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FRACP Shuyu > RPA cardiology > Flashcards

RPA cardiology Flashcards

1
Q

ECG

A

VT

more QRS complexes than p waves

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2
Q

most common cause of VT

A

old myocardial infarct

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3
Q

VT not compromised management

A

12 lead ECG

carotid sinus/adenosine

Drugs - sotalol, lignocaine (if acute ischaemic), amiodarone

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4
Q

tiered therapy for

bradycardia

VT

resistant VT

VF

A

bradycardiac - pacing

VT - overdrive pacing

resistant VT - DC cardioversion

VF - DC shock

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5
Q

cardioversion vs defibrillation

A

defbrillation shocks on command where as cardioversion times the shock away from the t wave

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6
Q

Use of antharrythic drugs in ICD patients

A

not unless required or getting lots of shocks

sotalol decreases risk of death and defibrillation

amiodarone less useful

https://www.nejm.org/doi/full/10.1056/NEJM199906173402402

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7
Q

when is ablation for VT first

A

“VT is a normal heart”

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8
Q

disadvantages of totally subcutaneous ICD

A

can’t pace for bradycardia or pace-terminate arrhythmias

useful for people who don’t need pacing (e.g. long QT) and people who need the device for many years

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9
Q

long term management of VT - with and without heart disease

A

with heart disease

  1. ICD + beta block
  2. if frequent episodes - add antharrhythmic
  3. If still frequent episodes - catheter ablation

without heart disease

beta blockers/verapamil

catheter ablation

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10
Q

3 criteria

primary prevention ICD indications

A

LVEF <0.35 despite optimal medical therapy

Expected longevity >2yr

>30 days after AMI

However, the DANISH study did not show efficacy of ICDs in people >60 who had symptomatic systolic heart failure NOT caued by coronary artery disease

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11
Q
A

AVNRT

narrow complex QRS without p wave

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12
Q
A

access pathway

p wave in ST segment SVT

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13
Q
A

p wave first then QRS (narrow complex tachycardia)

atrial tachycardia

suspected based on the shape of p waves (funny shape or different access)

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14
Q

pharmacological and ablation

SVT prevention

A

drugs not very effective

similar efficacy

used drugs with once daily dose: verapamil SR, dig, atenolol

reduce frequent but does not abolish them

most poeple have catheter ablation

90-95% cure rate

risks: vascular 1/100, heart block 1/200-500, death/AMI/CVA 1/2000

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15
Q
A

delta wave and abnormal repolarisation

WPW syndrome

AV node and accessory pathway. The impulse travels from the the SA to the AV and accessory pathway. The delta wave is the early excitation of the ventricle.

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16
Q

types of WPW

A

SVT antrograde over AP

atrial fibrillation

SVT anterograde over AP

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17
Q

Management of WPW w accessory pathway

A

amiodarone or flecanide

no AV blocking drugs or digoxin

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18
Q
A

WPW w abberant pathway

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19
Q

rate control in established AF

A

calcium blocker or beta blocker

consider adding amiodarone in difficult cases

then consider ablation AV node and pacemaker

acutely: verapamil or beta blocker

acute heart failure: dig, amiodarone

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20
Q

antiarrthmics for AF

A

sotalol

amiodarone

flecanide

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21
Q

which antiarrythmic should not be used in

severe impaired LVEF

severe ischaemic heart disease

A

flecanide

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22
Q

invasive management of AF

A

pulmonary vein isolation - via radiofrequency or cryobaloon technique

pulmonary veins contain cardiac muscle

a ring of scar tissue is produced around the vein

MACE procedure only used if another indication for open heart surgery

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23
Q

valvular AF definition

A

mitral stenosis or mechanial heart valves

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24
Q

AF bridging prior surgery

A

Probably need to consider CHADVA score and risk of bleeding.

Bridge study (NEJM 2015) showed similar rates of thromboembolism whether bridged with LMW heparin or not (0.3/0.4%) but contained mostly lower CHADVA score

https://www.nejm.org/do/10.1056/NEJMdo005029/full/

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25
Q

Atrial appendage closer in AF

A

Can use used when there is a contraindication to anticoagulation.

Protect-AF Lancet 2009 - atrial appendage non inferior to warfarin

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26
Q

where is ablation performed for AFlutter

A

catheter ablation between tricuspid valve and inferior vena cava

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27
Q

Indications for cardiac resynchronisation therapy

A

Class II, III or IV CCF

LVEF

QRS >130ms (more benefit w wider QRS)

AF is allowed

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28
Q

romano-ward syndrome

A

autosomal dominant long QT syndrome

KCNQ1, KCNH2, and SCN5A

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29
Q

ECG requirements for long QT

A

QTc >470 male

QTc >480 women

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30
Q

long QT precipitated by exercise, emotion

A

long QT 1

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31
Q

arrythmia precipitated by loud noises

A

Long QT 2

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32
Q

arrythmia in sleep long QT

A

long QT3

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33
Q

treatment of long QT

A

beta blockers

ICD if cardiac arrest, drug failure or preference

LQT1 - supervise swimming

LQT2 - avoid loud alarm vlocks

genetic testing and couselling (genetic defect found in 70%)

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34
Q
A

starting with short-long-short QRS intervals suggestive of torsades

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35
Q

most common gene in brugada

A

SCN5A

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36
Q
A

brugada syndrome

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37
Q

anticoagulation after AF ablation

A

yes

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38
Q

publication bias

A

not publishing negative result

thus metaanalysis exaggerates the true effect

Publication bias is perhaps the most vexing of the GRADE domains, because it requires making inferences about missing evidence. Several statistical and visual methods are helpful in detecting publication bias, despite having serious limitations. Publication bias is more common with observational data and when most of the published studies are funded by industry. A full discussion of publication bias is available in the GRADE guidelines series #5: rating the quality of evidence – publication bias.

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39
Q

retrospective cohort study pros and cons

A

when exposure is on database

but misses out on exposures

often used for vaccination studies

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40
Q

studies to assess harm

A

case control

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41
Q

clinical signs that are prognositc for heart failure

A

JVP

3rd heart sounds

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42
Q

calcium sensitisers ionotropes

A

levosimenden

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43
Q

EPLERENONE PBS indications and vs spironolactone

A

eplerenone has no gynaecomastia

Heart failure with a left ventricular ejection fraction of 40% or less:

The condition must occur within 3 to 14 days following an acute myocardial infarction,

AND

The treatment must be commenced within 14 days of an acute myocardial infarction.

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44
Q

beta blockers that can be used in HFrEF

A

nebivolol

Metoprolol succinate (SR)

carvedilol

bisoprolol

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45
Q

ARNI NOA

A

LCZ696

sacubitril+valsartan

a prodrug further metabolised into the neprilysin inhibitor LBQ657 (inhibits breakdown of BNP and enhances vasodilation)+ ARB (angiotensin I receptor blocker)

46
Q

why can’t BNP and pro-BNP be tested when the patient is on an ARNI?

A

BNP and pro-BNP are broken down by neprilysin inhibitor

only NTproBNP can be used

47
Q

biggest cause of mortality in NYHA II and III

A

sudden cardiac death

48
Q

DAPA-HF

A

dapagliflozin mortality benefit with or without diabetes

https://www.nejm.org/doi/full/10.1056/NEJMoa1911303

49
Q

see slildes

A

Apo-A/Apo-B ratio

50
Q

Lipid targets for high risk patients

A

TC <4

LDL <1.8

HDL >1.0

TG <1.1

51
Q

BP change during exercise prognostic marker in CAD

A

BP fall during exercise is a bad sign

52
Q

CTCA and MI

A

SCOT-hear study

reduced MI rate by 41%

53
Q

what can CTCA tell you about plaque

A

low density

positive remodelling

spotty calficiation - activity in the plaque

^these 3 features show vulnerable plaque (100% negative predictive value)

napkin ring sign

so it can show if the plaque is more vulnerable

54
Q

limitation of coronary angiography

A

plaque distribution and extent

positive remodelling

plaque composition

% stenosis often overestimate

can undersize stent

55
Q

FFR and IVUS/OCT

A

FFR is physiologic detail; reduce need for unnecessarily PCR

distal pressure / proximal pressure

FFR < 0.8 (drop of pressure >20%) suggests physiologic significance

OCT is anatomical detailing

assessing plaque composition and used for sizing up stents

56
Q

stable angina

syntax score

A

low = PCI and Bypass equivalent

high = CABG better

57
Q

women and STEMIs

A

less likely to present but worse outcomes

58
Q

culprit-SHOCK trial

A

only fix culprit lesion

https://www.nejm.org/doi/full/10.1056/NEJMe1713341

59
Q

non culprit lesions in non shock STEMI

A

fix all lesions at initial angio

60
Q

canakinumab

A

IL-1b

results in CRP production

reduced MACE independent of LDL lowering

not on PBS

confirms inflammatory effect

CANTOS trial

61
Q

genetic basis of HCM

A

genes affecting sarcomeres or z-disc

(beta myosin heavy chain and myosin-binding protein C gene defects affect up to 50% of all affected HCM patients)

62
Q

most likely inheritance pattern of genetic heart condition

A

autosomal dominant

63
Q

HCM only treatment that has evidence to preventing SCD

A

ICD

64
Q

Dilated cardiomyopathy genes affecting

A

abnormalities in the cytoskeleton

LMNA (lamina) makes up 5% of all DCM

presents with arrhythmias

AF, sinus brady, CHB

Titin is second most common genetic defect

65
Q

arrythmogenic RV cardiomyopathy genetic basis

A

disease of the desmosome - abnornal signalling between the cells

PKP2 (plakophilin 2)

66
Q

causes of sudden death in young people aged 1-35

A

unexplained in 40% (negative autopsy)

2nd is coronary artery disease

67
Q

3 most common genes for LQTS

A

KCNQ1 - triggered by exericise (especially swimming); responds well to BB

HERG (also potassium channel) - auditory triggers; also responds well to BB

SCN5A - sleep; doesnt respond well to BB because it’s sodium, mexiletine (antiarrhythmic agent (Class Ib)) can work; GAIN OF FUNCTION

makes up 70% of LQTS

68
Q

Brugada syndrome genetics

A

only 1 proven gene

SCN5A - LOSS OF FUNCTION

69
Q
A

CPVT - Catecholaminergic polymorphic ventricular tachycardia

Bidirectional Ventricular Tachycardia degenerating to Ventricular Fibrillation

exercise stres test for diagnosis

genetics

RYR2

Mx - beta blockers, sympathectomy, ICD therapy

70
Q

indication for ICD in syncope

A

class I - patient swith cardioinhibitory or mixed carotid sinus syndrome

other management:

  • midodrine (alpha agonist)

pacing would not work if it was a vasopressor response

71
Q

tilt table testing

A

differentiate between pure vasodepressor vs cardioinhibitory (carotid sinus hypersensitivity)

72
Q

hypersensitivity carotid sinus syndrome ICD indications

A

recurrent syncope caused by spontaneous occuring carotid sinus stimulation

73
Q

PCSK9 MOA

A

chaperones LDL receptor for destruction so increases circulating LDL

so PCSK9 inhibitors would decrease LDL

74
Q

RYR2 gene

A

changes in the structure and function of the RYR2 channel disrupt the careful control of calcium ion flow in myocytes, which can trigger an abnormal heart rhythm in people with CPVT

75
Q

the purpose of metoprolol in using both flecainide and metoprolol in rapid AF

A

to prevent 1:1 conduction if AFlutter occurs

76
Q

fractional shortening

A

end diastole to end systole diameter ratio

surrogate measure for EF but less accurate because it is 1 dimension

reduced fractional shortening suggest systolic dysfunction

77
Q

end diastolic left ventricular diameter

A

dilated LVs can develop diastolic failure but is it not a strict marker for diastolic dysfunction

78
Q

E/A

A

measure of velocity across mitral valve

the E wave is diastolic filling of the ventricle

A is the atrial kick (late diastole)

A is normally lower compared to the passive filling velocity (E)

in mild diastole failure, there is less velocity in passive dilling , then the atrium is contracting against a stiffer ventricle so the A increases

however, in mod to severe forms, the E becomes a lot more than A so the ratio reverses again

79
Q

pulsus paradoxus

A

an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as pulsus paradoxus

Caused by decreased compliance in septum causing RV to buldge into LV and decreased cardiac output

80
Q

which valve defect is caused by the tetraology of fallot surgery

A

pulmonary regurgitation due to the access to fix the RVOT

81
Q

tetraology of fallot defects

A
82
Q

predominant mechanism of atrial fibrillation

A

triggered by the pulmonary vein

83
Q

what does this left heart cath show

A

mitral stenosis

during diastole the pressures between the left atrium and ventricle should match up

84
Q

what does this left heart cath show

A

aortic stenosis

because during systole, the LVP and AORTIC PRESSURE should match up

85
Q

when is the CT coronary calcium score more useful

A

most value in intermediate risk patients (10-20% absolute 10 year CVS risk) who are asymptomatic, do not have known CAD and aged 45-75 where it can reclassify patients

can be considered in low risk who have a strong family history or other concerning features or high risk people who convince them to comply with therapy

86
Q

when is CTCA inappropriate

A

asymptomatic population

inpatients with typical angina symptoms who have a high risk of coronary artery disease

87
Q

PCI in stable angina

A

●Patients with unacceptable angina

●Patients likely to have a survival benefit from revascularization, based upon the location and severity of the lesion, the number of diseased vessels, and the presence of left ventricular dysfunction.

88
Q

BNPR2

A

type 1 pulmonary hypertension - familial

89
Q

non cyanotic (6) vs cyanotic congenital heart diseases (2)

A

(left to right shunts)

VSD, ASD, PDA,

Obstructive lesions : AS, PS, aortic coarctation

Cyanotic: TGA, tetralogy of fallot

90
Q

what does restrictive VSD mean

A

the VSD is smaller to restrict flow so LV pressure > RV pressure

91
Q

extra-cardiac manifestations of eisenmenger syndrome

A

cyanosis

polycythemia

gout

gallstones (high bilirubin)

scoliosis/acne

92
Q

clubbing in toes bbut not fingers

A

EIsenmenger PDA because blue blood only travels to lower limbs not upper limbs

93
Q

most common position of ASD

A

ostium secundum

94
Q

primum ASD ECG features

secondum ASD ECG

A

Primum: extreme left axis deviation (due to not going through the AV load)

first degree heart block

secondum: RA/ volume and hypertrophy

95
Q

what side of the heart is enlarged in PDA

A

left heart chambers big

due to extra blood aorta -> pulmonary artery -> PV -> LA -> LV

96
Q

murmur in PDA

A

machine gun murmur throughout systole and diastole

97
Q

complication of coarctation of aorta

A

bicuspid aortic valve

recoarctation or aneurysm coarctation during aneurysm repair

hypertension by age of 40

ascending aorta dilatation

98
Q

pathogenesis of ToF

A

anterior displacement of the infundibular septum

  • RVOT obstrution
  • RV hypertrophy
  • VSD
  • Pulmonary stenosis
99
Q

pathology in rheumatic mitral valve disease

A

commissure fusion

100
Q
  1. Most common cause of mitral regurg in <65 yr
  2. Most common cause of mitral regurg in >65 yr
A
  1. mitral valve prolapse

a part of the valve in systole that’s going above the plane in the normal valve annulus. Causes a mid-late systolic murmur

  1. Chornic myocardiac disease causing functional MR

Anything that can cause LV dilatation

101
Q

Indications for MR repair/replacement

A

Always repair > replacement

1) asymptomatic patients
- dilated left ventricle
- LVEF <60%; LVEDD >60mm

2)

102
Q

when is the mitral clip indicated

A

generative mitral valve disease (so antyhign aside from mitral valve dilatation)

if they cannot tolerate open heart surgery

103
Q

how to assess mitral stenosis

A

Pressure difference between LA and LV pressure

LA pressure is measured from PCW pressure

104
Q

when to do surgical aortic valve replacement

A

<1cm and under 75 yr

105
Q

AR aortic surgery

A

operate before LVESF >55mm

or LVEF <55%

106
Q

PAH definition

A

mean PA pressure >20

PCWP <15 mmHg

107
Q

sign of RV enlargement on CXR

A

need lateral film

108
Q

best scan for chronic PE

A

VQ scan due to microvascular involvement

109
Q

what improves survivals in PAH

A

IV prostaglandins

110
Q

pathogenesis of PAH

A

too much endothelin

decreased nitric oxide (sildenafil)

Decreased prostacyclin

111
Q

PAH treatment

A

upfront dual therapy

(not on PBS)

FRACP Shuyu (65 decks)

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