acute coronary syndrome Flashcards
acute myocardial infarction
ruptured plaque + thrombus
infarction = blood flow disruption is prolonged OR blood flow disruption is total
monitor ECG changes - STEMI or NSTEMI
*elevated troponin
unstable angina
ruptured plaque + thrombus
NO infarction = clot dissolves OR partial occlusion
ECG changes? maybe ischemic changes for short time
cardiac enzymes elevated? NO
NSTEMI
no ST elevation
increased troponin
= MI
STEMI
ST elevated
troponin elevated
= MI
prinzmetal angina
variant/vasospastic angina
cause:
coronary artery spasm, endothelial dysfunction
characteristics:
*may or may not have CAD
*occurs with rest, minimal exertion, night
*elevated ST
unstable plaque
- large lipid core
- active inflammation
- smooth muscle cells proliferate into intima (increase plaque rupture)
unstable angina
acute v. chronic
acute:
chest pain occurring for first time –> myocardial ischemia
chronic:
chest pain more severe than usual –> new regions of heart undergoing myocardial ischemia
EMERGENCY
theory of plaque rupture
- increased SNS activity –> increases BP, HR, force of contraction –> increases force of coronary artery blood flow –> increases force exerted against injured endothelium
- plaque rupture –> platelets adhere to ruptured plaque –> release substances that attract more platelets and contribute to vasospasm
- clot forms
ACS vs. stable angina
ACS:
>15min
no relief with nitrates
more severe pain, chest tightness begins to feel like ‘elephant’ on chest, diaphoretic, sense of pending doom
stable:
lasts ~5min, gone within 15 minutes
relief with ntirates
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
MI in women
sudden dizziness
heartburn-like feeling
cold sweat
unusual tiredness
N/V
MI in men
discomfort or tingling in arms, back, neck, shoulder or jaw
chest pain
SOB
what is an acute MI?
ACS with prolonged ischemia without recovery
heart cells suffer irreversible tissue death
ischemia –> infarction (patho)
when O2 decreases, ATP (energy) decreases –> function stops
irreversible injury occurs within 30 min to 4 hours
tissue death begins at 4 hours
dead tissue cleared away by 1-2 weeks –> tough fibrous (scaR) tissue replaces dead tissue ~6 weeks
electrical impulses have difficulty moving through scar tissue
three zones of damage
infarction: necrosis/death - cant recover tissue, but can stop progression
injury: some recover possible - can perfuse it and restore to become viable, not dead yet
ischemia: full recovery possible
the extent of damage to the heart during an MI is influenced by what factors?
- location/level of occlusion in coronary artery
- length of time that coronary artery has been occluded
- hearts availability of collateral circulation
STEMI
elevated ST
elevated troponin
peaked, then inverted T wave
wide QRS, develops over several hours
NSTEMI
no elevation or depressed ST segment
elevated troponin
inverted T wave
normal QRS
left anterior descending artery (LAD)
supplies left ventricle
most commonly involved in MI
“widowmaker”
left main artery
if occluded, entire L ventricle compromised
MAIN WIDOWMAKER
supplies the LAD and L circumflex artery
diagnostics for acute MI
serum:
-cholesterol, LDL, HDL, triglycerides
-electrolytes
-glucose
-homocysteine
ECG
CRP
cardiac enzymes; CPK
cardiac troponin (cTn)
CXR
Ca CT scan
cardiac angiogram and catheterization
ECHO
MONA b.
immediate acute MI tx
morphine
oxygen (#1)
nitroglycerin
aspirin
beta blockers
*thrombolytic agent (if clot is occluding vessel and w/in 4-6hr of beginning of MI)
why morphine for acute MI?
decrease pain
reduce preload and after load (amt of blood coming in and force to get it out)
dilates blood vessel - helps with blood flow
helps preserve ischemic tissue
why ASA for acute MI?
prevent clots by decreasing stickiness of platelets
CHEW first dose
decreases mortality **
why nitroglycerin for acute MI?
vasodilator - decreases preload and afterload to heart (amt of blood coming in and force to get it out)
SL, IV if tolerated
limits infarct size
does NOT reduce mortality**
why beta blocker for acute MI
reduce HR, contractility, oxygen demand
reduces pain, infarct size, and mortality
fibrinolytic therapy
alteplase (tPA) for a STEMI
MOA: dissolves clot by converting plasminogen into plasmin
*most effective in 30-70 minutes
*SE: BLEEDING
what is tPA always given with?
heparin and antiplatelet therapy (ASA, clopidogrel, ticagrelor)
nitroglycerin considerations
can cause severe hypotension and h/a
do NOT give with sildenafil or with other nitrates
interventions for reperfusion
- angioplasty and atherectomy
- angioplasty and stent replacement
- coronary artery bypass graft (CABG)
reperfusion injury
rapid restoration of blood flow to the myocardium also contributes to injury because of myocardial stunning
caused by oxidized free radicals generated by WBCs and the cellular responses to restored blood flow
dysrhythmias can occur (Vfib and Vtach)
