Cardio Pathology Part 1- Hillard Flashcards
LAD infarction leads to death of which parts of the heart
Apex
LV anterior wall
anterior two thirds of septum
Left Circumflex infarction leads to death of which parts of the heart
LV lateral wall
RCA infarction leads to death of which parts of the heart
RV free wall
LV posterior wall
posterior third of septum
CAD is….
leading cause of death
Risk factors of atherosclerosis
increasing age, male gender, HTN, hyperlipidemia, cigarette smoking, diabetes
most sensitive AND specific biomarkers of myocardial damage
Troponin T and I (cTnT and cTnI)
time to elevation of CKMB, cTnT and cTnI
3-12 hours
time to normalization of CKMB
48-72 hours
time to normalization of cTnI and cTnT
> 5 days
transient occlusion leads to what type of infarct
regional subendocardial infarct
global hypotension (shock) leads to what type of infarct
circumferential subendocardial infarct
small intramural vessel occlusions (drug users) leads to what type of infarct
microinfarcts
coronary artery blood flow direction?
from the outside towards the myocardium then the endocardium
the area at most risk with CA occlusion
the innermost layer of the heart, myocardium, is first impacted.
The endocardium will still be viable although it is the most innermost layer.
30 min-4hr irreversible injury leads to
waviness of fibers at border
4-12hrs of irreversible injury leads to
early coagulation necrosis; edema
12-24hrs of irreversible injury leads to
ongoing coagulation necrosis; pyknosis of nuclei; myocyte hypereosiniophilia; contraction band necrosis
1-3 days of irreversible injury leads to
a yellow-tan infarct center (gross) and coagulation necross with loss of nuclei; infiltrate of neutrophils
3-7 days of irreversible injury leads to
a hyperemic border (gross) and disintegration of dead myofibers; early phagocytosis of dead cells by macrophages at infarct border
7-10 days of irreversible injury leads to
yellow-tan and soft depressed red-tan margins (gross) and well-developed phagocytosis and granulation tissue at margins
10-14 days of irreversible injury leads to
collage deposition
2-8 weeks of irreversible injury leads to
gray-white scar (gross) and increased collagen deposistion
> 2 months of irreversible injury leads to
dense collagenous scar
the early complications of a MI are
life threatening arrhthmyia and cardiac dysfunction (shock)
arrhythmias occur within
1 hour of onset of myocardial infaction
the fatal arrhythmia is (V fib)
cardiogenic shock depends on
size of infarct and associated loss of function which leads to cardiogenic shock
early complications (time frame)
within 24 hours
intermediate complications (time frame)
1-3 days
the intermediate complications of a MI are
Septal, Free Wall, Papillary muscle rupture; acute pericarditis (fibrinous, serofibrinous)
myocardial rupture typically requires a
transmural infarct 2-4 days post MI (typically fatal)
which muscle is the most common one to rupture
the papillary muscles
what are the risk factors to myocardial rupture
increase in age, first MI, absence of LV hypertrophy
rupture of free wall can lead to
blood accumulating in the pericardial space –> acute pericardial tamponade (the heart can’t fully relax during diastole and puts strain on the heart)
ventricular septal rupture leads to
anterior infarctions
papillary muscle rupture leads to
mitral regurgitation
late complications of MI occur after
2 weeks
3 main late complications of MI
chronic pericarditis (Dressler syndrome), ventricular aneurysm, life-threatening arrhthmyias, progressive congestive heart failure
what is Dressler syndrome
a fibrinous pericarditis that is due to an immune response to myocardial proteins in blood. Pt will be FEBRILE.
angina pectoris
recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction
what causes the pain in angina pectoris
pain caused by adenosine and bradykinin release
what is a stable angina
stenotic occlusion of coronary artery
relieved by rest OR vasodilators
induced by physical activity, stress
what is a Prinzmetal variant angina
episodic coronary artery spasm, often occurs at rest
relieved with vasodilators
unrelated to physical activity, HR or BP
have recurrent episodes every 3 to 6 months and feel normal between those episodes
what is an Unstable angina
present at REST
“Crescendo pattern” increasing in severity or duration
crescendo-type can be caused by progressive mechanical obstruction
what test is used for stable angina
exercise stress test
pathophysiology of unstable angina if the symptoms are acute chest pain with activity and rest
this is due to a ruptured plaque with non-occlusive thrombus
pathophysiology of unstable angina if the symptoms are “crescendoing angina” that does not occur at rest
this is due to a progressive mechanical obstruction
stable angina leads to
demand ischemia, no infarct
unstable angina leads to
supply ischemia, no infarct
NSTEMI leads to
subendocardial infarct
STEMI leads to
transmural infarct
traumatic heart injury
leads to pericardial tamponade due to blunt force
weak point of the aorta is where it is tethered to the pulmonary artery which is….
the ligamentum arteriosum
life-threatening hemorrhage and most common way people die due to car crash
tearing or shearing of the ligamentum arteriosum
first common cause of death in MVA
head trauma
second common cause of death in MVA
hemorrhage of aorta
causes of arrhythmias
abnormalities in gap junctions
abnormalities of spacial relationships of myocytes
cardiac causes of arrhythmias
ischemic heart disease--> MOST important cause cardiomyopathies myocarditis valvular disease familial/congenital disorders
what is Sick sinus syndrome
SA node damaged–> bradycardia
this happens bc the AV node now takes over and the AV node is slower than SA node
Bradycardia defined as
less than 50-60 beats/min
what is Atrial fibrillation?
myocytes depolarize independently and sporadically due to atrial dilation, with variable transmission in AV node
causes an irregular, irregular HR
can cause thrombus formation, risk of thromboembolism
what is heart block
dysfunctional AV node
first degree heart block
prolonged PR interval
second degree heart block
intermittent transmission
third degree heart block
complete failure
increased length of ventricular depolarization to repolarization is called…
Long QT syndrome
what is Long QT syndrome caused by
usually due to abnormal ion channels causing arrhythmogenic disease (hereditary channelopathies)
what is Torsades des Pointes
It’s Long QT Syndrome that leads to syncope and sudden cardiac death
conditions that cause dilated cardiomyopathy
excessive alcohol use
myocarditis
certain drugs
iron overload
volume overload can cause
systolic dysfunction (heart can’t pump out enough blood)
CHF may result from
loss of ability to fill the ventricles during diastole (diastolic dysfunction)
loss of myocardial contractile function (systolic dysfunction)
most common side for CHF (right vs left)
left sided heart failure
left sided heart failure (systolic failure) causes
ischemic heart disease htn aortic stenosis dilated cardiomyopathy DECREASED ejection fraction
left sided heart failure (diastolic failure) causes
htn aortic stenosis hypertrophic cardiomyopathy restrictive cardiomyopathy NORMAL ejection fraction
right sided heart failure causes
Cor pulmonale (lung disease/dysfunction)
left sided heart failure main causes
ischemic heart disease
htn
left-sided valve disease
