5. Acute Coronary Syndrome and MI Flashcards
Acute coronary syndrome describes a spectrum of what 3 conditions?
Define MI.
What are the 2 different categories of MI pathophysiology?
Unstable angina, NSTEMI, STEMI
- *Rise and/or fall of troponin** with at least one value >99th percentile of the URL, plus at least one of:
- cardiac chest pain
- ECG changes (new ST-T change or new LBBB)
1) Unstable angina/NSTEMI: ruptured coronary plaque with subocclusive thrombus. ECG nondiagnostic - may be normal or show ST depression/T waves in region of infarct. Dx needs troponin analysis
2) STEMI: ruptured coronary plaque with occlusive thrombus. ECG diagnostic - regional ST elevation or new LBBB indicating emg reperfusion tx, preferably with PPCI. CAN’T DELAY TX!
Explain the following AMI classifications and give examples:
a) Type 1
b) Type 2
c) Type 3
d) Type 4a
e) Type 4b
f) Type 5
a) Spontaneous AMI - plaque rupture.
b) Ischaemic imbalance - coronary spasm, embolism, dissection, hypotension etc.
c) Cardiac death - presumed AMI
d) Related to PCI - >5 times URL for troponin
e) Caused by stent thrombosis - confirmed at angiography or autopsy
f) Related to CABG - > 10 times URL for troponin
NB: AMI tx pathway from calling emg services to discharge should take 2-7days.
In-hospital and post-discharge deaths are related to infarct size. What are some determinants of infarct size?
What are the main vessels responsible for
a) Inferior STEMI?
b) Anterior STEMI?
c) Lateral STEMI?
- *1) Anatomical** - distribution of occluded artery, promixity of coronary occlusion, collateralisation of occluded artery
- *2) Physiological** - thrombotic response to plaque rupture, effeciveness of endogenous thombolysis
- *3) Logistical** - time to call for help/arrive at hospital/deliver reperfusion
- *4) Therapeutic** - reperfusion therapy (thrombolysis vs PPCI), antiplatelet drugs, drugs to protect against LV remodelling
a) RCA
b) LAD
c) Cx
What is used to rapidly rule out AMI in AandE?
AMI: what are some emergency treatments of STEMI?
List some P2Y12 receptor antagonists.
Is the probability of dying greater after presentation with NSTEMI or STEMI?
How is low, medium and high risk NSTEMI managed?
High sensitivity troponin assay.
Aspirin + ticagrelor. GP IIb/IIIa inhibitor. Unfractioned/LMW heparin. PPCI.
Clopidogrel. Prasugrel. Ticagrelor. -> increasing antiplatelet activity and faster onset.
NSTEMI (pic)
Low risk -> aspirin/fondaparinux/ticagrelor -> conservative management.
Medium/high -> aspirin/fondaparinux/ticagrelor -> coronary angiography within 96 hrs -> PCI or CABG.
AMI complications: what are some in hospital treatments of:
1) Heart failure
2) Bradyarrhythmias (HR <60bmp) - 2 types
1. Diuretics: IV frusemide, haemofiltration if diuretic resistant
RAS inhibition: ACE-I or ARB, Eplerenone
Inotropes (+ve): Noradrenaline, dobutamine.
LV support device: balloon pump? LVAD?
NB. -vly inotropic agents weaken force of muscular contractions. +vly inotropic agents increase strength of muscular contraction.
-
Intermittant/complete AVN block - atropine if slow rate. Pacing rarely needed. Spontaneous recovery in <7d. Good prognosis.
* *Intermittant/complete block of both bundle branches** - pacing mandatory. No spontaneous recovery. Poor prognosis.
AMI complications: what are some in hospital treatments of tachyarrhythmias (AF, VT, VF)?
Once discharged from hospital, what are some 2o prevention methods for future AMI?
AF: rate control with β-blocker. DC cardioversion if haemodynamic compromise. If arrhythmia persists need anticoag with later consideration of rate vs rhythm control.
VT, VF: rhythm control - DC shock. Usually occur in first 12-24 hours when, if corrected, only have minor prognostic impact. If occur >24 hours after presentation = bad prognostic sign, predictive of sudden death in 1st year.
Lifestyle: smoking, diet, exercise
Drugs: aspirin, P2Y12 receptor antagonist e.g. clopidogrel, statin, β-blocker, ACE-I
Devices: ICD ( implantable cardioverter defibrillator)
Treatement for life (except P2Y12 antagonist)
What are the life saving strategies in the following AMI cases:
1) Pre-hospital death from 1o VF - 33% of all deaths
2) Hospital death from LVF - directly related to infarct size
3) Late deaths - variably related to infarct size
a) Recurrent ischaemic events
b) Lethal arrhythmias
1) Get pt to defibrillator ASAP
2) Initiate reperfusion therapy ASAP
3a) 2o prevention therapy
3b) Implantable defibrillator in selected cases
What is troponin and how is it useful?
How would you treat a suspected ACS in A and E?
Highly specific and sensitive biomarker of cardiac necrosis (regardless of underlying pathology). Isoforms I and T. Now higher sensitivity assays. Increased level = heart disorder. Complex of three regulatory proteins (C,I,T) integral to muscle contraction in skeletal muscle and cardiac muscle, but not smooth muscle.
Rapid evaluation/consider alternative sinister illness.
Initiate basic care (IV/O2/monitor/ECG/blood/aspirin/GTN)
If STEMI -> PPCI ASAP
If unstable angina/NSTEMI -> any high risk features?
If nondiagnostic -> continue evaluation.
What does this ECG show?
Normal
What does this ECG show?
Anterior STEMI
What does this ECG show?
Inferior STEMI. No P wave
What does this ECG show?
LBBB in a stable pt. Not MI!
W in V1/V2, M in V5/V6
What does this ECG show?
Pacemaker pt - normal rhythm.
Tiny spikes in V2-V5/6 = pace artefact.
What does this ECG show?
STEMI in the context of LBBB.
Inferior leads look abnormal. V1-V6 = inappropriate concordance STE.
What does this ECG show?
Hypertrophic obstructive cardiomyopathy. Normal for the pt.