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CPR Exam 1 > Cardiac Pathology Part I > Flashcards

Cardiac Pathology Part I Flashcards

1
Q

what valvular changes occur with age?

A

fibrous mitral valve –> atrial dilation and arhythmia
calcium deposits –> aortic stenosis and CHF
lambl excrescenses

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2
Q

what changes occur to the chambers of the heart with age?

A

left ventricular hypertrophy secondary to HTN

atrial dilation

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3
Q

what atherosclerotic changes occur with age?

A

stenosis –> MI, aortic dissection, etc.

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4
Q

what changes occur to the epicardium and myocardium with age?

A 
increased epicardial fat
lipofuscin accumulation
basophilic degeneration
myocyte loss
amyloid deposition –> senile amyloidosis –> CHF
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5
Q

what causes pump failure?

A 
inadequate contraction (systole)
inadequate filling (diastole)
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6
Q

what causes flow obstruction?

A

increased resistance pressure (stenosis, HTN)

decreased blood flow (atherosclerosis, ischemia)

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7
Q

what causes regurgitant flow?

A

incompetent valve

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8
Q

what causes shunted flow?

A 
congenital disease (VSD, ASD or PDA)
post-MI
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9
Q

what causes cardiac conduction abnormalities?

A

ischemic injury

heritable arrhythmias

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10
Q

what causes vessel rupture?

A

aortic dissection

trauma (MVC)

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11
Q

what occurs with MVC trauma reguarding the heart?

A

blow to the chest may cause tearing of the ligamentum arteriosum

results in aortic dissection

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12
Q

what is the most important measurement in cardiomegaly?

A

weight NOT wall thickness

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13
Q

what is congestive heart failure (CHF)?

A

progressive pump failure causing poor blood delivery

diastolic –> inability to fill ventricles
systolic–> inability to empty ventricles

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14
Q

what causes systolic dysfunction?

A

ischemic injury
dilated cardiomyopathy
valve regurgitation

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15
Q

what EF changes are consistent with systolic dysfunction?

A

decreased EF

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16
Q

what causes diastolic dysfunction?

A 
HTN --> LVH
aortic stenosis --> LVH
hypertrophic cardiomyopathy
fibrosis
restrictive cardiomyopathy
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17
Q

what EF changes are consistent with diastolic dysfunction?

A

normal EF but lower total volume due to less filling

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18
Q

what causes left CHF?

A

myocardial ischemia
HTN
left valve disease (aortic/mitral)

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19
Q

what is the clinial presentation of left CHF?

A 
pulmonary congestion (crackles)
low tissue perfusion
paroxysmal nocturnal dyspnea
orthopnea
dyspnea on exertion 
cyanosis
confusion due to low cerebral perfusion
azotemia due to low renal perfusion
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20
Q

what would be seen on CXR for a patient with left CHF?

A

Kerley B lines

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21
Q

what histologic findings would be seen on a patient with left CHF?

A

hemosiderin-laden macrophages

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22
Q

what is the most common cause of right CHF?

A

left CHF

*increases pulmonary pressure which results in right CHF

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23
Q

what causes isolated right CHF?

A

parenchymal lung disease (most common)
lung thromboemboli
primary pulmonary HTN (rare)

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24
Q

what is the clinical presentation of right CHF?

A 
HSM (nutmeg liver)
distended veins
LE edema
exertional dyspnea
ascites
weight gain
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25
Q

what is the most common congenital heart disease?

A

septal defects (ASD or VSD)

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26
Q

which septal defect is most common?

A

VSD

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27
Q

what is the most common cause of genetic heart disease?

A

Down syndrome

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28
Q

what defects are associated with down syndrome?

A

VSD or ASD

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29
Q

what is marfan syndrome and what cardiac defects are associated with it?

A

Fibrillin-1 mutation causing defective TGF-B activity

aortic aneurysm
aortic dissection
mitral or aortic valve prolapse

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30
Q

what is DiGeorge syndrome?

A

CATCH-22

cardiac abnormalities
abnormal facies
thymic aplasia
cleft palate
hypocalcemia
22q11 deletion
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31
Q

what cardiac defects are associated with DiGeorge syndrome?

A

tetrology of Fallot
transposition of great vessels
ASD
VSD

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32
Q

what cardiac defects are associated with Turner syndrome (45, XO)?

A

coarctation of the aorta

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33
Q

what cardiac defects are associated with Trisomy 18 and 13?

A

PDA
VSD
ASD

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34
Q

what are examples of a left-to-right shunt?

A

ASD
VSD
PDA

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35
Q

how do patients with a left-to-right shunt present?

A

asymptomatic without cyanosis

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36
Q

what are examples of a right-to-left shunt?

A

Tetralogy of Fallot
Transposition of the great arteries
Tricuspid atresia

37
Q

how do patients with a right-to-left shunt present?

A

cyanosis
hypertrophic osteoarthropathy
hypoxemia

38
Q

what is a paradoxical embolus?

A

a venous embolism that passes through an ASD or VSD and gains access to arterial circulation

39
Q

when can a paradoxical embolus occur?

A

during a L-R shunt when a pressure differential occurs (valsalva, BM, coughing, sneezing)

VSD, ASD, PDA or PFO

40
Q

what are the clinical features of ASD?

A

usually asymptomatic until adulthood
ejection systolic murmur
low mortality

41
Q

what are the clinical features of VSD?

A

holosystolic murmur

effects depend on size and presence of other heart defects:

  • symptoms as children often have other defects
  • 50% close spontaneously
42
Q

if a VSD large enough, what can occur?

A

right ventricular hypertrophy
pulmonary HTN
shunt reversal (Eisenmenger syndrome)

43
Q

what is shunt reversal/Eisenmenger syndrome?

A
  1. L-R shunt
  2. increased pulmonary blood flow
  3. endothelial dysfunction and pulmonary vascular remodeling
  4. increase in pulmonary vascular resistance
  5. inversion of shunt (R-L)
  6. poorly oxygenated blood enters systemic circulation
44
Q

what might cause a ductus arteriosis to remain open?

A

infant hypoxia

defects associated with increased pulmonary vascular pressure (VSD)

45
Q

what is heard on ausculation with a PDA?

A

harsh, machinery-like murmur

46
Q

what is tetralogy of fallot?

A

R-L shunt

  1. VSD
  2. R ventricular hypertrophy
  3. pulmonary valve stenosis
  4. overriding aorta
47
Q

what is the clinical presentation of ToF?

A

cyanotic at birth
VSD causes holosystolic murmur
pulmonic stenosis causes systolic ejection murmur
Tet spell = cyanosis/syncope during emotional distress
compensatory squatting

48
Q

what can be seen on CXR in ToF?

A

boot shaped heart

concave pulmonary arterial segment

49
Q

what is transposition of the great arteries?

A

aorta and pulmonary artery swap places
incompatible with life unless shunt is present (VSD, PDA or PFO)
presents as cyanosis and trouble breathing

50
Q

what can be given at birth to keep a ductus arteriosis open?

A

prostaglandin E1

51
Q

what is tricuspid atresia?

A

complete occlusion of the tricuspid valve
oxygenation must be maintained by an ASD/PFO AND a VSD
severe cyanosis at birth
high mortality

52
Q

what is the infantile form of coarctation of the aorta?

A

coarctation with a PDA

cyanosis in the lower half of the body
absent femoral pulses
heart failure/shock

53
Q

what is the adult form of coarctation of the aorta?

A

coarctation without PDA

usually asymptomatic
HTN in UE, hypo in LE
possible concentric left ventricular hypertrophy

54
Q

what can be seen on CXR with coarctation of the aorta?

A

rib notching

55
Q

what is the result of aortic stenosis/atresia?

A

left ventricular hypertrophy

seen in hypoplastic left heart syndrome

56
Q

what are the primary causes of ischemic heart disease?

A

artherosclerosis (>90%)
coronary artery emboli
vasculitis
vessel spasm

57
Q

what are the clinical features of MI?

A 
prolonged substernal CP (crushing, stabbing, squeezing)
radiation to neck, shoulder or jaw
rapid, weak pulse
profuse sweating
nausea and vomiting
dyspnea
58
Q

what are the most sensitive and specific biomarkers for myocardial damage?

A

Troponin T and I

59
Q

what other biomarkers can indicated myocardial damage?

A

CK-MB
CK
Myoglobin

60
Q

what is the time to elevation of Troponin and CKMB?

A

3-12 hours

peak at 24 hours

61
Q

what is the time to normalization of Troponin and CKMB?

A

CKMB back to normal in 48-72 hrs

Troponin >5 days

62
Q

why is it important to get serial troponins?

A

a person can present with an acute MI without having elevated cardiac enzymes

EKG is diagnostic at this time

63
Q

what are the transmural infarcts?

A

LAD
Left circumflex
Right coronary

64
Q

what area of the heart is affected by a LAD infarct?

A

anterior apex

65
Q

what area of the heart is affected by a circumflex infarct?

A

lateral left ventricle

66
Q

what area of the heart is affected by a right coronary infarct?

A

right posterior

67
Q

what causes subendocardial infarcts?

A 
reperfusion of transmural infarct (regional)
global hypotension (circumfrential)
68
Q

what causes microinfarcts?

A

small intramural vessel occlusion

COCAINE!!

69
Q

what morphologic changes are seen 30 mins-4 hrs post-infarct?

A

waviness of fibers

70
Q

what morphologic changes are seen 4-12 hrs post-infarct?

A

edema

early coagulative necrosis

71
Q

what morphologic changes are seen 12-24 hrs post-infarct?

A

monocyte hypereosinophilia

contraction band necrosis

72
Q

what morphologic changes are seen 1-3 days post-infarct?

A

coagulation necrosis with loss of nuclei

neutrophil infiltration

73
Q

what morphologic changes are seen 3-7 days post-infarct?

A

phagocytosis of dead cells with macrophages

74
Q

what morphologic changes are seen 7-10 days post-infarct?

A

granulation tissue

75
Q

what morphologic changes are seen 10-14 days post-infarct?

A

collagen deposition

*collagen formation continues until scar is fully formed at 2 months post-infarct

76
Q

what are the early complications (24 hrs) associated with MI?

A

life threatening arrhythmias (V fib)

cardiogenic shock

77
Q

what are the intermediate complications (2-4 days) associated with MI?

A 
myocardial rupture (septal, free wall or papillary)
acute pericarditis and tamponade
78
Q

what are the late complications (2 weeks+) associated with MI?

A

Dressler syndrome
ventricular aneurysm
life threatening arrhythmias
progressive CHF

79
Q

what is Dressler syndrome?

A

fibrinous pericarditis due to immune reaction to myocardial proteins in the blood

80
Q

what is the clinical presentation of Dressler syndrome?

A

fever
pleuritic pain
pericardial effusion

81
Q

what is angina pectoris?

A

transient, recurrent CP induced by myocardial ischemia

pain caused by release of adenosine and bradykinin

82
Q

what is stable angina?

A

stenotic occlusion of coronary artery
induced by physical activity or stress
relieved by rest or vasodilators

83
Q

what is prinzmental variant angina?

A

episodic coronary artery spasm
relieved with vasodilators
unrelated to physical activity, HR or BP

84
Q

what is unstable angina?

A

present at rest
crescendo pattern of pain

usually caused by rupture of artherosclerotic plaque with partial thrombus

85
Q

what EKG pattern and tropinin levels will be seen with stable angina?

A

normal EKG

normal troponins

86
Q

what EKG pattern and tropinin levels will be seen with unstable angina?

A

normal or inverted T waves or ST depression on EKG

normal troponins

87
Q

what EKG pattern and tropinin levels will be seen with NSTEMI?

A

normal or inverted T waves or ST depression on EKG

elevated troponins

88
Q

what EKG pattern and tropinin levels will be seen with STEMI?

A

hyperacute T waves or ST elevation on EKG

elevated troponins

CPR Exam 1 (19 decks)

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