Cardio Flashcards
posterior MI ECG findings
which vessel
lead v1-3
Op of STEMI:
horizontal ST depression
Tall Broad R waves
upright T waves
dominent R wave in v2
Basically if st depression in leads V1-V4 = do 2 extra leads V&V9 bc something going on posterior
LCX or RCA
? PE investigation CKD or pregnant
V&Q scan
instead of CTPA
malignant hypertention
BP> 180/120
end organ damage
hypokal ECG
prolonged PR ( 1st degree Hb)
Prominent U waves
flateneed t wave and st depression
HOCM hart sound
s4
when to stop anticoag consider alternative diagnosis with PE
2-level PE Wells score </= 4
-ve d-dimer
NSTEMI scoring scale and Mx
GRACE SCORE
<3% = conservative management
> 3% = PCI in 72hrs
haem unstable = PCI now
Conservative management NSTEMI
aspirin fondaparinux ticagrelor
clopidgrel if high bleedinig risk (ie on anti coags)
pulmonary embolism abg
resp alkalosis
bc hypervent = low co2
criteria for infective endocarditis
duke criteria
risk of bleeding af and on anticoags
ORBIT score
PE with haemodynaic instability
thrombolysis
mitral stenosis
mc cause
path
sx
tx
rheumatic fever
(blood backflow in left atrium) heart failure sx and af bc atrial stretch
malar flush
haemoptysis
tx af w mitral stenosis = anticiag
ASx = monitor w echo every 6-12 mths
sx = baloon valvotomy or perc mitral commissurotomy
mitral stenosis sounds
mid diastolic rumble (best in exp)
at apex
loud s1
opening snap
pt w PE that can be managed as outpatients
PESI score
(pe severity index)
aortic regrug causes and presentation
infection - infective endocarditis, rheuamtic fever
infarction
aortic dissection
spondoarthrop
RA, SLE , marfans and ehler danlos
acute = cardiogenic shock
chronic = CHF and chest pain maybe
aortic regurg signs
early diastolic rumble (increase by handgrip)
collapsing pulse
wide pulse pressure
quincke
de mussets
severe = mid diastolic austin flint murmur
quinckes sign
nailbed pulsation in aortic regrug
de mussets sigm
head bobbing in aortic regurg
what is austin flint murmur
severe aortic regurg
due to partuial closure of anterior mitral valve cusps bc regurg stream
aortic stenosis sx
chestpain dysponea syncope (exertional dizziness)
aortic stenosis causes and tx
calcification
ie old pt w athersclerosis
process sped up if bicuspid valve = ypunger pt
williams syndrome (supravalv aotic sten)
post rheumatic disease
HOCM
Asx = monitor
Sx = valve replacement
aortic stenosis murmur
what if severe
ejection systolic
radiates to carotids
decreased by valsalva manouvre
crescendo descrescendo
severe =
soft absent s2
s4 sound
slow rising pulse
narrow pulse pressure
causes mitral regurg
Post MI/ ACS ( bc papillary muscles/chordea tendinae affected)
mitral valve proplapse
infective endo
rheumatic fever
congenital
mitral regurg sx
often stays asx unless gets too bad = present w failure of Left vent, arythmia, or pul htn
ie fatigue SOB oedema
mitral regrug murmir
what if severe
pansystolic mumur
hollow high pitched blowing sound
apex and radiates to axilla
widely split S2 if severe
medical mx acute mitral regurg
nirates duiretics inotropes intraaortic balloon pump
if in heart failure maybe ace inhibitors n bb m spirinolactone
severe = replacement
making murmurs worse/better
murmur louder bc more blood in the heart
therefore
valsalva = dec venous return = improve
leg lift and squatting = increased venous return therefore worsens murm
hocm genes and path
autosomal dominant
diastolic dyfxn
left v hypertrophy -> decreased compliance -> decreased cardiac output
hcm presentation
murmur
extertional sob
young
syncope post exercise
sudden death bc vent arythmia
ejection systolic murmur
(made worse by vals and better by squatting)
hocm echo MR SAM ASH
MR SAM ASH
mitrak regurg
systolic antieror motion (of ant mitral valve leaflet)
assymetic hypertophy
mitral valve prolapse causes features
usually idiopathuc ie congenital
midsystolic click (occurs later if pt standing)
late systolic murmur (longer if pt standing)
basically similar murmur to mitral regurg but improves with blood in the heart
angina tx
bb or ccb first line
if only ccb used = verpamil or diltazem
if on monotherapy still sx and cannot tolerate either bb or ccb = long acting nitreate. nicorandil, ivabradine
hyperaldoesteronism presentation
hypertension
hypokalaemia
metabolic alkalosis
hyperaldost 1stline investigtiion how to differentiate btween 1 and 2ndry
aldoesterone renin ratio
high = primary (in adrenals bc aldosterone being produced indepedant of renin)
low ratio = secondary (inc aldos bc renin raised ie problem in axis )
primary hyperaldosterone ix
1st aldosterone renin ratio (high ald = primary)
2nd high resolution ct abdo
(to see uni lat or bilat cause)
if normal/inconc = AVS
3rd adrenal venous sampling (AVS)
if aldos inc in both veins = bilateral cause
causes of primary hyperaldos
unilat adrenal adenoma
bilateral adrenal hyperplasia
Post MI complication pericarditis
2-3 days bc post transmural MI
Post Mi complications Dressler’s syndrome
2-6weeks post MI
autoimmune reactuion to proteins as myocardium recovers
fever pleuritic pain pericardial effusion
raised ESR
Tx - nsaids
after 5 days complications of post MI
RUPTURE ie
free wall = sx cardiac tamponade
VSD septal rupture = hf sx (pansystolic murm)
papllary muscle damage = mitral regurg and hf sx (early to mid systolic murm)
poorly controlled htn already on acei, ccb, and thiazide
if k<4.5 = add spironolactone
ccb SE gums
gingival hyperplasia = gum bleed