Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
90 Cards in this Set
- Front
- Back
|
why is ischemia worse than hypoxia
|
ischemia brings with it a defecit in metabolites as well as oxygen, so it is worse
|
|
|
what is the most prevalent cause of ischemic heart disease
|
reduced blood flow due to atherosclerotic plaques in coronary arteries
|
|
|
IHD usually presents with what 4 signs
|
MI, Angina Pectoris, Chronic IHD with heart failure and sudden cardiac death
|
|
|
how does tachycardia stress IHD
|
increases oxygen demand of myocardial tissue and reduces perfusion time
|
|
|
what is the dominant cause of IHD syndrome
|
insufficient coronary perfusion relative to myocardial demand due to chronic atherosclerotic narrowing of the epicardial coronary arteries
|
|
|
what percentage blockage is required to give symptoms of IHD
|
75% or greater
|
|
|
what percent blockage will cause problems at rest
|
90%
|
|
|
where do most lesions occur in the coronary arteries
|
first few centimeters
|
|
|
what types of injury in are most regarded to result in IHD
|
plaque change or plaque disruption
|
|
|
stable angina IHD
|
where oxygen demands outstrip supply, not associated with plaque disruption
|
|
|
unstable angina IHD
|
associated with plaque rupture, disruption or downstream thomboemboli
|
|
|
MI
|
thrombotic occlusion resulting in myocardial death
|
|
|
sudden cardiac failure
|
MI of a regional area inducing a fatal arrhythmia
|
|
|
angina pectoris
|
substernal or precordial transiently occuring chest pain, falls short of inducing myocyte necrosis
|
|
|
three types of angina pectoris
|
stable, unstable, variant
|
|
|
stable AP
|
oxygen supply outstrips demand relative to cardiac demand, occurs under increased workload
|
|
|
variant AP
|
AP induced by vasospasm, PTs with this can still have atherosclerotic arteries, but it is unrelated to that
|
|
|
unstable AP
|
pattern of increasing frequent pain that even occurs at rest at progressively lower levels of physical activity - preinfarct angina
|
|
|
most common form of death for elderly women
|
IHD
|
|
|
what is most likely the main driving event behind an MI
|
coronary artery occlusion due to a sudden change of a plaque, microthrombi formation, vasoapasm, or thrombus formation
|
|
|
delaying of angioplasty untill 12-24 hours post MI shows what
|
less occlusion due to fibrinolysis or relaxation of vasospasm
|
|
|
how can MI occur without vascular pathology
|
vasospasm, emboli/paradoxical emboli, or disorders of small intramural coronary vessels
|
|
|
what is the early biochemical consequence of MI
|
cessation of aerobic metabolism - leads to no ATP production and a build up of metabolites
|
|
|
how long after MI is contracility lost
|
60 seconds
|
|
|
how long does it take for permanent necrosis to develop
|
20 to 30 minutes
|
|
|
what event marks the first sign of myocyte necrosis
|
sarcolemmal membrane disruption allowing intracellular molecules to leak out
|
|
|
in most cases of MI, permanent, nonreversible myocardial damage occurs when post MI
|
2 to 4 hours
|
|
|
what part of the heart succumbs to ischemic necrosis first
|
subendocardial region
|
|
|
what does the left anterior descending branch supply (LAD)
|
apex, anterior left ventricle, anterior 2/3 of IV septum
|
|
|
what perfuses a majority of the left ventricular myocardium
|
LAD, LCX
|
|
|
how can you tell if a heart is right or left dominant
|
by which artery perfuses the back side, RCA = right dominant, LCX = left dominant (RCA is most popular)
|
|
|
RCA in right dominant
|
supplies entire right ventricle, posterior aspect of right ventricle and posterior one third of IV septum
|
|
|
collateral flow of coronary arteries
|
normally not too much flows through these, but occlusions can force distensions and arteriogenesis
|
|
|
transmural infarction
|
full wall thickness infarct, results in an ST elevation
|
|
|
subendocardial infarction
|
only inner one third to 2/3rd infarct, seen as an ST depression
|
|
|
partial wall infarct resulting from a partial occlusion to one coronary artery
|
regional subendocardial infarct
|
|
|
partial wall infarct resulting in a full ventricular necrosis of the inner 1/3 of myocardium
|
global subendocardial infarct (hypotension)
|
|
|
nearly all transmural infarcts involve what damage
|
damage to the left ventricle in some form (IV septum)
|
|
|
RCA obstruction is commonly associated with
|
posterior wall of the septal portion of the left ventricle to the adjacent right ventricular wall
|
|
|
order in which coronary arteries will block
|
LAD, RCA, LCX
|
|
|
what is the predominant form of necrosis in MI
|
ischemic coagulative necrosis
|
|
|
what stain will give a red color to noninfarcted tissue
|
phenyltetrazolium chloride
|
|
|
what is one of the first histological signs of MI that occurs in the first 6 to 12 hours
|
wavy fibers at the periphery of the infarct
|
|
|
how do infarcts heal
|
outside inwards
|
|
|
most effective way to rescue ischemic tissue
|
reperfusion
|
|
|
what is one of the most important measures on the benefits of reperfusion
|
the extent of vascular correction done to the initial thrombus (thrombolysis fixes the problem but not the cause, angioplasty does both)
|
|
|
what is characteristic of myocytes that are irreversibly injured
|
contraction bands
|
|
|
how do contraction bands occur
|
exaggerated contractions when reexposed to perfusion, permanantly alters cellular morphology
|
|
|
what is one of the main negatives of reperfusion
|
high chance of reperfusion injuries
|
|
|
no-reflow
|
when inflammation due to reperfusion injuries obstruct vessels
|
|
|
when are silent MI's commonplace
|
elderly patients and those with diabetes mellitus
|
|
|
what is the most specific biomarker of MI
|
troponin I and T
|
|
|
describe the rise and fall of troponin I and T
|
begin to rose at 2 to 4 hours post MI, peak at 48 hours
|
|
|
why is CK-MB not always indicative
|
because it is located in skeletal muscle as well as cardiac muscle
|
|
|
describe the rise and fall of CKMB
|
begins to rise at 2 to 4 hours, peaks at 24, returns to normal in 72 hours
|
|
|
elevated levels of troponin I and T can last for how long
|
7 to 10 days
|
|
|
unchanged levels of CKMB after how long exclude MI
|
2 days/48 hours
|
|
|
role of aspirin and heparin in MI treatment
|
prevent further thrombosis
|
|
|
role of oxygen in MI treatment
|
prevent ischemia
|
|
|
role of nitrates in MI treatment
|
reduce vasospasm and induce vasodilation
|
|
|
role of beta blockers in MI treatment
|
reduce oxygen demand on the heart and to reduce chance of arrythmias
|
|
|
role of ACE inhibitors in MI treatment
|
reduce ventricular dilation
|
|
|
cardiogenic shock
|
pump failure - large infarct reduces pumping efficiency
|
|
|
myocardial irritibility
|
when conduction problems associated with MI induce arrythmias
|
|
|
which part of the heart is most suceptable to myocardial rupture
|
ventricular free walls
|
|
|
what is the most common site for post-infarction rupture
|
anterolateral wall at midventricular level
|
|
|
dressler syndrome
|
pericarditis that occurs after acute transmural infarct
|
|
|
right vent. infarct
|
uncommon, causes pooling of systemic bood, accompanies posterior left ventricle and IV septal injury
|
|
|
infarct extension
|
where new necrosis occurs adjacent to an existing one
|
|
|
infarct expansion
|
where infarcted muscle expands due to pressure
|
|
|
mural thrombosis
|
combination of abnormal contracility with endocardial damage creating a thrombogenic surface
|
|
|
ventricular aneurysm
|
where infarcted tissue thins and eventually ruptures
|
|
|
papillary muscle dysfunction
|
usually related to postinfarct mitral regurg, caused by infarcted underlying myocardial tissue or severe ventricular dilation
|
|
|
which type of injury usually causes conduction blocks
|
posterior wall mural infarct
|
|
|
what type of injury usually causes free wall rupture or aneurysms
|
anterior wall mural infarct
|
|
|
which is worse, anterior or posterior infarct
|
anterior infarcts are worse
|
|
|
ventricular remodeling
|
where non injured tissue undergoes hypertrophy to compensate
|
|
|
how can you lessen the ventricular dilation (and associated pathlogy post MI)
|
ace inhibitor
|
|
|
primary prevention
|
preventing first MI
|
|
|
secondary prevention
|
preventing reoccuring MI
|
|
|
chronic IHD
|
progressive heart failure as a result of chronic ischemic myocardial damage
|
|
|
when does chronic IHD usually occur
|
post MI, due to already lessened functionality of myocardium
|
|
|
physical manifestation of chronic IHD
|
heavy heart due to left vent hypertrophy and dilation
|
|
|
sudden cardiac death SCD
|
unexpected death from cardiac causes in individuals without symptomatic heart disease
|
|
|
what is SCD related to
|
usually comes as a consequence of chronic IHD
|
|
|
what is the most common trigger for fatal arrythmias
|
acute myocardial ischemia
|
|
|
what is commonplace in SCD
|
critical >75% stenosis involving one or more of the coronary arteries
|
|
|
why does death occur during MI
|
not enough compensatory flow to make up for ischemia
|
|
|
SCD is brought on by what genetic condition
|
channelopathies - disorders that hinder normal ion channel funtion
|
|
|
long QT syndrome
|
indicative of ventricular damage, increased suceptability to vent arrythmias,
|
