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ICSM Year 6 > Medicine - Cardiology > Flashcards

Medicine - Cardiology Flashcards

1
Q

Recall 2 observations about a person’s pulse that may be seen if they have aortic stenosis vs aortic regurgitation

A

Aortic stenosis: NARROW pulse pressure, slow rising pulse

Aortic regurgitation: WIDE pulse pressure, ‘waterhammer’ pulse (Corrigan’s pulse)

Pulse pressure = SBP-DBP (eg if BP = 120/80, PP = 40)

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2
Q

How would you describe the heart sounds that are auscultated in aortic stenosis vs regurgitation?

A

Aortic stenosis = soft S2 +/- S4

Aortic regurgitation = soft S2 +/- S3

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3
Q

What is the difference in cause between an S3 and S4 heart sound?

A

S3 heart sound is caused by blood filling against a non-compliant ventricle, whereas S4 is blood filling against a compliant ventricle

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4
Q

How can you hear the difference between an S3 and S4 heart sound?

A

S3 is early diastolic

S4 is late diastolic

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5
Q

What clinical examination findings can help differentiate aortic stenosis caused by valve sclerosis from aortic stenosis caused by HOCM?

A

In HOCM, the valsalva manoevre increases the volume of the murmur, whereas squatting decreases it

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6
Q

What might a CXR reveal in aortic stenosis?

A

Left ventricular hypertrophy
Pulmonary oedema
Valve calcification

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7
Q

What is the most useful investigation for assessing the severity of aortic stenosis?

A

Echo +/- doppler

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8
Q

Recall some general principles of management of heart valve disease

A

QRISK3 score to stratify risk
Manage risk with a statin (eg atorvastatin) and an antiplatelet (aspirin/ clopidogrel)
Manage coexistent HTN/ angina etc

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9
Q

Recall some indications for open replacement of the aortic valve (rather than cath lab procedure)

A

Symptomatic
Non-symptomatic with a low EF
Severe undergoing CABG

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10
Q

What does CABG stand for?

A

Coronary artery bypass graft

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11
Q

What are the 2 main types of artificial aortic valve?

A

Ball-in-cage

Bileaflet/ tilting disc

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12
Q

Recall some pros and cons of TAVI

A

Pros: no bypass required, no large scars, no GA required
Cons: higher risk of stroke compared to open replacement

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13
Q

What is a balloon aortic valvuloplasty

A

Procedure which stretches the aortic valve to improve symptoms of aortic stenosis

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14
Q

When is the aortic stenosis murmur heard vs aortic regurgitation?

A

AS: Ejection systolic
AR: Early diastolic

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15
Q

What is an Austin Flint murmur?

A

‘Rumbling diastolic murmur’

  • Associated with severe aortic regurgitation
  • Best auscultated in 5th ICS in MCL
  • Caused by blood flowing back through the aortic valve and over the mitral valve
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16
Q

When in the heart cycle is an Austin flint murmur heard, and what causes it?

A

Mid-diastole
Caused by regurgitant jet that runs over the mitral valve leaflets

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17
Q

Which heart murmurs are best heard on expiration?

A

Left heart murmurs

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18
Q

Where is the aortic regurgitation murmur best auscultated?

A

Erb’s point - Left 3rd ICS parasternal

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19
Q

Where is the main site of production of BNP?

A

Left ventricle (not actually brain, as name may suggest)

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20
Q

What is the advantage of measuring NT-proBNP over BNP?

A

NT-proBNP has a much longer half life as it is inactive - BNP, being an active hormone, has a much shorter half life

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21
Q

What can an echo and doppler be used to determine in cases of aortic regurgitation?

A

Severity
LV function
Cause

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22
Q

What is the mainstay of medical management for aortic regurgitation (other than managing cardiac risk with statins etc)?

A

Reduce afterload - can use:
ACE inhibitors (eg enalopril/ captopril)
Beta blockers (bisoprolol etc)
Diuretics (furosemide etc)

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23
Q

Which 2 antihypertensives are contra-indicated in aortic stenosis?

A 
Beta blockers (don't want to depress LV function)
Nitrates (may precipitate life-thretening hypotension)
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24
Q

Which heart murmur is most associated with atrial fibrillation?

A

Mitral stenosis

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25
Q

Which of the left heart murmurs will NOT produce a displaced apex beat?

A

Mitral stenosis (causes atrial hypertrophy not ventricular)

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26
Q

By what mechanism can heart valve disease cause a parasternal heave, and which murmurs can cause this?

A

Right ventricular hypertrophy (RVH) is cause of PSH (right ventricle is most anterior chamber of the heart so can cause heave)
MS and MR can cause RVH - as increased left atrial pressure –> pulmonary HTN –> RVH

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27
Q

Why might the apex beat be displaced in mitral regurgitation?

A

Left ventricle is pumping the stroke volume AND the regurgitant volume

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28
Q

Differentiate the timing of mitral stenosis and mitral regurgitation

A

Mitral stenosis is a MID DIAstolic murmur
Mitral regurgitation is a pan SYStolic murmur

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29
Q

Which of the heart murmurs might radiate to the axilla?

A

Mitral regurgitation

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30
Q

Recall some clinical signs of pulmonary hypertension

A

Malar flush
Raised JVP
Right ventricular (parasternal) heave
Loud S2

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31
Q

What might be seen on an ECG in mitral valve disease

A 
Atrial fibrillation 
P mitrale (bifid 'm-shaped' p waves in lead II as well as V1-V6)
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32
Q

What is the mainstay of medical management for mitral stenosis, other than heart disease risk modification eg statins?

A

RhF prophylaxis with benzylpenicillin
AF (rate control + DOAC)
Diuretics for symptomatic relief

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33
Q

What is the first line surgical treatment for mitral stenosis?

A

Balloon valvuloplasty

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34
Q

What is the mainstay of medical management for mitral regurgitation (other than managing cardiac risk with statins etc)?

A

Like AR, reduce afterload - can use:
ACE inhibitors (eg enalopril/ captopril)
Beta blockers (bisoprolol etc)
Diuretics (furosemide etc)

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35
Q

Describe briefly the NYHA classifications

A

1 - no limitation on activity
2 - comfortable at rest but dyspnoea on ordinary activity
3 - marked limitation on ordinary activity
4 - dyspnoea at rest

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36
Q

Recall the broad approach to medically managing heart failure

A

BASHeD up by the heart:
(Beta blocker or
ACE inhibitor)
Spironolactone
Hydralazine (+ nitrate)
Digoxin

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37
Q

Which extra immunisations should be offered in patients with heart failure?

A

Annual influenza
Pneumococcal

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38
Q

What must be monitored whilst patients are on spironolactone?

A

Potassium (as is a potassium-sparing diuretic)

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39
Q

Recall some drugs that are contra-indicated in heart failure

A

Thiozolidinediones (type 2 diabetes)
Verapamil (as is negative inotrope)
NSAIDs (can cause fluid retention)
Glucocorticoids (can cause fluid retention)
Flecainide (negative inotrope, arrhythmogenic)

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40
Q

How quickly should GTN spray relieve angina pain?

A

Within 5 minutes

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41
Q

What is the first line investigation for angina in stable patients, and what score is this investigation used to calculate?

A

CT coronary angiography
Calcium score

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42
Q

What are some pharmacological options for preventing angina (NOT symptomatic relief)?

A

Aspirin (75mg, OD)
Atorvastatin (80mg, ON)
ACE inhibitor (especially if co-existent DM)
Antihypertensives

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43
Q

What calcium score would be classified as low risk, and what score would be high risk?

A

Low risk < 100
High risk > 400

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44
Q

What care needs to be taken when prescribing CCBs and BBs together?

A

If you prescribe a non-dihydropyrimidine CCB (eg verapamil) with a BB it can cause complete heart block

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45
Q

What are some medical options for managing angina symptoms?

A

1st line: GTN (spray or sublingual) + beta blocker or CCB (if CCB used as monotherapy, use a rate limiting one like verapamil or dilitiazem)
2nd line: GTN + BB AND CCB
3rd line options:
- Long-acting nitrates eg Isosorbide mononitrate
- Ivabradine

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46
Q

What are the 3 types of AF?

A

Acute (<48 hours)
Paroxysmal (self-limiting, <7 days, recurs)
Persistent (>7 days, may recur even after cardioversion)

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47
Q

How does anti-clotting drug choice differ following a stroke, depending on whether or not they have AF?

A

If they have AF –> anti-coagulant (DOAC or warfarin if DOAC is CI)

If they do NOT have AF –> anti-platelet

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48
Q

Why are anti-platelets not used in AF?

A

Anti-platelets are specifically for artherogenic causes of clots eg atheroma

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49
Q

Within what window of AF beginning can it be treated differently to longer-standing AF? What is this different treatment? Why is it so difficult to treat within the initial window of time?

A

AF <48 hours duration and HAEMODYNAMICALLY UNSTABLE can be cardioverted electrically

Difficult to establish onset of AF as patient may not have palpitations, or may be unsure as to when they started

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50
Q

For how long before and after cardioversion for arrhythmia should a patient be anti-coagulated?

A

3w before and 4w after OR lifelong (if CHA2DS2VASc high or if paroxysmal AF)

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51
Q

How can chadsvasc score be used to determine the need for longterm anticoagulation?

A

Score:
0 = no need for longterm anticoagulation
1 = anticoagulate if male, do not anticoagulate if female
2 or more: anticoagulate

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52
Q

What is the main contraindication to be aware of for all CCBs?

A

Peripheral oedema (increased capillary hydrostatic pressure that results from greater dilation of pre-capillary than post-capillary vessels)

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53
Q

What are the 1st, 2nd and 3rd line options for rate control in AF?

A

1st line: beta blocker or CCB (verapamil is better than dilitiazem)
2nd line: digoxin
3rd line: amiodarone

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54
Q

With what waveform on the ECG should DC cardioversion be synchronised?

A

R wave
If synchronised with T wave it can cause VT

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55
Q

Recall 2 options for chemical cardioversion, and any important indications/ contra-indications for each

A

Flecainide - if young and no structural heart disease
Amiodarone - in structural heart disease (eg HF)

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56
Q

Recall 2 surgical options for managing AF

A
  1. Radiofrequency ablation of AV node
  2. Maze procedure
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57
Q

Recall the components of the CHA2DS2VASc score

A

CHF
HTN
Age >75
DM
Stroke
Vascular disease
Age 65-74
Sex Category (female)

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58
Q

In HTN, what BP is defined as ‘severe’?

A

>180/110

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59
Q

What is the first line treatment for HTN for diabetics?

A

ACE inhibitor

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60
Q

What is the first line treatment for HTN for black Africans?

A

CCB

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61
Q

What is the first line treatment for HTN for under vs over 55s who are not diabetic or Black African?

A

Under 55: ACE inhibitor or ARB
Over 55: CCB

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62
Q

Recall some side effects of ACE inhibitors

A

Angioedema (for around 4 weeks), cough, hyperkalaemia

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63
Q

Recall the name of one thiazide-like diuretic

A

Indapamide
nb bendoflumethiazide is thiazide, not thiazide-like

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64
Q

Why do CCBs cause oedema?

A

Cause dilation of arterioles but not venules

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65
Q

What is the atorvastatin dose for primary vs secondary prevention?

A

Primary prevention: 20mg OD
Secondary prevention: 80mg OD

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66
Q

What is the most commonly affected heart valve in infective endocarditis when the patient is an IVDU?

A

Tricuspid

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67
Q

What is the most common pathogen to cause an acute presentation of infective endocarditis?

A

Strep epidermidis

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68
Q

How does strep viridans infective endocarditis most commonly present?

A

Subacute presentation, most commonly in the developing world

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69
Q

What is Libman-Sacks endocarditis?

A

Non-infective endocarditis caused by SLE

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70
Q

Differentiate the empirical antibiotics used in native vs prosthetic valves affected by infective endocarditis

A

Native valve: amoxicillin +/- gentamicin
Prosthetic valve: vancomycin + rifampicin + gentamicin

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71
Q

How far apart should blood cultures be taken to investigate infective endocarditis?

A

12 hours

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72
Q

What is the most likely pathogen to cause rheumatic fever?

A

GAS (strep pyogenes)

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73
Q

What is the broad pathophysiology of rheumatic fever?

A

AB cross reactivity with myosin, muscle glycogen and VSMC

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74
Q

What is the latent period between pharyngeal infection and onset of rheumatic fever?

A

2-6 weeks

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75
Q

Recall some of the key symptoms of rheumatic fever

A

Pericarditis
Polyarthritis
Erythema marginatum

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76
Q

What are sydenham’s chorea?

A

Unwanted jerky movements that appear 2-6 months following rheumatic fever

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77
Q

Recall the Duckett-Jones diagnostic criteria

A

For diagnosing rheumatic fever:
CASES (major) FRAPP (minor)
Carditis
Arthritis
Sydenham’s chorea
Erythema marginatum
Subcutaneous nodules

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78
Q

What is the antibiotic treatment recommended in rheumatic fever?

A

Phenoxymethylpenicillin QDS 10/7

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79
Q

What drugs can be used to treat sydenham’s chorea?

A

Haloperidol
Diazepam

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80
Q

How long does penicillin treatment need to continue following an episode of rheumatic fever to prevent rheumatic heart disease?

A

If carditis and residual heart disease: 10 years or until age 40 (whichever is longer), possibly lifetime

If carditis but NO residual heart disease: 10 years or until age 21 (whichever is longer)

If NO carditis: 5 years or until age 21 (whichever is longer)

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81
Q

What is ‘fibrinous’ pericarditis?

A

Pericarditis caused by uraemia

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82
Q

Recall some signs and symptoms of pericarditis

A

Pleuritic chest pain
Non-productive cough
Dyspnoea
Flu-like symptoms
Pericardial rub
Tachypnoea + tachycardia

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83
Q

What are the typical ECG findings in pericarditis?

A

Widespread PR depression or saddle-shaped ST elevation

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84
Q

How should pericarditis be broadly managed?

A

Treat cause
NSAIDs and colchicine

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85
Q

Recall some cardiac causes of clubbing

A

Atrial myxoma
Cyanotic heart disease
Infective endocarditis

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86
Q

What can cause a collapsing pulse other than aortic regurgitation?

A

Pregnancy
Thyrotoxicosis
Anaemia

87
Q

What do the S1 and S2 heart sounds represent?

A 
S1 = mitral valve closure 
S2 = aortic valve closure
88
Q

What would cause a split S1?

A

Mitral and tricuspid valve closing at different times - normal in some

89
Q

What are the 2 types of purely genetic primary cardiomyopathy?

A

HOCM
Arrhythmogenic right ventricular dysplasia

90
Q

What are the 2 types of purely acquired primary cardiomyopathy?

A

Peripartum cardiomyopathy
Takotsubo cardiomyopathy

91
Q

Recall 2 types of primary cardiomyopathy that have mixed genetic/ acquired causes?

A

Dilated cardiomyopathy
Restrictive cardiomyopathy

92
Q

Recall 4 possible causes of dilated cardiomyopathy

A

Alcohol
Cocksackie B
Wet beri beri
Doxorubicin

93
Q

Recall 3 possible causes of restrictive cardiomyopathy

A

Amyloidosis
Post-radiotherapy
Loeffler’s endocarditis (due to eosinophillic infiltration)

94
Q

What is the most common gene mutation causing HOCM?

A

Beta-myosin heavy chain protein mutation

95
Q

What would the following echo findings be suggestive of:
Mitral regurgitation
Systolic anterior motion of the anterior mitral valve
Asymmetrical septal hypertrophy

A

HOCM

96
Q

What is arrhythmogenic right ventricular dysplasia?

A

Replacement of right ventricular myocardium with fatty and fibrofatty tissue

97
Q

What is the following description of an abnormal ECG most suggestive of:
Abnormalities in V1-3, typically T wave inversion. Possible epsilon wave.

A

Arrhythmogenic right ventricular dysplasia

98
Q

What would the following echo findings be suggestive of:
All 4 heart chambers dilated
Tricuspid and mitral regurgitation

A

Dilated cardiomyopathy

99
Q

What condition does the following describe: “transient, apical ballooning of the myocardium”?

A

Takotsubo cardiomyopathy

100
Q

Recall some causes of secondary cardiomyopathy

A

Infiltration (eg amyloidosis )
Inflammation (eg sarcoidosis)
Storage (eg haemochromatosis)
Deficiencies (eg beri beri)
Neuromuscular (eg Friedereich’s ataxia, duchenne-becker musculdystrophy)
Infective (cocksackie B, chagas)
Endocrine (thyrotoxicus, diabetes mellitis, acromegaly)

101
Q

Why is long QT syndrome dangerous?

A

Can cause VT –> death

102
Q

Recall 2 causes of congenital long QT syndrome, and how they can be differetiated?

A

Jervell-Lange-Nielsen syndrome (deafness)
Romano-Ward syndrome (no deafness)

103
Q

Recall some drugs that can cause long QT syndrome

A

METH CATS
Methadone
Erythromycin
Terfenadine
Haloperidol

Clarithromycin
Amiodarone/ arythromycin
TCAs
SSRIs (especially citalopram)

104
Q

What is the 1st line management of torsades de pointes?

A

IV magnesium sulphate

105
Q

What is torsades de pointes?

A

A type of polymorphic VT that is associated with QT prolongation

106
Q

How much does BP have to drop on standing to classify as ‘orthostatic hypertension’?

A

Over 3 mins, BP needs to fall by 20/10

107
Q

What is pulsus paradoxus, and in which conditions would it be seen?

A

>10mmHg fall in SBP during inspiration
Seen in severe asthma and cardiac tamponade - why?:
Inspiration –> reduced intrathoracic pressure –> blood pulled into right side of heart
Interventricular septum bulges into the left side of the heart –> reduced CO –> transient BP drop
You will feel varying strength of the pulse with inspiration and expiration

108
Q

What is pulsus alternans and in which condition is it seen?

A

Regular alternation of the force of the arterial pulse
Seen in severe LVF

109
Q

In which disease might a ‘jerky’ pulse be felt?

A

HOCM

110
Q

What is the inheritance pattern of HOCM?

A

Autosomal dominant

111
Q

How can HOCM cause sudden death?

A

Can cause spontaneous VF/VT

112
Q

How might the JVP be abnormal in a patient with HOCM?

A

Large a waves

113
Q

What are the 3 key features of HOCM on echo?

A

Mitral regurgitation
Systolic anterior motion (SAM)
Asymmetric hypertrophy

114
Q

Recall some general principles of HOCM management

A

A to E
Amiodarone
Beta blockers
Cardioverter defibrillator
Dual chamber pace maker
Endocarditis prophylaxis

115
Q

What are the classical clinical signs of pulmonary oedema?

A

Reduced exercise tolerance
Raised jugular venous pressure
Audible third heart sound

116
Q

Which electrolyte abnormalities may cause torsades de pointes?

A

Hypocalcaemia
Hypokalaemia
Hypomagnesaemia

117
Q

Name 2 drugs that can increase the effect of warfarin

A

Metronidazole
Sertralline

118
Q

Name one drug that can decrease the effect of warfarin

A

Phenobarbital

119
Q

When should DC cardioversion be attempted before chemical cardioversion for a tachyarrhythmia?

A

If SBP <90

120
Q

What should an inferior MI + aortic regurgitation raise suspicion of?

A

Ascending aortic dissection

121
Q

When would thrombolysis be the first line for treating PE, rather than anticoagulative medicines?

A

If circulatory collapse - eg hypotension

122
Q

What is the antibiotic of choice in native valve infective endocarditis?

A

IV amoxicillin

123
Q

What should the initial management be for patients with bradycardia and signs of shock?

A

500micrograms of atropine (repeated up to max 3mg)

124
Q

What ECG abnormality is most likely in hypercalcaemia?

A

Lengthened QT interval

125
Q

What are prominent V waves in the JVP indicative of?

A

Tricuspid regurgitation

126
Q

What are cannon A waves in the JVP indicative of?

A

Complete heart block

127
Q

What is a prominent x descent in the JVP indicative of?

A

Can be caused by:
Acute cardiac tamponade
Constrictive pericarditis

128
Q

Which 2 beta blockers have been proven to be effective in stable heart failure?

A

Carvedilol and bisoprolol

129
Q

What are the 3 most-commonly used drugs for treating NSTEMI medically?

A

Aspirin, ticagrelor, and fondaparinux

(Take special care to avoid GTN in hypotensive patients)

130
Q

When would you NOT use flecainide for rate control?

A

In structurally abnormal hearts (which includes those with a PMH of ischaemic heart disease)

131
Q

What is Beurger’s disease also known as?

A

Thromboangiitis obliterans

132
Q

What are the symptoms of Beurger’s disease?

A

Raynaud’s syndrome, intermittent claudication and finger ulcerations

133
Q

What is the biggest risk factor for Beurger’s disease?

A

Smoking

134
Q

What is the medical management of choice for conservative management of an NSTEMI?

A

Dual antiplatelet therapy:
Aspirin + clopidogrel/ ticagrelor
Clopidogrel if high bleeding risk, ticagrelor if low bleeding risk

135
Q

What is the biggest risk factor for renal impairment following prescription of an ACE inhibitor?

A

If the patient already has bilateral renal artery stenosis it can cause significant renal impairment

136
Q

What is radiofemoral delay a sign of?

A

Aortic coarctation

137
Q

Which congenital condition is strongly associated with aortic coarctation?

A

Turner’s

138
Q

In which arrhythmia is verapamil contraindicated and why?

A

Ventricular tachycardia
Verapamil is a CCB - may reduce cardiac contractility

139
Q

Recall the location on the praecordium where each valve is best auscultated

A

Aortic: Right 2nd ICS
Pulmonary: Left 2nd ICS
Tricuspid: left 4th ICS at sternal border
Mitral: left 5th ICS, MCL

140
Q

Where is aortic regurgitation best auscultated

A

Tricuspid area: left 3rd ICS parasternally (Erb’s point)

141
Q

At what point in the breathing cycle is aortic regurgitation best auscultated, and in which position?

A

End expiration
Sat up and forward
Put stethoscope at Erb’s point

142
Q

Why are right-sided murmurs louder on inspiration?

A

Increased venous return to the RHS

143
Q

Recall 2 types of murmur that are louder when there is LESS blood flow across the affected area

A

HOCM murmurs
Mitral valve prolapse

144
Q

Which murmur is best auscultated when the patient is in the left lateral decubitus position?

A

Mitral stenosis

145
Q

Which murmurs can radiate? Where do they radiate to?

A

Aortic stenosis –> carotids
Mitral regurgitation –> axilla

146
Q

Describe the meaning of each of the 6 grades of heart murmur

A

Grade 1 - Difficut to hear
Grade 2 - Quiet
Grade 3 - Easy to hear
Grade 4 - Easy to hear with a palpable thrill
Grade 5 - Easy to hear with stethoscope barely touching chest
Grade 6 - Easy to hear with stethoscope away from patient

147
Q

How does mitral stenosis vs regurgitation affect the heart structurally and why?

A

Stenosis –> atria have to work really hard to push blood through valve –> hypertrophic left artium

Regurgitation –> backflow of blood into atria stretches chamber –> left atrial dilatation

148
Q

What are the 2 main possible causes of mitral stenosis?

A

Rheumatic heart disease is the most common (learn!)
Infective endocarditis

149
Q

Why do you get a loud S1 in mitral stenosis?

A

Thickened valve needs a large systolic force to shut - once this systolic threshold is met the valve will shut very suddenly

150
Q

What is the cause of malar flush in patients with mitral stenosis?

A

Backflow of blood into the pulmonary system –> rise in CO2 and vasodilation

151
Q

What is the link between mitral regurgitation and congestive heart failure?

A

Backflow of blood –> reduced ejection fraction
–> backlog of blood waiting to pass through left side of heart

152
Q

What are the possible causes of mitral regurgitation and which of them is most common?

A

Age-related weakening is most common
Also associated with:
- IHD
- Infective endocarditis
- Rheumatic heart disease
- Connective tissue disease (EDS/Marfan’s)

153
Q

Which type of valve disease is associated with exertional syncope and why?

A

Aortic stenosis
Difficulty perfusing brain

154
Q

What is the most common cause of aortic stenosis?

A

Idiopathic age-related calcification

155
Q

What is Corrigan’s pulse?

A

Also known as collapsing pulse
Pulse rapidly appears and then disappears

156
Q

Recall 2 causes of aortic regurgitation

A

Age-related calcification
Connective tissue disease

157
Q

What is paroxysmal nocturnal dyspnoea?

A

Waking up suddenly in the night feeling acutely SOB with a really bad cough/ wheeze
They have to get up and gasp for air
Symptoms typically improve after a few minutes

158
Q

What is the mechanism of PND (3 aspects)?

A
  1. Lying flat –> fluid settling across large surface area of lungs
  2. Respiratory centre in the brain is less responsive during sleep - so lungs can become much more congested that they would normaly do before they wake up
  3. Adrenaline levels are much lower at night so myocardium is more relaxed –> reduced CO
159
Q

Recall the immediate management of rheumatic fever

A

Aspirin prn
Benzylpenicillin IM stat
10 day course of benzylpenicillin PO

160
Q

When in the course of rheumatic fever/heart disease is valve imcompetence most likely?

A

Acutely

161
Q

Which murmur is best heard at the apex with the bell of the stethoscope?

A

Mitral stenosis

162
Q

Is pericarditis more commonly viral or bacterial?

A

Viral

163
Q

ST elevation in which leads would represent an anteroseptal STEMI?

A

V1-V4

164
Q

In the setting of acute pulmonary oedema post MI, how can severe hypotension be managed?

A

CPAP - it effectively pushes fluid out of your lungs

165
Q

Which artery is occluded in an anterior MI?

A

Left anterior descending

166
Q

Which artery is occluded in an anterolateral MI?

A

Left anterior descending

167
Q

Which artery is occluded in inferior MI?

A

Right coronary artery (RV branch included)

168
Q

Which artery is occluded in a posterior MI?

A

Circumflex

169
Q

In which leads would you see ST elevation in an inferior STEMI?

A

II, III, aVF

170
Q

In which leads would you see ST elevation in an anterior STEMI?

A

V3, V4

171
Q

In which leads would you see ST elevation in a lateral STEMI?

A

I, aVL, V5, V6

172
Q

What is always the first thing to do in an acute exacerbation of heart failure?

A

Sit up and give 60-100% O2

173
Q

Which valve is most commonly affected by strep viridians infective endocarditis, and why?

A

Mitral
Strep viridians usually associated with teeth (commensal there)
Affects mitral valve as this valve is under higher pressures than in right side of heart and so is under higher pressure

174
Q

What is the most likely pathogen in infective endocarditis in IVDUs?

A

Staphylococcus

175
Q

Recall some causes of atrial fibrillation

A

PIRATES:
Pulmonary cancer
Ischaemic heart disease
Rheumatic heart disease
Atrial myxoma/ alcohol binge
Thyrotoxicosis
Embolus
Sepsis

176
Q

If you see a Q wave as well as ST elevation on an ECG, what does that mean?

A

Tissue death

177
Q

What may appear to be an anterior STEMI on an ECG post-MI, that is not actually an anterior STEMI?

A

Left ventricular aneurysm

178
Q

What class of drug is ticagrelor?

A

P2 Y12 inhibitor

179
Q

When would heparin be used in MI management?

A

In cath lab prior to PCI to prevent thrombosis

180
Q

Why does ticagrelor work more quickly than clopidogrel?

A

Clopidogrel is a pro-drug and so takes longer to work

181
Q

Recall one diuretic that improves prognosis post-MI and one that isn’t proven to

A

Improves prognosis: eplerenone
Does not improve prognosis: furosemide

182
Q

How long can someone not drive for post-MI?

A
  • Patients who are completeley revascularised with okay LVEF = 1 week
  • Patients with severely reduced LVEF = 4 weeks
183
Q

Recall 3 uses of SGLT2 inhibitors

A

Diabetes mellitus
Chronic kidney disease
Symptomatic chronic heart failure with reduced ejection fraction

184
Q

What is sacubitril with valsartan used for?

A

Improves LVF in patients who are already on other heart failure therapy

185
Q

How long after an MI might an ICD (implantable cardioverter defibrillator) be indicated?

A

40 days

186
Q

Which drug should be held 48 hours before and after angiogram?

A

Metformin

187
Q

How do you manage atrial flutter?

A
  1. Treat underlying cause
  2. Anticoagulate as you would for atrial fibrillation

If haemodynamically unstable: rate control or cardioversion

188
Q

How would you manage SVT in an asthmatic patient in whom vagal manoevres have failed?

A

IV verapamil

189
Q

How do you differentiate between aortic stenosis and sclerosis?

A

Aortic sclerosis is:

  • normal in the elderly
  • has a normal pulse (not narrow pulse pressure)
  • No radiation
190
Q

Recall 5 causes of raised JVP other than right-sided heart disease

A

Tricuspid regurgitation
Complete heart block
CCF
Pericardial effusion
SVC obstruction

191
Q

Recall 5 complications of a prosthetic valve

A

Failure
Infection
Bleeding
Anaemia
Thromboembolic

192
Q

Recall 3 causes of an irregularly irregular pulse that aren’t AF

A

Ventricular etopics
Atrial flutter
Sinus arrhythmias

193
Q

If in a suspected DVT the D-dimer is positive but the the USS is negative, what should you do?

A

Stop anticoagulation and repeat scan in one week

194
Q

What is the most appropriate anti-anginal treatment in a pateint with known heart failure?

A

Bisoprolol (verapamil CI in the case of CF)

195
Q

In ALS, when would 3 shocks be given instead of 1?

A

If arrest witnessed in the cath lab/ CCU/ critical care and rhythmn is VF/pVT

196
Q

What should be the initial drug treatment for patients with low EF heart failure?

A

Bisoprolol + ramipril

197
Q

Which class of abx can cause torsades de pointes?

A

Macrolides eg azithromycin

198
Q

Why is a pericardial friction rub heard in pericarditis?

A

The inflammed visceral and parietal pericardium rub against each other

199
Q

What is the basic pathophysiology of Sydenham’s chorea?

A

Autoimmune reaction against the basal ganglia

200
Q

What drug should be added to CPR for a patient in cardiac arrest if pulomnary emboli are suspected?

A

Alteplase

201
Q

When would you not use IV beta blockers to treat fast AF, and hwat would you do instead?

A

In fast atrial fibrillation not associated with shock, syncope, myocardial ischaemia or heart failure - do up to 3 synchronised DC shocks instead

202
Q

How can nitrate tolerance be prevented when prescribing isosorbide mononitrate?

A

Asymmetric dosing regimen

203
Q

What complication of MI does the following describe: sudden heart failure, raised JVP, pulsus parodoxus

A

Left ventricular free wall rupture

204
Q

What is the most useful blood test for detecting re-infarction post-MI?

A

CK-MB

205
Q

What long-term anticoagulation is required for mechanical heart valves?

A

Warfarin

206
Q

Where are vegetations most commonly seen in IV drug users with infective endocarditis?

A

Tricuspid valve

207
Q

How should AF (first presentation) be managed in the community?

A

If <48hrs symptoms (from first episode):
* Haemodynamically unstable - immediate referral to acute medial unit for emergency cardioversion
* Haemodynamically stable - consider Mx in community or refer to secondary care for cardioversion depending on clinical judgement

If >48hrs symptoms:
* Manage in community with rate control medications (e.g. beta blockers or CCB)
* Start anticoagulation

208
Q

What are the options for rate control of AF?

A
  • Beta blockers
  • Rate-controlling CCBs (e.g. verapamil)
209
Q

What are some options for rate control in patients that beta blockers are contraindicated in?

A

Rate-controlling calcium channel blockers (e.g. verapamil or diltiazem)

210
Q

What are the two different types of CCBs?

A
  • Rate controlling - diltiazem, verapamil
  • Non-rate controlling - amlodipine
211
Q

What scores can be used to determine risk of stroke after AF?

A

CHADS-VASc score + ORBIT score

212
Q

How does reversal of warfarin and DOACs differ?

A

It is quite easy to give Vit K to reverse warfarin, but with DOACs they only have a few approved reversal agents (that tend to be quite expensive)

213
Q

What is Beck’s triad?

A

Muffled heart sounds + raised JVP + hypotension = cardiac tamponade

ICSM Year 6 (21 decks)

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