Cardiology Flashcards

1
Q

What is the definition of orthostatic hypotension?

A

Orthostatic hypotension can be diagnosed when there is a drop in SBP of at least 20 mmHg or a drop in DBP of at least 10 mmHg after 3 minutes of standing.

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2
Q

What scroing system is used in assessment of suspected obstructive sleep apnoea?

A

Epworth Sleepiness Scale

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3
Q

What scoring system is uses to determine whether and AF patient needs anticoagulation=

A

The CHA2DS2-VASc

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4
Q

What is the most common cause of aortic stenosis in:

a) patients <65 years old
b) >65 years old

A

Patients <65 years old: Bicuspid aortic valve

Patients >65 years old: calcification

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5
Q

What ECG changes migh you expect in a hypothermic patient provided their electorlytes are all normal?

A
  • Bradycardia
  • J-wave (small hump at end of QRS complex see image)
  • First degree heart block
  • Long QT interval
  • Atrial and ventricular arrhythmias
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6
Q

Describe the murmur you would expect to hear with mitral regurgitation.

A
  • Pansystolic murmur
  • The murmur is best heard at apex (5ht ICS mid-clavicular line).
  • It radiates to the axilla.
  • Soft S1 due to incomplete closure of mitral valve
  • Severe MR: Widely split S2 as pressure in pulmonary circulation is high
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7
Q

List the causes of mitral regurgitation

A
  • Post MI: papillary muscle rupture/chordae tendiniae rupture
  • Mitral valve prolapse: Occurs when the leaflets of the mitral valve are slightly deformed.
  • Infective endocarditis: the infective vegitations prevent the valve form closing properly
  • Rheumatic fever
  • Congenital. E.g. Collagen Disorders are predisposed to mitral regurgitation
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8
Q

Name the symptoms a patient with mitral regurgitation might complain of.

A
  • Often asymptomatic
  • Symptoms of heart failure
  • Arrhythmias
  • Breathlessness/cough
  • Fatigue
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9
Q

What do the heartsounds S3 and S4 indicate?

A

S3: Commonly heard in heart failure. Indicates rapid ventiruclar filling, usually associated with volume overload as part of congestive cardiac failure.

S4: less commonly heard in heart failure. Thought to be due to contraction of the atria against a stiff ventricle.

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10
Q

What is the target blood pressure in DM?

A

If end organ damage (e.g. renal disease, retinopathy): < 130/80

Otherwise: < 140/80

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11
Q

What is the first line investigation for stable chest pain (i.e. on exertion exclusively) of suspected coronary artery aetilogy?

A

CT coronary angiography.

Then, do non-invasive cardiac imaging (look for reversible myocardial ischaemia) and after this, invasive coronary angiography.

(Examples of non-invasive functional cardiac imaging: Myocardial perfusions scintigraphy with single photon emission CT, MPS with SPECT; Stress echo; Contrast cardiac MRI)

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12
Q

What is the name given to abnormally large drop in BP during inspiration?

In what condition might you see this?

A

This is called puslus paradoxus. (a drop in BP > 10 mmHg with inspiration). Mechanism: there is normal increased venous return to the righ heart during inspiration. As the right ventricle cannot dilate in constrictive pericarditis or cardiac tamponade, the pressure is exerted onto the septum, so the left ventricle fills less and decrease in stroke volume, therefore lower BP during inspiration.

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13
Q

What is Kussmaul’s Sign?

In what condition might you see this?

A

Kussmaul’s Sign is the abnormal rise in JVP with inspiration. This typcially occurs in constrictive pericarditis, and very rarely in Cardiac Tamponade.

Mechanism of Kussmaul’s Sign: usually, during inspiration, the intrathoracic pressure decreases. The decrease in right atrial pressure, as well as the increased abdominal pressure, leads to increased venous return. A normal heart accommodates by increasing filling of the right ventricle and increasing heart rate. In constrictive pericarditis, the hear cannot dilate and therefore the increased venous pressure backs up to the JVP.

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14
Q

Describe the diagnostic pathway for hypertension.

A
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15
Q

Describe the management of primary hypertension in primary care.

A

Conservative: lifestyle advie (low sodium diet aiming for < 6g btu ideally <3g/day. Reduce caffeine intake. Smoking cessation, exercise, diet etc.)

Medical: see flowchart

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16
Q

If a patient with warfarin and on target INR for AF (2-3) suffers from a haemorrhagic stroke, what do you do with regards to the warfarin?

A

In any patient on warfarin with INR 2-3 that suffers from major bleed (such as intracranial haemorrhage):

Stop the warfarin, give 5mg of Vit K IV and give prothrombin complex concentrate IV. (if PCC nto available, give FFP).

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17
Q

What is the treatment protocol for a patient on warfarin that suffers from a major bleed?

A

In any patient on warfarin with INR 2-3 that suffers from major bleed (such as intracranial haemorrhage or GI haemorrhage):

Stop the warfarin, give 5mgof Vit K IV and give prothrombin complex concentrate IV. (if PCC nto available, give FFP).

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18
Q

What is the treatment protocol for a patient on warfarin that has an INR of >8.0 and suffers from a minor bleed?

A

If INR >8.0 and minor bleed:

  • Stop warfarin
  • 1-3 mg IV Vitamin K
  • Repeat INR after 24 hours; if still high -> repeat vitamin K
  • Restart warfarin when INR < 5.0
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19
Q

What is the treatment protocol for a patient on warfarin that has an INR of >8.0 with no bleed?

A

If INR >8.0 and no bleed:

  • Stop warfarin
  • 1-5 g Vitamin K PO
  • Repeat INR after 24 hours; if still high -> repeat vitamin K
  • Restart warfarin when INR < 5.0
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20
Q

What is the treatment protocol for a patient on warfarin that has an INR of 5.0-8.0 with minor bleeding?

A

When INR 5.0-8.0 and minot bleeding:

  • Stop warfarin
  • 1-3mg Vitamin K IV
  • Restart warfarin when INR < 5.0
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21
Q

What is the treatment protocol for a patient on warfarin that has an INR of 5.0-8.0 with no bleed?

A

If INR 5.0-8.0 with no bleed:

  • Withold 1-2 doses of warfarin
  • Re-titrate maintenance dose subsequently (likely needs to be reduced)
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22
Q

What are the side effects of ACE-inhibitors?

A
  • Cough (15% of patients, due to increased bradykinin levles)
  • Angioedema: after up to a year of starting treatment
  • Hyperkalaemia (if ≥6mmol/L should cessate ACEi in patient with CKD)
  • First-dose hypotension (more common if also taking diuretics)
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23
Q

What are causes of RBBB?

A
  • Normal variant - more common with increasing age
  • Right ventricular hypertrophy
  • Myocardial infarction - new onset RBBb should be concerning
  • Atrial septal defect
  • Pulmonary embolism
  • Cardiomyopathy/myocarditis
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24
Q

What are the features of RBBB on ECG?

A

Broad QRS (>120 ms)

rSR pattern in V1-3 (“M” shaped QRS)

Wide, slurred S wave in latearl leads (aVL, V5-6; “W” shaped)

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25
Q

Describe the drug management of stable angina.

A
  • All patients should receive 75mg Aspirin daily and a statin (unless contraindicated)
  • Sublingual GTN spray PRN
  • Offer beta-blocker OR calcium-channel-blocker (based on patients preference/co-morbidities/contraindications)
    • If CCB used as monotherapy: use rate-limiting, e.g. diltiazem ro verapamil
    • If CCB used together with beta-blockers: use long-acting dihydropyridine CCB, e.g. nifedipine
    • NEVER use verapamil together with beta-blockers due to risk of complete heart block
  • If patient still symptomatic after monotherapy, add the other one
  • If this is not tolerated, keep the original drug and add:
    • A nitrate (e.g. modified release isoborbide mononitrate)
    • Ivabradine (funny channel inhibitor)
    • Nicorandil
    • Ranolazine
  • If a patient is taking beta-blockers + CCB only add a third drug if awating assessment for PCI/CABG
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26
Q

In which rheumatic condition would you not give thiazide diuretics, and why?

A

Thiazide diuretics are contraindicated in gout as they increase absorption of uric acid.

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27
Q

Explain which ECG leads are affected in the different MI locations

A
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28
Q

What are the side effect of statins?

A

Myopathy: rare and overdiagnosed. Myalgia, myositis and rhabdomyolysis. Raised CK.

Liver impariment: check LFTs baseline, 3 and 12 months after starting treatment. Discontinue if raise to 3x ULN

Small evidence that statins raise risk of intracerebral haemorrhage in those that previously had a stroke. (not if used as primary prevention)

Contraindications:

  • Macrolide ABx: stop statins until course of ABx completed
  • Pregnancy (teratogenicity and cholesterol synthesis of newborn disturbed)
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29
Q

What is Wellen’s Syndrome?

A

Wellen’s syndrome is a critical occlusion of the LAD coronary artery.

On ECG:

Deep T wave inversion or biphasic T waves in V2-V3 is highly specific for critical stenosis of LAD. This is indicative of Wellen syndrome.

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30
Q

What is a pulsus alternans, and what is this indicative of?

A

Pulsus alternans is when the upstroke of the pulse alternatives between strong and weak.

It indicates systolic dysfunction and is seen in patients with heart failure.

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31
Q

What are the adverse effect of warfarin?

A
  • Main side effect is haemorrhage (titrate to INR)
  • Teratogenicity (but safe in breastfeeding)
  • Skin necrosis: due to the inital pro-coagulant effect of warfarin (protein C is reduced), there can be thrombosis in the venules leading to skin necrosis
  • Purple toes (same mechanism as above)
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32
Q

What are the ECG features of hypokalaemia?

A
  • U-waves (see image)
  • Small or absent T-waves (occasinally inverted)
  • prolonged PR interval
  • ST depressopm
  • Long QT

“In Hypokalaemia U have no Pot and no T, but a long PR and a long QT”

(no Pot = no POTassium)

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33
Q

What are the ECG changes that would indicate thrombolysis or PCI?

A
  • ST elevation of >2mm (2 small sqaures) in 2 or more consecutive anterior leads (V1-V6) OR
  • ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR
  • New LBBB
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34
Q

What does a rased BNP indicate?

A

BNP is a hormone mainly produced by the left ventricular myocardium in response to strain, i.e. heart failure, myocardial ischaemia and valvular disease (former most common).

Raised levels may also be seen in chornic kidney disease.

Factors which reduce BNP:

  • ACEis
  • ARBs
  • Diuretics
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35
Q

List some poor prognostic factors acute coronary syndrome.

A
  • Age >65
  • Development (or history) of heart failure and cardiogenic shock
  • Peripheral vascular disease
  • Reduced systolic blood pressure
  • Initial raised serum creatinine
  • Elevated initial cardiac markers
  • Cardiac arrest on admission
  • ST segment deviation
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36
Q

What is the main investigation of choice in a patient with suspected PE?

A

CTPA is the recommended initial lung-imaging modality in a non-massive PE. (easier to perform and quicker than V/Q scans).

V/Q scan is used if there is renal impairment (as no contrast is used).

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37
Q

What are the ECG changes seen with a PE?

A
  • S1Q3T3: S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III
  • RBBB and right axis deviation
  • Sinus tachycardia - probably the most common finding
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38
Q

What are the ECG changes seen with pericarditis?

A
  • Global/widespread saddle-shaped ST-elevation and PR depression (most specific ECG marker for pericarditis)
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39
Q

What are the causes of pericarditis?

A
  • Infectious:
    • Viral (coxsackie, influenza, HIV, EBV)
    • Bacterial (e.g. TB)
  • Inflammatory:
    • Post-MI
    • Dressler’s syndrome
  • Metabolic:
    • Uaraemia
    • Hypothyroidism
  • Neoplastic
  • Trauma
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40
Q

What are the clinical features of pericarditis?

A
  • Chest pain (often “pleuritic” - i.e. worse on inspiration and relieved by sitting forward)
  • Non-productive cough, dyspnoea, flu-like
  • Pericardial friction rub on ausculation
  • Tachpnoea
  • Tachycardia
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41
Q

Summarise the management of long QT syndrome.

A

Long QT is defined as a QT interval of >430 ms in males and >450 ms in females. It represents delayed ventricular repolarisation and is associated with sudden collapse and sudden death.

Management summmary:

  • Avoid precipitants (certain drugs/medications and strenuous exercise)
  • Beta blockers
  • In high risk cases (e.g. >500 ms or previous cardiac arrest): Implantable cardioverter defibrillator
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42
Q

What is a better pnemonic for CHA2DS2-VASc score?

A

SAD CHAVS - the first 2 (Stroke and age >75) give you 2 points - all others 1.

Stroke

Age >75

Diabetes

Congestive heart failure

HTN (or on HTN treatment)

Age 65-74

Vascular disease (prior MI, PAD)

Sex female

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43
Q

What ECG change would you expect in a patient with hypothermia?

A
  • J-waves (see image)
  • Bradycardia
  • First degree heart block
  • Long QT interval
  • Atrial and ventricular arrhythmias
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44
Q

What class of ABx is associated with QT prolongation?

A

The macrolides (erythromycin, clarithromycin, azithromycin) as well as ciprofloxacin.

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45
Q

What are the DVLA rules for returning to driving after percutaneous coronary intervention?

A

For private vehicles, patients do not need to notify the DVLA following PCI and may resume driving 4 weeks after (providing there is no other disqualifying condition).

Bus or lorry drivers must notify the DVLA and may not drive for 6 weeks. After 6 weeks, the DVLA wil reassess to determine whehter it is safe to reinstate the license for Bus/lorry.

46
Q

How do you manage Torsade de pointes in a patient that isn’t in shock?

A

Torsade de pointes is managed with IV Magnesium sulphate 2g IV over 10 minutes. Also stop all drugs that cause a long QT syndrome.

If the patient is shocked, this is treated as VT (TdP is a polymorphic VT) of the ALS algorithm, and therefore synchronised DC shocks should be given.

47
Q

How to you treat symptomatic bradycardia?

A

IV atropine 500 mcg IV. Given 6 times, before moving to external pacing.

After this, isoprenaline/adrenaline infusion titrated to response may be trialled.

48
Q

What medications should a patient be on for 2° prevention following an MI?

A

All patients should be offered the following drugs after and MI:

  • Dual anti-platelet therapy: Aspirin + ticagrelor (or clopidogrel) (aspirin life-long, second agent for 12 months)
  • Statin (usually atorvastatin 80mg)
  • Beta-blocker
  • ACE inhibitor
  • If Clinical heart failure: add aldosterone antagonist
49
Q

What is the normal left ventricular ejection fraction?

A

It is 55-70%.

50
Q

Summarise the New York Heart Association classification of heart failure.

A

I -No limitations on ordinary physical activity

II - Normal at reast. Ordinary physical actuvity causes breathlessness

III - Normal at reast. Less-than-ordinary activity causes breathlessness

IV - Symptoms at rest

51
Q

Summarise the doses of adrenaline, hydrocortisone and chlorpheniramine during anaphylaxis for children of different ages.

A
52
Q

How long after an anaphylactic reaction should patients be observed for, and why?

A

There is a risk of rebound anaphylaxis, or biphasic reaction. This occurs in up to 20% of patients.

For this reason, patients are observed for 6-12 hours from onset of symptoms.

53
Q

What is the mechanism of action of adenosine?

A

Adenosine causes transient hear block in the AV node. It does so by agonising the A1 receptor in the AV node, which inhibits adenylyl cyclase, thus reducing cAMP and causing hyperpolarisation by increasing outward K+ flux.

It has a very short half life of 8-10 seconds.

54
Q

What is the indication for adenosine, and how should it be administered?

A

Adenosine is used to terminate supraventricular tachycardias.

If should be given via a large bore cannula due to the short half-life. Start with 6mg, then 12mg, then another 12mg.

It shouldn’t be given to asthmatics (risk of bronchospasm). Use verapamil instead

55
Q

What is the mode of inheritance of HOCM?

A

Autosomal dominant mutation, most commonly of the beta-myosin heavy chain.

56
Q

What is the effect of thaizide diuretics and loop diretics (e.g. furosemide) on blood clacium levels?

A

Thiazide diruetics decrease urinary excretion of calcium, and therefore increase plasma levels.

Loop diuretics do the opposite: they increase urinary calcium excretion, and therefore lower plasma levels.

57
Q

What artery supplies the AV node, and why is this fact important?

A

The AV node is supplied by the posterior interventricular artery, which in the majority of patients is a branch of the right coronary artery. In the remainder of patients the posterior interventricular artery is supplied by the left circumflex artery.

Ther fore, an MI in the RCA can lead to complete heart block.

58
Q

Why might patients with diabetes suffer from postural hypotension?

A

Diabetes can lead to autonomic dysfunction, which includes a dysfunction in the sympathetic nervous system which would increase BP on standing.

59
Q

What are the features of diabetic autonomic dysfunction?

A

Orthostatic hypotension

Erectile dysfunction

60
Q

What is Takotsubo Cardiomyioathy?

A

Takotsubo cardiomyopathy is a type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium. It may be triggered by stress.

Features

  • chest pain
  • features of heart failure
  • ST elevation
  • normal coronary angiogram

Treatment is supportive.

61
Q

What is Boerhaave syndrome?

A
  • Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.
  • The rupture is usually distally sited and on the left side.
  • Patients usually give a history of sudden onset of severe chest pain that may complicate severe vomiting.
  • Severe sepsis occurs secondary to mediastinitis.
  • Diagnosis is CT contrast swallow.
  • Treatment is with thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin.
  • Delays beyond 24 hours are associated with a very high mortality rate.
62
Q

What are the side effets of GTN spray?

A
  • Headache
  • Tachycardia (reflex due to vasodilation)
  • Hypotension (vasodilatory effect)
63
Q

If pharmacological cardioversion for AF is required, what are the agents of choice?

A

If no underlying structural or ischaemic heart disease: flecainide or amiodarone.

If underlying heart disease: amiodarone.

64
Q

What bloodtests should be done when starting someone on a statin?

A

LFTs at baseline, 3 months and 12 months.

A fasting lipid profile may also be checked during monitoring to assess response to treatment.

65
Q

Which electrolyte disturbances are associated with a long QT syndrome?

A
  • Hypokalaemia
  • Hypomagnesaemia
  • Hypocalcaemia
66
Q

When should patients take statins?

A

Last thing in the evenings

67
Q

What baseline investigations should you do before starting a patietn on amiodarone?

A

Befors starting:

  • TFTs (thyroid dysfunction, bothy hypo and hyper)
  • LFTs (risk of liver fibrosis/hepatitis)
  • U&Es (to detect hyperkalaemia)
  • CXR (risk of pulmonary fibrosis/pneumonitis)
68
Q

What are the adverse effects of amiodarone?

A
  • Thyroid dysfunction
  • Pulmonary fibrosis/pneumonitis
  • Liver fibrosis/hepatitis
  • Peripheral neuropathy, myopathy
  • Photosensitivity
  • Slate-grey skin appearance
  • Bradycardia
  • Legthens QT interval
69
Q

What is the name of the prognostic scoring system used for risk-stratifying patients with suspected TIA?

Whad does it entail?

A

ABCD2. Indicates risk of stroke in the near future. (No longer recommended by NICE)

  • Age: 1 point for >60
  • BP: 1 point for ≥140/90
  • Clinical features of TIA: unilateral weakness 2 points, speech disturbance 1 point
  • Duration of symptoms: 10-59 min: 1 point. ≥60 min 2 points
  • Diabets: 1 point if yes

Low risk: 0-3

Moderate risk: 4-5

High risk: 6-7

70
Q

Summarise the management of orthostatic hypotension.

A

Conservative:

  • Education and lifestyle measures (adequate hydration and salt intake)
  • Discontinuation of vasoactive drugs (e.g. nitrates, antihypertensives)
  • Compression stockings
  • Head-up tilt sleeping

Medical:

  • Fludrocortisone
  • Midodrine
71
Q

What are potential causes of torsade de pointes?

A

Torsade de points is a form of polymorphic VT associated with long QR. Causes for long QT include:

  • Congenital
  • Drugs:
    • Antiarryhtmetics (amiodarone, sotalol)
    • TCAs, antipsychotics
    • Chloroquine
    • Erythromycine
  • Metabolic:
    • Hypocalcaemia, hypokalaemia, hypomagnesaemia
    • Hypothermia
  • Inflammation: myocarditis
  • Subarachnoid haemorrhage
72
Q

How often can IM adrenaline be repeated during anaphylaxis?

A

Adrenaline can be repeated every 5 minutes if necessary.

73
Q

What are the modified Duke criteria?

A

Duke criteria: infective endocarditis diagnosed if:

  • Pathological criteria +ve
  • 2 major criteria
  • 1 major and 3 minor
  • 5 minor

Major criteria:

  • Blood cultures:
    • 2 +ve blood cultures showing typical organisms (S. viridans, HACEK)
    • Persistent bacteraemia from cultures taken ≥12 horus apart, or ≥3 cultures with less specific organism (S. aureus, S. epidermidis)
    • +ve serology for Coxiella burnetii, Bartonella, Chlamydia psitacci
    • Positive molecular assays for specific gene targets
  • Endocardial involvement
  • +ve echocardiogram
  • New valvular regurgitation

Minor criteria:

  • Predisposing heart condition
  • Microbiological evidence that doesn’t meet major criteria
  • Fever >38°
  • Vascular phenomena (emboli, splenomegaly, splinter haemorrhages, Janeway lesions)
  • Immunological phenomena (glomerulonephritis, Osler’s nodes, Roth spots)
74
Q

What are the ECG features of hypercalcaemia?

A

Shortened QT interval.

75
Q

What do you do if the INR of a patient on warfarin falls below 2?

(and they require anti-coagulation e.g. due to AF)

A

As the INR is <2, the requre immediate anti-coagulation with LMWH.

Warfarin dose should be increased and INR monitored. LMWH discontinued when INR adequate.

76
Q

How soon after an ischeamic stroke + AF should a patient be started on anticaigulation therapy?

A

14 days after, due to the risk of haemorrhagic transformation if the anticoagulation is started earlier.

77
Q

What valvular abnormality is associated with polycystic kidney disease?

A

PCKD patients have incrased occurrence of cardiac valve abnormalities.

Mitral valve prolapse and mitral regurgitation are the most common. (1 in 4 affected)

78
Q

Which drugs have shown to improve mortality in patients with chronic heart failure?

A
  • ACE inhibitors
  • Spironolactone
  • Beta-blockers
  • Hydralazine with nitrates (hydralazine is a smooth-muscle relaxant, thereby relaxing vasculature)

(ACEi and beta-blockers have no effect on mortality on heart failure with oreserved ejection fraction)

79
Q

Summarise the treatment for chronic heart failure?

A

First-line:

  • ACE inhibitors
  • plus Beta-blockers (start one at a time)

Second-line:

  • Aldosterone Antagonist
  • OR Angiotensin II RB (don’t give ACEi + ARB together)
  • OR hydralazine plus nitrate

If symptoms persist:

  • Cardiac resynchronisation therapy
  • Digoxin
  • Ivabradine
  • Sucubitril valsartan (if still symptomatic on ACEi or ARBs)
    • Initiate following washout period of ACEi/ARBs

(note: this is the management for patients with reduced EF. For CHF patients with preserved EF, conservative management is recommended by NICE.)

80
Q

Differentiate between the half-life of troponin and CK-MB in the diagnosis of MI.

A

Troponin (T + I) are the most commonly used cardiac markers in today’s clinical practice; Trop T rises after 4-6 hours, peaks at 12. Because it returns to normal in 10 days, it isn’t useful to detect reinfacrction.

CK-MB begins to rise after 2-6 hours, peaks at 16-20 hours. It falls to normal after 2-3 days. This makes it useful to detect reinfarction in the 4-10 days after the infarct.

Myoglobin rises first (1-2 hours) but is not used in clinical pratice.

AST is non-specific and shouldn’t be used.

81
Q

What is the first-line investigation in suspected infective endocarditis?

A

Transthoracic echocardiography is the first-line Ix.

If this is negative, then perform a trans-oesophageal echo.

82
Q

Which arteries (and therfore which ECG leads) are likely to be affected in an MI that presents with arrythmias?

A

Right coronary artery (II, III, aVF) supplies the AV node, and ischaemia in this are can therefore lead to arrhythmias.

83
Q

Summarise the managment of an NSTEMI.

A

All patients should be given:

  • Aspirin 300 mg
  • Nitrates ± morphine to relieve chest pain
  • 2nd anti-platelet agent: ticagrelor or prasugrel (continue for 12 months, but take into account bleeding risk)
  • Antithrombin:
    • angiography planned within 24 hours: >264µmol of unfractionated heparin
    • angiograpy not planned within 24 hours: fondaparinux

Then assess GRACE score (6 month mortality after ACS).

Low (< 3%): conservative management. Assess for ischaemia before discharge.

High (> 3%):

  • Schedule for coronary angiography within 96 hours of hospital admission. (asap for unstable patients)
  • IV Gp IIb/IIIa receptor antagonists (eptafibatide or tirpfiban) if angiography planned.
84
Q

Summarise the MoA of drugs commonly used in the management of acute coronary snydrome.

A
85
Q

Summarise the post-stroke management in patients with AF.

A

In acute stroke patients:

  • In the absence of haemorrhage, anticoagulation therapy should be started 2 weeks after the stroke.
    • Warfarin or DOAC
  • Aspirin should be given at 300 mg OD for 2 weeks
86
Q

What is the first line investigation for PE? Name advantages of this method.

A

CTPA is first-line investigation for PE. Reasons for its superiority are:

  • Easier to perform, esp. out of hours
  • Reduced need for further imaging
  • Possibility of providing alternative diagnosis

V/Q scanning may be used initially if the appropriate facilities exist, the CXR is normal and there is no significant symptomatic concurrent cardiopulmonary disease.

V/Q scanning is also first-line in regally impaired patients as it doesn’t require contrast.

87
Q

Summarise the most common organisms implicated in infective endocarditis and in what patients they most commonly occur.

A

Streptococcus viridans:

  • Linked to poor dental hygiene/following a dental procedure

Streptococcus bovis:

  • Most commonly linked with colorectal cancer

Coxiella burnetii:

  • Causes Q fever, an infection caught most commonly from farm animals

Staphylococcus epidermidis:

  • Most commonly in those having undergone prosthetic valve surgery

Staphylococcus aureus

  • Most common cause of infective endocarditis
  • Esp. Common in IVDU
88
Q

What is the mode of inheritance for HOCM?

A

HOCM has an autosomal dominant inheritance pattern.

89
Q

What does this ECG of a 23 year old male show?

What is the likely underlying diagnosis?

A

This ECG shows LVH and T-wave inversion - both typical features of HOCM.

90
Q

Which beta blockers have evidence to reduce mortality in heart failure?

A

carvedilol, metoprolol, and bisoprolol

91
Q

What is the management of a patient in VT?

A

Haemodynamically stable:

  • IV amiodarone 300 mg IV bolus (followed by 900 mg infusion over 24 hours)
  • Elective DC cardioversion if above unsuccessful

Haemodynamically unstable:

  • Corret underlying causes, if possible
  • Immediate resuscitation
  • Emergency DC cardioversion
92
Q

What drugs are given to an adult patient in presumed anaphylaxis (state doses)?

A

Adrenaline 500 mcg (0.5 mL of 1:1000) IM.

Hydrocortisone 200 mg IV.

Chlorphenamine 10 mg IV.

Flluid bolus.

(Alphabetical order:
- Adrenaline 0.5 mg
- Chlorphenamine 10mg
- Hydrocortisone 200mg
Each dose is 20 times the previous dose.)

93
Q

What are the first-line investigations carried out in a patient with suspected heart failure?

A

All patients with suspected heart failure should have their N-terminal pro-B-type natriuretic peptide (NT-proBNP) measured first-line.

  • If levels are high: refer to specialist (including TTE) within 2 weeks
  • If levels are raised: arrange specialist assessment (incl. TTE) within 6 weeks

Other useful Ix include:

  • ECG
  • Bloods: FBC, U&E, LFT, (TFTs)
  • CXR
  • Spriometry (for DDx of dyspnoea)
94
Q

Summarise the management of Aortic Dissection.

A

Stanford Type A:

  • Immediate surgical repair (either endovascular of open)
  • Until surgery, control BP in 100-120 mmHg range.

Stanford Type B:

  • If uncomplicated: conservative with analgesia and BP control (100-120 mmHg)
  • If complicated: surgery
95
Q

What are the side effects commonly experienced wtih ivabradine?

A
  • Visual effects (particularly luminous phenomena)
  • Headache
  • Bradycardia, hart block
96
Q

What is cor pulmonale?

What are signs of cor pulmonale?

A

Cor pulmonale describes the hypertrophy of the right ventricle and right heart failure that are caused by pulmonary arterial hypertension.

Signs:

  • Raised JVP
  • Ankle oedema
  • Hepatomegaly

Long-standing R sided heart failure can lead to L heart failure as well.

97
Q

How should you manage the diabetes mediaction of a T2DM patient following an MI?

A

There are clear benefits of tight glucose control after an MI.

Type 2 diabetics are converted to IV insulin in the period immediately following an MI. Should aim for < 11.0 mmol/l.

98
Q

What blood test should be monitored with statins?

A

LFTs should be monitored.

Treatment with statins should be discontinued if serum transaminase concentrations rise to and persis at 3 times the upper limit of the reference range.

99
Q

What is Beck’s triad?

A

Beck’s triad:

  • Falling BP
  • Rising JVP
  • Muffled heart sounds

is indicative of cardiac tamponade.

100
Q

What does this ECG show, and what could the underlying diagnosis be?

A

This ECG shows Electrical alternants.

This is seen in cardiac tamponade.

101
Q

How should amiodarone ideally be administered?

A

IV amiodarone should ideally be given into central veins to reduce the risk of injection site reactions.

102
Q

What are the NICE recommendations with regards to rate vs rhythm control in AF?

A

NICE guideline advise:

Offer rate control as the first-line strategy to people with atrial fibrillation, except in people:

  • Whose AF has a reversible cause
  • Coexistant heartfailure
  • First-onset AF
103
Q

What is Buerger’s Disease?

A

Thromboangiitis obliterans is a small and medium vessel vasculitis that is strongly associated with smoking.

Features:

  • Extremity Ischaemia: intermittent claudication, ischaemic ulcers
  • Superficial thrombophlebitis
  • Raynaud’s phenomenon
104
Q

What is carotid sinus hypersensitivity?

A

Carotid sinus hypersensitivity is the hypersensitivity of the carotid plexus as defined by a ventricular pause of >3s or a fall in SBP of more than 50 mmHg.

105
Q

Which anti-diabetic medication is contraindicated in heart failure?

A

Thiazoledinediones such as pioglitazone are contraindicated in heartfailure as they can cause fluid retention.

106
Q

What are the potassium sparing diuretics?

A

Potassium sparing diuretics are the ones that act on the Na/K exchange transporter in the collecting duct. The transporters are increased by aldosterone.

  • Aldosterone antagonists: spironolactone, eplenerone
  • Angiotensin 2 receptor blockers: losartan, candesartan
107
Q

What cardiac abnormality can occur in carcinoid syndrome?

A

Pulmonary stenosis and tricuspid insufficiency.

Carcinoid syndrome is a neuroendocrine tumour. There are many locations that they can occur in such as in the GI tract, in the respiratory tract and many other places. They can secrete serotonin.

The syndrome is associated with right-sided valvular pathology. The most common pathology is tricuspid insufficiency and pulmonary stenosis. The best way to remember is the acronym ‘TIPS’.

108
Q

What is Löffler endocarditis?

A

Löffler endocarditis is a restrictive cardiomyopathy caused by eosinophilic infiltration.

109
Q

What is familial hypercholesteraemia?

When should you diagnose it?

A
  • Autosomal dominant condition
  • High LDL-levels

Diagnosis:

  • Adults total cholesterol >7.5 mmol, LDL >4.9
  • Tendon xanthomata
  • OR 1st/2nd degree relatives
  • OR genetic evidence
110
Q

How is Mitral stenosis linked to haemoptysis?

A

It is thought that secondary to the rupture of the bronchial veins, due to the rise in left atrial pressure, there can be haemoptysis.