Acute coronary syndrome refers to a range of conditions associated with sudden reduced blood flow to the heart. Such conditions include:
STEMI – a very serious MI during which one of the heart’s major arteries is more than 70% blocked. An ST segment elevation is an abnormality detected on the 12-lead ECG in STEMI. Treat immediately!
NSTEMI – non-ST elevation MI: may progress to STEMI so treat with importance.
MINIMAL MYOCARDIAL NECROSIS – cardiomyocytes cell death related to irreversible myocardial injury.
UNSTABLE ANGINA – experiencing pain even when resting (may progress to STEMI if undiagnosed or not treated in time).
STABLE ANGINA – experiencing pain during exacerbating physical activity.
Plaque Rupture Triggers
- Vulnerable Plaque – eg. Statin therapy causes plaque to become vulnerable
- Inflammatory Cytokines
- Emotional Stress – can change the physiological status of the body through high BP, increased heart rate etc.
- Physical Stress – strenuous exercise in unfit individuals
- Plaque Rupture – thin fibrous cap with lipid beneath makes plaque susceptible to rupture
Myocardial injury extent depends on facturs such as the oxygen demand of the affected tissue, tissue response (younger individuals usually respond better and deal in a better way with an MI than older individuals), rate of flow etc.
Myocardial Infarction Symptoms
- pain, pressure and heat sensation usually in the chest area but possibly radiating to the jaw, back, left arm or both arms;
- sweating, clammy cold skin, tachycardia
- weakness, nausea and vomiting
- mild fever
- dyspnoea
NOTE: an individual may experience a MI but still be asymptomatic!
Diagnosis of an Acute MI
- Obtain information directly from patient; ask questions regarding family history (parents or siblings), degree of pain, how it all started, etc.
- Assess symptoms to make sure they are coronary-related
- Monitor for ECG changes: check for signs of Ischaemia and MI
- Monitor serum cardiac biomarkers: necrosis causes sarcolema disruption, releasing macro-molecules in circulation
- Monitor Troponin I & T (absent in healthy individuals, rise 3-4hrs after a MI and peak at 18-36hrs before declining slowly within 10-14 days)
- Monitor Creatinine Kinase (CK): injury to the heart is marked as an elevation in CK; CK-MB rises 4-8hrs post MI and peak by 24hrs before returning to normal in 48-72hrs; a 2nd CK-MB indicates a re-infarction (can be noticed easier as CK-MB returns to normal quicker)
Acute Coronary Syndrome Treatment
- Morphine: decrease anxiety and pain associated with ACS
- Oxygen: monitor SP02 and administer Oxygen on demand
- Anti-Ischaemic Therapy: Beta-Blockers, Nitrates and Calcium Channel Blockers (CCB are not to be administered in case of heart block or heart failure)
- Anti-Thrombotics – Aspirin (300gm) & Clopidogrel (300-600mg loading dose, then 75mg): balance platelet aggregation
- Anti-Coagulants – Enoxaparin OR IV Heparin OR Fondaparinux OR Bivalirudin (the latter only for patients undergoing Percutaneous Coronary Intervention)
- Statin: anti-cholesterol drug that reduces infarction and mortality
- ACEi: helps control blood pressure – excellent drug for patients with low ejection fraction
Percutaneous Coronary Intervention VS Thrombolytics
Myocardial Infarction Complications
Cardiogenic Shock
Cardiogenic shock is caused by either a massive Myocardial Infarction or a valve issue. If a patient presents with a prominent jugular vein, low blood pressure and high heart rate consider as emergency…monitor closely!
Below you can find a collection of videos that can help provide a more visual approach to Acute Coronary Syndrome.
Acute Coronary Syndrome Detailed Overview
Special thanks to the creator of the featured videos on this post, specifically Youtube Channel Armando Hasudungan and Thrombosis Adviser.
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