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Finals Revision > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Physical signs of infective endocarditis.

A

Changing murmur (90%), Pyrexia (90%), Microscopic haematuria (70%), Petechiae (50%), Roth spots, Janeway lesions, Osler’s nodes, splinter haemorrhages, clubbing

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2
Q

What are the main organisms that cause Infective Endocarditis?

A

Staphylococcus from IVDU (aureus, epidermidis), Strep viridans (50-70%)

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3
Q

What increases risk of infective endocarditis due to strep viridans?

A

Damaged valve e.g. rheumatic heart disease, older age. Strep viridans is usually wiped out by immune system. Increases risk of other valvular disorders as well.

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4
Q

What organism causes acute rheumatic fever?

A

Group A strep causes strep throat. A few weeks later you get an autoimmune reaction that attacks self tissue.

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5
Q

What causes chronic rheumatic heart disease?

A

Fibrosis of heart valves (MS, AR) occurs ~20 years later.

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6
Q

Why do IVDUs get infective endocarditis? What side of the heart is mostly affected?

A

Get Staph infection entering the venous drainage which enters the right heart (tricuspid and pulmonary valves affected)

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7
Q

What side of the heart is commonly affected by strep viridans in infective endocarditis patients?

A

Left side. Older patients as they have damaged mitral valves as it’s pummelled by the highest amount of pressure.

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8
Q

Features of acute rheumatic fever? (major criteria for Duckett Jones criteria)

A

Carditis, polyArthritis, Sydenham’s chorea, Erythema marginatum, Subcutaenous nodules along the extensor surfaces

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9
Q

Which murmur causes mitral facies?

A

Mitral stenosis

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10
Q

What murmur causes a loud second HS?

A

Mitral stenosis

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11
Q

Why might you not hear mitral stenosis? What can you do to hear it?

A

Raised cardiac output is required to hear the murmur. Won’t hear it if inactive. Exercise the patient to hear the murmur.

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12
Q

What signs would be present in mitral stenosis?

A

malar flush, usually middle aged woman, AF, tapping apex (palpable heart sound), non-displaced apex, right ventricular heave, blowing mid diastolic murmur with presystolic accentuation

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13
Q

What signs would be present in mitral regurgitation?

A

Displaced apex, apical thrill, S1 quiet, pansystolic murmur radiating to axilla. S3 Present.

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14
Q

What signs would be present in aortic regurgitation?

A

Collapsing pulse, Corrigan’s sign, De Musset’s sign, Quincke’s sign, dynamic apex, early diastolic murmur at left sternal edge, systolic flow murmur, Luetic/Marfans/Ank spondylitis/Reiter/endocardiis/old rheumatic fever signs

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15
Q

What does this image show?

A

Malar flush

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16
Q

What does this image show?

A

Erythema marginatum- acute rheumatic fever

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17
Q

What does this ECG show?

A

atrial fibrillation

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18
Q

Causes of AF?

A
  1. Ischaemic heart disease
  2. Rheumatic heart disease
  3. Thyrotoxicosis
  4. PE
  5. Cardiomyopathy
  6. Ca bronchus
  7. Alcohol
  8. lone AF
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19
Q

What does this ECG show?

A

R wave progression which is normal and means there’s unlikely to be PMH of MI

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20
Q

What does this ECG show? Why is not pericarditis? Where is the pathology likely to be?

A

Full thickness acute MI. V1-V6 ST elevation.

Not pericarditis as the ST elevation is not global.

LCA occlusion causes this pattern.

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21
Q

What does this ECG show?

A

ST elevation in leads II, III and aVF. This suggests an inferior MI.

There is also ST depression in leads aVL, V1, V2, V3. Some ST change in V4 and V6. These are non-specific so suggest ischaemic changes.

The bradycardia could be due to arrhythmia (issue in SAN) or on beta blockers for past MI.

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22
Q

What does this ECG show?

A

ST depression in leads aVL, and V2 leads. This is actually an upside down ST elevation of the posterior wall. Likely due to an infarction with true posterior extension. Posterior infarction by itself is unlikely.

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23
Q

What does this ECG show? It is a 47 year old man with severe central crushing chest pain.

A

ST elevation MI with Type I heart block

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24
Q

How do you manage complete heart block? Is it regular or irregular?

A

Needs pacing, attach an external pacemaker. It is regular as there is a new ventricular origin of heart beat.

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25
Q

What is the main complication of a RCA occlusion? and LCA occlusion?

A

RCA: atria are affected so can get arrhythmias: heart block or abnormal atrial rhythm.

LCA: heart failure as you lose the pump.

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26
Q

Main principles of management in acute MI?

A
  • Call for help
  • Take A-E approach
  • Assuming airway patent/managed, start on morphine 5mg orally. Don’t forget antiemetics (metoclopramide 10mg). Can also give diamorphine IV 2.5-5mg but harder to get hold of.
  • Start them on nitrates sublingual
  • Aspirin 300mg, then second antiplatelet (ticragelor 180mg or clopidogrel but ticragelor better)
  • Streptokinase 1.5 MU over 1hr
  • Beta blockage if not in heart failure
  • Aspirin and nitrates reduce tissue death so must be done rapidly.
  • If NSTEMI can heparinize them (fondaparinux subcut), don’t heparainize if STEMI as going to PCI and they can do controlled heparin.
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27
Q

If patient with acute MI goes into VF what do they need rapidly?

A

Shock them, if you wait more than ~4minutes then its difficult to recordinate tissue.

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28
Q

Complications of MI?

A
  • Arrhythmia (inc VF and death)
  • Cardiac failure
  • Embolism
  • Rupture/aneurysmal dilatation
  • Pericarditis
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29
Q

When would you get early pericarditis following MI?

A

Full thickness anterior MI (common), presents as positional chest pain day after MI better sitting forward. Use NSAIDs

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30
Q

What is Dressler’s syndrome?

A

Pericarditis developing ~6 weeks after MI due to immune response

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31
Q

What does this CXR show? What ECG changes would you expect?

A

Enlarged LV- LV aneurysm in someone who had an MI a year ago. These patients have persistent ST elevation in LV segment.

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32
Q

What does this pulmonary angiogram show?

A

Massive pulmonary embolism. There is blockage of pulmonary vasculature to the right lung and the upper left lung.

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33
Q

What changes are present on the ECG of this lady with a PE?

A

S1Q3T3- suggests severe PE

  • Large S wave in lead I
  • Q wave in lead III
  • Inverted T wave in lead III
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34
Q

What ECG changes could you expect in a person with PE? (common to uncommon)

A
  1. Completely normal
  2. Sinus tachycardia
  3. Right ventricular strain
  4. Inverted T waves in V1 to V4
  5. S1Q3T3
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35
Q

What are the signs of heart failure?

A
  • 3rd heart sound is most common
  • tachycardia
  • tachypnoea
  • wheeze “cardiac asthma”
  • bilateral crepitations
  • raised JVP
  • ankle/sacral oedema
36
Q

What causes S3?

A

Rapid ventricular filling. Normal in young people (<35y), heart failure, MR, constrictive pericarditis

37
Q

What causes S4 heart sound?

A

Atrial contraction against stiff ventricle: hypertension, aortic stenosis

38
Q

Define heart failure

A

Condition where cardiac output is insufficient to meet tissue demands

39
Q

Define shock

A

Severe life threatening hypotension

40
Q

Define cardiogenic shock

A

Heart failure is so severe, that there is not enough pressure to perfuse even the heart muscle and brain alone.

41
Q

How do you manage cardiogenic shock?

A

Escalate to ITU. They will give inotropes: dobutamine or dopamine. Dobutamine is an analogue of dopamine that only has the medium dose effect of dopamine on the heart. (At low ‘renal’ doses it improves renal perfusion, at medium dose it’s a cardiac stimulant, at high doses is causes peripheral vasoconstriction which is dangerous)

42
Q

What causes a displaced apex beat?

A

Left ventricular dilatation NOT hypertrophy

43
Q

Causes of left ventricular dilatation?

A

aortic regurg, mitral regurg, ASD/VSD

44
Q

Causes of concentric hypertrophy?

A

aortic stenosis, hypertension, coarctation of the aorta

45
Q

When do you expect ST elevation after MI? Is the damage reversible?

A

First 4-12 hours. Reversible potentially

46
Q

When do you expect Q waves following MI? Is the damage reversible?

A

After about 6 hours. Indicate irreversible damage?

47
Q

When do T waves appear after MI?

A

As STs normalise

48
Q

What changes to look for on exercise ECG? How would you manage if changes are present?

A

ST depression on exertion: ischaemia on exertion. Patient will need a blocked vessel to be unblocked (PCI or CABG/angiogram). Proximal lesions easier to remove. Aspirin to prevent MI and GTN to maange symptoms. Clopid and statins as well.

49
Q

What does this ECG show? How would you manage this patient?

A

SVT

  1. Carotid sinus massage- stimulates vagus nerve, releases ACh, slows heart down
  2. Valsalva maneouvres
  3. Give adenosine (6mg->6mg->12mg)
50
Q

What does this ECG show? How do you manage this?

A

Wolff-Parkinson-White syndrome- look for delta waves. Looks like RBBB but actually eraly left BBB.

  1. ablation of accessory pathway (Bundle of Kent)
51
Q

What does cachexia in a patient indicate?

A

important prognostic sign of heart failure

52
Q

What cardiac abnormalities is Marfan’s associated with?

A

aortic reurg (aortic dissection)

53
Q

What cardiac abnormalities is Down’s associated with?

A

ASD, VSD

54
Q

What cardiac abnormalities is Turner’s associated with?

A

Coarctation of the aorta

55
Q

What cardiac abnormalities are spondyloarthropathies associated with?

A

aortic reurg

56
Q

What do xanthoma indicate?

A

familial hypercholesterolaemia

57
Q

What is Wenckebach’s phenomenon?

A

Increasing time between each pulse until one is missed and then cycle repeats. Indicates type I AV block

58
Q

What is a regular pulse with ectopics?

A

difficult to feel and be sure of without ECG, normal regular HR may be intermittently interrupted by a beat that is out of step. Almost feels irregularly irregular

59
Q

Where can a waterhammer pulse be felt?

A

Feel for collapsing pulse when raising the arm

60
Q

How does hypertrophic cardiomyopathy affect the pulse?

A

pulse may feel normal at first but peters out quickly, often described as jerky

61
Q

What does proptosis indicate?

A

hyperthyroidism due to Graves- can cause AF

62
Q

What do xanthelasma indicate?

A

High cholesterol- indicative of same things as corneal arcus

63
Q

What is the source of the pulse seen in JVP?

A

Jugular veins connect SVC and right atria without any intervening valves, so any pressure changes in the right atrium are transmitted up to these veins. By measuring the height of this impulse, the pressure in the right side of circulation can be expressed in cm

64
Q

Why is the internal JV used rathen than the external JV?

A

EJV has a more tortuous course making transmission of pulses less reliable/ready

65
Q

What is Kussmaul’s sign?

A

JVP will reduce during inspiration in normal state. Kussmaul’s is when JVP rises during inspiration in presence of pericardial constriction, right ventricular infacrtion or rarely cardiac tamponade.

66
Q

What does a midline sternotomy scar indicate?

A

Previous CABG, congenital heart defect correction, heart transplant. Midline sternotomy allows access to contents of mediastinum

67
Q

What does a left lateral thoracotomy scar indicate?

A

Closed mitral valvotomy, resection of coarctation, or ligation of a PDA

68
Q

What would an ICD or pacemaker indicate?

A

ICD- life-threatening arrhythmia risk (VT or VF), pacemaker- arrhythmias of other kinds

69
Q

What are systolic thrills caused by?

A

aortic stenosis, VSD or mitral regurg

70
Q

What are diastolic thrills caused by?

A

mitral stenosis

71
Q

Where else would you check if no apex beat was felt on the left?

A

on the right for dextrocardia

72
Q

What would an impalpable apex beat indicate?

A

emphysema, obesity, pericardial effusion, death

73
Q

Where does myocardial blood supply arise from?

A

L and R aortic sinuses, found within the aorta behind the L and R flaps of the aortic valve

74
Q

What do the LCA split into?

A

LAD, LCX, left marginal

75
Q

What does the LAD supply?

A

both ventricles and intraventricular septum

76
Q

What does the LCX supply?

A

left atrium and inferior part of the left ventricle- lateral heart

77
Q

What does the left marginal artery supply?

A

left ventricle

78
Q

What the RCA supply?

A

RA, RV

79
Q

Non-infective causes of endocarditis?

A

SLE (Libman Sacks endocarditis), marantic (adenocarcinoma), primary APLS

80
Q

How could aortic stenosis present? (6)

A
  1. Breathlessness
  2. Syncope
  3. Palpitations
  4. Orthopnoea
  5. PND
  6. Chest pain
81
Q

Signs of aortic stenosis? (6)

A
  1. Slow rising pulse of small volume
  2. BP- narrow pulse pressure
  3. Heaving but indisplaced apex and thrill in aortic area
  4. Reverse split of S2
  5. Opening click due to stiffened ventricle
  6. Ejection systolic murmur
82
Q

Differentials for a systolic murmur?

A
  1. Aortic stenosis
  2. Aortic sclerosis
  3. Pulmonary stenosis/mitral regurg
  4. ASD
  5. HOCM
83
Q

Further investigations to order if suspecting oartic stenosis? (beside, bloods, imaging, special)

A

Bedside

  1. ECG- conduction problems and left ventricular hypertrophy
  2. Urine dipstick for haematuria (infective endocarditis)
  3. Fundoscopy (Roth spots in infective endocarditis)

Bloods

  1. FBC- anaemia (Heyde’s)
  2. CRP, ESR- infective endocarditis
  3. U&Es- renal function in context of cardiac and anti-hypertensive medications

Imaging

  1. CXR: left sided heart failure with pulmonary oedema, cardiomegaly, effusions, Kerley B lines, calcified valve
  2. Echo: confirm diagnosis, assess severity, assess left ventricular function

Special tests

  1. coronary angiogram- directly measures pressure gradients across the valve
  2. Assess for co-existing coronary artery disease that could cause similar symptoms and/or be managed with a CABG at the same time as valve replacement
84
Q

Conservative, medical and surgical management of aortic stenosis?

A

Conservative: educate patient, report symptoms of angina/syncope/dyspnoea, regular follow-up with echo

Medical: manage cardio co-morbidities/complications.

Surgical: balloon valvuloplasty, valve replacement, Ross procedure, TAVI

85
Q

Clinical indicators of severe aortic stenosis?

A
  • Narrow pulse pressure
  • Quiet S2, presence of S4
  • Heaving apex or palpable thrill
  • Late peaking of murmur
  • Bi-basal creps on auscultation
86
Q

Indications for valve replacement in aortic stenosis?

A
  • Symptomatic with angina/dyspnoea/syncope
  • Deterioration in their ejection fraction to <40% of gradient >50mmHg or valve area
87
Q
A

Finals Revision (9 decks)

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