Myocardial Infarction: STEMI Flashcards
(29 cards)
What is a STEMI?
Acute myocardial infarction is 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.
A STEMI is diagnosed clinically when there is new (or increased) and persistent ST-segment elevation.
What risk factors are asscociated with a STEMI?
- Smoking
- Hypertension
- Diabetes
- Obesity
- Dyslipiademia
- Metabolic syndrome
- Established coronary artery disease
- Family history of premature coronary artery disease
What is Acute Coronary Syndrome?
Historically ACS has been divided into three clinical categories according to the presence or absence of ST-segment elevation on a presenting ECG and on elevations of cardiac troponin T or I.
- ST-elevation myocardial infarction (STEMI): ECG shows persistent ST-segment elevation in at least two anatomically contiguous leads.
- Non-STEMI (NSTEMI): ECG does not show ST-segment elevation, but cardiac biomarkers are elevated. The ECG may show ischaemic changes such as ST-segment depression, T-wave inversion, or biphasic T waves.
- Unstable angina pectoris: non-specific ischaemic ECG changes, but cardiac biomarkers are within the normal range.
Briefly differentiate the pathophysiology between a STEMI and NSTEMI
STEMI: transmural infarction
NSTEMI: subendocardial infarction
What are the symptoms of a STEMI?
- Chest pain
- Dyspnoea
- Nausea and vomiting
- Pallor
- Diaphoresis
How does chest pain present in a STEMI?
- Classically retrosternal, crushing, heavy, severe and diffuse in nature.
- Might be described by the patient as ‘pressing or squeezing’.
- May occur at rest or on activity.
- May be constant or intermittent or wax and wane in intensity.
- Sometimes radiating to the left arm, neck or jaw.
What are the signs of a STEMI?
- Abnormal beath sounds (e.g. rales and crackles)
- Additional heart sounds (e.g. muffled)
- Signs of cardiogenic shock
- Hypotension
What are the signs of cardiogenic shock?
- Altered mental status/reduced consciousness
- Tachypnoea
- Severe dyspnoea
- Tachycardia
- Orthopnoea
- Cool peripheries
- Grey, ashen, pale appearance
Briefly describe the diagnosis of cardiogenic shock
Cardiogenic shock is primarily a clinical diagnosis supported by haemodynamic measures. It is defined as persistent hypotension (systolic blood pressure [SBP] <90 mmHg) together with signs of end-organ hypoperfusion.
What investigations should be ordered in a STEMI?
- ECG
- Cardiac troponin
- Glucose
- FBC
- Electrolytes, urea, creatinine and eGFR
- CRP
- Serum lipids
Why investigate ECG? And what may this show?
- Perform a 12-lead ECG within 10 minutes of first medical contact in any patient who presents with chest pain and/or other signs of possible STEMI.
- A STEMI is diagnosed in the appropriate clinical context (a patient with chest pain or other symptoms consistent with myocardial ischaemia) when there is new (or increased) and persistent ST-segment elevation in at least two contiguous ECG.
Why investigate cardiac troponin? And what may this show?
- Troponin I and T are the preferred biomarkers for definitive confirmation of an MI. Cardiac troponins are biological markers of cardiac muscle death (cardiomyocyte necrosis) that are released into the circulation when damage to cardiac muscle has occurred.
- Acute MI is definitively confirmed by a rise and/or fall in cardiac troponin (with at least one value >99th percentile of the upper reference limit) in a patient who has symptoms or signs of ischaemia.
Why investigate glucose? And what may this show?
- Hyperglycaemia is common in the setting of acute MI, with or without a history of diabetes.
- Normal or elevated plasma glucose.
Why investigate FBC? And what may this show?
- Look for anaemia, which may influence the duration of dual antiplatelet therapy prescribed.
- Normal range but can be elevated or reduced.
Why investigate electrolytes, urea, creatinine and eGFR? And what may this show?
- Potassium, calcium, and magnesium homeostasis is crucially important to prevent both bradyarrhythmias and tachyarrhythmias during the peri-infarct interval. Baseline renal function at the time of hospital admission will provide a benchmark.
- Normal range but can be elevated or reduced
Why investigate CRP? And what may this show?
- May be raised as a direct result of the acute-phase response to acute MI but may also point to a concomitant infection.
- Normal range or elevated.
Why investigate serum lipids? And what may this show?
- Not useful in the acute period of STEMI management but will inform assessment of the patient’s risk factor profile for recurrent cardiovascular events. Cholesterol levels may be lowered by high catecholamine levels mediated by an acute MI in its early phases.
- Normal range or elevated.
What are the 5 steps in acute management of a STEMI?
- Morphine
- Oxygen
- Nitrates
- Aspirin
- Coronary reperfusion therapy
What is the preferred reperfusion strategy to treat a STEMI?
Percutaneous coronary intervention (PCI)
When is fibrinolysis appropriate in the treatment of STEMI?
If percutanous coronary intervention (PCI) is a lack of access to timely PCI. Idelly PCI should be performed within 120 minutes.
What drugs are given in the dual anti-platelet treatment of a STEMI?
Aspirin plus a P2Y12 inhibitor (e.g. ticagrelor, prasugrel, or clopidogrel)
What must not be given if the patient is eligible for percutanous coronary intervention?
Anticoagulation with unfractionated heparin, enoxaparin, or bivalirudin will be started by the interventional cardiology team in the catheterisation laboratory.
What is the long term management following a STEMI?
- Beta-blocker or non-dihydropyridine calcium-channel blocker
- ACE-inhibitor or angiotensin-II receptor antagonist
- Statin
- Dual anti-platelet
What differentials should be considered for a STEMI?
- Unstable angina
- NSTEMI
- Aortic dissection
- Pulomary embolism
- Pneumothorax
