Week Two Flashcards
(81 cards)
Acute Coronary Syndrome (ACS) includes….
unstable angina
NSTEMI
STEMI
NON Modifiable Risk Factors for CAD
age
gender
ethnicity
family history
genetic predisposition
Modifiable RF for CAD
HTN
smoking
exercise (lack thereof)
obesity
diabetes
metabolic syndrome
psychologic state (stress)
homocysteine level
substance abuse
Stable (chronic, exertional) Angina
blockage of coronary artery
predictable
relieved by rest
ST depression or T wave inversion
TREATMENT: rest and NTG
Prinzmetal’s Angina (Variant)
different things cause the chest pain
vasospasm of a coronary artery
smoking, alcohol, caffeine
transient ST elevation during pain episodes
cardiac cath
TREATMENT: CCB (relax coronary artery)
Silent Ischemia
ischemia without the patient reporting pain
diabetes- neuropathy
elderly
woman (present different)
Women Presentation with angina
unusual fatigue
sleep disturbances
SOB
weakness
cold sweat
lightheadness
Nausea
dizziness
indigestion
Unstable (crescendo) Angina
atherosclerotic plaque instability and possible thrombus formation
ST depression or T wave inversion
unpredictable
TREATMENT: rest, NTG, drugs affecting platelets, re-vascularization (stents and bypass)
Acute Myocardial Infarction (AMI)
ischemia with myocardial cell death (necrosis) r/t disruption or deficiency of blood supply to coronary arteries
imbalance of O2 supply and demand
CM of ACS
chest pain
diaphoretic
skin (pale/ashen, cool and clammy)
syncope
N/V
dysrhythmias
fever in the 1st 24 hours
Initially increase in HR and BP but then BP drops because of decreased CO
crackles
JVD
S3 or S4 heard
new murmur
how to classify an MI
ECG changes
depth of heart damage
location of the area of the heart affected
progression of an AMI
ischemia (lack of O2)
- ST depression, T wave inversion, tall peaked T wave
injury (occlusion with ischemia)
- ST elevation
infarction (death)
- pathological Q wave - ain’t getting fixes
Transmural
full-thickness damage of the heart
endocardium, myocardium, epicardium
pathological Q wave from scarring
Non Transmural
limited damage of the myocardium (middle layer of heart)
most frequent site of MI
left ventricle
most frequent coronary artery of a MI
left vein coronary artery (widow maker)
Anterior MI
left anterior descending
V3-V4
septal
left anterior descending
V1-V2
lateral
left circumflex
1, aVL, V5-V6
inferior MI
right coronary artery
2, 3, aVF
posterior MI
left circumflex
V1- V3
MI healing
within 24 hours, leukocytes infiltrate the area of cell death
neutrophils and macrophages remove necrotic tissue by 4th day (there is a thin wall)
10-14 days scar tissue is still weak
very vulnerable to stress
by 6 weeks, scar tissue replaced
normally, the heart will hypertrophy and dilate in an attempt to compensate for dead tissue
management of AMI
O2 supply
decrease myocardial demand (MONA)
M: morphine
O: o2
N: NTG
A: aspirin
IN THIS ORDER: ONAM
medical management of AMI
Call 911
O2
coags
decrease HR (increase ventricular filling time)
decrease preload
decrease afterload
decrease myocardial oxygen
lipid-lowering agents
thrombolytics
intensive glucose therapy