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Medicine Y6 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

AF thromboembolic risk: scoring system

A

CHA2DS2-VASc

CCF

HTN

Age <65, 65-74 (1), 75+ (2)

DM

Stroke (2), TIA (1)

Vascular dx

Female

Score: 0=low risk 1=intermediate risk (anticoagulate if male) 2+=high risk (anticoagulate if female)

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2
Q

Anticoagulation major bleeding risk in AF: scoring system

A

HAS-BLED

HTN sBP>160

Abnormal renal function (Cr>200, dialysis, transplant)

Abnormal liver function (LFTs >3x normal, bili>2x)

Age >65

Stroke hx

Bleeding hx

Labile INR (<60% time in normal range)

EToH hx

Drug hx (NSAIDs, antiplatelets)

Score 3+ is high risk and indictes regular r/v if on oral anticoagulation

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3
Q

Infective endocarditis: diagnostic criteria

A

Duke’s Modified Criteria

Pathological: intracardiac or embolized vegetations/abscess on micro/histo

Major:

Blood cultures +ve (2+, 12h apart, typicals)

Endocardial involvement (echo showing abscess, new valve disease, regurg)

minor:

IVDU or predisposing heart disease

Fever >38

Vascular phenomena (Janeway lesions, spetic emboli)

Immunological phenomena (GN, Osler, Roth, RF+ve)

Blood culture +ve (not matching major criteria)

Score:

Definite = 1P, 2M, 1M3m, 5m

Possible = 1M1m, 3m

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4
Q

Identify the possible complications of myocardial infarction

A

Complications of MI: ‘MAP’

Mechanical:

  • Contractile dysfunction –> cardiogenic shock, CCF
  • Papillary muscle damage –> mitral regurgitation (+ or other murmurs)
  • Rupture –> haemopericardium, L-to-R shunt (depending on location of rupture)

Arrhythmias: occur in first 24h, 90% pts, can cause sudden death

Pericardial:

Pericarditis (dusky haemorrhagic tissue). Fibrous pericarditis if infarct in epicardium

Effusion –> cardiac tamponade

Dressler’s syndrome

(Path)

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5
Q

What features allow you to differentiate aortic sclerosis from aortic stenosis on examination?

A

Aortic sclerosis features:

  • No radiation
  • Normal pulse
  • Normal in elderly

(Mirza)

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6
Q

Raised JVP: differentials

A
  • Right sided HF (or CCF)
  • Complete heart block (R atrium contracting agaist closed tricuspid valve)
  • Tricuspid regurgitation
  • Pericardial effusion
  • SVC obstruction
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7
Q

Identify the possible complications of valve replacement

A

FIBAT

Failure (valve, operation)

Infection (IE)

Bleeding (warfarin)

Anaemia (haemolytic from valve, anaemia of chronic disease)

Thromboembolism

(Mirza)

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8
Q

Summarise the indications for valve replacement in aortic stenosis

A

American Heart Association recommendations for valve replacement in aortic stenosis:

  • Strongly indicated when
    • severe high-gradient (50mmHg) AS + sx or +ve exercise test
    • severe AS + LV ejection fraction <50%
    • severe AS undergoing other cardiac surgery
  • May be indicated when
    • severe AS + low surgical risk pt
    • severe AS + low exercise tolerance
    • severe low-gradient AS + sx

There is also a Society of Thoracic Surgeons risk calculator

(UpToDate)

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9
Q

Hypertension: diagnostic criteria

A
  • Stage 1: hypertensionClinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
  • Stage 2 hypertensionClinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
  • Severe hypertensionClinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg

(NICE)

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10
Q

Hypertension: what other investigations are available in pts with ?white coat HTN

A

NICE suggest offering ABPM or HBPM to any patient with a BP >= 140/90 mmHg.

  • Ambulatory blood pressure monitoring (ABPM): at least 2 measurements per hour during the person’s usual waking hours (for example, between 08:00 and 22:00). Use the average value of at least 14 measurements
  • Home blood pressure monitoring (HBPM): offered if ABPM not tolerated. 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.

(Passmedicine, NICE)

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11
Q

Hypertension: what factors indicate antihypertensive therapy in pts with stage 1 hypertension?

A

Age < 80 + any of the following:

  • target organ damage
  • established cardiovascular disease
  • renal disease
  • Q-score >20%

(Antihypertensives indicated in all Stage 2 and Severe HTN pts)

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12
Q

Hypertension: outline the choice of antihypertensive

A
  • Stage 3: NICE recommend clorthalidone or indapamide as D (thiazide-diuretic) of choice
  • (Passmedicine)*
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13
Q

Generate a management plan for angina pectoris (stable)

A
  • Conservative: pt education (can be triggered by exercise, stress, heavy meals, cold), lifestyle advice, safety netting
  • Medical
    • Sx relief - r/v at 2-4w
      • GTN PRN - on pain stop activity, take GTN, if no improvement on 5mins take 2nd dose, if no improvement call 999
      • 1st line: beta-blocker or CCB
      • 2nd line: combine BB + CCB (remember verapamil CI with BBs)
      • 3nd line: if BB or CCB is CI or not tolerated, consider monotherapy of
        • Isosorbide mononitrate
        • Nicorandil
        • Ivabradine or Ranolazine (specialist, Na blocker)
    • Risk modification
      • Antiplatelet: low dose aspirin (or continue clopidogrel if previous CVD / PVD)
      • ACE-inhibitor: if angina + T2DM/HF/CKD/HTN
      • Statin

(NICE)

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14
Q

Reynauld’s phenomenon: mx

A

Medical:

  • 1st line: CCB (nifedipine)
  • 2nd line: IV prsotacyclin (lasts for weeks/months)

(Passmedicine)

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15
Q

Generate a management plan for supraventricular tachycardia

A

Acute management

  • Conservative: vagal manoeuvres: e.g. Valsalva manoeuvre
  • Medical
    • 1st line: intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option
    • 2nd line: electrical DC cardioversion

Prevention

  • Beta-blockers
  • Radiofrequency ablation

(Passmedicine, Resuscitation Council)

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16
Q

Outline the managment of sinus bradycardia

A

(UK Resuscitation Council)

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17
Q

Generate a management plan for NSTEMI or unstable angina

A
  • Immediate:
    • Medical (ABCDE): MONAC
      • Morphine
      • Oxygen: if sats <94%
      • Nitrates
      • Aspirin 300mg
      • Clopidogrel 300mg (if GRACE score >1.5% + no CI). Consider stopping 5d before CABG if low CV risk
        • antithrombin therapy: fondaparinux (if low bleeding risk, no angiography in 24h), unfractionated heparin if due for angiography
        • eptifibatide/tirofiban IV (glycoprotein IIa/IIIb inhib) if GRACE score >3%)
    • Interventional cardiology:
      • Coronary angiography: if GRACE score >3.0% (or recurrent ischaemia, or +ve ischaemia testing), w/i 96h
        • abciximab as adjunct to PCI
        • PCI or CABG if indicated
  • Long-term (if NSTEMI):
    • Conservative: risk factor modification, cardiac rehabilitation
    • Medical: ABDS
      • ACE-inhibitor (once haemodynamically stable)
      • Beta-blocker (once haemodynamically stable –> 12m, or indefinitely if LVF)
      • Dual anitplatelet therapy (aspirin indefinitely + 12m clopidogrel/ticagrelor)
          • gut protection
      • Statin
        • aldosterone antagonist if HF 3-14d post MI

(NICE)

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18
Q

How is aortic dissection classified?

A

Stanford classification

type A - ascending aorta, 2/3 of cases

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

DeBakey classification

type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally

type II - originates in and is confined to the ascending aorta

type III - originates in descending aorta, rarely extends proximally but will extend distally

(Passmedicine)

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19
Q

Generate a management plan for STEMI

A
  • Immediate:
    • Coronary reperfusion therapy ASAP
      • Coronary angiography + PCI: if <12h since onset + can be done w/i 2h of when fibrinolysis could have been given (or >12h since onset but ongoing ischaemia/shock)
      • Fibrinolysis (if not suitable for PCI) + antithrombin
        • Do ECG 1h later: if continued ischemia do PCI
    • Medical: MONAC if ineligible for coronary reperfusion therapy
  • Long-term:
    • Conservative: risk factor modification (T2DM, HTN, cholesterol, smoking, diet), cardiac rehabilitation
    • Medical: ABDS
      • ACE-inhibitor (once haemodynamically stable)
      • Beta-blocker (once haemodynamically stable –> 12m, or indefinitely if LVF)
      • Dual anitplatelet therapy (aspirin indefinitely + 12m clopidogrel/ticagrelor)
          • gut protection
      • Statin
        • aldosterone antagonist if HF 3-14d post MI

(NICE)

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20
Q

What are the characteristic of Wolff-Parkinson-White Syndrome on ECG?

A

Possible ECG features include:

  • 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

(passmedicine)

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21
Q

What pathologies are associated with Wolff-Parkinson-White Syndrome?

A

Associations of WPW

  • HOCM
  • mitral valve prolapse
  • Ebstein’s anomaly (tricuspid valve malformation, causing atrialisation of the right ventricle)
  • thyrotoxicosis
  • secundum ASD

(passmedicine)

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22
Q

Generate a management plan for Wolff–Parkinson–White syndrome

A

Medical (ABCDE):

  • Manage SVT / VT as per UK Resusitaton Council guidelines (amiodarone / flecainide)
    • sotalol (CI in AF as may –> VF)
  • Definitive treatment: radiofrequency ablation of the accessory pathway

(Passmedicine)

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23
Q

What is the target INR for anticoagulation with warfarin in chronic AF (post TIA)?

A

INR 2-3

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24
Q

Identify the possible complications of varicose veins

A

7 complications:

  • oedema
  • bleeding
  • varicose eczema + pruritus
  • thrombophlebitis
  • haemosiderin deposition
  • lipodermatosclerosis
  • venous ulceration

(lecture)

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25
Q

Give 3 cause of thoracic outflow obstruction

+

What are the 3 types of thoracic outflow obstruction?

A

3 causes:

  • extra cervical rib
  • overgrowth of scalenus anterior muscle (body builders)
  • occupation where arms raised (musicians)

3 types: depends on which structures impinged

  • venous: upper limb DVT, long-term oedema
  • arterial: Raynauld’s, claudication, embolisation
  • neurological: pain, radiculopathy

(lecture)

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26
Q

What are the main investigations in thoracic outflow obstruction?

A
  • Depends on type (venous, arterial or neurological)
    • Imaging: MRI, MRA or MRV
    • Duplex in abduction
    • Nerve conduction studies
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27
Q

What is the classification system for chronic heart failure?

A

New York Heart Association (NYHA) classification is used to grade the severity of functional limitations:

  • Class I: no limitation of physical activity (includes asymptomatic left ventricular dysfunction)
  • Class II: slight limitation of physical activity (comfortable at rest). Ordinary physical activity results in fatigue, palpitation, breathlessness or angina pectoris (symptomatically ‘mild’ heart failure).
  • Class III: marked limitation of physical activity (comfortable at rest, symptomatically ‘moderate’ heart failure)
  • Class IV: inability to carry out any physical activity without discomfort(sx present even at rest, increased discomfort with any physical activity, symptomatically ‘severe’ heart failure)

(GPNotebook)

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28
Q

Outline which coronary territories correspond to which leads on an ECG

A

(passmedicine)

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29
Q

Outline the ALS algorithm for cardiac arrest

A

(UK Resusitation Council)

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30
Q

Generate a management plan for acute atrial fibrillation

A

Acute AF mx

  • Medical (ABCDE)
    • If haemodynamically unstable: short-acting GA + DC cardioversion (synchronised, 200J-400J) (UK Resuscitation Council)
    • Haemodynamically stable: depends on onset
      • <48h
        • Rate control: beta-blocker (metoprolol) and/or CCB (diltiazem)
        • Rhythm control: after TTE confirms no intracardiac thrombus
          • amiodarone (if structural heart dx, older pts), flecainide (younger pts) or DC cardioversion
        • Heparin IV (continue until starting oral anticoagulation. Keep with warfarin until INR 2-3, CI to use with NOAC)
      • >48h or uncertain
        • Rate control: beta-blocker and/or CCB
        • Anticoagulation 3w (warfarin):
          • Then rhythm control: amiodarone or flecainide
      • Oral anticoagulation therapy: Start when sinus rhythm achieved, if CHA2DS2-VASc 1(male) or 2(female). HAS BLED to assess bleeding risk. Continue OAC for 4+ weeks after cardioversion
        • Warfarin (target INR 2.5, esp use w mechanical valves)
        • NOAC (apixaban, rivaroxaban, dabigatran etexilate). Only requires yearly r/v. Indicated if 75+, CVA, HTN, DM, HF. CI in ESRF

(NICE, BMJ)

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31
Q

Define atrial fibrillation

A

Atrial fibrillation: supraventricular tachycardia characterised by uncoordinated atrial activity on ECG, with an irregularly irregular ventricular response when AV conduction is intact

(BMJ)

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32
Q

Give common causes of acute atrial fibrillation

A

Acute

Intracardiac: think myocardium, pericardium, valves

  • IHD (CAD or MI)
  • Valvular dx (mitral, often rheumatic HD)
  • CCF (or dilated cardiomyopathy)
  • Inflammation + infiltrative (pericarditis, myocarditis, amyloidosis)

Extracardiac: THE APPE

  • Thyrotoxicosis
  • HTN
  • Electrolyte (esp hypokalaemia)
  • Alcohol / caffeine
  • Pneumonia
  • Pulmonary Embolism

(AS, OHCM, BMJ)

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33
Q

Give risk factors for acute atrial fibrillation

A

Strong RFs: age, T2DM, HTN, CCF, CAD, valvular dx, other atrial arrhythmias, hyperthyroidism

Weak RFs: obesity, ETOH intoxication, hypoxic pulmonary conditions (COPD)

(BMJ)

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34
Q

Identify appropriate investigations for atrial fibrillation

A
  • Confirm diagnosis:
    • ECG
  • Identify cause:
    • Bloods: Trop, CK-MB, TFTs
    • Imaging: CXR
    • Exercise stress echo: if ?structural abnormalities
  • Plan managment:
    • Imaging: TTE or TOE

(BMJ)

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35
Q

Identify the possible complications of atrial fibrillation

A

Early: acute stroke, MI, CCF

(BMJ)

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36
Q

What are the definitions of paroxysmal, persistent and long-standing atrial fibrillation?

A

Chronic

  • Paroxysmal AF: recurrent AF (>1 episode >=30s duration) that terminates spontaneosly w/i 7d
  • Persistent AF: sustained AF for >7d (or <7d but required cardioversion)
  • Longstanding AF: sustained AF doe >1y

(BMJ)

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37
Q

Give common causes of chronic atrial fibrillation

A

Chronic

Intracardiac: acute + ACE

  • Acute causes (IHD, valvular, CCF, inflammatory)
  • Age-related fibrosis
  • Congenital heart disease
  • Electrophysiological abnormalities (sick sinus syndrome)

Extra-cardiac: PHAT

  • Pulmonary HTN (pulmonary fibrosis etc)
  • HTN
  • Alcohol / caffiene
  • Thyroid dx

(AS, BMJ)

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38
Q

What is the long-term therapy for paroxysmal atrial fibrillation

A
  • Oral anticoagulation therapy: Start when sinus rhythm achieved, if CHA2DS2-VASc 1(male) or 2(female).
    • Warfarin (target INR 2.5, esp use w mechanical valves)
    • NOAC (apixaban, rivaroxaban, dabigatran etexilate). Only requires yearly r/v
      • Indicated if 75+, CVA, HTN, DM, HF
      • CI in ESRF
  • Rate control
    • 1st: beta-blocker
    • 2nd: CCB (diltiazem, verapamil) or digoxin

(BMJ)

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39
Q

Outline the prognosis in paroxysmal AF

A

Chronic:

25% paroxysmal AF progress to more sustain form w/i 1.5y

30% higher risk of cardiovascular events

(BMJ)

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40
Q

Identify appropriate investigations for chronic cardiac failure

A

Chronic HF

1st line ix depends if pt has had previous MI

  • Previous MI: echo w/i 2w
  • No previous MI: BNP
    • If BNP high: echo w/i 2w
    • If BNP raised: echo w/i 6w

Assess RFs and DDx

  • Bloods: UEs, eGFR, TFTs, LFTs, FBC, lipids, glucose
  • Urinalysis
  • Spirometry
  • Imaging: ECG, CXR

(Passmedicine, NICE)

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41
Q

What factors can alter a B-natriuretic peptide (BNP) reading in ?heart failure?

A

Factors decreasing BNP

  • Obesity
  • HTN medication (diuretics, ACE-Is, ARBs, BBs)
  • Aldosterone antagonists

Factors increasing BNP

  • >70
  • IHD, COPD, T2DM, sepsis, cirrhosis

(NICE)

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42
Q

Generate a management plan for acute cardiac failure

A

Acute HF

  • Medical (ABCDE)
    • Supportive
      • Sit up, limit fluids
      • High flow O2
          • IV morphine (if distressed)
      • Diuretic
        • 1st line: loop diuretic (furosemide PO/IV)
        • 2nd line: spironolactone / eplerenone PO
      • Additional support (consult senior):
        • pulmonary oedema + sBP>90: vasodilator (GTN IV)
        • sBP<90: inotrope (dobutamine) / vasopressor
        • hypertensive crisis: IV beta-blocker + GTN, nitroprusside
      • Consider escalation
        • NIV: if severe dyspnoea, acidosis
        • Consult senior if may require intubation / ventilation (resp failure, reduced GCS, exhaustion)
      • Tx underlying cause
        • MI: aspirin +/- revascularisation (PCI / CABG)
        • Valvular dx: nitroprusside (reduces TPR + venous return)
        • R-sided HF: eg PE (thrombolysis etc)

Ongoing:

  • Conservative: low salt diet, regular wts, fluid balance
  • Medical: ABDS
    • ACE-I / ARB
    • Beta-blocker
    • Diuretics (loop +/- thiazide)
    • Spironolactone (or eplerinone)

(NICE, BMJ)

43
Q

Identify the possible complications of deep vein thrombosis (DVT)

A
  • Immediate: Pulmonary Embolism
  • Early: Heparin-related bleeding, thrombocytopenia
  • Late: Post-thrombotic syndrome:
    • DVT –> venous outflow obstruction + venous insufficiency –> chronic venous hypertension

(passmedicine, BMJ)

44
Q

Explain the aetiology / risk factors of deep vein thrombosis (DVT)

A

Virchow’s triad

  • Hypercoagulability: cancer, COCP, pregnancy, syndromes (antiphospholipid syndrome, Factor V Leiden)
  • Haemodynamics (stasis, turbulence): orthopaedic surgery, long distance
  • Endothelial injury: smoking, sepsis, obesity, HTN

(path)

45
Q

Generate a management plan for deep vein thrombosis (DVT)

A
  • Acute
    • Initial anticoagulation: LWMH or fondaparinux
      • For 5d or until INR 2+ for 24h
      • Unfractionated heparin instead in severe renal impairment or bleeding risk
    • Interventional:
      • Catheter-directed thrombolytic therapy: if iliofemoral DVT + <14d sx + low bleeding risk + >1y life expectancy + good funcitonal status
      • IVC filter (if ineligible for anticoagulation or recurrent)
  • Long-term
    • TED stockings on affected leg (1w after dx, recommend for 2y)
    • Long-term anticoagulation (BMJ recommends NOACs)
      • Warfarin - start w/i 24h. 3m if cause known, 3-6m if cause unknown, lifelong if recurrent.
      • LMWH: if active cancer (3-6m)

(Passmedicine, NICE)

46
Q

Recognise the signs of infective endocarditis on physical examination

A
  • Hands: clubbing, splinter haemorrhages, Osler’s nodes, Janeway’s lesions
  • Arm: injection points
  • Eyes: Roth spots
  • Chest: new murmur
  • Abdo: petechiae, splenomegaly, microscopic haematuria (urine dip part or O/E)
  • tachycardia, tachypnoea, high temp

(Meeran)

47
Q

What are the common causative organisms of infective endocarditis?

  • How do they enter blood stream usally?
  • Which valves to they affect?
A
  • Strep viridans. Mouth commensal, enters bloodstream in dental work. Settle on mitral valve with pre-existing disease.
  • Staphylococcus aureus. Skin commensal, enters bloodstream in IVDUs. Settle on first valve it encounters; tricuspid.

(Meeran)

48
Q

Summarise the diagnostic criteria for acute rheumatic heart disease

A

Duckett Jones criteria

  • Major
    • Carditis
    • Erythema marginatum
    • Subcutaneous nodules
    • Polyarthritis
    • Syndenham’s Chorea
  • Minor: fever, arthraligia, ESR up, WCC up, PR interval up, previous RF

(Meeran)

49
Q

Summarise the aetiology of acute rheymatic heart disease

A

strep throat in child –> autoAbs against strep –> Type II HR attacking skin / heart / brain / joints

(Meeran)

50
Q

What is pulmonary haemosiderosis?

A
  • In mitral stenosis, enlarged L atrium + valve disease causes haemolysis –> Fe deposition in lung
  • Rare now due to valve replacement
  • Appears on CXR as bilateral shadowing + dense opacities + L-atrial enlargement

(Meeran)

51
Q

Recognise the signs of mitral stenosis on physical examination

A

Malar flush , AF, tapping apex, non-displaced apex, R ventricular heave

Blowing soft mid diastolic murmur + loud S1

(Meeran)

52
Q

Generate a management plan for mitral stenosis

A
  • Mild/moderate stenosis: no tx required
  • Severe stenosis (gradient >5mmHg):
    • diuretics (frusomide): reduce LV pressure
    • balloon valvotomy (percutaneous)
    • valve replacement surgery

(BMJ)

53
Q

Identify the possible complications of mitral stenosis

A

Long term:

  • L-sided HF (–> CCF)
  • AF (–> CVA)
  • Complications of replacement (FIBAT)
    • Failure (heart, valve)
    • Infection (IE)
    • Bleeding (warfarin)
    • Anaemia (haemolysis, of chronic disease)
    • Thromboembolic

(BMJ, Mirza)

54
Q

Recognise the signs of mitral regurgitation on physical examination

A

Pansystolic murmur radiating to axilla

Displaced apex, apical thrill, S1 quiet, S3 (rapid ventrilucar filling)

Look for valvotomy scar (under breast, old procedure to turn MS into MR)

(Meeran)

55
Q

Give causes of mitral regurgitation

A
  • Ischaemic damage to papillary muscle (MI)
  • Infective (IE)
  • Cardiac dilatation (R-sided HF)
  • Acute rheumatic fever
  • Congenital
  • Degenerative

(BMJ)

56
Q

Generate a management plan for mitral regurgitation

A
  • Acute (or ejection fraction <60%):
    • Surgical: valvuloplasty or valve replacement
    • +/- medical ((ACE-Is + beta blocker)
  • Chronic:
    • Ejection fraction >60%: medical (ACE-Is + beta blocker)

(BMJ)

57
Q

Identify the possible complications of mitral regurgitation

A
  • L-sided HF (–> CCF)
  • AF (–> CVA)
  • Complications of replacement (FIBAT)
    • Failure (heart, valve)
    • Infection (IE)
    • Bleeding (warfarin)
    • Anaemia (haemolysis, of chronic disease)
    • Thromboembolic

(BMJ, Mirza)

58
Q

Summarise the prognosis for patients with mitral regurgitation

A

L-ventricular dysfunction 6-10y

1% reoperation risk for valve replacement

(BMJ)

59
Q

Recognise the signs of aortic regurgitation on physical examination

A
  • End diastolic murmur at left sternal edge, systolic flow murmur
  • Wide pulse pressure
  • Collapsing pulse, dynamic apex
  • ALL the signs eg
    • Corrigans - visible neck pulses
    • De musset’s - head nodding w heartbeat
    • Quincke’s - capillary pulsation in nail bed

(Meeran)

60
Q

Explain the aetiology of aortic regurgitation

A
  • Congenital (biscuspid valve)
  • Valve damage
    • Infective: endocarditis, post-rheumatic fever
  • Aortic root dilatation
    • Marfan’s
    • Inflammatory: ankylosing spondyltiis, Behcet’s
    • Infective: secondary syphilis
  • Aortic root dissection - acute

(BMJ)

61
Q

Generate a management plan for aortic regurgitation

A
  • Mild/moderate: monitor
  • Severe:if symptomatic or outflow <50%:Aortic valve replacement
    • Surgical (mechanic vs bioprosthetic)
    • Transcatheteric aortic valve implantation (TAVI)
    • +/- vasodilator (nifedipine)
    • +/- Ace-Inhibitor

(BMJ)

62
Q

Identify the possible complications of aortic regurgitation

A
  • R-sided HF (–> CCF)
  • AF (–> CVA)
  • Complications of valve replacement (FIBAT)
    • Failure (heart, valve)
    • Infective endocarditis
    • Bleeding (warfarin)
    • Anaemia (haemolysis, of chronic disease)
    • Thromboembolic

(BMJ, Mirza)

63
Q

Generate a management plan for varicose veins

A
  • Conservative
    • Risk factor modification: wt loss, light exercise, stop smoking, elevate legs when possible, warn to watch for complications
    • Compression stockings may help with symptoms
  • Medical (in secondary care, refer if complications)
    • Foam sclerotherapy –> irritant foam –> inflammation –> vein closure
    • Endothermal methods: radiofrequency or laser ablation
    • Surgery: stripping or ligation

(NICE)

64
Q

Give risk factors for varicose veins

A

Causative factors: previous DVT, genetic

Risk factors: pregnancy, female, age, obesity

65
Q

Summarise the prognosis for patients with varicose veins

A

treatment leads to resolution of symptoms in 95% cases

(BMJ)

66
Q

Generate a management plan for HOCM

A

HOCM

  • Conservative: reduce strenuous exercise
  • Medical
    • Asymptomatic: monitor
    • Symptomatic:
      • 1st line: beta-blocker
      • 2nd line: CCB
    • High risk sudden death (including asymptomatic): implantable cardioverter-defibrillator
  • Manage complications:
    • AF: eg add warfarin
    • CCF: eg add ABDS

(BMJ)

67
Q

Identify the possible complications of hypertrophich obstructive cardiomyopathy

A

Immediate: sudden death (if undetected)

Early: AF (–> CVA), WPW, ventricular ectopics

Late: L-sided heart failure (–> CCF)

(BMJ)

68
Q

Give common drugs that cause hyperlipidaemia

A

Think of the X-men

  • Corticosteroids (cerebro –> cerebral cortex –> cortico)
  • Ciclosporin (cyclops)
  • Isotretonoin (iceman)
  • Protease inhibitors (Professor X)
  • Antipsychotics (any of them)

(passmedicine)

69
Q

Outline the Vaughan Williams Classification for antiarrhythmic drugs

A
  • Class Ia: increases AP duration (quinidine, procainamide). Ia = Increases AP
  • Class Ib: decreases AP duration, blocks Na channels (lidocaine). Ib = Is brief
  • Class Ic: no affect on AP duration, blocks Na channels (flecainide). Ic = Is consistent
  • Class II: beta-blockers (atenolol, bisporolol, propranolol, misoprolol). II = -lol
  • Class III: blocks K+ channels (amiodarone, sotalol)
  • Class IV: blocks Ca2+ channels (verapamil, diltiazem)
70
Q

Give causes of pericarditis

A
  • Infarction: MI (fibrous pericarditis, Dressler’s syndrome)
  • Infection:
    • Viral: coxsackie, flu, EBV
    • Bacterial: pneumonia, rheumatic fever, TB
  • Inflammatory: SLE, RA, sarcoid
  • Drugs: isoniazid, penicillin, procainamide, hydralazine

(AS)

71
Q

Identify appropriate investigations for pericarditis

A
  • Confirm diagnosis
    • ECG: ST elevation widespread, PR depression
    • Bloods: FBC, ESR, trop, cultures, virology

(AS)

72
Q

Generate a management plan for pericarditis

A

Medical

  • Manage cause
  • Analgesia: WHO ladder
  • Consider steroids / immunosuppression

(AS)

73
Q

Identify the possible complications of pericarditis

A
  • Constrictive pericarditis: –> R-sided HF. Kussmaul’s sign (JVP raised on inspiration), S3, hepatosplenomegaly, ascites etc
  • Pericardial effusion–> cardiac tamponade
  • Tamponade = Beck’s triad (low BP, high JVP, quiet heart sounds), pulsus paradoxus, Kussmauls sign

(AS)

74
Q

Give potential causes of chronic heart failure

A
  • Low output: PEE
    • Pump-failure: IHD, cardiomyopathy (dilated, restrictive, HOCM), pericardial (constriction, effusion), arrhythmias
    • Excessive preload: fluid overload, AR, MR
    • Excessive afterload: AS, HTN, HOCM
  • High output: ATP
    • Anaemia, AVM
    • Thyrotoxicosis, Thiamine deficiency (beri-beri)
    • Pregnancy, Paget’s

(AS)

75
Q

What are the complications of having a pacemaker?

A
  • Insertion
    • Bleeding
    • Arrhythmia (due to lead displacement)
    • Pneumothorax
  • Post-insertion
    • Erosion of skin
    • Lead migration
    • Pocket infection
    • Malfunction
    • Pacemaker syndrome: AV asynchrony

(AS)

76
Q

What are the indications for a permanent pacemaker?

A
  • Heart blocks:
    • Complete AV block
    • Mobitz Type 2
  • Heart rate:
    • Symptomatic bradycardia: sick sinus syndrome
    • Drug resistant tachyarrhythmias
  • Heart failure, chronic (requires biventricular pacing)

(AS)

77
Q

What lifestyle advice should be given after implantation of a pacemaker?

A
  • No driving for a week
  • No arm elevation for 6 weeks
  • No contact sports
  • Minimal phone interference
  • Carry pacemaker card (shop alarms, metal detectors)

(AS, Adam)

78
Q

What do you check on a CXR after pacemaker insertion?

A
  • Lead position
  • Lead integrity
  • Lead tension (coiling)
  • Apical pneumothorax

(AS, Adam)

79
Q

What are the different types of pacemaker? When are they indicated?

A
  • Single lead:
    • Atrial pacemaker: bradycardias
    • Ventricular pacemaker: AF (featuring bradycardia or ventricular pause)
  • Dual lead: heart blocks (complete, Mobitz Type II)
  • Biventricular: chronic heart failure (NYHA II/IV, despite optimal treatment) = cardiac resynchronisation therapy

(AS, Adam)

80
Q

Which drugs lengthen the QT interval on ECG?

A

‘CAAAT

  • Ciprofloxacin
  • Amiodarone
  • Adenosine
  • Antipsychotics
  • TCAs

(passmedicine)

81
Q

Give the features of aortic stenosis O/E

A

Features of severe aortic stenosis

  • narrow pulse pressure
  • slow rising pulse
  • delayed ESM
  • soft/absent S2
  • S4
  • thrill
  • duration of murmur
  • left ventricular hypertrophy or failure

(passmedicine)

82
Q

What are the causes of aortic stenosis

A

Calcification (most common)

Congenital bicuspid valve

Rheumatic heart disease

(OHCM, BMJ)

83
Q

Identify appropriate investigations for aortic stenosis

A
  • Confirm diagnosis:
    • Imaging: Echo + doppler
  • Assess complications
    • ECG, CXR
    • Bloods: FBC, UE, BNP, lipids, glucose
    • consider
      • cardiac catheterisation: valve gradient
      • coronary angiography

(AS)

84
Q

What are the echocardiogram feaures of severe aortic stenosis?

A
  • Valve area <1cm^2
  • Pressure gradient >40mmHg
  • Jet velocity >4m/s

(AS, AHA)

85
Q

Generate a management plan for aortic stenosis

A
  • Conservative: MDT (cardiologist, GP, cardiothoracic surgeon, specialist nurse), RF modification (optimise CV health), regular r/v + echos
  • Medical:
    • RF modification: statins, antihypertensive, DM, anticoagulation
  • Surgical
    • Valve replacement (if symptomatic, EF <50% or having other cardiac surgery)
      • +/- CABG
      • life-long anticoagulation (warfarin, NOAC) if prosthetic
    • Transcatheteric aortic valve implantation (TAVI)
    • Balloon valvuloplasty: if not fit for the above

(AS)

86
Q

Identify the possible complications of aortic stenosis

A
  • LVF (–> CCF)
  • Ventricular arrhythmias –> sudden cardiac death
  • Valve replacement complications:
    • Failure (valve, heart, restenosis)
    • Infection (IE)
    • Bleeding (warfarin)
    • Anaemia (haemolytic mechanical, of chronic disease)
    • Thromboembolic

(BMJ, Mirza)

87
Q

Summarise the prognosis for patients with aortic stenosis

A

Severe AS:

  • angina: 50% dead in 5y
  • syncope: 50% dead in 3y
  • dyspnoea: 50% dead in 2y

(AS)

88
Q

Identify the possible complications of chronic cardiac failure

A

Early: AKI, acute heart failure

Late: chronic renal insufficiency, pleural effusion, anaemia

(BMJ)

89
Q

What are the features of chronic heart failure on CXR?

A

‘ABCDEF’

  • Alveolar shadowing
  • Kerley B lines
  • Cardiomegaly
  • Upper lobe diversion
  • Effusions
  • Fluid in fissures

(AS)

90
Q

Summarise the prognosis for patients with chronic heart failure

A

NYHA - annual mortality risk:

  • Class I: 5%
  • Class II: 10%
  • Class IV: 40-60%

Higher BNP indicates worse prognosis

(BMJ OHCM)

91
Q

Identify possible complications of acute heart failure

A
  • End organ hypoperfusion: arrythmias, AKI, MI
  • pulmonary oedema, pleural effusion –> Type 1 resp failure
  • Peripheral oedema
92
Q

Give potential causes of acute heart failure

A
  • New:
    • Left-ventricular HF (post-MI)
    • Arrythmias (electrolyte imbalance, post-MI)
    • Fluid overload
    • Neurogenic (eg head injury)
  • Acute exacerbation of CCF (see causes CCF: PEE + ATP)

(OHCM)

93
Q

Define peripheral vascular disease

A

Peripheral vascular disease involves atherosclerosis of the arteries leading to stenosis via a mulitfactorial process

(OHCM)

94
Q

Give risk factors for peripheral vascular disease

A

RFs:

  • Modifiable: smoking, BP, DM, hyperlipidaemia, reduced exercise
  • Non-modifiable: FHx, PMH, male, age, ethnicity

(OHCM)

95
Q

What is the classification system for peripheral vacular disease?

A

Fontaine Classification of peripheral vascular disease

  • Class 1: asymptomatic
  • Class 2: intermittent claudication
  • Class 3: ischaemic rest pain
  • Class 4: ulceration, gangrene, critical ischaemia

(OHCM)

96
Q

Identify appropriate investigations for peripheral vascular disease

A
  • Confirm diagnosis
    • ABPI +/- exercise ABPI (drop >0.2 = claudication)
      • >1.0 = calcified artery
      • 0.8-1.0 = normal
      • 0.6-0.8 = claudication (may only drop to this on exercise)
      • <0.6 = critical ischaemia
    • Colour duplex USS (B-mode USS + multidirectional Doppler probe)
  • Assess cause / complications
    • Bloods: FBC (anaemia worsens PVD), UEs (renovascular dx), glucose, lipids
    • ECG
  • Plan tx: Imaging:
    • CT/MRI gadolinium contrast
    • digital subtraction angiography (if therapeutic angioplasty or stenting)

(AS, lecture)

97
Q

Generate a management plan for peripheral vascular disease

A
  • Conservative:
    • walk through the pain, supervised exercise programmes
    • RF modification: smoking cessation, control HTN/lipids/BP, lose wt
    • Foot care
  • Medical:
    • Anticoagulation: clopidogrel (lifelong)
    • Statin
    • Interventional:
      • Percutaneous transluminal angioplasty +/- stenting
  • Surgical
    • Endarterectomy (short segment only)
    • Bypass grafting (artificial dacron vs autologous vein)
      • Anatomical: fem-pop, fem-distal, aortobifemoral
      • Extra-anatomical: axillo-(bi)fem, fem-fem crossover
    • Amputation: unsalvageable limb, below-knee, physiotherapy, gabapentin

(AS)

98
Q

What are the indications for venous grafting in peripheral vascular disease?

A
  • <100m claudication distance
  • Sx impacting QoL
  • Rest pain

(AS)

99
Q

Summarise the prognosis for patients with peripheral vascular disease

A

Morbidity: <3% pts with intermittent claudication have amputation w/i 5y

Vasculopaths: increased risk of IHD, CVA

(OHCM)

100
Q

Identify the possible complications of peripheral vascular disease

A
  • Early: acute-on-chronic limb ischaemia
    • ischaemia less bad due to collaterals
    • Mx: catheter directed thrombolysis
  • Long: progression, ulcers, tissue loss, gangrene (–> sepsis)

(lecture)

101
Q

What is typical and atypical angina?

A

Typical angina presents with all 3 of:

  • Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms.
  • Relieved by rest or glyceryl trinitrate (GTN) within about 5 minutes.
  • Precipitated by physical exertion.

Atypical angina has 2 of these features

(NICE)

102
Q

Identify appropriate investigations of ischaemic heart disease

A
  • Immediate
    • Bloods: FBC, Trop-I or T, UEs, glucose, clotting
    • Imaging: ECG +/- echo
  • Long-term
    • If CAD risk >30%:
      • Stress echo
      • Functional imaging: myocardial perfusion scintigraphy or MRI
    • If CAD risk >60%:
      • coronary angiography (if CI, functional imaging)
  • Monitor: BP, renal function

(OHCM)

103
Q

Summarise the prognosis in ischaemic heart disease

A

Morbidity: Aggressive lifestyle modification reduces complications risk

Mortality:

  • ACS: 50% of deaths occur w/i first 2h
  • Worse prognosis if elderly, LV failure, ST changes

(OHCM)

Medicine Y6 (14 decks)

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