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RACP 2024 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What management is indicated on calcium score from CT-cardiac?

A

<100 = diet + lifestyle
101-400 = aspirin + statin
101 -400 + 75th centile = move to high risk category, aspirin + statin
> 400 = aspirin + statin aiming LDL < 2, consider functional assessment (eg stress echo or ETT)

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2
Q

How do you interpret calcium score on CT cardiac?

A

0 = very low risk of death, <1% in 10y
1-100 = low risk of death, <10% in10y
101-400 = intermediate risk, 10-20%
101-400& >75th centile = moderately high risk, 15-20%
>400 = high risk, >20%

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3
Q

When is calcium scoring of CT-cardiac not recommended?

A

Very low risk individuals <5% 10y risk

High risk individuals >20% 10y risk as does not change management

Symptomatic or known CAD

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4
Q

What is the value of combined calcium score in CT cardiac?

A

Can assess 10y cardiac risk of ASYMPTOMATIC individual 45-75 with intermediate risk profile (ie can move them to high or low risk)

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5
Q

What is the triple rule out principle on CTCA?

A

When used in acute chest pain syndrome CTCA can rule out:
-CAD
-aortic dissection
-pulmonary embolism

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6
Q

What causes false positives on CTCA?

A

Calcified plaques which cause blooming effect- does not always correlate with obstructive plaque on invasive coronary angiogram (gold standard). This causes LOW PPV

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7
Q

What are the sensitivity, specificity, PPV and NPV for CTCA?

A

High sensitivity = low false negatives
High specificity = low false positives
High NPV = rules out CAD

Low PPV = presence of CAD and degree of stenosis does not always correlate to obstructive plaque on invasive coronary angio

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8
Q

What are the indications for CTCA?

A
  1. Evaluation of chest pain syndrome with uniterpretable or equivocal stress test (ETT, stress echo)
  2. Evaluation of chest pain syndrome with intermediate pre test probability of CAD, uninterpretable ECG or unable to exercise
  3. Acute chest pain with intermediate pre test probability of CAD, no ECG changes and negative serial enzymes
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9
Q

How should stable ischaemic chest pain be investigated?

A

Non invasively:
-exercise or stress ECG
- exercise or dobutamine stress echo
- dipyridamole/adenosine nuclear perfusion
- cardiac CT or MRI (non stress)

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10
Q

What are the risks of invasive coronary angiography?

A

1 in 1000 risk:
-stroke
-MI
- contrast anaphylaxis
- major surgery at puncture site
- emergency angioplasty or surgery
- death

1 in 100 risk of
- arrhythmia
- surgical repair at puncture site
- minor contrast reaction
- AKI

1 in 20 risk of major bruising
1 in 10 lose pulse at radial puncture site

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11
Q

What is the gold standard for anatomical assessment in coronary artery disease?

A

Invasive coronary angiography

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12
Q

Compare and contrast cardiac CT and cardiac MRI

A

CTCA better at assessing coronary artery anatomy than MRI

MRI better at assessing myocardium - gadolinium uptake identifies scar

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13
Q

Compare and contrast cardiac MRI and SPECT imaging

A

cMRI better spatial resolution so better at detecting scar (esp subendocardial)

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14
Q

What is the gold standard for assessing coronary ischaemia?

A

Invasive coronary angiogram (specifically through measurement of FFR)

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15
Q

What is involved in stress echo?

A
  1. Pre stress echo: evaluates LVEF, diastology, valves, wall motion
  2. Stress applied (exercise or drug) and assess ECG, symptoms, haemodynamics, exercise capacity
  3. Post stress echo: wall motion, diastology, RVSP
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16
Q

How is myocardial ischaemia defined in stress echo?

A

Exercise induced ST changes or exercise induced RWMAs

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17
Q

How is myocardial ischaemia defined in ETT?

A

ST segment abnormality

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18
Q

Why is a stress echo more sensitive and specific than ETT?

A

Able to assess RWMAs - degree of wall thickening (should increase > 50%) which precedes ECG changes on ischaemic cascade

Less false negatives

Less False positives with stress echo for women

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19
Q

Rank non invasive tests in terms of specificity and sensitivity

A

Least = ETT
Middle = stress echo, nuclear
Most = CTCA

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20
Q

What is LVH criteria?

A

S in V1orV2 + R in V6 >35
OR
S in V3 + R in aVL > 22

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21
Q

What complications associated with inferior STEMI?

A
  • RVMI (dependent on pre load so avoid B-blocker)
  • posterior wall MI
  • lateral wall MI
  • sinus and AV node dysfunction (Avoid B-blocker)

Major cause of mortality in iatrogenic hypotension

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22
Q

What is the most common valvular heart lesion?

A

Aortic stenosis
- most commonly degenerative
- 1% have bicuspid valve

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23
Q

Describe rheumatic AS

A

Fusion of commisures

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24
Q

How is severe AS defined?

A

AS jet velocity > 4 m/s
OR
Mean gradient >40 mmHg
OR AVA >1 cm2

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25
Q

What is a key feature of low flow severe AS?

A

Reduced stroke volume < 35 mL/m2

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26
Q

What is the only treatment that improves patient outcomes for severe AS?

A

Valve replacement
- low surgical risk = AVR
- intermediate risk = AVR or TAVR
- high risk = TAVR

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27
Q

What is the most common cause of AR?

A

Congenital abnormality such as bicuspid valve

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28
Q

Describe AR murmur

A

Early diastolic decrescendo murmur
- increased on full expiration
- loudest left sternal edge
- increased with handgrip or squat due to increased afterload

May also hear low pitche dmid diastolic rumbling of austin flint murmur (where AR jet impinges AVML)

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29
Q

How is severe AR defined?

A

-Flail leaflet or wide coaptation defect
- large jets
- steep decceleration
- holodiastolic flow reversal in aorta
- dialted LV

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30
Q

How is AR managed?

A

Severe: if symptomatic or have impaired LVEF should be managed with AVR

Moderate or severe and if otherwise having cardiac surgery

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31
Q

What are causes of acute severe AR?

A

Aortic dissection or endocarditis or trauma

Short diastolic murmur

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32
Q

What are the two types of MR?

A

Primary: degenerative caused by leaflet prolapse, chordae rupture, endocarditis, RHD

Secondary: functional, normal valve in presence of LV dysfunction

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33
Q

Describe MR murmur

A

holosystolic murmur +/- diasotlic murmur

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34
Q

What LVEF indicates reduced LV function in severe MR?

A

LVEF < 60% indicates reduced contractility as MR reduces work of LV

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35
Q

How is primary MR managed?

A

Severe MR with symptoms or LV dysfunction and low surgical risk = MVR

high surgical risk = mitraClip (transcatheter edge to edge MV repair

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36
Q

How is secondary MR managed?

A

Managed medically as for HF +/- CRT as first line

If refractory:
- LVEF > 50% = MVR
- LVEF < 50% = MitraClip
Concurrent CABG = MVR

Surgical management 1st line does not reduce hospitalisations or death

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37
Q

What is acute rheumatic fever?

A

Systemic immune response to beta-haemolytic strep

Cardiac manifestation: pancarditis incl PR prolongation

MSK: polyarthritis, erythema marginatum, nodules

Syndenham chorea

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38
Q

Which valve is most commonly involved in RHD?

A

Mitral valve - more commonly stenosis

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39
Q

Describe appearance of rheumatic MS

A

Fusion of commisures = fish mouth
Thickened + restricted AVML = hockey stick

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40
Q

Which rheumatic valve disease should you give anticoagulation for A Fib regardless of CHADSVASc?

A

Mitral stenosis

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41
Q

In which rheumatic valve disease should you given a B-blocker for tachycardia with pulmonary oedema?

A

Mitral stenosis

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42
Q

Describe MS murmur

A

Low pitch diastolic rumble
(bell in left lateral with full expiration)

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43
Q

How is severe MR defined?

A

Valve area < 1.5 cm2
OR Mean gradient > 10 mmHg
Or PAP > 50 mmHg

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44
Q

What scoring tool helps to guide MS treatment?

A

Wilkins score of mitral valve anatomy

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45
Q

How is rheumatic MS managed?

A

Balloon valvuloplasty for pliable vales with thrombus in severe or progressive MS

MVR for severe MR with severe symptoms and low surgical risk

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46
Q

What is the most common cause of tricuspid regurgitation?

A

80% are functional

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47
Q

Should isolated TR be managed surgically?

A

No - poor outcomes especially if RV dysfunction and pulmonary hypertension

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48
Q

What is Bernoulli equation and its use?

A

Change in pressure across orifice is proportional to square of velocity of fluid flowing through the orifice
DeltaP = 4Vsquared

Used to asses RVSP = 4x (TR velocity squared) + right atrial pressure

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49
Q

What is different about mixed valve disease?

A

Often does not progress to severe grade but associated with higher morbidity and mortality

Requires specialist team input to guide appropriate management

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50
Q

What are the Four acoustic windows of TTE?

A
  1. Parasternal - front of heart structures
  2. Apical - LV + RV
  3. Subcostal - pericardium + RV function + ASD
  4. Suprasternal - aortic arch, SVC, great vessels
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51
Q

How is LVEF calculated?

A

EF (%) = (LVEDV - LVESV)/LVEDV x 100

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52
Q

What is normal global longitudinal strain on TTE?

A

More than 20%

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53
Q

What information os gained from GLS on TTE?

A
  • Can indicate RWMAs
  • Early detection of cardiotoxicity in cancer therapies (earlier detection than LVEF)
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54
Q

How does HFpEF appear on ECHO?

A
  • Abnormal relaxation = A wave > E wave in mitral doppler, slower decceleration in pulmonary vein
  • Psuedo normal: E > A wave, shortened decceleration wave reflects overload
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55
Q

What is pre capillary pulmonary hypertension?

A

Where arterial tree is obstructed, PAP is greater than LA pressure

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56
Q

What is post capillary pulmonary hypertension?

A

Normal lung circulation but raised LA pressure causes high PAP

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57
Q

How is pulmonary hypertension measured on ECHO?

A

Doppler gradient across tricuspid valve + bernoulli equation to estimate RVSP

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58
Q

How is pulmonary hypertension defined?

A

PAP (equal to RVSP) > 20-25 mmHg

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59
Q

What is the significance of pre and post capillary hypertension with regard to management?

A
  • post capillary hypertension should be managed with diuresis
  • pre capillary should be treated with pulmonary vasodilator drugs
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60
Q

When is it safe to do DCCV for AFib?

A
  • presentation with < 48 hours onset symptoms
  • stabled on anticoagulation at least 4 weeks
  • TOE rules out LAA thrombus

Same risk of stroke between these groups

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61
Q

What are the four best known causes of congenital heart disease?

A
  1. Trisomy 21 - VSD/AVSD
  2. 22q11 deletion (Digeorge syndrome)- great artery malformation (tetralogy of Fallot)
  3. Lithium - Ebsetin anomaly, TV anomaly
  4. Rubella - peripheral PA stenosis
62
Q

What is the incidence in congenital heart disease if no parents affected?

A

Approximately 1%

63
Q

What is the complication of patent ductus arteriosus?

A

Failure to close causes left to right shunt (aorta -> pulmonary artery) which can cause LV failure

64
Q

Why is location of pulmonary valve stenosis significant?

A

If valvular is amenable to balloon valvuloplasty

Otherwise sub-valvular and spravalvular may require stenting

65
Q

What is Noonan syndrome?

A

Autosomal Dominant syndrome associated with RAAS/MAPK gene mutation

Wide set eyes
Low set ears
Short stature
Pulmonary stenosis

66
Q

What is Williams Syndrome?

A

Autosomal Dominant syndrome resulting from deletion of WBSCR of 7q11.23

-Developmental Delay and cognitive impairment
-Overfriendly and anxious
-Elastin arteriopathy: pulmonary stenosis and and supravalvular aortic stenosis
-Specific facies
- Poor growth
- Connective tissue abnormalities
- Endocrinopathies: early puberty, hypercalcaemia, hypercalciuria, hypothyroidism, diabetes

67
Q

What is a key feature of Ross operation for aortic stenosis?

A

Uses patients own pulmonary valve as autograft - grows with patient and has greater longevity than prosthetic valve

68
Q

What are the co-morbidities associated with Coarctation of the aorta?

A
  • biscuspid aortic valve
  • hypertension (even after repair)
  • Arch hypoplasia
  • cerebral aneurysms
  • aortic dissection
  • repair site aneurysms
69
Q

What are the 4 lesions of tetralogy of fallot?

A
  • VSD
  • RV hypertrophy
  • Over-riding aorta (shifted right)
  • Pulmonary stenosis
70
Q

What are complications seen post repair of tetrology of fallot?

A
  • pulmonary regurgitation (esp if transannular patch used in repair)
  • pulmonary stenosis
  • arrhythmias (atrial > ventricular)
  • RV/LV dysfunction
  • Aortic root dilatation (needs screening)
71
Q

What is transposition of great arteries?

A

Aorta comes of RV and PA comes of LV. Two types D and L

72
Q

What are complications of D-TGA?

A

No communication between left and right heart so incompatible with life in infancy unless associated with shunt such as PFO

73
Q

What are complications of atrial switch for D-TGA?

A
  • baffle stenoses or leaks
  • atrial arrhythmias
  • RV dilatation and dysfunction (as becomes systemic supply)
  • TV dysfunction (as becomes systemic supply)
74
Q

What are complications of arterial switch for D-TGA?

A

-Anastomotic stenosis
- coronary insufficiency
- aortic and/or pulmoanry regurgitation
- aortic root dilatation

75
Q

What is L-TGA?

A

RV and LV swap places anatomically (ventricles also transposed i.e. RV is now on the left but still gives rise to the aorta)
associated with VSD
Can develop TR and RV dilatation/dysfunction as systemic supplier
10-15% develop complete heart block

76
Q

Compare L-TGA and D-TGA in terms of when they present

A

D-TGA: often identified in utero, presents with cyanosis in early infancy

L-TGA: often not seen on screening, can present in early adulthood

77
Q

What is Ebstein’s anomaly?

A
  • ASD
  • Accessory pathways; 20% have WPW
  • Arrhythmia
  • TR
  • Abnormal RV (smaller than RA)
78
Q

What is truncus arteriosus?

A

Failure of aorta and pulmonary artery to separate during embryonic development resulting in single outflow track to both aorta and lungs

79
Q

What is the incidence of congenital heart disease if 1 sibling affected?

A

2.3%

80
Q

What is the incidence of congenital heart disease if 2 siblings affected?

A

7.3%

81
Q

What is the incidence of congenital heart disease if mother affected?

A

4-6%

82
Q

What is the incidence of congenital heart disease if father affected?

A

2.1%

83
Q

What is the inheritance and incidence of bicuspid aortic valve?

A

-Autosomal dominant
-2% live births

84
Q

What are non-cardiac complications of congenital heart disease?

A
  • psycho-scoial issues (depression, anxiety)
  • substance abuse
  • needle phobia
  • non-adherence with medications and follow up
85
Q

What is cyanotic heart disease?

A

Presence of right to left shunt resulting in deoxygenated blood entering systemic circulation. This results in chronic hypoxia

Causes include large ASD, large VSD, anomalous pulmonary vein drainage

86
Q

What are complications of cyanotic heart disease?

A
  • risk of embolism: DVT arises to arterial clots causing stroke or limb ischaemia, cerebral abscess
  • secondary erythrocytosis (distinct from polycythaemia does not require venesection)
87
Q

What is fontan circuit?

A

Surgical procedure for single chamber or right heart hypoplasia that connects IVC/SVC directly to pulmonary circulation

Palliative procedure where complete repair is not possible

88
Q

What is the implication of Laplace’s law in aortic dissection?

A

Laplace’s law states wall tension = pressure x radius

Wider the aorta and higher the BP increases risk of dissection

89
Q

What is the best imaging modality to image the aorta?

A

CT chest (3D reconstructed)

90
Q

What is the normal growth rate of the aorta?

A

Normal aorta: 0.1-0.2 mm/year

Aneurysmal aorta: 1 mm/year

91
Q

What are the key principles of medical management of aortic aneurysm?

A

Blood pressure control
-> 1st line is B-blocker, often poorly tolerated in young patients
-> ARB in Marfans as block TGFB1 signalling

Restrictions on weight lifting and exercise

Close monitoring in pregnancy/pre pregnancy repair

92
Q

What are the inherited causes of thoracic aortic anuerysms?

A
  • bicuspid aortic valve
  • Turner syndrome (also associated with bicuspid AV)
  • Ehler’s danlos
  • Familial thoracic aortic anuerysm (fast growth rate)
  • Loey’s Dietz (faster growth and higher dissection risk)
  • Marfan syndrome (fast growth rate)
  • Non specific connective tissue disorder
  • Cono-truncal anomalies (TOF, truncus arteriosus as have dilated aortic root)
93
Q

What are the indications for surgical repair of ascending aortic aneurysm?

A

-Any aortic anuerysm > 55 mm
-Biscuspid AV with risk factors (coarctation, FHx, growth >3-5 mm/year) > 50 mm
-Marfan > 50 mm
Loeys Dietz > 42 mm
Turner syndrome > 27 mm/m2

94
Q

What ECG findings suggest a cardiac cause for syncope?

A

Bifasicular block (RBBB + LAFB)
QRS > 120 ms
Mobitz II type 2 AV block
Sinus bradycardia (< 50 bpm, pauses > 3secs or >5secs with AFib)
NSVT
Pre-excitation
Features of channelopathy or cardiomyoptahy
Pathological Q waves

95
Q

What medications have evidence for the use in vasovagal syncope?

A

Midodrine (a1 receptor agonist)
Fludrocortisone (synthetic steroid with high mineralocorticoid receptor activity)
Paroxetine (SSRIs)

Not beta blockers

96
Q

What are the frequency of each type of SVT?

A

AVNRT 60%
AVRT 30%
Atrial tachycardia 10%
Junctional tachycardia 1%

97
Q

What are the 2 mechanisms of arrhythmia?

A
  1. Abnormal impulse conduction, usually due to re-entry (Flutter, ANVRT, AVRT)
  2. Abnormal impulse formation
    -from abnormal automaticity such as sinus tachycardia, atrial tachycardia, junctional, ectopy
    - from triggered activity, such as early and late depolarisation, ectopy, torsade de pointes, digoxin toxicity
98
Q

How do you assess an SVT (narrow complex tachycardia, QRS < 120 ms)?

A
  1. Irregular = Afib, Atach with variable conduction, MAT
  2. Regular without p-waves = AVNRT or other
  3. Regular with non- conducted p-waves = AFib or AFlutter
  4. Regular with conducted p-waves and RP interval < 90 ms = AVNRT
  5. Regular with conducted p-waves and RP < PR interval but greater than > 90 ms = AVRT, atypical AVNRT or Atach
  6. Regular with conducted p-waves and RP > PR interval = Atach, PJRT or atypical AVNRT
99
Q

How should SVT be treated?

A
  • unstable = DCCV
  • Stable = vagal manoeuvres, IV adenosine (not in severe asthma as causes bronchoconstriction), IV CCB or B-blocker (CCB never in broad complex or WPW)
100
Q

What is the mechanism of atrioventricular reciprocating tachycardia (AVRT)?

A

Presence of accessory pathway, which may manifest (e.g delta wave as pre excitation) on an ECG or be concealed (retrograde conduction)

101
Q

What is Wolff-Parkinson-White syndrome?

A

Pre-excitation as delta wave on ECG and tachyarrhythmia
95% are AVRT but can also conduct other arrhythmias down this pathway
Sudden death risk 1 in 1000 due to risk of VFib

102
Q

How should a delta wave in asymptomatic patients be assessed?

A

Treadmill testing, if delta wave intermittent unlikely to need EPS + ablation

103
Q

How should sustained wide complex tachycardias in WPW be managed?

A

DCCV or IV procainamide
Never CCB or AVN blocking agents due to risk of VFib

104
Q

What is AV node re-entry tachycardia (AVNRT) and ECG features?

A

Most common form of SVT
Associated with good prognosis, can be symptomatic
Two forms:
- Typical = slow fast with short RP, Psuedo r prime in V1 indicating short RP interval
- Atypical = fast slow with long RP

105
Q

What are features of focal atrial tachycardia?

A

HR 100-150 bpm
Irregular rhythm but discernible p waves of differing morphology
Responde to B-blocker or CCB
Resistant to DCCV

106
Q

How are SVTs managed in the long term?

A
  • Vagal manoeuvres if infrequent
  • catheter ablation for AVNRT, WPW, unifocal Atach, CTI-dependent flutter
    -pill in pocket flecainide 200-300 mg stat (need B-blocker cover)
  • medications: b-blocker, CCB, digoxin, Flecainide (need b-blocker), sotalol, amiodarone
107
Q

What are features of typical AFlutter?

A

Macro-reentrant circuit dependent on cavo-tricuspid isthmus
Rate 250-350, 150 bpm in 2: 1 block
Associated with HTN, CAD, valvulopathy, COPD, cardiomyopathies
ECG: negatively directed saw-tooth atrial deflections (f waves) seen in leads II, III, and aVF, with positively directed deflections in lead V1

108
Q

What are management strategies for AFlutter?

A
  • Anticoagulation
  • rate control with AV nodal blockade
  • Pharmacological cardioversion
  • DCCV
  • ablation
109
Q

What are features of atypical AFlutter?

A

ECG not meeting criteria for typical flutter (negative in V1 and positive in II, III and aVF
Usually seen post cardiac surgery or in structural heart disease

110
Q

What is the CHA2DSVASc2 score and when is anticoagulation indicated?

A

Score > 1

Congestive heart failure
Hypertension
Age: 1 if 65-74, 2 if >75
Diabetes
Stroke or TIA or previous arterial thromboembolism
Vascular disease (prior MI or PAD
Sc is for women

111
Q

What is the HAS-BLED score?

A

Yearly risk of bleeding

Hypertension
Alcohol, antiplatelets and anti-inflammatories
Stroke
Bleeding: major bleeding labile INR
Liver disease
Elderly: age > 65
Dialysis/end stage renal disease

112
Q

What anticoagulation should be used for AFib?

A
  • NOACs in non-valvular AFib, no benefit when switching over from warfarin in frail adults over 75 as per FRAIL-AF trial
  • warfarin in metallic heart valves and moderate to severe mitral stenosis (valvular AF)
113
Q

When should DOACs be held and restarted around surgery?

A

Low risk = 1 day before
High risk = 2 days before
EXCEPT dabigatran in CrCl < 50 when should be held 4 days before high risk and 2 days before low risk surgery

All can be restarted on days 2-3

114
Q

How is AFib managed?

A
  1. Rate control: 1st line is B-blockers, CCBs except in CHF, 2nd line is digoxin, 3rd line is rhythm control
  2. Rhythm control:
    in structural heart disease flecainide or sotalol is first line and amiodarone second line
    in structurally normal heart amioadrone is first line, 2nd line is sotalol or B-clocker
    3rd line is ablation
115
Q

What are indications for ablation in atrial fibrillation and what is the most common site ablated?

A
  • symptomatic pAF or refractory permanent AF
  • AFib in HFrEF

Pulmonary veins

115
Q

Does ablation for Afib improve mortality?

A

No

Reduces symptom burden and QoL
Evidence that reduces hospitalisation and death in HFrEF (CASTLE-AF trial)

116
Q

What are features of pathological AV block (Mobitz II type 2)

A
  • wide QRS
  • short PR
  • block worse on exertion
  • associated with anterior MI
  • associated with syncope
117
Q

What is sinus node dysfunction and indications for treatment?

A

< 50 bpm with sinus pauses > 3 seconds

Treatment indicated for chronotropic incompetence (failure to reach 80% predicted HR)

NB OSA common treatable cause of sinus node dysfunction

118
Q

What are the indications for PPM for bradycardia?

A

Absence of reversible cause in Mobitz II type or complete heart block

Symptomatic patients without reversible cause in patients with:
-sinus node dysfunction
- Afib with bradycardia
- bradycardia due to goal directed medical therapy e.g b-blocker in HF
- Mobitz I or 1st degree HB with clear correlation to symptoms

119
Q

When is CRT indicated?

A

In patients with symptomatic heart failure on medical therapy with LVEF < 35% and QRS > 150 ms
Shown to improve mortality in patients without AFib

120
Q

Who should be considered for PFO closure?

A

Stoke patients with high RoPE score

121
Q

When should Left atrial appendage occlusion be considered?

A

In patients with non-valvular AFib with contraindications to lifelong anticoagulation

122
Q

What are absolute contraindications to TOE?

A

Oesophageal tumour, stricture, fistula or perforation
Active upper GI bleed
Perforated bowel or bowel obstruction
Unstable C-spine
Uncooperative patient

123
Q

What are the indications for TOE?

A

Infective endocarditis
Pre DCCV or ablation
To exclude cardiac source of embolus
Aortic dissection
Non diagnostic TTE
Cardiac surgery/structural procedures

124
Q

What features on TOE support a diagnosis of infective endocarditis?

A

Vegetations (lobulated, echogenic, indepedently mobile)
Abscess (echolucent space)
New partial dehiscence of prosthetic valve8

125
Q

What is the definition of a narrow complex tachycardia?

A

QRS duration less < 110 ms represents synchronous + symmetrical conduction down right + left bundles

126
Q

What two features are required to diagnose SVT with aberrancy?

A

SVT + evidence of BBB (typically in V1 and V6)

127
Q

Through what mechanism does pre-excited Atrial Fibrillation generate a wide complex tachycardia? How is it managed?

A

Bypassing of AV node through bypass tract

High risk of turning into VF so defibrillated

128
Q

What is the maximum rate of 1:1 conduction of Atrial flutter and why is the complex broad?

A

230 bpm
Broad because conduction is slower through left bundle at this rate

129
Q

What is the most common form of VT presenting to hospital?

A

Scar-related re-entrant VT

130
Q

Through what mechanism does scar contribute to VT?

A

Surviving myocytes/Purkinje in the scar create a conducting channel through the scar which demonstrates slowed conduction creates and re-entrant circuit

130
Q

How is scar mediated VT managed?

A

-VT controlled with anti-arrhythmic or ablated
-Needs work up for structural heart disease: ECHO, MRI, angiogram
- ICD if indicated

130
Q

How is idiopathic VT managed?

A

VT suppression with medication
Can consider ablation if recurrent
(note will have structurally normal heart)

131
Q

What is the diagnostic criteria of heart failure?

A

Symptoms and/or signs of heart failure caused by a structural or functional cardiac abnormality and corroborated by at least one of:
- elevated BNP
- objective evidence of cardiogenic pulmonary congestion

132
Q

What are the subclassifications of HF?

A

HFrEF = LVEF < 40%
HFmrEF = LVEF 41-49%
HFpEF = LVEF > 50%
HFimpEF = improvement in LVEF with HFrEF

133
Q

Which investigations are indicated for the diagnosis of heart failure?

A

12 lead ECG
CXR
BNP
TTE

134
Q

What maintenance therapies should be used in heart failure?

A

HFrEF:
- ACEi/ARB/ARNi + Beta blocker + MRA + SGLT2i
- consider ivabradine if HR > 70 and LVEF <35%
- hydralazine in African patients
- IV iron if ferritin < 100 or if 100-300 with Tsat
< 20%

HFmrEF: ACEi/ARB + Beta blocker + MRA

HFpEF: low dose MRA, SGLT2i

135
Q

What is the mechanism of action of Sacubitril+valsartan?

A

Sacubitril = neprilysin inhibitor = increases natriuretic peptides which enhance natriuresis/diuresis, results in vasorelaxation

Valsartan = ARB = inhibits vasoconstriction, inhibits fibrosis

136
Q

What is the NYHA HF classification?

A

Class I - No symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc.

Class II - Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.

Class III - Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20—100 m).Comfortable only at rest.

Class IV - Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.

137
Q

How is goal directed medical therapy initiated in congested vs euvolaemic patients with HF?

A
  • Congested: ARNi/ACEi/ARB and SGLT2i, then add MRA, then B-blocker once euvolaemic

-euvolaemic: ARNi/ACEi and B-clocker, then add MRA and SGLT2i

138
Q

What is the mechanism of action of verciguat? Who is it indicated for?

A

soluble guanylate cyclase stimulator, restores the cyclic guanosine monophosphate (cGMP) under low nitric oxide conditions and oxidative stress, resulting in relaxation of cardiac muscle and vasodilation

Patients with HFrEF with worsening HF despite optimal medical therapy

139
Q

What is the mechanism of action of omecamtiv mecarbil?

A

Selective cardiac mysoin activator

140
Q

What is the goal for LDL in high risk individuals?

A

< 1.8 or > 50% reduction in LDL

141
Q

When should Lp(a) be measured and how should it be managed?

A

Measured in people with premature CVD or stroke

Aggressive LDL reduction (<1.5)
ACEi if proteinuric
Nicotinic acid

142
Q

What is the pathological basis of familial hypercholesterolaemia?

A

AD inherited
Increases LDL resulting in increased cholesterol deposit

143
Q

What is the mechanism of action of evolocumab?

A

PCSK9 inhibitor (mAb), reduces LDL cholesterol

144
Q

What is the treatment of hypercholesterolaemia?

A

1st line: statin
2nd line: statin + ezetimibe
3rd line = PCSK9i if high risk and LDL > 2.6 despite statin and ezetimibe

145
Q

What is the mechanism of action of ezetimibe?

A

Inhibits intestinal absorption of cholesterol

146
Q

What is the canadian cardiovascular society grade of chronic angina?

A

Grade I: angina with strenuous activity
Grade II: angina with moderate activity
Grade III: angina with mild exertion
Grade IV: angina at rest

147
Q
A

RACP 2024 (15 decks)

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