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Flashcards in Cardiovascular Deck (99):
1

what does the bulbis cordis become

smooth parts (outflow tract) of both ventricles

2

what does the primitive pulmonary vein become

smooth part of left atrium

3

what does the left horn of the sinus venosus become

coronary sinus

4

what does the right horn of the sinus venosus become

smooth part of the right atrium (sinus venarum)

5

what do the right common cardinal vein and right anterior cardinal vein become

SVC

6

blood supply for SA and AV nodes

RCA

7

effect of aortic regurgitation on pulse pressure

increased

8

effect of tamponade on pulse pressure

decreased

9

effect of exercise on pulse pressure

increased

10

effect of obstructive sleep apnea on pulse pressure

increased (increased sympathetic tone)

11

effect of aortic stenosis on pulse pressure

decreased

12

MOA for catecholamines increasing contractility

inhibition of phosphobalamban --> more intracellular Ca++

13

MOA for beta blockade decreasing contractility

lowers cAMP

14

which calcium channels are for myocardium

nondihydropyridine

15

LaPlace's Law

T = pr / 2t

16

effect of increased TPR on venous return given fixed MAP

decrease

17

JVP A: peak or descent? meaning?

peak. atrial contraction (absent in afib)

18

JVP C: peak or descent? meaning?

peak. RV contraction (while atrium is still contracted)

19

JVP X: peak or descent? meaning?

descent. atrial relaxation

20

JVP V: peak or descent? meaning?

peak. filling ("villing") of right atrium against closed tricuspid

21

JVP Y: peak or descent? meaning?

descent. emptYing of right atrium into RV

22

fixed spliting caused by

ASD

23

paradoxical splitting caused by

something delaying aortic closure e.g. aortic stenosis, LBBB

24

effect of hand grip (increased afterload) on auscultation

increase MR, AR, VSD murmurs
Decreased HCM murmurs
later onset of MVP click/murmur

25

effect of valsalva or standing up (decreased preload) on auscultation

decreased intensity of most murmurs (including AS)
Increased intensity of HCM murmurs
Earlier onset of MVP click/murmur

26

effect of rapid squatting (decreased after load, increase preload) on auscultation

increased intensity of AS
decreased intensity of HCM murmur
Later onset of MVP click/murmur

27

AS murmur

systolic crescendo-decrescendo

28

MR/TR murmur

holosystolic, blowing murmurs

29

AR murmur

early diastolic decrescendo, blowing murmur

30

MVP murmur

mid-systolic click and late crescendo murmur

31

VSD murmur

holosystolic, harsh-sounding, loudest at tricuspid

32

MS murmur

diastolic opening snap and late rumbling murmur

33

PDA murmur

continuous machine-like murmur, loudest at S2

34

U wave present in

hypokalemia and bradycardia

35

causes of long QT

hypokalemia, low magnesium
congenital long QT syndromes
drug induced

36

Congenital long QT syndromes

Romano-Ward: AD, pure cardiac

Jervell and Lange-Nielson: AR, sensorineural deafness

37

Drug-induced long QT

anti-arrhythmic (IA, III), antibiotics (e.g. macrolides), anti-psychotics (e.g. haloperidol), anti-depressants (e.g. TCAs), anti-emetics (e.g. ondansetron)

38

Brugada syndrome ECG pattern

pseudo RBBB and ST elevations in V1-V3

AD, MC in Asian males. Increased risk of ventricular tachyarrhythmia and sudden cardiac death

39

AV block 2nd degree, mobitz type I

lengthening PR interval

40

AV block 2nd degree, Mobitz type II

random dropping

41

congenital defects causing early cyanosis

truncus arteriorsus, transposition, tricuspid atresia, tetralogy of fallot, TAPVR (total anamalous pulmonary venous return)

42

4 abnormalities in tetralogy of fallot

VSD, overriding aorta, pulmonic stenosis, RVH

43

fetal alcohol syndrome: cardiac congenital defect association

ASD, VSD, PDA, Fallot

44

rubella: cardiac congenital defect association

septal defects, PDA, pulmonic stenosis

45

Down: cardiac congenital defect association

AV septal defect, ASD, VSD

46

maternal diabetes: cardiac congenital defect association

transposition

47

prenatal lithium: cardiac congenital defect association

Ebstein abnormality

48

Turner syndrome: cardiac congenital defect association

bicuspid aortic valve, coarctation of aorta

49

Williams: cardiac congenital defect association

supravalvular aortic stenosis

50

22q11 syndromes: cardiac congenital defect association

truncus arteriosus, Fallot

51

term for eyelid xanthoma

xanthelasma. note corneal arcus is a corneal lipid deposit

52

most likely papillary muscle to rupture

posteromedial

53

cardiomyopathy associated with Friedreich ataxia

HCM

54

hypovolemic shock: skin, preload, CO, afterload

cold/clammy, very low preload, low CO, high SVR

55

cardiogenic shock: skin, preload, CO, afterload

cold/clammy, increased preload, very decreased CO, increased afterload

obstructive has same picture

56

distributive shock

two forms. both have low preload and low SVR

1) septic - warm skin, low preload, high CO, very low SVR

2) neurogenic - dry skin, low preload, low CO, very low SVR

57

microbes in tricuspid IV drug endocarditis

s aureaus, pseudomonas, candida

58

culture-negative endocarditis

coxiella, bartonella, HACEK (haemophilus, aggregatibacter [formerly actinobacillus], cardiobacterium, eikenella, kingella)

59

Beck triad (cardiac tamponade)

hypotension, distant heart sound, distended neck veins

60

kussmaul sign

paradoxical increase in JVP on inspiration

Note: seen in constrictive pericarditis, RCMs, tumors

61

pulsus paradoxus

decrease in amplitude of systolic BP by more than 10 during inspiration.

seen in tamponade, croup, severe asthma, sleep apnea, endocarditis

62

anti-HTN medications to use in pregnancy

hydralazine, labetalol, methyldopa, nifedipine

63

CCB to use for subarachnoid hemorrhages

nimodipine

64

CCB to use for hypertensive emergency

clevidipine

65

AE DHP CCBs

gingival hyperplasia and peripheral edema

66

drugs to use in HTN emergency

clevidipine, fenoldopam (D1), labetalol, nicardipine, nitroprusside (releases CN)

67

partial beta agonists that are contraindicated in angina

pindolol, acebutolol

68

ranolazine MOA

inhibits late phase of sodium current to reduce diastolic wall tension. does not affect HR or contractility, but can cause long QT

69

ezetimibe MOA

prevents cholesterol absorption

70

bile resin unwanted effect

increases TGs

71

fibrates MOA

upregulate LPL and induce HDL synthesis via PPAR-alpha

72

AE fibrates

myopathy

73

niacin MOA

inhibits hormone sensitive lipase in adipose tissue and reduces hepatic VLDL synthesis

74

AE niacin

flushing. hyperglycemia. hyperuricemia

75

Digoxin AE

hyperkalemia

76

class I anti-arr are

sodium channel blockers

77

name IA anti-arr

quinidine, procainamide, disopyramide

78

use IA anti-arr

atrial and ventricular arrhythmias, especially ectopic SVT and VT

79

use IB anti-arr

acute ventricular arrhythmias, especially post-MI, or digitalis-induce d arrhythmias

80

name IB anti-arr

lidocaine, mexiletine, (phenytoin)

81

name IC anti-arr

flecainide, propafenone

82

use IC anti-arr

atrial fibrilation and SVTs

83

class II anti-arr are

beta blockers

84

class III anti-arr are

potassium channel blockers

85

class IV anti-arr are

CCBs

86

beta blocker that causes dyslipidemia

metoprolol

87

beta blocker that can exacerbate vasospasm in prinzmetal angina

propranolol

88

name class III anti-arr

amiodarone, ibutilide, dofetilide, sotalol

("AIDS")

89

AE sotalol and ibutilide

torsades

90

adenosine MOA for anti-arr

increases K+ efflux from cells to hyperpolarize and decreaes calcium influx

91

use adenosine anti-arr

diagnosing/terminating certain forms of SVT

92

use Mg2+ anti-arr

effective in torsades and digoxin toxicity

93

uworld: class IA predominant actions

slows AP conduction velocity, prolongs APD

94

uworld: class IB predominant actions

no effect on AP conduction velocity, shortens APD

95

uworld: class IC predominant actions

slow AP conduction velocity, minimal effect on APD

96

uworld: class II predominant actions

slows sinus node discharge rate, slows AV node conduction and prolongs refractoriness

97

uworld: class III predominant actions

no effect on AP conduction velocity, prolongs APD

98

uworld: class IV predominant actions

slows sinus node discharge rate, slows AV nodal conduction and prolongs refractoriness

99

which anti-arrhythmic drugs prolong APD

classes IA and III