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FRACP Shuyu > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the evidence for NOACs in the treatment of embolic stroke of undetermine source (ESUS)

A

NAVIGATE ESUS (NEJM 2018) Rivaroxaban was not superior to aspirin with regard to the prevention of recurrent stroke after an initial embolic stroke of undetermined source and was associated with a higher risk of bleeding.

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2
Q

What are MBS indications for loop recorders

A

1) Recurrent/unexplained syncrope 2) Cryptogeni stroke/ESUS

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3
Q

What level of ETOH is bad for AF

A

Any ETOH consumption

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4
Q

Treatment for AF and Heart Failure

A

Greater evidence that ablation for AF in heart failure is more beneficial. CASTLE AF (NEJM 2018) found that patients with NYHA II + HF with LVEF <35% and an implantable defibrillator benefited from ablation over medical therapy (rate or rhythm control) - they had lower rates of death or hospitalisation for worsening heart failure. CAMERA-MRI (JACC 2017) found that in patients with persistent AF and LVEF <45%, ablation (cf medical rate control) have increased rates of improvements of ventricular function, especially in the absence of ventricular fibrosis.

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5
Q
A

Brugada syndrome

Cardiac sodium channelopathy with incomplete penetrance autosomal dominant inheritance.

Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave.

It is often referred to as Brugada sign.

Should be in the right clinical setting (VF or polymorphic VT, family hx of sudden cardiac death <45, syncope).

ICD

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6
Q

Diagnosis of heart failure and classifications of HFrEF vs HFpEF

A

Clinical diagnosis

HFrEF = LVEF <50%

HFpEF = LVEF >50% and objective evidence of structural abnormalities or diastolic dysfunction (demonstrated by heart cath, ECHO, BNP/NT-proBNP, exercise testing)

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7
Q

What is recommended for T2DM and hF

A

SGLT2 inhibitors are recommended for patients with T2DM and cardiovascular disease who does not have sufficient glycaemic control with metformin.

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8
Q

Investigation for coronary artery disease in low-intermediate risk groups

A

Either computed tomography (CT) coronary angiography or cardiac magnetic resonance imaging (CMR) with late gadolinium enhancement (LGE) may be considered in patients with HF who have a low-to-intermediate pre-test probability of coronary artery disease

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9
Q

Patients with dilated cardiomyopathy (DCM) associated with conduction disease should get what investigation?

A

Genetic testing

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10
Q

When should the follow up TTE be performed after commencement of optimal medical therapy for HFrEF

A

3-6 months after the start of optimal medical therapy, or if there has been a change in clinical status, to assess the appropriateness for other treatments, including device therapy (implantable cardioverter defibrillator (ICD) or cardiac resynchronisation therapy (CRT), or both).

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11
Q

What is recommended for all HFrEF <40% unless not tolerated/contraindicated?

A
  1. ACE - I
  2. BB (once stabilised with no or minimal clinical congestion on physical examination)
  3. MRA
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12
Q

When are ARNIs recommended

A

Replacement for an ACE inhibitor (with at least a 36-hour washout window) or an ARB in patients with HFrEF associated with an LVEF of less than or equal to 40% despite receiving maximally tolerated or target doses of an ACE inhibitor (or ARB) and a beta-blocker (unless contraindicated), with or without an MRA, to decrease mortality and decrease hospitalisation.2

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13
Q

When is ivabradine indicated?

A

HFrEF associated with an LVEF of less than or equal to 35% and with a sinus rate of 70 bpm and above, despite receiving maximally tolerated or target doses of an ACE inhibitor (or ARB) and a beta-blocker (unless contraindicated), with or without an MRA, to decrease the combined endpoint of cardiovascular mortality and HF hospitalisation.

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14
Q

When is cardiac resynchronisation therapy recommended in HFrEF?

A

Sinus rhythm, an LVEF of less than or equal to 35% and a QRS duration of 150 ms or more despite optimal medical therapy to decrease mortality, decrease hospitalisation for HF, and improve symptoms.

They can be considered in LVEF <35% and QRS 130-149.

They can also be considered in patients with HFrEF associated with an LVEF of less than or equal to 50% accompanied by high-grade atrioventricular (AV) block requiring pacing, to decrease hospitalisation for HF.3

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15
Q

When is cardiac resynchronisation therapy contraindiated in HFrEF?

A

CRT is contraindicated in patients with QRS duration of less than 130 ms, because of lack of efficacy and possible harm.4

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16
Q

Indications for ICD in HFrEF

A

Strong recommendation: Primary prevention indication in patients with HFrEF associated with ischaemic heart disease and an LVEF of less than or equal to 35% to decrease mortality

Weak recommendation: HFrEF associated with dilated cardiomyopathy and an LVEF of less than or equal to 35%, to decrease mortality.

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17
Q

Treatment for central sleep apnoea

A

NOT adaptive servoventilation.

Aim is to treat the heart failure in predominant central sleep apnoea

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18
Q

How to treat iron deficiency in HFrEF in patients who have persistent symptoms

A

IV iron

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19
Q

ICH rates in thrombolysis

A

~1%

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20
Q

Timing for PCI in successful lysis of STEMI

A

3-24 hour coronary angiography

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21
Q

Example of a direct thrombin inhibitor

A

Dabigatran

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22
Q

Example of an indirect thrombin inhibitor

A

UFH

LMWH

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23
Q

Risk factors for excess bleeding risk when using prasugrel

A

Previous stroke, >75 years old, <60kg

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24
Q

How longs should DAPT ideally continue for post ACS

A

12 months (although several trials have shown non inferiority in 6 months)

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25
Q

Dual therapy vs triple therapy post PCI

A

Triple therapy had worse ischaemic and bleeding outcomes.

If someone needs the NOAC, drop the aspirin.

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26
Q

Timing of invasive management of NSTEACS

A

Reasonable to perform angio 48-72 hrs but earlier in high risk group

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27
Q

What anti hypertensive decreases risk of CV death, MI or stroke in high risk patients

A

ramipril

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28
Q

Patients with high CV risk with high triglycerides

A

NJEM 2019 trial showed high dose fish oil icosapent ethyl 2g daily

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29
Q

Effect of PCSK9 inhibitors (evolocumab/alirocumab) on lowering CVS risk

A

Mild improvement in cardiovascular outcomes. Right now only use for famiiial hypercholesterolaemia. Very expensive

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30
Q

Timeframe for ECG in acute chest pain presentation

A

<10min

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31
Q

TImeframe for symptom onset for which an eligible patient should recieve emergency reperfusion therapy (STEMI)

A

<12 hours

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32
Q

What is the timeframe for which patients should get PCI over fibrinolysis

A

If PCI can be performed within 90min of medical contact

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33
Q

When to immediately transfer for rescue angioplasty post fibrinolysis for STEMI

A

<50% ST recovery at 60-90 min and/or with haemodynamic instability

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34
Q

When is immediate invasive strategy (<2hr of admission) recommended in NSTEACS?

A

Patients with ongoing ischaemia, haemodynamic compromise, arrhythmias, mechanical complications of MI, acute heart failure, recurrent dynamic or widespread ST-segment or T-wave changes on ECG (high to very high risk)

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35
Q

Who to give aspirin in ACS

A

Everyone - 300mg initially then 100mg/day

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36
Q

Who to give DAPT initially in ACS and which antiplatelet is preferred

A

Intermediate to very high risk of recurrent ischaemic events

Ticagrelor and prasugrel is preferred

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37
Q

When is glycoprotein IIb/IIIa inihibition in combination with heparin recommended?

A

At time of PCI in high risk clinical and angiographic characteristics or for treating thrombotic complications among patients with ACS

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38
Q

How long should asprin be continued post ACS

A

Indefinitely unless it is not tolerated or an indication for anticoagulation becomes apparent

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39
Q

How long should DAPT be continued for post angio

A

Clopidogrel/ticagrelor up to 12 months regardless of whether coronary revascularisation was performed. The use of prasugrel should be confined to patients recieving PCI

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40
Q

Which antiplatelet should be used with fibrinolysis

A

Clopidogrel (no evidence re ticagrelor/prasugrel)

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41
Q

What is the compression to breath ration in BLS

A

30:2

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42
Q

What is the deal depth in chest compressions

A

>5cm

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43
Q

When to administer adrenaline in ALS (shockable vs non shockable)

A

after 2 min for shockable

immediately for non shockable

every 3-5min

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44
Q

When to give amiodarone

A

After 3 shocks

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45
Q

ALS 4Hs and 4Ts

A

Hypoxia

Hypo/hyperthermia

Hypovolaemia

Hypo/hyperkalaemia/metabolic

Tamponade

Tension

Thrombosis (pulmonary + cardiac)

Toxins

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46
Q

When to do rhythm check in ALS

A

As soon as the defibrillator is available

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47
Q

What are the standard energy levels for the defibrillators

A

200J biphasic or 360J monophasic

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48
Q

Bystander CPR: chest compression only vs standard cardiopulmonary resuscitation

A

Compression only improved survival (Hupfl Lancet 2010)

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49
Q

What is a risk factor for familial hypercholesterolaemia?

A

xanthomata

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50
Q

Management of familiar hypercholesterolaemia

A

Screen first degree relatives

Statins first line

LDL >3.3 then PCSK9 inhibitors

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51
Q

Familial combined hyperlipidaemia inheritance and phenotype

A

Polygenic inheritance

Combination of high cholesterol, high Tf and low HDL

LDL to apo-B ratio of <1.2

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52
Q

FCHL (familial combined hyperlipidaemia) management

A

statins to reduce apo-B

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53
Q

What lipid profile is diabetes associated with

A

Increased Tg, increased LDL, low HDL

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54
Q

Cholestatic liver disease, PBC

A

accumulation of lipoprotein X - SEE SLIDES

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55
Q

Hypothyroidism lipoprofile

A

Isolated raised LDL

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56
Q

Obesity lipid profile

A

Increases everything aside from HDL

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57
Q

Heavy ETOH intake lipid profile

A

Isolated raised triglycerides

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58
Q

Antipsychotics lipid profile

A

High Tgs

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59
Q

When to use ezetimibe

A

Intolerant to statins or in addition to meet targets

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60
Q

Mechanism of statins

A

HMG-COA reductase for endogenous cholesterol production

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61
Q

Mechanism action of PCSK9 inhibtors

A

Breaking down LDL receptors (increases uptake of LDL into hepatic cells)

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62
Q

Target for secondary prevention (cholesterol)

A

LDL <1.8

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63
Q

definition of HTN (SBP and DBP)

A

SBP >130

DBP >80

stage 1 for first 10mmHg of increase and stage 2 thereafter

must be done in 2 sittings

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64
Q

When to start a statin for primary prevention

A

LDL >4.9

DM and age 40-75

Others dependent on risk score (ASCVD)

Coronary artery calcium score

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65
Q

What antihypertension will affect the aldo:renin the most

A

Spironolactone bu increasing renin, increasing K+ and reducing Na

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66
Q

What medication is important to avoid in pheochromacytoma

A

Beta-blockers due to unopposed alpha stimulation and worsening hypertension

Should use alpha blocker first

(Can initiate beta blocker after the intiation of alpha blockers)

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67
Q

When to start treatment for stage I hypertension

A

If 10 year risk calculation is >10%

(stage one is 130-140 mmHg SBP)

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68
Q

What antihypertensive agent in DM

A

Diuretics (ALLHAT) - chlorthalidone

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69
Q

What BP treatment targets?

A

<130/80

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70
Q

What is the normal aldosterone:renin syndrome

A

<30

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71
Q

main mechanism of action of dihydropyridine calcium channel antagonist

A

dihydropyridine = peripheral

reduce vascular smooth muscle tone

72
Q

What are P-GP inhibitors vs substrates

A

P-glycoprotein are drug transporters that determine the uptake and efflux of a range of drugs.

Inhibitors increase bioavailability and inducers decrease bioavailability

inhibitors - verapamil, clarithromycin, erythromycin, ritonavir, amiodarone

inducers - rifampicin, St John’s wort

substrates - dig, dabigatran, calcineurin inhibitors, amliodipine, docetaxel, etoposide, protease inhibitors

73
Q

what antihypertensive causes constipation

A

calcium channel blockers

74
Q

factors causing false BP measurement

A

underestimates BP: smoking

Overestimates BP: caffeine, talking, small cuff, pseudohypertension (arterial stiffness), crossing legs, unsupported arms

Small cuff overestimates the most from that list

75
Q

What is the first line screening test for structural heart disease?

A

ECG

76
Q

What types of AV blocks are indications to PPM regardless of symptoms?

A

Mobitz type II AV block and third-degree AV block not caused by reversible or physiologic causes

77
Q

When are cardiac resynchronisation therapy and HIs bundle pacing preferred to right ventricular pacing?

A

LVEF 36-50% and AV block who have an indication for permanent pacing and are expected to requiring ventricular pacing more than 40% of the time

78
Q

Pacing requirements in an acute inferior infarct that results in complete heart block that has an early response to atropine?

A

Only temporary pacing if haemodynamic compromise. Permanent pacing often not required.

79
Q

Acute management of torsades de pointes secondary to bradycardia?

A
  1. Magnesium, isoprenaline
  2. Urgent temporary/permanent pacemaker insertion
80
Q

What is the ECG and the management?

A

Trifascicular block - AV block, RBBB, LAH

Progression to CHB is 0.6-0.8/year

Will need monitoring if requiring surgery

PPM is not necessary at this stage

81
Q

What is a trifascular block and what is the management of a patient with symptomatic trifascular block?

A

1st degree AV block, RBBB and LAD

Progression to CHD is 10%

PPM probably indicated

82
Q

Management of a patient with a history of aortic repair for severe AS who presents with syncope and the ECG shows complete heart block

A
  1. Inpatient cardiology review
  2. PPM indicated - class 2B indication for bundle of HIS/biventricular pacing. 2A indication if there is LV dysfunction
83
Q

Indications for ICD in primary prevention in ischaemic patients

A

Patients at least 40 days post-MI

  • LVEF ≤ 35% NYHA class II or III
  • LVEF ≤ 30% NYHA class I
  • LVEF ≤ 40% non-sust VT, inducible VT/VF at EPS
84
Q

Primary prevention ICD indications in non-ischaemic patients

A

LVEF <35%

NYHA class II or III

(DANISH study NEJM 2016 no mortality benefit in NICM patients but subgroup analysis showed benefit in patients <70yr)

85
Q

Cardiac MRI - Cine imaging “SSFP”

What does this sequence require and what does it do

A

No contrast

10 sec breath hold

86
Q

Cardiac MRI - Late Gadolinium enhancement

What does this sequence require and what does it do

A

6-20min after gadolilium.

Correlates with scar (As the gad takes longer to wash out). Increase enhancement is worse prognosis.

Relates to likelihood to improvement.

The distribution of LGE can be indicative of aetiology - e.g. ischaemia always involves the subendothelium (even if it’s transmural) but myocarditis might spare the subendothelium

Good for detecting cardiac involvement in systemic sarcoidosis

87
Q

Cardiac MRI - Spin ECHO (black blood) imaging:

What does this sequence require and what does it do?

A

Shows myocardial oedema

Vessel anatomy

88
Q

Cardiac MRI - Mapping - T1, T2, T2*

What does this sequence require and what does it do

A

T1 mapping - quantify diffuse processes e.g. interstitial fibrosis

T2 mapping - oedema

T2* - iron quantification

89
Q

Cardiac MRI - Flow quantification

What does this sequence require and what does it do

A

Get flow curves of things e.g. aortic regurg

90
Q

Cardiac MRI in congenital heart disease indications

A

Tetralogy of fallot - quality right ventricular size and volume. They often get severe residual pulmonary regurgitation. Required for criteria for surgical mx

91
Q

What is coronary calcium pathognemonic for?

A

Athersclerotic disease

92
Q

Limitations of CTCA

A

Heavy calcification of the vessel would not be alble to specify on CT whether or not there is a stenosis

It is also hard to see if the stenosis is causing angina

93
Q

What is CTCA better at seeing than angiogram

A

Non obstructive plaques

Data for benefit of starting statin

94
Q

What can cause false +ve in stress ECHO

A

LVH, LBBB

95
Q

What stress testing has the highest sensitivity

A

Nuclear (although MRI is probably also pretty good)

96
Q
A
97
Q

what is the bernoulli equation?

A

change in pressure approx equals 4velocity2

Used to measure the pulmonary artery pressure

98
Q

How to calculate the peak right ventricular systolic pressure from TR velocity and whats is its significance

A

It is a way to screen for pulmonary arterial hypertension with continuous wave doppler. >35mmHg would be abnormal.

RV pressure = 4 (TR velocity)2 + RA pressure

Make sure to use peak velocity figures

99
Q

What is the normal mitral valve orifice area?

A

4-6cm2

100
Q

Mitral stenosis severity by valve area

A

Mild > 1.5 cm2
Mod 1.0 - 1.5 cm2

Severe < 1.0cm2

101
Q

First line management of mod mitral valve stenosis in pregnancy with pulmonary oedema driven by tachycardia?

A

Beta blockers (metoprolol), balloon valvuloplasty next line

102
Q

Percutaneous Balloon Mitral Valvuloplasty indications

A
  • Moderate or severe MS (<1.5 cm2)
  • Suitable valve (pliable, non- calcified, minimal

subvalvar fusion)

  • >1.5cm2 if pulmonary arterial wedge pressure >25mmHg/mitral valvular gradient >15mmHg with exercise
  • asymptomatic new onset AF (pulmonary artery systolic pressure >50mmHg at rest)
  • before pregnancy
103
Q

Percutaneous balloon mitral valvuloplasty contraindications

A
  1. More than mild mitral regurgitation
  2. LA thrombus (?appendage)
  3. Heavy calcification of both commissures
  4. Predominant subvalvar involvement
104
Q

What is ejection fraction misleading in mitral regurgitation?

A

In the early stages, there is increased EF because the LV is ejecting into low pressure LA (decreased afterload)

In the later stages, increased LV size and interstitial fibrosis causes the EF to decrease again.

Even with normal EF, the LV contractility could still be reduced

105
Q

When is mitral valve surgery indicated in secondary MR?

A

Class IIb evidence for severe symptomatic secondary MR with persistent NYHA class III - IV symptoms

106
Q

When is mitral valve surgery indicated for primary MR?

A

Severe MR

Symptomatic

or

Asymptomatic and LVEF 30-60%

107
Q

How to treat acute severe aortic regurg

A

Aortic valve replacement

Avoid bradycardia (slow heart rate allows more time for regurg)

108
Q

When is aortic valve replacement for chronic aortic regurg indicated

A

Severe aortic regurgitation

Stage D (symptomatic)

OR

Stage C (asymptomatic) + LVEF <50% or LVEF >50% and LVESF >50mm or LVEDD >65mm

LVEF <50% is a stronger indication

109
Q

Aortic Stenosis severity

A
110
Q

Why might there is severe decreased aortic valve area in mild/mod aortic stenosis?

A

Pseudostenosis due to cardiomyopathy. The LV isn’t able to produce enough outflow to keep the valve open.

111
Q

When is aortic valve replacement (via TAVI or surgery) indicated?

A
  1. Severe AS (mean gradient >40 mmHg, AVA <1.0cm) and symptomatic or LVEF <50%
  2. Severe AS (mean gradient <40mmHg and AVA <1.0 but confirmed stenosis with low dose dobutamine stress ECHO)
112
Q

Adverse effects of TAVI vs SAVR

A

SAVR: AKI, new AF and major bleeding

TAVI:

Short term - Vascular cx., pacemaker, AR

Long term - Paravalvar regurgitation, valve thrombosis, prosthetic endocarditis, late bleeding

113
Q

Should preventative PCI be performed on non-infarct arteries with >50% stenosis during PCI for STEMI?

A

Yes - reduces CV mortality, non fatal MI, refractory angina

PRAMI, CvPRIT

The optimal timing of index procedure vs index admission is unclear - approach is to only perform if there is a very significant bystander stenosis

114
Q

Should thromboaspiration be performed in STEMIs?

A

No, 1 study (TAPAS) showed benefit but subsequent studies (taste, total) have not

115
Q

When to use femoral vs radial access for PCI?

A

Radial clearly better in STEMI group

Unclear for NSTEMI and Stable angina

Radial reduces major bleeding in all groups

Radial reduces major vascular complications in all groups but it’s a complication that is poorly captured in the registry

116
Q

Drug eluding stents vs balloon valvuloplasty stents

A

BVS was invented to combat risk of inflammation

DES better for target lesion failure

No difference for cardiac death

DES better for target vessel MI

DES better for stent thrombosis +++

117
Q

When to continue DAPT in balloon valvuloplasty stents

A

3 years due to risk of in stent thrombosis

118
Q

How deep should chest compressions be

A

5-6 cm

119
Q

Haemodynamially compromised ventricular tachycardia treatment

A

synchronised shock x3, O2, IV access, exclusion of reversible factor, amiodarone

120
Q

When is an ARNI indictaed in HFrEF ? (sacubitril-valsartan)

A

NYHA class II or III HFrEF (left ventricular ejection fraction [LVEF] ≤40 percent) with all of the following criteria:

current or prior elevated natriuretic peptide level, hemodynamic stability with systolic blood pressure (SBP) ≥100 mmHg, and no history of angioedema. Sacubitril-valsartan may be initiated as a component of initial therapy for HFrEF.

121
Q

Examination findings and ECG of HOCM

A
  • double or even triple apical impulse
  • evidence of heart failure
  • jerky pulse
  • S2 may be paradoxically split if very high LVOT gradient
  • prominent a wave on JVP due to decreased RV compliance
  • Systolic ejection murmur (due to LVOTO)

ECG:

  • > LVH critieria
  • > deep anterior lateral TWI
  • > dagger-like Q waves in infero-lateral leads
122
Q

Clinical characteristics of Arrhythmogenic Right Ventricular Cardiomyopathy and ECG findings

A

paroxysmal ventricular arrhythmias and sudden cardiac death.

normally autosomal dominant inheritance

symptoms due to ventricular ectopic beats or sustained ventricular tachycardia (with LBBB morphology) and typically presents with palpitations, syncope or cardiac arrest precipitated by exercise.

ECG:

Epsilon wave (most specific finding, seen in 30% of patients) - blip at the end of QRS

T wave inversions in V1-3 (85% of patients)

Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)

Localised QRS widening of 110ms in V1-3

Paroxysmal episodes of ventricular tachycardia with a LBBB morphology

123
Q

Mitral valve prolapse clinical features

A

Symptoms are non specific and unreliable - dyspnoea, palpitations, exercise intolerance

non-ejection click (single or multiple) and the murmur of mitral regurgitation

124
Q

ECG diagnosis and management

A

WPW w AF

Chaotic looking wide complex ECG

Do not use AV blocking agents (adenosine, BB, C-blocker) as those may trigger VF.

Stable atrial fibrillation patient with WPW, you can use procainamide or ibutilide or amiodarone to convert the rhythm to normal without an electrical cardioversion

Unstable - DCR

125
Q

When is genetic testing useful in Brugada syndrome

A
  • Patients with a clinical diagnosis of brugada syndrome (only type 1)
  • In relatives where pathological mutation identified in proband
126
Q

What gene is Brugada syndrome associated with and what kind of mutation is it?

A

SCN5A decrease in function

(SCN5A gain in function can cause long QT3)

Less commonly: cardiac L-type Ca+ channel alpha subunit, CACNA1c and the βsubunit, CACNB2b

127
Q

What are the clinical features of Catecholaminergic Polymorphic Ventricular Tachycardia and its genetic inheritance

A

adrenergic-induced bidirectional and polymorphic ventricular tachycardia (induced by exercise testing, isoproterenol infusion or emotion)

resting ECG normal

autosomal dominant (RyR2)[2] or recessive (CASQ2) inheritance

128
Q

ECG findings of Arrhythmogenic Right Ventricular Dysplasia

A

Epsilon wave (most specific finding, seen in 30% of patients)

T wave inversion in V1-3 (85% of patients)

Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)

Localised QRS widening of 110ms in V1-3

Paroxysmal episodes of ventricular tachycardia with LBBB morphology

129
Q

Is the y descent prominent in constrictive pericarditis or cardiac tamponade

A

constrictive pericarditis

In tamponade, the volume of the heart is confined by the pericardium, so the RV cannot expand further to accommodate the volume from the RA, so the RA doesn’t empty and there is no y descent. In constrictive pericarditis, the RV is adherent to the pericardium, so that when the RV relaxes the pericardium helps to expand it rapidly, “sucking” the blood out of the RA and leading to a rapid y descent.

130
Q

What is kussmaul’s sign more assocaited with

A

constrictive pericarditis > cardiac tamponade

131
Q

What’s troponin I, T and C

A

Troponins are regulatory proteins for heart muscles

I - inhibits actin (used at The Alfred)

T binds tropomysin

C binds to calcium ions

132
Q

When do patients with thrombolyss do best?

A

within the first hour (as good as PCI in that group)

133
Q

Adverse effects of ticagrelor (aside from bleeding)

A

Bradycardia, shortness of breath

134
Q

What is thromboxane inhibitor

A

aspirin (cox-1 inihibitor - precursor of TxA2)

135
Q

What area of infarction is at the highest risk of LV thrombus

A

Anterior infarct ( do not discharge prior TTE before discharge)

136
Q

What kind of ST depression morpholog is more sinister

A

Downsloping

137
Q

Wallen’s syndrome

A

Anterior T wave inversion

LAD lesion

138
Q

Mx of takasubo’s

A

beta blocker, ACE-I

repeat TTE at 6-8 weeks

139
Q

MOA of PCSK9

A

Stops LDL receptors from being put up out onto the cell

e.g. alirocumab and evolovumab

(injections)

140
Q

Differentiate VT from SVT w aberrancy

A

Extreme axis deviation AVR +ve, I/AVF negative

AV dissociation, capture beats, fusion beats

141
Q

Marriott’s sign

A
142
Q

Bidirectional tachycardia

A

Catecholaminergic polymorphic ventricular tachycardia

143
Q

2 types of monomorphic VT

A

RVOT VT:

  • LBBB
  • Rightward/inferior axis
  • Beta blocker 1st line
  • Can respond to vagal/adenosine

Fasciculat VT:

  • young ppl w no structural heart disease

Very responsive to verapamil

triggered by rest, exercise, beta agonist

RBBB (coming from L fasicle)

144
Q

Management for VT

A

see slides

145
Q

Flecanide contraindications

A

CI - IHD, cardiomyopathy

CLass Ic anyarrhtyhmic

146
Q

Orthodromic AVRT vs antidromic AVRT

A

Orthodromic - impulse travels down normal AV nodal pathway but comes back through accessory -> narrow appearance.

Antidromic - comes up AV node retrogradly and broad complex

147
Q

orthodromic AVRT vs AVNRT

A

AVRT is a bit slower

p wave is closer to QRS in AVNRT (pseudo R’ in V1)

148
Q

acute mx of 1) orthodromic AVRT, 2) anridromic AVRT, 3) AF WPW

A

Don’t use AV blocking agents in antidromic AVRT or AF w preexcitation

149
Q

Polymorphic VT 1st line management

A

Prolonged QT vs normal QT

prolonged QT: Magnesium

then isoprenaline, temporary pacing

For normal QT, ischaemic until proven otherwise

150
Q

positive concordance in VT

A
151
Q

biggest RF for arrhythmia after bypass

A

LV function

152
Q

Outflow tract VT

A
153
Q

What NOAC has a lower cut off for eGFR

A

NOAC is 25, others are 30

154
Q

Signs on ECG of AVNRT

A

very fast rates up to 200 bpm

pseudo R’ in V 1 (which is the retrograde p wave)

155
Q

What STEMIS are more likely to have permanent requirements for PPM

A

Anterior STEMI

156
Q

Management of pcaemaker mediated tachycardia

A

Magnet over device to turn the PPM into VVI

a sign that it is PMT is that the rate is really close to the upper tracking rate

157
Q

Where is the current delivered in cardiac resynchronisation

A

on the R wave

158
Q

Flecanide challenge

A

Unmask brugada

159
Q

When are abx given prophylactically prior procedure?

A

30min prior procedure

160
Q

Which side IE are more likely to get surgical management

A

left side

161
Q

Loud s1

A

MS, TS, epstein’s anomaly, ASD

162
Q

Tricuspid stenosis JVP

A

elevated a wave

163
Q

Fixed spliting of second heart sound

A

ASD

164
Q

Tetralogy of fallot

A

vsd, overriding aorta, pulmonary stenosis, RVTO

165
Q

most likely complication following tetralogy of fallot repair

A

PR (as the part of the surgery involve access to the myocardium through the pulmonary artery, stretching the pulmonary valve)

166
Q

primum ASD ECG feature

A

AV block due to the close assocaition with AV node

167
Q

The MR usually have 2 kicks - what condition causes the 2nd kick to disappear?

A

First is from early diastole and second is from the atrial kick which is absent in AF

168
Q

Most common cause of sudden cardiac death in young adults

A

coronary artery disease

(well actually unexplained is first)

169
Q

Diagnosis of HCM

A

imaging diagnosis

  • Wall thickness >15mm
  • Can have slightly thinner wall if there are other features
170
Q

What might HCM with syncope at rest suggest?

A

ventricular arrhythmias

(cf syncope w exertion is suggestive of LVOT)

171
Q

ARVC management

A

activity restriction

beta blockers

ICD (secondary prevention and high risk primary prevention)

172
Q

Romano-ward syndrome

A

autosomal dominant LQT syndrome

KCNQ1, KCNH2, SCN5A

173
Q

Jervell and Lange-Nielsen syndrome

A

autosomal recessive long QT syndrome associated with neurosensori hearing loss

KCNE1 and KCNQ1 genes

174
Q

which beta blockers for long QT

A

propranolol > atenolol > metoprolol

175
Q

diagnosis of type 2 brudaga

A

can consider flecanide challenge (not used in in type 1)

176
Q
A

FRACP Shuyu (65 decks)

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