Download STEMI (from Cameron)

STEMI (from Cameron, Dunn, little bit from Tint)
ANTERIOR
Commonest site
LAD or branches
Precordial leads V1-V4
Reciprocal ST depression in 30% (?which leads…?posterior - no)
May have marked sympathetic stimulation & require rate control to control ischaemia
Large anteriors result in LV dysfunction
Prone to mural thrombus
May be associated INFERIOR infarction
POOR PROGNOSTIC SIGNS:
Bradycardia
Heart block
Note:
Antero-septal: ST V1-V4
Anterior: rS in V1, ST V2-V4, low R amplitude V1-V4
Anterolateral: ST V4-V6, I and aVL
INFERIOR
Inferior leads: II, III, aVF
Reciprocal changes in V1-V3 in 80%
ST depression in aVL = earliest sign
Occasionally Left axis
Due to occlusion in:
RCA (ST greater in III than II)
NB: Proximal RCA lesion (ST V1/V4R) = right ventricular infarction)
OR:
Circumflex (suggested by ST V5/V6/I/aVL) = infero-lateral
NB Reciprocal ST depression in V1-V4 are present in both RCA & Circumflex
infarctions
Less impairment of LV cf Anterior AMI
If associated with RECIPROCAL ST depression in ant leads (V1-V4) likely to have
additional LAD disease, poor LV function/incr risk CCF,
May present with epigastric pain/n/v (from vagal overactivity)
At risk for early complications:
Arrhythmias (especially bradycardias – more common in inferiors)
Heart Block
Cardiogenic Shock
RIGHT VENTRICULAR MI
In isolation = < 3% of all AMI’s
BUT occurs in association with approx 50% of INFERIOR MI’s
RCA occlusion prox to marginal branches
Or: Circumflex occlusion in left dominant circulation
RV Leads RV4-6 ST elevation confirms Dx
All patients with Inferior AMI + RHF: ie
Hypotension
Clear Lung fields
Raised JVP
Should have RV leads performed
RV Infarction complications
Shock
Heart Block (usually with Inferior)
AF
PE from RV thrombus
TR
Pericarditis
Must maintain preload in RV Infarction
Adequate filling
Avoid nitrates/diuretics
Maintain Sinus rhythm
Inotrope: Dobutamine (after adequate filling)
If associated with LV dysfunction:
May require IABP or arterial vasodilators (nitroprusside) to reduce afterload
POSTERIOR AMI
20% of AMI’s
ST Depression or peaked T’s in V1-3, with upright T’s
Initial tall wide R in V1-2 (R:S ratio >1)
ST elevation in posterior leads V7-9
Usually associated with inferior or lateral AMI
In Inferior: less ST elevation in II than III/aVF
R/S ratio > 1 in V1-2 without RAD
LATERAL AMI:
ST elevation in V4-6, I & aVL
“High lateral”
Changes in I, aVL but not V5-6
Can move leads up one intercostal space – may help make Dx
More prone to free ventricular rupture
NON STEMI
“subendocardial”
NSTMI
= 40% of AMI’s
Tend to be smaller than transmural
Better LVEF
Less likely to produce new onset CCF
Lower in hospital mortality
Higher risk of post infarct angina an recurrent infarction
CLINICAL FEATURES:
Often missed in:
Young patients
unsuspected
2-6% occur in age < 40
Elderly:
Atypical Syx (weakness, syncope, confusion, CVA)
Painless: 60-70% of AMI’s over age 85
Difficult Diagnosis in:
LBBB
Diabetic (autonomic neuropathy)
Alt consc state
DIAGNOSIS OF AMI:
AT LEAST 2 OF:
1) Typical ischaemic chest pain for >30 min
2) ECG: ST ELEVATION
a. At least 2mm in 2 or more consecutive chest leads
b. At least 1mm in 2 limb leads
c. New LBBB
3) Elevation of cardiac markers
ECG:
70% Sensitive,
increased with repeat ECG
incr 10% if RV & Post leads done
99% Specific
ST Elevation
Mimics:
LV Aneurysm: Concave initial ST segment
Q waves usually present in same leads as ST elevation
Loss of R waves
Benign Early Repolarisation
Greatest in precordial leads (V2-V5) Usually < 2mm
Minimal in limb leads, Usually < 0.5mm
Concave shape
J point elevated
No reciprocal changes, T waves shouldn’t evolve/change, no Q waves
Pericarditis/Myocarditis: PR depression
Generalised ST changes, not regional
LVH: ST similar morphology to BER
LBBB (+/- AMI)
Hypothermia – Osborne wave
Hypertrophic cardiomyopathy
Pacemaker
Normal variation
Serial ECG’s:
15% of Pt’s with initial normal ECG will develop criteria for reperfusion in
subsequent 24-48hrs
Every 30min if painfree, every 15min with pain
ST Depression:
In ACS
Usually >1mm below J point
Usually flat or downsloping
Regional (not generalised)
May represent
NSTMI
Posterior AMI
Reciprocal changes
Ischaemia without infarction
ST Depression Mimics:
Hypokalaemia
Digoxin
Cor pulmonale/RH strain
BER
LVH
Paced
LBBB
ST Depression/T inversion:
LV Strain
Downsloping ST depression
No J point depression
Asymmetrically inverted T wave
T inversion more marked in V6 than V4
Digoxin
Reverse tick
More prominent in lateral leads
T inversion Mimics:
Persistent juvenile pattern
Stokes-Adams syncope/seizures
Post tachycardia
Post pacemeker
Intracranial pathology
Mitral Valve Prolapse
Pericarditis
PE
PTX
Myocardial contusion
LBBB
RBBB
Q Waves:
Pathological if:
Q’s in 2 contiguous leads V1-3
30ms or more in width
1mm or more in depth in I, II, aVL, aVF, V4-6
LBBB & AMI
15% of Pt with chest pain & LBBB = AMI
Higher mortality than non-LBBB
“Normal LBBB”
ST & T wave will be in opposite direction to QRS (“normal discordance”)
LBBB & AMI
ST & T will be in SAME direction as QRS (ie CONCORDANT)
Sgarbossa Criteria for reperfusion in LBBB:
ST elevation 1mm or more in same direction as QRS (concordance)
ST depression of 1mm or more in V1-V3
ST elevation >5mm in V1-V3
“New LBBB”
new compared to old ECG
“Indeterminate LBBB”
= when no old ECG available
“Old LBBB”
proven to have been present on old ECG
PACEMAKERS
ECG criteria of paced rhythm = same as for LBBB
Can try to establish natural rhythm
Magnet
Atropine to increase rate
Dangerous as may increase O2 consumtion
NB Troponin:
No difference in sensitivity or specificity comp to CKMB at 6 hours
But: Troponin stays elevated longer so at 24 hrs:
Troponin = 100% sensitive
CKMB = 57% sensitive
Troponin In Unstable Angina
Only 50% sensitive
BUT PREDICTIVE (IF ELEVATED) OF:
30 day cardiac complications
1 year prognosis
CHEST XRAY:
Only use – rule out dissection
Cameron: “CxR should not delay administration of thromblytics”
MANAGEMENT
ABC/IV/O2/Monitoring
Aspirin
Treat arrhythmias/CCF
Reperfusion
Therapies that reduce mortality:
Aspirin
Nitrates
B-blockers
ACEI
Reperfusion (thrombolysis/PTCA)
Therapies that don’t reduce mortality:
Ca2+ blockers
GP IIb/IIIa inhibitors (Abciximab, Tirofiban) – unclear
THROMBOLYSIS
Most commonly used reperfusion technique
Max benefit if started within 1 hour of Syx
After 6 hours: some benefit
After 12 hours: NO benefit
Good idea for ED’s to record & audit “door to needle time”
Plasminogen activators (PA’s) or SK?
No difference between PA’s
(alteplase, reteplase, tenecteplase, lanoteplase)
Newer ones have increased fibrin specificity, longer T1/2, and resistance to PA
inhibitor.
tPA vs SK:
tPA better in:
Age < 75
Anterior AMI
Presenting within 4 hours
(ie give SK to older Pt with anterior AMI)
INDICATIONS FOR THROMBOLYSIS:
Typical pain >30min but < 6hrs
ECG criteria as above for Dx of AMI
No contraindications
CONTRAINDICATIONS FOR THROMBOLYSIS:
ABSOLUTE:
Uncontrolled HT (>180/120mmHg)
Bleeding diathesis
Recent GI bleed
Haemorrhagic stroke (<6mths)
Neurosurgery (<6mths)
Trauma, surgery, organ biopsy (<6 wks)
Pregnancy (up to 1wk post partum)
Aortic dissection
Acute pancreatitis
RELATIVE
Non-compressible vessel puncture site
Hx of cerebrovascular disease
Controlled HT
Acute ventricular thrombus
Endocarditis
Non-traumatic CPR
If any of these prewent – need to balance risks/benefits
COMPLICATIONS:
1) Cerebral haemorrhage: 0.5-1.5%
Greater when
SBP >150mmHg
Age > 65
Low body wt
tPA
Most other bleeding complications are relatively minor
2) Allergy/Anaphylaxis
SK = bacterial protein
Previous Strept infection or SK use (ie high Ab titres)
More likely to have allergic reaction
SK less effective
Anaphylaxis < 0.5%
Serum sickness may develop – treat in usual way
3) Hypotension
Due to kinin release during SK use, related to rate of administration
Treatment: Slow infusion, Fluid bolus
4) Reperfusion arrhythmias:
usually self terminating
Seldom require specific therapy
Occurrence often signals reperfusion if irritable myocardium
PCI/REVASCULARISATION
Mild angina & lesser degree of coronary atheroma
Medical Mx better
Significant LAD stenosis
Triple vessel disease (regardless of Syx)
Angina that fails to respond to medical Mx
ANGIOPLASTY VS CABG?
No clear advantage of one vs other in morbidity/mortality
PCI better for high risk surgical candidates
ANGIOPLASTY
85-90% success depending on site of lesion
Restenosis/stent occlusion: 50% in 2-3 years
Preferred for:
Previous PTCA or CABG
NSTMI
CABG
Preferred for LAD/triple vessel disease:
MEDICAL THERAPY
ASPIRIN:
Reduces death or MI in unstable angina/NSTMI
Reduces death in STMI if given early
Aspirin + SK = better than either treatment alone
Minimum effective dose/formula unknown
No benefit in coronary spasm
BETA-BLOCKERS
Improve survival after AMI
Antiarrhythmic
Decrease infarct size
Earlier is better
Blunt CVS response to adrenergic stimulation
CI:
Heart block
Symptomatic bradycardia
Low output/LVF/Acute CCF
May precipitate coronary spasm
So Ca2+ blocker preferred if spasm thought to be cause of ischaemia
In Stable Angina:
Reduce symptoms – especially with exercise/increased symp activity
BUT: Do not reduce AMI rate or mortality
ACEI
Reduce mortality post AMI
Early use after AMI = 6.5% reduction in mortality
NITRATES
Reduce: VR & LVEDP & myocardial O2 consumption
Coronary dilatation – improves flow to sub-endocardium & epicardium
Dilate stenotic segments
Improve collateral flow
May have anti-thrombotic effects
Post MI reduce ventricular dilation
Reduce pulmonary congestion & MR
Early short-term (4-6wk) use may reduce mortality
Ca2+ BLOCKERS
Do not reduce mortality during/after AMI
Useful if can’t tolerate B-Blockers for relief of ischaemic pain/antiarrhytmic
GP IIb/IIIa INHIBITORS
Abciximab
Tirofiban
Eptifibatide
Lamifiban
Efficacy in USA/NSTMI unclear
Mixed results for mortality/long term benefit
USA/NSTMI – GpIIb/IIIa + PCI = beneficial combination
STMI
Beneficial when combined with aspirin/heparin/tPA
BUT: increased bleeding complications
ADP Inhibitors
Clopidogrel
Ticlopidine