Ischemic Heart Disease Flashcards
O2 supply/demand mismatch for the whole body
shock
O2 supply/demand mismatch for the heart
ischemic heart disease
common symptom of ischemia
angina (chest pain)
high-risk plaque; can rupture
vulnerable (unstable) plaque
development of blood vessels
angiogenesis
development of new blood vessels from a pre-existing vasculature
neoangiogenesis
why does tachycardia produce ischemia (why intense workout can elicit MI)
diastole shortens
ischemic heart disease (IHD) aka
coronary artery disease (CAD)
3 main types of IHD/CAD
- vasospastic
- stable (chronic)
- thromboembolic
type of IHD/CAD very prone to rupture
thromboembolic
type of IHD/CAD not likely to rupture
stable IHD (stable angina)
another name for vasospastic IHD
Variant angina
spastic coronary artery restricts flow and decreases O2 supply=
ischemia; Supply Angina
during exercise, stenotic coronary artery can’t meet O2 demand=
ischemia; Demand Angina
thrombus/thromboembolism occludes coronary flow=
ischemia; Acute Coronary Syndromes (ACS)
thromboembolic occlusion of coronary flow can lead to what 4 things
unstable angina
NSTEMI
STEMI
sudden cardiac death
type of angina due to vasoconstriction “Supply angina”
Prinzmetal (variant) angina
type of angina due to increased cardiac workload “Demand angina”
stable angina
leading cause of death nationally and internationally
Ischemic Heart Disease/Coronary Artery Disease
most common etiology of IHD
atherosclerotic obstruction
4 other non-atherosclerotc obstruction leading to IHD
myocardial bridging
microvascular angina
Prinzmetal
radiation-induced
coronary artery prematurely enters myocardium
myocardial bridging
total occlusion in the absence of collaterals </= 20 min
reversible damage
total occlusion in the absence of collaterals > 20 min
permanent damage
3 main ECG findings with ischemia
T inversion
ST elevation
ST depression
discomfort location of angina/MI patient
retrosternal pain
radiation of angina where
interscapular, arm
epigastric location of angina seen in
elderly and women
retrosternal _____ caused by myocardial ischemia due to stenosis or spasm of coronary arteries
discomfort
4 cardinal clinical features of angina discomfort
character
site/radiation
provocation factors
duration
lasts b/t 2-5 min
angina
provoked by exertion/stress
angina
relieved by rest/nitroglycerin
angina
clenched fist over the sternum (sign of angina)
Levine’s sign
does not radiate to trapezius m. unlike in pericarditis
angina
3 main provocation factors for angina
exertion
emotion
rest
2-3 min of discomfort
Prinzmetal angina
stable angina duration
2-5 min
unstable angina duration (thromboembolic)
5-10 min
chest discomfort for 20-29 min at rest or at night
NSTEMI
chest discomfort for >/=30 min at rest or night
STEMI
dyspnea, nausea, fatigue, and faintness
Anginal equivalents
symptoms of myocardial ischemia other than angina
Anginal equivalents
Angina or Not angina: sharp/fleeting pain/dull, prolonged ache in L submammary area
not angina
3 main labs that will show risk factors for CAD/IHD
dyslipidemia
blood glucose
CRP
vasoconstriction w/ dynamic coronary stenosis (Supply angina)
Prinzmetal (variant) anginawhat
transient ST elevation seen in what type of angina
Prinzmetal angina
patients experiencing prinzmetal angina may also have other vasospastic disorders such as
Migraine, Raynaud’s
Prinzmetal angina
both vasoconstriction and increased cardiac workload lead to this angina (but mostly “demand” angina)
Stable angina
2-5 min discomfort; exertional, predictable timing
Stable angina
T inversion and ST depression seen with this angina
Stable Angina
Stable Angina
ST depression is suggestive of what
Coronary Artery Disease
how does stress test help identify CAD
vascular (coronary) steal syndrome
explain vascular steal syndrome
artery w/ plaque is max dilated, on exertion, blood is stolen by other arteries; artery w/ plaque robbed of it’s blood flow and O2
due to thromboembolic occlusion (2 names)
Acute Coronary Syndrome (ACS); unstable angina
rupture; unpredictable timing; 5-10 min discomfort
Unstable angina
this angina experiences ST depression
Unstable angina
unpredictable timing, plaque rupture; 20-29 min pain/discomfort; ST depression; necrosis
NSTEMI
severe angina, ST elevation; >/=30 min pain/discomfort; myocardial wall dies w/in 12-24 hrs
STEMI
heaviness of chest/pressure; 20-29 min or >/=30 min attack; unrelieved by rest or nitroglycerin
Myocardial Infarction
symptoms of this include: sob, sweating, weakness, nausea, vomiting, chest pressure
myocardial infarction
S wave in lead I, Q wave present and inverted T wave in lead III pattern sign of
pulmonary embolism
chest pain is often not present w/ what condition (99% not diagnosed)
pulmonary embolism
no Q wave seen most of the time in what
NSTEMI
exacerbated by vigorous exercise, experiences substernal chest PAIN
STEMI
presents w/ sweating, nausea, vomiting, sense of impending doom
STEMI
confusion, profound weakness, and hypotension
STEMI
anxious and restless; moving around; pain for >/=30 min + diaphoresis (sweating)
STEMI
what to order to diagnose STEMI
ECG and cardiac imaging
STEMI
ST elevation in leads II, III, aVF
acute inferior MI
ST elevation in leads (V1-V6)
acute anterior MI
ST elevation specifically seen in V4 and V5
Acute RV MI
preload dependent; so do NOT give nitroglycerin in this case b/c would precipitate hypotension
acute RV MI
ST elevation in V1-V3
acute posterior MI
cardiac biomarkers for cell death
Troponin I
myoglobin
CK-MB
cardiac biomarkers for inflammation
BNP
CRP
risk factor cardiac biomarkers
LDL, HDL, TG’s
lipoprotein A
myoglobin elevated
cell death from MI within hours
troponin I elevated
cell death from MI within 1-2 days
CK-MB elevated
cell death from MI w/in a day
what biomarker to determine re-infarction
CK-MB
CK-MB is marker for what structure
myocardium
what can cardiac imaging show
perfusion defect
shows depolarization of interventricular septum; if present in V1-V3=
Q wave; injury to myocardium
autoimmune post-infarction syndrome that presents with fever and leukocytosis
Dressler Syndrome
Rx Dressler Syndrome
Aspirin
heart not responding after MI, but resolves within 24 hours
stunning
heart takes up to 7 days to recover from MI
hibernation
in obstruction, coronary channels open and develop into real arterioles due to blood flow creating pressure
arteriogenesis
body makes and degrades this through ubiquitin/proteosome degradation
HIFa
no oxygen w/ ischemia, HIF-1a will bind what and end up producing VEGF
HIF-1a binds HIF-1b
exercise does not improve _____ in humans
coronary collaterals