Cardio Flashcards
Why do you give AV node blockers with flecanide when cardioverting AF?
Flecanide organises AF into macro circulations and often leads to flutter. It also increases the capacity of the AV node to conduct so can lead to 1:1 conduction of flutter i.e HR 300bpm–> VF. B-blocker prevents this.
What is target HR in majority of patients wqith AF?
<110bpm - the fewer agents necessary the better. Inc risk of complete HB + PPM requirement with increased number of agents
When is AF ablation indicated?
For symptomatic AF refractory to medications, and AF with heart failure, doesn’t improve outcomes or need for anticoag
What effect does pulmonary vein isolation have on AF patients with heart failuer?
Marked reduction in CHF hospitalisation and all cause mortality.
No benefit shown in people without CHF in ablation vs drug therapy however
What associations should you make if young patient wiyth AF? (19-30y/o)
Structural heart disease ( HOCM) and chanellopathies (e.g brugada)
Where does the electrical circuit run in A flutter?
in the RA, around the tricuspid ishthmus
What is the treatment for flutter?
Ablation - at the tricuspid isthmus
Anticoag same as for AF
Beware of 1:1 conduction with flecanide
In what situations is warfarin used over NOAC for AF anticoagulation?
Mechanical heart valves, and rheumatic valvular heart disease. - excess of thrombotic AND bleeding events seen.
If there are retrograde P waves after QRS whatdoes this indicate?
AV node re-entrant tachycardia - normal beat down fast pathway, ectopic beat conducted down slow (but short refractory time) pathway and back up fast pathway.
If there is broad complex tachycardia with irregular R-R intervals what is the underlying rhythm ( looks like VT)
Need to think about AF with conduction down an accessory pathway . VT is regular!
What features mean a broad complex tachy is definitely VT?
AV dissociation, fusion and capure beats
Is patients with non-ischaemic cardiomyopathy, which benefit from CRT device?
Broad complex QRS - >120ms ~ 10% risk reduction.
No role for antiarthmis other than b-clockers. No evidence for narrow QRS
What patients with ischaemic heart disease benefit from ICD?
Post MI B-blockers reduce VT and sudden cardiac death by 30%
Patients with LVEF <35% more than 40 days post acute MI
what are the common HOCM ECG findings?
infrolateral TWI +/- Q waves (in 90%)
What factors are taken in HCM risk of SCD stratification?
Age, max LV wall thickness, Left atrial size, max LVOT gradient, fam hx SCD, non-sustained VT, unexplained syncope.
If risk <3-4 % not recommend defib > than than - ICD
What is the screening for someone who has a 1st degree relative with HOCM?
if can identify gene then genetic screening ( 50-60% have identifieable gene).
Otherwise annual ECG + ECHO age 11-20, 2-3 yearly age 21-30, and 3-5 yearly >31.
What genes commonly cause Long QT? (AD inheritance)
KCNQ1, KCH2, SCN5A ( LQT1-3)
What are the characteristics of the 3 LQT syndromes
LQT1 - normal but long - tri by exercise/emotional stress
LQT2 - biphasic T wave -trig by emotion/ loud noises
LQT3 - late peaking T wave - trig in sleep/loud noises
What is the greatest risk of developing arrythmia in LQT?
QTc >500
What is treatment for long QT?
B-blockers, ICD for high risk
What are the ECG changes for brugada syndrome?
Septal downslping ST elevation - may be elicited with flecanide challence. (v1-V3)
What is the inheritence of brugada?
AD
“Imapaired longitudinal strain with apical sparing” on myocardial strain indicates what? ( bullseye pattern)
Cardiac amyloid
What are indications for cardiac MRI?
Assessment of suspected infiltrative disease - Fabry disease, myocarditis, amyloid, sarcoidosis, haemochromatosis. Should be considetred in dilated cardiomyopathy to determine if ischanemic or non-ischaemic
What is fabry disease?
It is glycosphingolipid metabolic pathway that results in lysosomal accumulation of globotriaosylceramide (Gb3).
Cardiac manifestations: left ventricular hypertrophy (LVH), aortic and mitral regurgitation, conduction defects, coronary artery disease, hypertension, and aortic root dilation
What are :
- Increased extracellular volume
- Abnormal gadolinum kinetics
- Late gadolinium enhancement
typical features of?
Cardiac Amyloid
What amyloid affects the heart more?
TTR (transtheyretin) amyloid.
Protein misfolding leading to dissociated monomores which aggregate and form amyloid fibrils. Fibrils deposit in the myocardium
What happens in the L) heart during diastole?
Mitral valve open, passive filling, then atrial contraction for active filling.
Passive filling on dopler represented by E wave and active/atrial contraction filling represented by A wave
What is the echo doppler findings with normal diastolic function?
Dominant E wave. - passive filling
What is the echo doppler findings with mild diastolic function?
E/A wave reversal; - most filling by active atrial contraction.
Pseudonormal in Moderate and restrictive pattern in severe
What do you use a bone scintigraphy for in cardiology?
Will have cardiac uptake in cardiac amyloid
What are indications to investiate for cardiac amyloid?
Heart failure with wall thickness >12mm AND age >65 or a red flag symptom (polyneuropathy, dysautonomia, skin bruisin macroglosia, renal failure, family history ect)
What is tafamidis?
Used to treat TTR cardiac amyloidosis - stabilises TTR monomers.
in What patients is a TOE contraindicated?
Eosophageal abnormalities - tumour, stricture, fistula, perforation, active UGIB, perforated bowel, unstable C-spine, uncooperative pt.
relative contraindication: Barrets, active oesophagitis, neck immobility, coagulopathy, high grade oesophageal varices or active peptic ulcer disease
Why is TOE better than TTE in infective endocarditis?
higher SPECIFICITY ( tests that are negative are truely negative)
What is Libman-sacks endocarditis?
Non-infective mitral vegetations, seen in Lupus and APS, myeloproliferative disorders
How long after cardioversion do patients need to have anticoagulation?
Min 4 weeks to prevent thrombus formation in the cardiac stunning phase post DCCV
What are indicaytions for intervention in severe AS?
Asymptomatic patients with EF <50%, asymptomatic patients with symptoms on exercising, Sustained fall in BP >20mmHg during exercise, LVEF <55% without other cause
Which patients with severe AS should have intervention?
Symptomatic patient, asymp with EF <55%, asymptomatic but symptoms with exercise.
Which patients should have valver replace vs TAVI
TAVI - >75y/o, high risk (Euro score II >8%) or unsuitable for surgery
SAVR: <75y/o, low risk, or can’t do AVI
When do you use Baloon aortic valvotomy?
In patients with severe AS requiring intervention as a bridge to SAVR or TAVI in haemodynamically unstable patients
Which valve disease should have intervention even only at moderate impairment?
Mitral stenosis ( Valve area 1-1.5cm)
What are the cut offs for mitral valve stenosis?
MILD: Valv area: >1.5cm^2, mean gradient <5, PASP <30
MOD: Area: 1-1.5, Gradient 5-10, PASP 30-50
SEV: Area <1, Mean grad > 10, PASP >50
What patients with asymptomatic MR should have surgery?
Severe primary MR with EF <60, >40
What is primary vs secondary MR?
Primary - valve problem
Secondary - something else pulling valve apparet ( e.g scarred chordae, dilated LV, dilated atrium)
