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USMLE Step 1: Part 1 COPY > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Review the embryology of the heart:

  • truncus arteriosus
  • bulbus cordis
  • endocardial cushion
  • primitive atria
  • primitive ventricle
  • primitive pulmonary vein
  • sinus venosus
  • common cardinal veins
A
  • TA: aorta and pulmonary arteries
  • BC: smooth part of right atrium
  • EC: atrial and ventricular septum
  • PA: trabeculated part of right atrium
  • PV: trabeculated part of right ventricle and left ventricle
  • PPV: smooth part of right atrium
  • SV: pulmonary veins and coronary sinus
  • CCV: vena cavae
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2
Q

The heartbeat develops at __________.

A

week 4

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3
Q

The __________ forms a valve for the foramen ovale. Which way does it allow blood to flow?

A

septum secundum; right-left

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4
Q

Describe the clinical utility of knowing that a patient has a patent foramen ovale?

A

Most people are asymptomatic, but if big enough they can allow venous emboli to enter the arterial circulation.

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5
Q

The most common congenital heart abnormality results from a defect in which embryonic structure?

A

VSD –membranous septum

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6
Q

What does the membranous septum fuse with?

A

The aorticopulmonary septum

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7
Q

What causes conotruncal abnormalities (and what are conotruncal abnormalities)?

A

Conotruncal abnormalities are disorders of the aortic trunk, pulmonic trunk, and the truncus arteriosus; they result from failure of neural crest cell migration.

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8
Q

What embryonic tissue gives rise to the valves?

A

Endocardial cushions

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9
Q

By what two ways does deoxygenated blood bypass the fetal lungs?

A

The foramen ovale allows R-L flow in the atria and the ductus arteriosus allow R-L flow in the pulmonary artery and aorta.

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10
Q

The ___________ vein carries oxygenated blood from the placenta to the baby.

A

umbilical

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11
Q

What main artery gives rise to the umbilical artery (which takes deoxygenated blood to the placenta)?

A

The internal iliac artery

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12
Q

What is the purpose of the ductus venosus?

A

It takes oxygenated and detoxified blood from the placenta and bypasses the liver.

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13
Q

What is the name for the non-patent foramen ovale?

A

Fossa ovalis

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14
Q

In addition to the increase in left atrial pressure (from the pulmonary circulation increase), what else causes the foramen ovale to close?

A

The placenta produces prostaglandins which help keep the FO patent. When the placenta separates, the prostaglandins decrease.

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15
Q

What do these develop into in adults?

  • ductus arteriosus
  • ductus venosus
  • foramen ovale
  • notochord
  • umbilical arteries
  • umbilica vein
A
  • DA: ligamentum artiosum
  • DV: ligamentum venosum
  • FO: fossa ovalis
  • N: nucleus pulposus
  • UA: medial umbilical ligaments
  • UV: ligamentum teres hepatis
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16
Q

The term “right-dominant,” in reference to the heart, means that the ___________ artery arises from the right coronary. Most people are this.

A

posterior descending

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17
Q

The ____________ arises from the left coronary.

A

left circumflex (left anterior descending is also a valid answer)

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18
Q

Describe the layers of the pericardium.

A

There are three. From outside to inside they are fibrous, parietal, and visceral. The pericardial cavity is between the parietal and visceral.

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19
Q

Recall that pericardial blood flows peaks during ___________.

A

diastole (because that is when the myocardium relaxes and eases its pressure on the coronary arteries)

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20
Q

Mean arterial pressure is equal to ________________.

A

2/3 x diastolic + 1/3 x systolic

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21
Q

The main determinant of pulse pressure is _______________.

A

stroke volume

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22
Q

What arteries arise from the aorta inferior to the diaphragm?

A
  • Inferior phrenic
  • Middle suprarenal
  • Celiac trunk
  • Superior mesenteric
  • Testicular / ovarian
  • Common iliac
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23
Q

Describe the three layers of arteries.

A
  • Tunica intima: endothelium and internal elastic lamina
  • Tunica media: smooth muscle, collagen, and elastic fibers
  • Tunica adventitia: vaso vasorum, nerves, and lymphatics
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24
Q

What two genetic disorders predispose someone to AAA?

A

Marfan’s and Ehlers-Danlos

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25
Q

True or false: tissue factor is made by the liver.

A

False. It is a transmembrane receptor made by the walls of blood vessels.

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26
Q

Hypertension increases risk of __________, while atherosclerotic plaques increase risk of ___________.

(Both abdominal aortic pathologies.)

A

aortic dissection; AAA

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27
Q

Catecholamines increase contractility by _______________.

A

inhibiting phospholambin (“catecho-LAM-IN-es = lam inhibitors”)

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28
Q

Why does contractility increase with decreased extracellular sodium?

A

Because with decreased extracellular sodium, the Na/Ca exchanger activity decreases and Ca accumulates in the cytosol (which increases contractility)

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29
Q

Myocardial oxygen demand increases with ______________.

A

contractility, HR, wall diameter, and afterload

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30
Q

Nitrates predominantly affect _____________.

A

veins

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31
Q

Ejection fraction ___________ in systolic heart failure.

A

decreases (this being dilated cardiomyopathy)

32
Q

Which medications affect contractility?

A

Beta-blockers and non-dihydropyridine calcium-channel blockers

33
Q

Which blood vessels hold the most blood?

A

The veins

34
Q

Which blood vessels have the most resistance?

A

The arterioles

35
Q

True or false: S4s are normal in some young women.

A

False. S4s are always pathologic, indicating hypertrophy. S3s in children and young women is sometimes normal.

36
Q

What is the A wave?

A

Right Atrial contraction

37
Q

What is the C wave?

A

Right ventriCular contraction

38
Q

The ______ (a part of S2) is slightly delayed upon inspiration.

A

P2

39
Q

Differentiate wide-splitting S2 that changes upon inspiration from fixed-split S2.

A

Wide-splitting: pulmonic stenosis or right-bundle-branch block
Fixed-split: ASD

40
Q

Explain paradoxical splitting.

A

Any condition that delays A2 can delay it so that it occurs after P2 during expiration. Inspiration allows more blood into the right ventricle and delays P2 such that A2 and P2 occur together, thus eliminating the split.

*Note: this is called paradoxical, because usually there is no split during expiration and a split during inspiration.

41
Q

Where can you hear aortic and pulmonic regurgitation the best?

A

Left sternal border between the 3rd and 4th ribs (beneath the normal pulmonic auscultation spot)

42
Q

In addition to the fixed-split S2, what else can you listen for in ASD?

A

A diastolic murmur heard over the tricuspid area (because there will be increased diastolic flow through the tricuspid valve)

43
Q

Valsalva and ____________ both decrease preload. What is the utility in this?

A

standing up; they will decrease the intensities of all heart murmurs with the exception of HCM

44
Q

What is a common cause of mitral regurgitation?

A

Ischemic heart disease (post-MI)

45
Q

What murmur will be present in VSD?

A

A “harsh” holosystolic sound over the tricuspid area

46
Q

There are only two murmurs heard only during diastole: ________________.

A

mitral stenosis (being a mid-diastolic click) and aortic regurgitation (early diastolic decrescendo murmur)

47
Q

In cardiac myocytes, phase 4 is dominated by _____________.

A

baseline efflux of potassium

48
Q

Cardiac myocyte contraction is directly stimulated by _______________.

A

calcium entering the cytosol and binding to sarcoplasmic calcium-gated calcium channels

49
Q

How does the action potential pass from one cardiac myocyte to another?

A

Gap junctions!

50
Q

Why is the phase 0 upstroke of pacemaker neurons determined by voltage-gated calcium channels (as opposed to voltage-gated sodium channels)?

A

The pacemaker neurons have a less negative resting potential, so the VSSCs remain permanently inactive.

51
Q

Which action potential phases are absent in the pacemaker neurons?

A

Phases 1 and 2

52
Q

What channels allow the AV node to be automatic?

A

The I(f) –”I funny” – current that allows a gradual inward current of sodium and potassium, thus depolarizing the cell. These are also altered by catecholamines to increase heart rate.

53
Q

Where are the AV and SA nodes?

A

The SA node is on the superior aspect of the right atrium, and the AV node is on the posteroinferior aspect of the right atrium.

54
Q

True or false: inverted T-waves indicate hypokalemia.

A

False! U waves (which indicate hypokalemia) are additional waves after T waves –not inverted T-waves. Inverted T-waves indicate recent MI.

55
Q

What usually supplies the AV node?

A

The RCA

56
Q

Both cardiac pacemaker nodes have automaticity. Which has a faster basal rate?

A

The SA node is faster. This is so because the SA node needs to direct the AV node. If the AV node were faster, then the AV node could beat autonomously.

57
Q

When does ventricular contraction occur (based on ECG waves)?

A

In the QT interval

58
Q

How much time is represented by one small box on an ECG?

A

0.04 seconds (so five of them, which is demarcated by bold lines, is 0.2 seconds)

59
Q

First Aid has a good mnemonic for drugs that can cause torsades de pointes. What is it?

A

The anti-ABCDEs:

  • antiArrhythmics (IA and III)
  • antiBiotics (macrolides)
  • antipsyChotics (haldol)
  • antiDepressants (TCAs)
  • antiEmetics (ondansetron)
60
Q

There are two electrolyte abnormalities that can cause torsades de pointes: _______________.

A

hypokalemia and hypomagnesemia (hence, you give magnesium to stop torsades)

61
Q

In terms of cardiac effects, what do hyperkalemia and hypokalemia cause?

A 
Hyper = cardiac arrest 
Hypo = arrhytmia
62
Q

What congenital disorders can cause torsades?

A

The long QT syndromes:

  • Romano-Ward: purely cardiac; AD
  • Jervell and Lange-Nielsen: cardiac and sensorineural deafness; AR
63
Q

Describe Brugada syndrome.

A

An autosomal dominant disorder (common in Asian males) in which there is ST-elevation and pseudo-right bundle branch block; this requires cardioversion to avoid sudden cardiac death

64
Q

In general, what causes atrial fibrillation?

A

Damaged atrial tissue causing additional firing nodes

Stretching of the atria can lead to this because the transmitting calcium channels are stretch-sensitive. Thus, anything that stretches the atria –such as hypertension, CHF, or valvular disease –can trigger atrial fibrillation.

65
Q

What causes atrial flutter?

A

Re-entrant circuits in the atria

66
Q

What is cardioversion?

A

Restoration of normal cardiac rhythm using drugs or devices

67
Q

What infection can cause third-degree heart block?

A

Lyme disease

68
Q

Which kinds of heart block require pacemaker?

A

Second-degree Mobitz II and third-degree

69
Q

What effects do ANP and BNP have?

A

They increase cGMP which causes vasodilation, increased GFR (from constricted efferent arteriole and dilated afferent arteriole), and decreased sodium resorption.

70
Q

Which nerves mediate the afferent information to changes in blood pressure?

A

The glossopharyngeal nerve senses changes from the carotid bifurcation and the vagus nerve senses changes in the aortic arch.

71
Q

Why does carotid massage generate a vagal response?

A

Massaging the carotids stretches the nerve terminals of the glossopharyneal nerve which causes increased action potential firing. The increased firing mimics the response to hypertension, so the sympatholytic pathways are activated!

72
Q

True or false: transposition of the great vessels is always fatal.

A

True, but some infants can survive outside the womb provided they have a persistent communication between the two circuits (such as a PFO, PDA, or VSD)

73
Q

Tricuspid atresia requires what other defects to be viable?

A

ASD and VSD! Think about it: the ASD allows deoxygenated blood returning from the body to enter the left atrium and be pumped through the VSD back to the lungs.

74
Q

What is total anomalous pulmonary venous return?

A

When the pulmonary veins drain back into the right atrium. This requires ASD and/or PDA to be viable.

75
Q

What structure forms the smooth parts of the ventricular outflow tracts?

A

The conus cordis (which leads to the truncus cordis)

76
Q

What structure gives rise to the vena cavae?

A

The sinus venosus

77
Q

What does Ebstein’s anomaly ultimately cause?

A

“Atrialization” of the right ventricle –bascially, excessive tricuspid regurgitaiton –with right heart failure resulting

USMLE Step 1: Part 1 COPY (243 decks)

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