Acute Coronary Syndrome Flashcards
types of angina
–Printzmetal’s Variant Angina
–Chronic Stable Angina
–Unstable Angina
Printzmetal’s Variant Angina
–vasospasm
–supply ischemia
–not due to atherosclerosis
Unstable Angina
–thrombus
–supply ischemia
–due to atherosclerosis
causes of variant/vasospastic angina (Prinzmetal angina)
–coronary artery spasm
–endothelial dysfunction
characteristics of variant/vasospastic angina
–CAD may or may not be present
–onset: rest, minimal exertion, night
–elevated ST segment
characteristics of unstable plaque causing ACS
–large lipid core
–active inflammation
–smooth muscle cell proliferation into intima
–thin fibrous cap
specifics of unstable angina
–chest pain occurring for the first time
–chest pain more severe than usual with chronic angina
–new regions of the heart are undergoing myocardial ischemia
–emergency situation
why is there no infarction with unstable angina?
–occlusion is partial
–thrombus dissolves
EKG 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
–plaque rupture
–thrombus formation
components of increased SNS activity leading to plaque rupture
–increased BP, HR, and force of contraction
–increased force of coronary artery blood flow
–increased force exerted against injured endothelium
components of plaque rupture leading to thrombus formation
–platelets adhere to ruptured plaque
–release substances that (1) attract more platelets and (2) contribute to vasospasm
contributing factors to increased SNS activity leading to plaque rupture
–psychological stress
–exercise
–circadian rhythms
signs of MI in men
–discomfort or tingling in arms, back, shoulder, or jaw
–chest pain
–SOB
signs of MI in women
–sudden dizziness
–heartburn-like feeling
–cold sweat
–unusual tiredness
–nausea or vomiting
general 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 MI?
ruptured plaque + thrombus
why do infarctions occur?
–blood flow disruption is prolonged
OR
–blood flow disruption is total
EKG changes with MI?
yes
cardiac enzyme elevation with MI?
yes
acute MI
acute coronary syndrome with prolonged ischemia without recovery
importance of ATP with ischemia/infarction
–decreased O2 = decreased ATP
–decreased ATP = decreased contractility
when does irreversible injury to cardiac muscle occur?
within 30 min to 4 hours
when does tissue necrosis begin?
by 4 hours
when is necrotic tissue cleared away?
by 1-2 weeks
when does tough fibrous scar tissue replace necrotic tissue?
by 6 weeks
three zones of tissue damage
–ischemia
–injury
–infarction
infarction
–necrosis
–MI, dead cells
–beyond hope of recovery but can stop from increasing
injury
–some recovery possible
–can still perfuse it and restore it to become viable
–not dead yet
ischemia
full recovery possible
how to prevent extension of infract?
–increase oxygen
–decrease the demand on the heart
what influences the extent of damage in a MI?
–location or level of occlusion in the coronary artery
–length of time that the coronary artery has been occluded
–heart’s availability of collateral circulation
ST segment in STEMI v. NSTEMI
STEMI = elevated
NSTEMI = depression or normal
QRS in STEMI v. NSTEMI
STEMI = usually pathologic (wide), develops over hours
NSTEMI = normal
T wave in STEMI v. NSTEMI
STEMI = peaked, then inverted
NSTEMI = inverted
Trop in STEMI v. NSTEMI
STEMI = elevated
NSTEMI = elevated
size of infarct in STEMI v. NSTEMI
STEMI = larger
NSTEMI = smaller
outcomes of STEMI v. NSTEMI
STEMI = poor
NSTEMI = better
left anterior descending artery
–supplies the left ventricle
–most commonly involved in MIs
three main arteries that supply the heart with blood
–right coronary artery
–left circumflex artery
–left anterior descending artery
diagnostics for acute MIs
–serum cholesterol, LDL, HDL, triglycerides
–ECG
–serum electrolytes
–serum glucose
–CRP
–serum homocysteine
–cardiac enzymes
–CXR
–CT scan
–cardiac angiogram and cardiac cath
–ECHO
initial treatment of acute MIs
–oxygen
–morphine
–ASA
–nitro
–beta blocker
–thrombolytic agent
when are thrombolytic agents used?
within 4-6 hours of beginning of MI
reason for giving oxygen with MIs
increase O2 delivery to ischemic myocardium
reason for giving ASA with MIs
suppresses platelet aggregation
–decreases mortality
–chew first dose
reason for giving morphine with MIs
decreases pain
reduces preload and afterload
–helps preserve ischemic tissue
reason for giving beta blocker
reduce HR and contractility
–reduces pain, infarct size, and mortality
reason for giving nitro
reduces preload and afterload
limits infarct size
–does not reduce mortality
example of fibrinolytic therapy
Alteplase (tPA)
MOA of alteplase (tPA)
dissolves clot by converting plasminogen into plasmin
advantages to alteplase (tPA)
most effective
disadvantages to alteplase (tPA)
works best within 30-70 minutes
main adverse effect of alteplase (tPA)
bleeding
what is tPA always given with?
heparin and antiplatelet therapy
side effects of nitro
–hypotension
–headache
–flushing
what shouldn’t be given with nitro?
sildenafil (Viagra) –> severe hypotension
interventions for reperfusion
stent/balloon angioplasty
myocardial stunning
contributes to injury through rapid restoration of blood flow to the myocardium
what is reperfusion injury caused by?
oxidized free radicals generated by WBCs and the cellular response to restored blood flow
who suffers silent, asymptomatic MIs?
–diabetics
–older than age 65
major causes of MI death
–hesitation
–delayed request for emergency care
drug therapy post-MI
–ASA
–beta blocker
–ACE inhibitor
–statin
