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Acute Myocardial Infarction (Risk factors (Male, History of premature…
Acute Myocardial Infarction
Definition
Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial ischaemia due to COMPLETE occlusion of artery by thrombus
Two types
Non ST elevation MI (NSTEMI) or Non-Q infarction
This causes partial thickness damage of heart muscle
A RETROSPECTIVE diagnosis made after troponin results and sometimes other investigation results are available
Occurs by developing a complete occlusion of a MINOR or a partial occlusion of a major coronary artery previously affected by atherosclerosis
ST depression/T wave inversion
STEMI is the most common medical emergency
ST elevation MI (STEMI)
Usually diagnosed on ECG at presentation
Tall T waves
This causes full thickness damage of heart muscle
ST elevation and subsequent pathological Q wave
Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis
May present as new left bundle branch block (LBBB) on ECG
COMPLETE
Differential diagnosis
Stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis and MSK chest pain
Epidemiology
STEMI results in 5/1000 deaths per annum in the UK
Worse prognosis in the elderly and those with left ventricular failure
Pathophysiology
This results in platelet aggregation, adhesion, local thrombosis, vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial necrosis within 15-30 mins in a STEMI (since major artery occluded fully)
STEMI
The sub-endocardial myocardium is initially affected but, continued ischaemia, the infarct zone extend through the sub-epicardial myocardium, producing a transmural Q wave MI
Early repercussion may salvage regions of the myocardium - reducing future mortality and morbidity
Rupture or erosion of vulnerable fibrous cap of coronary artery atheromatous plaque
Risk factors
Male
History of premature coronary heart disease
Age
Premature menopause
Diabetes Mellitus
Smoking
Hypertension
Hyperlipidaemia
Obesity and sedentary lifestyle
Family history of IHD - MI in first degree relative below 55
Clinical Presentation
Any patient presenting with severe chest pain lasting more than 20 minutes may be suffering from an MI
Breathlessness
Fatigue
Distress and anxiety
Pale, clammy and marked sweating
Significant hypotension (low BP)
Chest pain
Pain DOES NOT usually respond to sublingual GTN spray - opiate analgesia is required
Pain described as substernal pressure, squeezing, aching, burning or even sharp pain
Pain may radiate to left arm, jaw or neck
Associated with: sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations
Severe central ongoing pain, lasting more than 20 mins
Bradycardia or tachycardia
Diagnosis
ECG
Performed on admission to A&E
Continuous monitoring required due to high likelihood of significant cardiac arrhythmias
ECG changes confined to leads that FACE INFARCTION
Evolution of STEMI on ECG
After the first few minutes, the T waves become tall, pointed and upright, and there is ST segment elevation
After the first few hours, the T waves invert, the R-wave voltage decreases and Q waves develop
After a few days, the ST segment returns to normal
After weeks or months, the T wave may return to upright by the Q WAVE REMAINS
Troponin I or T increased
NSTEMI
Diagnosis is retrospective made after troponin results etc.
ST depression and T wave inversion
Myoglobin increased
STEMI
Tall T waves
L bundle branch block (LBBB)
ST elevation
T wave inversion and pathological Q waves follow
Diagnosed on presentation
Transthoracic echocardiography (TTE) may be helpful to confirm MI, as wall-motion abnormalities are detected early in STEMI
Treatment
Fibrinolysis - enhance the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin
Risk factor modification
Lose weight and exercise daily
Stop smoking
Healthy diet
Treat hypertension and diabetes
Low fat diet with statins
Coronary revascularisation
PCI
Presented to all patients who present with an acute STEMI who can be transferred to a primary PCI centre WITHIN 120 minutes of first medical contact
If not possible then give patient fibrinolysis and then transfer to PCI centre after infusion
CABG
Hospital
Oxygen if their sats are below 95% or are breathless
Beta blocker - Atenolol
IV Morphine
P2Y12 inhibitor - Clopidogrel
Secondary prevention
Statins
Aspirin - long term
Warfarin if large MI
Beta blockers
ACE inhibitors
Pre-hospital
GTN (sublingual)
Morphine
Aspirin 300mg chewable
Five types of MI
Type 2 - MI secondary to ischaemia due to increased O2 demand or decreased supply such as in coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension
Type 3, 4, 5 - MI due to sudden cardiac death, related to PCI and related to CABG respectively
Type 1 - spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection