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MRCP: Cardiology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Mechanism of ACEi?

A

inhibit the conversion angiotensin I to angiotensin II
ACE inhibitors are activated by phase 1 metabolism in the liver

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2
Q

What are the side effects of ACEi?

A

Cough (15% - Bradykinin)
Angioedema: may occur up to a year after starting treatment
Hyperkalaemia
First-dose hypotension: more common in patients taking diuretics

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3
Q

Cautions and contraindications of ACEi?

A

Pregnancy and breastfeeding - avoid
Renovascular disease (e.g. renal artery stenosis)
Aortic stenosis - may result in Hypotension
Hereditary of idiopathic angioedema
Potassium > 5

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4
Q

What are acceptable U&E changes when starting ACEi?

A

Creatinine rise of 30% from baseline
Increase in potassium up to 5.5

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5
Q

Outcomes of formation of coronary atheroma?

A
  1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen reaching the myocardium during exertion
  2. The risk of sudden plaque rupture. The fatty plaques which have built up in the endothelium may rupture leading to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.
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6
Q

What are unmodifiable risk factors for ischaemic heart disease?

A

Increasing age
Male gender
Family history

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7
Q

What are modifiable risk factors for ischaemic heart disease?

A

Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity

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8
Q

Stages of atheroma formation?

A
  1. Initial endothelial dysfunction
  2. Results in pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
  3. Fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
  4. Monocytes migrate from the blood and differentiate into macrophages.
    5.These macrophages then phagocytose oxidized LDL - propagate the inflammatory process.
  5. Smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
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9
Q

Anterior leads and artery?

A

V1-V4
LAD

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10
Q

Inferior leads and artery?

A

II, III, aVF
Right coronary

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11
Q

Lateral leads and artery?

A

I, V5-6
Left circumflex

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12
Q

Management of STEMI?

A

Aspirin + second anti platelet
PCI

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13
Q

Secondary prevention in STEMI?

A

Aspirin
Second antiplatelet if appropriate (e.g. clopidogrel)
Beta-blocker
ACE inhibitor
Statin

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14
Q

ECG STEMI criteria?

A

2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)

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15
Q

When should PCI be attempted?

A
  1. Should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
  2. If patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
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16
Q

What do patients require with PCI and radial access?

A

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

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17
Q

What do patients require with PCI and femoral access?

A

bivalirudin with bailout GPI

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18
Q

Mnx of NSTEMI?

A
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19
Q

How is the grace score calculated?

A

Predicts mortality in 3 months

age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

<1.5 - low
3-6 intermediate
>9% - high

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20
Q

What grace score NSTEMI patient should get a follow up PCI?

A

> 3%
Or clinically unstable

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21
Q

Choice of second line antipaltelet in NSTEMI ?

A

if the patient is not at a high risk of bleeding: ticagrelor
if the patient is at a high risk of bleeding: clopidogrel

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22
Q

What is the Killip risk stratification?

A

Stratifies 30 mortality risk post MI

Killip class Features 30 day mortality

I No clinical signs heart failure 6%
II Lung crackles, S3 17%
III Frank pulmonary oedema 38%
IV Cardiogenic shock 81%

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23
Q

Features of acute pericarditis?

A

chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia

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24
Q

Causes of pericarditis?

A

viral infections (Coxsackie)
tuberculosis
uraemia (causes ‘fibrinous’ pericarditis)
trauma
post-myocardial infarction, Dressler’s syndrome
connective tissue disease
hypothyroidism
malignancy

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25
Q

ECG changes in pericarditis?

A

Global ST saddle shaped elevation

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26
Q

How should pericarditis be treated?

A

Colchicine + NSAID

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27
Q

In which patients should adenosine be avoided?

A

Ashtmatics - bronchospasm

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28
Q

What drugs enhance adenosine? What drug reduces the effect of adenosine?

A

Enhances: dipyridamole (antiplatelet agent)
Diminish: Theophylline

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29
Q

What is the mechanism of action of adenosine?

A
  1. Causes transient heart block in the AV node
  2. Agonist of the A1 receptor in the atrioventricular node.
  3. Inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux

Adenosine has a very short half-life of about 8-10 seconds

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30
Q

Side effects of adenosine?

A

Chest pain
Bronchospasm
Transient flushing

Can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

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31
Q

What are examples of ADP inhibitors?

A

Clopidogrel
Prasugrel
Ticagrelor
Ticlopidine

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32
Q

What is the mechanism of ADP inhibitors?

A
  1. Adenosine diphosphate (ADP) is one of the main platelet activation factors, mediated by G-coupled receptors P2Y1 and P2Y12.
  2. The main target of ADP receptor inhibition is the P2Y12 receptor, as it is the one which leads to sustained platelet aggregation and stabilisation of the platelet plaque.
  3. Inhibitors block this
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33
Q

Which ADP inhibitors should be considered in high risk patients?

A

Long term complications reduced with prasugel + aspirin

rather than clopidogrel

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34
Q

How long should high risk PCI patients continue DAPT for?

A

12 months

post acute coronary syndrome (medically managed): add ticagrelor to aspirin, stop ticagrelor after 12 months
post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months

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35
Q

Side effect of ticagrelor?

A

Dyspnoea
Impaired clearance of adenosine

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36
Q

What are absolute contraindications for prasugrel?
What should you use instead?

A

Stroke
TIA
High risk bleeding

Ticagrelor. IF NOT THEN CLOPI

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37
Q

What are contraindications for ticagrelor?

A

high risk of bleeding, those with a history of intracranial haemorrhage, and those with severe hepatic dysfunction

caution in asthmatics and COPD

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38
Q

What are the shockable rhythms?

A

VF
Pulseless VT

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39
Q

In non-shockable rhythms, when should adrenaline be given?

A

adrenaline 1 mg as soon as possible for non-shockable rhythms

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40
Q

When should adrenaline be given in shockable rhythms?

A

After third shock

repeat adrenaline 1mg every 3-5 minutes whilst ALS continues

1ml of 1;1000

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41
Q

When should amiodarone be given in shockable rhythms?

A

300 mg After third shock

300mg after fifth shock

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42
Q

When should thrombolytic drugs be considered in CPR?

A

If attempts are 60-90 mins

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43
Q

What are the H’s?

A

Hypoxia
Hypovolaemia
Hypothermia
Hyperkalaemia

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44
Q

What are the T’s?

A

Toxins
Tamponade
Thrombosis
Tension pneumothorax

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45
Q

Mechanism of amiodarone?

A

Class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias.
Blocks potassium channels that inhibit repolarisation
Prolongs the action potential.

Amiodarone also has other actions such as blocking sodium channels (a class I effect)

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46
Q

Issues with amiodarone?

A
  • Long half life 20-100 days
  • Give into central veins, causes thrombophlebitis
  • Can be pro arrhythmic, as prolongs QT
  • P450 inhibitor
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47
Q

Side effects of amiodarone?

A

thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
‘slate-grey’ appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval

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48
Q

Medical management of angina?

A
  1. Aspirin
  2. GTN
  3. Consider beta blocker or CCB first line.
    - If mono therapy CCB then use diltiazem / verapamil
    - If used with beta blocker, CCb must be dihydroperidine
  4. Titrate up doses if poor response rate
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49
Q

What adjunct medication can be added in for angina?

A

a long-acting nitrate
ivabradine
nicorandil
ranolazine

only add a third drug whilst a patient is awaiting assessment for PCI or CABG

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50
Q

How should nitrates be prescribed?

A

asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate

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51
Q

Mechanism of angiotensin receptor blockers?

A

block effects of angiotensin II at the AT1 receptor

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52
Q

Treatment of anti platelets and duration in medical treated MI?

A

Aspirin (lifelong) & ticagrelor (12 months)

If aspirin contraindicated, clopidogrel (lifelong)

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53
Q

Treatment of anti platelets and duration in PCI?

A

Aspirin (lifelong) & prasurgrel or ticagrelor (12 months)

If aspirin contraindicated, clopidogrel (lifelong)

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54
Q

Treatment of anti platelets and duration in TIA?

A
  1. Clopidogrel (lifelong)
  2. Aspirin (lifelong) & dipyridamole (lifelong)
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55
Q

Treatment of anti platelets and duration in ischaemic stroke?

A
  1. Clopidogrel (lifelong)
  2. Aspirin (lifelong) & dipyridamole (lifelong)
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56
Q

Treatment of anti platelets and duration in peripheral vascular disease?

A
  1. Aspirin
  2. Clopidogrel
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57
Q

Features of aortic dissection

A

Sharp tearing pain
- chest pain type A
- back pain type B
Pulse deficit
- absent brachial, carotid, femoral
- > 20 mmHg drop
Aortic regurgitation

If involved:
coronary arteries → angina
spinal arteries → paraplegia
distal aorta → limb ischaemia

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58
Q

How are aortic dissections classified?

A

type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases

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59
Q

ECG changes in aortic dissection?

A

In a minority of patients, ST-segment elevation may be seen in the inferior leads

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60
Q

Risk factors for aortic dissection ?

A

hypertension: the most important risk factor
trauma
bicuspid aortic valve
collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
Turner’s and Noonan’s syndrome
pregnancy
syphilis

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61
Q

What investigations should be done for aortic dissection?

A

CXR –> widened mediastinum

CT angiography of the chest, abdomen and pelvis is the investigation of choice
suitable for stable patients and for planning surgery
a false lumen is a key finding in diagnosing aortic dissection

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

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62
Q

What is the management of Type A aortic dissection?

A

Surgical
keep BP 100-120 - labetaolol

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63
Q

Causes of aortic regurgitation due to valve disease?

A

Rheumatic fever: the most common cause in the developing world
calcific valve disease
Infective endocarditis
Connective tissue diseases e.g. Rheumatoid arthritis/SLE
Bicuspid aortic valve (affects both the valves and the aortic root)

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64
Q

Causes of aortic regurgitation due to aortic root disease?

A

Bicuspid aortic valve (affects both the valves and the aortic root)
Aortic dissection
Spondylarthropathies (e.g. ankylosing spondylitis)
Hypertension
Syphilis
Marfan’s, Ehler-Danlos syndrome

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65
Q

Clinical findings of aortic regurgitation?

A

Early diastolic murmur (increases with handgrip )
Collapsing pulse
Wide pulse pressure

  1. Quincke’s sign (nailbed pulsation)
  2. De Musset’s sign (head bobbing)
    mid-diastolic Austin-Flint murmur in 3. severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
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66
Q

What are indications for treatment of aortic regurgitation?

A

surgery: aortic valve indications include
symptomatic patients with severe AR
asymptomatic patients with severe AR who have LV systolic dysfunction

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67
Q

Symptoms associated with aortic stenosis?

A

Chest pain
Dyspnoea
Syncope / presyncope (e.g. exertional dizziness)
murmur

an ejection systolic murmur (ESM) is classically seen in aortic stenosis
classically radiates to the carotids
this is decreased following the Valsalva manoeuvre

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68
Q

Features of severe aortic stenosis?

A

narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
left ventricular hypertrophy or failure
Displaced apex beat

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69
Q

Causes of aortic stenosis?

A

Degenerative calcification (most common cause in older patients > 65 years)
Bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM

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70
Q

When should aortic stenosis be treated?

A

If symptomatic valve replacement

if asymptomatic but > 40 mmHg consider valve surgery

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71
Q

What surgical options are there for aortic stenosis?

A

AVR surgical replacement in younger people
CVS may be co-existant - should complete angiogram
Balloon valvuloplasty used in children

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72
Q

What is arrhythmogenic right ventricular cardiomyopathy (ARVC) ?

A

Autosomal dominant condition
Right ventricle myocardium replaced by fatty / fibrous tissue

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73
Q

What is the typical mutation in ARVC?

A

Desomosomal

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74
Q

ECG changes notably seen on ARVC?

A

ECG abnormalities in V1-3, typically T wave inversion.
Epsilon wave

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75
Q

What echo changes as seen in ARVC?

A
  • Thin walled right ventricle
  • ## Hypokinetic right ventricle
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76
Q

Best imaging for ARVC?

A

Cardiac MRI

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77
Q

Management of ARVC

A

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

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78
Q

What is Naxos disease?

A

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

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79
Q

Define paroxysmal AF?

A

Self terminating episodes of AF

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80
Q

Define persistent AF?

A

arrhythmia is not self-terminating
> 7 days

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81
Q

What is permanent AF?

A

Persistent AF - despite cardioversion

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82
Q

How is AF managed?

A

Rate control
- Beta blocker or diltiazem

Rhythm control
- Digoxin after rate control failed

Then try combination of beta blocker, diltazem or digoxin

Assess if anticoagulation is needed

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83
Q

When can cardioverion be carried out?

A

Anticoagulated for 3 weeks prior to cardioversion
AF for only 48 hours

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84
Q

What is the CHAD VASC score?

A

C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age >= 75 years 2
Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1
S Sex (female) 1

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85
Q

What CHAD VASC score merit anticoagulation?

A

1: If male anticoagulant. If female do not
2 or more: Anticoagulant

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86
Q

How should assessment of bleeding risk be carried out?

A

ORBIT scoring system:

Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females 2
Age > 74 years 1
Bleeding history (GI bleeding, intracranial bleeding or haemorrhagic stroke) 2
Renal impairment (GFR < 60 mL/min/1.73m2) 1
Treatment with antiplatelet agents 1

Provides risk of bleeding out of 100

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87
Q

What type of anticoagulant should be used in AF?

A

First line: DOAC
Second line: Warfarin

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88
Q

Types of cardioversion and indications?

A
  1. Electrical cardioversion as an emergency if the patient is haemodynamically unstable
  2. Electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.
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89
Q

How long should a patient be anti coagulated post cardioversion?

A

4 Weeks

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90
Q

what agents can cardiovert AF?

A

Amiodarone
Felcanide ( If not structural heat disease)

Less effective agents
beta-blockers (including sotalol)
calcium channel blockers
digoxin
disopyramide
procainamide

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91
Q

When should you anticoagulant in TIA?

A

Immediately once imaging has excluded haemorrhage

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92
Q

In acute stroke patients when should anticoagulation start?

A

Start after 2 weeks - anti platelet therapy should be started
Large strokes may need to delay

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93
Q

What does the rate of atrial flutter depend on ?

A

Degree of AV block

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94
Q

What is the management of atrial flutter?

A

Same as AF - although less effective
Cardioversion requires less joules
Radiofrequency ablation of tricuspid valve isthmus is curative

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95
Q

What are the echo findings of a atrial myxoma?

A

Auscultation: Mid-diastolic + Tumour plop
pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum (Commonly left atrium)

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96
Q

What is the most common congenital abnormality found in adulthood?

A

Atrial septal defect
- Osmium secundum is the most common

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97
Q

What is osmium secundum and osmium primum ASD?

A

Ostium primum: The septum Primus does not grow down completely
Osmium secundum: The septum does not close (foramen oval valve to rostrum secundum does not close at birth)

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98
Q

Murmur associated what ASD?

A

ejection systolic murmur, fixed splitting of S2

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99
Q

Complications with ASD?

A

embolism may pass from venous system to left side of heart causing a stroke

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100
Q

ECG changes and features of ostium Primus ASD?

A

Ostium primum
present earlier than ostium secundum defects
associated with abnormal AV valves
ECG: RBBB with LAD, prolonged PR interval

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101
Q

ECG changes and features of ostium secundum ASD?

A

Ostium secundum (70% of ASDs)
associated with Holt-Oram syndrome (tri-phalangeal thumbs)
ECG: RBBB with RAD

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102
Q

What is atrioventricular block ?

A

atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles. There are three types

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103
Q

Features of first degree heart block?

A

PR interval > 0.2 seconds
asymptomatic first-degree heart block is relatively common and does not need treatment

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104
Q

Types of type 2 AV node block?

A

type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs

type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

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105
Q

Features of complete heart block?

A

there is no association between the P waves and QRS complexes

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106
Q

Mechanism of atropine?

A

Muscarinic receptor antagonist
- Used in bradycardia
- Used in organophosphate poisoning

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107
Q

Side effects of atropine?

A

tachycardia
mydriasis
atropine may trigger acute angle-closure glaucoma in susceptible patients

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108
Q

What produces BNP and what is it effect?

A

Left ventricle myocardium

Diuretic
Suppresses renin-angiotensn system
Vasodilator

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109
Q

What level of BNP makes heart failures unlikely?

A

< 100

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110
Q

Side effects of beta blockers?

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

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111
Q

Contraindications of beta blockers?

A

uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia

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112
Q

Features of bicuspid aortic valve?

A

Normally asymptomatic in childhood
Normally patients get aortic stenosis or regard

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113
Q

Associations with bicuspid aortic valve

A

Left dominant coronary artery system
Turner’s syndrome

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114
Q

Features suggesting VT rather than SVT with aberrant conduction?

A

AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms

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115
Q

Inheritance in burgada syndrome? Most common mutation?

A

Autosomal dominant
Mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein

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116
Q

ECG features of brugada syndrome?

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

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117
Q

Management in brugara?

A

Implantable cardiac defibrillator

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118
Q

What is Buerger disease?

A

Middle vessel vasculitis
Strong association with smoking

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

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119
Q

O2 saturations through cardiac circuit?

A

The right atrium (RA), right ventricle (RV) and pulmonary artery (PA) normally have oxygen saturation levels of around 70%
the lungs oxygenate the blood to a level of around 98-100%. The left atrium (LA), left ventricle (LV) and aorta should all, therefore, have oxygen saturation levels of 98-100%

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120
Q

How would ASD affect O2 saturations in cardiac circuit?

A

Higher O2 saturtions in RA
85%

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121
Q

How would VSD affect O2 saturations in cardiac circuit?

A

High O2 saturations in RV
85%

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122
Q

What cardiac markers can be used, instead of troponin ?

A

Myoglobin
CK-MB
CK
Trop T
AST
LDH

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123
Q

What is the first cardiac marker to rise?

A

Myoglobin

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124
Q

What cardiac marker should be used if consider re-infarction?

A

CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)

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125
Q

What is a SPECT scan used for in cardiac imaging?

A

assess myocardial perfusion and myocardial viability
Identify areas of ischaemia

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126
Q

What is MUGA used for ?

A

Multi Gated Acquisition Scan, also known as radionuclide angiography
radionuclide (technetium-99m) is injected intravenously
the patient is placed under a gamma camera
may be performed as a stress test
can accurately measure left ventricular ejection fraction. Typically used before and after cardiotoxic drugs are used

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127
Q

What is a cardiac CT used for?

A

Calcium score
Correlation between plaque and future ischaemic event
Allow view of coronary artery lumen

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128
Q

Best imaging for structural heart disease?

A

Cardiac MRI
Myocardial perfusion can also be done by gadolinium

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129
Q

What are the features of cardiac tamponade?

A

Classical features - Beck’s triad:
hypotension
raised JVP
muffled heart sounds

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

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130
Q

Cardiac tamponade vs constrictive pericarditis?

A

Cardiac tamponade Constrictive pericarditis
JVP Absent Y descent X + Y present
Pulsus paradoxus Present Absent
Kussmaul’s sign Rare Present
Characteristic features / Pericardial calcification on CXR

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131
Q

Features of hypertrophic obstructive cardiomyopathy?

A

Leading cause of sudden cardiac death in young athletes
Usually due to a mutation in the gene encoding β-myosin heavy chain protein
Common cause of sudden death
Echo findings include MR, systolic anterior motion (SAM) of the anterior mitral valve and asymmetric septal hypertrophy

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132
Q

Features of Arrhythmogenic right ventricular dysplasia?

A

Right ventricular myocardium is replaced by fatty and fibrofatty tissue
Around 50% of patients have a mutation of one of the several genes which encode components of desmosome
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 comple

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133
Q

Caused of dilated cardiomyopathy?

A

Classic causes include
alcohol
Coxsackie B virus
wet beri beri
doxorubicin
Selenium deficiecny

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134
Q

Causes of restrictive cardiomyopathy?

A

Classic causes include
amyloidosis
post-radiotherapy
Loeffler’s endocarditis

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135
Q

Features of permpartum cardiomyopathy?

A

Typical develops between last month of pregnancy and 5 months post-partum
More common in older women, greater parity and multiple gestations

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136
Q

Features of takotsubo cardiomyopathy?

A

Stress’-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
Transient, apical ballooning of the myocardium
Treatment is supportive

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137
Q

Infective causes of cardiomyopathy?

A

Coxsackie B virus
Chagas disease

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138
Q

Infiltrative causes of cardiomyopathy?

A

Amyloidosis

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139
Q

Storage causes of cardiomyopathy?

A

Haemochromatosis

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140
Q

Toxicity causes of cardiomyopathy?

A

Alcohol
Doxorubicin

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141
Q

Inflammatory causes of cardiomyopathy?

A

Sarcoidosis

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142
Q

Endocrine causes of cardiomyopathy?

A

Diabetes mellitus
Thyrotoxicosis
Acromegaly

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143
Q

Nutritional causes of cardiomyopathy?

A

Wet Beriberi (thiamine)

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144
Q

Autoimmune causes of cardiomyopathy?

A

SLE

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145
Q

Features of Catecholaminergic polymorphic ventricular tachycardia

A

Autosomal dominant
defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum

exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope
sudden cardiac death
symptoms generally develop before the age of 20 years

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146
Q

Management of catecholaminergic polymorphic VT ?

A

beta-blockers
implantable cardioverter-defibrillator

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147
Q

Centrally acting anti-hypertensives?

A

methyldopa: used in the management of hypertension during pregnancy
moxonidine: used in the management of essential hypertension when conventional antihypertensives have failed to control blood pressure
clonidine: the antihypertensive effect is mediated through stimulating alpha-2 adrenoceptors in the vasomotor centre

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148
Q

Chronic heart failure medication?

A
  1. ACEI + Beta blocker
  2. Adjunct Aldosterone antagonist

Third line:
Ivabradine
Digoxin
Sacubitril-valsartan
Hydralazine

Cardiac resychronisation therapy ( biventricular pacing)

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149
Q

Criteria for ivabradine in heart failure?

A

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

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150
Q

Criteria for sucubitril valsartan?

A

criteria: left ventricular fraction < 35%
is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
should be initiated following ACEi or ARB wash-out period

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151
Q

What vaccinations should be commenced in heart failure?

A

annual flue
One off pneumococcal

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152
Q

In preserved LV heart failure, do ACEI and beta blocker work?

A

No

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153
Q

Features of cholesterol embolism?

A

eosinophilia
purpura
renal failure
livedo reticularis

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154
Q

Indication CRT in heart failure?

A

For patients with heart failure and wide QRS
Not tolerating medical conersvative management

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155
Q

NYHA classifcation of heart failure?

A

NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

NYHA Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

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156
Q

What drug class of clopidogrel belong to?

A

thienopyridine

prasugrel
ticagrelor
ticlopidine

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157
Q

Mechanism of action of clopiodgrel?

A

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

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158
Q

Acceptable PPI use in antiplatelets?

A

Lansoprazole

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159
Q

Features of coarctation of the aorta?

A

infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over 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

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160
Q

Associations of coarctation?

A

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

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161
Q

If a patient has an MI, and is anticoagulated. How long should they remain on anticoagulation and antiplatelet?

A

triple therapy (2 antiplatelets + 1 anticoagulant) for 4 weeks-6 months after the event and dual therapy (1 antiplatelet + 1 anticoagulant) to complete 12 months

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162
Q

How to manage VTE while on DAPT?

A

an ORBIT score should be calculated. Those with a low risk of bleeding may continue antiplatelets. In patients with an intermediate or high risk of bleeding consideration should be given to stopping the antiplatelets

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163
Q

Causes of constrictive pericarditis?

A

any cause of pericarditis
particularly TB

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164
Q

What is the eponymous sign for constrictive pericarditis?

A

Kussmaul’s sign - rise in JVP on inspiration

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165
Q

Features of constrictive pericarditis?

A

dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul’s sign is positive

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166
Q

Explain the coronary vasculature?

A

left aortic sinus → left coronary artery (LCA)
right aortic sinus → right coronary artery (RCA)
LCA → LAD + circumflex
RCA → posterior descending
RCA supplies SA node in 60%, AV node in 90%

Coronary arteries fill in diastole

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167
Q

Mechanism of dabigitran ?

A

Direct thrombin inhibitor
- Cannot be used in prosthetic heart valves
- Reduce dose in kidney disease
- Can be used in non-valvular AF

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168
Q

What is the first line anti-hypertensive and diabetes?

A

ACEI / ARB

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169
Q

Features of dilated cardiomyopathy?

A

classic findings of heart failure
systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
S3
‘balloon’ appearance of the heart on the chest x-ray

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170
Q

Cannot drive for how long post angioplasty (elective)?

A

angioplasty (elective) - 1 week off driving

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171
Q

CABG how long off driving?

A

CABG - 4 weeks off driving

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172
Q

Acute coronary syndrome with successful angioplasty - how long off driving?

A

4 weeks off driving if no angiplasty
1 week if angioplasty

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173
Q

ICD how long off driving ?

A

6 months
Having an ICD results in a permanent bar for Group 2 drivers

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174
Q

What is ebstein anomaly?

A

congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle
- Also referred to atrialisation

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175
Q

If ebstein anomaly present what other associations are likely?

A

Patent foramen ovale or ASD in 80%
Wolfe parking white

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176
Q

Clinical features of ebstain anomaly?

A

cyanosis
prominent ‘a’ wave in the distended jugular venous pulse,
hepatomegaly
tricuspid regurgitation
pansystolic murmur, worse on inspiration
right bundle branch block → widely split S1 and S2

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177
Q

Causes of left deviation?

A

left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people

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178
Q

Causes of right axis deviation?

A

right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome* - left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people

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179
Q

Posterior MI changes?

A

V1-V3 changes

Reciprocal changes of STEMI are typically seen:
horizontal ST depression
tall, broad R waves
upright T waves
dominant R wave in V2

Must confirm in positions V7-9

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180
Q

ECG changes in digoxin toxicity?

A

down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia

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181
Q

ECG changes of hypokalaemia?

A

U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT

U have no Pot and no T, but a long PR and a long QT

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182
Q

ECG changes 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

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183
Q

Causes of new LBBB?

A

myocardial infarction
hypertension
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

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184
Q

What are sgarbossa criteria?

A

Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)
Concordant ST depression > 1 mm in V1-V3 (score 3)
Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

Score >3 - suggestive of MI

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185
Q

Normal egg variations in an athlete?

A

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

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186
Q

What is suggestive of P wave with increased amplitude?

A

Cor pulmonale

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187
Q

P waves that are broad or notched? ( bifid)

A

often most pronounced in lead II
a sign of left atrial enlargement, classically due to mitral stenosis

188
Q

What type of PR interval is seen in WPW?

A

Short PR interval

189
Q

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

190
Q

Causes of RBBB?

A

normal variant - more common with increasing age
right ventricular hypertrophy
chronically increased right ventricular pressure - e.g. cor pulmonale
pulmonary embolism
myocardial infarction
atrial septal defect (ostium secundum)
cardiomyopathy or myocarditis

191
Q

Causes of ST depression?

A

secondary to abnormal QRS (LVH, LBBB, RBBB)
ischaemia
digoxin
hypokalaemia
syndrome X

192
Q

ST elevation causes?

A

myocardial infarction
pericarditis/myocarditis
normal variant - ‘high take-off’
left ventricular aneurysm
Prinzmetal’s angina (coronary artery spasm)
Takotsubo cardiomyopathy
rare: subarachnoid haemorrhage

193
Q

T wave inversion?

A

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

194
Q

?Peaked T waves

A

> 5mm in limb leads
10mm in precordial

hyperkalaemia
myocardial ischaemia

195
Q

What are the features of eclampsia?

A

condition seen after 20 weeks gestation
pregnancy-induced hypertension
proteinuria

196
Q

Management of eclampsia?

A

Magnesium sulphate 4g over 5-10 minutes

197
Q

What is eisenmenger’s syndrome?

A

reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension

uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

198
Q

Features of eisenmenger’s reaction?

A

original murmur may disappear
cyanosis
clubbing
right ventricular failure
haemoptysis, embolism

199
Q

What are contraindications to exercise tolerance testing?

A

myocardial infarction less than 7 days ago
unstable angina
uncontrolled hypertension (systolic BP > 180 mmHg) or hypotension (systolic BP < 90 mmHg)
aortic stenosis
left bundle branch block: this would make the ECG very difficult to interpret

200
Q

Positive exercise tolerance test?

A

exhaustion / patient request
‘severe’, ‘limiting’ chest pain
> 3mm ST depression
> 2mm ST elevation.Stop if rapid ST elevation and pain
systolic blood pressure > 230 mmHg
systolic blood pressure falling > 20 mmHg
attainment of maximum predicted heart rate
heart rate falling > 20% of starting rate
arrhythmia develops

201
Q

Physiological changes in exercise?

A

systolic increases, diastolic decreases
leads to increased pulse pressure
in healthy young people the increase in MABP is only slight

increase in cardiac output may be 3-5 fold
results from venous constriction, vasodilation and increased myocardial contractibility, as well as from the maintenance of right atrial pressure by an increase in venous return
heart rate up to 3-fold increase
stroke volume up to 1.5-fold increase

202
Q

How is heart failure define with ejection fraction?

A

Heart failure with reduced ejection fraction - < 35-40%
(typically systolic dysfunction)

Heart failure with preserved ejection fraction
(typically diastolic dysfunction)

203
Q

Systolic dysfunction heart failure?

A

Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias

204
Q

Diastolic dysfunction heart failure?

A

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

205
Q

Features of left sided heart failure?

A

pulmonary oedema
dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles

206
Q

Features of right sided heart failure?

A

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

207
Q

What does high output heart failure refer to?

A

High-output heart failure refers to a situation where a ‘normal’ heart is unable to pump enough blood to meet the metabolic needs of the body.

208
Q

Causes of high output heart failure?

A

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

209
Q

What causes heart sound 1 ?

A

closure of mitral and tricuspid valves
soft if long PR or mitral regurgitation
loud in mitral stenosis

210
Q

What causes heart sound 2 ?

A

closure of aortic and pulmonary valves
soft in aortic stenosis
splitting during inspiration is normal

211
Q

What causes heart sound 3?

A

caused by diastolic filling of the ventricle
considered normal if < 30 years old (may persist in women up to 50 years old)
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

212
Q

What causes heart sound 4 ?

A

may be heard in aortic stenosis, HOCM, hypertension
caused by atrial contraction against a stiff ventricle
therefore coincides with the P wave on ECG
in HOCM a double apical impulse may be felt as a result of a palpable S4

213
Q

Where should pulmonary valve be listened to?

A

Left second intercostal space, at the upper sternal border

214
Q

Where should aortic valve be listened to?

A

Right second intercostal space, at the upper sternal border

215
Q

Where should mitral valve be listened to ?

A

Left fifth intercostal space, just medial to mid clavicular line

216
Q

Where should tricuspid valve be listened to?

A

Left fourth intercostal space, at the lower left sternal border

217
Q

What causes a loud S1?

A

mitral stenosis
left-to-right shunts
short PR interval, atrial premature beats
hyperdynamic states

218
Q

What causes a soft S1?

A

mitral regurgitation

219
Q

What causes a loud S2?

A

hypertension: systemic (loud A2) or pulmonary (loud P2)
- loudest at pulmonary (P2) –> pulmonary hypertension
- loudest at aortic(A2) –> systemic hypertension
hyperdynamic states
atrial septal defect without pulmonary hypertension

220
Q

What causes a soft S2?

A

Aortic stenosis

221
Q

What causes a split S2 ?

A

deep inspiration
RBBB
pulmonary stenosis
severe mitral regurgitation

222
Q

Mechanism of hydralazine?

A

cGMP leading to smooth muscle relaxation in arterioles rather than veins

223
Q

Contraindicaitons for hydralazine?

A

systemic lupus erythematous
ischaemic heart disease/cerebrovascular disease

224
Q

Adverse effects of hydralazine?

A

tachycardia
palpitations
flushing
fluid retention
headache
drug-induced lupus

225
Q

What are the features of hypercalcaemia?

A

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

226
Q

Features and causes of eruptive xanthoma?

A

high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)

Causes of eruptive xanthoma
familial hypertriglyceridaemia
lipoprotein lipase deficiency

227
Q

Causes of tendon xanthoma?

A

familial hypercholesterolaemia
remnant hyperlipidaemia

228
Q

When is aspirin used in pregnancy?

A

High risk pregnancies - from week 12 until birth

hypertensive disease during previous pregnancies
chronic kidney disease
autoimmune disorders such as SLE or antiphospholipid syndrome
type 1 or 2 diabetes mellitus

229
Q

Criteria for hypertension in pregnancy?

A

systolic > 140 mmHg or diastolic > 90 mmHg
or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic

230
Q

Features of severe pre-eclampsia?

A

hypertension: typically > 160/110 mmHg and proteinuria as above
proteinuria: dipstick ++/+++
headache
visual disturbance
papilloedema
RUQ/epigastric pain
hyperreflexia
platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome

231
Q

Definition of pre-eclampsia?

A

Pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours)

Oedema may occur but is now less commonly used as a criteria
other organ involvement (see list below for examples): e.g. renal insufficiency (creatinine ≥ 90 umol/L), liver, neurological, haematological, uteroplacental dysfunction

232
Q

You get a high blood pressure reading… now what?

A
233
Q

What are stages of hypertension?

A

Stage 1: Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
Stage 2: Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
Stage 3: Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

234
Q

Features of phaechromocytoma?

A

labile or postural hypotension, headache, palpitations, pallor and diaphoresis

235
Q

How is a ambulatory blood pressure calculated?

A

2 blood pressures per hour
Average of 14

236
Q

How should home blood pressure monitoring be completed?

A

for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated
BP should be recorded twice daily, ideally in the morning and evening
BP should be recorded for at least 4 days, ideally for 7 days
discard the measurements taken on the first day and use the average value of all the remaining measurements

237
Q

Renal diseases that cause hypertension?

A

glomerulonephritis
pyelonephritis
adult polycystic kidney disease
renal artery stenosis

238
Q

Endocrine causes of hypertension?

A

phaeochromocytoma
Cushing’s syndrome
Liddle’s syndrome
congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
acromegaly

239
Q

Drug causes of hypertension?

A

steroids
monoamine oxidase inhibitors
the combined oral contraceptive pill
NSAIDs
leflunomide

240
Q

What is the pathophysiology in HOCM?

A

Autosomal dominant condition (generally)
gene encoding β-myosin heavy chain protein or myosin-binding protein C
results in predominantly diastolic dysfunction
left ventricle hypertrophy → decreased compliance → decreased cardiac output
characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy

241
Q

Signs found in HOCM?

A

jerky pulse, large ‘a’ waves, double apex beat
ejection systolic murmur
increases with Valsalva manoeuvre and decreases on squatting
hypertrophic cardiomyopathy may impair mitral valve closure, thus causing regurgitation

242
Q

What is HOCM associated with?

A

Friedreich’s ataxia
Wolff-Parkinson White

243
Q

Echo findings associated with HOCM?

A

MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)

244
Q

ECG changes of HOCM?

A

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

245
Q

Indications for implantable defibrillators?

A

long QT syndrome
hypertrophic obstructive cardiomyopathy
previous cardiac arrest due to VT/VF
testing and ejection fraction < 35%
Brugada syndrome

246
Q

Best antihypertensive in afrocaribean diabetic firstling?

A

ARB

247
Q

How does blood pressure chain throughout pregnancy?

A

blood pressure usually falls in the first trimester (particularly the diastolic), and continues to fall until 20-24 weeks
after this time the blood pressure usually increases to pre-pregnancy levels by term

248
Q

Management of HOCM?

A

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

249
Q

What drugs should be avoided in HOCM?

A

nitrates
ACE-inhibitors
inotropes

ACE inhibitors can reduce afterload which may worsen the LVOT gradient. The patient in this scenario has the characteristic signs of HOCM on his echocardiogram; mitral regurgitation, systolic anterior motion of the anterior mitral valve leaflet, asymmetric hypertrophy.

250
Q

Major criteria of Dukes?

A

Cultures:
- Two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
- Persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
- Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
- Positive molecular assays for specific gene targets

Endocarditis:
- Positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or
new valvular regurgitation

251
Q

Minor Duke’s criteria?

A

predisposing heart condition or intravenous drug use
microbiological evidence does not meet major criteria
fever > 38ºC
vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots

252
Q

Duke’s diagnosis criteria for infective endocarditis?

A

Infective endocarditis diagnosed if
pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria

253
Q

Poor prognostic factors for endocarditis?

A

Staphylococcus aureus infection (see below)
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels

254
Q

Initial blind therapy: Endocarditis + unsure what organism abx?

A

Native valve
amoxicillin, consider adding low-dose gentamicin

If penicillin allergic, MRSA or severe sepsis
vancomycin + low-dose gentamicin

If prosthetic valve
vancomycin + rifampicin + low-dose gentamicin

255
Q

Native valve endocarditis + Staph?

A

Flucloxacillin

If penicillin allergic or MRSA
vancomycin + rifampicin

256
Q

Prosthetic valve endocarditis caused by staphylococci?

A

Flucloxacillin + rifampicin + low-dose gentamicin

If penicillin allergic or MRSA
vancomycin + rifampicin + low-dose gentamicin

257
Q

Endocarditis +Strep (full sensitive) ?

A

Benzylpenicillin

If penicillin allergic
vancomycin + low-dose gentamicin

258
Q

Endocarditis + Strep (less sensitive) ?

A

Benzylpenicillin + low-dose gentamicin

If penicillin allergic
vancomycin + low-dose gentamicin

259
Q

Indications for surgery?

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

260
Q

How to investigate arrhythmias?

A
  1. ECG
  2. Holter monitor
  3. External loop recorder
  4. Internal loop recorder
261
Q

Mechanism of ivabradine?

A

Anti-anginal
acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.

262
Q

What are the side effects of ivabradine?

A

visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block

263
Q

What does the A wave in JVP correspond with?

A

Atrial contraction
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in atrial fibrillation

264
Q

When are cannon A waves seen in JVP and why:?

A

caused by atrial contractions against a closed tricuspid valve
are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

265
Q

What causes the c wave in JVP?

A

‘c’ wave
closure of tricuspid valve
not normally visible

266
Q

What causes the V wave in jvp?

A

‘v’ wave
due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation

267
Q

What causes the X wave in JVP?

A

‘x’ descent = fall in atrial pressure during ventricular systole

268
Q

What causes the Y wave in JVP?

A

‘y’ descent = opening of tricuspid valve

269
Q

Types of cannon A waves?

A

Regular cannon waves
ventricular tachycardia (with 1:1 ventricular-atrial conduction)
atrio-ventricular nodal re-entry tachycardia (AVNRT)

Irregular cannon waves
complete heart block

270
Q

Features of Kawasaki disease?

A

high-grade fever which lasts for > 5 days. Fever is characteristically resistant to antipyretics
conjunctival injection
bright red, cracked lips
strawberry tongue
cervical lymphadenopathy
red palms of the hands and the soles of the feet which later peel

271
Q

Management of Kawasaki disease?

A

Management
1. high-dose aspirin
- Kawasaki disease is one of the few indications for the use of aspirin in children. Due to the risk of Reye’s syndrome aspirin is normally contraindicated in children
2. intravenous immunoglobulin

echocardiogram (rather than angiography) is used as the initial screening test for coronary artery aneurysms

272
Q

What is the major complication in kawaski disease?

A

Coronary artery aneurysm

273
Q

What is long Qt syndrome?

A

Delayed depolarisation of the ventricles
defects in the alpha subunit of the slow delayed rectifier potassium channel

274
Q

Normal QTc?

A

< 430 females
<450 males

275
Q

Congenital causes of long QT?

A

Jervell-Lange-Nielsen syndrome
- includes deafness and is due to an abnormal potassium channel

Romano-Ward syndrome
- no deafness
RomaNO deafness

276
Q

What are the three types of long QT?

A

Long QT1 - usually associated with exertional syncope, often swimming
Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
Long QT3 - events often occur at night or at rest
sudden cardiac death

277
Q

Management of long QT?

A
  1. avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)
  2. beta-blockers*** ( sotalol can make it worse)
  3. implantable cardioverter defibrillators in high risk cases
278
Q

Mechanism of loop diruretic?

A

inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.

279
Q

Adverse effects of loop diuretic?

A

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

280
Q

What are the features of malignant hypertension?

A

classically: severe headaches, nausea/vomiting, visual disturbance
however chest pain and dyspnoea common presenting symptoms
papilloedema
severe: encephalopathy (e.g. seizures)

281
Q

What is the pathophysiology of malignant hypertension?

A

fibrinoid necrosis of blood vessels, leading to retinal haemorrhages, exudates, and proteinuria, haematuria due to renal damage (benign nephrosclerosis).
can lead to cerebral oedema → encephalopathy

282
Q

Treatment of malignant hypertension?

A

reduce diastolic no lower than 100mmHg within 12-24 hrs
bed rest
most patients: oral therapy e.g. atenolol
if severe/encephalopathic: IV sodium nitroprusside/labetolol

283
Q

What are the associations of mitral valve prolapse?

A

congenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Marfan’s syndrome, Fragile X
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease

284
Q

Features of mitral valve prolapse?

A

Complain of atypical chest pain or palpitations
mid-systolic click (occurs later if patient squatting)
late systolic murmur (longer if patient standing)

285
Q

What is multi-focal atrial tachycardia?

A

Irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves

286
Q

How can multi-focal atrial tachycardia be managed?

A

correction of hypoxia and electrolyte disturbances
rate-limiting calcium channel blockers are often used first-line
cardioversion and digoxin are not useful in the management of MAT

287
Q

Ejection systolic + Louder on expiration?

A

aortic stenosis
hypertrophic obstructive cardiomyopathy

288
Q

Ejection systolic + Louder in inspiration?

A

pulmonary stenosis
atrial septal defect

289
Q

Holosytolic murmur + High pitch?

A

mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral stenosis
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole

290
Q

Late systolic murmur?

A

mitral valve prolapse
coarctation of aorta

291
Q

Early diastolic mumur + high pitch blowing?

A

aortic regurgitation (high-pitched and ‘blowing’ in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)

292
Q

Mid-late diastolic murmur?

A

mitral stenosis (‘rumbling’ in character)
Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)

293
Q

Myocardial infarction complications?

A

Left ventricle aneurysm
- Ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation.
- This is typically associated with persistent ST elevation and left ventricular failure.
- Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Left ventricle free wall rupture

VSD

Acute mitral regurgitation

294
Q

When can sildenafil be used after MI?

A

6 Months

295
Q

Causes of myocarditis?

A

viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin

296
Q

Clinical findings of myocarditis?

A

usually young patient with an acute history
chest pain
dyspnoea
arrhythmias

↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP

297
Q

Complications of myocarditis?

A

heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy: usually a late complication

298
Q

Mechanism of nicorandil?

A

potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

299
Q

Adverse effects of nicorandil?

A

headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration

300
Q

Mechanism of nitrates?

A

nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels

301
Q

Side effects of nitrates?

A

hypotension
tachycardia
headaches
flushing

302
Q

Indications for temporary pacing?

A

Indications for a temporary pacemaker
symptomatic/haemodynamically unstable bradycardia, not responding to atropine
post-ANTERIOR MI: type 2 or complete heart block*
trifascicular block prior to surgery

303
Q

Symptomatic bradycardia treatment?

A

Atropine (500mcg IV) is the first line treatment in this situation.

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

304
Q

Management of regular broad complex tachycardia?

A

assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
loading dose of amiodarone followed by 24 hour infusion

305
Q

Management of irregular broad complex tachycardia?

A

atrial fibrillation with bundle branch block - the most likely cause in a stable patient
atrial fibrillation with ventricular pre-excitation
torsade de pointes

306
Q

Management of narrow complex regular tachycardia?

A

vagal manoeuvres followed by IV adenosine
if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. beta-blockers)

307
Q

Management of irregular narrow complex tachycardia?

A

probable atrial fibrillation
if onset < 48 hr consider electrical or chemical cardioversion
rate control: beta-blockers are usually first-line unless there is a contraindication

308
Q

Hypertension in pregnancy management?

A
  1. Labetaolol

Nifedipine if asthmatic
Hydralazine may also be used

309
Q

Choice for treatment of PE in renal failure?

A

if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA

310
Q

PE in antiphospholipid?

A

if the patient has antiphospholipid syndrome (specifically ‘triple positive’ in the guidance) then LMWH followed by a VKA should be used

311
Q

Duration of anticoagulation for PE?

A

provoked: 3 months
unprovoked: 6 months

312
Q

Management of PE with haemodynamic instability?

A

Thrombolysis

313
Q

Management of recurrent PE?

A

IVC filter

314
Q

What type of pulse can be associated with severe asthma?

A

Pulsus paradoxus

315
Q

Slow rising pulse?

A

aortic stenosis

316
Q

Collapsing pulse?

A

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

317
Q

Jerk pulse?

A

HOCM

318
Q

Causes of restrict cardiomyopathy?

A

amyloidosis (e.g. secondary to myeloma) - most common cause in UK
haemochromatosis
post-radiation fibrosis
Loffler’s syndrome: endomyocardial fibrosis with a prominent eosinophilic infiltrate
endocardial fibroelastosis: thick fibroelastic tissue forms in the endocardium; most commonly seen in young children
sarcoidosis
scleroderma

319
Q

Pathogenesis of rheumatic fever?

A

Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells
B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated
there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry
the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries
this response leads to the clinical features of rheumatic fever
Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

320
Q

How is rheumatic fever diagnosed?

A

2 major criteria
or
1 major with 2 minor criteria

321
Q

Major criteria for rheumatic fever?

A

erythema marginatum
Sydenham’s chorea: this is often a late feature
polyarthritis
carditis and valvulitis (eg, pancarditis)
subcutaneous nodules

322
Q

Minor criteria rheumatic fever?

A

raised ESR or CRP
pyrexia
arthralgia (not if arthritis a major criteria)
prolonged PR interval

323
Q

Mnx of rheumatic fever?

A

antibiotics: oral penicillin V
anti-inflammatories: NSAIDs are first-line
treatment of any complications that develop e.g. heart failure

324
Q

Management of supra ventricular tachycardia?

A
  1. Valsalva
  2. rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
    contraindicated in asthmatics - verapamil is a preferable option
  3. Electrical cardio version
325
Q

Syndrome X?

A

Features
angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography

Management
nitrates may be beneficial

326
Q

Contraindications of thrombolysis

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

327
Q

Stages of valsalva?

A
  1. Increased intrathoracic pressure
  2. Resultant increase in venous and right atrial pressure reduces venous return
  3. The reduced preload leads to a fall in the cardiac output (Frank-Starling mechanism)
  4. When the pressure is released there is a further slight fall in cardiac output due to increased aortic volume
  5. Return of normal cardiac output
328
Q

Management of VT?

A

< 90 mmHg - cardiovert

Drug therapy
amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

329
Q

Management of warfarin INR 5.0-8.0
No bleeding

A

Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

330
Q

INR 5.0-8.0
Minor bleeding

A

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

331
Q

INR > 8.0
No bleeding

A

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

332
Q

INR > 8.0
Minor bleeding

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

333
Q

ECG changes on ?

A

short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway*
right axis deviation if left-sided accessory pathway*

334
Q

Management of WPW?

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

335
Q

Anti-biotic prophylaxis in tooth extract with valve disease?

A

Nope

336
Q

What is QRISK score?

A

Risk of stroke or heart attack in 10 years
If <10 this is acceptable

337
Q

Who should primary prevention be given to?

A

QRISK score > 10% should get a statin (20 mg atorvastatin)

338
Q

What is the dose for secondary prevention ?

A

80 mg atorvastatin

339
Q

Features of tricuspid regurgitation?

A

pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave

340
Q

Causes of tricuspid regurgitation?

A

right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein’s anomaly
carcinoid syndrome

341
Q

In complete heart block, what sign can be elicited?

A

Variable intensity of S1
Widened pulse pressure

342
Q

What is suggestive of a split fixed S2 ?

A

ASD

343
Q

AF + Old person + lots of falls = ? should you anticoagualte?

A

Assessing using the orbit score
Risk of falls or old age alone is not sufficient reasoning to withhold anticoagulation

344
Q

Pathophyiology behind aortic stenosis by age?

A

Risk of falls or old age alone is not sufficient reasoning to withhold anticoagulation

345
Q

Choice of imaging for PE if renal failure?

A

VQ scan
- contrast media

346
Q

What gives you pulses alternates?

A

severe lv function

347
Q

What gives a bisferiens pulse?

A

‘double pulse’ - two systolic peaks
mixed aortic valve disease

Hock

348
Q

?Target INR for mechanical aortic valve

A

3.0

349
Q

?Target INR for mechanical mitral valve

A

3.5

350
Q

Features of tetralogy of fallout?

A

ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta

351
Q

Treatment of hypertension

A
352
Q

What classifies as pulmonary hypertension?

A

Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of >= 25 mmHg

353
Q

Features of pulmonary hypertension ?

A

progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis
right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation

354
Q

How should treatment be guided in pulmonary hypertension

A

Acute vasodilator testing

355
Q

Pulmonary hypertension + positive vasodilator test treatment?

A

If there is a positive response to acute vasodilator testing (a minority of patients)
oral calcium channel blockers

356
Q

Pulmonary hypertension + negative vasodilator testing treatment?

A

If there is a negative response to acute vasodilator testing (the vast majority of patients)
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists: bosentan, ambrisentan
phosphodiesterase inhibitors: sildenafil
Combination therapy helpful

357
Q

How to measure pressure in left ventricle?

A

easured is similar to that of the left atrium (normally 6-12 mmHg).

balloon tipped Swan-Ganz catheter which is inserted into the pulmonary artery.

358
Q

What are the drugs cause long QT?

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron

359
Q

Dipyridamole mechanism?

A

phosphodiesterase inhibitor and decreases cellular uptake of adenosine

360
Q

Reasons to cease ACEi ?

A

A potassium above 6mmol/L should prompt cessation of ACE inhibitors in a patient with CKD

361
Q

MI long time ago + AF - not anticoagualted, on anti platelet. Management?

A

Stop antiplatelets
Put on anticoagulant

362
Q

Drugs liscenced for peripheral vascular disease and mechanism?

A

Drugs licensed for use in peripheral arterial disease (PAD) include:
naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life - 5HT2 antagonist
cilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICE

363
Q

Features of left ventricle aneurysm?

A

Persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

364
Q

Features of left ventricle free wall rupture?

A

acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

365
Q

What drug is contraindicated in broad complex tachycardia?

A

Verapamil

366
Q

Prognostic factors in HOCM?

A

syncope
family history of sudden death
young age at presentation
non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring
abnormal blood pressure changes on exercise

367
Q

Why does ticagrelor give you dyspnea?

A

Dyspnoea in ticagrelor-treated patients is due to the impaired clearance of adenosine

368
Q

Most common heart diseases at birth?

A

Congenital heart disease
cyanotic: TGA most common at birth, Fallot’s most common overall
acyanotic: VSD most common cause

369
Q

What drug improves long term prognosis in angina?

A

Aspirin

370
Q

Mitral valve repairs?

A

Percutaneous mitral commissurotomy is the intervention of choice for severe mitral stenosis
Mitral valve balloon

371
Q

Mechanism of tirofabn ?

A

GpIIa/IIIb inhibitor

372
Q

Grace score of < 1.5% management?

A

Aspirin 12 months

373
Q

Grace 1.5 - 3% ?

A

Aspirin + Clopidogrel for 12 months & outpatient perfusion/stress imaging

374
Q

Grace 3-6 % ?

A

Glycoprotein inhibitor & angiography within 96 hours

375
Q

When should 3 back to back shocks be given?

A

If already on continuing monitoring and note sudden change into VT

376
Q

In hypertension treatment, should thirazide like or thiazide diuretics be given?

A

Thiazide like - e.g. indapamide

377
Q

What heart valve issues does carcinoid syndrome cause?

A

Right heart valve stenosis

378
Q

Features of a 2 level well score? And what does this mean?

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) 1

Clinical probability simplified scores
PE likely - more than 4 points
PE unlikely - 4 points or less

379
Q

Mechanism of heparin?

A

Activates anti-thrombin 3

380
Q

Most common cause of infective endocarditis?

A

Staphylococcus aureus
now the most common cause of infective endocarditis
particularly common in acute presentation and IVDUs

381
Q

Endocarditis related to dental issues?

A

Strep viridans

382
Q

Strep viridans is the name of a group, rather than the organisms. what two notable cause dental plaque endocaridits?

A

Streptococcus mitis and Streptococcus sanguinis

383
Q

Most common endocarditis post valve surgery, or from line insertions ?

A

coagulase-negative Staphylococci such as Staphylococcus epidermidis

After two months post - bugs return to normal. ie. staph aureus most likely organism

384
Q

Endocariditis most commonly associated colon malignancy?

A

Strep bovis
- strep gallactoganis is a type of Boris

385
Q

Culture negative endocarditis?

A

prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

386
Q

What drug can increase calcium by decreasing calcium secretion by the kidney?

A

Thiazide diuretics can cause hyponatraemia, metabolic alkalosis, hypokalaemia and hypocalciuria

This doesn’t improve bones

387
Q

What should target INR be if recurrent DVT
‘s?

A

3.5

388
Q

Congenital causes of VT?

A

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)

389
Q

Drug causes of VT?

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron

390
Q

If high risk of cardio version failure, while anticoagulating what should also be offered?

A

Amiodarone

391
Q

Rate control should be offered to people, except?

A

whose atrial fibrillation has a reversible cause
who have heart failure thought to be primarily caused by atrial fibrillation
with new‑onset atrial fibrillation (< 48 hours)
with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
for whom a rhythm‑control strategy would be more suitable based on clinical judgement

392
Q

Agents used to control rate in AF?

A

Beta blockers
CCB
Digoxin
- not considered first-line anymore as they are less effective at controlling the heart rate during exercise
- should only be considered if he person does no or very little physical exercise or other rate‑limiting drug options are ruled out because of comorbidities
- may have a role if there is coexistent heart failure

393
Q

Agents used for rhythm control in AF?

A

beta-blockers
dronedarone: second-line in patients following cardioversion
amiodarone: particularly if coexisting heart failure

394
Q

Success rate of cardio version?

A

around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who’ve had a single procedure remain in sinus rhythm. Of patients who’ve undergone multiple procedures around 80% are in sinus rhythm

395
Q

Features of takayasu arteritis?

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%)

396
Q

What vessels are affected in takayasu arteritis?

A

large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse

397
Q

Imaging seen on takayasu arteritis?

A

vascular imaging of the arterial tree is required to make a diagnosis of Takayasu’s arteritis
either magnetic resonance angiography (MRA) or CT angiography (CTA)

398
Q

What factors may falsely elevated BNP?

A

Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis

399
Q

What factors may reduced BNP levels?

A

Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists

400
Q

Statin adverse effects?

A

myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase.

401
Q

Risk factors for rhabdomyolysis from statin?

A

female sex, low body mass index and presence of multisystem disease such as diabetes mellitus
Advanced age

402
Q

What statins are more likely to give myalgia?

A

Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

403
Q

xProphylaxis in supraventricualr tachycardia?

A

Beta blocker

404
Q

Eruptive xanthomata is associated with?

A

Familial hypertriglyceridaemia

405
Q

What does a bicuspid aortic valve develop into?

A

Aortic regurgitation or stenosis

406
Q

Associations of aortic stenosis?

A

associated with a left dominant coronary circulation (the posterior descending artery arises from the circumflex instead of the right coronary artery) and Turner’s syndrome
around 5% of patients also have coarctation of the aorta

407
Q

Erythromycin prolongs QT by affecting what channel?

A

Potassium channels

408
Q

why is a prolonged loading regimen needed in amiodarone?

A

Amiodarone has a long half-life - it is highly lipophilic and widely absorbed by tissue, which reduces its bioavailability in serum. Therefore, a prolonged loading regime is required to achieve stable therapeutic levels

409
Q

What is the best test for a stable patient with chest pain

A

Contrast-enhanced CT coronary angiogram is the first line investigation for stable chest pain of suspected coronary artery disease aetiology

Do not use stress ECG

410
Q

Loud S2?

A

Hypertension
- pulmonary or systemic

411
Q

Soft S2?

A

Aortic stenosis

412
Q

Fixed split S2?

A

ASD

413
Q

Reversed split S2?

A

Pulmonary valve closes before aortic
Severe aortic stenosis
LBBB

414
Q

SVT + asthmatic?

A

Verapamil

415
Q

Dentistry+ warfarin?

A

check INR 72 hours before procedure, proceed if INR < 4.0

416
Q

Patent ductus arterioles features?

A

left subclavicular thrill
continuous ‘machinery’ murmur
large volume, bounding, collapsing pulse
wide pulse pressure
heaving apex beat

417
Q

Complications of VSD?

A

aortic regurgitation
Eisenmenger’s complex
Eisenmenger’s complex is an indication for a heart-lung transplant
right heart failure
pulmonary hypertension
pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortality

418
Q

How do you determine if a patient will benefit from CRT?

A

ECG - broad complex
Echo - <35% ejection fraction

419
Q

What LV function bans you from driving lorries?

A

< 40%

420
Q

In thrombolysis treatment of STEMI:

A

After 90 minutes assess if greater than 50% resolution
If not rescue PCI > thrombolysis

421
Q

Indications for surgery in 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

422
Q

What drug may cause ulceration in the GI tract?

A

Nicorandil

423
Q

Left ventricle aneurysm features?

A

Persistent ST elevation following recent MI, no chest pain - left ventricular aneurysm

424
Q

What should be monitored while giving magnesium IV in treatment of pre-eclampsia’?

A

urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment

425
Q

Mechanism of thiazide diuretics?

A

Thiazides/thiazide-like drugs (e.g. indapamide) - inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

426
Q

What should be monitored in endocarditis/?

A

PR interval - aortic root abscess

427
Q

What cardiovascular disease should mean pregnancy is contraindicated?

A

Pulmonary hypertension

428
Q

What causes transpoition of the great vessels?

A

Transposition of great vessels is due to the failure of the aorticopulmonary septum to spiral

429
Q

Causes of tornado dev point?

A

congenital
Jervell-Lange-Nielsen syndrome
Romano-Ward syndrome
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage

430
Q

Thiazide side effects?

A

Common adverse effects
dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence

Rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis

431
Q

What is the most common mutation in HOCM?

A

gene encoding β-myosin heavy chain protein or myosin-binding protein C

432
Q

When should statins be stopped if causing transaminitis

A

3 X the upper limits of normal

433
Q

Can warfarin be used breat feeding?

A

Yes

434
Q

Amiodarone side effects?

A

You should check if there is hypokalaemia before starting
Coexistent hypokalaemia significantly increases this risk.

thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
‘slate-grey’ appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval

435
Q

ECG changes in pericarditis

A

ECG changes
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis

436
Q

What test should be done for pericarditis patients?

A

Echocardiogram

437
Q

How is bleeding reversed on dabigitran?

A

idarucizumab

438
Q

If an ICD is inserted prophylactically, driving?

A

1 month

439
Q

Mechanism of sacubitril?

A

Prevents degradation of patriotic peptides BNP and ANP

440
Q

What is paradoxical embolus?

A

For a right-sided thrombus (e.g. DVT) to cause a left-sided embolism (e.g. stroke) it must obviously pass from the right-to-left side of the heart

cardiac lesions may cause such events
patent foramen ovale - present in around 20% of the population
atrial septal defect - a much less common cause

441
Q

How should PFO be investigated?

A

Transoesphageal echo

442
Q

What should be avoided in right ventricle myocardial infarction?

A

Nitrates should be avoided in the likely diagnosis of right ventricular myocardial infarct due to causing reduced preload

443
Q

Mechanism of fondaparinux?

A

Antithrombin 3 activation

444
Q

What conditions may form eisenmengers?

A

Associated with
ventricular septal defect
atrial septal defect
patent ductus arteriosus

445
Q

Assoications of Wolffe Parkinson white?

A

HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD

446
Q

Drugs to avoid in WPW?

A

Verapamil and digoxin should be avoided in patients with Wolff-Parkinson White as they may precipitate VT or VF

447
Q

What hsitological findings are found in rheumatic fever?

A

Aschoff bodies

448
Q

Management for uraemia pericarditis ?

A

Haemodialysis

449
Q

When should you anticoagulant a paroxysmal AF?

A

Anticoagulant for life after second episode

450
Q

Mechanism of simvastatin?

A

Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis
Decreases intrinsic hepatic cholesterol synthesis

451
Q

Side effects of ivabradine?

A

Ivabradine use may be associated with visual disturbances including phosphenes and green luminescence

visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block

452
Q

Function of troponin in cardiac muscle?

A

COmponent of thin filaments

453
Q

Antithrombotic therapy in different valves?

A

Prosthetic heart valves - antithrombotic therapy:
bioprosthetic: aspirin
mechanical: warfarin + aspirin

454
Q

Why do thiazides cause hypokalaemia?

A

Thiazides/thiazide-like drugs (e.g. indapamide) - inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

455
Q

Why electrolyte disturbance can a bisphosphonate infusion lead to?

A

Hypocalcaemia

456
Q

In aortic dissecrtion what can be seen on CXR?

A

Widened mediastinum

457
Q

Main symptom of pulmonary hypertension?

A

Exertional dyspnoea

458
Q

Organism that causes leading cause of mortality in endocarditis?

A

Staph

459
Q

What rhythms develop from an inferior MI?

A

Atrioventricular block

460
Q

Management of aortic dissection?

A

type A - ascending aorta - control BP (IV labetalol) + surgery
type B - descending aorta - control BP(IV labetalol)

461
Q

What type of shunt is there in tetralogy of fallout?

A

Right to left shunt

462
Q

What is prinzmetal angina? Treatment?

A

From the SIGN guidelines: Prinzmetal (vasospastic) angina is a rare form of angina in which pain is experienced at rest rather than during activity. It is caused by narrowing or occlusion of proximal coronary arteries due to spasm and cannot be diagnosed by coronary angiography. Beta blockers should not be used in
this form of angina because they may worsen the coronary spasm. Patients with this condition may be treated effectively with a dihydropyridine derivative CCB such as amlodipine.

463
Q

Criteria for surgery for aortic stenosis

A

Gradient >40mmHg
Symptoms

464
Q

STEMI + diabetes. Management?

A

Intravenous insulin

465
Q

Careful in hypertension questions, if give ejection fraction consider treatment for heart failure

A

See above

MRCP: Cardiology (2 decks)

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