Cardio Flashcards

1
Q

INR target for replacement aortic valve

A

3.0

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1
Q

INR target for replacement mitral valve

A

3.5

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2
Q

which pathway timing is most affected by warfarin

A

PT

as predominately affects factor VII

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3
Q

Initial blind therapy for native valve endocarditis

A

amoxicillin

consider adding low-dose gentamicin

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4
Q

Initial blind therapy If penicillin allergic, MRSA or severe sepsis in endocarditis

A

vancomycin + low-dose gentamicin

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5
Q

Initial blind therapy If prosthetic valve endocarditis [3]

A

vancomycin + rifampicin + low-dose gentamicin

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6
Q

Native valve endocarditis caused by staphylococci : treatment

A

Flucloxacillin

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7
Q

Native valve endocarditis caused by staphylococci treatment if pen allergic or MRSA

A

vancomycin + rifampicin

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8
Q

Prosthetic valve endocarditis caused by staphylococci: treatment

A

Flucloxacillin + rifampicin + low-dose gentamicin

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9
Q

Prosthetic valve endocarditis caused by staphylococci: treatment if pen allergic or MRSA [3]

A

vancomycin + rifampicin + low-dose gentamicin

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10
Q

Endocarditis caused by fully-sensitive streptococci (e.g. viridans) treatment

A

Benzylpenicillin

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11
Q

Endocarditis caused by fully-sensitive streptococci (e.g. viridans) treatment if pen allergic

A

vancomycin + low-dose gentamicin

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12
Q

Endocarditis caused by less sensitive streptococci

A

Benzylpenicillin + low-dose gentamicin

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13
Q

Endocarditis caused by less sensitive streptococci if pen allergic

A

vancomycin + low-dose gentamicin

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14
Q

CHADS-VASC components

A

Congestive Heart Failure
Hypertension
Age
Diabetes
Stroke, TIA, thromboembolism hx
Vascular disease
Sex

SADCHAVS

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15
Q

which components of CHADS-VASC score 2 points

A

Age >75
and
previous stroke, TIA, thromboembolism

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16
Q

normal QRS

A

80-120 ms

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17
Q

normal QTc

A

<450 female
<430 male

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18
Q

normal PR

A

120-200 ms

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19
Q

indication for cardiac resynchronisation therapy in heart failure

A

a widened QRS (e.g. left bundle branch block) complex on ECG

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20
Q

vaccines offers in heart failure

A

offer annual influenza vaccine
offer one-off pneumococcal vaccine

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21
Q

summary of drugs in HF [4]

A

BASH

beta blockers
ace inhibitors
spirinolactone
hydralazine, SGLT-2 and co

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22
Q

Modified Dukes Criteria for Infective Endocarditis

A

A useful mnemonic to remember the criteria is ‘BE FIVE PM’:

Major Criteria:
- Blood Cultures (2 cultures, 12 hours apart)
- Evidence of Endocardial Involvement: Echo shows new murmur; abscess

Minor Criteria:
- Fever >38
- Immunological phenomena: Roth spots, splinter haemorrhages or Olser’s nodes
- Vascular phenomena
- Echocardiogram minor criteria
- Predisposing features: valvular disease, IVDU, prosthetic valves
- Microbiological evidence that does not meet major criteria.

For a definitive diagnosis of IE two major criteria, or one major and three minor criteria, or all five minor criteria must be present.

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23
Q

5 medications that need to be started post MI

A

2 antiplatelets (aspirin + ticagrelor if medically managed)
ACEi
Beta blocker
Statin

might use prasugrel after PCI

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24
Q

reduced ejection fraction (HF-rEF) percentage

A

<35-40%

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25
Q

4 causes of Systolic dysfunction HF

A

Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias

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26
Q

4 causes of Diastolic dysfunction HF

A

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

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27
Q

which type of ejection fraction do
- systolic HF
- diastolic HF

have?

A

HF-rEF in systolic HF

HF-pEF in diastolic HF

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28
Q

signs of LVHF

A

pulmonary oedema:
dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles

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29
Q

signs of RVHF

A

peripheral oedema
ankle/sacral oedema
raised jugular venous pressure
hepatomegaly
weight gain due to fluid retention
anorexia (‘cardiac cachexia’)

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30
Q

causes of high output cardiac failure (normal heart with not enough blood to pump to meet metabolic needs) [6]

A

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

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31
Q

pulse pressure in aortic regurg

A

wide

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32
Q

pulse pressure in aortic stenosis

A

narrow

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33
Q

which murmur has an opening snap

A

mitral stenosis

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34
Q

in which murmurs is S3 likely to be heard

A

mitral regurgitation
aortic regurgitation

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35
Q

where is S4 likely to be heard

A

aortic stenosis

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36
Q

main ECG findings in pericarditis

A

main: PR depression
ST elevation everywhere

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37
Q

which murmur has a displaced apex heart sound

A

aortic regurgitation

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38
Q

aortic regurgitation murmur

A

end diastolic on LLSE (Erb’s point)

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39
Q

signs of severe aortic regurg [3]

A

collapsing pulse
wide pulse pressure
LVF

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40
Q

chronic causes of aortic regurgitation [4]

A

bicuspid aortic valve
RHD
CTD
ankylosing spondylitis

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41
Q

acute causes of aortic regurg [2]

A

infective endocarditis
aortic dissection

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42
Q

heart sounds in mitral stenosis

comment on the apex beat

A

loud S1 due to opening snap
tapping apex beat

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43
Q

murmur in mitral stenosis

A

mid diastolic in left lateral position at end expiration radiates to the axilla

low pitch rumbling

low pitch= low velocity

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44
Q

causes of mitral stenosis [2]

A

RHD
Austin-flint murmur

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45
Q

1st line surgical treatment of mitral stenosis (symptomatic)

A

balloon valvuloplasty

CI: LAA thrombus, calcified valve

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46
Q

murmur in mitral regurgitation

A

pan systolic murmur in left lateral position on end expiration radiates into axilla

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47
Q

chronic causes of mitral regurgitation [4]

A

mitral valve prolapse
RHD
calcification
CTDs

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48
Q

how can AR and MR be medically manageed

A

reduce the after load e.g. rate control and BP reduction, fluid reduction with diuretics

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49
Q

management of heart failure [4 lines]

A

1st line:
ACEi or Beta blocker (HFrEF)
Diuretic (HFpEF)

2nd line:
Spironolactone
SGLT-2 inhibitor (for HFrEF)

3rd line:
Hydralazine + nitrate
(other: ivabradine, digoxin, sacubitirl-valsartan)

4th:
cardiac resychronisatfon therapy

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50
Q

1st line treatment of stable angina

A

beta blocker or non-DHP CCB (along with GTN)

non DHP CCB e.g. verapamil or diltiazem

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51
Q

2nd line treatment of stable angina

A

beta blocker AND DHP CCB (along with GTN)

DHP CCB: amlodipine, nifedipine as these can be given with beta blcokcers

never prescribe non-DHP CCBs with beta blockers

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52
Q

3rd line options for stable angina [4]

A

long acting nitrate
ivabradine
nicorandil
ranolazine

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53
Q

1st line investigation of stable angina

A

CT coronary angiography

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54
Q

treatment of stroke without AF

A

antiplatelets i.e. clopidogrel (+ statin)

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55
Q

treatment of stroke with AF

A

anti coagulant i.e. DOAC

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56
Q

NICE guidelines (2021) suggest all patients with AF should have rate control as first-line, except with: [4]

A
  • A reversible cause for their AF
  • New onset atrial fibrillation (within the last 48 hours)
  • Heart failure caused by atrial fibrillation
  • Symptoms despite being effectively rate controlled

i.e. all of these people need rhythm control

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57
Q

1st line rate control option for AF

A

beta blocker (bisoprolol or atenolol)

or

non DHP CCB (diltiazem or verapamil)

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58
Q

contraindication for CCB [2]

A

peripheral oedema, heart failure

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59
Q

2nd line rate control of AF

A

digoxin

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60
Q

3rd line rate control of AF

A

amiodarone

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61
Q

which patients need rhythm control [4]

A
  • have a reversible cause of AF
  • have heart failure with AF
  • new onset AF
  • inadequately managed by rate control
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62
Q

1st line rhythm control of AF

A

electrical cardioversion (synchronised)

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63
Q

2nd line rhythm control of AF

A

pharmacological cardio version

depends on presence of structural heart disease

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64
Q

pharm rhythm control in someone with structural heart problems

A

amiodarone

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65
Q

pharm rhythm control in someone with NO structural heart disease

A

flecainide

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66
Q

two methods of rhythm control

A

cardio version (immediate or delayed) and long term drugs

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67
Q

2 types of immediate cardioversion

A

electrical and pharmacological

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68
Q

indications for immediate cardio version [2]

A

Present for less than 48 hours
Causing life-threatening haemodynamic instability

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69
Q

when is delayed cardio version used. How it is done.

A

if the atrial fibrillation has been present for more than 48 hours and they are stable.

The patient should be anticoagulated for at least 3 weeks before delayed cardioversion.
They are rate controlled whilst waiting for cardioversion.

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70
Q

1st line long term rhythm control

A

Beta blockers

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71
Q

2nd line long term rhythm control

A

Dronedarone

second-line for maintaining normal rhythm where patients have had successful cardioversion

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72
Q

3rd line long term rhythm control

A

Amiodarone

is useful in patients with heart failure or left ventricular dysfunction

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73
Q

1st line investigation of hypertension

A

ambulatory BP monitoring

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74
Q

what BP is severe hypertension requiring admission; what are the signs [5]

A

> =180/110

retinal haemorrhage
papilloedema
confusion
AKI
chest pain

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75
Q

example of thiazide LIKE diuretic

A

indapamide

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76
Q

what needs to be monitoring before and during ACEi treatment

A

U&Es

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77
Q

most commonly affected valve in infective endocarditis

A

mitral

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78
Q

most commonly affected valve in infective endocarditis caused by IVDU

A

tricuspid

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79
Q

treatment approach for paroxysmal AF

A

pill in pocket with flecainde

Paroxysmal atrial fibrillation refers to episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.

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80
Q

Investigation for suspected paroxysmal AF [2]

A

24-hour ambulatory ECG (Holter monitor)
Cardiac event recorder lasting 1-2 weeks

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81
Q

most common causative agent of infective endocarditis

A

staph aureus

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82
Q

Key investigations in infective endocarditis [3]

A

1) blood cultures: x3, 6hr apart
2) trans-oesophageal echo
3) 18F-FDG PET/CT for prosthetic heart valve

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83
Q

what replaces amoxicillin in infective endocarditis treatment if pen-allergic or MRSA

A

vancomycin and Low dose gentamicin

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84
Q

what replaces flucloxacillin in infective endocarditis treatment if pen-allergic or MRSA

A

vancomycin and rifampicin

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85
Q

treatment duration of native valve infective endocarditis

A

4 weeks

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86
Q

treatment duration of prosthetic valve infective endocarditis

A

6 weeks

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87
Q

causative organism of rheumatic fever

A

group A beta haemolytic strep i.e. strep pyogenes

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88
Q

2 histological findings in rheumatic heart disease

A

Anitschkow myocytes and Aschoff bodies

89
Q

Rheumatic fever major criteria: CASES

A

C- carditis
A- Arthritis
S- Sucutaneous nodules
E- Erythema marginatum
S- Syndenham’s chorea (presents 2-6m later)

90
Q

Rheumatic fever minor criteria: FRAPP

A

F- Fever
R- Raised ESR/CRP
A- Arthralgia
P- Prolonged PR
P- Previous rheumatic fever

91
Q

diagnostic investigations of rheumatic fever [3]

A

throat culture and rapid streptococcal antigen test

ISO titre

92
Q

management of rheumatic fever [3]

A
  • bed rest
  • analgesia (NSAIDs for joint painand aspirin for carditis)
  • phenoxymethylpenicillin (Pen V, for sore throat, 10 days)
93
Q

prophylactic antibiotic for rheumatic fever

A

IM benzathine penicillin or PO phenoxymethylpencillin

94
Q

infective causes of pericarditis [4]

A

HIV
TB
coxsackie
EBV

95
Q

autoimmune causes of pericarditis [2]

A

SLE
RA

96
Q

investigations for pericarditis [3]

A

bloods for inflammatory markers
ECG
Echo for effusion

97
Q

acute management of pericarditis and long term management

A

NSAID e.g. aspirin or ibuprofen
steroids in severe cases

colchicine (longer term to reduce reoccurrence)

98
Q

which patients are at risk of silent MI

A

diabetics

99
Q

ECG changes in stemi [2]

A

ST-segment elevation
New left bundle branch block

100
Q

ECG changes in NSTEMI [2]

A

ST segment depression
T wave inversion

can be normal just like in unstable angina but will have raised crops

101
Q

ECG leads representing the Left coronary artery

A

I, aVL, V3-6

102
Q

ECG leads representing the Left anterior descending

A

V1-4

103
Q

ECG leads representing the Circumflex

A

V5-6, I, aVL

104
Q

ECG leads representing the Right coronary artery

A

II, III, aVF

105
Q

two options for a STEMI presenting within 12 hours

A

Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)

Thrombolysis (if PCI is not available within 2 hours)

106
Q

medication given before PCI

A

aspirin and prasugrel

107
Q

what are angiography, angioplasty and stent

A

catheter into the patient’s radial or femoral artery (radial is preferred), feeding it up to the coronary arteries under x-ray guidance and injecting contrast to identify the area of blockage (angiography).

Blockages can be treated using balloons to widen the lumen (angioplasty) or devices to remove or aspirate the blockage.

Usually, a stent is inserted to keep the artery open.

108
Q

examples of fibrinolytic used in thrombolysis [3]

A

streptokinase, alteplase and tenecteplase.

109
Q

BATMAN management of NSTEMI

A

B – Base the decision about angiography and PCI on the GRACE score

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)

M – Morphine titrated to control pain

A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)

N – Nitrate (GTN)

110
Q

what GRACE score is considered low risk

A

<=3%

111
Q

what GRACE score is considered medium to high risk

how are they treated

A

> 3%

angiography with PCI within 72 hours

112
Q

how are unstable NSTEMI patients treated

A

angiography

113
Q

which CCB must ivabradine not be given with

A

verapamil (rate limiting CCB) as it can lead to bradycardia

114
Q

4H’s and 4T’s of reversible causes of PEA

A

hypovolaemia, hypoxia, hyper/hypokalaemia, hyper/hypothermia, toxicity, tension pneumothorax, tamponade, thromboembolism

115
Q

how can aortic dissection have neuro deficits

A

due to involvement of the carotid artery

116
Q

in which type of dissection is chest pain more common

A

Type A

117
Q

in which type of dissection is upper back pain more common

A

Type B

118
Q

treatment of acute pulmonary oedema

A

IV loop diuretics e.g. furosemide or bumetanide

119
Q

treatment of heart failure with respiratory failure

A

add CPAP

120
Q

when should GTN be given in acute heart failure [3]

A

normally not routinely given

only if there is concurrent myocardial ischaemia, severe hypertension or AR/MR

121
Q

what is pulsus paradoxus

causes of pulsus paradoxus

A

greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration

severe asthma, cardiac tamponade

122
Q

cause of slow rising pulse

A

aortic stenosis

123
Q

causes of collapsing pulse [4]

A

aortic regurgitation
patent ductus arteriosus
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

124
Q

what is Pulsus alternans

cause of Pulsus alternans

A

regular alternation of the force of the arterial pulse

severe LVF

125
Q

what is Bisferiens pulse

cause of bisferiens pulse

A

double pulse’ - two systolic peaks

mixed aortic valve disease, HOCM occasionally (a jerky pulse)

126
Q

investigation of choice in aortic dissection

A

CT angio of chest, abdo pelvis

Transoesophageal echocardiography (TOE) more suitable for unstable patients who are too risky to take to CT scanner

127
Q

1st line investigation in aortic dissection

A

Chest X-ray

shows widened mediastinum

128
Q

treatment of Type A dissection

A

IV labetalol aim for 100-120 systolic and surgery

129
Q

treatment of Type B dissection

A

IV labetolol and conservative

130
Q

ECG feature of cardiac tamponade

A

electrical alternans (QRS big small big small)

131
Q

which ejection systolic murmurs are heard louder on expiration [2]

A

aortic stenosis and HOCM

132
Q

which ejection systolic murmurs are heard louder on inspiration [2]

A

ASD and pulmonary stenosis

133
Q

which murmur is associated with carcinoid heart disease (Hedinger syndrome).

A

mid-ejection systolic murmur due to pulmonary stenosis

134
Q

what drug can make clopidogrel less effective

A

PPI

lansoprazole should be okay tho

135
Q

what are the risk factors for asystole in bradycardia [4]

A

complete heart block with broad complex QRS
recent asystole
Mobitz type II AV block
ventricular pause > 3 seconds

136
Q

treatment of bradycardia

A

initially atropine 500mcg
atropine, up to a maximum of 3mg
transcutaneous pacing
isoprenaline/adrenaline infusion titrated to response

transvenous pacing if no response to the above

137
Q

contraindications for thrombolysis [8]

A

active internal bleeding
recent haemorrhage, trauma or surgery (including dental extraction)
coagulation and bleeding disorders
intracranial neoplasm
stroke < 3 months
aortic dissection
recent head injury
severe hypertension

138
Q

MoA of thrombolytic drugs

A

convert plasminogen to plasmin, plasmin degrades fibrin that makes up the thrombus

139
Q

difference between aortic sclerosis and aortic stenosis

A

aortic sclerosis produced an ejection systolic murmur that does not radiate to the carotids and produces a normal ECG

140
Q

what finding would suggest an ascending aorta dissection over a descending

A

new early diastolic murmur suggesting aortic valve involvement

141
Q

ST elevation requirement in anterior leads and inferior leads in order to do PCI or thrombolysis

A

ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR

ST elevation of > 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR

New Left bundle branch block

142
Q

cause of inverted T waves [6]

A

myocardial ischaemia
digoxin toxicity
subarachnoid haemorrhage
arrhythmogenic right ventricular cardiomyopathy
pulmonary embolism (‘S1Q3T3’)
Brugada syndrome

143
Q

features of takayasu arteritis [6]

A

systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit and tenderness
absent or weak peripheral pulses
upper and lower limb claudication on exertion
aortic regurgitation (around 20%)

144
Q

investigation and management of takayasu arteritis

A

Investigations
vascular imaging of the arterial tree -either magnetic resonance angiography (MRA) or CT angiography (CTA)

Management
steroids

145
Q

which vessel is typically affected in Takayasu

A

aorta

146
Q

which antibiotic should statins not be co-prescribed with

A

macrolides due to risk of rhabdomyolysis

147
Q

what is Kussmaul’s sign and where is it seen

A

JVP will rise on inspiration

seen in constrictive pericarditis

148
Q

which diuretic can worse glucose tolerance

A

thiazides

149
Q

Beck’s Triad in cardiac tamponade

A

hypotension
raised JVP
muffled heart sounds

other features: pulsus paradoxus - an abnormally large drop in BP during inspiration

150
Q

in acute heart failure, when are inotropes and vasopressors used

A

in severe hypotension/ cardiogenic shock

151
Q

Following basic ABC assessment, patients are classified as being stable or unstable according to the presence of any adverse signs:

A

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

152
Q

monitoring of amiodarone
- before treatment
- during treatment

A

before: TFT, LFT, U&E, CXR prior to treatment
during: TFT, LFT every 6 months

153
Q

normal QRS in seconds

A

0.12-0.20

154
Q

4 causes of raised JVP

A
  • heart failure
  • fluid overload
  • constrictive pericarditis
  • cardiac tamponade
155
Q

management of WPW Syndrome

A

definitive treatment: radiofrequency ablation of the accessory pathway

medical therapy: sotalol***, amiodarone, flecainide
sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

156
Q

which drug is contraindicated in VT

A

verapamil

can precipitate cardiac arrest.

157
Q

atorvastatin dose in primary prevention of MI

A

20mg

158
Q

what three things make up a trifasicular block

A

RBBB +left anterior or posterior hemiblock (ventricular strain) + 1st-degree heart block

159
Q

features of 2 level Wells score

A

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative)

160
Q

what makes the ejection systolic murmur in HOCM quieter and louder

A

Increases with Valsalva manoeuvre and decreases on squatting

161
Q

which two conditions is HOCM associated with

A

Friedreich’s ataxia
Wolf-Parkinson White

162
Q

anti-anginal associated with GI ulceration

A

nicorandil

163
Q

anti-anginal at risk of developing tolerance

what should be done if this happens

A

isosorbide mononitrate

patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance

164
Q

what does the opening snap in MS indicate

A

valve is still mobile

165
Q

which anti anginal can cause cold peripheries

A

beta blockers

166
Q

age threshold for ACEi/ARB in hypertension

A

< 55

167
Q

causative agent of endocarditis in post prosthetic valve op patients ( < 2 months)

A

staph epidermidis

168
Q

causative agent of endocarditis associated with colorectal cancer

A

strep bovis

169
Q

causative agent of endocarditis associated with poor dental hygiene

A

step viridans

170
Q

which abx can precipitate torsade de pointes

A

macrolides

171
Q

ECG features of HOCM [4]

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
172
Q

when can consecutive shocks be given in defibrillation

A

if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend ‘up to three quick successive (stacked) shocks’, rather than 1 shock followed by CPR

173
Q

when is a further dose of amiodarone given in defibrillation

A

a further dose of amiodarone 150 mg should be given to patients who are in VF/pulseless VT after 5 shocks have been administered

174
Q

First degree heart block

A

constantly prolonged PR interval

there is delayed conduction through the atrioventricular node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex.

175
Q

Second degree heart block

A

some atrial impulses do not make it through the atrioventricular node to the ventricles. There are instances where P waves are not followed by QRS complexes. There are two types of second-degree heart block:

Mobitz type 1 (Wenckebach phenomenon)
Mobitz type 2

176
Q

Mobitz type 1
what is the pathophysiology and what is the ECG finding

A

conduction through the atrioventricular node takes progressively longer until it finally fails, after which it resets, and the cycle restarts.

increasing PR interval until a P wave is not followed by a QRS complex.

177
Q

Mobitz type 2
what is the pathophysiology and what is the ECG finding

A

Intermittent failure of conduction through the atrioventricular node, with an absence of QRS complexes following P waves.

The PR interval remains normal.

178
Q

what is the complication of Mobitz type 2 and third degree heart block

A

risk of asystole

179
Q

Third degree heart block

A

There is no observable relationship between the P waves and QRS complexes

180
Q

3 causes of sudden cardiac death in the young

A

most common: HOCM
2nd most common : Arrhythmogenic right ventricular cardiomyopathy (ARVC, also known as arrhythmogenic right ventricular dysplasia or ARVD
Brugada syndrome (common in Asians)

181
Q

inheritance of ARVC/ARVD

A

autosomal dominant pattern with variable expression

Naxos disease
an autosomal recessive variant of ARVC
a triad of ARVC, palmoplantar keratosis, and woolly hair

182
Q

pathology in ARVC

A

right ventricular myocardium is replaced by fatty and fibrofatty tissue

183
Q

investigations for ARVC [3]

A

ECG
abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex

echo
changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall

magnetic resonance imaging
is useful to show fibrofatty tissue

184
Q

treatment of ARVC [3]

A

drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator

185
Q

curative treatment for patients who get atrial flutter

A

radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

186
Q

where do atrial myxomas develop

A

75% occur in left atrium, most commonly attached to the fossa ovalis

more common in females

187
Q

most common ASD found in adulthood

what ECG finding?

A

ostium secundum

ECG: RBBB with RAD

188
Q

features of ASD [2]

A

ejection systolic murmur
fixed splitting of S2

189
Q

ECG changes in Brugada syndrome [2]

administration of which medications make these changes more apparent

A

-convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
- partial right bundle branch block

the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome

190
Q

management of Brugada syndrome

A

implantable cardioverter-defibrillator

191
Q

treatment of HOCM

A

Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

192
Q

drugs to avoid in HOCM

A

nitrates
ACE-inhibitors
inotropes

193
Q

drug causes of Long QT (METH CATS)

A

Methadone
Erythromycin
Terfenadine
Haloperidol
Clarithromycin / chloroquine
Amiodarone / Azithromycin
TCAs
SSRIs (esp. citalopram) / Sotolol

194
Q

ECG findings in dextrocardia [3]

A

inverted P wave in lead I
right axis deviation
loss of R wave progression

195
Q

how is asymptomatic mitral stenosis treated

A

observation every 6-12 months with echo

196
Q

side effects of beta blockers [5]

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

197
Q

Long QT syndrome: what channel is the issue

A

loss of function of K+ channels

198
Q

which murmur can present with haemoptysis

A

mitral stenosis

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

199
Q

which medication is contraindicated in treating breathlessness associated with aortic stenosis

A

nitrates

theoretical risk of profound hypotension

200
Q

management of AF post TIA and stroke: when is a DOAC started

A

post TIA- immediately once haemorrhage has been excluded

post stroke- if not haemorrhage, after 14 days of aspirin

201
Q

what BP is defined as severe hypertension

A

180 sys or 120 dia

202
Q

which conditions are associated with coarctation of the aorta

A

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

203
Q

features of coarctation of the aorta

A

infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over the back
apical click from the aortic valve
notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

204
Q

ECG features in hypothermia

A

bradycardia
‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias

205
Q

common cause of aortic stenosis in young patients

A

bicuspid aortic valve

206
Q

stage 1 HTN: clinic and ABPM

A

clinic >= 14//90

ABPM >=135/85

207
Q

stage 2 HTN: clinic and ABPM

A

clinic >=160/100

ABPM >=150/95

208
Q

when are LFTs monitored with statins

A

at baseline, 3 months then 12 months

209
Q

reversal agent for dabigatran

A

idarucizumab

210
Q

reversal agent for heparin

A

protamine

211
Q

reversal agent for DOAC

A

andexanet alfa

212
Q

treatment of subclavian steal syndrome

A

percutaneous transluminal angioplasty or a stent.

213
Q

NSTEMI (managed conservatively) antiplatelet choice

A

aspirin, plus either:
ticagrelor, if not high bleeding risk
clopidogrel, if high bleeding risk

+fondaparniux

214
Q

which type of heart failure are SGLT-2 inhibitors used for

A

HFrEF

215
Q

features of a bifascicular block

A

the combination of RBBB with left anterior or posterior hemiblock
e.g. RBBB with left axis deviation

216
Q

indication for emergency valve replacement surgery in infective endocarditis

A

severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy

217
Q

adverse effects of thiazide diuretics

A

dehydration
postural hypotension
hypokalaemia
due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions
hyponatraemia
hypercalcaemia
the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones
gout
impaired glucose tolerance
impotence

Rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

218
Q

treatment of aortic stenosis:
- asymptomatic
- symptomatic
- young person
- high risk operative
- not fit for valve replacement

A
  • asymptomatic: observe unless valve gradient >40 –> consider valve replacement
  • symptomatic: valve replacement
  • young person : surgical AVR
  • high risk: transcatheter AVR
    • not fit for valve replacement: balloon valvuloplasty
219
Q

for how long can’t you drive post mi

A

4 WEEKS

unless angioplasty done, then its one week

220
Q

Wellen syndorme

A

ECG pattern that is typically caused by high-grade stenosis in the left anterior descending coronary artery.

biphasic or deep T wave inversion in V2-3
minimal ST elevation
no Q waves

221
Q

management of AF with mitral stenosis

A

warfarin