acute MI Flashcards
ACS
acute coronary syndrome: acute presentation of coronary artery disease and there are loads of them ! ie -unstable angina -acute non STEMI -STEMI
AMI
acute myocardial infarction
chronic stable angina
fixed stenosis, demand led ischaemia, predictable, safe
ask patients to : sit and breath !
only comes along with increased demand
cardiac chest pain
often described as:
heavy feeling
weight on chest
pressure, tightness
nonSTEMI and STEMI
have the same pathogenic trigger > take safe atherosclerotic plaque > make it unsafe ie with plaque rupture + thrombosis = dynamic stenosis»_space; supply led ischaemia»_space; leading to symptoms at rest
risk factor for stemi/nonstemi
spontaneous plaque rupture !! ie platelet cascade
factors affecting plaque rupture / fissure
- lipid content of plaque
- thickness of fibrous cap
- sudden changes in intraluminal pressure or tone
- bending and twisting of an artery during
- each heart contraction
- plaque shape
- mechanical injury
chronic stable angina is :
predictable, safe
is demand led ischaemia
fixed stenosis
ACS is : (ua / mi)
unpredictable and dangerous
is supply led ischaemia
dynamic stenosis (subtotal or complete occlusion)
PCI
percutaneous coronary intervention ! angioplasty damages endothelium, exposing sub endothelial tissue and body will react as an injury … platelet cascade etc
treatments (2)
aspirin > inhibit cyclooxyrgenase and stops the production of thromboxane A2
clopidogrel, prasugrel, ticagrelor > are ADP receptor antagonist
blocks , and so prevent the binding of ADP to the platelet surface
after an MI - left sided heart failure
even if a patient survives an MI, the tissue that suffered from the infarct, scar tissue will form - the muscle is damaged
the volume within the LV cavity increased and so heart function will decrease
left sided heart failure
causes : dizziness orothpnea paraxysmal nocturnal dysopnea 5 year survival rate : death due to HF (25%)
diagnosis of STEMI
history !
of ..
severe crushing central chest pain
radiating to jaw and arms - left is worse
similar to angina but more severe, prolonged and not relived by GTN (glyceryl trinitrate)
associated with sweating, nausea and often vomitting
diagnosis of STEMI (3)
history !
of ..
severe crushing central chest pain
radiating to jaw and arms - left is worse
similar to angina but more severe, prolonged and not relived by GTN (glyceryl trinitrate)
associated with sweating, nausea and often vomitting
ECG !
ST elevation
-more than or 1mm ST elevation in 2 adjacent limb leads
or
- more than or 2mm ST elevation in at least 2 continuous precordial leads
or
-new onset bundle branch block
T wave inversion
Q waves
cardiac enzymes and proteins markers !
but ..
may be normal at presentation
and do not have time to wait for results
>CK - creatinine kinase
>troponin - Tn (what is preferred)
anatomical site of MI (ECG)
inferior : II III AVF
anterior : v1-v6
anteroseptal v1-v4
anterolateral I avL V1-V6
early treatment of STEMI (1)
> clopidogrel etc blocks the action of ADP on platelet surface
aspirin is good at inhibition COX system thus prevention the product of thromboxane A2
> use aspirin in combination with clopidogrel/prasugrel/ticagrelor
aspirin
300mg
patients asked to chew
thrombolysis
breaks up clot
|»_space; can get prehospital thrombolysis ie paramedics
indications for PCI / thrombolysis
-
risks of thrombolytic therapy
- failure to re-perfuse (mortality risk doubled if artery didn’t open
- haemorrhage (minor, major, intracranial)
- hypersensitivity
treatment of STEMI with regards to time
if : TS elevation ACS they should b treated immediately with PCI
if : PCI cannot be provided within 120m of ECG diagnosis then patients should receive immediate / prehospital thrombolytic therapy
early treatment of STEMI (2)
> analgesia - diamorphine IV -reduces workload of heart and reduced infarct size
anti emetic - IV (treats motion sickness)
aspirin - 300mg AND ticegralor 180mg/clopidogrel 600mg to start as a loading dose for anti-platelet work
can considerGTN if bp > 90mmHg
oxygen if hypoxic
primary angioplasty
thrombolysis (if angioplasty not available within 2 hours)
complications of AMI
death, arrhythmic complications
structural complications
functional complications
arrhythmic complications
> ventricular fibrillation
structural complications
> cardiac rupture >ventricular septal defect >mitral valve regurgitation -LV aneurysm formation -mural thrombus (sometimes with systemic emboli) -inflammation -acute pericarditis -dressler's syndrome
dressler’s syndrome
inflammation of the pericardium
functional complications
> mainly just ventricular function …
acute ventricular failure of LV/RV/both
chronic cardiac failure
cardiogenic shock
killip classification
1 - no signs of heart failure
2 - crepitations <50 % of lung fields
3 - crepitations >50% of lung fields
4 - cardiogenic shock
acute NSTEMI and UA
the pathogenic trigger is the spontaneous plaque rupture and so antiplatelets are the solution ie clopidogrel and aspirin (standard therapy)
»associated with poorer outcomes , potentially have a higher risk than STEMI
diagnosis of NSTEMI
history - heart pain
ECG - it may be normal !!
biomarker of troponin - can reflect microscopic zone of myocyte necrosis (actin and myosin)
treatment of NSTEMI
>in the presence of an ischaemic ECG changes or elevation of cardiac troponin patents with ACS should be treated immediately with both aspirin 300mg and ticagrelor 180mg > patients with ACS should be considered for aspirin and clopidogrel where the risks outweigh the benefits of ticagrelor and prasugrel >in the presents of an ishaemic ECG changes or elevation of cardiac markers patients with ACS should be treated immediately with fondaparinux or LMWH > in the absence of bradycardia or hypotension, patients with ACS in killip class 1 should be considered for immediate IV and oral beta blockers
GP IIb - IIa
open another receptor on platelet starting synthesis of fibrinogen which would them go on to aggregate more platelets > so can get GP IIb - a inhibitors
troponin-itis
misdiagnosis of an ACS based solely off of troponin levels .. troponin levels are also elevate in a series of other conditions ie CCF hypertensive crisis renal failure PE sepsis stroke/tia pericarditis/myocarditis post arrhythmia
task force criteria for the diagnosis of MI
detection of a rise/fall of carina biomarker values w at least one value above the 99th percentile upper reference limit and with one of the following :
- symptoms of ischaemia
- new or presumed new significant ST segment - T wave changes on the left branch block
- imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
- identification of an intracoronary thrombus by angiography or autopsy
diagnosis of type II of myocardial infarction
is secondary to an ischaemic imbalance .. increased myocardial demand for oxygen ie sustained tachycardia significant hypertension marker LVH hypertrophic cardiomyopathy valvular disease ... reduced myocardial oxygen / blood supply anaemia hypoxia and resp. failure bradycardia hypotension vasospasm coronary embolism
type I vs type II MI
I = sudden symptoms major ECG changes no obvious other cause higher trop. with rise then fall severe CAD on angiography II = less chest pain minor ECG changes tach/low bp/illness smaller more static troponin mild moderate coronary disease
non ischaemic myocardial injury with necrosis
not type II cos they don’t have a coronary artery disease … ie pacing , cardiac contusion , received chemotherapy
mechanisms of aspirin
it inhibits cyclooxyrgenase, preventing the production of prostaglandins and thromboxane A2 from arachnoid acid, TXA2 promotes the expression of the GP IIb/IIIa binding site on the platelet - allowing fibrinogen to bind
mechanism of clopidogrel (thienopyridine)
is a potent inhibitor of ADP-induced platelet aggregation
irreversibly inhibiting the binding of ADP to its platelet membrane receptor
(ADP binding is necessary for activation of the GP IIb/IIIa receptor, which is the binding site for fibrinogen)
Clopidogrel thus ultimately inhibits the activation of the GP IIb/IIIa receptor and its binding to fibrinogen.
