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ICSM Year 6 + edits > 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
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

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87
Q

What do the S1 and S2 heart sounds represent?

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

What would cause a split S1?

A

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

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89
Q

What are the 2 types of purely genetic primary cardiomyopathy?

A

HOCM
Arrhythmogenic right ventricular dysplasia

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90
Q

What are the 2 types of purely acquired primary cardiomyopathy?

A

Peripartum cardiomyopathy
Takotsubo cardiomyopathy

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91
Q

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

A

Dilated cardiomyopathy
Restrictive cardiomyopathy

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92
Q

Recall 4 possible causes of dilated cardiomyopathy

A

Alcohol
Cocksackie B
Wet beri beri
Doxorubicin

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93
Q

Recall 3 possible causes of restrictive cardiomyopathy

A

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

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94
Q

What is the most common gene mutation causing HOCM?

A

Beta-myosin heavy chain protein mutation

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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

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96
Q

What is arrhythmogenic right ventricular dysplasia?

A

Replacement of right ventricular myocardium with fatty and fibrofatty tissue

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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

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98
Q

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

A

Dilated cardiomyopathy

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99
Q

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

A

Takotsubo cardiomyopathy

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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)

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101
Q

Why is long QT syndrome dangerous?

A

Can cause VT –> death

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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)

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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)

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104
Q

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

A

IV magnesium sulphate

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105
Q

What is torsades de pointes?

A

A type of polymorphic VT that is associated with QT prolongation

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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

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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

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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

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109
Q

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

A

HOCM

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110
Q

What is the inheritance pattern of HOCM?

A

Autosomal dominant

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111
Q

How can HOCM cause sudden death?

A

Can cause spontaneous VF/VT

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112
Q

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

A

Large a waves

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113
Q

What are the 3 key features of HOCM on echo?

A

Mitral regurgitation
Systolic anterior motion (SAM)
Asymmetric hypertrophy

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114
Q

Recall some general principles of HOCM management

A

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

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115
Q

What are the classical clinical signs of pulmonary oedema?

A

Reduced exercise tolerance
Raised jugular venous pressure
Audible third heart sound

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116
Q

Which electrolyte abnormalities may cause torsades de pointes?

A

Hypocalcaemia
Hypokalaemia
Hypomagnesaemia

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117
Q

Name 2 drugs that can increase the effect of warfarin

A

Metronidazole
Sertralline

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118
Q

Name one drug that can decrease the effect of warfarin

A

Phenobarbital

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119
Q

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

A

If SBP <90

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120
Q

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

A

Ascending aortic dissection

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121
Q

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

A

If circulatory collapse - eg hypotension

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122
Q

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

A

IV amoxicillin

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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)

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124
Q

What ECG abnormality is most likely in hypercalcaemia?

A

Lengthened QT interval

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125
Q

What are prominent V waves in the JVP indicative of?

A

Tricuspid regurgitation

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126
Q

What are cannon A waves in the JVP indicative of?

A

Complete heart block

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127
Q

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

A

Can be caused by:
Acute cardiac tamponade
Constrictive pericarditis

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128
Q

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

A

Carvedilol and bisoprolol

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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)

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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)

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131
Q

What is Beurger’s disease also known as?

A

Thromboangiitis obliterans

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132
Q

What are the symptoms of Beurger’s disease?

A

Raynaud’s syndrome, intermittent claudication and finger ulcerations

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133
Q

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

A

Smoking

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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

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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

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136
Q

What is radiofemoral delay a sign of?

A

Aortic coarctation

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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

Why can non-dihydropyridine and beta blockers be put together?

A

Risk of bradycardia

206
Q

If a patient is on monotherapy and cannot tolerate addition of CCB / BB what should be added?

A

a long-acting nitrate
ivabradine
nicorandil
ranolazine

207
Q

What are the side effects of Loop Diuretics?

A

hypotension
hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
ototoxicity
hypocalcaemia
renal impairment (from dehydration + direct toxic effect)
hyperglycaemia (less common than with thiazides)
gout

208
Q

What are ECG signs of Mitral Stenosis?

A

P - mitrale = LAH (bifid P wave)

209
Q

Heart failure with reduced LVEF should be given what for first line?

A

BB + ACEi

210
Q

If new onset AF is within 48 hrs and has a reversible cause what should be done

A

DC Cardioversion

211
Q

Factors that potentiate warfarin

A

liver disease
P450 enzyme inhibitors e.g. antibiotics
cranberry juice
drugs which displace warfarin from plasma albumin, e.g. NSAIDs
inhibit platelet function: NSAIDs

212
Q

If a patient is haemodynamically stable in SVT and does not respond to vagal manoeuvres - what should be done?

A

IV Adenosine - rapid IV 6mg - then 12mg - 18mg (verapamil in asthmatics)

213
Q

In ALS once adrenaline has been given what should happen next?

A

Adrenaline again in 3-5 minutes if ALS continues

214
Q

When should Ivabradine be considered for Heart Failure?

A

sinus rhythm > 75/min and a left ventricular fraction < 35%

Not responding to ACEi, BB and aldosterone antagonist therapy

215
Q

Major bleeding on warfarin what should be done?

A

Stop warfarin, give IV VitK 5mg, prothrombin complex concentrate

216
Q

Drug therapy for broad complex tachycardia and haemodynamically stable

A

Amiodarone - central line

217
Q

Persistent ST elevation following MI with no chest pain

A

Ventricular aneurysm - need anticoagulation

218
Q

If a person with NSTEMI and grace score of 10% what should be done?

A

patients with a GRACE score > 3% should have coronary angiography within 72 hours of admission

medical therapy of aspirin, pain relief, anti-emetic, nitrates and oxygen in the interim

219
Q

If a strong suspicion of PE but a delay in scan what should be done?

A

Start treatment of DOAC whilst awaiting V/Q (if allergy to CTPA)

220
Q

Side effects of Beta Blockers

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

221
Q

Best DUAP post MI

A

Aspirin + Ticagrelor / prasugrel (infinitely + 12 months)

if not then Clopidogrel e.g. patient has undergone thrombolysis

222
Q

`Which condition is associated with congenital aortic stenosis?

A

Williams Syndrome

223
Q

How common is depression post MI?

A

20%

224
Q

What is a seatbelt sign characteristic of?

A

Aortic Rupture

225
Q

Infective endocarditis: How should blood cultures be taken?

A

3 sets of blood cultures from different venous sites 1 hour apart before antibiotics

226
Q

What antibiotic is given for Staphylococcus in IE?

A

Flucloxacillin

227
Q

Treatment for Wolff Parkinson white

A

Radiofrequency ablation

228
Q

What are the ECG changes in Hypokalaemia?

A

ST depression
QT interval prolongation
increased PR interval
visible U waves
T wave flattening/ inversion.

229
Q

If atropine does not work in bradycardia what should be done

A

transcutaneous pacing
isoprenaline infusion

230
Q

Main investigation for aortic dissection

A

CT angiography - finding the false lumen - TOE if risky

231
Q

Why is Labetalol given pre aortic dissection?

A

To control blood pressure and reduce stress on aortic walls

232
Q

If a patient with heart failure has poor renal function what should be done?

A

Escalating doses to achieve the concentration

233
Q

What are shockable rhythms?

A

ventricular fibrillation/pulseless ventricular tachycardia (VF/pulseless VT)

234
Q

What are non-shockable rhythms?

A

‘non-shockable’ rhythms: asystole/pulseless-electrical activity (asystole/PEA)

235
Q

When is adrenaline given in ALS?

A

1mg - asap in non-shock
after third shock - in shockable
repeat every 3-5 minutes during

236
Q

When should amiodarone be given during ALS?

A

300mg - shockable after 3 shocks
further 150mg - after 5 shocks

237
Q

Reversible causes of cardiac arrest

A

Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia

Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins

238
Q

In AF, if a CHA2DS2-VASc score suggests no need for anticoagulation what should be done

A

Echo for VHD - transthoracic

239
Q

What is a Epsilon wave characteristic of?

A

arrhythmogenic right ventricular dysplasia (ARVD)

(a small positive deflection at the end of the QRS complex)

240
Q

What are posterior MI changes?

A

v1-v3
reciprocal changes
ST depression
Tall broad R waves and upright T waves
posteior leads v7-v9
left circumflex

241
Q

Benefit of switching standard release isosorbide mononitrate to modified

A

Gives a nitrate free period, decreasing the change of nitrate tolerance occuring

242
Q

What patients can get a MI without chest pain?

A

Elderly, diabetic and female

243
Q

What type of drug is candesartan?

A

Angiotensin receptor blocker

244
Q

Why is CPAP useful in heart failure?

A

increases the intrathoracic pressure, which reduces venous return to the heart and lowers preload, as well as decreases afterload by decreasing the pressure difference between the left ventricle and the extrathoracic arteries. These pressure changes increase stroke volume and promote the movement of fluid from the interstitial fluid compartment into the intravascular fluid compartment, reducing oedema and alleviating symptoms of dyspnoea

245
Q

Order of therapies for heart failure

A
  1. BB + ACEi
  2. Aldosterone antagonist / SGLT2 inhibitors
  3. Ivabradine / hydralazine etc
246
Q

What drug is particularly useful in afro c patients in heart failure

A

Hydralazine

247
Q

What is a indication for cardiac resynchronisation therapy in heart failure?

A

Widened QRS e.g LBBB

248
Q

What type of drug is bumetanide?

A

Loop diuretic - inhibit Na/k/cl cotransporter in ascending limb
reduce absorption of NaCl

249
Q

If patients treated with PCI for MI are experiencing pain or haemodynamic instability post PCI: what should be commenced

A

CABG

250
Q

When giving DUAP prior to PCI when is each one given?

A

Prasugrel - not already on a AC
Clopidogrel - if they are

251
Q

If QRISK3 is higher than 10% what should be offered in addition to ACEi in hypertension

A

Statin

252
Q

What would make Aortic stenosis quieter?

A

Left ventricular systolic dysfunction

n.b it is a consideration for arotic valve replacement surgery

decreased flow rate across aortic valve

253
Q

Can LBBB be considered normal?

A

Always pathological - left ventricle takes longer to polarise

254
Q

What are causes of LBBB?

A

MI
HTN
AS
Cardiomyopathy

William Marrow

255
Q

NSTEMI management, if grace score more than 3% what should be done?

A

Coronary angiogram within 72 hrs of admission

256
Q

What should be given to all ACS patients?

A

Aspirin 300mg
Oxygen if low sats
Morphine if severe pain (IV)
Nitrates

Nitrates = caution if hypotensive

257
Q

STEMI criteria: heights

A
  • clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
  • 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
  • 1.5 mm ST elevation in V2-3 in women
  • 1 mm ST elevation in other leads
  • new LBBB (LBBB should be considered new unless there is evidence otherwise)
258
Q

STEMI management: When should PCI be offered compared to fibrinolysis?

A

PCI: presents within 12 hrs of symptoms and can be given in 120 minutes of time when fibrinolysis could be given

radial access, using drug eluding stents

259
Q

PCI using a drug eluding stent what should be given before?

A

unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)

260
Q

How long do you repeat a ECG after fibrinolysis for a MI

A

60-90 minutes
if it persists do PCI

261
Q

What are the normal heart variants in athletes?

A

sinus bradycardia
junctional rhythm
first degree heart block
Mobitz type 1 (Wenckebach phenomenon)

262
Q

Prosthetic valve anti-thrombotics

A

Bioprosthetic: aspirin
mechanical: warfarin + aspirin

Mechanical valves have an increased risk of thrombosis

263
Q

Target INR in mitral and aortic valves

A

aortic: 3.0
mitral: 3.5

264
Q

In AF, if a CHA2DS2-VASc score suggests no need for anticoagulation what should be done?

A

echo to look for valvular heart disease

24-holter for symptomatic AF

265
Q

Treatment for acute heart failure

A

IV loop diuretics

+oxygen, nitrates (MI, AR, MR, HTN)

266
Q

Treatment for acute heart failure with hypotension

A

Inotropic agents e.g dobutamine - left ventricular failure

267
Q

When should beta blockers be stopped during acute heart failure

A

heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock

268
Q

Reversal agent to DOAC

A

Andexanet alfa

half if renal failure / aki

269
Q

Bleeding on dabigatran

A

Idarucizumab

270
Q

Metallic valve warfarin level

A

Warfarin INR 3-4

271
Q

NT-proBNP levels

A

<400 - HF unlikely
400-2000 - refer for echo + specialist review < 6 weeks
2000< - echo + specialist < 2 weeks

bloods, cxr, echo

272
Q

Initial management of all ACS

A

IV opiate analgesia
antiemetics
aspirin 300mg
o2 if hypoxic
gtn infusion uncontrolled pain / htn / pulmonary oedema

273
Q

Types of MI

A

1 = acute plaque rupture
2 = supply over deamnd mismatch

274
Q

Complications post MI

A

DARTH VADER
Death
Arrythmia
Ruptured aneurysm
Thrombus
Heart Failure

VSD
Another MI
Dresslers syndrome
Embolus
Regurgitant valve

275
Q

Cold peripheries and poor urine output

A

Cardiogenic shock

276
Q

Bradycardia & AV nodal block

A

Inferior MI

277
Q

Clinic BP 140/90

A

ABPM monitoring

180/120 - same day assessment and treatment

278
Q

ABPM - < BP 135/85

A

recheck in 5 yrs

279
Q

ABPM 135/85 - 150<95

A

Treat if:
-10 yr CVD risk >10%
- End-organ damage
- diabetes / CVD / CKD

280
Q

ABPM > 150/95

A

treat + assess secondary causes if <40yrs

281
Q

Causes of secondary hypertension

A

Renovascular - renal artery stenosis
Primary kidney disease
Sleep apnoea syndrome
Endocinre
- primary hyperaldosteronism
- cushing syndrome
- hypothyroidism
- pheochromocytoma

282
Q

Accerlated / malignant HTN

A

180/120< - retinal haemorrhages or papilloedema

283
Q

Management for malignant HTN

A

Reduce BP slowly, aiming <160/120 over hrs to days
- IV nitroglycerin (GTN)
- IV nitroprusside
- IV beta blocker e.g. labetolol
- oral - amlodipine if no end organ damage

284
Q

Side effects of aldosterone antagonists

A

Hyperkalaemia
Gynaecomastia

285
Q

Headache, sweating, palpitations with severe HTN

A

Phaeo

286
Q

Pedal oedema resistant to diuretics

A

Calcium channel blocker S/E

287
Q

ECG features of HOCM

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen - bifid p waves for atrial hypertrophy

288
Q

Interpret this ECG

A

100bpm (3 large squares between each QRS)
sinus rhythm (regular p-waves preceding each QRS)and has a normal axis
p-waves: they are present and regular - the ‘m-shaped’ or bifid p-waves in multiple leads which likely represent left atrial enlargement
PR interval is ~120-160ms (normal)
extremely high-voltage QRS complexes which represent extreme left ventricular hypertrophy (LVH).
high-voltage R-waves in the precordial leads (V1-V6) which suggest septal hypertrophy
ST depression in the precordial leads and T-wave inversion in the anterolateral leads (I/avL/V2-V6) which may represent ischaemia secondary to LVH.

HOCM

289
Q

What is HOCM associated with?

A

Friedreichs ataxia
Wolff parkinson white

290
Q

Drugs to avoid in HOCM management

A

nitrates
ACE-inhibitors
inotropes

291
Q

Wedge-shaped opacification on CXR

A

Pulmonary embolism

pulmonary infarction due to the clot occluding the blood flow and oedema due to the local inflammatory response to lung tissue necrosis

292
Q

Features of hypercalcaemia

A

‘bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension

293
Q

How is haemopytsis a symptom of mitral stenosis

A

due to pulmonary pressures and vascular congestion
may range from pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins

294
Q

Patients with mechanical heart valves what is used for AF

A

Warfarin

295
Q

inferior myocardial infarction and AR murmur

A

ascending aorta dissection

296
Q

Features of right BBB

A

broad QRS > 120 ms
rSR’ pattern in V1-3 (‘M’ shaped QRS complex)
wide, slurred S wave in the lateral leads (aVL, V5-6)

297
Q

Why are lung crackles bad asuculataion with MI

A

cardiogenic shock - indicate heart failure has occured and leading to pulmonary oedema

298
Q

causes of heart failure with reduced systolic dysfunction (reduced ejection fraction)

A

Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias

299
Q

causes of heart failure with preserved ejection (reduced diastole function)

A

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

300
Q

Causes of high output heart failure

A

anaemia
arteriovenous malformation
Paget’s disease
Pregnancy
thyrotoxicosis
thiamine deficiency (wet Beri-Beri)

normal heart unable to meet metabolic needs

301
Q

3 things to classify angina

A

constricting discomfort front of chest
worse on exercise
relieved by rest or nitrates withing 5 minutes

if only 2 = atypical angina

302
Q

What should be given with aspirin in ACS

A

PPI

303
Q

Side effects of Amiodarone

A

thyroid
PS
PF
Liver toxicity
blue skin
myocarditis

304
Q

Side effects of SGLT2 inhibitors

A

weights loss
reurrent genital thrush
euglycaemia diabetic ketoacidosis

305
Q

Describe pulsus paradoxus

A

-normal inspiration produces a decrease in
intrathoracic pressure, this increases preload
-as the pulmonary vasculature expands, less
blood enters the left circulation, which causes a
drop in blood pressure during inspiration
(NORMAL)
-in tamponade, the increased preload in the RV
results in bowing of the ventricular septum in to
the LV, resulting in reduced cardiac output

306
Q

Collapse is indicative of what type of heart problem

A

Arrythmogenic

307
Q

How is orthostatic hypotension diagnosed?

A

A drop by 20 in BP from 3 minutes of standing

308
Q

What pulse isexpected in mixed aortic valve disease?

A

bisferiens

309
Q

In acute stroke that was caught late when should AC be started

A

2 weeks time

310
Q

Normal variants in athletes

A

sinus bradycardia
junctional rhythm
first degree heart block
Mobitz type 1 (Wenckebach phenomenon)

311
Q

Side effects of statins

A

myopathy - check CK
t2dm
haemorrhagic strokes

312
Q

Mx of stable angina

A

RAMP
refer to cardiology
advise of diagnosis and safety net
medical treatment
procedural / surgical interventions

313
Q

GTN for stable

A

take prn, if pain not go after 5 minutes, re do, if still present call ambulance

314
Q

NSTEMI

A

ST depression
deep t wave inversion
pathological q waves

315
Q

Alternatives of raised troponins

A

chronic renal failure
sepsis
myocarditis
aortic dissection
PE

316
Q

Complications of MI

A

DREAD
death, rupture of heart septum, oedema, arrhythmia and aneurysm, dresslers

317
Q

Dressler diagnosis

A

ecg - st elevevation and t wave incersion
echo - periocardial effusion
rasied inflammatory markers

nsaids +/- pericardiocentesis

318
Q

Triggers of acute LVF

A

sepsis
aggressive iv fluids
MI
arrhythmias

rapid onset breathlessness

319
Q

What type of resp failure does LVF cause

A

type 1 - low oxygen

320
Q

treatment acute heart failure

A

pour sod

stop iv fluids
oxygen
diuretics - iv furosemide
monitor fluid balance

321
Q

Patho of malar flush

A

back pressure of blood into pulmonary system causing a rise in CO2 and vasodilation

322
Q

Valve with highest risk of thrombus formation

A

starr edwards - ball in cage

INR 2.5-3.5

323
Q

af vs vent ectopic

A

make do exercise, vent ectopics disappear once a certain threshold is met

324
Q

Side effects of HTN drugs

A
325
Q

Why are ARBs better than ACE for afro c patients second line htn

A

reduced incidence of cardiovascular events and reduced adverse effects.

326
Q

Becks triad

A

hypotension
raised jvp
muffled heart sounds

327
Q

```

Features of cardiac tamponade

A

Becks
dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans

328
Q

Treatment of tamponade with malignancy

A

Percutaneous balloon pericardiotomy

329
Q

Benefit of using drug-eluting stents in PCI

A

anti-proliferative drugs that significantly decrease the likelihood of restenosis

330
Q

Patients nitrates should be used in caution with

A

hypotensive

331
Q

Prefered vessel for PCI access

A

radial

unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI

332
Q

criteria for angina - 2 of = atypical

A
  1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
  2. precipitated by physical exertion
  3. relieved by rest or GTN in about 5 minutes
333
Q

ECG signs of HOCM

A

left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen

334
Q

persistent st elevation

A

ventricular aneurysm

335
Q

right bundle branch block and left axis deviation

A

bifasciular block

336
Q

Sudden heart failure, raised JVP, pulsus parodoxus, recent MI

A

left ventricular wall free rupture

337
Q

what marker is useful for re-infarction

A

CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days

338
Q

Causes of LBBB

A

New LBBB is always pathological. Causes of LBBB include:
myocardial infarction
diagnosing a myocardial infarction for patients with existing LBBB is difficult
rhe Sgarbossa criteria can help with this - please see the link for more details
hypertension
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

339
Q

Main poor prognostic indicator in ACS

A

cardiogenic shock

340
Q

Digoxin signs

A

ECG Features:
- Down-sloping ST depression (‘reverse tick’, ‘scooped out’)
- Flattened/inverted T waves
- Short QT interval
- Arrhythmias e.g., AV block, bradycardia

ICSM Year 6 + edits (28 decks)

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