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EH 2 Flashcards

1
Q

CHF with decreased EF (<55%)

A

systolic heart failure

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2
Q

*** causes of systolic heart failure

A

viral, ETOH, cocaine, Chagas, idiopathic (essentially, heart becomes ischemic and then dilated)

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3
Q

What is the EF is diastolic or preserved EF heart failure?

A

> 55%

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4
Q

*** Causes of diastolic heart failure

A

HTN, amyloidosis, hemachromatosis

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5
Q

*** CHF treatment

A

ACEi, bb, spironolactone, furosemide, digoxin

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6
Q

*** ACEi role in CHF

A

prevents heart remodeling by blocking aldo

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7
Q

*** BB role in CHF

A

prevents remodeling by blocking epi/norepi

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8
Q

Furosemide role in CHF

A

improve sx (SOB, crackles, edema)

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9
Q

Digoxin role in CHF

A

Decrease sxs and hospitilization

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10
Q

*** Which two CHF meds improve survival

A

ACEi and BB

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11
Q

Does digoxin improve survival in those with CHF?

A

NO

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12
Q

heart > 50% AP diameter, cephalization, Kerly B lines, interstitial edema

A

CHF

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13
Q

*** thickened peri-tracheal stripe and splayed carina bifurcation

A

LA enlargement (severe mitral stenosis) or CA with mediastinal pathology

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14
Q

Can mitral stenosis cause LA enlargement?

A

YES

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15
Q

complications of cocaine use

A

aortic dissection, cranial hemorrhage, acute MI

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16
Q

first 3 things to do in cardiac arrest

A

CPR, oxgen, and assess rhythm

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17
Q

*** When to shock cardiac arrest?

A

v fib or pulseless v tachycardia

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18
Q

*** Do you defibrillate or shock patients in PEA or asystole?

A

NO - use continuous CPR or epinephrine for vasopressor

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19
Q

*** Ortne syndrome

A

when mitral stenosis becomes SO severe that LA enlarges and begins to compress surrounding structures, specifically the laryngeal nerve resulting in hoarse voice

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20
Q

*** dyspnea, orthopnea, PND, hemoptysis, voice hoarseness, mid-diastolic rumble with opening snap, predisposes to a fib with resultant thromboemboli

A

MS

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21
Q

Why dyspnea, orthopnea, PND and hemoptysis in severe MS?

A

increased left atrial pressures results in increased pulmonary pressure and thus pulmonary vascular congestion

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22
Q

*** low amounts of which electrolytes can result in torsades?

A

low K, Mg, Ca

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23
Q

*** first line tx for torsades

A

mag sulfate

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24
Q

when to use adenosine

A

tx of paroxysmal SVT

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25
Q

*** use this for tx symptomatic bradycardia or AV block

A

atropine

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26
Q

months after MI with CHF-like sx, EKG with persistent ST elevations and deep Q waves, echo with thinned, dyskinetic myocardial wall

A

left ventricular aneurysm

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27
Q

can someone get dilated cardiomyopathy (systolic HF) secondary to viral myocarditis?

A

YES

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28
Q

hypokinesis of inferior wall of heart

A

inferior MI (RCA, II III and avF)

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29
Q

*** mid diastolic click, opening snap, left atrial hypertrophy

A

MS

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30
Q

ST pattern in anterolateral infarction (left main, LAD +LCx)

A

elevated in I, aVL, V2-V6 and depressed in II, III and avF

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31
Q

if EKG confirms MI, do you need cardiac enzymes?

A

Nope

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32
Q

rheumatic fever

A

MS

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33
Q

why a fib in MS

A

causes left atria to dilate, which stretches fibers and disrupts normal conduction resulting in afib

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34
Q

taring chest pain radiating to back in setting of severe HTN

A

aortic dissection

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35
Q

*** restrictive cardiomyopathy, proteinuria, easy bruising, neuropathy, hepatomegaly, macroglossia

A

amyloidosis

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36
Q

fixed splitting S2

A

ASD

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37
Q

pulsus paradoxus

A

tamponade

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38
Q

bounding pulses

A

AR

39
Q

pulsus parvus et tardus

A

AS

40
Q

*** tx of chronic stable angina

A

BB, CCB, nitrates, ranolazine

41
Q

role of nitrates in angina tx

A

decrease preload

42
Q

*** two first line rx for chronic stable angina

A

BB and nondihydropyridine CCB (amlodipine, nifedipine)

43
Q

how do BB (metoprolol, atenolol) and non-dihydropyridine CCB (amlodipine, nifedipine) work to relieve sx of angina

A

decrease myocardial contractility and HR, resulting in lower oxygen demand of heart

44
Q

*** physical exam findings of chronic severe MR

A

displaced apical impulse, holosystolic murmur, third heart sounds, afib 2/2 atrial enlargement

45
Q

isolated systolic HTN

A

result of decreased elasticity or increased stiffness of arterial walls

46
Q

ddx for exertional dyspnea

A

ventricular arrhythmias (MI) and outflow obstruction (AS, HCOM)

47
Q

delayed and diminished carotid pulse

A

pulsus parvus et tardus of AS

48
Q

continuous murmur at the left interscapular area due to turbulent flow across

A

coarctation of the aorta

49
Q

prominent capillary pulsations in the fingertips or nail beds

A

AR, finding due to widened pulse pressure

50
Q

> 10 change in SBP with inspiration

A

pulsus paradoxus of cardiac tamponade

51
Q

tx of complete AV disassociation/3rd degree AV block

A

cardiac pacing, prevents asystole

52
Q

decreased CO, increased SVR, increased LVEDV

A

CHF

53
Q

Can LV systolic dysfunction result in LV dilation and MR?

A

YES

54
Q

is MR heard as a holosystolic murmur at the apex with radiation to the axilla?

A

YES

55
Q

what to do with pt whose triglycerides are > 1000

A

fibrates, fish oil, abstinence from alcohol –> GOAL IS TO PREVENT PANCREATITIS

56
Q

*** triglycerides 150-500

A

lifestyle modification (wt loss, exercise, alcohol decrease) and manage CVD risk (statin)

57
Q

name two fibrate medications used for triglyceride lowering

A

gemifibrozil, fenofibrate

58
Q

does niacin + statin lead to SE?

A

YES, mostly GI

59
Q

murmur made louder upon standing and valsalva, AD inheritance

A

HOCM

60
Q

Why outflow obstruction in HCOM?

A

contact between the mitral valve and the thickened septum during systole

61
Q

myxomatous degeneration of the mitral valve and/or chordae tendineae

A

MV prolapse

62
Q

dilation of MV annulus

A

dilated cariomyopathy or ischemic cardiomyopathy leading to MR

63
Q

pleuritic chest pain, dyspnea, tachycardia

A

worry about PE

64
Q

30 y/o woman presents with atypical CP, should she be evaluated for CAD?

A

NO

65
Q

*** how does dobutamine work in decompensated HF?

A

as an INOTROPE, improves heart contractility by binding to beta-1 receptors

66
Q

when to hospitalize HTN?

A

severe with end organ damage (AMS, retinal hemorrhage etc)

67
Q

who should be screened for secondary causes of HTN?

A

if resistant HTN (3 or more meds and not controlled) and young < 30 non-obese, non-black patients

68
Q

treatment of WpW patient who presents with stable a fib

A

procainamide

69
Q

*** what do these meds have in common: digoxin, bb, ccb, adenosine

A

AV node blockers (do not use in WpW patients)

70
Q

prolonged standing, pallor, sinus bradycardia with arrest, passing out

A

vasovagal syncope

71
Q

progressive edema, ascites, elevated JVP, pericardial knock (mid-diastolic sound), pericardial calicifications on CXR

A

constrictive pericarditis

72
Q

nephrotic range proteinuria

A

> 3.5 g/day

73
Q

*** pulmonary HTN, dilated RV, TR

A

cor pulmonale

74
Q

what is cor pulmonale

A

RV failure as a result of pulmonary HTN due to severe lung disease, pulmonary vascular disease or OSA

75
Q

old man with HTN who has sudden severe “tearing” pain that radiates to the back

A

aortic disease - disseciton, intramural hematoma

76
Q

what does ST elevation turn into?

A

T wave inversion

77
Q

can diffuse T wave inversions be seen in someone with pericarditis?

A

yes, as evolution of ischemic changes

78
Q

recent catheterization, now mottling of LE skin, and labs with elevated creatine, eosinophils, and low complement

A

cholesterol emboli

79
Q

*** physical exam findings suggestive of severe AS

A

pulsus parvus and tardus
mid to late peaking systolic murmur
quiet S2 as valve becomes too stiff to shut quickly

80
Q

why is S2 soft in severe AS

A

S2 is due to sudden AV closure, with severe AS the aortic valve is stiff and slow to close

81
Q

how does the murmur of mild-moderate AS differ from that of severe AS?

A 
mild-mod = early-peaking systolic murmur
severe = late-peaking
82
Q

how severe is AS if pt has exertional presyncope and delayed carotid upstroke

A

SEVERE - would expect late-peaking systolic murmur with a soft S2

83
Q

what conditions produce S3 heart sound

A

severe MR, chronic aortic reguritation, HF, high CO states like thyrotoxicosis or pregnancy

84
Q

*** plasma aldo: renin > 20:1, hypokalemia, resistant HTN

A

primary hyper-aldosteronism

85
Q

how does tension pneumothorax lead to hypotension?

A

obstructs the vena cava and thus blood flow return to RA

86
Q

is PCWP and CI low in pneumothorax?

A

YES

87
Q

can MI lead to cardiogenic shock?

A

YES

88
Q

narrow complex tachycardia, hemodynamic instability with hypotension and poor perfusion

A

unstable SVT = provide synchronized cardioversion

89
Q

inferior leads

A

II, III, avF (RCA)

90
Q

inferior infarction

A

RCA, primarily affects R ventricle

91
Q

pt comes in with CP and vomiting, found to have ST elevations in II, III, and avF - what DON’T you give them?

A

nitroglycerin - can worsen hypotension

92
Q

are pt with inferior infarct preload dependent and need fluids in addition to MI tx?

A

YES

93
Q

MI treatment regimen

A 
Oxygen if <90%
PCI within 90 minutes of medical contact
Nitrates (cautious with RV infarction)
Antiplatelet (ASA + clopidogrel)
Anticag (heparin, warfarin)
BB
Statin
94
Q

*** ascites, peripheral edema, hepatomeagly, splenomegaly

A

portal hypertension

IM (17 decks)

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