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Exam 2: Physio-Ischemic heart disease
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Terms in this set (75)
_______________ is a result of a failure
of the coronary blood to supply enough O2 to meet cardiac demand
Ischemic heart disease
Synonyms for ischemic heart disease
CAD, CHD
The only real common symptom among ischemic heart syndromes is chest pain, aka _____________
angina
____________ is the most common serious chronic illness in U.S.
Ischemic heart disease
O2 supply to the myocardium is determined by the _________ of the blood to hold O2
and the ________ at which blood is delivered
capacity, rate
Rate of blood delivery is the coronary artery BQ ___________
~ 250 mL/min
The amount of oxygen the myocardium consumes
25 mL O2/min
Normal adult cardiac O2 demand
Resting: ____________
Heavy exercise: ______________
~ 25 mL O2/min
~200mL O2/min
Four major factors determine myocardial O2 demand:
HR, SBP (afterload), Tension in myocardial wall (preload), contractility
Coronary artery blood flow depends on
Coronary artery diameter, tone, Perfusion pressure, HR, Length of diastole and systole
flow is much
reduced during systole due
to strong ventricular
contraction compressing
small vessels in
myocardium
LAD
flow not effected by
systole due to much lower
pressure generated
RCA
Two main ischemic heart disease syndromes
Angina, MI
Classify patients on presentation as
Chronic/ Stable
Acute/ Unstable/MI
9 causes of ischemic heart disease
Vasospasm, Stenosis of coronary ostia, embolism, arteritis, thrombotic disease, Trauma, Aneurysms/ dissections occluding ostia, compression (tumors/ tension pneumothorax), atherosclerosis
Most common cause of ischemic heart disease
atherosclerosis
The fibrous cap is comprised of:
smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization
The necrotic center is comprised of:
cell debris, cholesterol crystals, foam cells, Ca+
When occlusion reaches _______%, pt will experience symptoms during exercise
75
When occlusion reaches _______%, pt will experience symptoms during rest
90
Death usually result of
thromboembolism
This vessel, if occluded, is called the widow maker
LAD
List in order of severity, the vessels most commonly blocked as a result of atherosclerosis
LAD>RCA>LCX
Worst location to get a blockage because it produces the largest area of ischemia
coronary ostia
Put the Mechanism of Atherosclerosis development in order of occurrence:
A. Chemokines attract monocytes, T-cells & activate macrophages and smooth muscle cells
B. Macrophages release growth factors (PDGF) which stimulate smooth muscle proliferation and connective tissue capsule formation
C. Endothelial cells release chemokines
D. Damage to endothelium
E. Smooth muscle cells change into secretory type smooth muscle and create more connective tissue capsule formation
D. Damage to endothelium
C. Endothelial cells release chemokines
A. Chemokines attract monocytes, T-cells & activate macrophages and smooth muscle cells
B. Macrophages release growth factors (PDGF) which stimulate smooth muscle proliferation
E. Smooth muscle cells change into secretory type smooth muscle and create more connective tissue capsule formation
Carried in blood attached to
lipoproteins
Two lipoproteins identified as playing major role in
CHD
_______: "good"
_______: "bad"
HDL, LDL
Good readings:
• Total cholesterol __________ mg/dL
• LDL ________mg/dL
• HDL ________ mg/dL
< 125 - 200, < 100 , > 40
Delivers cholesterol to cells for use in membranes,
steroid hormones, etc.
Binds to specific LDL receptors on cells that need cholesterol
LDL
clears cholesterol from body by sending it to bile for excretion
HDL
If cholesterol levels are high, _________ can remain in circulation a long time
LDLs
If LDLs remain in circulation a long time, it allows accumulation of ________ form of cholesterol
oxidized
Oxidized LDL picked up by "________________" on
macrophages
scavenger receptors
scavenger receptors on _________ pick up oxidized LDLs
macrophages
Cholesterol builds up in macrophages and they
become
foam cells
As macrophages die, form __________ in atheroma
necrotic core
Before macrophages die, they release cytokines that
contribute to ______________ and ____________
fatty streak, atheroma
Plaque progression from mild to severe:
Normal artery----->___________, or ___________---->advanced vulnerable plaque
Fatty streak, fibrofatty plaque
Clinical phase atherosclerosis
aneurysm and rupture
occlusion by thrombus
critical stenosis
When a capsule ruptures, it exposes collagen to blood, activating the __________ cascade, and forming an unstable blood clot that can ______ the artery.
clotting, occlude
If velocity exceeds __________ number threshold,
blood flow will become turbulent. _________ flow increases chance of embolism.
Reynolds, turbulent
Clinical syndrome arising from transient
myocardial ischemia
Angina
Angina is characterized by _____________ and _____________
attacks of substernal/precordial chest
discomfort (knife-like, choking, squeezing)
paroxysmal, recurrent
Angina pain is due to buildup of _____________ in
myocardium
metabolic waste
Pain receptors piggy-back on __________ pain receptors in same _______________
somatic, dermatome
Three types of angina
Stable
Unstable
Prinzmetal
Stable angina
chest pain that occurs when a person is active or under severe stress
Stable angina relieved with ________ or __________
rest, nitroglycerine
Stable angina has no elevation in cardiac ______________
enzymes
unstable angina
chest pain at rest or chest pain of increasing frequency
Unstable angina also called __________
preinfarction angina
This angina occurs at rest, is unrelated to physical activity
heart rate or BP. Due to sudden vasospasm of
coronary artery.
Prinzmetal angina
Prinzmetal angina is due to _______________ of coronary artery
vasospasm
Prinzmetal angina responds to _________ and __________ channel blockers
vasodilators, Ca+
Result of an embolism lodging in and occluding a
coronary artery
MI
infarction implies some ____________
necrosis
After an MI, damaged tissue initially composed of a _______________ surrounded by a ___________ (or border) zone
that may or may not recover
necrotic core, marginal
_______________ may be an important site of
arrhythmiogenesis until it recovers or dies
Border zone
Infarcted tissue does not contribute to tension
generation, therefore, can compromise ventricular
__________________
function
Damage from MI encompasses the entire thickness of the wall (transmural)
STEMI
Damage from MI limited to subendocardial surface
NSTEMI
NSTEMI damage from MI limited to ___________________
subendocardial surface
STEMI damage from MI encompasses
entire thickness of wall, transmural
Diagnosis of MI based on presence of cardiac enzyme isoforms:
Creatine kinase (CK-MB)
Troponin T (TnT)
Troponin I (TnI)
Weak wall due to MI can show up as cardiac
_______________
aneurysm
_______________ begins to rise within 3 to 12 hours, peak at ~30 hours post-MI
Serum cardiac troponin-I
Serum cardiac troponin-I remains elevated 5 - 10 days, _____________returns to normal in 48 - 72 hours
CK-MB
Because it can be detected for longer time, ______________ is replacing ________ as marker for MI
cardiac troponin, CK
All MI patients should receive _____________ immediately
aspirin
Sublingual ________________ if the blood pressure is adequate
nitroglycerin
Treatment for STEMI: Immediate reperfusion with _______________________, if not available or contraindicated use IV
_______________ agent
percutaneous coronary intervention (PCI), thrombolytic
Treatment for NSTEMI: Managed with _______________ therapy
antiplatelet
percutaneous coronary intervention (PCI) and IV
thrombolytic agents treat:
STEMI
Antiplatelets are used to treat
NSTEMI
Long-term consequences of MI include ventricular
____________
remodeling
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