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need to knows > Cards (F.A.) > Flashcards

Cards (F.A.) Flashcards

1
Q

what is the embryological derivative of the Ligamentum Teres? (Round ligament(

A

Umbilical Vein

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2
Q

Where is the Ligamentum Teres found

A

Falciform ligament

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3
Q

What is the embryological derivative of the MediaN ligament and the MediaL ligament

A

MediaN- Allantois/urachus

MediaL- Umbilical A

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4
Q

an RCA infarction will present in which EKG leads?

A

II, III, avF

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5
Q

a LCX infarction will present in which EKG leads?

A

I, V5, V6, avL

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6
Q

an LCA infarction will present in which EKG leads

A

V1,V2 - interventricular septum

V3, V4- anterior LV

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7
Q

what are the (2) equations to determine Cardiac Output?

A 
CO= HR * SV 
CO = rate of O2 consumption/ (arterial O2 - venous O2)
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8
Q

what are (2) equations to calculate MAP

A 
MAP= 2/3 DBP + 1/3 SBP 
MAP = CO * TPR
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9
Q

how to calculate Pulse Pressure

A

SBP- DBP

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10
Q

how to calculate Stroke Volume?

A

SV= EDV- ESV

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11
Q

what 3 factors affect SV

A

contractility, afterload, preload

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12
Q

how do you calculate wall tension

A

wall tension = pressure * radius

hence, tension increases with increasing radius

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13
Q

how do you calculate wall stress

A

Pressure * radius / 2* wall thickness

wall tension/ 2* wall thickness

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14
Q

Driving Pressure in a vessel=

A 
P= Q * R
Pressure= Flow rate * Resistance
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15
Q

how are size of the vessel and flow through the vessel related

A

Q= (P1-P2/ nL) * r^4

so in radius is cut in half (1/2), flow decreases by (1/16)

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16
Q

what is an S3 sound related to

A

dilated ventricle or increased filling pressure (like bc of MR)
think- SYSTOLIC dysfunction

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17
Q

what is an S4 sound related to

A

stiff ventricle

think - DIASTOLIC dysfunction

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18
Q

JVP tracing: a wave (1)

absent in??

A

R. atrial contraction

absent in Afib

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19
Q

JVP tracing: c wave (2)

A

R. ventricular contraction

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20
Q

JVP tracing: x descent (3)

A

ventricular ejection, caused by downward motion of Tricuspid

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21
Q

JVP tracing: v wave (4)

A

“villing” -increase in atrial pressure due to diastolic filling

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22
Q

JVP tracing: y descent (5)

absent in??

A

RA emptYing into RV

absent in constrictive pericarditis

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23
Q

normal splitting
what is it?
why does it happen?

A

a normal split in S2, with P2 coming after A2 during inspiration
- increased VR in inspriration causes delayed Pulmonic valve closing

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24
Q

Wide splitting
what is it?
why does it happen?

A

an abnormal split in S2- with P2 coming MUCH after A2 in inspiration due to conditions that delay P2 closure
- RBBB or pulmonic stenosis which is exaggerated by the increased VR in inspiration causes wide split

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25
Q

Fixed Splitting
what is it?
why does it happen?

A
  • an abnormal split in S2- with P2 coming after A2 in inspiration and expiration
  • ASD, causes Right heart volume overload all the time, so always causing delayed pulmonic valve closure
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26
Q

paradoxical splitting
what is it
why does it happen

A
  • an abnormal split in S2- with A2 coming before P2 usually. But on inspiration, the split is actually reduced bc P2 closure is delayed
  • caused by delays in aortic valve closure-LBBB and aortic stenosis
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27
Q

AS- describe the murmur

A

crescendo- decrescendo systolic ejection murmur, with presence of possible ejection click

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28
Q

MR/TR- describe the murmur

A

holosystolic, high pitched, blowing murmur

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29
Q

MVP - desrcibe the murmur

A

late crescendo murmur with midsystolic click

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30
Q

VSD- describe the murmur

A

holosystolic, harsh sounding murmur

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31
Q

AR - describe the murmur

A

early diastolic decrescendo murmur, blowing, high pitched

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32
Q

MS - describe the murmur

A

diastolic, OS followed by diastolic delayed rumble

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33
Q

PDA- describe the murmur

A

constant and machine like

34
Q

pulsus parvus et tardis is associated with which murmur

A

AS

35
Q

inspiration makes which murmurs louder?

why?

A

all right heart murmurs

- bc increased VR to RH

36
Q

handgrip makes which murmurs louder?

why?

A
  • MR, AR, and VSD

- because increase in afterload

37
Q

handgrip softens or delays which murmurs

A
  • AS, and click of MVP as well as HOCM

- it increases afterload, which increases LV vol

38
Q

valsalva/standing up does what to HOCM murmur?

A

it increases HOCM murmur because it decreases preload

39
Q

valsalva does what to MVP click

A

it makes MVP click earlier bc it decreases preload making LV vol smaler

40
Q

what does rapid squatting do? whats the murmur it makes better?

A

it increases preload and afterload.

makes HOCM better, because it increases preload, it also makes MVP happen later for same reason

41
Q

Romano Ward Syndrome

A

congenital QT prolongation
AD
pure cardiac phenotype

42
Q

Jervell and Lange-Lielsen

A

congenital QT prolongation
AR
accompanied by sensineural deafness

43
Q

Brugada syndrome

A

AD in asian males
pseudo RBBB and St elevations in V1-V3
risk of V tach and SCD

44
Q

1st degree AV block

A

prolonged PR (>200 msec) benign

45
Q

2nd degree AV block, type I (Mobitz I)

A

regularly irregular
progressive PR lengthening until dropped beat
asymptomatic

46
Q

2nd degree AV block, type II ( Mobitz II)

A

randomly dropped beats, theres no change or progressive PR interval length preceding it
may become type 3 heart block, may need pacing

47
Q

3rd degree AV block

A

atria and ventricles beat separately

48
Q

capillary fluid exchange formula

A

Flow out of capillary = ( hydrostatic capillary P - oncotic capillar pressure) - (hydrostatic interstitial P- oncotic interstitial P)

49
Q

hyperplastic arteriosclerosis seen in

A

extreme hypertension

50
Q

hyaline arteriosclerosis seen in

A

diabetes, maybe low levels of hypertension

51
Q

list most common sites of atherosclerosis

A

abdominal aorta > CORONARY As > popliteal A > carotid As

52
Q

claudication symptoms caused by

A

atherosclerosis

53
Q

what is AAA associated with, how about Thoracic Aortic Aneurysm?

A

AAA- atherosclerosis

TAA- cystic medial degeneration

54
Q

unstable angina vs NSTEMI vs STEMI

A

UA- no cardiac biomarker elevation
NSTEMI- cardiac biomaker elevation but ST DEPRESSION due to SUBendocardial infarct
STEMI- cardiac biomarker elevation but ST ELEVATION due to TRANSmural infarct

55
Q

MI: first 4 hours

A

no change

56
Q

MI: 4-12 hours

A

wavy fibers w/ edema, hemorrhage, and start of coag necrosis

57
Q

MI: 12-24 hr

A

cytopia and neutrophils begin to appear

58
Q

MI: 1-3 days

A

extensive coagulative necrosis

acute inflammation with neurtophil abundance

59
Q

MI: 3- 14 days

A 
granulation tissue (collagen III) 
macrophages
60
Q

MI: 2 wks- months

A

scar tissue complete (collagen I)

61
Q

an infarct in PDA will show changes in which EKG leads?

A

V7-V9 has elevations ( note depression in V1-V3)

62
Q

MI complication: within the first few days

A 
arrhythmia (death before 24 hr) 
postinfarction pericarditis (1-3 days) - note this is not autoimmune, and it only overlies area of necrosis
63
Q

MI complication: before first week

A

Papilary Muscle Rupture - usually posteromedial papillary and will cause MR
Interventricular septal rupture - causes VSD, is macrophage mediated

64
Q

MI complication: within first two weeks

A

ventricular pseudoaneurysm - contained free wall rupture

free wall rupture- causes cardiac tamponade

65
Q

Mi complication: several weeks following

A

true ventricular aneurysm- outward bulge w contraction and assn with fibrosis
Dressler Syndrome- autoimmune fibrinous pericarditis

66
Q

Kussmaul Sign

A

increase JVP on inspiration
sign of constrictive pericarditis, restrictive cardiomyopathy, or ventricular tumor
you would expect JVP to decrease on inspiration bc drop in transthoracic pressure, but an increase suggests that the drop in transthoracic pressure is not transmitted to heart

67
Q

vasculitides with focal granulomatous inflammation

A

Large Vessel- GCA and Takayasu

68
Q

vasculitides affecting Medium size vessels

A

Polyarteritis Nodosa, Thromboangiitis Obliterans (Buerger) and Kawasaki

69
Q

PAN key features?

A

segmental transmural inflammation with fibrinoid necrosis
spares pulmonary As
Hep B assn
renal microaneurysms form

70
Q

Kawasaki key features?

A 
risk of: coronary artery aneurysms 
CRASH& BURN 
C- conjunctival injection 
R- rash 
A- adenopathy
S- strawberry tongue 
H- hand and foot changes 
BURN- fever
71
Q

Thromboangiitis Obliterans (Buerger) key features?

A

young male HEAVY smoker
- gangrene and Raynaud’s
“segmental thrombosing vasculitis”

72
Q

What are the small vessel vasculitides?

A
  • Wegener’s
  • Churg- Strauss
  • Henoch Schonlein
  • Microscopic Polyangitis
73
Q

Wegener’s (Granulomatosis with Polyangitis) Vasculitis

A

granulomas in lung+ glomerulonephritis + “focal necotizing vasculitis”

c-ANCA (aka pr3 ANCA)

74
Q

Churg Strauss (Eosinophilic Granulomatosis with polyangitiis)

A

asthma + peripheral neuropathy (foot drop)

p-ANCA (MPO ANCA)

75
Q

Henlock Schonlein Vasculitis

A

triad: GI disturbance + Arthralgia + palpable purpura on legs and butt

IgA complex deposition

76
Q

Osler-Weber- Rendu syndrome

A

AD disorder of blood vessels. Telengiectasias (blanching), recurrent nosebleeds/ GI bleeds/ hematuria, AVMs

77
Q

Leukocytoclastic Vasculitis

A

a drug response (penicillin)
nonblanching palpable purpura
sm vessel vasculitis

78
Q

which vasculitis are p-ANCA (MPO ANCA) positive?

A

microscopic polyangitis

churg strauss

79
Q

Ranolazine

A

used in refractory angina

inhibits late phase sodium current without affecting contractility or HR

80
Q

Ivabradine

A

selective inhibition of funny Na+ current which slows phase 4 depol in nodes WITHOUT ionotropy
used for stable angina for pts who cant take B blockers
ae: visual brightness, htt, bradycardia

81
Q

How to calculate Flow Rate?

A

Q= CSA * velocity of flow

need to knows (31 decks)

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