RPA cardiology Flashcards
ECG
VT
more QRS complexes than p waves
most common cause of VT
old myocardial infarct
VT not compromised management
12 lead ECG
carotid sinus/adenosine
Drugs - sotalol, lignocaine (if acute ischaemic), amiodarone
tiered therapy for
bradycardia
VT
resistant VT
VF
bradycardiac - pacing
VT - overdrive pacing
resistant VT - DC cardioversion
VF - DC shock
cardioversion vs defibrillation
defbrillation shocks on command where as cardioversion times the shock away from the t wave
Use of antharrythic drugs in ICD patients
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
when is ablation for VT first
“VT is a normal heart”
disadvantages of totally subcutaneous ICD
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
long term management of VT - with and without heart disease
with heart disease
- ICD + beta block
- if frequent episodes - add antharrhythmic
- If still frequent episodes - catheter ablation
without heart disease
beta blockers/verapamil
catheter ablation
3 criteria
primary prevention ICD indications
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
AVNRT
narrow complex QRS without p wave
access pathway
p wave in ST segment SVT
p wave first then QRS (narrow complex tachycardia)
atrial tachycardia
suspected based on the shape of p waves (funny shape or different access)
pharmacological and ablation
SVT prevention
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
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.
types of WPW
SVT antrograde over AP
atrial fibrillation
SVT anterograde over AP
Management of WPW w accessory pathway
amiodarone or flecanide
no AV blocking drugs or digoxin
WPW w abberant pathway
rate control in established AF
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
antiarrthmics for AF
sotalol
amiodarone
flecanide
which antiarrythmic should not be used in
severe impaired LVEF
severe ischaemic heart disease
flecanide
invasive management of AF
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
valvular AF definition
mitral stenosis or mechanial heart valves
AF bridging prior surgery
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/
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
where is ablation performed for AFlutter
catheter ablation between tricuspid valve and inferior vena cava
Indications for cardiac resynchronisation therapy
Class II, III or IV CCF
LVEF
QRS >130ms (more benefit w wider QRS)
AF is allowed
romano-ward syndrome
autosomal dominant long QT syndrome
KCNQ1, KCNH2, and SCN5A
ECG requirements for long QT
QTc >470 male
QTc >480 women
long QT precipitated by exercise, emotion
long QT 1
arrythmia precipitated by loud noises
Long QT 2
arrythmia in sleep long QT
long QT3
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%)
starting with short-long-short QRS intervals suggestive of torsades
most common gene in brugada
SCN5A
brugada syndrome
anticoagulation after AF ablation
yes
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.
retrospective cohort study pros and cons
when exposure is on database
but misses out on exposures
often used for vaccination studies
studies to assess harm
case control
clinical signs that are prognositc for heart failure
JVP
3rd heart sounds
calcium sensitisers ionotropes
levosimenden
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.
beta blockers that can be used in HFrEF
nebivolol
Metoprolol succinate (SR)
carvedilol
bisoprolol
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)
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
biggest cause of mortality in NYHA II and III
sudden cardiac death
DAPA-HF
dapagliflozin mortality benefit with or without diabetes
https://www.nejm.org/doi/full/10.1056/NEJMoa1911303
see slildes
Apo-A/Apo-B ratio
Lipid targets for high risk patients
TC <4
LDL <1.8
HDL >1.0
TG <1.1
BP change during exercise prognostic marker in CAD
BP fall during exercise is a bad sign
CTCA and MI
SCOT-hear study
reduced MI rate by 41%
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
limitation of coronary angiography
plaque distribution and extent
positive remodelling
plaque composition
% stenosis often overestimate
can undersize stent
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
stable angina
syntax score
low = PCI and Bypass equivalent
high = CABG better
women and STEMIs
less likely to present but worse outcomes
culprit-SHOCK trial
only fix culprit lesion
https://www.nejm.org/doi/full/10.1056/NEJMe1713341
non culprit lesions in non shock STEMI
fix all lesions at initial angio
canakinumab
IL-1b
results in CRP production
reduced MACE independent of LDL lowering
not on PBS
confirms inflammatory effect
CANTOS trial
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)
most likely inheritance pattern of genetic heart condition
autosomal dominant
HCM only treatment that has evidence to preventing SCD
ICD
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
arrythmogenic RV cardiomyopathy genetic basis
disease of the desmosome - abnornal signalling between the cells
PKP2 (plakophilin 2)
causes of sudden death in young people aged 1-35
unexplained in 40% (negative autopsy)
2nd is coronary artery disease
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
Brugada syndrome genetics
only 1 proven gene
SCN5A - LOSS OF FUNCTION
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
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
tilt table testing
differentiate between pure vasodepressor vs cardioinhibitory (carotid sinus hypersensitivity)
hypersensitivity carotid sinus syndrome ICD indications
recurrent syncope caused by spontaneous occuring carotid sinus stimulation
PCSK9 MOA
chaperones LDL receptor for destruction so increases circulating LDL
so PCSK9 inhibitors would decrease LDL
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
the purpose of metoprolol in using both flecainide and metoprolol in rapid AF
to prevent 1:1 conduction if AFlutter occurs
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
end diastolic left ventricular diameter
dilated LVs can develop diastolic failure but is it not a strict marker for diastolic dysfunction
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
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
which valve defect is caused by the tetraology of fallot surgery
pulmonary regurgitation due to the access to fix the RVOT
tetraology of fallot defects
predominant mechanism of atrial fibrillation
triggered by the pulmonary vein
what does this left heart cath show
mitral stenosis
during diastole the pressures between the left atrium and ventricle should match up
what does this left heart cath show
aortic stenosis
because during systole, the LVP and AORTIC PRESSURE should match up
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
when is CTCA inappropriate
asymptomatic population
inpatients with typical angina symptoms who have a high risk of coronary artery disease
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.
BNPR2
type 1 pulmonary hypertension - familial
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
what does restrictive VSD mean
the VSD is smaller to restrict flow so LV pressure > RV pressure
extra-cardiac manifestations of eisenmenger syndrome
cyanosis
polycythemia
gout
gallstones (high bilirubin)
scoliosis/acne
clubbing in toes bbut not fingers
EIsenmenger PDA because blue blood only travels to lower limbs not upper limbs
most common position of ASD
ostium secundum
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
what side of the heart is enlarged in PDA
left heart chambers big
due to extra blood aorta -> pulmonary artery -> PV -> LA -> LV
murmur in PDA
machine gun murmur throughout systole and diastole
complication of coarctation of aorta
bicuspid aortic valve
recoarctation or aneurysm coarctation during aneurysm repair
hypertension by age of 40
ascending aorta dilatation
pathogenesis of ToF
anterior displacement of the infundibular septum
- RVOT obstrution
- RV hypertrophy
- VSD
- Pulmonary stenosis
pathology in rheumatic mitral valve disease
commissure fusion
- Most common cause of mitral regurg in <65 yr
- Most common cause of mitral regurg in >65 yr
- 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
- Chornic myocardiac disease causing functional MR
Anything that can cause LV dilatation
Indications for MR repair/replacement
Always repair > replacement
1) asymptomatic patients
- dilated left ventricle
- LVEF <60%; LVEDD >60mm
2)
when is the mitral clip indicated
generative mitral valve disease (so antyhign aside from mitral valve dilatation)
if they cannot tolerate open heart surgery
how to assess mitral stenosis
Pressure difference between LA and LV pressure
LA pressure is measured from PCW pressure
when to do surgical aortic valve replacement
<1cm and under 75 yr
AR aortic surgery
operate before LVESF >55mm
or LVEF <55%
PAH definition
mean PA pressure >20
PCWP <15 mmHg
sign of RV enlargement on CXR
need lateral film
best scan for chronic PE
VQ scan due to microvascular involvement
what improves survivals in PAH
IV prostaglandins
pathogenesis of PAH
too much endothelin
decreased nitric oxide (sildenafil)
Decreased prostacyclin
PAH treatment
upfront dual therapy
(not on PBS)
