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Jenna's Shit List > Shit - Cardio UWorld > Flashcards

Shit - Cardio UWorld Flashcards

1
Q

Epi vs. NE receptors

A

Epi b > a

NE a1 > a2 > b1

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2
Q

Beta blocker selectivity

A

A-M olol = b1

N-Z olol = b1 and b2

ilol/alol = a and b

*nebivolol = b1 block and b3 stimulate (activate NOS)

*sotalol = K+ and b blocker

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3
Q

Most common hear defect in turners

A

Bicuspid aortic valve (early systolic high-pitched click)

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4
Q

Effects of dobutamine:

Use:

A

1) Inotropic (increased contractility is most useful effect)
2) slight chronotropy (increases O2 consumption with inotropic, so bad, can cause ischemia)
3) increases conduction velocity (bad; arrythmyas)

Used for heart failure with decreased contractility i.e. MI cardiogenic shock

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5
Q

Front of heart =

Back of heart (against esophagus) =

A

front = right ventricle

back = left atrium

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6
Q

diastolic rumble with an opening snap

A

Mitral stenosis

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7
Q

Which vessel in the body has the lowest O2?

A

Coronary sinus (heart extracts 80-90% of the O2)

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8
Q

Rheumatic heart disease timeline post-strep throat

A

1-8 months

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9
Q

bounding pulses =

weak pulses =

(valve defects)

A

bounding = AR = Corrigan’s/water-hammer

Weak = AS = pulsus parvus et tardus

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10
Q

most important aspect of nitrates

A

decreased preload

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11
Q

MI collagen 1 w vs few months

A

1w = type III

months = type I

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12
Q

MCC NVBE and MV valve

A

MVP, mitral valve

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13
Q

Maintenance dose =

A

Cp x CL x dosage interval

DI i.e. ever 6 hours = 60min/hr x 6hrs

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14
Q

pulsus paradoxus: sign and mechanism and causes

A

> 10mmHg fall in SBP upon inspiration.

Mechanism: increase in RVP during inspiration (VR and pulmonary retrigrade flow) causes RVP>LVP → IVS pushed into LV decreasing filling → decreased CO and thus SBP

Causes: cardiac tamponade, asthma, OSA, pericaditis, croup

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15
Q

Hepatic Angiosarcoma

A

Vinyl chloride, arsenic, thorotrast

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16
Q

Daptomycin AE

A

Rhabdo and myopathy

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17
Q

Fates of embryonic veins:

Cardinal

Vitelline

Umbilical

A

Cardinal = systemic venous system

Vitellin = portal venous system

Umbilical = degenerate

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18
Q

highest oral bioavailable nitrate

A

isosorbide mononitrate

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19
Q

Biventricular pacemakers: path of LV lead

A

SVC, RA, coronary sinus (in A-V groove in post heart), LV

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20
Q

Blood supply to diaphragmatic part of the heart

A

posterior interventricular branch (85% of people via RCA)

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21
Q

AA creating NO

A

Arginine

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22
Q

Aortic arch baro-receptors to NTS via what nerve?

A

X (vagus)

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23
Q

carotid sinus baro-receptors to NTS via what nerve?

A

IX (glossopharyngeal)

[actually branch called hering’s nerve]

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24
Q

Sign of pulsus paradoxus

A

Lose pulse sounds with BP cuff during inspiration

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25
Q

Irreversible change associated with wide fixed splitting of S2

A

Pulmonary hypertension (via ASD)

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26
Q

Stable angina vessel profile

A

AS plaque obstructing >75% of lumen, no thombus

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27
Q

Decrease platelet aggregation AND vasodilate arteries: drug names and condition they treat

A

Cilostazole and dipyridamole. Intermittent claudication (PVD), angina, prevent stroke/TIA

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28
Q

CCB toxicity

A

flush, edema, AV block, constipation (verapamil)

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29
Q

Orthopnea specific for:

A

LHF (dyspnia while supine relieved by sitting up)

Could also be mitral stenosis

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30
Q

2 major regulators of coronary flow, and the vessel size they work best on

A

Adenosine = arterioles

NO = large arteries and pre-arteriolar

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31
Q

Dilated coronary sinus indicates:

A

Increased RAP i.e. RHF or pulmonary hypertension

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32
Q

Thiazide AE

A

Hyper GLUC (glycemia, lipidemia, uricemia, calcemia)

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33
Q

Cardiac structures anterior and posterior to esophagus

A

anterior = LA

posterior = descending aorta

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34
Q

phenoxybenzamine vs phentolamine

A

phenoxybenzamine = irreversible a-antag, for pheo

Phentolamine = reversible a-antag, for MAO pts with cheese reaction

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35
Q

effects of increased vs decreased baro-R firing:

A

Increased (i.e. HTN, valsalva, carotid massage) = slowed AV node by increasing refractory perior

Decreased (i.e. low BP or BV) = increase HR, BP, contractility, vasocontriction

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36
Q

Chronic pericarditis causes + key features

A

Causes: TB, radiation, cardiac surgery

Pericardial Knock: just after S2 (confused with MS opening snap), from chronic pericarditis

Sharp y-descent, depper/steeper with inspiration

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37
Q

What does b2 vs glucagon do to alter myocardial contractility

A

BOTH INCREASE cAMP!

(just have different receptors)

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38
Q

cause of janeway lesions

A

Septic emboli to cutaneous vessels

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39
Q

mutations in genetic DCM vs HCM

A

DCM = mitochondrial enzymes for ox phos and cardiac cytoskeletal element

HCM = beta myosin heavy chains

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40
Q

holosystolic murmur =

A

MR

TR

VSD

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41
Q

anti-hyperlipidemia drug causing flushing, warmth, and itching. What is drug and what mediates this AE?

A

Niacin (B3)

Prostaglandins (reduce with asprin)

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42
Q

Fenoldopam MOA

A

selective D1-agonist, causes arteriolar dilation and naturesis

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43
Q

Leads II, III and AvF

Specific s/s

A

RCA (inferior heart; inf wal of LV)

Bradycardia (RCA supplies SA and AV nodes)

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44
Q

Familial hyperchylomicronemia (type I hyperlipoproteinemia):

  • Dx
  • complications
A

LPLase deficiency, milky plasma on standing via chylomicrons

Hypertriglyceridemia, recurrent acute pancreatitis, lipidema retinalis, erruptive xanthomas

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45
Q

Nitroprusside action

A

VS BOTH arterioles and veins, so decreases preload AND afterload, maintaining SV

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46
Q

Diastolic HF: LVP, LVV, LVEF

A

LVP increased

LVV normal (increase pressure ot achieve normal volume)

LVEF normal

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47
Q

polymorphic QRS complexes (varying amplitude and cycle length) with prolonged QT =

causes =

A

torsades des pointes V tach

causes = class Ia + III (not amiodarone) antiarythmics + TCAs

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48
Q

substitute for asprin allergy in angina + MOA

A

Clopidogrel; irreversibly blocks platelet ADP-Rs

49
Q

SCD: cause and predisposing factors

A

Cause = ventricular arrythmia

Predispose = CAD (70%), cardiomyopathies, channelopathies

50
Q

Adenosine MOA

A

K+ efflux from nodal tissues (prolongs phase 4), as well as Ca++ influx (phase 0)

51
Q

Small ventricular space, sigmoid shaped septum, brown pigments =

A

normal aging

52
Q

Distance from A2 to OS: disease and what it tells you

A

Mitral stenosis Severity: decreased time = worse. Tighter stenosis = higher LAP needed to overcome it = LAP > LVP sooner (during LV isovolumetric relaxation) = valve opens sooner thus closer to aortic valve shutting

53
Q

Calcific aortic stenosis via:

A

dystrophic calcification: abnormal organ calcification via damage (i.e. longterm hemodynamic stress os AS), with NORMOcalcemia

54
Q

Hibernating myocardium

A

Ischemia so that myocardium doesn’t work, but they make enough ATP to survive. If oxygen is returned with CABG or angioplasty, the hibernating myocardium wakes up and s/s improve (overs hrs-months)

55
Q

Myocardial stunning

A

Less severe version of hibernation. Ischemia

56
Q

Anti-arythmic specific for rapidly depolarizing and repolarized myocytes (i.e. ischemic cells in v. tach)

A

Lidocaine

57
Q

Best beta blocker for decreasing M/M in CHF; and its function

A

Carvedilol. B1, B2, A1 antagonist

58
Q

Sotalol Special properties

A

Only class III (K+ blocker, prolong Q-T) with beta-antagonist effects (so will also cause bradycardia)

59
Q

what part of the wave do beta blockers alter and how

A

Increased PR interval by slowing down AV node conduction

60
Q

Drugs producing dilated cardiomyopathy

A

Anthracyclines = doxorubicin and daunorubucin. Prevent with dexrazoxane

61
Q

Nesiritide

A

BNP analog

62
Q

SVT DOC

A

Adenosine (especially paroxysmal SVT)

63
Q

Adenosine AE

A

Flushing, burning chest pain, sense of impending doom, bronchospasm, hypotension

64
Q

Drug for chemical stress test

A

Adenosine

65
Q

HOCM heart changes (gross)

A

Asymmetrical septal hypertrophy, leading to systolic anterior motion (SAM) of anterior mitral valve leaflet

66
Q

Class III antiarythmics

A

Amiodarone, Ibutilide, dofetilide, sotalol

67
Q

how do vegetations form in bacterial endocarditis

A

Bug binds —> expresses tissue factor (thomboplastin/Factor III, extrinsic coagulation pathway)—> activates platelets and fibrin deposition —> vegetation

68
Q

Osler-Weber-Rendu

A

Hereditary hemorrhagic telangectasias. AD. spider nevi with bleeds i.e. epistasis

69
Q

Sturge-Weber

A

Facial, leptomeningeal, seizures, hemiplegia, skull tram track opacities

70
Q

Conduction speed

A

Purkinje > atria > ventricles > AV

71
Q

a fib ECG:

A

Lose P-waves, narrow QRS and irregularly spaced, variable RR

72
Q

Hypercoaguable paraeoplastic: name, cause, s/s

A

Trousseau’s syndrome. Pancreatic, colon, lung adenocarcinomas. Make thromboplastin-like substance that causes migratory thrombophlebitis (and non-bacterial thrombotic endocarditis)

73
Q

Aortic isthmus

A

tethered by ligamentum arteriosum, so injured during accel-deccel injuries

74
Q

young woman with RVH

A

Cor pulmonale from primary pulmonary hypertension

75
Q

What sets ventricle pace in 3rd degree block?

A

AV node = 45-55bpm

76
Q

Coronary steal

A

giving adenosine or dipyridamole (coronary vasodilators) when there is a blocked vessel exacerbates it

77
Q

Who has more compliant LA, chronic or acute MR?

A

Chronic; allows for room for blood to prevent acute pulmonary edema (seen in acute)

78
Q

beck triad: what and when

A

What: severe hypotension, muffled heart sounds, distended neck veins. Via pericardial tamponade

79
Q

Rx for AS with a fib

A

Cardioversion: they need the atrial kick to get blood into hypertrophied LV, and ot prevent acute pulmonary edema

80
Q

Distance from A2 to OS: disease and what it tells you

A

Mitral stenosis

Severity: decreased time = worse. Tighter stenosis = higher LAP needed to overcome it = LAP > LVP sooner (during LV isovolumetric relaxation) = valve opens sooner thus closer to aortic valve shutting

81
Q

Calcific aortic stenosis via:

A

dystrophic calcification: abnormal organ calcification via damage (i.e. longterm hemodynamic stress os AS), with NORMOcalcemia

82
Q

Hibernating myocardium

A

Ischemia so that myocardium doesn’t work, but they make enough ATP to survive. If oxygen is returned with CABG or angioplasty, the hibernating myocardium wakes up and s/s improve (overs hrs-months)

83
Q

Myocardial stunning

A

Less severe version of hibernation. Ischemia

84
Q

Anti-arythmic specific for rapidly depolarizing and repolarized myocytes (i.e. ischemic cells in v. tach)

A

Lidocaine

85
Q

Best beta blocker for decreasing M/M in CHF; and its function

A

Carvedilol. B1, B2, A1 antagonist

86
Q

Sotalol Special properties

A

Only class III (K+ blocker, prolong Q-T) with beta-antagonist effects (so will also cause bradycardia)

87
Q

what part of the wave do beta blockers alter and how

A

Increased PR interval by slowing down AV node conduction

88
Q

Drugs producing dilated cardiomyopathy

A

Anthracyclines = doxorubicin and daunorubucin. Prevent with dexrazoxane

89
Q

Nesiritide

A

BNP analog

90
Q

SVT DOC

A

Adenosine (especially paroxysmal SVT)

91
Q

Adenosine AE

A

Flushing, burning chest pain, sense of impending doom, bronchospasm, hypotension

92
Q

Drug for chemical stress test

A

Adenosine

93
Q

HOCM heart changes (gross)

A

Asymmetrical septal hypertrophy, leading to systolic anterior motion (SAM) of anterior mitral valve leaflet

94
Q

Class III antiarythmics

A

Amiodarone, Ibutilide, dofetilide, sotalol

95
Q

how do vegetations form in bacterial endocarditis

A

Bug binds —> expresses tissue factor (thomboplastin/Factor III, extrinsic coagulation pathway)—> activates platelets and fibrin deposition —> vegetation

96
Q

Osler-Weber-Rendu

A

Hereditary hemorrhagic telangectasias. AD. spider nevi with bleeds i.e. epistasis

97
Q

Sturge-Weber

A

Facial, leptomeningeal, seizures, hemiplegia, skull tram track opacities

98
Q

Conduction speed

A

Purkinje > atria > ventricles > AV

99
Q

a fib ECG:

A

Lose P-waves, narrow QRS and irregularly spaced, variable RR

100
Q

Hypercoaguable paraeoplastic: name, cause, s/s

A

Trousseau’s syndrome. Pancreatic, colon, lung adenocarcinomas. Make thromboplastin-like substance that causes migratory thrombophlebitis (and non-bacterial thrombotic endocarditis)

101
Q

Aortic isthmus

A

tethered by ligamentum arteriosum, so injured during accel-deccel injuries

102
Q

young woman with RVH

A

Cor pulmonale from primary pulmonary hypertension

103
Q

What sets ventricle pace in 3rd degree block?

A

AV node = 45-55bpm

104
Q

Coronary steal

A

giving adenosine or dipyridamole (coronary vasodilators) when there is a blocked vessel exacerbates it

105
Q

Who has more compliant LA, chronic or acute MR?

A

Chronic; allows for room for blood to prevent acute pulmonary edema (seen in acute)

106
Q

beck triad: what and when

A

What: severe hypotension, muffled heart sounds, distended neck veins. Via pericardial tamponade

107
Q

Rx for AS with a fib

A

Cardioversion: they need the atrial kick to get blood into hypertrophied LV, and ot prevent acute pulmonary edema

108
Q

Functions of ANP

A

Kidney: dilates afferent arteriole, prevents Na+ resorption, inhibits renin secretion

Adrenal: restricts aldosterone secretion

Blood vessels: vasodilation and increases capillary permeability to decrease circulating BV

109
Q

Pressures in the heart

A
110
Q

Maneuvers for murmurs

A
111
Q

Best way to hear S3

A

Lateral decubitus and exhaled to decrease lung volume and bring heart closest to chest

112
Q

Resistance =

A

nL/r4

113
Q

When is AS murmur the loudest?

A

When Aorta-LV pressure gradient is the largest, so mid-systole (hence the crescendo-decrescendo)

114
Q

Response to arteriole vasodilators (minoxidil and hydralazine)

A

Decreased arterial BP causes baro-R firing causes increased SNS:

Reflex tachycardia/FOC

RAS causing fluid retention cuasing edema and Na+ retention

115
Q

Congenital heart diseae causing toe cyanosis and clubbing

A

PDA

(deO2 blood from PA into descending aorta (past the 3 branches)

116
Q

Signal for migration (and the proliferation) of smooth muscle cells into tunica intima

A

PDGF

From pletelets, endothelium, macrophages

117
Q

Aortic aneurism vs aortic dissectoin major RF

A

aneurism = AS

dissection = HTN

118
Q

effects of 5HT of the heart:

A

endocardial fibrosis

Jenna's Shit List (23 decks)

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