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1 - MSRA > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Anteroseptal MI ECG leads

A

V1-4

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2
Q

Anteroseptal MI coronary artery

A

Left anterior descending

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3
Q

Inferior MI ECG leads

A

II, III, aVF

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4
Q

Inferior MI coronary artery

A

Right coronary

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5
Q

Anterolateral MI ECG leads

A

V1-6, aVL

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6
Q

Anterolateral MI coronary aretery

A

Proximal left anterior descending

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7
Q

Lateral MI ECG leads

A

I, aVL, +/- V5-6

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8
Q

Lateral MI coronary artery

A

Left circumflex

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9
Q

Posterior MI ECG leads

A

V1-3

Reciprocal changes typically seen

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10
Q

Reciprocal changes in posterior MI

A
  • Horizonal ST depression
  • Tall, broad R waves
  • Upright T waves
  • Dominant R wave in V2
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11
Q

Coronary artery in posterior MI

A

Usually left circumflex, also right coronary

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12
Q

Use of ACEi

A

First line hypertension in under 55’s
Heart failure
Diabetic nephropathy
Secondary prevention IHD

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13
Q

SEs ACEi

A

Cough
Angiodema
Hyperkalaemia
First dose hypotension (more common if on diuretics)

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14
Q

Cautions ACEi

A

Pregnancy/breastfeeding - avoid
Renovascular disease
Aortic stenosis
Hereditary idiopathic angioedema
K ≥5

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15
Q

Interactions ACEi

A

High dose diuretics (>80mg furosemide/day) - increased risk of hypotension

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16
Q

Monitoring ACEi

A

U&E before treatment started and after increaseing dose

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17
Q

Acceptable blood changes when starting ACEi

A

Serum creatinine 30% inc from baseline
Increase in K up to 5.5mmol/LWh

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18
Q

When might ACEi cause significant renal impairment

A

In patients with undiagnosed bilateral renal artery stenosis

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19
Q

Secondary prevention after ACS

A

Aspirin
Second antiplatelet if appropriate, aka clopidogrel
Beta blocker
ACEi
Statin

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20
Q

Common management all patients ACS

A

Aspirin 300mg
Oxygen to maintain sats <94%
Morphine if severe pain
Nitrates - SL or IV

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21
Q

STEMI criteria

A

Clinical symptoms of ACS ≥20mins, >20mins ECG features in ≥2 contiguous leads of:
- 2.5mm ST elevation in V2-3 in men under 40 years, or 2mm in men over 40
- 1.5mm ST elevation in V2-3 in women
- 1mm ST elevation in other leads
- New LBBB

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22
Q

Criteria PCI

A

Presentation in 12 hours of onset of symptoms
PCI can be delivered in 120mins of time fibrinoysis could be given

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23
Q

Criteria fibrinolysis

A

Presentation within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120mins

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24
Q

Antiplatelets given prior to PCI

A

If patient not taking oral anticoagulant - prasugrel
If patient taking oral anticoagulant - clopidogrel

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25
Q

Drug therapy used for PCI

A

If radial access - unfractionated heparin
If femoral access - bivalirudin

Both give glycoprotein IIb/IIIa inhibitor if inadequate response

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26
Q

Other procedures during PCI

A

Thrombus aspiration
Complete revascularisation if multivessel CAD without cardiogenic shock

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27
Q

Assessment of success of fibrinolysis

A

ECG repeated 60-90 min after. If persistent myocardial ischaemia, consider PCI

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28
Q

Risk assessment NSTEMI patients

A

GRACE

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29
Q

What factors included in GRACE score

A
  • Age
  • HR and BP
  • Cardiac and renal function (creatinine)
  • Arrest on presentation
  • ECG findings
  • Troponin levels
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30
Q

Categories of risk based on predicted 6 month mortality

A

1.5% or below - lowest
> 1.5 - 3% - low
> 3 - 6% - intermediate
> 6 - 9% - high
over 9% - highesthi

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31
Q

Which patients with NSTEMI/unstable angina should have immediate coronary angiography?

A

Clinically unstable patients

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32
Q

Which patients with NSTEMI/unstable angina should have coronary angio within 73 hours

A

GRACE score >3% aka intermediate, high, or highest risk

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33
Q

What antithrombin treatment NSTEMI/unstable angina

A

Fondaparinux if not high risk of bleeding and not having immediate angio
Unfractionated heparin if immediate angio planned or Cr >265

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34
Q

Drug therapy prior to PCI in patients with NSTEMI/unstable angina

A

If not taking oral anticoagulant, prasugrel or ticagrelor
If taking oral anticoagulant, clopidogrel

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35
Q

Drug therapy PCI in NSTEMI/unstable angina

A

Unfractionated heparin

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36
Q

Conservative management NSTEMI/unstable angina

A

If patient at high risk of bleeding, clopidogrel
If patient not at high risk of bleeding, ticagrelor

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37
Q

Role of adenosine

A

Terminate SVT

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38
Q

Adverse effects adenosine

A

Chest pain
Bronchospasm (avoid in asthmatics)
Transient flushing
Can enhance conduction down accessory pathways, resulting in increased ventricular rate e.g. in WPW

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39
Q

What drug enhances effect of adenosine

A

Dipyridamole

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40
Q

What drug inhibits affects of adenosine

A

Theophyllines

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41
Q

When to give adrenaline ALS

A

ASAP non-shockable
Once chest compressions restarted after 3rd shock in VF/VT
Every 3-5 mins whilst ALS continues

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42
Q

Dose adrenaline ALS

A

1mg

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43
Q

When to give amiodarone ALS

A

VF/pulseless VT after 3 shocks
Further dose after 5 shocks

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44
Q

Dose amiodarone ALS

A

After 3 shocks - 300mg
After 5 shocks - 150mg

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45
Q

Alternative to adenosine ALS

A

Lidocaine

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46
Q

Role of thrombolytic drugs ALS

A

Should be given if PE suspected
If given, CPR continued for 60-90 minutes

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47
Q

Reversible causes cardiac arrest

A

Hypoxia
Hypovolaemia
Hyper/hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade
Toxins

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48
Q

Monitoring amiodarone

A

TFT, LFT, U&E, CXR prior to treatment
TFT and LFT every 6 months

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49
Q

Adverse effects amiodarone

A

Thyroid dysfunction
Corneal deposits
Pulmonary fibrosis/pneumonitis
Liver fibrosis/hepatitis
Peripheral neuropathy, myopathy
Photosensitivity
‘Slate grey’ appearance
Thrombophlebitis and injection site reactions
Bradycardia
Lengthens QT interval

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50
Q

First line treatment angina

A

Aspirin and statin
Sublingual GTN as needed
Beta blocker or calcium channel blocker

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51
Q

What calcium channel blocker angina

A

If monotherapy, rate limiting e.g. verapamil or diltizem
If in combo with beta blocker, dihydropyridine e.g. amlodipine, MR nifedipine

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52
Q

Second line treatment angina

A

If on beta blocker add CCB and vice versa

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53
Q

Options if patient cannot tolerate addition of beta blocker/CCB in angina

A

Long acting nitrate
Ivabradine
Nicorandil
Ranolazine

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54
Q

When to add third drug angina

A

Only whilst awaiting assessment for PCI

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55
Q

How to avoid nitrate tolerance

A

If taking SR ISMN, asymmetric dosing interval to maintain daily nitrate free time of 10-14 hours

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56
Q

Use of ARBs

A

Generally when ACEi not tolerated usually due to cough

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57
Q

Examples ARBs

A

Candesartan
Losartan
Irbesartan

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58
Q

SEs ARBs

A

Hypotension
Hyperkalaemia

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59
Q

1st line antiplatelet ACS (medially treated)

A

Aspirin (lifelong) and ticagrelor (12 months)

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60
Q

What if aspirin contraindicated in ACS (medically treated)

A

Lifelong clopi

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61
Q

1st line antiplatelet after PCI

A

Asprin (lifelong) and prasurgrel or ticagrelor (12 months)

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62
Q

What if aspirin contraindicated after PCI

A

Clopidogrel (lifelong)

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63
Q

1st line antiplatelet after TIA

A

Clopidogrel

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64
Q

2nd line antiplatelet after TIA/stroke

A

Aspirin and dipyridamole lifelong

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65
Q

1st line antiplatelet peripheral arterial disease

A

Clopidogrel (lifelong)

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66
Q

2nd line antiplatelet peripheral arterial disease

A

Aspirin (lifelong)

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67
Q

Risk factors aortic dissection

A

Hypertension
Trauma
Bicuspid aortic valve
Marfans and Ehlers-Danlos syndrome
Turner’s and Noonan’s sydnrome
Pregnancy
Syphilis

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68
Q

Features aortic dissection

A

Chest/back pain
Pulse deficit - weak/absent pulse, variation >20mmHg between arms
Aortic regurgitation
Hypertension

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69
Q

Features aortic dissection involving coronary arteries

A

Angina

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70
Q

Features aortic dissection involving spinal arteries

A

Paraplegia

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71
Q

Features aortic dissection involving distal aorta

A

Limb ischaemia

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72
Q

ECG changes aortic dissection

A

Majority have no or non-specific ECG changes
In minority, ST elevation in inferior leads

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73
Q

Classification aortic dissection

A

Type A - ascending aorta (more likely chest pain)
Type B - descending aorta (more likely back pain)

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74
Q

CXR aortic dissection

A

Widened mediastinum

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75
Q

Investigation of choice aortic dissection

A

CT angio CAP (suitable for stable patients and planning surgery)

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76
Q

CT angio CAP findings aortic dissection

A

False lumen

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77
Q

Management type A aortic dissection

A

Surgical management
BP control systolic 100-120mmHg whilst awaiting intervention

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78
Q

Management type B aortic dissection

A

Conservative management
Bed rest
IV labetalol

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79
Q

Complications backwards aortic dissection

A

Aortic incompetence/regurgitation
MI - inferior pattern

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80
Q

Complications forward aortic dissection

A

Stroke
Renal failure

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81
Q

Causes of chronic presentation of aortic regurgitation due to valve disease

A

Rheumatic fever
Calcific valve disease
Connective tissue disease, e.g. RA, SLE
Bicuspid aortic valve

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82
Q

Causes of acute presentation aortic regurgitation due to valve disease

A

Infective endocarditis

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83
Q

Causes of chronic presentation aortic regurgitation due to aortic root disease

A

Bicuspid aortic valve
Spondyloarthropathies, e.g. ankylosing spondylitis
Hypertension
Syphilis
Marfans, Erlers Danlos

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84
Q

Causes of acute presentation of aortic regurgitation due to aortic root disease

A

Aortic dissection

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85
Q

Features aortic regurgitation

A

Early diastolic murmur, increased by handgrip
Collapsing pulse
Wide pulse pressure
Quincke’s sign
De Musset’s sign

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86
Q

What is Quincke’s sign

A

Nailbed pulsation

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87
Q

What is De Musset’s sign

A

Head bobbing

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88
Q

Aortic regurg surgery indications

A

Symptomatic with severe AR
Asymptomatic with severe AR and LV dysfunction

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89
Q

Features aortic stenosis

A

ESM, radiates to carotids, decreased following Valsalva
Narrow pulse prsesure
Slow rising pulse
Delayed ESM
Soft/absent S2
S4
Thrill

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90
Q

Causes aortic stenosis

A

Degenerative calcification (most common >65)
Bicuspid aortic valve (most common <65)
Williams syndrome
Post-rheumatic disease
HOCM

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91
Q

Management aortic stenosis

A

If asymptomatic, observe
If symptomatic or valvular gradient >40mmHg and features of LV dysfunction, consider surgeryS

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92
Q

Surgical options aortic stenosis

A

Surgical AVR for young, low/medium risk patients
Transcatheter AVR for high operative risk

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93
Q

Role of balloon valvuloplasty aortic stenosis

A

Children with no aortic valve calcification
Adults with critical AS who not fit for valve replacement

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94
Q

Inheritence pattern arrythomogenic right ventricular cardiomyopathy (ARVC)

A

Autosomal dominant

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95
Q

Pathology ARVC

A

Right ventricular myocardium replaced with fibrous/fatty tissue

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96
Q

ECG ARVC

A

Abnormalities in V1-3, typically T wave inversion
Epsilon wave in 50% - terminal notch in QRS complex

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97
Q

Echo ARVC

A

Often subtle changes in early stages
Enlarged, hypokinetic right ventricle with thin free wall

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98
Q

Management ARVC

A

Sotalol
Catheter ablation
ICD

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99
Q

What is Naxos disease

A

Autosomal recessive variant of ARVC

ARVC, palmoplantar keratosis, woolly hair

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100
Q

First line rate control AF

A

Beta blocker or rate limiting CCB (e.g. diltiazem)

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101
Q

Second line rate control AF

A

Combination therapy with any 2 of:
Beta blocker
Diltiazem
Digoxin

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102
Q

CHADVASC score

A

Congestive HF - 1
Hypertension - 1
Age ≥75 - 2
Age 65-74 - 1
Diabete - 1
Prior stroke, TIA, or thromboembolism - 2
Vascular disease - 1
Female - 1

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103
Q

Anticoagulation based on CHADVASC

A

0 - no treatment
1 - consider anticoagulation if male
2 - offer anticoagulation

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104
Q

HASBLED score

A

Hb <130 males, <120 for females - 2
Age >74 - 1
Bleeding history (GI, intracranial) - 2
GFR <60 - 1
Antiplatelets - 1

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105
Q

Interpretation HASBLED

A

0-2 low risk
3 medium risk
4-7 high risk

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106
Q

First line anticoagulant AF

A

DOACs

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107
Q

Indications for cardioversion AF

A

If haemodynamically unstable (emergency)
If rhythm control strategy preferred (elective)

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108
Q

Anticoagulation prior to cardioversion

A

If definitely less than 48 hours, patients should be heparinised
If more than 48 hours, needs anticoagulation for at least 3 weeks prior to cardioversion (or TOE to exclude left atrial appendage thrombus - if neg, treat as less than 48h)

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109
Q

Cardioversion options when onset AF <48 hours

A

Electrical cardioversion
Chemical cardioversion

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110
Q

Drugs used for chemical cardioversion

A

Amiodarone if structural heart disease
Flecainide or amiodarone if no structural heart disease

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111
Q

Cardioversion options AF onset >48 hours

A

Electrical cardioversion

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112
Q

Management of AF with high risk of cardioversion failure

A

At least 4 weeks of amiodarone or sotalol prior to electrical cardioversion

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113
Q

Management post electrical cardioversion

A

If AF was <48 hours duration, no anticoagulation necessary
If AF >48 hours, at least 4 weeks of anticoagulation

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114
Q

Anticoagulation in AF post stroke

A

Warfarin or direct thrombin (rivaroxaban, apixaban, edoxaban) or factor Xa inhibitor (dabigatran)

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115
Q

When should anticoagulation for AF be started in TIA patients

A

Immediately (once haemorrhage excluded)

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116
Q

When should anticoagulation for AF be started in acute stroke patients

A

After 2 weeks (antiplatelets in intervening period)

Delayed if imaging shows very large cerebral infarction

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117
Q

When should rhythm control strategy be employed in AF

A

AF has reversible cause
Heart failure thought to be primarily caused by AF
New onset AF (<48hours)
Flutter suitable for ablation
More suitable based on clinical judgement

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118
Q

Role of digoxin rate control for AF

A

Not first line as less effective at controlling heart rate during exercise, only considered if person does no or very little exercise and other rate-limiting drugs ruled out due to co-morbidities
Good if co-existent heart failure

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119
Q

What drugs can be used to maintain sinus rhythm in patients with history of AF

A

Beta blockers
Dronedarone
Amiodarone

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120
Q

When is catheter ablation used in AF

A

If have not responded to or wish to avoid anti-arrhythmic medication

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121
Q

Anticoagulation around catheter ablation for AF

A

4 weeks before and during procedure

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122
Q

Limitation of catheter ablation for AF

A

Does not reduce stroke risk, even if patients remain in sinus rhythm, so still need anticoagulation based on chadvasc

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123
Q

Complications catheter ablation AF

A

Cardiac tamponade
Stroke
Pulmonary vein stenosis

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124
Q

Features first degre heart block

A

PR interval >0.2s
Often asymptomatic - if so doesnt need treatment

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125
Q

Features second degree heart block type 1

A

Progressive prolongation of PR interval until dropped beat occurs

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126
Q

Features second degree heart block type 2

A

PR interval constant, but P wave often not followed by QRS

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127
Q

Features third degree heart block

A

No association between P waves and QRS complexes

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128
Q

Causes raised BNP

A

Heart failure
Left ventricular hypertrophy
Ischaemia
Tachycardia
RV overload
Hypoxaemia
GFR <60
Sepsis
COPD
Diabetes
Age >70
Cirrhosis

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129
Q

Factors reducing BNP (false lows)

A

Obesity
Diuretics
Drugs

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130
Q

Drugs reducing BNP

A

ACEi
Beta blockers
ARBs
Aldosterone antagonists

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131
Q

What is bivalirudin

A

Reversible direct thrombin inhibitor used as anticoagulant in management of ACS

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132
Q

Inheritance Brugada syndrome

A

Autosomal dominant

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133
Q

ECG changes Brugada syndrome

A

Convex ST segment elevation >2mm in >1 of V1-3, followed by negative T wave
Partial RBBB

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134
Q

Investigation of choice Brugada syndrome

A

Give flecainide or ajmaline - ECG changes become more pronounced

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135
Q

Management Brugada syndrome

A

ICD

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136
Q

What is Buerger’s disease

A

Small and medium vessel vasculitis, strongly associated with smoking

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137
Q

Features Buerger’s disease

A

Extremity ischaemia - intermittent claudication, ischaemic ulcers
Superficial thrombophlebitis
Raynaud’s phenomenon

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138
Q

Features cardiac tamponade

A

Hypotension
Raised JVP
Muffled heart sounds

Dyspnoea
Tachycardia
Pulses paradoxus
Absent Y descent on JVP

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139
Q

ECG cardiac tamponade

A

Electrical alternans

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140
Q

Causes restrictive cardiomyopathy

A

Amyloidosis
Post-radiotherapy
Loeffler’s endocarditis

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141
Q

When does peripartum cardiomyopathy occur

A

Last month of preg - 5 months PP

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142
Q

Risk factors peripartum cardiomyopathy

A

Older women
Greater parity
Multiple gestations

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143
Q

Features Takotsubo cardiomyopathy

A

Stress induced
Transient, apical ballooning of myocardium
Supportive treatment

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144
Q

Infective causes of cardiomyopathy

A

Coxsackie B
Chagas disease

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145
Q

Infiltrative causes of cardiomyopathy

A

Amyloidosis

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146
Q

Storage causes of cardiomyopathy

A

Haemochromotosis

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147
Q

Toxic causes of cardiomyopathy

A

Doxorubicin
Alcoholic

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148
Q

Inflammatory causes of cardiomyopathy

A

Sarcoidosis

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149
Q

Endocrine causes of cardiomyopathy

A

Diabetes mellitus
Thyrotoxicosis
Acromegaly

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150
Q

Neuromuscular causes of cardiomyopathy

A

Friedreich’s ataxia
Duchenne/Beckers muscular dystrophy
Myotonic dystrophy

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151
Q

Nutritional causes of cardiomyopathy

A

Beriberi (thiamine)

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152
Q

Autoimmune causes of cardiomyopathy

A

SLE

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153
Q

What is Boerhaaves syndrome

A

Spontaneous rupture of oesophagus occurring as result of repeated episodes of vomiting

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154
Q

Presentation Boerhaaves syndrome

A

Sudden onset severe chest pain with severe vomiting
Severe sepsis secondary to mediastinitis

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155
Q

Diagnosis Boerhaaves syndrome

A

CT contrast swallow

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156
Q

Treatment Boerhaaves syndrome

A

Thoracotomy and lavage
If less than 12 hours from onset, primary repair feasible. If more, insertion of T tube to create controlled fistula between oesophagus and skin

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157
Q

First line investigation suspected heart failure

A

BNP

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158
Q

Interpretation BNP as first line in suspected heart failure

A

If >400, specialist assessment inc transthoracic echo within 2 weeks
If 100-400, specialist assessment including transthoracic echo within 6 weeks

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159
Q

BNP → NTproBNP conversion

A

BNP >400 = NTproBNP >2000
BNP 100-400 = NTproBNP 400-2000

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160
Q

First line treatment heart failure

A

ACEi and beta blocker

Start one at a time, judgement to decide which

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161
Q

Second line treatment heart failure

A

Aldosterone antagonist, e.g. spironolactone and eplerenone

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162
Q

Role of SGLT-2 inhibitors in heart failure

A

Reduce hospitalisation and cardiovascular death
Add dapagliflozin to optimised standard care

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163
Q

Third line treatment heart failure

A

Should be initiated by specialist
Options:
- Ivabradine
- Sacubitril-valsartan
- Hydralazine with nitrate
- Digoxin
- Cardiac resync therapy

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164
Q

Criteria ivabradine heart failure

A

Sinus rhythm >75/min
LV fraction <35%

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165
Q

Criteria sacubitril-valsartan heart failure

A

LV fraction <35
Symptomatic on ACEi/ARB
Initiated following ACEi/ARB wash out period

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166
Q

Use of digoxin in heart failure

A
  • Improves symptoms due to inotropic properties
  • Strongly indicated if co-existent AF
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167
Q

Who is hydralazine with nitrate useful for in heart failure

A

Afro-Caribbean patients

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168
Q

Indications cardiac resync therapy in heart failure

A

Widened QRS (LBBB)

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169
Q

Vaccinations in heart failure

A

Annual flu
One of pneumococcal

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170
Q

Who needs 5 yearly pneumococcal vaccine

A

Asplenia or splenic dysfunction
CKD

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171
Q

NYHA class I heart failure

A

No symptoms, no limitation on ordinary physicla exercise

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172
Q

NYHA class II heart failure

A

Mild symptoms, slight limitations of physical activity, comfortable at rest but ordinary activity results in fatigue, palpitations, or dyspnoea

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173
Q

NYHA class III heart failure

A

Moderate symptoms
Marked limitation of physical activity, comfortable at rest but less than ordinary activity results in symptoms

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174
Q

NYHA class IV heart failure

A

Severe symptoms, unable to carry out any physical activity without discomfort, symptoms present at rest

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175
Q

Associations coarctation of aorta

A

Turner’s syndrome
Bicuspid aortic valve
Berry aneurysms
Neurofibromatosis

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176
Q

Features coarctation of aorta

A

In infancy, heart failure
In adults, hypertension
Radiofemoral delay
Mid-systolic murmur, maximal over back
Apical blick from aortic valve
Notching of inferior border of ribs (due to collateral vessels)

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177
Q

Features complete heart block

A

Syncope
Heart failure
Regular bradycardia (30-50)
Wide pulse pressure
JVP - cannon waves in neck
Variable intensity S1

178
Q

First line anti-hypertensive in diabetics

179
Q

Considerations anti-hypertensives diabetics

A

Autonomic neuropathy may result in more postural symptoms
Routine use of beta blockers should be avoided as can cause insulin resistance, impair insulin secretion, and alter autonomic response to hypoglycaemia

180
Q

Causes dilated cardiomyopathy

A

Idiopathic (most common)
Myocarditis
IHD
Peripartum
Hypertension
Iatrogenic
Substance abuse
Inherited
Infiltrative

181
Q

Causes of myocarditis → dilated cardiomyopathy

A

Coxsackie B
HIV
Diptheria
Chagas

182
Q

Drugs causing dilated cardiomyopathy

A

Doxorubicin

183
Q

Substance abuse causing dilated cardiomyopathy

A

Alcohol
Cocaine

184
Q

Infiltrative causes dilated cardiomyopathy

A

Haemochromatosis
Sarcoidosis

185
Q

Features dilated cardiomyopathy

A

Classic features of heart failure
Systolic murmur
S3

186
Q

CXR dilated cardiomyopathy

A

Balloon appearance of heart

187
Q

DVLA hypertension

A

Can drive unless treatment causes unacceptable side effects, no need to notify DVLA

If group 2, can’t drive if BP consistently over 180mmHg systolic or 100mmHg diastolic

188
Q

Angiography (elective) DVLA

A

1 week off driving

189
Q

CABG DVLA

A

4 weeks off driving

190
Q

ACS DVLA

A

4 weeks off driving, 1 week if successfully treated by angioplasty

191
Q

Angina DVLA

A

Can’t drive if symptoms at rest/at the wheel

192
Q

Pacemaker insertion DVLA

A

1 week off driving

193
Q

ICD DVLA

A

If implanted for sustained ventricular arrhyhtmia - 6 months off
If prophylactic - 1 month

Permanent ban for group 2

194
Q

Successful catheter ablation for arrhythmia DVLA

A

2 days off

195
Q

Aortic aneurysm DVLA

A

If 6cm or more, notify DVLA - yearly review of licensw
If over 6.5cm, can’t drive

196
Q

Heart transplant DVLA

A

Can’t drive 6 weeks, no need to notify DVLA

197
Q

Causes left axis deviation

A

Left anterior hemiblock or left bundle branch block
Inferior MI
WPW (right sided pathway) - majority of cases
Hyperkalaemia
Congenital - ostium primum ASD, tricuspid atresia
Minor in obese

198
Q

Causes of right axis deviation

A

Right ventricular hypertrophy
Left posterior hemiblock
Lateral MI
Chronic lung disease → cor pulmonale
Pulmonary embolism
Ostium secundum ASD
WPW (left sided pathway)

Minor in tall
Normal in <1yo

199
Q

ECG digoxin toxicity

A

Down-sloping ST depression
Flattened/inverted T waves
Short QT
Arrhythmias, e.g. AV block, bradycardia

200
Q

ECG hypokalaemia

A

U waves
Small or absent T waves
Prolong PR
ST depression
Long QT

201
Q

ECG hypothermia

A

Bradycardia
J wave
First degree heart block
Long QT interval
Atrial and ventricular arrhythmias

202
Q

ECG LBBB

A

W in V1, M in V6

203
Q

ECG RBBB

A

M in V1, W in V6

204
Q

Causes LBBB

A

MI
Hypertension
Aortic stenosis
Cardiomyopathy
Idiopathic fibrosis
Digoxin toxicity
Hyperkalaemia

205
Q

ECG normal variants in athlete

A

Sinus bradycardia
Junctional rhythm
First degree heart block
Mobitz type 1

206
Q

Causes of increased P wave amplitude

A

Cor pulmonale

207
Q

Causes of bifid (broad, notced) P waves

A

Left atrial enlargement, classically due to mitral stenosis

208
Q

Causes prolonged PR interval

A

Idiopathic
Ischaemic heart disease
Digoxin toxicity
Hypokalaemia
Rheumatic fever
Aortic root pathology, e.g. abscess secondary to endocarditis
Lyme disease
Sarcoidosis
Myotonic dystrophy

209
Q

Causes short PR interval

A

Wolff-Parkinson-White syndrome

210
Q

Causes of right bundle branch block

A

Normal variant
Right ventricular hypertrophy
Chronically increased right ventricular pressure, e.g. cor pulmonale
Pulmonary embolism
Myocardial infarction
Atrial septal defect
Cardiomyopathy or myocarditis

211
Q

Causes ST depression

A

Secondary to abnormal QRS (LVH, LBBB, RBBB)
Ischaemia
Digoxin
Hypokalaemia
Syndrome X

212
Q

Causes ST elevation

A

Myocardial infarction
Pericarditis/myocarditis
Normal variant (high take off)
Left ventricular aneurysm
Prinzmetal’s angina (coronary artery spasm)
Takotsubo cardiomyopathy
Subarachnoid haemorrhage

213
Q

Causes peaked T waves

A

Hyperkalaemia
Myocardial ischaemia

214
Q

Causes inverted T waves

A

Myocardial ischaemia
Digoxin toxicity
Subarachnoid haemorrhage
Arrythmogenic right ventricular cardiomyopathy
Pulmonary embolism
Brugada syndrome

215
Q

Acute heart failure treatment for all patients

A

IV loop diuretics, e.g. furosemide or bumetanide

216
Q

Role of vasodilators (nitrates) in acute heart failure

A

May be used if concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease

217
Q

Treatment of acute heart failure patients with resp failure

218
Q

Treatment of hypotension/cardiogenic shock in acute heart failure

A

Inotropic agents, e.g. dobutamine
Vasopressor agents, e.g. norepinephrine
Mechanical circulatory assistance, e.g. intra-aortic balloon counterpulsation

219
Q

Role of inotropic agents in acute heart failure

A

Should be considered for patients with severe left ventricular dysfunction who have potentially reversible cardiogenic shock

220
Q

Role of vasopressor agents in acute heart failure

A

Normally only used if insufficient response to inotropes and evidence of end-organ hypoperfusion

221
Q

Should regular medications for heart failure be continued in acute heart failure

A

Yes
Beta blockers should be stopped if HR under 50, 2nd or 3rd degree block, or shock

222
Q

Causes of soft S1

A

Prolonged PR
Mitral regurgitation

223
Q

Causes of loud S1

A

Mitral stensois

224
Q

Causes of soft S2

A

Aortic stenosis

225
Q

Causes of S3

A

Normal if <30
LVF
Constrictive pericarditis
Mitral regurgitation

226
Q

Causes of S4

A

Aortic stenosis
HOCM
Hypertension

227
Q

What is remnant hyperlipidaemia

A

Also called type 3 hyperlipoproteinaemia
Rare inherited condition causing high levels of cholesterol and triglycerides in the blood

228
Q

Causes palmar xanthoma

A

Remnant hyperlipidaemia
Less commonly, familial hypercholesterolaemia

229
Q

What are eruptive xanthomas

A

Multiple red/yellow vesicles on extensor surfaces, e.g. elbows, knees

230
Q

Causes of eruptive xanthomas

A

Familial hypertriglyceridaemia
Lipoprotein lipase deficiency

231
Q

Causes of tendon xanthoma, xanthelasma

A

Familial hypercholesterolaemia
Remnant hyperlipidaemia

232
Q

What are xanthelasma

A

Yellowish papules and plaques caused by localised accumulation of lipid deposits commonly seen on eyelid

233
Q

Management options xanthelasma

A

Surgical excision
Topical tricholoroacetic acid
Laser therapy
Electrodesiccation

234
Q

Stage 1 hypertension criteria

A

Clinic BP ≥140/90 and ABPM/HBPM ≥135/85

235
Q

Stage 2 hypertension criteria

A

Clinic BP ≥160/100 and ABPM/HBPM ≥150/95

236
Q

Severe hypertension criteria

A

Clinic BP systolic ≥180 or diastolic ≥120

237
Q

When should ABPM/HBPM be offered

A

Any BP ≥140/90

238
Q

Management BP ≥180/120

A

Consider need for urgent referral
Urgent investigation for end-organ damage - bloods, urine, ACR, ECG

239
Q

Who needs urgent referral BP ≥180/120

A

Signs of retinal haemorrhage or papilloedema
Life threatening symptoms, e.g. new onset confusion, chest pain, signs of heart failure, AKI
If phaeochromocytoma suspected

240
Q

What to do if BP ≥180/120 and target organ damage identified on investigation

A

Consider starting anti-hypertensive drugs immediately, wtihout waiting for results of ABPM/HBPM

241
Q

What to do if BP ≥180/120 and target organ damage not identified on investigation

A

Repeat clinic BP within 7 days

242
Q

How is ABPM carried out

A

At least 2 measurements per hour during persons usual waking hours, average value of at least 14 measurements

243
Q

When is HBPM offered

A

If ABPM not tolerated or declined

244
Q

How is HBPM carried out

A

For each BP recording, 2 consecutive measurements, at least 1 min apart and with patient seated
Record BP BD, ideally morning and evening
Recorded for at least 4 days, ideally 7 days.
Discard all measurements from first day, and use average of all remaining measurements

245
Q

When to defo offer drug treatment in stage 1 hypertension

A

Age under 80 and:
- Target organ damage
- CVD
- Renal disease
- Diabetes
- 10 year CVD risk ≥10%

246
Q

When to consider offering drug treatment in stage 1 hypertension

A

Age over 80 and clinic BP >150/90
Age under 60 and 10 year CVD risk <10%

247
Q

What to do stage 1 hypertension in under 40’s

A

Consider specialist evaluation of secondary causes

248
Q

How to manage stage 2 hypertension

A

Lifestyle advice and drug treatment

249
Q

Causes secondary hypertension

A

Primary hyperaldosteronism (5-10% of cases of hypertension
Renal disease
Endocrine disorders
Drugs
Pregnancy
Coarctation of aorta

250
Q

Drugs causing hypertension

A

Steroids
MAOI
COCP
NSAIDs
Leflunomide

251
Q

Inheritance HOCM

A

Autosomal dominant

252
Q

Features HOCM

A

Often asymptomatic
Exertional dyspnoea
Angina
Syncope, typically following exercise
Sudden death
Jerky pulse, large A waves, double apex beat
Systolic murmur - ESM or pansystolic

253
Q

Conditions associated with HOCM

A

Friedreich’s ataxia
Wolff-Parkinson White

254
Q

Echo findings HOCM

A

Mitral regurgitation
Systolic anterior motion of anterior mitral valve leaflet
Asymmetric hypertrophy

255
Q

ECG HOCM

A

Left ventricular hypertrophy
Non-specific ST segment and T wave abnormalities, progressive T wave inversion
Deep Q waves
Occasionally AF

256
Q

Drugs to avoid HOCM

A

Nitrates
ACE-i
Inotropes

256
Q

Management HOCM

A

Amiodarone
Beta blockers or verapamil
Cardioverter defib
Dual chamber pacemarker
Endocarditis prophylaxis

257
Q

Most common pathogen infective endocarditis

A

Staphylococcus aureus

258
Q

Streptococcus viridans endocarditis associated with…

A

Developing countries (most common cause)
Poor dental hygiene or following dental procedure

259
Q

Most common organism causing endocarditis after valve surgery/indwelling lines

A

Coag neg Staphylococci, e.g. staphylococcus epidermidis

After 2 months, staph aureus most common cause again

260
Q

Infective endocarditis caused by Streptococcus bovis associated with…

A

Colorectal cancer

261
Q

Causes non-infective endocarditis

A

SLE
Malignancy (marantic endocarditis

262
Q

Culture negative causes of endocarditis

A

Prior ABx therapy
Coxiella burnetii
Bartonella
Brucella
HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella)

263
Q

Ivabradine use

A

Anti-anginal

264
Q

Adverse effects ivabradine

A

Visual effects, particularly luminous phenomena
Headache
Bradycardia, heart block

265
Q

Cause non-pulsatile JVP

A

Superior vena cava obstruction

266
Q

What is Kussmaul’s sign, and when seen

A

Paradoxical rise in JVP during inspiration
Seen in constrictive pericarditis

267
Q

What forms the a wave of JVP

A

Atrial contraction

268
Q

Cause of large A waves

A

Atrial pressure - tricuspid stenosis, pulmonary stenosis, pulmonary hypertension

269
Q

Cause of absent A waves

270
Q

What are Cannon a waves, and what causes?

A

Atrial contraction against closed tricuspid valve
Seen in:
- Complete heart block
- Ventricular tachycardia/ectopics
- Nodal rhythm
- Single chamber ventricular pacing

271
Q

Cause of V wave JVP, and when abnormal

A

Due to passive filling of blood into atrium against closed tricuspid valve
Giant V waves in tricuspid regurgitation

272
Q

How does long QT cause death

A

May lead to ventricular tachycardia/torsades de pointes → collapse and sudden death

273
Q

Congenital causes long QT

A

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

274
Q

Drugs causing long QT

A

Amiodarone, sotalol
TCAs, SSRIs (esp citalopram)
Methadone
Chloroquine
Terfenadine
Erythromycin
Haloperidol
Ondansetron

275
Q

Electrolyte disturbances causing long QT

A

Hypocalcaemia
Hypokalaemia
Hypomagnesaemia

276
Q

Other causes long QT

A

Acute MI
Myocarditis
Hypothermia
SAH

277
Q

Feaetures long QT1

A

Usually associated with exertional syncope, often swimming

278
Q

Features long QT2

A

Often assocaited with syncope occurring following emotional stress, exercise, or auditory stimuli

279
Q

Features long QT3

A

Events often occur at night or rest

280
Q

Management long QT

A

Avoid drugs that prolong QT interval and other precipitants as appropriate
Beta blockers
Implantable cardioverter defib in high risk cases

281
Q

Examples loop diuretics

A

Furosemide
Bumetanide

282
Q

Indications loop diuretics

A

Herat failure
Resistant hypertension

283
Q

Adverse effects loop diuretics

A

Hypotension
Hyponatraemia, hypokalaemia, hypomagnesaemia, hypocalcemia, hypochloraemic alkalosis
Ototoxicity
Renal impairment
Hyperglycaemia
Gout

284
Q

Risk factors mitral regurgitation

A

Female
Low BMI
Age
Renal dysfunction
Prior MI
Prior mitral stenosis or valve prolapse
Collagen disorders, e.g. Marfans, Ehlers-Danlos

285
Q

Causes mitral regurgitation

A

Papillary muscle or chordae tendinae damage after cardiac insult
Mitral valve prolapse
Infective endocarditis
Rheumatic fever
Congenital

286
Q

Symptoms MR

A

Most asymptomatic

Symtptoms of:
- Left ventricular failure
- Arrhythmias
- Pulmonary hypertension

287
Q

Signs MR

A

Pansystolic murmur described as blowing - best heard at apex and radiates to axilla
S1 quiet
Severe MR - widely split S2

288
Q

ECG findings MR

A

Broad P wave

289
Q

CXR findings MR

A

Cardiomegaly, enlarged LA and ventricle

290
Q

Medical management MR

A

Nitrates
Diuretics
Positive inotropes
Intra-aortic balloon pump

291
Q

Indications for surgery MR

A

Acute, severe regurgitation

292
Q

Surgical options MR

A

Repair > replacement in degenerative
When not possible, valve replacement - artificial or pig

293
Q

Causes mitral stenosis

A

Rheumatic fever (most common)
Mucopolysaccharoidoses
Carcinoid
Endocardial fibroelastosis

294
Q

Symptoms mitral stenosis

A

Dyspnoea
Haemoptysis

295
Q

Cause of dyspnoea and haemoptysis in mitral stenosis

A

Increased left atrial pressure → pulmonary venous hypertension
This can lead to rupture of thin walled and dilated bronchial veins

296
Q

Signs mitral stenosis

A

Mid-late diastolic murmur, best heard in expiration
Loud S1
Opening snap
Low volume pulse
Malar flush
AF

297
Q

Change in murmur in severe mitral stenosis

A

Length of murmur increases
Opening snap becomes close to S2

298
Q

CXR mitral stenosis

A

Left atrial enlargement

299
Q

Management asymptomatic mitral stenosis

A

Regular echo monitoring

300
Q

Management symptomatic mitral stenosis

A

Percutaneous mitral balloon valvotomy or mitral valve surgery (commissurotomy or valve replacement)

301
Q

Management AF in mitral stenosis

302
Q

Associations mitral valve prolapse

A

CHD - PDA, ASD
Cardiomyopathy
Turners syndrome
Marfans syndrome
Fragile X
Osteogenesis imperfecta
WPW
Long-QT
Ehlers Danlos
PKD

303
Q

Festures mitral valve prolapse

A

Mid-systolic click
Late systolic murmur, longer if patient standing

304
Q

Cause of ESM louder on expiration

A

Aortic stenosis
HOCMC

305
Q

Cause of ESM louder on inspiration

A

Pulmonary stenosis
ASD

306
Q

Cause of pansystolic murmur

A

Mitral/tricuspid regurgitation (louder during inspiration in tricuspid)
VSD (harsh)

307
Q

Cause of late systolic murmur

A

Mitral valve prolapse
Coarctation of aorta

308
Q

Cause of early diastolic murmur

A

Aortic regurgitation
Pulmonary regurgitation

309
Q

Cause of mid-late diastolic murmur

A

Mitral stenosis (rumbling)
Severe aortic regurgitation

310
Q

Cause of continuous machine like murmur

311
Q

Most common cause of death after MI

A

Cardiac arrest

312
Q

Management cardiogenic shock after MI

A
  • Inotropic support
  • Intra-aortic balloon pump
313
Q

What kind of MI is bradycardia more common following

A

Inferior MI (AV block)

314
Q

Time frame pericarditis after MI

A
  • First 48 hours
  • Dresslers syndrome occurs 4-6 weeks after
315
Q

Features pericarditis after MI

A

Common after transmural MI
Typical pericarditis pain
Pericardial rub
Pericardial effusion on echo

316
Q

Cause Dresslers syndrome

A

Autoimmune reaction against antigenic proteins formed as myocardium recovers

317
Q

Features Dresslers syndrome

A

Fever
Pleuritic pain
Pericardial effusion
Raised ESR

318
Q

Treatment Dresslers syndrome

319
Q

Features left ventricular aneurysm following MI

A

Persistent ST elevation
Left ventricular failure

320
Q

Treatment left ventricular aneurysm following MI

A

Anticoagulation (thrombus may form → stroke)

321
Q

Timeframe left ventricular free wall rupture post MI

A

1-2 weeks after

322
Q

Presentation left ventricular free wall rupture post MI

A

Acute heart failure secondary to tamponade - raised JVP, pulsus paradoxus, diminished heart sounds

323
Q

Treatment left ventricular free wall rupture

A

Urgent pericardiocentesis and thoracotomy

324
Q

Timeframe VSD post MI

A

First week

325
Q

Features VSD post MI

A

Acute heart failure
Pansystolic murmur

326
Q

Treatment VSD post MI

A

Urgent surgical correction

327
Q

What kind of MI is acute mitral regurg more common with

A

Infero-posterior

328
Q

Presentation acute mitral regurg post MI

A

Acute hypotension
Pulmonary oedema
Early to mid systolic murmur

329
Q

Treatment acute mitral regurgitation post MI

A

Vasodilator therapy
Often need emergency surgical repair

330
Q

Secondary prevention drugs after MI

A

DAPT
ACEi
Beta blocker
Statin

331
Q

Lifestyle recommendations post MI

A

Mediterranean style diet, switch butter and cheese for plant based products
Exercise 20-30 min/day until slightly breathless

332
Q

Sexual activity post MI

A

May resume 4 weeks post uncomplicated MI

333
Q

Use of PDE5 inhibitors (e.g. sildenafil) post MI

A

Can be used 6 months post MI
Avoid if on nitrates or nicorandil

334
Q

DAPT choice post medically managed ACS

A

Aspirin (lifelong) + ticagrelor (12 months)

335
Q

DAPT choice post PCI

A

Aspirin (lifelong) + prasugrel or ticagrelor (12 months)D

336
Q

Role of aldosterone antagonists post MI

A

In patients acute MI with symptom/signs of heart failure and LV systolic dysfunction, start eplerenone within 3-14 days of MI, pref after ACEi

337
Q

Use of oxygen therapy in COPD patients with MI

A

If at risk of hypercapnic respiratory failure, aim 88-92% until ABG available

338
Q

Agent of choice in thrombolysis

A

Tissue plasminogen activator (tPA)

339
Q

Glycaemic control in MI

A

Use dose-adjusted insulin infusion with regular monitor of blood glucose aiming under 11

340
Q

Nicorandil use

341
Q

Adverse effects nicorandil

A

Headache
Flushing
Skin, mucosal, and eye ulceration (GI ulcers including anal)

342
Q

Contraindications nicorandil

A

Left ventricular failure

343
Q

Nicotinic acid use

A

Hyperlipidaemia

344
Q

Adverse effects nicotinic acid

A

Flushing
Impaired glucose tolerance
Myositis

345
Q

Use nitrates

A

Angina
Acute treatment of heart failure

346
Q

SEs nitrates

A

Hypotension
Tachycardia
Headaches
Flushing

347
Q

Adverse signs with bradycardia

A
  • Shock - hypotension, pallor, sweating, cold/clammy extremities, confusion, impaired consciousness
  • Syncope
  • Myocardial ischaemia
  • Heart failure
348
Q

First line treatment bradycardia with adverse features

A

Atropine 500mcg IV

349
Q

Second line treatments bradycardia with adverse features

A

Atropine, up to 3mg
Transcutaneous pacing
Isoprenaline/adrenaline infusion titrated to response

350
Q

Third line treatment bradycardia with adverse features

A

Specialist advice for consideration of transvenous pacing

351
Q

Risk factors for asystole in bradycardia (need to consider transvenous pacing)

A

Complete heart block with broad complex QRS
Recent asystole
Mobitz type II AV block
Ventricular pause >3 seconds

352
Q

Management tachycardia with adverse features

A

Up to 3 synchronised DC shocks

353
Q

What is considered broad QRS in tachycardia

354
Q

Cause regular broad complex tachycardia

A

Ventricular tachycardia

355
Q

Treatment regular broad complex tachycardia

A

Loading dose amiodarone followed by 24 hour infusion

356
Q

Treatment irregular broad complex tachycardia

A

Expert help

357
Q

Cause irregular broad complex tachycardia

A

AF with bundle branch block (most likely in stable patient)
AF with ventricular pre-excitation
Torsades de pointes

358
Q

Treatment regular narrow complex tachycardia

A
  1. Vagal manoeuvres
  2. IV adenosine

If unsuccessful, consider diagnosis of atrial flutter - control rate (e.g. beta blockers)

359
Q

Treatment irregular narrow complex tachycardia

A

Probably AF - if onset <48h, consider cardioversion. If not, rate control - beta blockers first line

360
Q

Who usually gets bioprosthetic heart valves

A

Older patients (>65 in aortic, >70 in mitral)

361
Q

Advantage bioprosthetic valves

A

Long-term anticoagulation not needed - warfarin for 3 months, then low-dose aspirin

362
Q

Disadvantage bioprosthetic valve

A

Structural deterioration and calcification over time

363
Q

Anticoagulation mechanical heart valves

A

Warfarin
Aspirin if additional indication, e.g. IHD

364
Q

INR target mechanical heart valves

A

Aortic 3.0
Mitral 3.5

365
Q

Pulmonary embolism rule out criteria

A

Age 50+
HR ≥100
Oxygen sats ≤94%
Previous DVT or PE
Recent surgery or trauma in past 4 weeks
Haemoptysis
Unilateral leg swelling
Oestrogen use, e.g. HRT, contraceptives

If all criteria ABSENT, low chance of PE

366
Q

Wells score

A

Clinical signs/symptoms of DVT (leg swelling, pain on palpation of deep veins) - 3
Alternative diagnosis less likely than PE - 3
HR >100 - 1.5
Immobilisation for more than 3 days, or surgery in past 4 weeks - 1.5
Previous DVT/PE - 1.5
Haemoptysis - 1
Malignancy - 1

367
Q

Interpretation of Wells score

A

PE likely if 4+
PE unlikely if 4 or less

368
Q

Management PE likely Wells score

A

Immediate CTPA
If delay in getting CTPA, interim therapeutic anticoagulation (apixaban or rivaroxiban)
If CTPA negative, consider proximal leg vein USS if DVT suspected

369
Q

Management PE unlikely Wells score

A

D-dimer test - if positive, CTPA. If negative, stop anticoag and consider alternative diagnosis

370
Q

Use of V/Q scanning

A

Investigation of choice in renal impairment

371
Q

ECG changes PE

A

Large S wave in lead I
Large Q wave in lead III
Inverted T wave in lead III
RBBB
Right axis deviation
Sinus tachy

372
Q

CXR PE

A

Usually normal
Sometimes wedge-shaped opacification

373
Q

Other causes of V/Q mismatch

A

Old PE
AV malformations
Vasculitis
Previous radiotherapy

374
Q

First line anticoagulant PE

A

Apixaban or rivaroxiban

375
Q

Second line anticoagulant PE

A

Dabigatran or edoxaban
LMWH → warfarin

376
Q

Anticoagulant PE with severe renal impairment (<15)

A

LMWH → warfarin

377
Q

Anticoagulant PE in antiphospholipid syndrome

A

LMWH → warfarin

378
Q

Length of anticoagulant PE

A

3 months if provoked (3-6 months if acitive cancer)
6 months if unprovoked

379
Q

Treatment PE with haemodynamic instability

A

Thrombolysis

380
Q

Treatment repeated PEs on anticoagulation

A

Consider IVC filter

381
Q

What is pulsus paradoxus

A

Greater than 10mmHg fall in systolic BP during inspiration, presenting as faint or absent pulse in inspiration

382
Q

Causes pulsus paradoxus

A

Severe asthma
Cardiac tamponade

383
Q

Causes slow-rising/plateau pulse

A

Aortic stenosis

384
Q

Causes collapsing pulse

A

Aortic regurgitation
PDA
Hyperkinetic states, e.g. anaemia, thyrotoxic, fever, exercise, pregnancy

385
Q

Causes pulsus alternans

A

Severe LVF

386
Q

What is bisferiens pulse

A

Two systolic peaks

387
Q

Causes bisferiens pulse

A

Mixed aortic valve disease

388
Q

Causes jerky pulse

389
Q

Adverse effects statins

A

Myopathy
Liver impairment
Some evidence of increased risk of intracerebral haemorrhage in previous stroke patients

390
Q

Risk factors myopathy caused by statins

A

Female
Low BMI
Multisystem disease, e.g. diabetes mellitus

391
Q

Which statins more likely to cause myopathy

A

Simvastatin, atorvastatin

392
Q

Liver monitoring statins

A

LFTs at baseline, 3 months, 12 months

393
Q

Management of deranged LFTs with statins

A

Treatment discontinued if serum transaminase concentrations rise to and persist 3x upper limit of normal

394
Q

Interactions statins

A

Macrolides, e.g. erythromycin, clarithromycin - stop statins until course complete

395
Q

Who should be on statin

A

Everyone with established cardiovascular disease, e.g. stroke, TIA, IHD, PAD
Anyone with 10 year cardiovascular risk ≥10%
Patients with T1DM diagnosed over 10 years ago or 40+ or established nephropathy

396
Q

Time of day to take statins

A

Night (when majority of cholesterol synthesis occurs)

397
Q

First line statin primary prevention

A

20mg atorvastatin

398
Q

First line statin secondary prevention

A

80mg atorvastatin

399
Q

When to increase dose statin primary prevention

A

If non-HDL not reduced ≥40%

400
Q

Management SVT

A

Vagal manoeuvures
IV adenosine - rapid bolus 6mg → 12mg → 18mg
Electrical cardioversion

401
Q

Who can’t have adenosine in SVT

A

Asthmatics - give verapamil instead

402
Q

Prevention of SVT

A

Beta blockers
Radio-frequency ablation

403
Q

Types of syncope

A
  • Reflex
  • Orthostatic
  • Cardiac
404
Q

Causes reflex syncope

A

Vasovagal
Situational, e.g. cough, micturition, GI
Carotid sinus

405
Q

Causes orthostatic syncope

A

Primary autonomic failure
Secondary autonomic failure
Drug-induced
Volume depletion, e.g. haemorrhage, diarrhoea

406
Q

Causes primary autonomic failure → syncope

A

Parkinsons disease
Lewy body dementia

407
Q

Causes secondary autonomic failure → syncope

A

Diabetic neuropathy
Amyloidosis
Uraemia

408
Q

Drug causes of orthostatic syncope

A

Diuretics
Alcohol
Vasodilators

409
Q

Causes cardiac syncope

A

Arrhythmias
Structural - valvular, MI, HOCM
PE

410
Q

What is Takayasu’s arteritis

A

Large vessel vasculitis, typically causing obstruction of aorta

411
Q

Risk factors Takayasu’s arteritis

A

Younger females (10-40)
Asian people

412
Q

Features Takayasu’s arteritis

A

Systemic features of vasculitis, e.g. malaise, headache
Unequal BP in upper limbs
Carotid bruit and tenderness
Absent or weak peripheral pulses
Upper and lower limb claudication on exertion
Aortic regurgitation

413
Q

Conditions associated with Takayasu’s arteritis

A

Renal artery stenosis

414
Q

Investigations Takayasu’s arteritis

A

Vascular imaging of arterial tree - either MRA or CTA

415
Q

Management Takayasu’s arteritis

416
Q

Use thiazide diuretics

A

Mild heart failure (but loop diuretics better)
Hypertension (but now recommended to use thiazide-like diuretics instead)

417
Q

Common adverse effects thiazide diuretics

A

Dehydration
Postural hypotension
Hypokalaemia, hyponatraemia
Hypercalcaemia
Gout
Impaired glucose tolerance
Impotence

418
Q

Rare adverse effects thiazide diuretics

A

Thrombocytopenia
Agranulocytosis
Photosensitivity rash
Pancreatitis

419
Q

Contraindications thrombolysis

A

Active internal bleeding
Recent haemorrhage, trauma, or surgery
Coagulation and bleeding disorders
Intracranial neoplasms
Stroke <3 months
Aortic dissection
Recent head injury
Severe hypertension

420
Q

SEs thrombolysis

A

Haemorrhage
Hypotension
Allergic reactions with streptokinase

421
Q

What is torsades de pointes

A

Form of polymorphic ventricular tachycardia associated with a long QT interval

422
Q

Management ventricular tachycardia with adverse signs

A

Immediate synchronised cardioversion

423
Q

Management ventricular tachycardia without adverse signs

A

Amiodarone
Lidocaine (caution in severe LV impairment)
Procainamide

424
Q

Management ventricular tachycardia if drug treatment fails

A

Electrophysiological study
ICD

425
Q

INR target VTE

A

2.5, 3.5 if recurrent

426
Q

INR target AF

427
Q

Factors increasing action of warfarin

A

Liver disease
P450 enzyme inhibitors, e.g. amiodarone, ciprofloxacin
Cranberry juice
NSAIDs

428
Q

SEs warfarin

A

Haemorrhage
Teratogenic
Skin necrosis
Purple toes

429
Q

Warfarin and breastfeeding

A

Can be used

430
Q

Management of major bleeding on warfarin

A

Stop warfarin
Give IV vitamin K 5mg
Give prothrombin complex concentrate (if not available then FFP)

431
Q

Management INR >8.0 minor bleeding

A

Stop warfarin
Give IV vitamin K 1-3mg, repeat dose if INR still high after 24 hours
Restart warfarin when INR <5.0

432
Q

Management INR >8.0 no bleeding

A

Stop warfarin
Give vitamin K 1-5mg, using IV preparation orally, repeat dose if INR still too high after 24 hours
Restart when INR <5.0

433
Q

Management INR 5.0-8.0 minor bleeding

A

Stop warfarin
Give IV vitamin K 1-3mg
Restart warfarin when INR <5.0

434
Q

Management INR 5.0-8.0 no bleeding

A

Withhold 1 or 2 doses warfarin
Reduce subsequent maintenance

435
Q

What is WPW

A

Syndrome caused by congenital accessory conducting pathway between the atria and ventricles leading to AVRT

436
Q

ECG features WPW

A

Short PR interval
Wide QRS complexes with slurred upstroke - delta wave
Left axis deviation if right sided pathway (and vice versa)

437
Q

Type A vs type B WPW

A

Type A (left sided) - dominant R wave in V1
Type B (right sided) - no dominant R wave in V1

438
Q

Conditions associated with WPW

A

HOCM
Mitral valve prolapse
Ebstein’s anomaly
Thyrotoxicosis
Secundum ASD

439
Q

Definitive management WPW

A

Radiofrequency ablation of accessory pathway

440
Q

Medical management WPW

A

Sotalol (avoid if AF)
Amiodarone
Flecainide

1 - MSRA (23 decks)

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