acute coronary syndrome Flashcards
Unstable angina (UA)
new or changing chest pain caused by ischemia.
those with angina for the first time are diagnosed with UA until cause of chest pain is determined.
more severe than normal.
STEMI
ST segment elevation myocardial infarction
NSTEMI
non-ST segment elevation myocardial infarction
Variant/Vasospastic Angina is also known as?
Prinzmetal angina
causes of Variant/Vasospastic Angina
Coronary artery spasm.
Endothelial dysfunction.
characteristics of Variant/Vasospastic Angina
CAD may or may not be present
Onset timing: Rest, minimal exertion, night.
Specific ECG changes: Elevated ST segment.
treatment for Variant/Vasospastic Angina
nitrates- relaxes spasms.
Unstable plaque leads to ACS: size of lipid core, inflammation, smooth muscle cells?
size of lipid core= large. inflammation= active; check CRP levels
smooth muscle cells= proliferation into intima
with unstable angina why is there no infarction?
the Occlusion is partial OR Thrombus dissolves.
are there any ECG changes with unstable angina?
Might see ischemic changes, typically transient
are cardiac enzymes elevated with unstable angina?
no
theory of plaque rupture
INCREASED SNS ACTIVITY: epi/norepi is released; ↑ BP, HR, & force of contraction, ↑ force of coronary artery blood flow, ↑ force exerted against injured endothelium.
PLAQUE RUPTURE.
Platelets adhere to ruptured plaque; Release substances that 1) attract more platelets
and 2) contribute to vasospasm.
THROMBUS FORMATION.
contributing factors to increased SNS activity
Psychological stress
Exercise
Circadian rhythms
signs of UA in men
discomfort in arms, back, neck, shoulder, or jaw.
chest pain, SOB
signs of UA in women
sudden dizziness
heartburn-like feeling
cold sweat
unusual tiredness
N/V
S/S of MI
Diaphoresis
Dyspnea
Extreme anxiety
Levine’s sign (fist to chest)
Pallor
Retrosternal crushing chest pain that radiates to shoulder, arm, jaw, or back
Weak pulses
What is an acute myocardial infarction?
Ruptured plaque + thrombus.
Acute coronary syndrome (ACS) with prolonged ischemia without recovery.
MI: Why is there an infarction?
Blood flow disruption is prolonged OR Blood flow disruption is total.
Are there ECG changes with an acute MI?
yes
are cardiac enzyme levels elevated during an acute MI?
Yes
Myocardial cells suffer _ _ _.
irreversible ischemic necrosis.
Irreversible injury occurs within …..
30 minutes to 4 hours
tissue necrosis begins by _ hours
4
necrotic tissue is cleared away by _ weeks
1-2
Tough fibrous scar tissue replaces necrotic tissue by _ weeks?
6
3 zones of damage
ischemia= full recovery possible
injury= some recovery possible, can still perfuse it & restore it to become viable
infarction= necrosis
The extent of damage influenced by three factors:
location or level of occlusion
Length of time
Heart’s availability of collateral circulation.
STEMI: describe ST segment, QRS, T wave, troponin, size of infarct, outcomes
ST segment: elevation
QRS: usually pathologic (wide), develops over hours
T wave: peaked then inverted
troponin: elevated
size of infarct: large
outcomes: poor
NSTEMI: describe ST segment, QRS, T wave, troponin, size of infarct, outcomes
ST segment: depressed or normal
QRS: normal
T wave: inverted
troponin: elevated
size of infarct: smaller
outcomes: better
which artery is most commonly involved in myocardial infarction?
Left Anterior Descending (LAD) Artery
