Cardiology Flashcards
stable angina investigation
coronary angiogram
treatment of stable angina
dual antiplatelet therapy
Investigation for a STEMI
already done an ECG so straight to angiogram as a troponin would take so long to come back
stable angina
ORBIT trial between PCI and medical therapy is on going.
stent if 70% stenosed with PCI
IHD investiation in stable
functional and anatomical
functional test for ischaemia like ETT
Anatomical Coronary angiogram
IHD ivx acute or unstable IHD
Serial ECG
Blood markers
Further tests
if no ST elevation and normal trop what could it be still and what would you do
unstable angina
aspirin/clopi/LMWH
no st elevation and raised trop
NSTEMI
IHD STABLE management catergories
Lifestyle
Medical Therapy
Revascularisation
Medical Therapy of STABLE IHD further categories
Preventative - antiplatelet
Symptoms - GTN spray, long acting nitrates
Alternative antianginals - BB
Types of revascualrisaiton of heart
PCI - baloons and stents
CABG
UNSTABLE IHD Mx
Pain - analgesia + oxygen
Ischaemia - aspirin and clopi plus antithrombotic treatment LMWH
Serial ECG
HF - Reduced ejection fraction is what type of failure
Systolic
HFrEF
Preserved ejection fraction is what type
HFpEF
diastolic failure
Chronic Heart Failure causes
Myocardial
Pressure
Arrhythmias
Myocardial causes of HF
IHD Tocins Infectious INfiltrative metabolic genetic
Pressure causes for HF
HTN valvular disease pericardial disease high output volume overload
importance of diastolic heart failure
with something like AF where this no atrial contraction it relies on sucking from ventricles relaxing. This won’t happen! Need BB to slow AF?
How IHD causes HF
Frank starling mechanism - increasing end diastolic pressure to try and increase output
hypertrophy from La Place relationship due to increase wall stress. More muscle fibre.
This hits a limit
then heart dilates
heart can’t maintain blood pressure with cardiac output so increasing Total preipheral resistance
salt and water retention to increase pre load.
RAAS - angiotenisin II to retain water and aldosterone release
Anit diuretic hormone from baroreceptors due to decreased BP
Adrenergic response to increase Peripheral vasculature through increased sympathetic tone of blood vessels
continuous sympathetic stimulation to increase HR - more cell death from ischaemia
eventually prelkoad is too much for heart - congested
the high levels of angiotensin/aldosterone increase cytokine production and get adverse heart remodelling
signs of CHF
JVP Hepatojugular reflux Gallop Displaced apex Murmur
