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USMLE Step 1 Random Facts > Cardio > Flashcards

Cardio Flashcards

1
Q

cardiac tissue conduction velocity

A

purkinje system –> atrial muscle –> ventricular muscle –> AV node

“Park AT VENTura AVenue”

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2
Q

P-wave

A

atrial depolarization

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3
Q

PR interval

A

conduction delay thru AV node (<200 ms)

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4
Q

QRS complex

A

ventricular depolarization (<120 ms)

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5
Q

QT interval

A

mechanical contraction of ventricles (depol + repol)

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6
Q

T-wave

A

ventricular repolarization

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7
Q

T-wave inversion indicates?

A

recent MI

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8
Q

ST segment

A

ventricles depolarized

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9
Q

U-wave caused be?

A

hypokalemia, bradycardia

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10
Q

preference for Pacemaker activity?

A

SA > AV > bundle of His/Purkinje/ventricles

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11
Q

conduction pathway of heart?

A

SA node –> atria –> AV node –> common bundle –> bundle branch –> Purkinje fibers –> ventricles

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12
Q

AV node delay?

A

100 ms –> allow for ventricular filling

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13
Q

how do ventricles depolarize?

A

from apex to base and endocardium to epicardium

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14
Q

ST elevation indicates?

A

transmural MI

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15
Q

QRS interval prolongation indicates?

A

ventricular dyssynchrony or slowed intraventricular impulse conduction

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16
Q

prolonged QT interval

A

torsades de pointes

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17
Q

no discrete P-waves

A

Afib

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18
Q

“sawtooth” appearance of waves

A

atrial flutter

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19
Q

no identifiable waves

A

Vfib

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20
Q

common cause of Vfib in <30 y.o pt

A

hypertrophic cardiomyopathy

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21
Q

PR interval prolonged

A

1st degree AV block

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22
Q

P-wave not followed by QRS complex

A

2nd degree AV block = Mobitz type I = Wenckebach

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23
Q

distinguishing feature of Wenckebach

A

progressive lengthening of PR interval until beat “dropped”

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24
Q

2 or more P-waves to 1 QRS complex

A

Mobitz type II

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25
Q

distinguishing feature of Mobitz type II

A

not preceded by lengthening of PR intervals

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26
Q

narrow QRS complex

A

3rd degree AV block (complete)

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27
Q

atria and ventricles beat independently of each other (P waves have no relation to QRS complex)

A

3rd degree AV block (complete)

atrial rate faster (SA node) than ventricular rate (AV node)

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28
Q

uses accessory pathway (bundle of Kent)

A

WPW synd

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29
Q

early ventricular depolarization w/ delta waves at beginning of QRS complex

A

WPW synd

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30
Q

where does ANP work?

A

medullary collecting tubule

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31
Q

what presents w/ sharp chest that is worsened by inspiration and relieved by sitting up/leaning forward?

A

acute pericarditis

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32
Q

striking physical finding of acute pericarditis

A

friction rub

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33
Q

kussmaul’s sign description + seen in?

A

INC in JVP on INSPIRATION instead of NORMAL DEC

constrictive pericarditis
restrictive cardiomyopathies
RA/ventricular tumors
right-sided HF
tricuspid stenosis
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34
Q

pulsus paradoxus description + seen in?

A

dec in amplitude of systolic BP by >= 10 mmHg during INSPIRATION

severe cardiac tamponade
asthma
obstructive sleep apnea
pericarditis
croup
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35
Q

bifurcation of abd aorta @ what level?

A

L4

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36
Q

IVC courses through what?

A

abdomen and inferior thorax in location ANTERIOR to the right half of the vertebral bodies

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37
Q

renal veins join IVC @ what level?

A

L1/L2

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38
Q

common iliac veins merge to become IVC @ level

A

L4

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39
Q

fibrinous pericarditis caused by?

A

Dressler’s synd
uremia
radiation

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40
Q

serous pericarditis caused by?

A

viral pericarditis

SLE, RA, etc. (noninfectious inflamm dz)

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41
Q

suppurative/purulent pericarditis caused by?

A

bacterial infections

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42
Q

cardiac tamponade triad?

A

hypotension
increased venous pressure (JVD)
muffled heart sounds

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43
Q

“tree-bark” appearance of aorta

A

tertiary syphilis (disrupts vasa vasorum)

44
Q

cardiac myxomas are ass w/?

A

multiple syncopal episodes

45
Q

V1-V4 leads w/ Q waves implies infarct in?

A

anterior wall (LAD)

46
Q

V1-V2 leads w/ Q waves implies infarct in?

A

anteroseptal (LAD)

47
Q

V4-V6 leads w/ Q waves implies infarct in?

A

anterolateral (LCX)

48
Q

I, aVL leads w/ Q waves implies infarct in?

A

lateral wall (LCX)

49
Q

II, III, aVF leads w/ Q waves implies infarct in?

A

inferior wall (RCA)

50
Q

Cardiac Output (CO) = ?

51
Q

Fick principle?

A

CO = rate of O2 consumption/(arterial - venous O2)

52
Q

PT for? PTT for?

A 
PT = extrinsic
PTT = intrinsic

“my PET uPITT caused me to BLEED”
PET = PT extrinsic (PT less letter, less factors)
PITT = PTT intrinsic (PTT more letters, more factors)

53
Q

reduced LV compliance indicates what?

A

diastolic dysfunction (“stiff ventricle”)

54
Q

predom mechanism of HF in restrictive cardiomyopathy

A

diastolic dysfunction (“stiffer ventricle”)

55
Q

predom mechanism of HF in dilated cardiomyopathy

A

systolic dysfunction

56
Q

what can lead to dilated cardiomyopathy?

A

viral myocarditis
alcohol toxicity
diphtheric myocarditis
doxorubicin/danorubicin tx

57
Q

S1 =

A

mitral/tricuspid closure

loudest @ mitral area

58
Q

S2 =

A

aortic/pulmonary valve closure

loudest @ left sternal border

59
Q

S3 =

A

EARLY diastole
rapid ventricular filling phase
ass w/ increased filling pressures (mitral regurg, CHF) + common in dilated ventricles
normal in children + pregnant women

60
Q

S4 =

A

“atrial kick”
LATE diastole
ass w/ ventricular hypertrophy
high atrial pressure (LA must push against stiff LV wall)

61
Q

truncus arteriosus forms?

A

ascending aorta + pulm trunk

62
Q

bulbis cordis forms?

A

SMOOTH parts of left/right ventricles (outflow tract)

63
Q

primitive ventricle forms?

A

TRABECULATED left/right ventricles

64
Q

primitive atria forms?

A

TRABECULATED left/right atria

65
Q

left horn of sinus venosus forms?

A

coronary sinus

66
Q

right horn of sinus venosus forms?

A

SMOOTH part of RA (sinus venarum)

67
Q

SVC formed from?

A

right common cardinal vein and right anterior cardinal vein

68
Q

mean arterial output =

69
Q

pulse pressure is proportional to?

A

stroke volume

70
Q

factors that increase SV

A

increased PRELOAD
decreased AFTERLOAD
increased CONTRACTILITY

71
Q

contractility and SV increased by

A

catecholamines
increased INTRAcell Ca
decreased EXTRAcell Na
Digitalis (blocks Na/K pump)

72
Q

contractility and SV decreased by

A 
beta blockade
HF
acidosis
hypoxia/hypercapnia
non-dihydropyridine CCB
73
Q

afterload =

74
Q

histo in temporal (giant cell) arteritis?

A

focal granulomatous inflamm (branches of carotid a.)

75
Q

histo in Takayasu’s arteritis

A

granulomatous thickening (of media of aortic arch @ branch pts)

76
Q

histo in polyarteritis nodosa (PAN)

A

transmural inflamm of arterial wall w/ fibrinoid necrosis (except in lungs)

77
Q

weird tx in Kawasaki dz

A

aspirin (bc never given to children)

78
Q

histo in Buerger’s dz (thromboangiitis obliterans)

A

segmental thrombosing vasculitis (necrotizing vasculitis involving digits) - often of tibial/radial a.

79
Q

histo in microscopic polyangiitis

A

segmental fibrinoid necrosis (can be caused by AB use - penicillins)
NO granulomas

80
Q

histo in Wegeners granulomatosis (granulomatosis w/ polyangiitis)

A

focal necrotizing vasculitis
necrotizing granulomas in lung
necrotizing glomerulonephritis

81
Q

histo in Churgg-Strauss synd

A

granulomatous necrotizing vasculitis w/ eosinophilia (diff from MP)

82
Q

histo in Henoch-Schonlein purpura

A

vasculitis 2ndary to IgA complex depositions

83
Q

ECG changes in V1-V4, V5

A

LAD (anterior wall)

84
Q

ECG changes in V1-V2

A

LAD (anteroseptal)

85
Q

ECG changes in I, aVL

A

LCX (lateral wall)

86
Q

ECG changes in V4-V6

A

LCX (anterolateral)

87
Q

ECG changes in II, III, aVF

A

RCA (inferior wall)

88
Q

common cause of death BEFORE reaching hospital in MI pts

A

arrhythmia (Vfib)

89
Q

common cause of death in pt hospitalized for MI

A

cardiogenic shock (esp if large infarct)

90
Q

cardiac tamponade in post-MI pt

A

ventricular wall rupture (up to 14 days after)

91
Q

severe mitral regurg in post-MI pt

A

papillary muscle rupture

92
Q

new VSD in post-MI pt

A

interventricular septum rupture

93
Q

embolus from mural thrombus in post-MI pt

A

ventricular aneurysm formation (common 1 wk after)

94
Q

friction rub 1-3 days after MI

A

fibrinous pericarditis

95
Q

pulmonary wedge pressure is pretty equivalent to?

A

LA pressure

96
Q

murmurs heard @ right 2nd ICS adjacent to sternum (aortic area)

A

SYSTOLIC MURMURS!
aortic stenosis (radiates to neck [carotids])
flow murmur
aortic valve sclerosis

97
Q

murmurs heard @ left sternal border

A

systolic murmurs:
hypertrophic cardiomyopathy

diastolic murmurs:
aortic regurg (if caused by aortic root dilation, heard best @ RIGHT sternal border)
pulmonic regurg

98
Q

murmurs heard @ left 2nd ICS adjacent to sternum (pulmonic area)

A

systolic ejection murmurs!
pulmonic stenosis
flow murmur (ex. ASD [mid-systolic ejection murmur])

99
Q

murmurs heard @ left 4th ICS adjacent to sternum (aka “left lower sternal border” or the tricuspid area)

A

pansystolic murmurs:
tricuspid regurg (radiates to right sternal border)
VSD

diastolic murmur:
tricuspid stenosis
ASD

100
Q

murmurs heard @ left 5th ICS at midclavicular line (apex of heart) (mitral area)

A 
systolic murmur:
mitral regurg (radiates toward axilla)
MVP (late systolic crescendo w/ midsystolic click; loudest @ S2)

diastolic murmur:
mitral stenosis

101
Q

murmur heard @ left infraclavicular region

102
Q

valsalva increases intensity of what murmurs

A

MVP, hypertrophic cardiomyopathy

103
Q

rapid squatting decreases the intensity of what murmurs

A

MVP, hypertrophic cardiomyopathy

104
Q

in pacemaker action potential, what phase determines HR and how

A

slope of phase 4 (Na channels)

105
Q

increasing afferent baroreceptor firing does what to HR?

A

decreases HR

106
Q

Cushing reaction triad

A

HTN
resp depression
BRADYcardia! (due to reflex baroreceptor-induced)

USMLE Step 1 Random Facts (35 decks)

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