ST Elevation Myocardial Infarction (STEMI)
Introduction
Acute myocardial infarction is a myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand. In the case of ST- elevation myocardial infarction (STEMI) this is caused predominantly by complete atherothrombotic occlusion of a coronary artery.
In the appropriate clinical context, a STEMI is diagnosed clinically when;
there is new or presumed new ST-segment elevation in at least two contiguous leads of > 1mm in all leads other than leads V2-V3
In leads V2-V3 = ≥2.5 mm in men < 40 years old, ≥2 mm in men > 40 years old and ≥1.5 mm in women .
The presence of reciprocal ST depression helps confirm the diagnosis
In addition to patients with ST-elevation on the ECG, two other groups of patients with an ACS may have an STEMI: those with new or presumably new LBBB and those with a true posterior MI.
Contiguous ECG leads lie next to each other anatomically and indicate specific myocardial territory.
Risk Factors
Modifiable Risk Factors
Elevated cholesterol levels
Smoking
Hypertension
Diabetes mellitus
Obesity
Physical inactivity
Cocaine use
Non -Modifiable Risk Factors
Age
Male sex
Family history - MI in 1st- degree relative <55 years
Clinical Features
Symptoms
Pain
Chest pain. Acute, dull, central, crushing, worse on exertion
Radiation - into either or both arms, the neck, the jaw, the back.
Chest pain is usually a presenting feature but not always. This is especially the case in women and diabetics
Associations
SOB, nausea, pre-syncope, palpitations, belching, indigestion, fatigue.
Signs
Appearance
Distressed, anxious, clutching chest, pale, diaphoretic
Signs of shock
Hypotension, tachycardia, bradycardia, delayed CRT
Signs of heart failure
Hypoxia, increased WOB, tachypnoea, 3rd or 4th heart sound, gallop rhythm, basal creps, elevated JVP
Differential Diagnosis
STEMI is a life threatening, time critical diagnosis. Consider differential diagnoses but the priority is out STEMI first by performing urgent ECG. Potential alternative diagnoses are listed below.
Cardiac
Other ACS i.e. NSTEMI, Unstable angina
Angina pectoris
Pericarditis
Myocarditis
Gastrointestinal
GORD
Gastritis
PUD
Oesophageal spasm
Vascular
Aortic dissection
Musculoskeletal
Costochondritis
Precordial catch syndrome
Trauma
Respiratory
Pneumothorax
Pulmonary embolism
Pneumonia
Neuropathic
Herpetic Neuralgia
Cervical Neuropathy
Clinical Investigations
Bedside
ECG
12 lead ECG and interpretation within 10 mins of arrival to ED
VBG
? lactic acidosis implying shock.
Check BM
POCUS
Skilled operator may be able see regional wall motion abnormality
Evidence of complications e.g. pericardial effusion, papillary muscle rupture
Evidence of underlying heart disease e.g. LVF, LVH
Laboratory
Troponin
Do not delay coronary reperfusion (Cardiology referral) to wait for troponin results.
Levels usually begin to rise around 2 -3 hours after onset of myocardial ischaemia.
Levels peak at approx 18 hours post pain and remain elevated for 14 days
FBC
elevated WCC not unusual. ? Low Hb as contributing factor to AMI
Routine U&E, LFT, Coag
Ca, Mg, K
Decrease risk of cardiac arrhythmias by ensuring normal levels
Radiology
CXR
To exclude alternative causes and to aid indirect assessment of cardiac function.
Do not delay definitive treatment for Chest x-ray
The ECG in STEMI
In patients with a STEMI the ECG usually evolves through a sequence.
Not often seen but the first change is hyper acute or peaked T Waves.
Elevation of the J point (junction of the end of QRS complex and the beginning of ST segment).
ST elevation becomes more prominent and becomes convex or rounded upwards
Over time (several hours to weeks) ST segment eventually returns to isoelectric baseline
R wave amplitude becomes markedly reduced and T waves become inverted in contigious leads
Q waves deepen indicating transmural infarction
The ECG can be used to localize the MI, and at times, predict the infarct-related artery.
Inferior STEMI
Usually due to RCA stenosis. Sometimes LCx
ST elevation in II, III, aVF
ST depression in aVL
Posterior STEMI accompanies ~ 20% of inferior/lateral STEMI. Isolated posterior STEMI = <10% of STEMIs
Horizontal ST depression in V1-V3.
Tall broad R Waves in V2 + V3
Anterior STEMI
Occlusion of LAD. Highest mortality
ST elevation with Q waves in chest leads. V1-V4
Reciprocal ST depression in inferior leads
Often accompanied with Lateral STEMI
ST elevation I, aVL and V5 + V6
Lateral STEMI
Occlusion of diagonal branch of LAD or LCx
ST elevation in I, AVL, V5 + V6
Reciprocal ST depression in inferior leads
Can occur on it’s own = smaller branches of LAD or LCx
more commonly occurs as Anterolateral STEMI (LAD occlusion) or Inferolateral STEMI (LCx Occlusion)
Management and Disposition
Once a working diagnosis of STEMI is made a reperfusion therapy needs to be initiated as soon as possible. The organisation of this should happen concurrently while initial resuscitation and symptomatic treatment is occurring.
The established cornerstone of STEMI management is a combined strategy of primary PCI or thrombolysis plus dual antiplatelet therapy.
Initial Resuscitation
All STEMI patients should be managed in a resuscitation environment
Continuous ECG monitoring
Manage ABC as indicated
O2 to keep sats > 92%
In case of RV infarction (i.e. Inferior STEMI) hypotension is best treated initially with cautious boluses of fluid to preserve preload on RV.
Persistent hypotension and shock is best treated with emergency revascularisation. If delay to PCI patient should have CVC inserted and be commenced on inotropes e.g. noradrenaline
Symptomatic Treatment
Pain relief as required – intravenous opioid usually first line
Intravenous anti-emetic PRN
GTN
sublingual route initially. May help with pain by decreasing myocardial work
consider IV infusion if signs of CCF or severe hypertension
avoid nitrates in inferior STEMI as they work by reducing myocardial workload by reducing preload. Decreased preload in RV infarction can cause profound hypotension
Specific Treatment
Primary PCI is the preferred reperfusion strategy in patients with STEMI within 12hrs of symptom onset.
If the patient is not within 90 minutes of a primary PCI centre IV thrombolysis can be initiated pending transfer.
In ED give a loading dose of dual anti-platelet therapy (Aspirin plus P2Y12 Inhibitor)
Aspirin 300 mg PO
Ticagrelor 180 mg PO
Disposition
Once the diagnosis of STEMI has been made the Cardiology service need to be consulted urgently to facilitate transfer to the local primary PCI cath lab.
The patient should be transferred from the ED to the Cath lab for urgent PCI. From there they should be admitted to CCU or ICU as clinically indicated .
Report of the National Clinical Programme for Acute Coronary Syndrome (ACS) on standardising treatment of patients with STEMI in 2016
References
Ibanez B, James S, Agewall S, et al; ESC Scientific Document Group. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018 Jan 7;39 (2):119-77
B Wilkinson I, Raine T, Wiles K, Goodhart A, Hall C, O’Neill H. (2017) Oxford Handbook of Clinical Medicine. Oxford, UK: Oxford University Press.
Faselis C, Lieber J, Noto F. (2017) Step 2 CK Lecture Notes 2017: Internal Medicine. New York, US: Kaplan Medical.
Reeder G et al. Diagnosis of acute myocardial infarction. Uptodate.com
This blog was written by Dr Maria Garcia and was last updated in Nov 2020