Acute MI Flashcards
What is an atheroma?
Build up of a fatty, fibrous plaque in the endothelium of the artery, narrowing the lumen and restricting blood flow
What is chronic stable angina?
Chronic chest pain due to ischaemic cardiac tissue. Fixed stenosis (narrowing) Only occurs on demand. Predictable, safe
What does a patient do for chronic stable angina?
- Stop activity - Sit - Use GTN spray
Where is central chest pain felt? Where can it radiate to?
Left sided usually. Rough area. Radiates to left arm Can radiate to the back Or up the neck into the jaw. Felt as “heavy weight”, “pressure, tightness”
What is acute coronary syndrome?
Acute presentation of any coronary artery disease. Umbrella term for - unstable angina - Acute Non STEMI - STEMI
What are the factors for ACS, compared to chronic stable angina?
- Dynamic stenosis - Supply led ischaemia - Unpredictable, dangerous
What are the main steps underlying the pathogenesis of ACS?
- Endothelial injury 2. Platelet activation 3. Platelet aggregation 4. Thrombus formation 5. Vascular blockage (MI, Stroke, death)
How are platelets taken to the site of endothelial injury?
- Endothelial injury exposes collagen - Collagen binds to Glycoprotein Ia/IIb on platelets. Von Willebrand factors also attract platelets. - Platelets recruited and adhere to site of injury. - Platelets join together= Forms a Monolayer
What key mediators cause platelet activation?
Platelet adhesion leads to activation Platelets release ADP and thromboxane A2, which are picked up by receptors of circulating Platelets. Process amplified, leading to platelet aggregation.
How does platelet aggregation lead to thrombus formation?
- Platelets express receptors for leukocytes. - Leukocytes attach to the platelets - Other factors (II, V, X) involved - Thrombin converts fibrinogen to fibrin - Fibrin meshes activated platelets together. - Result is a Thrombus or a blood clot.
What is the result of an acute coronary occlusion?
Acute STEMI
What is the result of a person with an acute STEMI who survives?
- Cardiac tissue beyond the occlusion is starved of blood. - Eventually dies and loss of muscle layer - Increased stretch of ventricles causes dilation. - End result= thin layer of scar tissue, dilated ventricle. Diagnosis- Heart failure (usually left)
What are some things in a patients history who have an STEMI?
- Central, crushing chest pain - Often radiates to neck, jaw and left arm - Similar but more severe than angina, not relieved by GTN - Nausea, vomiting
Difference in symptoms between angina and STEMI?
- More sever pain - Lasts longer - Not relieved by GTN - Associated with vomiting, nausea - Onset at rest, not exertion
What is a NON cardiac diagnosis for chest pain?
Pneumothorax
What are the key ECG changes in acute STEMI?
- ST elevation (1st few hours) 2. T wave inversion (after a day) 3. Q waves (after the MI)
What ST changes are required to diagnose STEMI?
>1mm STE in 2 adjacent limb leads >2mm STE in 2 contiguous precordial leads new onset of Left bundle branch block
What anatomical sites are linked with the ECG leads?
- Right Coronary artery- II,III,avF
- LAD- V1,V4
- Circumflex- I,avL, V5-6
What cardiac proteins and enzymes are useful for MI diagnosis?
- enzyme- Creatinine Kinase 2. protein marker- Troponin: detects any myocardial necrosis. Will be elevated in MI. May not have time to have these checked in acute MI.
What is the immediate treatment for acute STEMI?
- Aspirin (300mg) 2. Clopidogrel (300mg) Both stop platelet aggregation in the coagulation cascade
What other medical interventions are used in early treatment of MI?
- Analgesia- dimorphine IV. Antiemitic 2. Oxygen if hypoxic 3. Aspirin + Clopidogrel 4. GTN 5. Angioplasty 6. Thrombolysis- if angioplasty unavailable after 90min
Summarise the complications (4) that can arise from an MI?
- Death - Arrhythmic complications - Structural “ - Functional “
Main arrhythmic complication in MI? What is its treatment?
Ventricular fibrillation- disordered ventricular output. Loss of CO. Death v likely. Infarcted muscle is a substrate for VF. Treatment- Defibrilator
Some structural complications of MI?
- Ventricular septal defect (recurrent chest pain, shock, low CO) - Mitral valve regurgitation (presents as pulmonary oedema) - Cardiac rupture - Left ventricular aneurysm formation - Dresslers syndrome - Inflammation - Acute pericarditis - Mural thrombus
Functional complications of MI?
- Acute ventricular failure (left, right, both) - Chronic cardiac failure - Cardiogenic shock
Routine things that need to be observed in these patients?
- Cardiac monitor - Patients feelings - Pulse and BP - Heart sounds, specially Added - Any murmurs - Pulmonary crepitations - Fluid balance (urine output)
Examples of fibrniolytics?
tissue plasminogen activator Streptokinase
What is the difference of pathogenesis in STEMI compared to NSTEMI?
Thrombus or clots formed in the vessel and broken down by natural thrombolytics (Plasmin) which breaks down fibrin. Thus no vessel occlusion. NB- NSTEMI is a type of ACS.
Three most important things in diagnosing NSTEMI?
- History (detail of chest pain) - ECG, MAY BE NORMAL. could see ST depression or T wave inversion - Troponin investigations: highly specific to cardiac muscle. Can detect microscopic levels of myocyte necrosis. (can be a marker for other problems, CCF, Arrhythmia, pericarditis)
Main treatment for NSTEMI?
- Aspirin 2. Clopidogrel for 3 months onwards. (often Ticagrelor used instead)
What are some methods of achieving coronary revascularisation in these patients?
- Putting a balloon in the artery to dilate it - If there is a ruptured plaque, a stent pushes it outwards allowing blood flow.
