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CPR II > Cardio Pathology Part 1- Hillard > Flashcards

Cardio Pathology Part 1- Hillard Flashcards

(75 cards)

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1
Q

LAD infarction leads to death of which parts of the heart

A

Apex
LV anterior wall
anterior two thirds of septum

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2
Q

Left Circumflex infarction leads to death of which parts of the heart

A

LV lateral wall

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3
Q

RCA infarction leads to death of which parts of the heart

A

RV free wall
LV posterior wall
posterior third of septum

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4
Q

CAD is….

A

leading cause of death

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5
Q

Risk factors of atherosclerosis

A

increasing age, male gender, HTN, hyperlipidemia, cigarette smoking, diabetes

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6
Q

most sensitive AND specific biomarkers of myocardial damage

A

Troponin T and I (cTnT and cTnI)

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7
Q

time to elevation of CKMB, cTnT and cTnI

A

3-12 hours

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8
Q

time to normalization of CKMB

A

48-72 hours

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9
Q

time to normalization of cTnI and cTnT

A

> 5 days

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10
Q

transient occlusion leads to what type of infarct

A

regional subendocardial infarct

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11
Q

global hypotension (shock) leads to what type of infarct

A

circumferential subendocardial infarct

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12
Q

small intramural vessel occlusions (drug users) leads to what type of infarct

A

microinfarcts

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13
Q

coronary artery blood flow direction?

A

from the outside towards the myocardium then the endocardium

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14
Q

the area at most risk with CA occlusion

A

the innermost layer of the heart, myocardium, is first impacted.

The endocardium will still be viable although it is the most innermost layer.

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15
Q

30 min-4hr irreversible injury leads to

A

waviness of fibers at border

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16
Q

4-12hrs of irreversible injury leads to

A

early coagulation necrosis; edema

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17
Q

12-24hrs of irreversible injury leads to

A

ongoing coagulation necrosis; pyknosis of nuclei; myocyte hypereosiniophilia; contraction band necrosis

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18
Q

1-3 days of irreversible injury leads to

A

a yellow-tan infarct center (gross) and coagulation necross with loss of nuclei; infiltrate of neutrophils

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19
Q

3-7 days of irreversible injury leads to

A

a hyperemic border (gross) and disintegration of dead myofibers; early phagocytosis of dead cells by macrophages at infarct border

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20
Q

7-10 days of irreversible injury leads to

A

yellow-tan and soft depressed red-tan margins (gross) and well-developed phagocytosis and granulation tissue at margins

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21
Q

10-14 days of irreversible injury leads to

A

collage deposition

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22
Q

2-8 weeks of irreversible injury leads to

A

gray-white scar (gross) and increased collagen deposistion

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23
Q

> 2 months of irreversible injury leads to

A

dense collagenous scar

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24
Q

the early complications of a MI are

A

life threatening arrhthmyia and cardiac dysfunction (shock)

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25
arrhythmias occur within
1 hour of onset of myocardial infaction | the fatal arrhythmia is (V fib)
26
cardiogenic shock depends on
size of infarct and associated loss of function which leads to cardiogenic shock
27
early complications (time frame)
within 24 hours
28
intermediate complications (time frame)
1-3 days
29
the intermediate complications of a MI are
Septal, Free Wall, Papillary muscle rupture; acute pericarditis (fibrinous, serofibrinous)
30
myocardial rupture typically requires a
transmural infarct 2-4 days post MI (typically fatal)
31
which muscle is the most common one to rupture
the papillary muscles
32
what are the risk factors to myocardial rupture
increase in age, first MI, absence of LV hypertrophy
33
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)
34
ventricular septal rupture leads to
anterior infarctions
35
papillary muscle rupture leads to
mitral regurgitation
36
late complications of MI occur after
2 weeks
37
3 main late complications of MI
chronic pericarditis (Dressler syndrome), ventricular aneurysm, life-threatening arrhthmyias, progressive congestive heart failure
38
what is Dressler syndrome
a fibrinous pericarditis that is due to an immune response to myocardial proteins in blood. Pt will be FEBRILE.
39
angina pectoris
recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction
40
what causes the pain in angina pectoris
pain caused by adenosine and bradykinin release
41
what is a stable angina
stenotic occlusion of coronary artery relieved by rest OR vasodilators induced by physical activity, stress
42
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
43
what is an Unstable angina
present at REST "Crescendo pattern" increasing in severity or duration crescendo-type can be caused by progressive mechanical obstruction
44
what test is used for stable angina
exercise stress test
45
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
46
pathophysiology of unstable angina if the symptoms are "crescendoing angina" that does not occur at rest
this is due to a progressive mechanical obstruction
47
stable angina leads to
demand ischemia, no infarct
48
unstable angina leads to
supply ischemia, no infarct
49
NSTEMI leads to
subendocardial infarct
50
STEMI leads to
transmural infarct
51
traumatic heart injury
leads to pericardial tamponade due to blunt force
52
weak point of the aorta is where it is tethered to the pulmonary artery which is....
the ligamentum arteriosum
53
life-threatening hemorrhage and most common way people die due to car crash
tearing or shearing of the ligamentum arteriosum
54
first common cause of death in MVA
head trauma
55
second common cause of death in MVA
hemorrhage of aorta
56
causes of arrhythmias
abnormalities in gap junctions | abnormalities of spacial relationships of myocytes
57
cardiac causes of arrhythmias
``` ischemic heart disease--> MOST important cause cardiomyopathies myocarditis valvular disease familial/congenital disorders ```
58
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
59
Bradycardia defined as
less than 50-60 beats/min
60
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
61
what is heart block
dysfunctional AV node
62
first degree heart block
prolonged PR interval
63
second degree heart block
intermittent transmission
64
third degree heart block
complete failure
65
increased length of ventricular depolarization to repolarization is called...
Long QT syndrome
66
what is Long QT syndrome caused by
usually due to abnormal ion channels causing arrhythmogenic disease (hereditary channelopathies)
67
what is Torsades des Pointes
It's Long QT Syndrome that leads to syncope and sudden cardiac death
68
conditions that cause dilated cardiomyopathy
excessive alcohol use myocarditis certain drugs iron overload
69
volume overload can cause
systolic dysfunction (heart can't pump out enough blood)
70
CHF may result from
loss of ability to fill the ventricles during diastole (diastolic dysfunction) loss of myocardial contractile function (systolic dysfunction)
71
most common side for CHF (right vs left)
left sided heart failure
72
left sided heart failure (systolic failure) causes
``` ischemic heart disease htn aortic stenosis dilated cardiomyopathy DECREASED ejection fraction ```
73
left sided heart failure (diastolic failure) causes
``` htn aortic stenosis hypertrophic cardiomyopathy restrictive cardiomyopathy NORMAL ejection fraction ```
74
right sided heart failure causes
Cor pulmonale (lung disease/dysfunction)
75
left sided heart failure main causes
ischemic heart disease htn left-sided valve disease

CPR II (3 decks)

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