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Cardiology Finals Revision Andrew Degnan PALI Wednesday 12 th September 2012.

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Presentation on theme: "Cardiology Finals Revision Andrew Degnan PALI Wednesday 12 th September 2012."— Presentation transcript:

1 Cardiology Finals Revision Andrew Degnan PALI Wednesday 12 th September 2012

2 Why Cardiology?

3 2005 – Paper 1-Heart failure – Paper 2-Unstable angina – Resit 1-Aortic stenosis – Resit 2-Infective endocarditis and pericarditis 2006 – Paper 1-Heart failure – Paper 2-Primary prevention 2007 – Paper 1-Heart failure and pericarditis – Paper 2-None 2010 – Paper 1-None – Paper 2-Postural hypotension – Resit 1-Aortic stenosis – Resit 2-Infective endocarditis 2011 – Mock-Heart failure – Paper 1-None – Paper 2-Infective endocarditis and heart failure – Resit 1-Acute MI – Resit 2-Postural hypotension 2012 – Paper 1-None – Paper 2-Unstable angina and postural hypotension

4

5 2012 Mock Paper Unstable Angina

6 MEQ 1.8 A 39 year old Asian man was admitted to the medical admissions unit with pains in his chest and neck. He admitted to smoking 20 cigarettes per day and a blood cholesterol had been measured at 7.2mmol/L (reference range mmol/L). His average HR on admission was 90 bpm and his blood pressure was 170/100mmHg. An initial diagnosis of unstable angina was made. (a)  What are his risk factors for coronary artery disease? (2 marks)

7 MEQ 1.8 A 39 year old Asian man was admitted to the medical admissions unit with pains in his chest and neck. He admitted to smoking 20 cigarettes per day and a blood cholesterol had been measured at 7.2mmol/L (reference range mmol/L). His average HR on admission was 90 bpm and his blood pressure was 170/100mmHg. An initial diagnosis of unstable angina was made.

8 Risk Factors for CVD Unmodifiable Factors Male Increasing age Asian decent Post-menopause Family History Modifiable Risk Factors Smoking Hyperlipidaemia Obesity (diet and exercise) Diabetes Hypertension Stress

9 (b)  You decide to admit him to hospital. What drug therapy could he be started on? List 4 potentially beneficial drugs (2 marks) and give a reason for prescribing each (2 marks).

10 Immediate Treatment of NSTEMI and UA Anti-ischaemic therapy (decrease myocardial oxygen demand) – Nitrates (GTN  IV), venodilation, decrease venous return – Beta-blockers, decrease sympathetic drive and so decrease O2 demand Anti-thrombotic therapy (prevent further development of partially occluded thrombus) – Aspirin, prevents platelet aggregation and activation – Clopidogrel, alternative action on platelets. Can be used in combitaion with or in place of aspirin – Heparin, usually LMWH, breaks down any clots

11 Results of blood tests revealed a Troponin T of 0.35ng/ml (normal=unrecordable), peak CK was 180iu/ml (reference range: iu/ml) on day 2 (c)  List the 2 cardinal ECG features of an acute full thickness anterior myocardial infarction and outline their electrophysiological cause (4 marks)

12 The Easy Bit

13 The Hard Bit Is it enough to answer with “It just does”?

14 ST Elevation – Changes in the action potentials produced by necrotic tissue – Abnormal firing of action potentials leads to early repolarisation secondary to ischaemia, causing this abnormal wave Pathological Q Waves – Any initial downward movement of the QRS is a Q wave. – Pathological Q waves are Q waves developing after MI which have a width of ≥ 1 small box and a depth > 25% of the total QRS height – Develop from living tissue behind the infarct which is picked up by the ECG as a downward movement as impulses move away from the anterior leads

15 Cardiac Enzymes

16 Discussion Points?

17 2005 Paper 1 Left Ventricular Failure

18 MEQ 1.2 A 78 year old man had a large anterior myocardial infarction three years ago. Initially he made a good recovery, but has had to take a diuretic for ankle swelling since. In the last 2 months he has become short of breath on exertion. You suspect that he has developed left ventricular failure (a)  Give 2 additional symptoms that would support this diagnosis (2 marks)

19 MEQ 1.2 A 78 year old man had a large anterior myocardial infarction three years ago. Initially he made a good recovery, but has had to take a diuretic for ankle swelling since. In the last 2 months he has become short of breath on exertion. You suspect that he has developed left ventricular failure (a)  Give 2 additional symptoms that would support this diagnosis (2 marks)

20 Left Heart Failure Exertional dyspnoea Orthopnoea Paraxysmal nocturnal dyspnoea Fatigue and weakness Poor exercise tolerance Cardiac wheeze Nocturnal cough with frothy pink sputum Impaired urine output during the day and nocturia at night Impaired metal status Cold peripheries Right Heart Failure Peripheral oedema Abdominal discomfort Weight gain Anorexia and nausea

21 Left Heart Failure Exertional dyspnoea Orthopnoea Paraxysmal nocturnal dyspnoea Fatigue and weakness Poor exercise tolerance Cardiac wheeze Nocturnal cough with frothy pink sputum Impaired urine output during the day and nocturia at night Impaired mental status Cold peripheries Right Heart Failure Peripheral oedema Abdominal discomfort Weight gain Anorexia and nausea

22 Left Heart Failure Cachexia Cyanosis Sweating Tachopnoea Tachycardia Pulses alternans Bilateral basal crackles Displaced apex beat Extra heart sounds and murmurs (depends on cause) Right Heart Failure Cachexia Oedema Increased JVP with positive hepatojugular reflex RV heave Hepatomegaly Ankle oedema Sacral oedema Ascities

23 (b)  You arrange for a chest X-ray. Give four features that would support the diagnosis of left ventricular failure (4 marks)

24 Adapted from

25 Adapted from Pulmonary%20edema-CHF/caseoftheweek267page.html

26 Adapted from

27 Adapted from diagnosis-6/

28 (c)  Give 2 neurohormonal mechanisms which may be activated in heart failure (2 marks)

29 4 Neurohormonal Mechanisms 1.Sympathetic Nervous System Activity – Fall in CO detected by baroreceptors, sympathetic drive increases, ↑ HR and BP 2. RAAS – Decreasing renal perfusion activates RAAS which ↑ PVR (angiotensin II) and blood volume (aldosterone) which both play a role in ↑ BP 3. ADH – Released in response to low BP and release of angiotensin II. ↑ blood volume and hence BP 4. Natriuretic Peptides – Both ANP and BNP. Both inhibit RAAS and so ↓ blood volume and BP. Beneficial effect, but not released in sufficient enough quantities. BNP=prognostic marker

30 These all have an effect on…? Frank Starling Mechanism Improved venous return improves LV contraction Preload vs. afterload And this combination leads to Symptoms of LV HF Hypertrophy

31 (d)  If starting this patient on an ACE inhibitor, what precautions would you take? (3 marks)

32 Side-effects First dose hypotension Persistent cough Hyperkalaemia Renal impairment Headache Dizziness Fatigue Nausea Contra-indications and Cautions Hypersensitivity Bilateral renal artery stenosis Pregnancy Impaired renal function Aortic stenosis Cardiac outflow obstruction Hypovolaemia Haemodialysis

33 Other Precautions Check baseline BP (first dose hypotension) and Us+Es (hyperkalaemia, renal dysfunction) Start low, tritrate dose up Continue to monitor Us+Es Drug interactions

34 Discussion Points?

35 2011 Paper 2 (also 2005 Resit 1 and 2010 Paper 2) Infective Endocarditis

36 MEQ 2.6 A 32 year old woman, who is a known alcoholic and abuser of intravenous drugs, presents to A+E complaining of gradual onset malaise, fever, weight loss and night sweats. She is pyrexial (38.5°). She has a pansystolic murmur which is thought to be a new finding and you suspect she has a diagnosis of infective endocarditis (a)  Name 4 additional clinical signs that may be found on examination in this patient (2 marks)

37 MEQ 2.6 A 32 year old woman, who is a known alcoholic and abuser of intravenous drugs, presents to A+E complaining of gradual onset malaise, fever, weight loss and night sweats. She is pyrexial (38.5°). She has a pansystolic murmur which is thought to be a new finding and you suspect she has a diagnosis of infective endocarditis (a)  Name 4 additional clinical signs that may be found on examination in this patient (2 marks)

38 orrhage.jpg

39 Signs of Infective Endocarditis Hands – Splinter haemorrhages – Janeway lesions – Osler’s nodes – Clubbing

40 Signs of Infective Endocarditis Hands – Splinter haemorrhages – Janeway lesions – Osler’s nodes – Clubbing Eyes – Roth Spots

41

42 Signs of Infective Endocarditis Hands – Splinter haemorrhages – Janeway lesions – Osler’s nodes – Clubbing Eyes – Roth Spots Heart – New murmur – Signs of HF Others – Abscess – Splenomegaly – Petechia

43 AgentRoute Strep. ViridansDental procedures Staph. aureusIVDU/Thoracotomy/Peripheral lines EnterococciUTI CandidaPeripheral lines/catheters Strep. BovisColorectal carcinoma (b) Name the 2 most likely organisms likely to be implicated in infective endocarditis (2 marks)

44 Blood (microhaematuria) Pathology – Micro-emboli from vegetation on heart valve – Can block vessels in the glomerulus, causing glomerularnephritis and ARF. – Micro-emboli cause other clinical signs (c) Your FY2 asks you to dip the urine. What would you expect to find and what is the pathology behind this abnormality? (2 marks)

45 (d)  Name two investigations that are mandatory to confirm your diagnosis (1 mark)

46 Blood Cultures – 3 sets – Different times – Different places Major Criteria (x2) Positive blood culture – Typical organism in 2 separate cultures – Persistently +’ve over time Echo evidence of valvular involvement New valvular regurgitation (murmur) Echo – Trans-oesophageal more sensitive – >2mm for trans-thoracic Minor Criteria (x5) Risk factors Fever Vascular phenomenon Immunological phenomenon Positive blood cultures not meeting requirement for major criteria Echo evidence not meeting requirement for major requirement Dukes Criteria 1 Major + 3 Minor

47 Environment favourable to Infection IVDU Dental surgery Thoracotomy Catheterisation Peripheral/central lines Immunosuppression Allow Implantations and Growth of Organism Prosthetic heart valve Pre-existing valvular disease – Rheumatic – Acquired – Congenital (e) Other than IVDU, name 4 risk factors for this condition (2 marks)

48 On further examination you can also hear the pansystolic murmur. This is loudest at the left sternal edge and you demonstrate the JVP is elevated with giant “v” waves. In addition she also has tender pulsatile hepatomegaly. (f)  What is the most likely cardiac lesion to be responsible for this, given the above history and examination? (1 mark)

49 On further examination you can also hear the pansystolic murmur. This is loudest at the left sternal edge and you demonstrate the JVP is elevated with giant “v” waves. In addition she also has tender pulsatile hepatomegaly. (f)  What is the most likely cardiac lesion to be responsible for this, given the above history and examination? (1 mark) Tricuspid Regurgitation

50 Murmurs Systolic Loud Radiate Ejection Systolic – Aortic Stenosis Pansystolic – Mitral Regurge Diastolic Quiet Accentuated by manoeuvres Early-mid diastolic – Aortic regurge Late diastolic – Mitral stenosis Remember DARMS

51 Discussion Points?

52 Thank You!


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