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CR - ischaemic heart disease (i) (intro (MI usually reflects a coronary…
CR - ischaemic heart disease (i)
intro
95% caused by CAD
primary atheroma (fibrolipid plaque with inflamm cells)
can be complicated by fibrosis (fibrolipid plaque + inflamm cells)
other rare causes: shock, LVH
sudden acute left ventricular failure - paroxysmal nocturnal dyspnoea
serum troponin differentiates MI from angina (no necrosis)
MI usually reflects a coronary art occlusion
dynamic process
can be txed by stenting (coronary reperfusion)
rare causes of coronary occlusion
vasculitis
thrombus secondary to hypercoagulability
vasospasm (cocaine)
trauma
almost never emboli
evaluating heart @ autopsy: assess coronaries + myocardium
massive cardiac hypertrophy predisposes heart to MI (increased O2 requirements)
ankle oedema caused by increased pressure in IVE due to RHF
use ECG to distinguish STEMI vs NSTEMI (NB as Tx is different)
vital signs = HR, BP, RR, O2 sat
use cardiac markers to distinguish MI + angina
3 main coronary arts
left
left circumflex
interventricular LAD (left ant descending) - supplies apex, ant 2/3 of septum, ant wall of left ventricle
1.5 cm long
if occlusion in 1st 1cm instant death - Widowmaker's disease
right
supplies post septum
looks inf/post on ECG
end arts in normal hearts / hearts with mild atheroma - no collat circulation
paradox: patients who were previously well before coronary occlusion tend to have more catastrophic outcomes (ACS)
collat circulation may develop in abnormal hearts
MI consequences/complications
arrhythmia
ventricular tachycardia within 48hrs post MI
sudden death
v fib
LVF - aneurysm (weakening of scarred area) - chronic heart failure, arrhythmias, mural thrombosis (+ then systemic emboli) or rupture after 4 days - haemopericardium
pul oedema
papillary muscle/chordae tendonae infarct/rupture - valvular disease (rare)
endo/myo/peri carditis
infection/sepsis
rheumatic heart disease (non-infectious, post-infection immune response)
Dressler's syndrome (pericarditis after 12 wks due to immune reaction to myocardial injury)
can be acute or chronic
cariogenic shock due to inadequate blood flow (poor pump - low CO)
important to know these, understand + anticipate them so you can look for them + tx them in good time
Angina Pectoris
cardiac markers not elevated
stable
chest pain caused by exercise + relieved by rest
reflects significant atheroma (>75% stenosis in 1 vessel or 50% in 2 vessels)
assess via Hx + angiography (finds % stenosed)
predictable onset pattern
tx with sublingual vasodilator
long survival
on postmortem: microscopic myocardial fibrosis often seen (tiny microscopic infarcts, not detectable on angiograph)
worsened by anaemia (decreased oxygenation) + hypertrophy (increased cardiac mass)
unstable
progressively increasing frequency - precipitated with progressively less effort
unpredictable pattern - sometimes @ rest
caused by
plaque disruption/rupture (prevented with statins)
secondary thrombus
patient @ increased risk of MI
Sudden cardiac death (SCD) from ischaemia
within 1 hr of symptoms (often instantaneous)
caused by
arrhythmias (most common esp in post/inf MIs - 50% dead before arrival)
sudden large coronary thrombosis on ruptured atheromatous plaque
certain plaques more likely to thrombus -> lipid rich with fibrous cap cracks
coronary art spasm (cocaine)
cardiac rupture -> haemopericardium/cardiac tamponade -> heart can't pump
MI presentation
crushing central chest pain
unrelieved by rest (ddx unstable angina not stable)
commonly radiates to left shoulder + jaw
weakness, sweating (diaphoresis), nausea, vomitting
can be atypical (abdo symptoms) - mistaken for indigestion (mimics gallstones + oesophageal spasm)
need a high index of suspicion
can be painless (esp in elderly/DM)