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FRACP written exam preparation > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define pulmonary hypertension

Define mild/mod/severe

A

mPAP >25mmHg at rest.

Mild mPAP >25
Moderate mPAP >35
Severe mPAP >45

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2
Q

Name two congenital causes of LQTS and the difference between the two.

A

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

Romano-Ward syndrome (no deafness)

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3
Q

What is the minimal amount of following nutrients required in ICU setting?

  1. Carbohydrate
  2. Amino acid mixture
  3. Lipids
A
  1. 2g/kg per day
  2. 1.3-1.5g/kg IBW/day
  3. 1-2g/kg IBW/day
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4
Q

3 causes of restrictive cardiomyopathy

A
  1. Idiopathic
  2. Post radiation
  3. Infiltrative - Amyloidosis, sarcoidosis, haemochromatosis
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5
Q

What is the role of P2Y12 receptor?

A

When bound by ADP, stimulates the activation of GP 2b/3a receptor resulting in enhanced platelet degranulation and TXA production and prolonged platelet aggregation.

GP 2b/3a receptors are involved in cross linking of platelets via binding to fibrinogen.

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6
Q

Describe the rate control aim in AF as per RACE II trial.

What is the most effective treatment?

A

RACE II trial looked into lenient <110 bpm vs strict <80 bpm. There was no difference in mortality, heart failure, stroke or serious arrhythmias. There were many more visits in the strict group where as less therapy with the lenient group achieved nearly as good control.

Therefore anything below <110 is fine.

Beta blockers are the most useful, followed by CCBs (verapamil > diltiazem)
Digoxin only adds minimal benefit (~1%) when added to beta blockers or CCBs.

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7
Q

Mortality risk for the following:

  1. Isolated aortic or mitral valve surgery
  2. Concurrent CABG with valve surgery
  3. 2x valve surgery (aortic and mitral valve)
  4. Double valve and CABG
A
  1. Around 1-2% in a patient <80 who is relatively well
  2. Above risk is doubled
  3. Above risk is double
  4. Above risk is quadrupled (ie 8%)
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8
Q

4 criteria for CRTD therapy

What are its benefits?

A

NYHA symptoms 3-4 on treatment
Dilated heart failure with LVEF <35%
QRS >120 ms
Sinus rhythm

Reduces symptoms and HF related deaths and sudden deaths
Also reverses remodelling

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9
Q

What is the significance of mobitz type II block?

A

Significant risk of progression to complete heart block.

PPM is indicated if symptomatic, or asymptomatic but very bradycardic.

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10
Q

Comorbidities associated with AF

What kind of lifestyle activities can reduce AF?

A
  1. Hypertension
  2. Obesity
  3. Diabetes
  4. HTN - 1.5x risk
  5. Structural heart disease such as HOCM, valvular disease
  6. Hyperthyroidism

Note: no clear association with IHD with exception of AMI or heart failure

Weight loss and increased fitness can reduce incidence of AF.

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11
Q

Mechanism of action of ticagrelor

A

Direct acting P2Y12 inhibitors which change conformation of P2Y12 receptors resulting in REVERSIBLE, concentration dependent inhibition

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12
Q

Indications for cardiac transplantation

A

Low EF by itself is NOT an indication.

  1. Severe symptomatic heart failure despite maximum medical therapy, mechanical cardiac support
  2. Cardiogenic shock
  3. Frequent discharges from AICD
  4. Intractable angina despite optimal management - very rare
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13
Q

Young man with fast AF with deep TWI over inferolateral leads - what should you think about?

A

HOCM.

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14
Q

Safest medication to use for recurrent SVT in pregnancy?

A

Metoprolol. (although can cause IUGR)

Amiodarone is associated with teratogenicity and neonatal goitres.

Adenosine and verapamil can cause decreased uterine blood flow.

Flecainide is associated with hyperbilirubinaemia.

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15
Q

2 roles of right heart catheterization in pulmonary hypertension

A
  1. Define relationship to LAP and to calculate PVR in order to determine the cause of pulmonary hypertension
  2. Check vasodilator response with IV adenosine/inhaled nitroprusside
    - ?predict response to vasodilator therapy
    - Assessment prior to heart +/- lung transplantation
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16
Q

3 associations with coarctation of aorta?

A
  1. Bisucspid aortic valve + aortopathy
  2. Berry aneurysms in 10%
  3. Other congenital heart diseases - VSD, PDA
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17
Q

When should atrial septal defects be closed?

When shouldn’t it be closed?

A
  1. Haemodynamically significant shunt determined by symptoms, RV enlargement, Qp:Qs ratio >1.5
  2. Paradoxical embolism
  3. Platypnea-orthodeoxia syndrome

Do not close if already developed eisenmenger physiology.

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18
Q

Most common mutations involved in HOCM

A

β-myosin heavy chain protein or myosin binding protein C

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19
Q

5 Indications for AICD in HOCM?

A
  1. Cardiac arrest
  2. Sustained VT
  3. Family history of sudden death
  4. Unexplained syncope
  5. LVH thickness >30mm

For all other cases such as NSVT on Holter monitoring and abnormal exercise BP, think about other HOCM SCD risk variables then use risk calculator…

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20
Q

Describe primary prophylaxis of VT in IHD

A
  1. Beta blockers reduce VT and SCD by 30%
  2. Revascularize if possible
  3. AICD is indicated if LVEF <35% after more than 40 days post AMI

No other antiarrhythmics are of benefit

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21
Q

What is the estimated mortality rate for chronic severe symptomatic AR or chronic asymptomatic AR with LV dysfunction? (LVESD >50mm)

A

20% per annum.

Therefore key factors in determining timing of valve surgery is symptoms and LVESD.

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22
Q

PCI timing on the basis of symptom onset:

A

If symptom onset <1hr - PCI within 60min
If symptom onset 1-3 hours - PCI within 90 minutes
If symptom onset 3-12 hours, PCI within 2 hours

PCI can remain effective upto 12 hours.

If PCI is not possible within 2 hours, thrombolysis first then immediate transfer to PCI centre for evaluation of success of lysis. If unsuccessful lysis - rescue PCI.
If successful lysis via thrombolysis, coronary angiography within 3-24 hours.

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23
Q

How does Ivabradine work?

A

Inhibition of If channel (funny channels) consisting of mixed sodium and potassium channels found in spontaneously active regions of the heart such as SA node and are triggered by hyperpolarisation.

Inhibition of these channels delays depolarisation in the SA node and selectively slows heart rate.

SE includes transient luminous phenomenon.

Metabolized by CYP3A4.

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24
Q

How would you make a decision of choosing tissue valve replacemnet over mechanical heart valve replacement?

A

Generally, bioprosthetic AVR if >60, bioprosthetic MVR if >65.

Warfarin is not needed for tissue AVR, but needed for MVR if prior history of AF, LA/LV thrombus, prior embolism. Otherwise aspirin but pretty much if you are in doubt, use warfarin…

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25
Q

4 causes of PCWP > LVEDP

A

Usually PCWP should estimate LVEDP.

  1. Mitral stenosis
  2. Cor triatriatum - congenital defect in which left or right atrium is subdivided by a thin membrane resulting in 3 atrium
  3. Atrial myxoma
  4. Pulmonary vein stenosis
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26
Q

Write Bernoulli’s equation.

A

P = 4Vsquared

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27
Q

3 causes of predominantly hypercholesterolaemia?

A
  1. Nephrotic syndrome
  2. Cholestasis
  3. Hypothyroidism
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28
Q

How does ezetimibe work?

A

Reduces absorption of dietary and biliary cholesterol by inhibiting its transport across the intestinal wall, leading to upregulation of low density lipoprotein receptors on the surface of cells and increased LDL cholesterol uptake into cells.

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29
Q

What does kussmaul’s sign indicate?

A

Paradoxical rise of RA pressure or lack of decline in RA pressure during inspiration.

Indicates constriction or RV ischaemia.

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30
Q

4 potential conditions which affect valve gradient

A
  1. Anaemia
  2. Sepsis
  3. Tachycardia
  4. Thyrotoxicosis

Basically any loading conditions can affect the valve gradient, hence echo evaluating the severity of the valve lesion should be done when patient is stable.

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31
Q

Most common cause of Eisenmenger syndrome?

A

PDA > VSD > ASD

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32
Q

ECG changes in dextrocardia?

A
  1. R axis deviation
  2. Positive QRS complexes in aVR with upright P and T waves
  3. Inversion of all complexes with global negativity in lead 1
  4. Absent R wave progression in the chest leads

Accidental reversal of L and R arm electrodes may produce a similar picture to dextrocardia in the limb leads only (but with normal apperance in the praecordial leads)

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33
Q

What is the agent of choice in fast AF with rapid ventricular response via accessory pathway?

A

Flecainide. Slows conduction through normal and accessory pathway and has a greater effect at higher atrial rates.

Potent inhibitor of sodium channels and therefore slows conduction.

ECG will show lengthening of PR interval and widening of QRS complex on the ECG.

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34
Q

Timing of:

  1. Stent thrombosis
  2. Restenosis
A

Stent thrombosis - 1-2% most commonly in the first month

Restenosis - most commonly in first 3-6 months, occurs in 5-20% of patients

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35
Q

Duration of DAPT post PCI and CABG in stable IHD and post ACS

Duration of DAPT post fibrinolysis?

A

In STABLE IHD:
Minimum of 1 month in BMS, 6 months in DES
Longer if minimal bleeding risk

Post ACS:
At least 12 months regardless of DES/BMS

CABG: DAPT with aspirin and P2Y12 inhibitors for 12 months post ACS

Fibrinolysis: Aspirin and clopidogrel for minimum of 14 days and ideally at least 12 months

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36
Q

3 indications for aortic balloon valvuloplasty

A
  1. In children it is effective
  2. Bridging therapy in pregnant women with severe AS or in non-emergent surgery in older patients (eg: hip replacement)
  3. Assessment of symptoms whether it relates to the severity of the valve lesion as opposed to other factors such as COPD prior to definitive treatment

note: cardiopulmonary bypass in pregnancy has 20-30% chance of fetal loss.

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37
Q

How long do you treat for rheumatic fever?

A

Either upto age of 40, or at least 10 years, whichever is the longest.

Ie, if Pt develops rheumatic fevre at age of 5, needs to continue antibiotic prophylaxis for 35 years!!

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38
Q

Why are beta blockers not used as a first line therapy in blood pressure management?

A

Increases risk of developing diabetes
Increased incidence of stroke particularly in smokers.
Therefore not used unless there is a compelling reason such as heart failure or ischaemic heart disease.

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39
Q

What is the role of biventricular pacing in heart failure?

A

Previous DAVID trial showed that RV pacing alone resulted in increase in heart failure and mortality.

Subsequently NEJM 2013 article showed that biventricular pacing in heart failure with heart block is effective in reducing combined end point by 26%:

  1. Class I - III HF with LVEF <50%
  2. Narrow complex
  3. Pacing indication present
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40
Q

Where is BNP produced and what is its role?

A

BNP is produced by left ventricle in response to strain. Acts as a vasodilator, diuretic and natriuretic.
Suppresses both sympathetic tone and RAA system.

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41
Q

How do you calculate Qp:Qs?

A

Qp:Qs = Aorta O2 - Mixed venous O2 / Pulmonary vein O2 - Pulmonary artery O2

Anything more than 7% is considered step up.

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42
Q

How do you treat cyanide intoxication?

A

Hydroxycobalamin or sodium thiosulphate.

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43
Q

Name 5 risk factors for unsuccessful discontinuation of mechanical ventilation.

A
  1. Age >65
  2. Chronic heart failure
  3. Pneumonia as a cause of respiratory failiure
  4. Partial pressure of PaCO2 >45 mmHg after extubation
  5. Upper airway stridor at extubation.
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44
Q

6 Drug causes of prolonged QTc

A
  1. Amiodarone
  2. Sotalol
  3. TCA
  4. Fluoxetine
  5. Class 1a antiarrhythmic drugs
  6. Erythromycin
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45
Q

How would you assess whether the accessory pathway needs to be ablated with EP study?

A

Exercise testing with a bike.

If delta wave disappears in response to exercise (HR >130) it means that it doesn’t conduct at higher HR.

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46
Q

What is the significance of late gadolinium enhancement on cardiac MRI?

A

LGE identifies regional but not diffuse myocardial fibrosis.

Patients with NICM with LGE+ did the worst in terms of requiring device therapy much earlier compared to those without LGE!

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47
Q

What are the side effects of flecainide?

A
  1. Bradycardia and hypotension (negatively inotropic)
  2. Visual blurring
  3. Oral paraesthesia.
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48
Q

What are clinical signs of severity of AR?

A 
Low diastolic BP
Wide pulse pressure
Displaced apex, S3, LVF
Waterhammer pulse
Long duration of murmur
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49
Q

What are 3 key issues with clopidogrel?

A
  1. Delayed onset of action depending on the loading dose given (slower if 300mg given compared to 600mg - 2-6hrs vs 12-24 hours)
  2. Poor metabolizers specifically CYP2C19
  3. Drug interaction with PPIs

Therefore prasugrel is preferred over clopidogrel - prasugrel has earlier production and greater concentration of the active metabolite compared to clopidogrel.

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50
Q

Name 5 contraindications for TAVI.

A
  1. Unsuitable anatomy
  2. Endocarditis
  3. LV thrombus
  4. Life expectancy <1 year
  5. Other conditions which may not alleviate symptoms eg COPD, pulmonary hypertension
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51
Q

What is the significance of mobitz type 1 block?

A

Usually benign
Seen in young fit individuals and reflect high vagal tone
No indication for PPM

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52
Q

What valve disease is more predominant as you age? mitral or aortic valve?

A

Mitral. Aortic valve disease is second.

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53
Q

How do you calculate pulmonary vascular resistance?

A

PVR = mPAP - mLAP / Qp (pulmonary blood flow)

PVR is measured in Wood’s unit = mmHg/L/min

Anything below <5 WU is low and suggests that there is no significant pulmonary vascular disease (ie left heart driven disease)

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54
Q

Mechanism of action of aspirin

A

Irreversible inhibition of COX-1 which is required to make thromboxane, which is required to facilitate platelet aggregation. Because platelets do not have a nucleus, effect persists until its death 7-10 days.

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55
Q

Cardiac manifestations of Marfan’s Syndrome

A

Aortic sinus dilatation leading to aortic aneurysm, dissection, regurgitation. (90%)

Also mitral valve prolapse in 75%

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56
Q

ECG signs of hypokalaemia

A
  1. U waves
  2. small or absent T waves (occasionally inversion)
  3. prolong PR interval
  4. ST depression
  5. long QT
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57
Q

3 causes causing predominantly hypertriglyceridaemia?

A
  1. Diabetes
  2. Obesity
  3. Alcohol
58
Q

Most common cardiac defect of Downs syndrome

A

endocardial cushion defect (c. 40%, also known as atrioventricular septal canal defects)
ventricular septal defect (c. 30%)
secundum atrial septal defect (c. 10%)

59
Q

How does fibrates work?

A

Activates peroxisome proliferator activated nuclear receptors and modulate lipoprotein synthesis and catabolism. Reduces TGL, moderately increase HDL and have a variable effect on LDL concentration.

60
Q

What is the role of magnesium in muscle contraction?

A

Magnesium stimulates calcium reuptake via calcium activated ATPases

61
Q

Mechanism of action of Dipyridamole

Side effects?

A

Both antiplatelet and vasodilating properties by inhibiting activity of adenosine deaminase and phosphodiesterase, causing accumulation of adenosine, adenine nucleotides, and cAMP.

Side effects include headache, dizziness, nausesa, diarrhoea, worsening of angina

62
Q

Describe the disease causing the following changes to JVP waveform:

Absent a wave
Cannon a wave
Large a wave
Large v wave
Steep y descent
A

Absent a wave - AF
Cannon a wave - complete heart block - atrial contracts against closed tricuspid valve
Large a wave - increased resistance in ventricular filling eg pulmonary hypertension, tricuspid stenosis
Large v wave - tricuspid regurgitation - increased volume into R atria during atrial diastole
Steep y descent - constrictive pericarditis due to restriction in adequate stretch of the cardiac wall.

63
Q

4 features of tetralogy of Fallot

A
  1. VSD
  2. Overriding aorta
  3. Pulmonary stenosis causing RVOTO
  4. RVH
64
Q

What is the role of neprilysin?

A

Neprilysin degrades natriuretic peptides such as ANP, BNP and CNP which cause vasodilatation, decreases cardiac fibrosis/hypertrophy, and increases natriuresis and diuresis which are all beneficial effects in HF.

Therefore neprilyn blockade allows beneficial effects to persist.

Neprilysin inhibition must be accompanied by simultaneous RAAS blockade as neprilysin also metabolizes AT I/II and inhibition of neprilysin alone results in increase of AT II, counteracting the potential benefits.

65
Q

Describe Ebstein anomaly

A

Atrialisation of the RV due to apical displacement of the septal leaflets resulting in RA hypertrophy and relatively small RV.

Also commonly associated with concurrent ASD/PFO and 20% have accessory pathway resulting in tachyarrhythmias

66
Q

What are the key symptoms of AS which denotes prognosis? (3)

A

In descending order of severity:

  1. Angina
  2. Syncope
  3. Heart failure (worst)
67
Q

Indications for transvenous pacing due to high risk of asystole:

A
  1. CHB with broad complex QRS
  2. Recent asystole
  3. Mobitz type 2 AV block
  4. Ventricular pause >3sec
68
Q

5 criterias for use of ivabradine

A

A direct sinus node inhibitor.

Class II to IV NYHA heart failure
For CHF with impaired systolic function <35%
Recent HF hospitalization within 12 months
Sinus rhythm >70 bpm
Despite maximum tolerated beta blockers.

Showed that it reduces hospitalization for heart failure but not CV death (does reduce mortality if HR >77 bpm)

It is NOT a beta blockade substitute, but aids HF management if:

  1. If HR remains high >77 bpm despite adequate BB use as it reduces mortality in this subgroup
  2. If asthma precludes use of beta blockers
  3. Beta blockers are truly not tolerated due to side effects
69
Q

How do you distinguish between constrictive and restrictive cardiomyopathy?

A

Ventricular interdependence is seen in constrictive pericarditis.

Discordance in LV/RVSP with respiration. While RVSP increases during inspiration, LVSP pressure decreases. These changes reverse during expiration.

In restrictive cardiomyopathy, these changes are CONCORDANT.

This is because in constrictive cardiomyopathy, the pericardium is fibrosed while the septum is not involved. Therefore inspiration causes increased RV filling with IV septum to bulge into the LV, causing reduced LV filling.

70
Q

3 indications for surgery in infective endocarditis

A
  1. Prevention of embolism
    - Vegetation >10mm AFTER embolic event despite appropriate antibotic therapy
    - Embolism is rare after at least 2 weeks of antibiotic therapy
  2. Heart failure
  3. Failure of local control with development of abscess, fistula, enlarging vegetation. Also fungal infection.
71
Q

What does 4th heart sound correlate with?

A

P wave.
Atrial contraction against the stiff ventricles.

Seen in HTN, HOCM, AS.

72
Q

Indications for antibiotic prophylaxis for endocarditis?

A

In high risk individuals defined by:

  1. Prosthetic valve - either biological or mechanical
  2. Previous endocarditis
  3. Cyanotic congenital heart disease
  4. High risk lesions such as PDA
  5. Rheumatic heart disease

Undergoing procedures which involve:

  1. Gingival tissue or tooth root manipulation
  2. Perforation of the oral mucosa
  3. Tonsillectomy/adenoidectomy
  4. GI/GU procedure with intercurrent infections

Choice of antibiotics:

  1. Amoxycillin PO/IM/IV, 1hr/30min/immediately before procedure
  2. Clindamycin if amoxicillin is contraindicated or already taking long term penicillin prophyalxis
73
Q

Action of bivalirudin?

A

Reversible direct thrombin inhibitor.

Used as an adjunct therapy in primary PCI

74
Q

How does noradrenaline exert its effect?

A

Through a1, a2 and beta1 receptors.
Unlike epinephrine which also triggers b2 receptors, noradrenaline has a stronger vasoconstrictive action.

Combination of a1 and b1 stimulation increases systemic and pulmonary blood flow, myocardial contractility and cardiac output.

Heart rate can decrease due to intense alpha 1 stimulation.

Potent a2 agonist effect can cause intense peripheral vasoconstriction resulting in organ hypoperfusion and ischaemia.

75
Q

In aortic stenosis, what are the 3 indices which denotes severe disease?

A
  1. mean gradient >40mmHg
  2. valve area <1cm
  3. Dimensionless index <0.25
76
Q

5 causes of constrictive pericarditis

A
  1. TB
  2. Recurrent pericarditis of any cause
  3. Previous radiotherapy
  4. Uraemia
  5. CTD
77
Q

Management of symptomatic VT with structural heart disease (sustained VT, pre/syncope due to VT, unexplained syncope)

A
  1. ICD

2. No prognostic benefit from anti-arrhythmics (only for symptom control and ICD discharge prevention)

78
Q

What is responsible for the plateau phase of the myocardial action potential?

A

Calcium influx, potassium efflux

79
Q

In adult comatose patients after cardiac arrest, what is the most reliable predictor of poor outcome?

A

Absence of pupillary light and corneal reflexes at 72 hours.

Absence of vestibulo-ocular reflexes at 24 hours or longer and Glasgow coma motor score of 2 or less at 72 hours or longer are less reliable.

Myoclonus status in adults was strongly associated with poor outcome, but rare cases of good neurological recovery have been described and accurate diagnosis can be difficult.

80
Q

Management of LQTS

A
  1. Beta blockers in all patients - most benefit in LQTS 1
  2. Avoid QTc prolonging drugs
  3. If previous VT or high risk for VT (QTc >500ms, LQTS1-3, male gender) - ICD
81
Q

What is Gallavardin phenomenon?

A

Usually murmur of AS should be loudest at the second right ICS radiating to carotids.

In Gallavardin phenomenon, murmur is loudest at the apex like MR but without classical radiation to the axilla. Due to stiff ventricles.

82
Q

Mechanism of action of clopidogrel

A

Thienopyridine. Binds irreversibly binds to ADP - P2Y12 receptor, therefore inhibiting binding of ADP to its platelet receptor.

83
Q

Familial hypercholesterolaemia

A

Autosomal dominant
Due to LDL receptor mutation - liver uptake of LDL via LDL receptor is affected.
Homozygous or heterozygous - homozygous generally die by age 30s unless drastically managed eg with liver transplant, ileal bypass, LDL apheresis.

84
Q

Steps in development of atherosclerosis

A
  1. Infiltration of LDL into the tunica intima and subsequent oxidization of LDL
  2. Oxidized LDL causes release of MCP-1 from endothelial and resident SMC to attract monocytes
  3. Monocytes differentiate into macrophages and takes up oxidized LDLs to form foamy macrophages
  4. Foam cells stimulate smooth muscle proliferation
  5. Smooth muscles deposit collagen to form fibrous cap
85
Q

3 roles of HDL

A

1) HDL inhibits oxidation of LDL
2) HDL promotes cholesterol efflux from foam cell
3) HDL inhibits adhesion molecule expression

86
Q

3 factors which increase the gradient across LVOT in HOCM

A
  1. Reduction in preload
  2. Reduction in afterload
  3. Increase in contractility

Therefore anything which causes above such as cilazapril, GTN infusion, frusemide etc will worsen LVOT.

87
Q

Most common valve lesion after repair of ToF?

A

Pulmonary regurgitation

88
Q

Describe LQT1, LQT2, LQT3.

A

LQT1 - K channelopathy. Execise induced arrhythmia. Fail to shorten QT with HR. If homozygous, will present as Jervell-Lange-Nielsen syndrome with associated deafness. Treated with beta blockade. Events are highest for LQT1. Gene involved KCNQ1

LQT2 - also K channelopathy. Seecond most common type. Precipitant mostly emotional reaction or startle. Respond to beta blockade. KCNH2

LQT3 - Na channelopathy. Events mainly occur during sleep. Beta blockade CONTRAINDICATED. If male with LQT3, need to have ICD inserted. Gene involved SCN5A (gain of function mutation. Loss of function mutation leads to Brugada syndrome)

LQT3 gets least events but they are more likely to be fatal.

89
Q

ECG signs of RV infarction

A
  1. Inferior STEMI pattern
  2. ST elevation higher III>II
  3. ST elevation in V1>V2 or ST depression in V2 (highly specific for RV infarction)
  4. Place VR4 leads to check for ST elevation

V1 is the only standard lead which looks directly into RV.

90
Q

6 causes of dominant R wave in V1

A
  1. RVH
  2. RBBB
  3. WPW
  4. Posterior infarction
  5. Muscular dystrophy
  6. Normal variant in infants and young adults
91
Q

5 Contraindications for ETT

A
  1. myocardial infarction less than 7 days ago
  2. unstable angina
  3. uncontrolled hypertension (systolic BP > 180 mmHg) or hypotension (systolic BP < 90 mmHg)
  4. severe aortic stenosis
  5. left bundle branch block: this would make the ECG very difficult to interpret
92
Q

4 risk factors for in-stent stenosis

Cigarette smoking paradox in instent restenosis

A
  1. Post-procedural vessel diameter
  2. Long lesion/plaque
  3. Diabetes
  4. Chronic renal failure

Cigarette smokers require target lesion revascularization (TLR) significantly less frequently than nonsmokers (6.6 versus 10.1 percent in one study)

Despite this difference in clinical restenosis, the angiographic restenosis rate does not differ between the groups and the rates of subsequent death and myocardial infarction are significantly higher for smokers.

Explanations for this paradox include a reduced sensitivity to restenosis or a greater reluctance to seek medical attention for recurrent angina in smokers.

93
Q

Three presentations of angina which suggests ACS

A
  1. Rest angina more than 20min duration
  2. New onset angina that markedly limits physical activity
  3. Increasing angina that is more frequent, longer in duration, or occurs with less exertion than previous angina
94
Q

Difference between unstable angina and NSTEMI

A

Differ primarily in whether the ischaemia is severe enough to cause sufficient myocardial damage to release detectable quantities of troponins.

Prior to availability of troponins, clinically difficult to distinguish between the two.

95
Q

Compare GRACE, TIMI and PURSUIT risk scores in ACS

A

All are used to identify those who are at highest risk for further cardiac event who may benefit from more aggressive therapeutic approach.

If composite end point of death or MI at 1 year is used, GRACE is better than TIMI and PURSUIT.

If composite end point of death or MI at one year and area under the survival curve and need or urgent revascularisation at 30 days, all three predictors were comparable with TIMI somewhat better than GRACE and PURSUIT.

96
Q

7 predictors in TIMI risk score

A
  1. Age >65
  2. Presence of at least 3 risk factors for CAD (HTN, DM, dyslipidaemia, smoking, family history of early MI)
  3. Prior coronary stenosis >50%
  4. ST deviation on admission ECG
  5. At least 2 anginal episode over past 24 hours
    6 Elevated troponin
  6. Use of aspirin in prior seven days (probably a marker for more severe CAD)
0-2 = low risk
3-4 = intermediate risk
5-7 = high risk
97
Q

Which NSTEACS patients benefit from immediate angiography and revascularisation?

A
  1. Haemodynamic instability/cardiogenic shock
  2. Severe LV dysfunction/heart failure
  3. Recurrent/persistent rest angina despite intensive medical therapy
  4. New/worsening MR or new VSD
  5. Sustained ventricular arrythmia
98
Q

Differences in electrophysiologic properties between oral and IV amiodarone

A

Oral amiodarone:

  1. Prolonged QTc due to potassium channel blockade without proarrythmic activity
  2. Inhibits inactivated sodium channel of phase 0, primarily seen at rapid heart rate (class I effect)
  3. Non-competitive beta receptor blockade causing sympathetic activity (class II effect)
  4. Also some class IV effect with blockage of slow calcium channels

IV amiodarone:
1. Compared to PO dosing, produces much smaller increase in action potential duration and refractory period in atrial and ventricular myocardium, therefore little to no increase in QTc/QRS duration

  1. Little or no slowing of the sinus rate
  2. More potent and rapid antiadrenergic activity
  3. Blocks sodium channel activity to a lesser extent than PO dosing
99
Q

5 main Indications for oral amiodarone

A
  1. Maintenance of rhythm control in pAF
  2. Post-cardiac surgery AF prophylaxis
  3. Treatment of ventricular arrhythmias and NSVT in CHF (does not increase mortality even in severe heart failure)
  4. Primary prevention of SCD in ischaemic cardiomyopathy who cannot or refuse to have ICD (not used for secondary prevention as ICD is much superior)
  5. Decrease in shock burden in patients with ICD

Not usually used for other atrial arrhythmias such as A flutter/atrial tachycardia as there are other drugs available with lower toxicity rates and high success rates of ablative therapy.

100
Q

3 main indications for IV amiodarone

A
  1. Restoration and maintenance of sinus rhythm in critically ill patients with hemodynamically unstable atrial fibrillation (AF)
  2. Rate control in critically ill patients with AF with rapid ventricular response in whom the tachycardia is contributing to hemodynamic compromise (when standard rate controlling therapies have been unsuccessful or contraindicated due to hypotension)
  3. Prevention of AF following cardiac surgery
101
Q

What are the two major modifiable risk factors for heart failure as identified from Framingham heart study?

A
  1. Hypertension - responsible for 39% of HF in men, 59% in women
  2. Coronary artery disease - 34% in men, 13% in women

Effect of diabetes and obesity is largely mediated through hypertension.

102
Q

Beta blockers in COPD and asthma

A

Carvedilol was shown to be safe in COPD despite its non-selective nature, therefore beta blockers can be used in COPD.

Howevre asthma still remains a contraindication to beta blockade.

Should do lung function test to test for reversible bronchospasm - if <15% reversibility, can undergo careful supervised initiation. In asthma, need to use cardioselective beta blockers (bisoprolol, metoprolol, nebivolol).

103
Q

Indications for spironolactone/epleronone

A

In class III or IV heart failure with EF <30% provided CrCl >30 ml/min and K <5 mmol/L

Associated with decrease in CV death and heart failure hospitalization.

104
Q

One specific genotype of HOCM associated with significant mortality

A

Arg719Trp mutation which is involved in beta-myosin heavy chain mutation.

105
Q

6 factors which needs to be met for CRTD therapy

A
  1. Ischaemic/dilated cardiomyopathy with LVEF <35%
  2. Sinus rhythm
  3. NYHA class III, IV
  4. LBBB with QRS >120ms
  5. NYHA II with LBBB, QRS >150 ms
  6. Symptomatic despite optimal medical therapy
106
Q

Characteristics of highest responders to CRTD therapy

A

Wider QRS
LBBB
Females
Non-ischaemic cardiomyopathy

107
Q

Role of biventricular pacing in heart failure

A

BLOCK-HF trial - included high degree AV block, NYHA class I-III, LVEF <50%, no indications for CRTD

Showed decrease in all cause death or hospitalization.

108
Q

Private vehicle driving restriction post NSTEMI

A

For PCI following MI - no driving for 2 weeks
Elective PCI - 2 days
CABG - 4 weeks

109
Q

Minimum LVEF required for driving in heart failure

A

Needs to have EF >40%

110
Q

When should you start screening for cardiovascular risk in Torres Strait/Aboriginals?

A

From age of 35

111
Q

What is the greatest risk factor for systemic embolism for AF?

A

Mitral stenosis (10-15% year)

112
Q

Pathophysiology of Brugada syndrome

A

In 10-30% of cases, mutations in the SCN5A gene, which encodes the cardiac voltage-gated sodium channel Nav 1.5, have been found.

These loss-of-function mutations reduce the sodium current (INa) available during the phases 0 (upstroke) and 1 (early repolarization) of the cardiac action potential.

This decrease in INa is thought to affect the right ventricular endocardium differently from the epicardium. Thus, it underlies both the Brugada ECG pattern and the clinical manifestations of the Brugada syndrome.

113
Q

Management of Brugada syndrome

A

Lifestyle changes:
Avoidance of drugs that may induce ST-segment elevation in right precordial leads
Avoidance of excessive alcohol intake and large meals
Prompt treatment of any fever with antipyretic drugs.

ICD implantation in patients who are survivors of an aborted cardiac arrest and/or have documented spontaneous sustained ventricular tachycardia (VT).

114
Q

ECG changes with flecainide therapy

When should you monitor flecainide level?

A

Increased PR and QRS duration.

Flecainide should be monitored if history of CKD, liver disease, concurrent amiodarone treatment.

115
Q

Low dose rivaroxaban post ACS

A

ATLAS-2 study showed that when low dose rivaroxaban was added to DAPT 4-5 days following ACS, it reduced the composite end point of CV death/MI/stroke but with increase in bleeding events (2x ICH events but no increase in fatal bleeding)

Normal dose of rivaroxaban showed similar result with more increase in bleeding events (mainly ICH but no increase in fatal bleeding event)

This reduction in composite end point is thought to be due to reduction in sudden death…

116
Q

How would you manage complete heart block secondary to inferior MI?

A

If it occurs early, usually vagally mediated and is responsive to atropine.
Temporary pacing is required only if HD compromise.
Permanent pacing is often not required.

117
Q

ICD indications for primary preventions for:

  1. Ischaemic cardiomyopathy
  2. Non ischaemic cardiomyopathy
  3. At risk of SCD due to genetic disorders
A
  1. Ischaemic cardiomyopathy
    - Needs to be at least 40 days post MI
    - LVEF <35% and NYHA class II or III
    - LVEF < 30% and NYHA class I
    - LVEF <40%, non sustained VT, inducible VT/VF at EP study
  2. Non-ischaemic cardiomyopathy
    - LVEF <35% and NYHA class II/III
    - Slight benefit in SCD rates but no overall mortality benefit.
    - If wide QRS, CRTD.
  3. SCD at risk patient
    eg: LQTS, Brugada, HOCM, ARVC

ICD should only be inserted if reasonable expectation of survival with a good functional status for more than a year.

118
Q

When should you close PDA?

A

PDA connects aorta to pulmonary artery.

Close if:

  1. Left chamber enlargement
  2. Pulmonary hypertension
  3. Previous endarteritis
  4. Audible murmur.

Late complications of PDA is CHF, endocarditis (10% lifetime risk)

119
Q

Coarctation of aorta and its common presentation, prognosis, indication to treat, and treatment method

A

Commonly presents with HTN of upper limbs, reduced femoral pulses, radio-femoral delay, arm-leg BP gradient. Also exercise intolerance with claudication/angina.

Prognosis is poor if untreated, with reduced life expectancy (75% die before age of 46 in one study)

Treatment is with percutaneous intervention if native and recurrent coarctation - stenting is better than balloon angioplasty.

Treatment is to prevent complications such as stroke, heart failure, aortic dissection.

Follow up is important - residual HTN in 30%, need to check for recurrence and aneurysm formation.

120
Q

3 predictors of sudden cardiac death in ToF

A

LVEDP >12 mmHg
NSVT
QRS >180ms

121
Q

5 most common complications following balloon mitral valvotomy

A
  1. Severe MR in 2-10%
  2. Cardiac tamponade
  3. ASD
  4. LV perforation upto 4%
  5. Embolic phenomena upto 3%
122
Q

Indications for percutaneous balloon mitral valvotomy

A

Moderate to severe MS (valve area <1.5 cm2)
Suitable valve anatomy (pliable, non calcified, minimal subvalvular fusion)

Symptomatic, OR,
Asymptomatic with new onset AF,
PASP >50mmHg at rest, >60mmHg with exercise

123
Q

4 contraindications for PBMV

A
  1. More than mild mitral regurgitation
  2. LA thrombus
  3. Heavy calcifications of both commissures
  4. Predominant subvalvar involvement
124
Q

Criteria for AVR in chronic severe AR

A
  1. Symptomatic (do exercise test)

In asymptomatic patients:

  1. Resting EF <50%
  2. Cardiac surgery required eg: CABG
  3. Resting EF >50% but LVEDD >65mm or LVESD >50
125
Q

How do you distinguish between true severe AS and low gradient AS?

A

In low gradient AS, AV area is reduced in relative fashion due to poor output across the valve. This may be due to low stroke volume or low/normal EF.

Do dobutamine stress echo - by increasing stroke volume in non severe AS, dobutamine will cause increased gradient and increased AV area, while as true severe AS will have increased gradient but unchanged AV area.

126
Q

Compare and contrast TAVI and surgical AVR.

A

TAVI and surgical AVR had similar 2 year survival.

TAVI is associated with greater TIA/CVA (5.5% vs 2.4%), vascular complications and paravalvar AR.

Surgical AVR is associated with more major bleeding and new AF.

127
Q

TAVI indications

4 Contraindications?

A

In symptomatic severe aortic stenosis who are at high risk for surgery.

4 contraindications are:

  1. Bicuspid aortic valve
  2. LV apical thrombus
  3. Peripheral vascular/thoracic aorta access issue
  4. Unsuitable anatomy
128
Q

When would you do concurrent CAGS and valve replacement?

A 
Class IC indication if stenosis >70%
Could also consider CAGS for moderate stenosis 50-70% at the time of valve surgery (class IIa C evidence)
129
Q

Risk of death in severe AS depending on symptoms?

A

If truly asymptomatic (confirmed with stress testing), then annual sudden death rate in SEVERE AS is less than 1%

However, once you develop any symptoms (angina, syncope, heart failure), <50% 5 year survival.

130
Q

4 class 1 indications for severe AS

A
  1. Symptomatic severe AS
  2. Asymptomatic AS who are having other cardiothoracic surgery
  3. Asymptomatic severe AS but with LV dysfunction thought to be related to the valve
  4. Severe asymptomatic AS but with abnormal stress test thought to be due to AS
131
Q

3 indications for AR surgery

A

Almost always done as a valve replacement

  1. Severe symptomatic AR
  2. Asymptomatic severe AR with LVEF <50%
  3. Having other cardiothoracic surgeries
132
Q

4 indications for aortic root/ascending aorta surgery, regardless of AR severity

A

Normal ascending aorta dimensions <35 mm

Surgery indicated if:

  1. Marfans with ascending aorta >50mm
  2. Marfans with >45mm with risk factors (eg: family history of rupture, ie operate earlier)
  3. Bicuspid >50mm with risk factors
  4. For everyone else, consider surgery >55mm
133
Q

Indications for TR/TS surgery

A

Severe TR is almost always the consequence of some other pathology (eg pulmonary hypertension). Therefore fixing the TR wont fix the underlying problem.

Pretty much if you are fixing the L sided valves then you may as well do the right side as well…
Isolated TV surgery is rare.

Also surgery is indicated in symptomatic patients with severe TS.

134
Q

Duke’s criteria of infective endocarditis

A

Requires 2 major criteria, or 1 major/3 minor criteria, or all 5 minor criteria.

Major criteria:

  1. Growth of appropriate organisms for at least 2 separate blood cultures
  2. Single positive for coxiella
  3. Imaging shows vegetation, abscess, perforation, new dehiscence of prosthetic valve, or abnormal PET/SPECT for valve >3 months since implantation

Minor criteria:

  1. Predisposition - heart disease, IVDU
  2. Fever
  3. Embolic phenomena
  4. Immunologic phenomena
  5. Microbiology not meeting major criteria
135
Q

Empiric antibiotic choice in severely unwell IE

A

Ampicillin + flucloxacillin + gentamicin

Vancomycin + gentamycin +/- rifampicin if prosthetic valve <12 months

136
Q

How would you manage R sided endocarditis?

A

Surgery is usually not indicated, and given high rates of IVDU, there are concerns about recurrence and anticoagulation etc.

Could consider surgery in:

  1. Difficult to eradicate organism or culture positivity after 7 days
  2. Persistent vegetation >20mm after PE
  3. Refractory RHF secondary to severe TR
137
Q

What do you do when you see non-obstructive plaques on CTCA?

A

Start them on statins if they are not on it already.
Shown to reduce mortality.
This is because non obstructive plaques actually matter - majority of MI occur on no-obstructive lesions.
3 vessel non-obstructive plaques have a HR of around 5.

In contrast, if you have a normal CTCA result, then you have a very low incidence of cardiac event of 0.17%/year, therefore have a ‘warranty’ period of 5 years.

138
Q

When to use CTCA - 5 indications

A

Most useful in excluding obstructive CAD.

  1. Equivocal stress test in a young patient
  2. Chest pain with intermediate risk of CAD, where exercise test will be precluded by uninterpretable ECG or unable to exercise
  3. Excluding CAD in cardiomyopathy
  4. Checking patency of bypass grafts (100% sensitivity for bypass graft stenosis) or coronary stents >3.5mm (eg left main stents)
  5. Assessment prior to non-coronary cardiac surgery
139
Q

Significance of mid wall late gadolinium enhancement in cardiac MRI for dilated cardiomyopathy

A

Mid wall LGE suggests interstitial fibrosis.

LGE predicts higher risk of MACE (death, heart failure, and ICD discharge) and also predicts lack of improvement in newly diagnosed DCM.

140
Q

Mechanism of action of ezetimibe?

A

Ezetimibe reduces the small intestinal enterocyte uptake and absorption of cholesterol by binding to Niemann-Pick C1 Like 1 (NPC1L1), which keeps cholesterol in the intestinal lumen for excretion.

FRACP written exam preparation (18 decks)

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