carribean patients tend to develop a low renin, salt sensitive hypertension. Diuretics and Ca antagonists are the most valuable. Following diuretic introduction, ACE inhibitors and beta blockers regain more therapeutic effect. BP is strongly linked with CVA, MI and mortality in many studies.

89. ) A 65 year old man with a history of severe heart failure on optimal treatment attends AAU with episode of pre-syncope. While under observation collapses with VT. The correct initial treatment is: a)Bolus of lignocaine b)Bolus of amiodarone. c)Bolus of beta blocker. d)Electrical cardioversion. e)See what happens.

90. The correct answer is (d) This is easy….. For any patient with significant hypotension due to a tachyarrhythmia, electrical cardioversion is the treatment of choice.

91. For the same man, the correct long term management strategy is: a)Addition of amiodarone. b)Switch beta blocker c)AICD insertion d)Electrophysiology studies. e)See what happens.

92. The correct answer is (c). Patients with heart failure remain at high risk of arrhythmic death, with approximately 50% of patients dying suddenly. AICD has consistently been shown to decrease mortality in patients with poor ventricular function.

93. Which of the following is false? a)A systolic murmur in pregnancy is frequently innocent. b)A large VSD may have an inaudible murmur. c)In aortic stenosis loss of the second heart sound indicates severe disease. d)A diastolic murmur in pregnancy is frequently innocent. e)The mumur of pulmonary stenosis radiates to the back.

94. The correct `false` answer is (d) During pregnancy expansion of the circulatory volume and increase in cardiac output often results in an innocent `flow murmur`. Flow across a VSD is related to the size, but faster more audible jets usually occur with small VSD, whereas larger shunts result in lower velocity flow, and quieter murmurs. Loss of A2 is a marker of significant AS, together with a slow rising pulse. A diastolic murmur in pregnancy requires full investigation as it is rarely innocent. Mitral stenosis may be unmasked by pregancy.

95. Concerning Amiodarone, which is true? a)It universally treats tachyarrhythmias irrespective of cause. b)It is a coronary artery dilator due to beta blocking effects. c)Thyroid dysfunction is its most serious side effect. d)It has a half life of 60 days e)It can cardiovert AF to sinus rhythm

96. The correct answer is (e). It has a wide range of uses, but should not be used as first line for VT related to a long QT interval, as it can lengthen it further. Amiodarone is a vasodilator, so should be used with caution in hypotensive patients. This is due its action as a calciumk antagonist. It also has beta and alpha blocking effects. It has a variable half life probably ranging from 90-180 days, While Amiodarone use usually results in rate control, cardioversion can occur in a minority of cases (1/3 or less).

97. Concerning Digoxin, which is true? a)It can cardiovert AF to sinus rhythm. b)It has a high therapeutic index c)It is an inotrope due to beneficial effects on intracellular calcium levels. d)When a loading dose is required, this is best given as a single IV bolus e)Digoxin use can protect against hypokalaemia

98. The correct answer is (c). Digoxin is a rate control agent It has a low therapeutic index. Loading is safest using a SPLIT oral regimen. Digoxin competes with cardiac K+ cellular transport, and may protect slightly against Hyperkalaemia. Digoxin has been recognised as a positive inotrope, as it has beneficial effects on the calcium dependant calcium transporter, resulting in higher free intracellular calcium (used for active contraction)

99. When differentiating between VT and SVT with aberrancy the following favours SVT: a)Previous myocardial infarction. b)Fusion or capture beats. c)History of heart block d)Positive deflection in V1 and V6 e)Irregular rate.

100. The correct answer is (e) a-d favour VT. VT is a regular rhythm. Any significant irregularity points to atrial fibrillation.

101. The following are not causes of QT prologation. a)Jervell-Lange-Neilsen syndrome b)Mitral valve prolapse c)Erythromycin d)Amiodarone. e)Lown-Ganong-Levine syndrome.

102. The correct answer is (e) The list of QT prolongers also includes Romano Ward syndrome (sensory deafness) IHD Hypo :calcaemia, thyroidism, thermia, kalaemia Quinidine, Tricyclics, phenothiazines some anthistimines. LGL is a syndrome with an accessory pathway similar to WPW, but with no delta wave (just a short PR)

103. For SBE : a)Staph. Epidermidis is the most frequent causative organism. b)Left untreated it has a mortality of 90%. c)Prosthetic valve disease accounts for the majority of cases. d)Septic emboli indicates early surgery. e)Tricuspid valve disease is usually as a result of rheumatic fever.

104. The correct answer is (d). Other indications for surgery include : CCF, Severe valve incompetence, Antibiotic resistance, and large vegetations. The most common organisms are Strep. Viridans and Staph.Aureus. Epidermidis is most common post valve replacement. Left untreated endocarditis has a mortality of 100%. Prosthetic valve BE accounts for 10% IV drugs 10% Congenital Heart disease 10% Rheumatic heart disease 30% Normal Hearts 40%

108. The correct answer is (c). The PV loops show a dilated failing heart. The volumes are larger than normal, and loops with larger end diastolic volumes do not eject enough blood to return to a normal end systolic volumes. There has been a failure of the normal compensatory mechanisms.

109. In acute severe heart failure : A)The patient needs IV diuretics due for fluid overload. B)NIPPV ventilation is the most effective mechanical treatment. C)The patient is sweating in an effort to lose fluid. D)Afterload reduction is the best treatment for patients with high systolic BP. E)Frusemide administration results in an increase in cardiac output.

110. The correct answer is (d) Patients with acute heart failure are rarely fluid overloaded….it is just in the wrong fluid compartment. If mechanical ventilation is requires continuous positive pressure should be used. Patients sweat due to reflex release of adrenaline and nor-adrenaline in an effort to maintain cardiac output. This is however detremental to the failing heart which can not cope with the resulting increase in blood pressure – afterload. Intravenous nitrates have shown significant benefit. Frusemide actually decreases cardiac output.

111. Which of the following statements regarding Fallot’s Tetralogy is not true A) Surgical treatment increases the risk of infective endocarditis B) Without treatment it is invariably fatal by the 4th decade C) They are often associated with ASD D) Pulmonary hypertension is rare E) It is the commonest cyanotic congenital heart disease.

112. The correct answer is (b)