Cardiology Flashcards
What is the evidence for NOACs in the treatment of embolic stroke of undetermine source (ESUS)
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.
What are MBS indications for loop recorders
1) Recurrent/unexplained syncrope 2) Cryptogeni stroke/ESUS
What level of ETOH is bad for AF
Any ETOH consumption
Treatment for AF and Heart Failure
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.
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
Diagnosis of heart failure and classifications of HFrEF vs HFpEF
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)
What is recommended for T2DM and hF
SGLT2 inhibitors are recommended for patients with T2DM and cardiovascular disease who does not have sufficient glycaemic control with metformin.
Investigation for coronary artery disease in low-intermediate risk groups
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
Patients with dilated cardiomyopathy (DCM) associated with conduction disease should get what investigation?
Genetic testing
When should the follow up TTE be performed after commencement of optimal medical therapy for HFrEF
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).
What is recommended for all HFrEF <40% unless not tolerated/contraindicated?
- ACE - I
- BB (once stabilised with no or minimal clinical congestion on physical examination)
- MRA
When are ARNIs recommended
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
When is ivabradine indicated?
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.
When is cardiac resynchronisation therapy recommended in HFrEF?
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
When is cardiac resynchronisation therapy contraindiated in HFrEF?
CRT is contraindicated in patients with QRS duration of less than 130 ms, because of lack of efficacy and possible harm.4
Indications for ICD in HFrEF
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.
Treatment for central sleep apnoea
NOT adaptive servoventilation.
Aim is to treat the heart failure in predominant central sleep apnoea
How to treat iron deficiency in HFrEF in patients who have persistent symptoms
IV iron
ICH rates in thrombolysis
~1%
Timing for PCI in successful lysis of STEMI
3-24 hour coronary angiography
Example of a direct thrombin inhibitor
Dabigatran
Example of an indirect thrombin inhibitor
UFH
LMWH
Risk factors for excess bleeding risk when using prasugrel
Previous stroke, >75 years old, <60kg
How longs should DAPT ideally continue for post ACS
12 months (although several trials have shown non inferiority in 6 months)
Dual therapy vs triple therapy post PCI
Triple therapy had worse ischaemic and bleeding outcomes.
If someone needs the NOAC, drop the aspirin.
Timing of invasive management of NSTEACS
Reasonable to perform angio 48-72 hrs but earlier in high risk group
What anti hypertensive decreases risk of CV death, MI or stroke in high risk patients
ramipril
Patients with high CV risk with high triglycerides
NJEM 2019 trial showed high dose fish oil icosapent ethyl 2g daily
Effect of PCSK9 inhibitors (evolocumab/alirocumab) on lowering CVS risk
Mild improvement in cardiovascular outcomes. Right now only use for famiiial hypercholesterolaemia. Very expensive
Timeframe for ECG in acute chest pain presentation
<10min
TImeframe for symptom onset for which an eligible patient should recieve emergency reperfusion therapy (STEMI)
<12 hours
What is the timeframe for which patients should get PCI over fibrinolysis
If PCI can be performed within 90min of medical contact
When to immediately transfer for rescue angioplasty post fibrinolysis for STEMI
<50% ST recovery at 60-90 min and/or with haemodynamic instability
When is immediate invasive strategy (<2hr of admission) recommended in NSTEACS?
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)
Who to give aspirin in ACS
Everyone - 300mg initially then 100mg/day
Who to give DAPT initially in ACS and which antiplatelet is preferred
Intermediate to very high risk of recurrent ischaemic events
Ticagrelor and prasugrel is preferred
When is glycoprotein IIb/IIIa inihibition in combination with heparin recommended?
At time of PCI in high risk clinical and angiographic characteristics or for treating thrombotic complications among patients with ACS
How long should asprin be continued post ACS
Indefinitely unless it is not tolerated or an indication for anticoagulation becomes apparent
How long should DAPT be continued for post angio
Clopidogrel/ticagrelor up to 12 months regardless of whether coronary revascularisation was performed. The use of prasugrel should be confined to patients recieving PCI
Which antiplatelet should be used with fibrinolysis
Clopidogrel (no evidence re ticagrelor/prasugrel)
What is the compression to breath ration in BLS
30:2
What is the deal depth in chest compressions
>5cm
When to administer adrenaline in ALS (shockable vs non shockable)
after 2 min for shockable
immediately for non shockable
every 3-5min
When to give amiodarone
After 3 shocks
ALS 4Hs and 4Ts
Hypoxia
Hypo/hyperthermia
Hypovolaemia
Hypo/hyperkalaemia/metabolic
Tamponade
Tension
Thrombosis (pulmonary + cardiac)
Toxins
When to do rhythm check in ALS
As soon as the defibrillator is available
What are the standard energy levels for the defibrillators
200J biphasic or 360J monophasic
Bystander CPR: chest compression only vs standard cardiopulmonary resuscitation
Compression only improved survival (Hupfl Lancet 2010)
What is a risk factor for familial hypercholesterolaemia?
xanthomata
Management of familiar hypercholesterolaemia
Screen first degree relatives
Statins first line
LDL >3.3 then PCSK9 inhibitors
Familial combined hyperlipidaemia inheritance and phenotype
Polygenic inheritance
Combination of high cholesterol, high Tf and low HDL
LDL to apo-B ratio of <1.2
FCHL (familial combined hyperlipidaemia) management
statins to reduce apo-B
What lipid profile is diabetes associated with
Increased Tg, increased LDL, low HDL
Cholestatic liver disease, PBC
accumulation of lipoprotein X - SEE SLIDES
Hypothyroidism lipoprofile
Isolated raised LDL
Obesity lipid profile
Increases everything aside from HDL
Heavy ETOH intake lipid profile
Isolated raised triglycerides
Antipsychotics lipid profile
High Tgs
When to use ezetimibe
Intolerant to statins or in addition to meet targets
Mechanism of statins
HMG-COA reductase for endogenous cholesterol production
Mechanism action of PCSK9 inhibtors
Breaking down LDL receptors (increases uptake of LDL into hepatic cells)
Target for secondary prevention (cholesterol)
LDL <1.8
definition of HTN (SBP and DBP)
SBP >130
DBP >80
stage 1 for first 10mmHg of increase and stage 2 thereafter
must be done in 2 sittings
When to start a statin for primary prevention
LDL >4.9
DM and age 40-75
Others dependent on risk score (ASCVD)
Coronary artery calcium score
What antihypertension will affect the aldo:renin the most
Spironolactone bu increasing renin, increasing K+ and reducing Na
What medication is important to avoid in pheochromacytoma
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)
When to start treatment for stage I hypertension
If 10 year risk calculation is >10%
(stage one is 130-140 mmHg SBP)
What antihypertensive agent in DM
Diuretics (ALLHAT) - chlorthalidone
What BP treatment targets?
<130/80
What is the normal aldosterone:renin syndrome
<30
main mechanism of action of dihydropyridine calcium channel antagonist
dihydropyridine = peripheral
reduce vascular smooth muscle tone
What are P-GP inhibitors vs substrates
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
what antihypertensive causes constipation
calcium channel blockers
factors causing false BP measurement
underestimates BP: smoking
Overestimates BP: caffeine, talking, small cuff, pseudohypertension (arterial stiffness), crossing legs, unsupported arms
Small cuff overestimates the most from that list
What is the first line screening test for structural heart disease?
ECG
What types of AV blocks are indications to PPM regardless of symptoms?
Mobitz type II AV block and third-degree AV block not caused by reversible or physiologic causes
When are cardiac resynchronisation therapy and HIs bundle pacing preferred to right ventricular pacing?
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
Pacing requirements in an acute inferior infarct that results in complete heart block that has an early response to atropine?
Only temporary pacing if haemodynamic compromise. Permanent pacing often not required.
Acute management of torsades de pointes secondary to bradycardia?
- Magnesium, isoprenaline
- Urgent temporary/permanent pacemaker insertion
What is the ECG and the management?
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
What is a trifascular block and what is the management of a patient with symptomatic trifascular block?
1st degree AV block, RBBB and LAD
Progression to CHD is 10%
PPM probably indicated
Management of a patient with a history of aortic repair for severe AS who presents with syncope and the ECG shows complete heart block
- Inpatient cardiology review
- PPM indicated - class 2B indication for bundle of HIS/biventricular pacing. 2A indication if there is LV dysfunction
Indications for ICD in primary prevention in ischaemic patients
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
Primary prevention ICD indications in non-ischaemic patients
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)
Cardiac MRI - Cine imaging “SSFP”
What does this sequence require and what does it do
No contrast
10 sec breath hold
Cardiac MRI - Late Gadolinium enhancement
What does this sequence require and what does it do
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
Cardiac MRI - Spin ECHO (black blood) imaging:
What does this sequence require and what does it do?
Shows myocardial oedema
Vessel anatomy
Cardiac MRI - Mapping - T1, T2, T2*
What does this sequence require and what does it do
T1 mapping - quantify diffuse processes e.g. interstitial fibrosis
T2 mapping - oedema
T2* - iron quantification
Cardiac MRI - Flow quantification
What does this sequence require and what does it do
Get flow curves of things e.g. aortic regurg
Cardiac MRI in congenital heart disease indications
Tetralogy of fallot - quality right ventricular size and volume. They often get severe residual pulmonary regurgitation. Required for criteria for surgical mx
What is coronary calcium pathognemonic for?
Athersclerotic disease
Limitations of CTCA
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
What is CTCA better at seeing than angiogram
Non obstructive plaques
Data for benefit of starting statin
What can cause false +ve in stress ECHO
LVH, LBBB
What stress testing has the highest sensitivity
Nuclear (although MRI is probably also pretty good)
what is the bernoulli equation?
change in pressure approx equals 4velocity2
Used to measure the pulmonary artery pressure
How to calculate the peak right ventricular systolic pressure from TR velocity and whats is its significance
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
What is the normal mitral valve orifice area?
4-6cm2
Mitral stenosis severity by valve area
Mild > 1.5 cm2
Mod 1.0 - 1.5 cm2
Severe < 1.0cm2
First line management of mod mitral valve stenosis in pregnancy with pulmonary oedema driven by tachycardia?
Beta blockers (metoprolol), balloon valvuloplasty next line
Percutaneous Balloon Mitral Valvuloplasty indications
- 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
Percutaneous balloon mitral valvuloplasty contraindications
- More than mild mitral regurgitation
- LA thrombus (?appendage)
- Heavy calcification of both commissures
- Predominant subvalvar involvement
What is ejection fraction misleading in mitral regurgitation?
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
When is mitral valve surgery indicated in secondary MR?
Class IIb evidence for severe symptomatic secondary MR with persistent NYHA class III - IV symptoms
When is mitral valve surgery indicated for primary MR?
Severe MR
Symptomatic
or
Asymptomatic and LVEF 30-60%
How to treat acute severe aortic regurg
Aortic valve replacement
Avoid bradycardia (slow heart rate allows more time for regurg)
When is aortic valve replacement for chronic aortic regurg indicated
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
Aortic Stenosis severity
Why might there is severe decreased aortic valve area in mild/mod aortic stenosis?
Pseudostenosis due to cardiomyopathy. The LV isn’t able to produce enough outflow to keep the valve open.
When is aortic valve replacement (via TAVI or surgery) indicated?
- Severe AS (mean gradient >40 mmHg, AVA <1.0cm) and symptomatic or LVEF <50%
- Severe AS (mean gradient <40mmHg and AVA <1.0 but confirmed stenosis with low dose dobutamine stress ECHO)
Adverse effects of TAVI vs SAVR
SAVR: AKI, new AF and major bleeding
TAVI:
Short term - Vascular cx., pacemaker, AR
Long term - Paravalvar regurgitation, valve thrombosis, prosthetic endocarditis, late bleeding
Should preventative PCI be performed on non-infarct arteries with >50% stenosis during PCI for STEMI?
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
Should thromboaspiration be performed in STEMIs?
No, 1 study (TAPAS) showed benefit but subsequent studies (taste, total) have not
When to use femoral vs radial access for PCI?
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
Drug eluding stents vs balloon valvuloplasty stents
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 +++
When to continue DAPT in balloon valvuloplasty stents
3 years due to risk of in stent thrombosis
How deep should chest compressions be
5-6 cm
Haemodynamially compromised ventricular tachycardia treatment
synchronised shock x3, O2, IV access, exclusion of reversible factor, amiodarone
When is an ARNI indictaed in HFrEF ? (sacubitril-valsartan)
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.
Examination findings and ECG of HOCM
- 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
Clinical characteristics of Arrhythmogenic Right Ventricular Cardiomyopathy and ECG findings
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
Mitral valve prolapse clinical features
Symptoms are non specific and unreliable - dyspnoea, palpitations, exercise intolerance
non-ejection click (single or multiple) and the murmur of mitral regurgitation
ECG diagnosis and management
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
When is genetic testing useful in Brugada syndrome
- Patients with a clinical diagnosis of brugada syndrome (only type 1)
- In relatives where pathological mutation identified in proband
What gene is Brugada syndrome associated with and what kind of mutation is it?
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
What are the clinical features of Catecholaminergic Polymorphic Ventricular Tachycardia and its genetic inheritance
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
ECG findings of Arrhythmogenic Right Ventricular Dysplasia
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
Is the y descent prominent in constrictive pericarditis or cardiac tamponade
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.
What is kussmaul’s sign more assocaited with
constrictive pericarditis > cardiac tamponade
What’s troponin I, T and C
Troponins are regulatory proteins for heart muscles
I - inhibits actin (used at The Alfred)
T binds tropomysin
C binds to calcium ions
When do patients with thrombolyss do best?
within the first hour (as good as PCI in that group)
Adverse effects of ticagrelor (aside from bleeding)
Bradycardia, shortness of breath
What is thromboxane inhibitor
aspirin (cox-1 inihibitor - precursor of TxA2)
What area of infarction is at the highest risk of LV thrombus
Anterior infarct ( do not discharge prior TTE before discharge)
What kind of ST depression morpholog is more sinister
Downsloping
Wallen’s syndrome
Anterior T wave inversion
LAD lesion
Mx of takasubo’s
beta blocker, ACE-I
repeat TTE at 6-8 weeks
MOA of PCSK9
Stops LDL receptors from being put up out onto the cell
e.g. alirocumab and evolovumab
(injections)
Differentiate VT from SVT w aberrancy
Extreme axis deviation AVR +ve, I/AVF negative
AV dissociation, capture beats, fusion beats
Marriott’s sign
Bidirectional tachycardia
Catecholaminergic polymorphic ventricular tachycardia
2 types of monomorphic VT
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)
Management for VT
see slides
Flecanide contraindications
CI - IHD, cardiomyopathy
CLass Ic anyarrhtyhmic
Orthodromic AVRT vs antidromic AVRT
Orthodromic - impulse travels down normal AV nodal pathway but comes back through accessory -> narrow appearance.
Antidromic - comes up AV node retrogradly and broad complex
orthodromic AVRT vs AVNRT
AVRT is a bit slower
p wave is closer to QRS in AVNRT (pseudo R’ in V1)
acute mx of 1) orthodromic AVRT, 2) anridromic AVRT, 3) AF WPW
Don’t use AV blocking agents in antidromic AVRT or AF w preexcitation
Polymorphic VT 1st line management
Prolonged QT vs normal QT
prolonged QT: Magnesium
then isoprenaline, temporary pacing
For normal QT, ischaemic until proven otherwise
positive concordance in VT
biggest RF for arrhythmia after bypass
LV function
Outflow tract VT
What NOAC has a lower cut off for eGFR
NOAC is 25, others are 30
Signs on ECG of AVNRT
very fast rates up to 200 bpm
pseudo R’ in V 1 (which is the retrograde p wave)
What STEMIS are more likely to have permanent requirements for PPM
Anterior STEMI
Management of pcaemaker mediated tachycardia
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
Where is the current delivered in cardiac resynchronisation
on the R wave
Flecanide challenge
Unmask brugada
When are abx given prophylactically prior procedure?
30min prior procedure
Which side IE are more likely to get surgical management
left side
Loud s1
MS, TS, epstein’s anomaly, ASD
Tricuspid stenosis JVP
elevated a wave
Fixed spliting of second heart sound
ASD
Tetralogy of fallot
vsd, overriding aorta, pulmonary stenosis, RVTO
most likely complication following tetralogy of fallot repair
PR (as the part of the surgery involve access to the myocardium through the pulmonary artery, stretching the pulmonary valve)
primum ASD ECG feature
AV block due to the close assocaition with AV node
The MR usually have 2 kicks - what condition causes the 2nd kick to disappear?
First is from early diastole and second is from the atrial kick which is absent in AF
Most common cause of sudden cardiac death in young adults
coronary artery disease
(well actually unexplained is first)
Diagnosis of HCM
imaging diagnosis
- Wall thickness >15mm
- Can have slightly thinner wall if there are other features
What might HCM with syncope at rest suggest?
ventricular arrhythmias
(cf syncope w exertion is suggestive of LVOT)
ARVC management
activity restriction
beta blockers
ICD (secondary prevention and high risk primary prevention)
Romano-ward syndrome
autosomal dominant LQT syndrome
KCNQ1, KCNH2, SCN5A
Jervell and Lange-Nielsen syndrome
autosomal recessive long QT syndrome associated with neurosensori hearing loss
KCNE1 and KCNQ1 genes
which beta blockers for long QT
propranolol > atenolol > metoprolol
diagnosis of type 2 brudaga
can consider flecanide challenge (not used in in type 1)
