This document discusses acute coronary syndrome and thrombolytic therapy for STEMI. It defines ACS as a spectrum ranging from unstable angina to STEMI depending on the degree of coronary occlusion. For STEMI, the goals of early management are pain relief, early reperfusion, and treating complications to minimize heart muscle loss. Thrombolytic therapy with drugs like streptokinase or tenecteplase is recommended if initiated within 12 hours of symptoms to restore blood flow. Factors that indicate successful reperfusion and guidelines for concomitant medications, complications, and contraindications to thrombolysis are also summarized.
3. ACUTE CORONARY SYNDROME
ACS is a clinical spectrum of ischaemic heart disease
ranging from unstable angina, non-ST segment
elevation myocardial infarction (NSTEMI) to STEMI
depending upon the degree and acuteness ofcoronary
occlusion. In unstable angina, myocardial injuryis
absent and cardiac biomarkers are normal. In
myocardial infarction (MI) [both NSTEMI and STEMI]
cardiac biomarkers are raised.
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4. Myocardial infarction
Clinical diagnosis based on the presence of myocardial injury or necrosis as
indicated by a rise and fall of serum cardiac biomarkers. There should be at
least one of the following:
i. Clinical history consistent with chest pain of ischaemic origin
ii. ECG changes of ST segment elevation or presumed new LBBB
iii. Imaging evidence of new loss of viable myocardium/new regional wall
motion abnormality
iv. Identification of an intracoronary (IC) thrombus by angiography or autopsy
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6. DIAGNOSIS
CHEST PAIN
Begins abruptly and lasts for more than 30min
Located in centre of chest. May radiate to jaw / left arm
May occur at rest / with activity
Usually describe as a pressure / sqeuazzing or severe
crushing pain with a sense of impending doom. Sometimes
the pain may be just a tightness or heaviness
a/w sweating, nausea, vomiting, sob
In elderly, females and diabetic pt, the index of suspicion
has to be high because they may present with atypical sx
eg unexplained fatigue, sob, dizziness, lightheadedness, or
syncope
7. Other important points to note in the history are the
presence of:
• Previous history of ischaemic heart disease, PCI or
CABG.
• Risk factors for atherosclerosis.
• Symptoms suggestive of previous transient ischaemic
attack (TIA) or other forms of vascular disease.
8. Pain differentiation
SYSTEM SYNDROME Clinical
description
Presenting
features
CARDIOVASCULAR Stable angina Retrosternal
pressure,
heaviness, burning;
may radiate to
arms, neck, jaw
Provoked by
physical
/emotional stress
Unstable angina Same as stable but
usually more
severe and
prolonged
Occur at rest or
with minimal
exertion
Acute MI Same as angina but
usually more
severe
Usually > 30min,
a/w dyspnea,
diaphoresis
Pericarditis Pleuritic pain,
worse in supine
position
Fever, pericardial
friction rub
GASTROINTESTINAL Peptic ulcer Burning
retrosternal &
Relieved by antacid
or food
9. ECG
12-lead ECG should be performed and interpreted
immediately within 10 minutes of first medical contact
The presence of ST elevation in two contiguous leads
The cut-off points for new or presumed new ST segment
elevation (in the absence of LVH and LBBB) is the
presence of ≥ 0.1 mV ST segment elevation in all leads
except leads V2-V3. In leads V2-V3, a cut-off point of ≥
0.25 mV (in males < 40 years), ≥ 0.2 mV (in males ≥ 40
years) and ≥0.15 mV in females is used.
The presence of a new onset or presumed new LBBB
Early stage of MI – hyperacute T wave. ECG should be
repeated at 15min intervals
10. Patients with inferior STEMI should have an ECG
recording of the right praecordial lead (V4R) to identify
concomitant right ventricular (RV) involvement.
In those with ST segment depression in leads V1-V3, it
is advisable to have an ECG recording of the posterior
chest wall (V7-V9) to identify a true infero-basal
(formerly known as infero-posterior)STEMI. The cut-off
point for ST segment elevation in the posteriorleads is ≥
0.05 mV (≥ 0.1 mV in men < 40 years).
19. UA/NSTEMI
Features suggestive of UA/NSTEMI are:
Dynamic ST/T changes
ST depression > 0.5 mm in 2 or more contiguous leads
T-wave inversion – deep symmetrical T-wave inversion
Other ECG changes include new or presumed new onset
bundle branch block (BBB)* and cardiac arrhythmias,
especially sustained ventricular tachycardia. Evidence
of previous infarctions such as Q waves may be present.
However, a completely normal ECG does not exclude
the diagnosisof UA/NSTEMI. Serial ECGs should be done
as the ST changes may evolve.
24. MANAGEMENT
Early management of STEMI is directed at:
Pain relief
Establishing early reperfusion
Treatment of complications
25. TIME LOST is
equivalent to
MYOCARDIUM LOST
A)
CPG – Management of acute STEMI 2014 – 3rd
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DBT – 90MIN
DNT – 30MIN
26. B) Contraindications to
fibrinolytic therapy
Absolute contraindications
Risk of intracranial haemorrhage
- History of intracranial bleed
- History of ischaemic stroke within 3 months
- Known structural cerebral vascular lesion (e.g AVM)
- Known intracranial neoplasm.
Risk of bleeding
- Active bleeding or bleeding diathesis (excluding menses)
- Significant head trauma within 3 months
- Suspected aortic dissection
CPG – Management of acute STEMI 2014 – 3rd
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27. B) Contraindications to
fibrinolytic therapy
Relative contraindications
Risk of intracranial haemorrhage
- Severe uncontrolled hypertension on presentation (BP > 180/110 mmH
- Ischaemic stroke more than 3 months
- History of chronic, severe uncontrolled hypertension
Risk of bleeding
- Current use of anticoagulation in therapeutic doses (INR > 2)
- Recent major surgery < 3 weeks
- Traumatic or prolonged CPR > 10 minutes
- Recent internal bleeding within 4 weeks
- Non-compressible vascular puncture
- Active peptic ulcer CPG – Management of acute STEMI 2014 – 3rd
edtion
28. C) High-risk patients
Large infarcts
Anterior infarcts
Hypotension and cardiogenic shock
Significant arrhythmias
Elderly patients
Post-revascularisation (post-CABG and post-PCI)
Post-infarct angina
CPG – Management of acute STEMI 2014 – 3rd
edtion
29. FIBRINOLYTIC AGENT
1) Streptokinase is antigenic and promotes the production of
antibodies. Thus the utilisation of this agent for reinfarction is less
effective if given between 3 days and 1 or even 4 years after the first
administration. PCI or fibrin specific agents should then be considered.
Regimen:
-1.5 mega units in 100 ml normal saline or 5% dextrose over 1 hour
2) Tenecteplase (TNK-tPA) causes more rapid reperfusion of the
occluded artery than streptokinase and is given as a single bolus dose
Regimen: single IV bolus 30 mg if < 60 kg
35 mg if 60 to < 70 kg
40 mg if 70 to < 80 kg
45 mg if 80 to < 90 kg
50 mg if > 90 kg
30. Indication of Tenecteplase
(TNK-tPA)
To reduce mortality associated with AMI
Patient < 50 years old
Patient have an anterior MI
Chest pain < 12 hours
31. Indicators of successful
reperfusion
Resolution of chest pain (may be confounded
by the use of narcotic analgesics)
Early return of ST segment elevation to
isoelectric line or a decrease in the height of
the ST elevation by 50% (in the lead that
records the highest ST elevation) within 60-90
minutes of initiation of fibrinolytic therapy
Early peaking of CK and CK-MB levels
Restoration and/or maintenance of
haemodynamic and/or electrical stability
32. Concomitant therapy
A) Oxygen - indicated in the presence of hypoxaemia
(SpO2 < 95%)
B) Antiplatelet agents – Aspirin, Clopidogrel
C) Antithrombotic therapy
33. Concomitant therapy
D) B-blocker
Contraindications to B-blockers:
1) Bradycardia < 60/minute
2) SBP < 100 mmHg
3) Pulmonary congestion with crepitations beyond the lung bases
4) Signs of peripheral hypoperfusion
5) Second or third degree atrio-ventricular (AV) block
6) Asthma or chronic obstructive airway disease
7) Severe peripheral vascular disease
34. Concomitant therapy
E) ACE-Is and ARBs
The benefits of ACE-Is are greatest in patients with: HF, Anterior infarcts,
Asymptomatic LV dysfunction [LV ejection fraction (LVEF)] < 40% on
echocardiography)
Contraindications to ACE-I and ARB therapy:
SBP < 100 mmHg
Established contraindications e.g. bilateral renal artery stenosis
35. Concomitant therapy
F) Statin – Early and intensive high dose statin in ACS have been
proven to produce superior benefits in reduction of major cardiac
events.
G) Calcium channel blocker
H) Nitrates
ACS is a clinical spectrum of ischaemic heart disease ranging from
unstable angina, non-ST segment elevation myocardial infarction
(NSTEMI) to STEMI depending upon the degree and acuteness of
coronary occlusion (See Figure 1). In unstable angina, myocardial injury
is absent and cardiac biomarkers are normal. In myocardial infarction
(MI) [both NSTEMI and STEMI] cardiac biomarkers are raised.
MI is a clinical diagnosis based on the presence of myocardial injury or
necrosis as indicated by a rise and fall of serum cardiac biomarkers. In
addition, there should be at least one of the following:4
i. Clinical history consistent with chest pain of ischaemic origin.
ii. ECG changes of ST segment elevation or presumed new LBBB.
iii. Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality.
iv. Identification of an intracoronary (IC) thrombus by angiography or
autopsy.
This new comprehensive definition of MI which utilises newer cardiac
biomarkers and imaging techniques is more sensitive in diagnosing
MI.5
‘Reinfarction’ is used for MI that occurs within 28 days of the incident
event while recurrent MI occurs after 28 days.4
Post lead
V7 – Left posterior axillary line, in the same horizontal plane as V6.
V8 – Tip of the left scapula, in the same horizontal plane as V6.
V9 – Left paraspinal region, in the same horizontal plane as V6.
Anterolateral mi
ST elevation is present in the anterior (V2-4) and lateral leads (I, aVL, V5-6).
Q waves are present in both the anterior and lateral leads, most prominently in V2-4.
[above]
Hyperacute anterolateral MI
hyperacute t wave v2 –v4, st-elevation v1,
Inferoposterolateral STEMI:
ST elevation is present in the inferior (II, III and aVF) and lateral leads (I, V5-6).
ST depression in V1-3 with tall, broad R waves and upright T waves and a R/S ratio &gt; 1 in V2 indicate concomitant posterior infarction (this patient also had ST elevation in the posterior leads V7-9).
Posterior ecg
ST depression I, II and V5-6
subtle ST elevation in V1-2 and aVR
TWI V1-V4
The benefits of early treatment – opening the blocked coronary
artery as soon as possible so as to limit myocardial damage to the
minimum and preserve heart function.
“TIME IS MYOCARDIUM.”
Pain relief - s/l GTN , IV morphine 2-5mg
Non entereric coated aspirin 300mg
Clopidogrel 300mg