Acute coronary syndrome Flashcards
what are the three conditions of ACS?
Unstable angina
NSTEMI
STEMI
what is caused by supply ischemia and leads to vasospasm?
printzmetals variant angina
unstable angina
New or changing chest pain caused by ischemia
Variant/vasospastic angina
prinzmetal angina
Caused by coronary artery spasm and endothelial dysfunction
when does variant angina occur?
Onset, timing is rest with minimal exertion may be at night
does ST segment elevation with variant angina?
Yes
treatment for variant angina
Nitrates to relax spasms
unstable plaques
Large, lipid core, thin cap
Active inflammation
Proliferation into intima of smooth muscle cells
t/f a small core with a thick cap is a more unstable plaque
False
can an infarction occur with a partial occlusion, or a dissolved thrombus?
No
ECG changes with unstable angina
Ischemic changes typically transient
do cardiac enzymes elevate with unstable angina?
No
theories of plaque rupture
increased SNS activity
Platelet aggregation
Thrombus formation
increased SNS activity
Increased BP, HR, force of contraction
Increased force of coronary artery blood flow
Increased force against injured endothelium
platelet aggregation
Platelets in here to ruptured plaque
Release substances that attract more platelets
Contribute to vasospasm
ACS
More severe chest pain last longer
No relief from nitrates
more symptoms - accompanying
Sense of impending doom
s/sx ACS
Chest pain, SOA
Discomfort in arms, back, neck, jaw, shoulders
diaphoresis, N/V
What are atypical symptoms with women?
heartburn
Sudden dizziness
s/sx MI
diaphoresis
Dyspnea
Extreme anxiety
Levine sign
Pale
Crushing chest pain
Weak peripheral pulses
Acute MI
Ruptured plaque plus thrombus
Blood flow disrupted, prolonged or total disruption
when do troponins levels increase with acute MI
With infarction, trends up
is an acute MI reversible?
prolonged ischemia with no recovery
Myocardial cells suffer, irreversible, ischemic, necrosis
Infarction
Tissue death
ischemia
Hearts blood supply doesn’t Meet bodies demands
transition from ischemia to infarction
ATP not able to be stored
Irreversible injury within 30 min-4hours
Tissue necrosis by four hours
Necrotic tissue cleared away by one to two weeks
Tough fibrous scar tissue replaces necrotic tissue by six weeks
infarction
MI, DEAD CELLS
Can’t recover
Try to stop progression
Injury
some recovery possible
Can still perfuse and restore to become viable
t/f the injury, phase of damage has dead cells
False
when is a full recovery possible?
Ischemia
what does the extent of an MI depend on
Location of occlusion
Length of time of occlusion
Hearts, availability of collateral circulation
STEMI
elevated ST
Wide, QRS
Peaked T waves then inverted
Elevated troponins
Larger infarct
Poor outcomes
NSTEMI
depression/normal ST
Normal QRS
Inverted T-wave
Elevated troponins
Smaller infarct
Better outcomes
which artery supplies the left ventricle with oxygenated blood
Left anterior descending artery
which artery supplies the left anterior descending artery and left circumflex
Left main artery
what occurs with a blockage at the beginning of the left anterior descending artery
Widowmaker
acute MI pharm
oxygen
Aspirin
Morphine
Beta blockers
Nitrates
oxygen
Increases oxygen to ischemic myocardium
aspirin
Suppresses platelet aggregation
** Chew
Morphine
decreases pain
Decreases pre-and afterload
Helps preserve tissue
Beta blockers
selective Beta one
decreases HR, contractility
decreases, oxygen demand
Decreases infarct size
Nitrates
decrees pre-and after load
Decreases infarct size
t/f nitrates affect, mortality rate with a cute MI
False
myocardial stunning
Rapid restoration of blood flow to myocardium contributes to reperfusion injury
Reperfusion injury
Oxidized, free radicals generated by wbc’s
Cellular response – restore blood flow
what type of dysrhythmias can occur from reperfusion?
Ventricular tachycardia
Ventricular fibrillation
