acute coronary syndrome

Question 1

acute myocardial infarction

Answer 1

ruptured plaque + thrombus

infarction = blood flow disruption is prolonged OR blood flow disruption is total

monitor ECG changes - STEMI or NSTEMI
*elevated troponin

Question 2

unstable angina

Answer 2

ruptured plaque + thrombus

NO infarction = clot dissolves OR partial occlusion

ECG changes? maybe ischemic changes for short time
cardiac enzymes elevated? NO

Question 3

NSTEMI

Answer 3

no ST elevation
increased troponin
= MI

Question 4

STEMI

Answer 4

ST elevated
troponin elevated
= MI

Question 5

prinzmetal angina

Answer 5

variant/vasospastic angina

cause:
coronary artery spasm, endothelial dysfunction

characteristics:
*may or may not have CAD
*occurs with rest, minimal exertion, night
*elevated ST

Question 6

unstable plaque

Answer 6

1. large lipid core
2. active inflammation
3. smooth muscle cells proliferate into intima (increase plaque rupture)

Question 7

unstable angina
acute v. chronic

Answer 7

acute:
chest pain occurring for first time –> myocardial ischemia

chronic:
chest pain more severe than usual –> new regions of heart undergoing myocardial ischemia

EMERGENCY

Question 8

theory of plaque rupture

Answer 8

1. increased SNS activity –> increases BP, HR, force of contraction –> increases force of coronary artery blood flow –> increases force exerted against injured endothelium
2. plaque rupture –> platelets adhere to ruptured plaque –> release substances that attract more platelets and contribute to vasospasm
3. clot forms

Question 9

ACS vs. stable angina

Answer 9

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

Question 10

S/S of MI

Answer 10

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

Question 11

MI in women

Answer 11

sudden dizziness
heartburn-like feeling
cold sweat
unusual tiredness
N/V

Question 12

MI in men

Answer 12

discomfort or tingling in arms, back, neck, shoulder or jaw
chest pain
SOB

Question 13

what is an acute MI?

Answer 13

ACS with prolonged ischemia without recovery

heart cells suffer irreversible tissue death

Question 14

ischemia –> infarction (patho)

Answer 14

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

Question 15

three zones of damage

Answer 15

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

Question 16

the extent of damage to the heart during an MI is influenced by what factors?

Answer 16

1. location/level of occlusion in coronary artery
2. length of time that coronary artery has been occluded
3. hearts availability of collateral circulation

Question 17

STEMI

Answer 17

elevated ST
elevated troponin
peaked, then inverted T wave
wide QRS, develops over several hours

Question 18

NSTEMI

Answer 18

no elevation or depressed ST segment
elevated troponin
inverted T wave
normal QRS

Question 19

left anterior descending artery (LAD)

Answer 19

supplies left ventricle
most commonly involved in MI
“widowmaker”

Question 20

left main artery

Answer 20

if occluded, entire L ventricle compromised
MAIN WIDOWMAKER

supplies the LAD and L circumflex artery

Question 21

diagnostics for acute MI

Answer 21

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

Question 22

MONA b.

Answer 22

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)

Question 23

why morphine for acute MI?

Answer 23

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

Question 24

why ASA for acute MI?

Answer 24

prevent clots by decreasing stickiness of platelets
CHEW first dose

decreases mortality **

Question 25

why nitroglycerin for acute MI?

Answer 25

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**

Question 26

why beta blocker for acute MI

Answer 26

reduce HR, contractility, oxygen demand

reduces pain, infarct size, and mortality

Question 27

fibrinolytic therapy

Answer 27

alteplase (tPA) for a STEMI

MOA: dissolves clot by converting plasminogen into plasmin

*most effective in 30-70 minutes
*SE: BLEEDING

Question 28

what is tPA always given with?

Answer 28

heparin and antiplatelet therapy (ASA, clopidogrel, ticagrelor)

Question 29

nitroglycerin considerations

Answer 29

can cause severe hypotension and h/a

do NOT give with sildenafil or with other nitrates

Question 30

interventions for reperfusion

Answer 30

1. angioplasty and atherectomy
2. angioplasty and stent replacement
3. coronary artery bypass graft (CABG)

Question 31

reperfusion injury

Answer 31

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)