Myocardial infarction/acute coronary syndrome Flashcards
1
Q
Pathogenesis of MI
A
- endothelial cell injury and inflammation
- plaque formation
- plaque rupture and thrombogenesis
- reduce blood supply and increase oxygen demand
- myocardial ischemia
- myocardial cell necrosis
- acute myocardial infarction
2
Q
MI Is result of prolonged ischemia - prolonged ischemia is result of
A
- most commonly = coronary thrombus
- prolonged vasospasm
- inadequate myocardial blood flow
- excessive metabolic demand
- embolic occlusion (not commonly from distal body)
- vasculitis/coronary artery dissection/trauma
- congenital abnormalities
- hematological disorders
- cocaine
3
Q
What does the arteries supply?
1. right coronary artery
2. left coronary artery
3. posterior circumflex artery
4. anterior interventricualr descending
A
- SA/AV node - right side of heart
- splits into circumstancesflex/LAD
- lateral and posterior heart
- left ventricle and septum
4
Q
SA/AV node blood supply
A
- variations exist in right and left coronary artery distribution
- in MOST people the RCA supplies both SA and AV node
- circumflex can supply SA/AV node in some people
5
Q
Patient presentation with MI
A
- sudden onset of chest discomfort
- may be described as crushing
- Levines sign: flexed forward slightly at hip and clutching chest
- dramatic surge in sympathetic nervosa system activity
- diaphoresis
- cool, clammy skin
- nausea/vomiting
- fever
6
Q
Diagnostic criteria for MI/ACS
A
- must have 2/3:
1. pain
2. ECG changes
3. Biochemical markers/presence of enzymes
7
Q
Pain with MI is located where?
A
- any place above the diaphragm
8
Q
EKG changes with MI
A
- ST segment
- Q-wave: larger
- T-wave - tall = hyperacute phase or inverted = fully evolved
- elevated ST segment = tissue death
ST elevation does not have to present for tissue death
9
Q
Cardiac enzymes with MI
A
- true indicators/appear with tissue death
- take a couple hours to later to look at how the levels are changing
- MI can develop over hours/days
- Troponin T/I = immediately increase
- CKMB = specific to cardiac muscle; increases with myocardial degeneration and clear quickly
- AST, LDH increase later on as troponin decreases
- before mobilizing make sure troponin levels are trending down
10
Q
Acute coronary syndrome stages
A
- Stage 1: stable angina
- Stage 2: unstable angina
- Stage 3: NSTEMI
- Stage 4: STEMI
11
Q
Stage 1: stable angina
A
- angina pain develops when there is increase in demand
- setting of a stable atherosclerotic plaque
- vessel is able to dilate enough to allow adequate blood flow to meet myocardial demand
- ECG/Troponins normal
12
Q
Stage 2: unstable angina
A
- The plaque ruptures and a thrombus forms around the ruptured plaque causing partial occlusion of vessel
- angina pain occurs at rest or progresses rapidly over short period of time
- ECG: inverted T-wave, normal or ST depression
- Troponin = normal
13
Q
Stage 3: NSTEMI
A
- plaque rupture and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium
- ECG = normal, inverted T-waves, or ST depression
- Troponin = elevated
14
Q
Stage 4: STEMI
A
- complete occupation of blood vessel
- results in transmural injury and infarction to myocardium
- ECG = hyperacute T-waves or ST elevation
- Troponins = elevated
- tissue death through whole depth of muscle
- lose contractility and conductibility
15
Q
Pathogenesis for MI once the blockage has occured
A
- a complete interruption of blood supply to an area of myocardium
- cells die and tissue becomes necrotic
- at risk are is within the Zone of perfusion
- the area of tissue death is called zone of necrosis
- if reperfused quickly then surrounding damaged tissue can be spared
