Deck 1 Flashcards
Angina grading
Canadian cardiovascular society 1-4
1 is on strenuous, 2 is on mod exertion, 3 is on mild exertion and 4 is at rest
Angina causes
Reduced perfusion (atheroma, embolus, iflammation, hypotension, spasm, thrombosis), reduced oxygenation (anaemia, carboxyhaemoglobinaemia) or increased tissue demands (LVH)
CTCA
First choice in new onset angina pain. Looks at whole vessel, not just lumen (can adequately assess plaque burden)
Use in NICE probability 61-90%
CT-FFR
Computer modelling to assess functional impact (if <0.8 then haemodynamically significant)
Use in NICE probability 31-60%
Clinical diagnosis of angina
At NICE probability >90%
Looks at age and symptom type
Angina Tx
Address RF
GTN spray, BB (or rate limiting CCB)
Can add nicorandil for refractory disease (vasodilator)
Give statin and low dose aspirin
Surgery required if large area at risk (>10%) or left main stem, or 2-3 vessel disease.
CABG good for diffuse disease, reduced LV function, recurrent stent stenosis and in diabetes.
PCI good for 1 or 2 vessel, frailty, advanced age or varicose veins.
Acute MI
Can be regional (90%) or circumferential (10%)
See trop rise (if ECG change only then unstable angina)
If Trop rise + ST elevation/LBBB then STEMI (full thickness)
If trop rise and no ST elevation then NSTEMI (partial thickness)
RCA supplies
Type of MI
Which leads
RA, RV, posterior septum - often AVN and SAN
Gives posterior/inferior MI
Leads II, III, avF
LCA (main stem) MI
Massive anteriolateral MI
Seen on I, aVL, V1-V6
LAD supplies
Which leads
LV and anterior septum
V1-V4
Circumflex supplies?
Type of MI
Leads?
LA and LV
Lateral MI
I, aVL and V5/6
DDX for acute coronary syndrome
Coronary artery spasm, pericarditis/myocarditis, aortic dissection, PE, pneumothorax, oesophageal disease (worse on leaning forwards), mediastinitis, costochondritis, trauma
Troponin peak
24h
ECG MI progression
Tall T waves at 5 mins ST elevation at 30 minutes T wave inversion, Q waves (2h) ST segment normal (days) T wave may return to normal, Q wave remains (WEEKS)
ACS management
Morphine (5mg + antiemetic), GTN/IV nitrates (unless hypotensive), 300mg aspirin, oxygen if <94%
PCI within 90 minutes if STEMI
If NSTEMI then GRACE score
AMI complications
Short term:
Arrythmias, Pulmonary oedema (LVF), cardiogenic shock, thromboembolism, ventriculoseptal defect (due to intracardiac rupture), ruptured cordae tendinae (mitral valve incompetence), ventricular wall rupture (leads to haemopericadium, cardiac tamponade and death)
Long term: HF, dressler (immune mediated pericarditis wit raised ESR and myocardial antibodies), ventricular aneurysm formation (distended scar)
IE risks
Damaged endocardium (valve disease, prostetic valves, congenital disease), sustained bacteraemias (IVDU, infected intravascular device, untreated abscess/collection)
Vascular IE phenomenom
Splinter haemorrahage, janeway lesion
Immunological IE phenomenon
Osler node, Roth spot, glomerulonephritis (microscopic haematuria)
Native valve IE causes
Streptococcus viridans, Streptococcus mitis
S. aureus in IVDU
Prosthetic valve IE causes
coagulase negative staphylococcus (e.g. s epidermidis for first 2 month)
IE causes: - Bowel malignany -GI/GU disease If culture negative If non infectious
Streptococcus bovis in bowel malignancy
Enterococcus in GI/GU tract
Coxiella burnetii, bartonella, brucella, HACEK (haemophilus, actinobacilus, cardiobacterium, eikenella, kingella)
Non infectious cause is libman sacks lesions (SLE)
IE investigations
Echo (ideally TOE)
FBC, CRP, ESR, BCx3, Urinalysis, ECG, CXR
Dukes IE criteria
Major is: atypical organism on 2 separate BCs, echo findings or new valvular regurgitation (worsening of existing not enough)
Minor is predisposition, pyrexia, vascular phenomena, immunological phenomena, positive BC
Can diagnose if 2 major 1 minor, 1 major 3 minor or 5 minor