• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/36

Click to flip

36 Cards in this Set

  • Front
  • Back
What are some of the clinical manifestations of ischemic heart disease?
angina pectoris
MI
Chronic IHD with heart failure
Sudden cardiac death
What are some of the causes of the ischemia?
Fixed coronary obstruction
acute plaque change - platelet aggregation
coronary thrombus
vasospasm
Fixed coronary obstruction
90% of patients
beginning of LAD and LCX
entire length of RCA
secondary epicardial branches
rare in intramural branches
Acute plaque change
rupturing or fissuring
erosion or ulceration

can be triggered by adrenergic stimulation

moderately stenotic are most dangerous
Coronary thrombus
can cause partial to total occlusion

vessel mural thrombus can embolize - cause partial occluusion and can embolism

activate smooth muscle growth related signals
Vasoconstriction
adrenergic agonists
platelet contetnts
impaired secretion of NO
mast cells causing inflamation
What is the cause of stable angina? Unstable?
Stable - decreased perfusion on exertment
Unstable - increasing in frequency, often at rest, due to distruption of atherosclerotic plaque with superimposed occluding thrombus

harbinger of acute MI
What is Prinzmetal angina?
due to coronary artery spasm
episodic, at rest
treat with Ca channel blocker and nitroglycerin
What are some common risk factors with MI?
Male, age,

females - after menopause
blacks same risk as whites
What is the pathogenesis of MI?
Active plaque disruption (hemorrhage, erosion, rupture)
platlets adehere to plaque site and release aggregators
vasospasm
extrinsic coagulation pathway
What is the myocardial response to ischemia?
cesssation of glycolysis
accumulation of breakdown products
loss of contractility
injury and arrhythmias
Transmural vs. subendocardial infarction
Most MI's are transumural
transmural - associated with coronary athersclerosis
acute plaque change
causes ST elevation on EKG

Subendocardial
inner walls
difuse stenosing coronary atherosclerosis
NO plaque disruption
NO superimpsed thrombus
from early lysed thrombus
from severe prolonged hypotension
Non ST elevated MI
What is the morphology process after an infarct?
12-24 hrs red-blue from trapped blood (necrosis and neutrophil infiltrate)
10 days - soft yellow
2 weeks - yellow zone inside red zone
past 8 weeks - scarring past this - can't tell
What are some treatments for MI?
Thrombolysis
Angioplasty with possible stent placementCoronary bypass graft
What is thrombolytic therapy and PTCA?
reestablishes flow through the occluded coronary artery salvages ischemic myocytes
PTCA + stent improves stenosis
CABG helps perfuse tissue past plaque
What is the morphology of a reperfused myocardium?
hemorrhagic
microscopic contraction bands (eosinophillic bands in sync with sarcomere's)

can have free radical damage
myocardium may be "stunned" - take several days to regain strength
What are some Lab tests done to diagnose MI?
CK: MM - muscle; BB - brain lungs; MB - myocardium
starts 2-4 hrs/ peaks at 24/ returns by 72
(CK-MB not myocardium specific, could be skeletal)

Troponins - cardiac specific
rise similar to CK-MB, but may remain elevated for a week
What are some imaging studies done to dianose MI?
ECHO
Radionucleotide angiography
What might post MI contractile dysfunction lead to?
hypotension
pulmonary congestion
cardiogenic shock
What arrhythmias or dysrhythmia are common post MI?
sinus brady
asystole
tachy
V-vib
premature Ventr.
V-tach
heart block
Consequences and Complications: Myocardial rupture
3-7 days after MI
rip in necrotic/inflamed tissue

Ventricular wall - most common
IV septum - causes shunting
papillary musce - causes mitral regurg
Consequences and Complications: Pericarditis
2-3 days
fibrous/hermorrhagic tissue overlying the myocardium
What are some infarct related complications post MI?
Right ventricular infarcts
infarct extension
infarct expansion
Mural thrombus
ventricular aneurysm
What complications arise from large transmural infacts?
cardiogenic shock
arrhythmias
late CHF
What complications arise from anterior transmural infarcts?
free wall rupture, mural thrombi, aneurysm

More severe clinical course
What are the complications of inferior transmural infarcts?
conduction blocks, right ventricular involvement
What is ventricular remodeling?
necrotic area thins - can aneurysm
non-infarcted area hypertrophys - seems good, but may lead to impairment

Goal is to minimize remodeling with medication
WHat are the most important factors in determining prognosis post MI?
quality of LV function
area necrosed
What are the preventative measures for MI?
aggressive risk factor modification
prevent reinfarction
Chronic Ischemic Heart Disease
often elderly
progressive heart failure
history of MI or bypass surgery
cardiac decompensation of hypertrophied myocardium
severe obstruction of coronary artery
What is the morphology of chronic ischemic heart disease?
heart is enlarged and heavy
coronary arteries severly stenosed
healed infarcts usually present
What is the clinical picture of someone with chronic ischemic heart disease?
previous MI
Angina
CHF
some patients are previously silent - only present with CHF

accounts for 1/2 of transplants
What are some causes of sudden cardiac death?
IHD
Congenital abnormalities
valvular problems
myocarditis
cardiomyopathy
What is the MOA of suden cardiac death?
formation of a lethal arrhythmia (v-fib)

#3 coronary syndrome (#1 - unstable angina, #2 MI)
What is the morphology of sudden cardiac death?
most have high great stenosis (>75%)
some have previous MI

prognosis improved with implantation of defibrilator
What is the common pathophysiology of the acute coronary syndromes?
atherosclerotic plaque disruption with thrombus formation