Myocardial Infarction Flashcards
chain of events leading to an MI
atherosclerosis plaque rupture platlet aggregation thrombus formation vessel occlusion vasospasm distal ischemia ischemic complications
classic symptoms of an MI
intense opressive chest pain/pressure radiating to left arm
other symptoms of MI
increased chest heaviness nausea dyspona ligthheadness sweating confusion
characteristics of a stable angina
transient (<30mins) episodic chest discomfort
predictable, reproducible
often follows physical excertion or emotional stress
ECG of stable angina
normal,
t wave changes
st depression
unstable angina
new onset
rest angina
angine worseing in severity or occuring with PA
ischemic ECG
assocaited with inverted t wave or st segment depression
Non-STEMI ECG
partial or intermittent blockage of the artery, may show ST depression
STEMI ECG
St segment elevation and t wave inversion
casued by complete and perishing blockage of the artery
how does ischemia reduce ATP availibilty
K+ channels open if Low ATP, thus K+ quickly leak out of cell = trigger deploarization
Ca and Na flood inwards
reduced K:Na pump activity
K builds up outisde, reducing gradient
cell stays positve for longer before repolarzing
effect MI on ST
depression
depolarises, ischemic region generates electrical current
pocket of +ive signal elevates baseline volatge
when ventricles become depolarized, all the muscle depolarises so 0 voltage is recorded
ST segment appears depresssed relative to baseline
potential charactersitics of ST depression
downsloping upsloping horizontal need to be >1mm below baseline seen in at least 2 leads
effect of MI Q wave
damage to left ventricle
dead area so no signal
non pathological q wave
q wave less than 2mm are normal
pathological q wave
q wave greater than 2mm
marker of historic heart attcak
deeper q wave
due to damage in the tissue
surivival of MI
60min golden window
irreversible injury typically requires 30 mins of ischemia
use of cardiac enzymes
allow clincians to document when hearrt attack started as each spike at different times
released when myocardial tissue dies causing cells to collapse and spill contents into blood
CPK peak and time
12-36 hours
raise 3-4 d
tropoin peak
peak 12-24
approx 8
anti- ischemics
oxygen
beta-blockers - slow HR, reduced O2 requirement
nitrates - vasodilator
morphine - pain relief
anti thrombotics
anti platelet agents
- tissue plasminogen activator
Post myocardial infarction
first 4-6 hours
poor contraction
loses systolic power
Post myocardial infarction
7 days
infarct dilation and remodling
inflammation
bruising
thinning of ventricles and enlargement of infarct site
Post myocardial infarction
6-12 weeks
necrosis may develop congestive heart failure
scarring
- scar tissue leads to increased stiffness
- partially resolves with time
types of blood thinners
asprin plus another antiplatelet therapy (warfrin)
novel oral anti-coagulents
effect of ACE Inhibitors
decrease peripheral resistance = reduce BP and less heart work
aids fibrin disolving
effect of Beta blockers
reduce heart work
adrenaline, epinephrin blocker
effect of statins
cholestrol lowering
effect of calcium channel blockers
decrease peripheral resistance = less heart work
effects of diruetics
reduce blood volume = reduces BP & heart work
aspects of a comprehensive cardiac rehab programme
exercise training psychological and stress counselling dietary advice advice on meds and treatment risk factor modification facilitating social reintegration
benefits of exercise based cardiac rehab
13-26% decrease in all cause mortality 10-36% decrease in cardiac mortality 20-50% decrease in reinfarction 10% risk decrease cardiac mortality 23-56% decrease in hopital readmission cost effective increase QoL
starting rehab
normally met in hospital
Post MI/PTCA rehab starts 2-4 weeks later
Post CABG - rehab starts 4-6 weeks
rehab stage 1
before discharge from hospital
- assessment
- lifestyle advice
- medication
- informative
rehab stage 2
early post discharge
- comperhensive assesment
- education
rehab stage 3
strucural exercise
maintain access to advice and support
rehab phase 4
long term maintenance
- long term advice
- referal onto other groups
- outside exercise
what is the best single measure of an individuals Cadio respiratory fitness
peak oxygen uptake
VO2 equation
VO2 = Q xA - VO2 Diff
peak vo2 of aerobically fit vs unfit
unfit is lower
peak vo2 of cardiac patient
CAD patients may have 50% lower peak VO2
stroke volume cardiac patients
increases with exercise
levels off at 50% peak vo2
dictated by venous return, TPR and myocardial contractility
why does SV decrease
scarring and ischemia - increases wall stiffness - hypokinectic myocardium decrease EDV decrease contractility - increase afterload decrease SV
why does Q decrease
coronary vasoconstriction
- exercise can cause locailised vasocon
reduces blood supply to myocardium making it hypokinetic
- subnormal production of endotheliam NO
- localised overproduction of endothelium
redistrubution in cardiac patients
do not redistrubute as effectively viseral blood flow as % resting value - normal 20% - cardiac 50% therefore less delivered to the muscles
