RPA cardiology Flashcards

(111 cards)

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
Atrial appendage closer in AF
Can use used when there is a contraindication to anticoagulation. Protect-AF Lancet 2009 - atrial appendage non inferior to warfarin
26
where is ablation performed for AFlutter
catheter ablation between tricuspid valve and inferior vena cava
27
Indications for cardiac resynchronisation therapy
Class II, III or IV CCF LVEF QRS \>130ms (more benefit w wider QRS) AF is allowed
28
romano-ward syndrome
autosomal dominant long QT syndrome KCNQ1, KCNH2, and SCN5A
29
ECG requirements for long QT
QTc \>470 male QTc \>480 women
30
long QT precipitated by exercise, emotion
long QT 1
31
arrythmia precipitated by loud noises
Long QT 2
32
arrythmia in sleep long QT
long QT3
33
treatment of long QT
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%)
34
starting with short-long-short QRS intervals suggestive of torsades
35
most common gene in brugada
SCN5A
36
brugada syndrome
37
anticoagulation after AF ablation
yes
38
publication bias
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.
39
retrospective cohort study pros and cons
when exposure is on database but misses out on exposures often used for vaccination studies
40
studies to assess harm
case control
41
clinical signs that are prognositc for heart failure
JVP 3rd heart sounds
42
calcium sensitisers ionotropes
levosimenden
43
EPLERENONE PBS indications and vs spironolactone
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.
44
beta blockers that can be used in HFrEF
nebivolol Metoprolol succinate (SR) carvedilol bisoprolol
45
ARNI NOA
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
why can't BNP and pro-BNP be tested when the patient is on an ARNI?
BNP and pro-BNP are broken down by neprilysin inhibitor only NTproBNP can be used
47
biggest cause of mortality in NYHA II and III
sudden cardiac death
48
DAPA-HF
dapagliflozin mortality benefit with or without diabetes https://www.nejm.org/doi/full/10.1056/NEJMoa1911303
49
see slildes
Apo-A/Apo-B ratio
50
Lipid targets for high risk patients
TC \<4 **LDL \<1.8** HDL \>1.0 TG \<1.1
51
BP change during exercise prognostic marker in CAD
BP fall during exercise is a bad sign
52
CTCA and MI
SCOT-hear study reduced MI rate by 41%
53
what can CTCA tell you about plaque
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
limitation of coronary angiography
plaque distribution and extent positive remodelling plaque composition % stenosis often overestimate can undersize stent
55
FFR and IVUS/OCT
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
# stable angina syntax score
low = PCI and Bypass equivalent high = CABG better
57
women and STEMIs
less likely to present but worse outcomes
58
culprit-SHOCK trial
only fix culprit lesion https://www.nejm.org/doi/full/10.1056/NEJMe1713341
59
non culprit lesions in non shock STEMI
fix all lesions at initial angio
60
canakinumab
IL-1b results in CRP production reduced MACE independent of LDL lowering not on PBS confirms inflammatory effect CANTOS trial
61
genetic basis of HCM
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
most likely inheritance pattern of genetic heart condition
autosomal dominant
63
HCM only treatment that has evidence to preventing SCD
ICD
64
Dilated cardiomyopathy genes affecting
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
arrythmogenic RV cardiomyopathy genetic basis
disease of the desmosome - abnornal signalling between the cells PKP2 (plakophilin 2)
66
causes of sudden death in young people aged 1-35
unexplained in 40% (negative autopsy) 2nd is coronary artery disease
67
3 most common genes for LQTS
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
Brugada syndrome genetics
only 1 proven gene SCN5A - LOSS OF FUNCTION
69
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
indication for ICD in syncope
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
tilt table testing
differentiate between pure vasodepressor vs cardioinhibitory (carotid sinus hypersensitivity)
72
hypersensitivity carotid sinus syndrome ICD indications
recurrent syncope caused by spontaneous occuring carotid sinus stimulation
73
PCSK9 MOA
chaperones LDL receptor for destruction so increases circulating LDL so PCSK9 inhibitors would decrease LDL
74
RYR2 gene
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
the purpose of metoprolol in using both flecainide and metoprolol in rapid AF
to prevent 1:1 conduction if AFlutter occurs
76
fractional shortening
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
end diastolic left ventricular diameter
dilated LVs can develop diastolic failure but is it not a strict marker for diastolic dysfunction
78
E/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
pulsus paradoxus
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
which valve defect is caused by the tetraology of fallot surgery
pulmonary regurgitation due to the access to fix the RVOT
81
tetraology of fallot defects
82
predominant mechanism of atrial fibrillation
triggered by the pulmonary vein
83
what does this left heart cath show
mitral stenosis during diastole the pressures between the left atrium and ventricle should match up
84
what does this left heart cath show
aortic stenosis because during systole, the LVP and AORTIC PRESSURE should match up
85
when is the CT coronary calcium score more useful
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
when is CTCA inappropriate
asymptomatic population inpatients with typical angina symptoms who have a high risk of coronary artery disease
87
PCI in stable angina
●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
BNPR2
type 1 pulmonary hypertension - familial
89
non cyanotic (6) vs cyanotic congenital heart diseases (2)
(left to right shunts) VSD, ASD, PDA, Obstructive lesions : AS, PS, aortic coarctation Cyanotic: TGA, tetralogy of fallot
90
what does restrictive VSD mean
the VSD is smaller to restrict flow so LV pressure \> RV pressure
91
extra-cardiac manifestations of eisenmenger syndrome
cyanosis polycythemia gout gallstones (high bilirubin) scoliosis/acne
92
clubbing in toes bbut not fingers
EIsenmenger PDA because blue blood only travels to lower limbs not upper limbs
93
most common position of ASD
ostium secundum
94
primum ASD ECG features secondum ASD ECG
Primum: extreme left axis deviation (due to not going through the AV load) first degree heart block secondum: RA/ volume and hypertrophy
95
what side of the heart is enlarged in PDA
left heart chambers big due to extra blood aorta -\> pulmonary artery -\> PV -\> LA -\> LV
96
murmur in PDA
machine gun murmur throughout systole and diastole
97
complication of coarctation of aorta
bicuspid aortic valve recoarctation or aneurysm coarctation during aneurysm repair hypertension by age of 40 ascending aorta dilatation
98
pathogenesis of ToF
anterior displacement of the infundibular septum - RVOT obstrution - RV hypertrophy - VSD - Pulmonary stenosis
99
pathology in rheumatic mitral valve disease
commissure fusion
100
1. Most common cause of mitral regurg in \<65 yr 2. Most common cause of mitral regurg in \>65 yr
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 2. Chornic myocardiac disease causing functional MR Anything that can cause LV dilatation
101
Indications for MR repair/replacement
Always repair \> replacement 1) asymptomatic patients - dilated left ventricle - LVEF \<60%; LVEDD \>60mm 2)
102
when is the mitral clip indicated
generative mitral valve disease (so antyhign aside from mitral valve dilatation) if they cannot tolerate open heart surgery
103
how to assess mitral stenosis
Pressure difference between LA and LV pressure LA pressure is measured from PCW pressure
104
when to do surgical aortic valve replacement
\<1cm and under 75 yr
105
AR aortic surgery
operate before LVESF \>55mm or LVEF \<55%
106
PAH definition
mean PA pressure \>20 PCWP \<15 mmHg
107
sign of RV enlargement on CXR
need lateral film
108
best scan for chronic PE
VQ scan due to microvascular involvement
109
what improves survivals in PAH
IV prostaglandins
110
pathogenesis of PAH
too much endothelin decreased nitric oxide (sildenafil) Decreased prostacyclin
111
PAH treatment
upfront dual therapy | (not on PBS)