Heart Attack Flashcards
(44 cards)
Describe roughly chronic stable angina?
Fixed stenosis of the vessel
Causing demand led ischaemia
Predictable and relatively safe
Stop, sit down (reduces CO) and use spray (improves coronary perfusion)
What is typical anginal pain?
Vague area over breastbone radiating down the arm
Heavy feeling
Weight on the chest
Pressure tightness
What is acute coronary syndrome?
Any acute presentation of coronary artery disease
Only a provisional diagnosis that covers a spectrum of conditions.
Describe the rough pathogenesis of acute coronary syndromes?
Normal Fatty streak Atherosclerotic plaque Fibrous plaque Plaque rupture/fissure + thrombosis
What is Plaque rupture/fissure + thrombosis usually associated with?
ACS
- unstable angina
- MI
- Sudden cardiac death
Roughly describe acute coronary syndromes ( unstable angina/MI)
Dynamic stenosis - an obstruction suddenly develops
Supply let ischaemia which is unpredictable and dangerous
What is the main pathogenesis of ACS?
Spontaneous plaque rupture
What are some of the factors affecting plaque rupture/fissure?
Lipid content of plaque
Thickness of fibrous camp
Sudden changes in intraluminal pressure or tone
Bending/twisting of arteries during contraction
Plaque share
Mechanical injury
What happens in PCI - in terms of the vessel wall damage?
A metal stent is fitted under high pressure
This disrupts the vessel wall and established the lumen
The vessel wall damage leads to exposed tissue elements (collagen and vWF)
Platelets react to these factors
They form a monolayer, starting the activation process and undergo a conformational change which encourages platelet clumping
What happens next in the platelet cascade - release of activators?
Platelets when activated release ADP ( from granules in the platelets) and thromboxane A2 (from cycloxygenase)
These bind to the platelets via receptors
Induces the conformational change
The platelet activation accelerates causing platelet aggregation
Inflammation is also set up - leukocytes are involved
Clotting network then forms the fibrin rich thrombus and blood clot
What happens in unstable plaque - in terms of platelets etc?
The plaque ruptures
Platelets react
Form a clump which further reduces the luminal AP causing restricted blood flow leading to ACS.
Briefly summaries the central pathway to platelet aggregation?
Activation
Activator release –> Aggregation –> Inflammation
Vascular blockage
Acute MI, stoke or death
What is management of ACS focused on?
Damping down the activation of platelets
What happens to the heart after an acute infarct if the patient survives?
The tissue downstream will die due to the blockage, leading to the acute infarct.
There will be scarring, loss of muscular function and dilatation.
Leading to a progressive reduction in blood that can be pumped by the centric;e
Eventually leading to cardiac failure
What would be a history diagnosis of STEMI?
Central crushing chest pain
Radiating to arm and jaw (left)
Like angina, but worse and not relieved by GTN
Nausea, sweating, vomitting
What would you look for on an ECG in a STEMI?
ST elevation
T wave inversion and Q waves
What are the values for ST elevation for diagnosis of a STEMI?
>= to 1mm of ST elevation in 2 adjacent limb leads >= 2mm of ST elevation in 2 contiguous precordial leads
New onset of LEFT bundle branch block (hard to tell on ECG if new onset, so chest pain in the history is CRUCIAL to diagnosis)
What is the sign of a previous MI?
Q waves
+/- T wave inversion
(?) What leads are inferior?
2, 3 AVF
(?) What leads are anterior?
V3,4
(?) What leads are septal?
V1,2
(?) What leads are lateral?
1, AVL, V5,6
Describe cardiac enzymes and protein markers in diagnosis of MI?
May be normal at presentation
May not have time to wait for results in STEMI
Describe the cardiac enzyme CK?
Creatinine kinase
Peaks in 24h
Also in skeletal muscle and brain
Not used so much
An elevated level of creatine kinase is seen in heart attacks, when the heart muscle is damaged, or in conditions that produce damage to the skeletal muscles or brain
