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Cardiovascular Flashcards

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1
Q

what does the bulbis cordis become

A

smooth parts (outflow tract) of both ventricles

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2
Q

what does the primitive pulmonary vein become

A

smooth part of left atrium

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3
Q

what does the left horn of the sinus venosus become

A

coronary sinus

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4
Q

what does the right horn of the sinus venosus become

A

smooth part of the right atrium (sinus venarum)

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5
Q

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

A

SVC

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6
Q

blood supply for SA and AV nodes

A

RCA

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7
Q

effect of aortic regurgitation on pulse pressure

A

increased

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8
Q

effect of tamponade on pulse pressure

A

decreased

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9
Q

effect of exercise on pulse pressure

A

increased

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10
Q

effect of obstructive sleep apnea on pulse pressure

A

increased (increased sympathetic tone)

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11
Q

effect of aortic stenosis on pulse pressure

A

decreased

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12
Q

MOA for catecholamines increasing contractility

A

inhibition of phosphobalamban –> more intracellular Ca++

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13
Q

MOA for beta blockade decreasing contractility

A

lowers cAMP

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14
Q

which calcium channels are for myocardium

A

nondihydropyridine

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15
Q

LaPlace’s Law

A

T = pr / 2t

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16
Q

effect of increased TPR on venous return given fixed MAP

A

decrease

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17
Q

JVP A: peak or descent? meaning?

A

peak. atrial contraction (absent in afib)

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18
Q

JVP C: peak or descent? meaning?

A

peak. RV contraction (while atrium is still contracted)

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19
Q

JVP X: peak or descent? meaning?

A

descent. atrial relaxation

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20
Q

JVP V: peak or descent? meaning?

A

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

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21
Q

JVP Y: peak or descent? meaning?

A

descent. emptYing of right atrium into RV

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22
Q

fixed spliting caused by

A

ASD

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23
Q

paradoxical splitting caused by

A

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

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24
Q

effect of hand grip (increased afterload) on auscultation

A

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

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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

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