Early medical management of MI
Myocardial Infraction
Myocardial infarction occurs when cardiac myocytes die due to prolonged myocardial ischaemia.
The diagnosis can be made in patients with an appropriate clinical history together with findings from repeated 12-lead ECGs and elevated biochemical markers - troponin I and T, CK-MB.
STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury.
This injury is produced or facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation.
A mural thrombus forms at the site of plaque disruption, and the involved coronary artery becomes occluded.
Histologic studies indicate that the coronary plaques prone to disruption are those with a rich lipid core and a thin fibrous cap.
Clinical Features
Symptoms
Prolonged cardiac pain: Chest, throat, arms, epigastrium or back (pain is not uniformly present in patients with STEMI).
Anxiety and fear of impending death
Nausea and vomiting
Breathlessness
Collapse/syncope
Physical signs
Signs of sympathetic activation
Pallor, sweating (The combination of substernal chest pain persisting for >30 min and diaphoresis strongly suggests STEMI), tachycardia
Signs of vagal activation (up to one-half with inferior infarction)
Vomiting, bradycardia
Signs of impaired myocardial function (physical signs of ventricular dysfunction )
Hypotension, oliguria, cold peripheries
Narrow pulse pressure
Raised jugular venous pressure
Third heart sound
Quiet first heart sound
Diffuse apical impulse
Lung crepitations
Signs of tissue damage
Fever
Signs of complications, e.g. mitral regurgitation, pericarditis.
Investigations
Electrocardiogram
Serum cardiac biomarkers-
Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI)
CKMB
Cardiac Imaging-
Echocardiography: estimation of left ventricular (LV) function is useful prognostically; detection of reduced function serves as an indication for therapy with an inhibitor of the renin-angiotensin-aldosterone system.
Identify the presence of right ventricular (RV) infarction, ventricular aneurysm, pericardial effusion, and LV thrombus.
Typical ECG changes in myocardial infarction (STEMI)
Cardiac biomarkers
Typical cardiac biomarkers that are used to evaluate patients with STEMI include the MB isoenzyme of CK (CKMB) and cardiac-specific troponins. The black horizontal line depicts the upper reference limit (URL) for the cardiac biomarker in the clinical chemistry laboratory.
Early medical management
brief history/risk factors. Examination
intravenous access + blood for markers (plus FBC, biochemistry, lipids, glucose)
12 lead ECG
intravenous opiate, e.g. morphine sulphate 5-10 mg or diamorphine 2.5-5 mg + anti-emetic, e.g. metoclopramide 10 mg
aspirin 150-300 mg chewed
sublingual glyceryl trinitrate 0.3-1 mg. Repeat
oxygen - nasal cannula 2-4 L/min
beta-blocker (if no contra-indication) for ongoing chest pain, hypertension, tachycardia
if primary PCI available give GP IIb/IIIa inhibitor. Alternatively give thrombolysis.
Fibrinolysis/Thrombolysis
Fibrinolytic agents enhance the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin.
The initial thrombolytic agent used in clinical trials was streptokinase. Others are tissue plasminogen activator (alteplase), Newer-generation analogues of tPA (tenecteplase (TNK))
This agent is derived from bacteria, which can lead to the development of neutralizing antibodies that limit its repeated use.
Given as early as possible: <30 mins of onset of symptoms.
Streptokinase, 1.5 million U in 100 ml of saline given as an intravenous infusion over 1 hour, is a widely used regimen.
Alteplase (human tissue plasminogen activator or tPA) is a genetically engineered drug that is not antigenic and seldom causes hypotension.
The standard regimen is given over 90 minutes (bolus dose of 15 mg, followed by 0.75 mg/kg body weight, but not exceeding 50 mg, over 30 minutes and then 0.5 mg/kg body weight, but not exceeding 35 mg, over 60 minutes).
Contraindications to thrombolysis
Primary percutaneous coronary intervention (PCI)
In institutions that are able to offer rapid access (within 3 hours) to a 24-hour catheter laboratory service, percutaneous coronary intervention is the treatment of choice.
In comparison to thrombolytic therapy, it is associated with a 50% greater reduction in the risk of death, recurrent myocardial infarction or stroke.
Intravenous thrombolytic therapy remains the first-line reperfusion treatment in many hospitals with advanced cardiac unit.
