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Cardiology Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the signs of tricuspid regurg?

A
  • Typically inaduible (due to low pressure in R heart)
  • Low frequency pansystolic murmur if RV pressure elevated
  • Elevated JVP
  • Giant c-V waves
  • Pulsatile liver edge
  • Peripheral oedema
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2
Q

What are the causes of severe TR?

A
  • Functional (RV dilatation)
  • Infection (from venous cannulation)
  • Carcinoid (nodular hepatomegaly and telangiectasia)
  • Post-rheumatic
  • Ebstein’s anomaly
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3
Q

What is Ebstein’s anomaly?

A

Tricuspid valve dysplasia with a more apical position to the valve; patients are cyanotic and there is an association with pulmonary atresia or ASD and, less commonly, congenitally corrected transposition

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4
Q

What causes tricuspid stenosis?

A

Rheumatic fever (with MV and AV disease)

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5
Q

What are the symptoms of tricuspid stenosis?

A

Fatigue, ascites, oedema

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6
Q

What are the signs of tricuspid stenosis?

A

LArge A waves, opening snap, EDM murmur at LLSE in inspiration

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7
Q

How do you manage tricuspid stenosis?

A

Diuretics, repair/replacement

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8
Q

What causes pulmonary regurg?

A

Any cause of pulmonary hypertension, or a Graham-Steell murmur (secondary to mitral stenosis)

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9
Q

What kind of murmur do you hear in pulmonary regurg?

A

Decrescendo end diastolic murmur at the upper left sternal edge

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10
Q

What are the causes of pulmonary stenosis?

A
  • Usually congenital: Turner’s, Fallot’s
  • Rheumatic fever
  • Carcinoid syndrome
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11
Q

What are the symptoms of pulmonary stenosis?

A
  • Dyspnoea
  • Fatigue
  • Ascites
  • Oedema
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12
Q

What are the signs of pulmonary stenosis?

A
  • Dysmorphia
  • Large A wave
  • RV heave
  • Ejection clic, soft P2
  • Murmur: ejection systolic, upper left sternal edge to left shoulder
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13
Q

What investigation findings indicate pulmonary stenosis?

A
  • ECG: P pulmonale, right atrial dilatation, RBBB
  • CXR: prominent pulmonary arteries (post stenotic dilatation)
  • Catheterisation: diagnostic
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14
Q

How do you manage pulmonary stenosis?

A

Valvuloplasty or valvotomy

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15
Q

What are the features of benign flow murmur?

A
  • Present in 30% children
  • Short, soft systolic murmur
  • Heard along left sternal edge to the pulmonary area
  • No other abnormalities
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16
Q

When can you hear a cervical venous hum and what does it indicate?

A
  • Continuous when upright, reduced when lying
  • Indicates hyperdynamic circulation or jugular vein compression
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17
Q

WHat kind of murmur can a large AV fistula cause?

A

Harsh flow murmur across the upper mediastinum

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18
Q

What are the causes of mid/late systolic murmurs?

A
  • Innocent murmur
  • Aortic stenosis/sclerosis
  • Coarctation of the aorta
  • Pulmonary stenosis
  • HCM
  • Papillary muscle dysfunction
  • ASD (due to high pulmonary flow)
  • Mitral valve prolapse
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19
Q

What are the causes of mid diastolic murmurs?

A
  • Mitral stenosis or ‘Austin Flint’ murmur due to aortic regurgitant jet
  • Carey Coombs murmur (rheumatic fever)
  • High AV flow states (ASD, VSD, PDA< anaemia, mitral regurgitation, tricuspid regurg)
  • Atrial tumours (particularly if causing AV flow disturbance)
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20
Q

What are the causes of continuous murmurs?

A
  • PDA
  • Ruptured sinus of Valsalva’s aneurysm
  • ASD
  • Large arteriovenous fistula
  • Anomalous left coronary artery
  • Intercostal arteriovenous fistula
  • ASD with mitral stenosis
  • Bronchial collaterals
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21
Q

How is mitral stenosis defined?

A
  • Normal MV - 4-6cm2
  • MS ≤2cm2
  • Severe MS ≤1cm2
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22
Q

What are the causes of mitral stenosis?

A
  • Chronic rheumatic heart disease (antibody cross reactivity to a streptococcal illness)
  • SLE
  • Carcinoid
  • Mucopolysaccharidoses (glycoprotein deposits on cusps)
  • Congenital (rare)
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23
Q

What is the pathophysiology of mitral stenosis?

A
  • Valvular narrowing causes increased LA pressure, therefore loud S1 and atrial hypertrophy followed by invariable AF
  • Increased pulmonary pressure causes pulmonary oedema
  • RV hypertrophy leads to left parasternal heave
  • TR causes large V waves
  • Eventual right heart failure causes raised JVP, oedema, ascites
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24
Q

What are the symptoms of mitral stenosis and when do they manifest?

A
  • When valve gets below 2cm2
  • Dyspnoea with minimal activity
  • Fatigue
  • Chest pain
  • AF, therefore palpitations
  • Dysphagia (due to LA enlargement)
  • Haemoptysis with rupture of bronchial veins
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25
Q

What are the signs of mitral stenosis?

A
  • Rumbling MDM at the apex, left lateral position in end expiration, radiates to the axilla
  • AF
  • Low pulse pressure
  • Long diastolic murmur and apical thrill (rare)
  • Very early opening snap i.e. closer to S2 (lost if valves immobile)
  • RV heave or loud P2
  • Pulmonary regurg (Graham Steell murmur)
  • Tricuspid regurg
  • Malar flush (low cardiac output leads to backpressure and vasoconstriction)
  • JVP can be raised late on
    • Prominent A waves: PHT
    • Large V waves: TR
    • Absent A waves: AF
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26
Q

What are the clinical indicators of severe mitral stenosis?

A
  • Mitral facies
  • Longer murmur
  • Opening snap closer to 2nd heart sound (high LA pressure forcing valve open early)
  • Decompensation: RVF
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27
Q

What are the complications of mitral stenosis?

A
  • Pulmonary hypertension
  • Emboli: TIA, CVA, PVD, ischaemic colitis
  • Hoarseness: recurrent laryngeal nerve palsy = Ortner’s syndrome
  • Dysphagia (oesophageal compression)
  • Bronchial obstruction
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28
Q

What investigation findings are consistent with mitral stenosis?

A
  • ECG: AF, P mitrale (if in sinus), RVH (ST depression and T wave inversion in V1-V2)
  • CXR
    • LA or RV enlargement
    • Splaying of subcarinal angle (>90 degrees)
    • Pulmonary congestion or hypertension
    • Pulmonary haemosiderosis
  • Echo
    • Doming of leaflets
    • Heavily calcified cusps
    • Orifice area <2cm2
    • USe TOE to look for LA thrombus if intervention considered
  • Cardiac catheterisation
    • Pulmonary capillary wedge end diastole to LV end diastolic pressure >15mmHg
    • LA pressures >25mmHg
    • Elevated RV and PA pressures
    • High pulmonary vascular resistance
    • Cardiac output <2.5L/min per m2 with exercise
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29
Q

How do you manage mitral stenosis?

A
  • Medical
    • Optimise risk factors: statins, antiHTN, diabetes
    • Monitor: regular follow up with echo
    • Consider prophylaxis against rheumatic fever e.g. penicillin V
    • AF: rate control and anticoagulate
    • Diuretics for symptom relief
  • Surgical
    • Indicated in moderate to severe MS (asymptomatic and symptomatic)
    • Percutaneous balloon valvuloplasty
      • Treatment of choice
      • Suitability depends on valve characteristics (pliable, minimally calcified)
      • Contraindicated if left mural thrombus
    • Surgical valvotomy/commissurotomy: valve repair
    • Valve replacement if repair not possible
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30
Q

What is functional mitral regurg?

A

MR caused by stretching of the annulus secondary to ventricular dilatation

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31
Q

What are the causes of mitral regurg?

A
  • Myxomatous degeneration
  • Functional
  • Mitral valve prolapse (Barlow syndrome)
  • Ischaemic papillary muscle rupture
  • Congenital heart diseases
  • Collagen disorders
  • Rheumatic heart disease
  • Endocarditis
  • Annular calcification -> contraction (elderly)
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32
Q

What are the symptoms of mitral regurg?

A
  • Dyspnoea
  • Fatigue
  • AF -> palpitations
  • Pulmonary congestion -> oedema
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33
Q

What are the signs of mitral regurg?

A
  • AF
  • Left parasternal heave (RVH)
  • Apex: displaced
  • Heart sounds: Soft S1, S2 not heart separately from murmur, loud P2 (if PHT)
  • Murmur:
    • Blowing, pan systolic
    • Apex
    • Left lateral position in end expiration
    • Radiates to axilla
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34
Q

Why is the apex displaced in mitral regurg?

A

Because of volume overload, as the ventricle has to pump forward SV and regurgitant volume leading to eccentric hypertrophy

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35
Q

What are the indicators of severe MR?

A
  • Small volume pulse
  • LV enlargement due to overload
  • Presence of S3
  • Atrial fibrillation
  • Mid diastolic flow murmur
  • PRecordial thrill, signs of pulmonary hypertension or congestion (cardiac failure)
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36
Q

What are the indications of predominant mitral regurgitation in mixed mitral valve disease?

A
  • Soft S1; S3 present
  • Displaced and hyperdynamic apex (LV enlargement)
  • ECG showing LVH and left axis deviation
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37
Q

What are the differentials for mitral regurg?

A

AS, TR, VSD

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38
Q

What investigation findings indicate mitral regurg?

A
  • ECG: AF, P mitrale (unless in AF), LVH
  • CXR:
    • LA and LV hypertrophy
    • Mitral valve calcification
    • Pulmonary oedema
  • Echo
    • Doppler to assess severity: multiple criteria
      • Jet width (vena contracta) >0.6cm
      • Systolic pulmonary flow reversal
      • Regurgitant volume >60ml
    • TOE to assess severity and suitability of repair/replacement
  • Cardiac catheterisation to confirm diagnosis and assess CAD
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39
Q

How do you manage mitral regurg?

A
  • Medical
    • Optimise risk factors (statin, HTN, DM)
    • Regular follow up with echo
    • AF: rate control and anticoagulate (also if Hx of embolism, prosthetic valve, additional MS)
    • Drugs to decrease afterload can help symptoms: ACEi, beta blockers (especially carvedilol), diuretics
  • Surgical
    • Valve repair or replacement
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40
Q

What are the indications for valve replacement/repair in mitral regurg?

A
  • Symptoms
  • Increasing LV dilatation
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41
Q

What causes Barlow syndrome and how common is it?

A

5% of the population (probably the commonest valve problem).

Often myxomatous degeneration and redundant valve tissue due to deposition of acid mucopolysaccharide material

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42
Q

What are the causes/conditions associated with Barlow syndrome?

A
  • Coronary artery disease
  • Polycystic kidney disease
  • Cardiomyopathy - dilated cardiomyopathy/HCM
  • Secundum ASD
  • WPW syndrome
  • PDA
  • Marfan’s
  • Pseudoxanthoma elasticum
  • Osteogenesis imperfecta
  • Myocarditis
  • SLE; polyarteritis nodosa
  • Muscular dystrophy
  • Left atrial myxoma (often young women)
  • Turner’s
  • Ehlers Danlos
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43
Q

What are the symptoms of Barlow syndrome?

A
  • Usually asymptomatic
  • Autonomic dysfunction: atypical chest pain, palpitations, anxiety, panic attack
  • Mitral regurg -> dyspnoea, fatigue
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44
Q

What are the signs of Barlow syndrome?

A
  • Mid systolic click ± late systolic murmur
  • Squatting increases the click
  • Standing increases the murmur
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45
Q

What are the complications of Barlow syndrome?

A
  • Mitral regurg
  • Embolic pehnomena including cerebral emboli
  • Rupture of mitral valve chordae
  • Dysrhythmias with QT prolongation
  • Sudden death
  • Cardiac necrosis
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46
Q

How do you manage mitral prolapse?

A

Beta blockers to relieve palpitations and chest pain, surgery if severe

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47
Q

What is the difference in presentation between acute and chronic aortic regurg?

A

Acute causes -> acute decompensation and profound heart failure

Chronic -> time for the LV to accommodate and gradually enlarge end diastolic volumes

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48
Q

What are the causes of aortic regurg?

A
  • Valve inflammation
    • Chronic rheumatic
    • Infective endocarditis
    • RA, SLE
    • Hurler’s syndrome
  • Aortitis
    • Syphilis
    • Ank spond
    • Reiter’s
    • Psoriatic arthropathy
  • Aortic dissection/trauma
  • Hypertension
  • Bicuspid aortic valve - associated with aortopathy and aortic root dilatation which can cause aortic regurg
  • Ruptured sinus of valsalva’s aneurysm
  • VSD with prolapse of right coronary cusp
  • Disorders of collagen
    • Marfan’s (aortic aneurysm)
    • Hurler’s
    • Pseudoxanthoma elasticum
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49
Q

What are the symptoms of aortic regurg?

A
  • LVF: exertional dyspnoea, PND, orthopnoea
  • Arrhythmias (especially AF) -> palpitations
  • Angina
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50
Q

What are the signs of aortic regurg?

A
  • End diastolic murmur
    • Upper right sternal edge and 3rd left intercostal space parasternal
    • Sitting forward in end expiration
    • ± ejection systolic flow murmur ± Austin Flint murmur
  • Collapsing pulse
  • Wide pulse pressure
  • Displaced apex (volume overload)
  • Heart sounds: soft/absent S2, ±S3
  • Underlying cause (high arched palate, spondyloarthropathy)
  • Various eponymous signs
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51
Q

What are the eponymous signs of aortic regurg?

A
  • Quincke’s sign - nail bed fluctuation of capillary flow
  • Corrigan’s pulse - ‘waterhammer’ collapsing radial pulse
  • Corrigan’s sign - visible carotid pulsation
  • De Musset’ ssign - head nodding with each systole
  • Duroziez’s sign - audible femoral bruits with diastolic flow (indicating moderate severity)
  • Traube’s sign - ‘pistol shots’ (systolic auscultatory finding of the femoral arteries)
  • Austin Flint murmur - functional mitral diastolic flow murmur
  • Argyll Robertson pupils - aetiological connection of syphilitic aortitis
  • Muller’s sign - pulsation of the uvula
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52
Q

What are the features of aortic regurg indicating a need for surgery?

A
  • Symptoms of dyspnoea/LV failure (reducing exercise tolerance)
  • Rupture of sinus of Valsalva’s aneurysm
  • Infective endocarditis not responsive to medical treatment
  • Enlarging aortic root diameter in Marfan’s syndrome with AR
  • Enlarging heart (as seen on echo/ECG changes)
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53
Q

Which investigation findings indicate aortic regurg?

A
  • ECG: LVH (R6 + S1 >35mm)
  • CXR
    • Cardiomegaly
    • Dilated ascending aorta
    • Pulmonary oedema
  • Echo
    • Aortic valve structure and morphology (e.g. bicuspid)
    • Evidence of infective endocarditis e.g. vegetations
    • Severity
      • Jet width (>65% of outflow tract = severe)
      • Regurgitant jet volume
      • Premature closing of the mitral valve
    • LV function: ejection fraction, end systolic dimension
  • Cardiac catheterisation
    • Coronary artery disease
    • Assess severity, LV function, root size
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54
Q

How do you manage aortic regurg?

A
  • Medical
    • Optimise risk factors
    • Follow up with echo
    • Manage systolic hypertension with ACEI, CCBs (decreased afterload -> decreased regurg)
  • Surgical
    • Aortic valve replacement is the definitive therapy
    • Acute severe AR won’t be tolerated for longby a normal ventricle so needs prompt surgery, except in infection where it can be delayed for antibiotic therapy where possible
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55
Q

How is aortic stenosis defined?

A

Normal valve area is >2cm2; severe AS is valve area <1cm2

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56
Q

What are the causes of aortic stenosis?

A
  • Senile calcification (60+)
  • Congenital
    • Bicuspid valve
    • William’s syndrome
    • Rheumatic fever
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57
Q

What are the symptoms of aortic stenosis?

A
  • Triad: angina, dyspnoea, syncope (especially with exercise)
  • LVF: PND, orthopnoea, frothy sputum
  • Sudden death
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58
Q

What are the signs of aortic stenosis?

A
  • Ejection systolic murmur at right 2nd intercostal space, sitting forward in end expiration, radiating to carotids
  • Arrhythmias
  • Slow rising pulse with narrow pulse pressure
  • Aortic thrill
  • Forceful, non displaced apex (pressure overload)
  • Heart sounds: quiet A2, early systolic ejection click if pliable (young) valve, S4 (forceful atrial contraction vs hypertrophied ventricle)
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59
Q

What are the indicators of severe AS?

A
  • Symptoms of syncope or LV failure
  • Signs of LV failure
  • Absent A2
  • Paradoxically split A2
  • Presence of praecordial thrill
  • S4
  • Slow rising pulse with narrow pulse pressure
  • Late peaking of long murmur
  • Valve area >0.5cm on echo
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60
Q

What are the differentials for the aortic stenosis symptoms?

A
  • Coronary artery disease
  • MR
  • Aortic sclerosis
    • Valve thickening - no pressure gradient
    • Turbulence -> murmur
    • ESM with no radiation and normal pulse
  • HOCM
    • ESM murmur which increases in intensity with Valsalva
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61
Q

What are the complications of aortic stenosis?

A
  • Systemic emboli if endocarditis
  • Sudden death
    • Can occur in AS or subvalvular stenosis due to ventricular tachycardia
    • Vulnerability to VT is due to LV hypertrophy
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62
Q

Which investigation findings indicate aortic stenosis?

A
  • ECG:
    • LVH
    • LV strain: tall R, ST depression, T inversion in V4-V6
    • LBBB or complete AV block (septal calcification); may need pacing
  • CXR
    • Calcified AV (especially on lateral films)
    • LVH
    • Evidence of failure
    • Post-stenotic aortic dilatation
  • Echo and doppler: diagnostic
    • Thickened, calcified, immobile valve cusps
    • Severe AS:
      • Pressure gradient >40mmHg
      • Jet velocity >4m/s (or increasing by 0.3m/s in a year)
      • Valve area <1cm2
  • Cardiac catheterisation + angiography
    • Can assess valve gradient and LV function
    • Assess coronaries in all patients planned for surgery
  • Exercise stress test
    • Contraindicated if symptomatic AS
    • May be useful to assess exercise capacity in asymptomatic patients
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63
Q

What is the management for aortic stenosis?

A
  • Medical
    • Optimise risk factors
    • Regular follow up with echo
    • Angina: beta blockers
    • Heart failure: ACEI and diuretics
    • Avoid nitrates
  • Surgical
    • All symptomatic patients should be considered for surgery
      • Mortality rate of surgery is related to the absence or presence of LV failure
      • Poor prognosis if symptomatic: 2-3 years with angina/syncope, 1-2 years with LVF
    • Mechanical or tissue valve
    • For unfit patients:
      • Balloon valvuloplasty (limited in adults as complication rate is high at >10% and restenosis occurs in 6-12 months)
      • Transcatheter aortic valve implantation
    • Strong association with IHD - 50% AS patients have important coronary disease so consider concomitant CABG at the time of valve replacement
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64
Q

What are the indications for valve replacement in aortic stenosis?

A
  • Severe symptomatic AS
  • Severe asymptomatic AS with decreased ejection fraction (<50%)
  • Severe AS undergoing CABG or other valve op
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65
Q

What happens in transcatheter aortic valve implantation (TAVI) and what are the pros/cons?

A
  • Folded valve deployed in aortic root
  • Increased perioperative stroke risk compared to replacement
  • Lower risk of major bleeding
  • Similar survival at 1 year
  • Little long term data
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66
Q

What is the difference between metallic and tissue valves?

A
  • Tissue valves don’t need lifelong anticoagulation; metal do
  • Metal valves are more durable
  • All replacements have a residual transvalvular gradient across them - in mechanical valves this can cause loud murmurs
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67
Q

What are the common kinds of metallic prosthetic valves?

A
  • Ball and cage valve
  • Single tilting disc
  • Bileaflet (most common); has two semi circular leaflets that open, creating a central and two peripheral orifices
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68
Q

What are the common kinds of tissue prosthetic valves?

A
  • Allografts: porcine or bovine three cusp valve
    • 3 months’ anticoagulation sometimes recommended until tissue endothelialisation
    • No need for long term anticoagulation if patient is in sinus rhythm
  • Homografts: usually cadaveric
    • Need no long term anticoagulation
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69
Q

What causes infection of prosthetic valves and what are the complications?

A
  • Within 6 months, usually due to staph epidermis
  • Mortality rate as high as 60% depending on organism
  • Septal abscesses can cause PR interval lengthening
  • Valvular sounds may be muffled by vegetations; new murmurs may occur
  • Mild haemolysis can occur - detected by presence of urobilinogen in the urine
  • Dehiscence is an ominous feature needing urgent intervention
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70
Q

What is the pathology in infective endocarditis?

A

Valves develop vegetations composed of bacteria and platelet-fibrin thrombus

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71
Q

What are the risk factors for infective endocarditis?

A
  • Cardiac disease - subacute
    • Prosthetic valves
    • Degenerative valvulopathy
    • VSD, PDA, CoA
    • Rheumatic fever
  • Normal valves - acute
    • Dental caries
    • Post op wounds
    • IVDU (tricuspid valve)
    • Immunocompromised (including diabetes mellitus)
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72
Q

Which organisms commonly cause infective endocarditis?

A
  • Culture positive
    • Strep viridans (50%)
    • Strep bovis
    • Staph aureus
    • Staph epidermidis
    • Enterococci
    • Pseudomonas
  • Culture negative
    • Haemophilus
    • Actinobacillus
    • Cardiobacterium
    • Eikenella
    • Kingella
    • Coxiella
    • Chlamydia
  • Non infective
    • SLE (Libman Sacks)
    • Marantic (metastatic related)
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73
Q

What are the clinical features of infective endocarditis?

A
  • Sepsis
    • Fever, rigors, night sweats
    • Weight loss
    • Anaemia, splenomegaly
    • Clubbing (late sign)
  • Cardiac
    • New/changing murmur: MR in 85%, AR in 55%
    • AV block
    • LVF
  • Embolic phenomena
    • Abscesses in brain, heart, kidney, splene, gut and lung (if right sided)
    • Janeway lesions (non painful)
  • Immune complex deposition
    • Microscopic haematuria due to glomerulonephritis
    • Vasculitis
    • Roth spots (retinopathy)
    • Splinter haemorrhages
    • Osler’s nodes (painful)
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74
Q

How do you diagnose infective endocarditis?

A

Duke’s criteria: diagnose if 2 major, or 1 major and 3 minor, or all 5 minor:

  • Major:
    • Positive blood culture
      • Typical organism in 2 separate cultures or
      • Persistently positive cultures e.g. 3 >12 hours apart
    • Endocardium involved
      • Positive echo: vegetation, abscess, valve dehiscence or
      • New valvular regurgitation
  • Minor
    • Predisposition: cardiac lesion, IVDU
    • Fever >38
    • Emboli: septic infarcts, splinters, Janeway lesions
    • Immune phenomea: glomerulonephritis, Osler nodes, Roth spots, rheumatic fever
    • Positive blood culture not meeting major criteria
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75
Q

What are the poor prognostic factors in infective endocarditis?

A
  • Prosthetic valve
  • Staph aureus infection
  • Culture negative endocarditis
  • Depletion of complement levels
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76
Q

What investigations should you do in infective endocarditis and what will they find?

A
  • Bloods:
    • Normochromic, normocytic anaemia
    • Raised ESR and CRP
    • ± Positive IgG for rheumatic fever
    • Cultures x3, >12 hours apart
    • Serology for unusual organisms
  • Urine: microscopic haematuria
  • ECG: AV block
  • Echo:
    • TTE detects vegetations >2mm
    • TOE is more sensitive (90-100% vs 50-60%)
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77
Q

How do you manage infective endocarditis?

A
  • Aim to sterilise the valve medically (4-6 weeks IV Abx) then assess whether needs replacement
  • Medical:
    • Empiric:
      • Acute severe: fluclox and gent IV
      • Subacute: benpen and gent IV
    • Streps: benpen and gent IV
    • Enterococci: amox and gent IV
    • Staphs: fluclox ± rifampicin IV
    • Fungi: flucytosine IV and fluconazole PO
      • Amphotericin if flucytosine resistance or aspergillus
  • Surgical
    • Earlier operations only if clinically necessary - outcomes are poorer
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78
Q

What are the indications for surgery in infective endocarditis?

A
  • Cardiac failure or haemodynamic compromise
  • Extensive valve incompetence
  • Large vegetations
  • Septic emboli
  • Septal abscess
  • Fungal infection
  • Antibiotic resistant endocarditis
  • Failure to respond to medical therapy
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79
Q

What is the prognosis in infective endocarditis?

A
  • 30% staphs
  • 14% bowel flora
  • 6% sensitive streps
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80
Q

What are the causes of acyanotic congenital heart disease?

A
  • WIth shunts:
    • Aortic coarctation (with VSD or PDA)
    • VSD
    • ASD
    • PDA
    • Partial anomalous venous drainage (with ASD)
  • Without shunts:
    • Congenital AS
    • Aortic coarctation
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81
Q

What are the causes of cyanotic congenital heart disease?

A
  • With shunts:
    • Tetralogy of Fallot (VSD)
    • Severe Ebstein’s anomaly (ASD)
    • Complete transposition of the great vessels (ASD, VSD/PDA)
  • Without shunts:
    • Tricuspid atresia
    • Severe pulmonary stenosis
    • Pulmonary atresia
    • Hypoplastic left heart
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82
Q

What is the pathophysiology of atrial septal defect?

A
  • Most common congenital defect found in adulthood
  • Defective or absent interatrial septum, allowing mixing of oxygenated and deoxygenated blood and shunting at the atrial level
  • Size of shunting and reduction in oxygenation depends on size of defect
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83
Q

What are the types of atrial septal defect?

A
  • Secundum (70%): central fossa ovalis defects
  • Primum (15%): sited above the AV valves
  • Sinus venosus (15%): defect in the upper septum
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84
Q

What are the clinical features of atrial septal defect?

A
  • Symptoms:
    • Dyspnoea
    • Pulmonary hypertension (fatigue etc)
    • Arrhythmia
    • Chest pain
  • Signs
    • AF
    • Raised JVP
    • Pulmonary ejection systolic murmur
    • Pulmonary hypertension leads to tricuspid regurgitation or pulmonary regurgitation
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85
Q

What are the complications of atrial septal defect?

A
  • Paradoxical emboli
  • Eisenmenger’s syndrome
    • Increased RA pressure causes a right to left shunt and cyanosis
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86
Q

Which investigation findings indicate atrial septal defect?

A
  • CXR: pulmonary plethora
  • ECG: secundum - RAD
  • Echo
    • Paradoxical septal motion
    • Septal defect
    • Right to left flow of contrast during venous injection with Valsalva’s manoeuvre
  • Catheter
    • Pulmonary hypertension
    • Raised RV pressures and steup up in oxygen saturation between various parts of the right circulation e.g. SVC to high right atrium
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87
Q

How do you manage atrial septal defect?

A

Transcatheter closure, indicated if:

  • Symptoms (dyspnoea)
  • Systemic embolism (typically stroke)
  • Chamber dilatation
  • Elevated right heart pressures
  • Significant L to R shunt
88
Q

What are teh features of bicuspid aortic valve?

A

No problems at birth but most eventually get stenosis ± regurg. Presisposes to IE/SBE

89
Q

What is the defect in coarctation of the aorta?

A

Severe narrowing of the aorta, usually just distal to the origin of the left subclavian

90
Q

What are the associations with coarctation of the aorta?

A
  • M>F
  • Cardiac
    • Bicuspid aortic valve (and thus AS±AR) in 10-20%
    • PDA
    • VSD
    • Mitral valve disease
  • Non-cardiac
    • Berry aneurysms in the Circle of Willis
    • Turner’s syndrome
    • Renal abnormalities
91
Q

What are the signs of coarctation of the aorta?

A
  • Hypertension
  • Radiofemoral delay of arterial pulse
  • Absent femoral pulses
  • Mid-systolic or continuous murmur (infraclavicular)
  • Subscapular bruits
92
Q

What are the complications of coarctation of the aorta?

A

Heart failure, infective endocarditis

93
Q

Which investigations are consistent with coarctation of the aorta?

A
  • CXR: rib notching, psot-stenotic aortic dilatation
  • ECG: LV strain
  • CT angio
94
Q

How do you manage coarctation of the aorta?

A
  • Balloon dilatation and stenting
  • Surgical or percutaneous
95
Q

What is the defect in ventricular septal defect and what causes it?

A
  • Hole connects the two ventricles
  • Most defects are small and just need observing
  • Most common isolated congenital heart defect
  • Spontaneous closure more common in muscular defects
  • Congenital or can occur post-MI
96
Q

What are the features of ventricular septal defect?

A
  • Severe heart failure in infancy OR incidental discovery in later life
  • Large defects allow significant left to right shunt, causing elevated right heart pressures and consequent pulmonary hypertension
  • Small holes which are haemodynamically less significant -> louder murmurs
    • Harsh, pansystolic murmur at the left sternal edge
    • Systolic thrill
    • Left parasternal heave
  • Other cardiac associations
    • PDA (10%)
    • AR (5%)
    • PUlmonary stenosis
    • ASD
    • Tetralogy of Fallot
    • Coarctation of the aorta
97
Q

What complications are associated with VSD?

A
  • Infective endocarditis
  • Pulmonary hypertension
  • Eisenmenger’s
98
Q

What investigations should you do in VSD?

A
  • ECG:
    • Small: normal
    • Large: LVH + RVH
  • CXR:
    • Small: mild pulmonary plethora
    • Large: cardiomegaly + marked pulmonary plethora
99
Q

How do you manage VSD?

A

Surgical or percutaneous closure if:

  • Significant L-R shunt
  • Associated with other defect requiring cardiotomy
  • Elevated R heart pressure causing pulmonary hypertension
  • Endocarditis
  • Membranous VSD causing AR
100
Q

In whom is PDA common?

A
  • Premature babies
  • Female infants born at high altitude
  • Maternal rubella
101
Q

What is the defect in PDA?

A

Connection between pulmonary trunk and descending aorta, usually just distal to origin of left subclavian

102
Q

What are the features of PDA?

A
  • Left subclavicular thrill
  • Enlarged left heart and apical heave
  • Continuous ‘machinery’ murmur
  • Wide pulse pressure and bounding pulse
103
Q

How do you manage PDA?

A
  • Indometacin closes the duct in about 90%
  • Prostaglandin may be needed to reverse closure e.g. when associated with coarctation, hypoplastic left heart, or transposition
  • Can be closed thoracoscopically or percutaneously
104
Q

What is Eisenmenger’s syndrome?

A

Any untreated congenital cardiac defect with intracardiac communication that leads to severe irreversible pulmonary hypertension, reversal of L to R shunts and cyanosis

105
Q

What is the pathophysiology in Eisenmenger’s?

A

Long standing L to R shunts e.g. large VSDs, ASDs, PDAs cause remodelling of pulmonary microvasculature, with raised pressures: this causes shunts to reverse, sending deoxygenated blood into the systemic circulation evident as cyanosis

106
Q

What are the signs of Eisenmenger’s?

A
  • Clubbing and central cyanosis
  • Decrease or original pansystolic (left to right) murmur
  • Decreasing intensity of tricuspid/pulmonary flow murmurs
  • Single S2 with loduer intensity, palpable P2; right ventricular heave
  • Appearance of Graham Steell murmur due to pulmonary regurgitation
  • Pansystolic murmur and v waves due to TR
107
Q

What are the complications of Eisenmenger’s?

A
  • RV failure
  • Massive haemoptysis
  • Cerebral embolism/abscess
  • Infective endocarditis (rare)
108
Q

What is the defect in tetralogy of Fallot and how common is it?

A
  • Commonest congenital cyanotic heart defect
  • Abnormal separation of truncus arteriosus into aorta and pulmonary arteries
109
Q

Which syndrome is Tetralogy of Fallot associated with?

A

Di George

110
Q

What are the features of tetralogy of Fallot?

A
  1. VSD
  2. Pulmonary stenosis
  3. RV hypertrophy
  4. Overriding aorta
    • 25% have right sided aortic knuckle
111
Q

What are the clinical features of tetralogy of fallot?

A
  • Presentation:
    • Infants: hypercyanotic episodes, squatting, clubbing
    • Adults:
      • Often asympto
      • Unoperated: cyanosis, ESM of PS
      • Repaired: dyspnoea, palpitations, RVF
  • Cyanotic attacks (pulmonary infundibular spasm)
  • Clubbing
  • Parasternal heave
  • Systolic thrill
  • Palpable A2
  • Soft ejection systolic murmur (inversely related to pulmonary gradient)
  • Single S2 (inadudible pulmonary closure)
  • ECG features of RV hypertrophy
112
Q

What investigations should you do in tetralogy of Fallot?

A
  • ECG: RVH + RBBB
  • CXR: Coeur en sabot
  • Echo: anatomy and degree of stenosis
113
Q

What are the possible complications of tetralogy of fallot?

A
  • Endocarditis
  • Polycythaemia
  • Coagulopathy
  • Paradoxical embolism
  • Cerebral abscess
  • Ventricular arrhythmias
114
Q

How do you treat tetralogy of fallot?

A
  • Surgical (usually before 1 year)
  • Closure of VSD
  • Correctionof pulmonary stenosis
  • Blalock-Taussig shunt (traditional palliative procedure) results in weaker pulses in the arm from which the subclavian artery is diverted to the pulmonary artery
115
Q

Which leads and vessel represent the inferior aspect of the heart?

A

Leads II, III, aVF

RCA

116
Q

Which leads and vessel represent the anterolateral aspect of the heart?

A

Leads: I, aVL, V5+V6

L circumflex

117
Q

Which leads and vessel represent the anteroseptal aspect of the heart?

A

leads V2-V4

LAD

118
Q

Which leads and vessel represent the anterior aspect of the heart?

A

Leads V2-V6

Left main stem

119
Q

Which leads and vessel represent the posterior aspect of the heart?

A

Leads V1, V2, V3 (recip)

RCA

120
Q

What is the rate of an ECG?

A

300/number of large squares

121
Q

What features are you looking for in the rhythm of an ECG?

A
  • P waves followed by QRS
  • AF: no discernable P waves, irregularly irregular QRS
  • Atrial flutter: saw tooth baseline
  • Nodal rhythm: regular QRS but no P waves
122
Q

How do you determine the axis of an ECG and what does it tell you?

A
  • I and II positive = normal axis
  • I positive and II negative (leaving) = LAD (-30 to -90)
    • Inferior MI
    • LVH
    • Left anterior hemiblock WPW
    • ASD primum
  • I negative and II positive (reaching) = RAD (+90 to +180)
    • Anterolateral MI
    • RVH
    • PE
    • Left posterior hemiblock WPW
    • ASD secundum
123
Q

What can you tell from the P waves in an ECG?

A
  • Absent: AF, SAN block, nodal rhythm
  • Dissociated: complete heart block
  • P mitrale: bifid P waves = LA hypertrophy
    • HTN, AS, MR, MS
  • P pulmonale: peaked P waves = RA hypertrophy
    • Pulmonary hypertension, COPD
124
Q

What can you tell from the QRS complex in an ECG?

A
  • Wide QRS (>120ms)
    • Ventricular initiation
    • Conduction defect
    • WPW
  • Pathological Q wave
    • >1mm wide and >2mm deep
    • Full thickness MI
  • RVH: dominant R wave in V1 and deep S wave in V6
  • LVH
    • R wave in V6>25mm
    • R wave in V5/V6 and S wave in V1 >35mm
125
Q

What can you tell from the PR interval in an ECG?

A
  • 120-200ms
  • STart of P wave to start of QRS
  • Long: heart block
  • Short:
    • Accessory conduction e.g. WPW
    • Nodal rhythm
    • HOCM
  • Depressed: pericarditis
126
Q

What can you tell from the QTc interval in an ECG?

A
  • 380-420ms
  • Start of QRS to end of T wave
  • Bazett’s formula: QTc = actual QT/root of R-R
  • Long (>420ms)
  • Short (<380ms)
127
Q

What are the causes of a prolonged QTc?

A

TIIMME:

  • Toxins
    • Macrolides
    • Anti arrhythmics: quinidine, amiodarone
    • TCAs
    • Histamine antagonists
  • Inherited: Romano-Ward, Jervell
  • Ischaemia
  • Myocarditis
  • Mitral valve prolapse
  • Electrolytes: low magnesium/potassium/calcium/temperature
128
Q

What are the causes of a short QTc?

A

Digoxin, beta blockers, phenytoin

129
Q

What are the causes of elevated and depressed ST segments?

A
  • Elevated: limbs >1mm, chest >2mm
    • Acute MI
    • Prinzmetal’s angina
    • Pericarditis: saddle shaped
    • Aneurysm: ventricular
  • Depressed: <0.5mm
    • Ischaemia: flat
    • Digoxin: down sloping
130
Q

When is T wave inversion abnormal?

A

Normal if inverted in aVR and V1, or V2-V3 as well in black people.

Abnormal if inverted in: I, II and V4-V6

131
Q

What are the causes of T wave inversion?

A
  • Strain
  • Ischaemia
  • Ventricular hypertrophy
  • BBB
  • Digoxin
  • Peaked in hyperkalaemia, flattened in hypokalaemia
132
Q

What are U waves and when are they seen on ECG?

A
  • After T wave
  • Hypokalaemia
133
Q

What are J/osborne waves and when are they seen on ECG?

A
  • Between QRS and ST segment
  • Causes:
    • Hypothermia <32 degrees
    • SAH
    • Hypercalcaemia
134
Q

How is 1st degree heart block defined on ECG?

A

PR >200ms

135
Q

How is 2nd degree heart block defined on ECG?

A
  • Wenckebach/mobitz I
    • Progressive lengthening of PR interval
    • One non-conducted P wave
    • Next conducted beat has a shorter PR interval
  • Mobitz II
    • Constant PR
    • Occasional non conducted P waves
    • Often wide QRS: block is usually in bundle branches of Purkinje fibres
  • 2:1 block:
    • Two P waves per QRS
    • Normal consistent PR intervals
136
Q

How is 3rd degree heart block defined on ECG?

A
  • P waves and QRS @ different rates - dissociation
  • Abnormally shaped QRS - ventricular origin (40bpm)
137
Q

How does right BBB appear on ECG and what are the causes?

A
  • Wide WRS and RSR pattern in V1
  • Causes:
    • Infarct - inferior MI
    • Normal variant
    • Congenital: ASD, VSD, Fallot’s
    • Hypertrophy - RVH (PE, cor pulmonale)
138
Q

How does left BBB appear on ECG and what are the causes?

A
  • Wide QRS with notched top
  • T wave inversion in lateral leads
  • Causes:
    • Fibrosis
    • LVH: AS, HTN
    • Infarct: inferior MI
    • Coronary HD
139
Q

How do bifascular and trifascicular blocks appear on ECG?

A
  • Bifascicular: RBBB + LAD
  • Trifascicular: RBBB + LAFB + 1st degree AV block
140
Q

How does an atrial escape appear on ECG?

A
  • SAN fails to depolarise
  • Abnormal P wave
  • Normal QRS
  • Rate 60-80bpm
141
Q

How does a junctional escape appear on ECG?

A
  • Usually no P waves (occasionally after QRS)
  • Normal QRS
  • 40-60bpm
142
Q

How does a ventricular escape appear on ECG?

A
  • Usually result of complete AV block therefore regular P waves are seen
  • May be SAN failure and therefore no P waves
  • Wide QRS
  • 20bpm
143
Q

How do you discern between the different kinds of extrasystole on ECG?

A
  • Atrial
    • Abnormal P wave, normal QRS
  • Nodal
    • P wave buried in QRS or sometimes immediately before/after QRS - may be negative
    • Normal QRS
  • Ventricular
    • No P wave
    • Wide QRS and abnormal T wave
144
Q

What are the kinds of narrow complex tachycardia and how do you distinguish between them on ECG?

A
  • AVNRT
    • P wave absent or immediately before/after QRS with normal QRS
  • AVRT
    • P waves usually visible between QRS, which may be narrow or wide, accessory conduction bundle
  • Atrial tachy
    • Abnormally shaped P waves, normal QRS, rate >150bpm, may be associated with AV block
  • Atrial flutter
    • Saw toothed baseline as atria contract at 300bpm; AVN can’t conduct >200bpm therefore AV block occurs e.g. 2:1 (15), QRS is normal
  • Atrial fib
    • No P waves - irregular line
    • Irregularly irregular QRS
145
Q

What are the ECG features of VT?

A

No P waves, regular, wide QRS, no T waves

146
Q

When is VT more likely if you’re considering if it’s VT or SVT with BBB?

A
  • History of recent infarction
  • Atrioventricular dissociation
  • Broad QRS complexes (>140ms)
  • Concordant QRS direction in V1-V6
  • Fusion and capture beats
147
Q

What’s the difference between P mitrale and P pulmonale?

A
  • P pulmonale - peaked P wave
    • RAH - pulmonary hypertension, tricuspid stenosis
  • P mitrale - broad, bifid P wave
    • LAH - mitral stenosis
148
Q

Which ECG features indicate RVH?

A
  • Tall R wave in V1
  • Deep S wave in V6
  • RAD
  • Normal QRS width
  • May be T Wave inversion in V1-V3
149
Q

Which ECG features indicate LVH?

A
  • S in V1 and R in V6 >35mm and/or R wave in V6>25mm
  • May be LAD
  • May be T wave inversion in II, aVL, V5, V6
150
Q

What are the ECG features of WPW?

A
  • Accessory conducting bundle
  • Short PR interval
  • Slurred upstroke of QRS called a delta wave (V3/4)
  • Can establish a re entrant circuit -> SVT (antidromic AVRT)
  • AF + WPW -> irregularly irregular broad QRS complexes
151
Q

What are the ECG features of Brugada syndrome?

A

RBBB, ST elevation in V1-3

152
Q

What are the ECG features of digoxin toxicity?

A

Reverse tick: down sloping ST depression, T wave inversion

153
Q

What are the ECG features of PE?

A
  • S1Q3T3
    • Deep S wave in I (RAD)
    • Pathological Q in 3
    • T wave inversion in 3
  • Right ventricular strain
    • RAD (S wave in I)
    • Dominant R wave and T wave inversion in V1-V3
154
Q

What are the ECG features of hyperkalaemia?

A
  • Tall tented T Waves
  • Widened QRS
  • Absent P waves
  • Sine wave appearance
155
Q

What are the ECG features of hypokalaemia?

A
  • Small t waves
  • ST depression
  • Prolonged QT interval
  • Prominent U waves
156
Q

What’s the difference between bradycardia and bradyarrhythmia?

A

Bradycardia is rate <60bpm.

Bradyarrhythmia is a pathological bradycardia

157
Q

What are the causes of bradyarrhythmias?

A

DIVISIONS:

  • Drugs:
    • Antiarrhythmics (type 1a, amiodarone)
    • Beta blockers
    • CCBs (verapamil)
    • Digoxin
  • Ischaemia/infarction (inferior MI)
  • Vagal hypertonia
    • Athletes
    • Vasovagal syncope
    • Carotid sinus syndrome
  • Infection
    • Viral myocarditis
    • Rheumatic fever
    • Infective endocarditis
  • Sick sinus syndrome
  • Infiltration: restrictive/dilated cardiomyopathy
    • Autoimmune
    • Sarcoid
    • Haemochromatosis
    • Amyloid
    • Muscular dystrophy
  • O
    • HypOthyroidism
    • HypOkalaemia (or hyperkalaemia)
    • HypOthermia
  • Neuro: Raised ICP
  • S
    • Septal defect (primum ASD)
    • Surgery or catheterisation
      *
158
Q

How does sick sinus syndrome present and how do you treat it?

A

Presents with SVT alternating with either sinus bradycardia ± arrest or SA/AV block

159
Q

How do you classify bradycardia?

A
  • Sinus
  • 1st degree AV block
    • PR interval>200ms is abnormal
  • 2nd degree heart block
    • Wenckebach/mobitz I
      • Progressive prolongation and then block of the PR interval
      • Can be normal in young, fit people
    • Mobitz II
      • More than one P wave per QRS
  • Complete heart block
    • AV dissociation
    • Junctional: narrow QRS ~50bpm
    • Ventricular: broad QRS ~40bpm
160
Q

What are the indications for pacing first degree AV block?

A

If with LBBB, RBBB with axis deviation or alternating LBBB + RBBB with syncope

161
Q

How do you manage bradycardia?

A
  • Asymptomatic and rate >40: no treatment needed
  • Urgent/rate <40
    • Treat underlying cause e.g. drugs, MI
    • Medical:
      • Atropine 0.6-1.2g (max 3g) IV
      • Isoprenaline IVI
    • Pacing: external
  • Elective: permanent pacing
    • Mobitz type II
    • Complete AV block
    • Sick sinus
    • AF
    • Drug resistant tachyarrhythmias
162
Q

What defines a narrow complex tachycardia?

A

Rate >100, QRS width <120ms

163
Q

What are the differentials for a narrow complex tachycardia?

A
  • Sinus
  • Atrial:
    • AF
    • Atrial flutter
    • Atrial tachy
  • AVNRT
    • Re entry circuit in and around the AV node
  • AVRT
    • Accessory pathway between teh atria and ventricles some distance from the AV node e.g. WPW and related
164
Q

What are the principles of managing SVT?

A
  • If compromised, sedate and DC cardiovert
  • Otherwise ID rhythm and treat accordingly
    • If AF, need to identify it as treatment is different
  • Vagal manoeuvres transiently increase AV block so may unmask underlying atrial rhythm
    • Carotid sinus massage
    • Valsalva
  • If unsuccessful, give adenosine while recording rhythm strip
    • Transient AV block, unmasking atrial rhythm
    • Cardioverts AVNRT/AVRT to sinus rhythm
  • If adenosine fails, choose from:
    • Digoxin
    • Atenolol
    • Verapamil (not if on beta blocker)
    • Amiodarone
  • If unsuccessful, DC cardiovert
165
Q

How much adenosine do you give for SVT?

A

6mg IV bolus, then 12mg, then 12mg

166
Q

What are the side effects, contraindications and interactions of adenosine in SVT?

A
  • Side effects: transient chest tightness, dyspnoea, flushing, headache
  • Relative contraindications: asthma, 2nd/3rd degree block
  • Interactions:
    • Increased by dipyridimole
    • Decreased by theophylline
167
Q

What prophylaxis can you give against SVT?

A
  • Beta blockers
  • AVRT: flecainide
  • AVNRT: verapamil
168
Q

What are the differentials for a broad complex tachy?

A
  • Ventricular tachycardia
  • Torsades de points
  • SVT with BBB
169
Q

What are the causes of VT?

A

I’M QVICK:

  • Infarction (especially with ventricular aneurysm)
  • Myocarditis
  • QT interval increased
  • Valve abnormality: mitral prolapse, AS
  • Iatrogenic: digoxin, antiarrhythmics, catheter
  • Cardiomyopathy (especially dilated)
  • K (hypokalaemia), hypomagnesaemia, hypoxia, acidosis
170
Q

How do you manage broad complex tachy?

A
  • O2 + IV access
  • Adverse signs (BP<90, HF, chest pain, reduced GCS, HR>150): sedate, synchronised cardiovert (200-300-360), then amiodarone:
    • 300mg over 20-60 mins
    • Then 900mg over the next 23h
  • If no, correct electrolyte problems (K/Mg)
    • K: max 60mM KCl at 20mmol/h
    • Mg: 4ml 50% MgSO4 in 30 mins
  • Then assess rhythm:
    • Regular (i.e. VT): amiodarone as above, or lignocaine 50mg over 2 mins
    • If irregular, diagnosis is usually:
      • AF with BBB
      • Pre excited AF: flec/amio
      • TDP: MgSO4 2g IV over 10 min
  • If failure, synchronised cardioversion
171
Q

How do you treat recurrent/paroxysmal VT?

A

Amiodarone, beta blockers, ICD

172
Q

What is the pathophysiology in AF?

A

Multiple wavelet propagation in different directions, which can be from myocardial tissues in the openings of the four pulmonary veins, which enter into the posterior aspect of the LA (particularly in younger patients with paroxysmal AF)

173
Q

What are the causes of AF?

A
  • Common:
    • IHD
    • Rheumatic heart disease
    • Thyrotoxicosis
    • Hypertension
  • Uncommon:
    • Alcohol: acute alcohol excess or chronic alcoholic cardiomyopathy
    • Pneumonia
    • PE
    • Post op (post CABG)
    • Hypokalaemia
    • RA
    • Pericarditis
    • Mitral valve disease
    • Atrial myxomas
    • LVH
    • ASD
    • Caffeine excess
    • Dilated LA >4.5cm
    • WPW
    • Bronchial malignancy
174
Q

What are the symptoms of AF?

A
  • Asymptomatic
  • Chest pain
  • Palpitations
  • Dyspnoea
  • Faintness
175
Q

What are the signs of AF?

A
  • Irregularly irregular pulse
  • Pulse deficit: difference between pulse and HS
    • Fast AF -> loss of diastolic filling -> no palpable pulse
  • Signs of LVF
176
Q

What are the risk factors for stroke with non valvular AF?

A
  • Previous history of CVA or TIA
  • Diabetes
  • HTN
  • Heart failure
177
Q

What are the risk factors for recurrence of AF after cardioversion?

A
  • Long duration (>1-3 years)
  • Rheumatic mitral valve disease
  • LA size >5.5cm
  • Older age (>75 years)
  • LV impairment
178
Q

How do you manage acute AF (≤48h)?

A
  • Haemodynamically unstable -> emergency cardioversion
    • 2nd line: IV amiodarone
  • Control ventricular rate
    • 1st line: diltiazem or verapamil or metoprolol
    • 2nd line: digoxin or amiodarone
  • Start LMWH
  • Cardioversion: only if acute AF <48
    • Electrical cardioversion or pharmacological
      • 1st line: flecainide (if no structural heart disease)
      • 2nd line: amiodarone
    • Long term anticoagulation not needed if sinus rhythm restored, no risk factors, and low recurrence risk
179
Q

How do you manage paroxysmal AF?

A
  • Self limiting, <7 days, recurs
  • Anticoagulate according to chadsvasc score
  • Pill in pocket - flecainide, propafenone
  • Prevention: beta blockers, sotalol, or amiodarone
180
Q

How do you manage persistent AF?

A
  • >7 days, may recur after cardioversion
  • Try rhythm control first line if:
    • Symptomatic or CCF
    • Younger (<65)
    • Presenting first time with lone AF
    • Secondary to treated precipitant
  • Rhythm control
    • TTE first to look for structural abnormalities
    • Warfarin for ≥3 weeks, or TOE to exclude intracardiac thrombus
    • PRe treat ≥4 weeks with sotalol or amiodarone if high risk of failure
    • Electrical or pharmacological cardioversion
    • ≥4 weeks anticoagulation after (target INR 2.5)
    • Maintenance anti arrhythmic
      • Not needed if successfully treated precipitant
      • 1st line: beta blocker (e.g. bisoprolol, metoprolol)
      • 2nd line: amiodarone
    • Other otpions:
      • Radiofrequency ablation of AV node
      • Maze procedure
      • Pacing
  • Rate control (target <90 bpm at rest)
    • 1st line: beta blocker or rate limiting CCB (not both)
    • 2nd line: add digoxin (don’t use as monotherapy)
    • 3rd line: consider amiodarone
181
Q

How do you manage permanent AF?

A
  • Failed cardioversion/unlikely to succeed
    • AF for >1 year, valve disease, poor LV function
  • Patient doesn’t want cardioversion
  • Rate control
182
Q

How do you manage atrial flutter?

A
  • As for AF
  • Anti AF drugs may not work but try
    • Amiodarone to restore sinus
    • Amiodarone or sotalol to maintain it
  • Cavotricuspid isthmus ablation is treatment of choice
183
Q

How does the chadsvasc score work?

A
  • Risk factors:
    • CCF
    • Hypertension
    • Age ≥75 (2 points)
    • Age 65-74
    • DM
    • Stroke/TIA/thromboembolism (2 points)
    • Vascular disease
    • Female gender
  • Scoring:
    • 0 - aspirin 300mg
    • ≥1: warfarin
  • Warfarin contraindicated in AF if bleeding diathesis, low platelets, BP>160/90
  • Can give NOACs
184
Q

What are the features of silent MI?

A
  • Elderly/diabetics
  • Syncope
  • Delirium
  • Post op oliguria/hypotension
185
Q

What are the ECG features of MI?

A
  • STEMI:
    • ST elevation and hyperacute (tall) T waves
    • Q waves: full thickness infarct
    • Normalisation of ST segments
    • T wave inversion
    • New onset LBBB also = STEMI
  • NSTEMI
    • ST depression
    • T wave inversion
  • No Q waves = subendocardial infarct
186
Q

What is troponin T/I and what is their significance?

A
  • Myofibrillar proteins linking actin and myosin
  • Elevated from 3-12h - need a 12 hour trop to exclude MI
  • Peak 24h
  • Baseline from 5d-14d
187
Q

What are the CXR features of MI?

A
  • Cardiomegaly
  • Pulmonary oedema
  • Widened mediastinum: aortic rupture
188
Q

Which conditions cause a troponin leak?

A
  • Critical illness - ICU/sepsis
  • Hypotension
  • Hypertensive crisis/pre eclampsia
  • Pulmonary embolism
  • Infective exacerbations of COPD
  • Ruptured AAA
  • GI bleeding
  • Chemotherapy: some directly cardiotoxic
  • Renal impairment
  • Neuro conditions: stroke, SAH, seizures
189
Q

How do you diagnose STEMI/NSTEMI/UA?

A
  • STEMI/LBBB: typical symptoms + ST elevation (/LBBB)
  • NSEMI: typical symptoms + no ST elevation + positive trop
  • UA: typical symptoms + no ST elevation + negative trop
190
Q

How do you manage MI?

A
  • STEMI: PCI or thrombolysis
  • NSTEMI/UA: medical treatment + elective angio ± PCI/CABG
191
Q

What is the prognosis in MI?

A
  • STEMI: 30 day mortality ~15%
  • NSTEMI: overall mortality 1-2%
192
Q

What are the complications of MI?

A
  • Death: VF, LVF, CVA
  • Pump failure
  • Pericarditis
  • Rupture: myomalacia cordis
  • Arrhythmias
    • Tachycardias: SVT, AF or flutter
    • Ventricular
      • Frequent premature ventricular contraction common after acute MI - no treatment
      • Sustained VT
      • VF
    • Bradycardias
      • Sinus brady (especially inferior MI)
      • AV block
      • Ventricular brady
  • Aneurysm: ventricular
  • Embolism
  • Dressler’s syndrome: pleuro-pericarditis
193
Q

How do you manage STEMI?

A
  • O2 2-4L aim for 94-98% SpO2
  • IV access bloods for FBC, U+E, glucose, lipids
  • Assess
  • Aspirin 300mg PO (then 75mg/d)
  • Clopidogrel 300mg PO (then 75mg/d)
  • Morphine 5-10mg IV
  • Metoclopramide 10mg IV
  • GTN 2 puffs or 1 tablet SL
  • Atenolol 5mg IV (CI: asthma, LVF)
  • LMWH: e.g. enoxaparin IV then SC
  • Admit to CCU
  • Primary PCI or thrombolysis
194
Q

What are the ECG criteria for thrombolysis in STEMI?

A
  • ST elevation >1mm in 2+ limbs or >2mm in 2+ chest leads
  • New LBBB
  • Posterior: deep ST depression and tall R waves in V1-V3
195
Q

What are the contraindications to thrombolysis in STEMI?

A
  • Aortic dissection
  • GI bleeding
  • Allergic reaction previously
  • Iatrogenic: recent surgery
  • Neuro: cerebral neoplasm or CVA history
  • Severe hypertension (200/120)
  • Trauma including CPR
196
Q

Which agents are given for thrombolysis in STEMI?

A

Streptokinase, alteplase, tenecteplase

197
Q

How do you manage NSTEMI?

A
  • O2
  • IV access, bloods, trop
  • Aspirin 300mg PO (then 75mg/d)
  • Clopidogrel 300mg PO
  • Fondaparinux 2.5mg SC
  • Morphine 5-10mg IV
  • Metoclopramide 10mg IV
  • GTN: 2 puffs or 1 tablet SL
  • Beta blockers: atenolol 50mg/24h PO
  • IV GTNif pain continues
  • Assess cardio risk
    • Intermediate/high risk: HPIIb/IIIa antagonist (tirofiban), angio ± PCI in 96hrs, clopidogrel 75mg/d for 1 year
    • Low risk: discharge if 12h trop negative, outpatient tests
198
Q

What are the types of angina?

A
  • Stable: induced by effort
  • Unstable: happens at rest/minimal exertion
  • Decubitus: induced by lying down
  • Prinzmetal’s/variant: occurs during rest due to coronary spasm
  • Syndrome X: angina pain and ST elevation on exercise test but no evidence of coronary atherosclerosis
  • Vincent’s - not cardiac - infection of the pharyngeal and tonsillar space
199
Q

What are the indications for CABG in angina?

A
  • Left main stem disease
  • Triple vessel disease
  • Refractory angina
  • Unsuccessful angio
200
Q

What are the complications of CABG?

A
  • MI
  • Stroke
  • Pericaridal tamponade or haemothorax
  • Postperfusion syndrome
  • Post op AF
  • Nonunion of sternum
  • Graft stenosis
201
Q

What is the pathophysiology of heart failure?

A
  • Reduced CO initially compensated for
    • Starling effect: dilates heart to enhance contractility
    • Remodelling -> hypertrophy
    • RAS and ANP/BNP release
    • Sympathetic activation
  • Progressive decrease in CO leads to decompensation
    • Progressive dilatation leads to impaired contractility and functional valve regurg
    • Hypertrophy causes relative myocardial ischaemia
    • RAS activation leads to sodium and fluid retention, increased venous pressure, oedema
    • Sympathetic excess increases afterload, decreasing CO
202
Q

What are the causes of low output heart failure?

A
  • CO decreases and fails to increase with exertion
  • Pump fialure
    • Systolic failure - impaired contraction
      • Ischaemia/MI (commonest)
      • Dilated cardiomyopathy
      • Hypertension
      • Myocarditis
    • Diastolic failure - impaired filling
      • Pericardial effusion/tamponade/constriction
      • Cardiomyopathy: restrictive, hypertrophic
    • Arrhythmias
      • Bradycardia, heart block
      • Tachycardias
      • Anti-arrhythmics e.g. beta blocker, verapamil
  • Excessive pre load
    • AR, MR
    • Fluid overload
  • Excessive afterload
    • AS
    • HTN
    • HOCM
203
Q

What are the causes of high output heart failure?

A
  • Increased needs cause RVF initially, then LVF
  • Anaemia
  • AVM
  • Thyrotoxicosis
  • Thiamine deficiency (beri beri)
  • Pregnancy
  • Paget’s
204
Q

What are the causes of RV failure?

A
  • LVF
  • Cor pulmonale
  • Tricuspid and pulmonary valve disease
205
Q

What are the clinical features of RV failure?

A
  • Symptoms:
    • Anorexia and nausea
  • Signs:
    • Raised JVP and jugular venous distension
    • Tender smooth hepatomegaly (may be pulsatile)
    • Pitting oedema
    • Ascites
206
Q

What are the causes of LV failure?

A
  • IHD
  • Idiopathic dilated cardiomyopathy
  • Systemic hypertension
  • Mitral and aortic valve disease
  • Specific cardiomyopathies
207
Q

What are the clinical features of LV failure?

A
  • Symptoms:
    • Fatigue
    • Exertional dyspnoea
    • Orthopnoea and PND
    • Nocturnal cough ± pink frothy sputum
    • Weight loss and muscle wasting
  • Signs
    • Cold peripheries ± cyanosis
    • Often in AF
    • Cardiomegaly with displaced apex
    • S3 + tachycardia = gallop rhythm
    • Wheeze (cardiac asthma)
    • Bibasal creps
208
Q

How do you diagnose heart failure?

A

Framingham criteria: 2 major or 1 major and 2 minor:

  • Major:
    • PND
    • Positive abdominojugular reflex
    • Neck vein distension
    • S3
    • Basal creps
    • Cardiomegaly
    • Acute pulmonary oedema
    • Raised CVP (>16mcH2O)
    • Weight loss >4.5kg in 5 days in response to treatment
  • Minor
    • Bilateral ankle oedema
    • Shortness of breath on exertion
    • Raised HR >120
    • Nocturnal cough
    • Hepatomegaly
    • Pleural effusion
    • 30% decreased vital capacity
209
Q

What are the CXR signs of heart failure?

A
  • Alveolar shadowing
  • Kerley B lines
  • Cardiomegaly
  • Upper lobe diversion
  • Effusions
  • Fluid in the fissures
210
Q

What is the NY Heart Association Classification?

A

For heart failure:

  1. No limitation of activity
  2. Comfortable at rest, dyspnoea on ordinary activity
  3. Marked limitation of ordinary activity
  4. Dyspnoea at rest, all activity causes discomfort
211
Q

How do you manage heart failure medically?

A
  • ACEI, beta blockers, and spironolactone reduce mortality
  • 1st line: ACEI/ARB + beta blockers + loop diuretic
    • Lisinopril or candesartan: hyralazine + ISDN if not tolerated
    • Carvedilol or bisoprolol
    • Furosemide or bumetanide
  • 2nd line: get specialist advice
    • Spironolactone/eplerenone (watch K)
    • ACEI + ARB
    • Vasodilators: hydralazine + ISDN
  • 3rd line:
    • Digoxin
    • Cardiac resynchronisationtherapy ±ISD
212
Q

What are the characteristic features of hypertrophic cardiomyopathy?

A
  • Jerky pulse with large tidal wave as outflow obstruction is overcome
  • Large a waves in the JVP
  • Double apical impulse (palpable atrial systle, S4, in sinus rhythm)
  • LSE systolic thrill (turbulence) with harsh ESM radiating to axilla
  • Often accompanied by mitral regurg
  • Often paradoxical splitting of second heart sound
  • ESM increases with Valsalva’s manoeuvre and decreases with squatting
213
Q

What are the genetics of hypertrophic cardiomyopathy?

A
  • AD in 1/2 (other 1/2 sporadic)
  • Beta myosin heavy chain mutation commonest
  • Assoc with chromosomes 1, 11, 14, or 15
  • Assoc with Friedrich’s ataxia, WPW, phaeo, familial lentiginosis
214
Q

What changes the murmur in hypertrophic cardiomyopathy?

A
  • Increases with GTN, digoxin and standing due to volume reduction in diastole
  • Decreases with squatting, beta blockers, Valsalva’s release, handgrip
215
Q

How do you treat hypertrophic cardiomyopathy?

A
  • Medical:
    • Negative inotropes: first line beta blocker,s second line verapamil
    • Amiodarone for arrhythmias
    • Anticoagulate if AF or emboli
  • Dual chamber pacing
  • Internal defibs
  • Surgical myomectomy
  • Therapeutic septal infarction
  • Avoid:
    • Digoxin (if in sinus rhythm)
    • Nitrates
    • Atropine
    • Inotropes
    • Diuretics (unless in LV failure)
216
Q

What can cause sudden death in hypertrophic cardiomyopathy?

A
  • Catecholamine driven extreme outflow obstruction
  • VR related to accessory pathway transmitted AF
  • Massive MI
217
Q
A

Medical Finals (11 decks)

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