Acute MI Flashcards Preview

Smoking and stress Alcohol - Hypertension Drug abuse- High cholesterol Age - Obesity Gender - Family history

Normal | } Clinically silent Fatty streak | Atheromatous plaque | } Angina and claudication Atherosclerotic plaque

Predictable Fixed stenosis Demand led ischaemia Safe

Stop Sit Spray (GTN)

Heavy feeling Weight on chest Pressure Tightness

T-he development of atheroma begins with the deposition of a fatty streak within the wall of a vessel. -Over time, this initial lesion develops firstly into an atheromatous plaque and subsequently to an area of atherosclerosis. These two stages are often completely asymptomatic, although the lesion may occlude the vessel lumen sufficiently to give rise to symptoms such as angina or claudication during exercise or to transient ischaemic attacks. - The atherosclerotic plaque, particularly when it is mature and calcified, is a relatively inflexible structure and is prone to fissuring and rupture. These events in turn may trigger the development of a thrombus which can cause acute vascular stenosis, leading to local ischaemia and possibly to infarction. Depending on the vessel involved, this can become manifest as a myocardial infarction, stroke, critical leg ischaemia, or even cardiovascular death.

ST elevation MI

Non ST elevation MI

Non ST elevation MI

- The arterial endothelium is damaged initially by uneven or high ‘shear forces’ in the blood (related to abnormal pressure/flow relationships and enhanced by hypertension, hypercholesterolaemia, smoking, diabetes, inflammation and immune processes). - Lipids accumulate within the intima of the artery at a site of damage. - Over the years, fatty streaks grow towards the media of the artery and may become fibrous because of the production of collagen. Plaques are formed. - If the plaque grows into the arterial lumen, it causes further uneven blood flow and increased shear stress. This increases the build-up of plaque and stenosis of the artery. - The first symptom of arterial stenosis may be pain or cramps at times when the blood flow cannot keep up with the body’s demand for oxygen. Typically, these symptoms develop gradually as the plaque slowly narrows the artery. - At some point, plaques with a high lipid content, which are soft and unstable, may rupture and cause an acute blockage. - During plaque rupture, the lipid core and underlying endothelium is exposed to platelets in the blood. These adhere to the injured surface and release mediators, such as adenosine diphosphate (ADP) and thromboxane A2 (TXA2), that trigger platelet aggregation. - Circulating platelets aggregate at the site of injury forming a platelet-rich thrombus through further platelet activation and recruitment. This process is known as atherothrombosis.

Unstable angina MI sudden Cardiac death

Acute presentation of CAD

Dynamic stenosis - subtotal or complete occlusion Supply led ischaemia Unpredictable Dangerous

Lipid content of plaque (higher = more likely to burst) Thickness of fibrous cap Sudden changes in intraluminal pressure or tone Bending/twisting of an artery in each heart contraction Plaque shape Mechanical Injury

Initiation - spontaneous plaque rupture Adhesion- Platelet recruitment and adhesion at the sit of injury - forming monolayer Activation- adhesion leads to this Release of activators- ADP etc is released through degranulation Surface receptors- ADP binds to receptors Amplification of platelet activation - this accelerates and leads to platelet aggregration Inflamattory cascade triggered-

Severe crushing central chest pain Radiating to jaw and arms especially left Similar to angina but more sever and prolonged- not relieved by GTN spray Sweating, nausea and vomiting

Angina MI - 10 mins -30 mins or longer - Onset=exertion -At rest - Severity usual pain -More severe - GTN= Relief -No effect - No associated symptoms -Sweating, nausea & vomiting

ST elevation T wave inversion Q wave formation

-ST elevation 1mm< in 2 adjacent limb leads - >2mm ST elevation in at least 2 contiguous precordial leads -New onset bundle branch block

Q waves +- inverted T waves

Inferior

V1-V6

V1-V4

Anterolateral

Protein Marker Highly specific for cardiac muscle damage Can detect tiny amounts of cardiac necrosis

ASA inhibits COX, preventing the production of prostaglandin and thromboxane A2 (TxA2) from arachidonic acid. TxA2 aids the expression of the GP IIb/IIIa binding site on the platelet, allowing fibrinogen to bind. Clopidogrel is a potent inhibitor of ADP-induced platelet aggregation, irreversibly inhibiting the binding of ADP to its platelet membrane receptors. ADP binding is necessary for activation of the GP IIb/IIIa receptor, which is the binding site for fibrinogen. Clopidogrel thus ultimately inhibits the activation of the GP IIb/IIIa receptor and its binding to fibrinogen. Due to the different mode of action of aspirin and clopidogrel, the initial interest was to determine which antiplatelet was most effective at reducing vascular events

Chest pain suggestive of acute MI ECG changes No contraindications

-Failure to perfuse - Haemorrhage - Hypersensitivity +

Analgesia - diamorphine (IV) Anti-emetic Aspirin GTN if BP is above 90mmHg Oxygen if hypoxic Primary angioplasty Thrombolysis if angioplasty not available within 2 hours