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First Aid Sections > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Beta Blockers

A

slow AV conduction, increase PR interval

decrease cAMP, Ca currents

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2
Q

Esmolol

A

very short acting

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3
Q

Metoprolol side effect

A

dyslipidemia

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4
Q

Nitroglycerin - molecular mechanism

A

NO –> increase cGMP –> decrease Ca/MLCK –> dephosphorylation –> SM relaxation (vasodilate!)

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5
Q

Nitrates - sympomatic relief by

A

decrease cardiac preload/LV volume

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6
Q

NO/Nitrates primarily work on

A

VEINS

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7
Q

Nitrate with highest bioavailability

A

isosorbide mononitrate

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8
Q

Beta Blockers affect preload/afterload

A

afterload

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9
Q

Ca Channel blocker mechanisms

A

block L type channels
reduce muscle contractility
(slow diastolic depolarization)

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10
Q

Digoxin side effects

A

N/V, blurry vision
ECG changes
hyperkalemia

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11
Q

autoregulation of coronary blood flow

A

NO

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12
Q

Causes of Pulsus Paradoxus

A

acute cardiac tamponade
constrictive pericarditis
restrictive cardiomyopathy
severe obstructive lung dz

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13
Q

milrinone

A

vasodilation

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14
Q

maintenace dose

A

Cpss x CL / bioavailability fraction

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15
Q

cause of tetralogy of fallot

A

abnormal neural crest cell migration

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16
Q

trauma affects

A

aortic arch rupture

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17
Q

CO =

A

SV x HR

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18
Q

MAP

A

CO x TPR

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19
Q

preload

A

ventricular EDV

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20
Q

Preload increases with

A

exercise
increased BV
sympathetics

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21
Q

Afterload

A

mean arterial pressure

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22
Q

venodilators

A

nitroglycerin

decrease preload

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23
Q

vasodilators

A

hydralazine

decrease afterload

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24
Q

EF =

A

SV / EDV

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25
Q

increase handgrip, murmur at LSB

A

VSD

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26
Q

Bicuspid Aortic Valve

A

aortic stenosis

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27
Q

Severe Aortic Stenosis

A

LV hypertrophy, reduced LV compliance

decrease in LV preload

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28
Q

Mitral Stenosis Severity

A

S2 to opening snap interval

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29
Q

Ventricular Action Potential

A 
Phase O - Na
1 - K influx
2 - Ca
3 - K efflux (close Ca channels)
4 - K permeability
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30
Q

Pacemaker Action Potential

A

0 - VG Ca channels open
3 - inactivate Ca channels, increase K efflux
4 - slow diastolic depolarization, inward Ca

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31
Q

heart rate determined by

A

slope of phase 4 in SA node

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32
Q

U wave

A

hypokalemia, bradycardia

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33
Q

Jervell and Lange-Nielsen syndrome

A

congenital long QT syndrome
defects in cardiac sodium or potassium channels
congenital sensorineural deafness

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34
Q

ANP

A

released in response to increase BV and atrial pressure
causes relaxation, decreased Na reabsorption
constricts efferent renal arterioles
dilates afferent renal arterioles
“escape from aldosterone”

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35
Q

PCWP

A

apprxoimation of LAP

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36
Q

LAD

A

anterior wall

V1-4

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37
Q

LCX

A

lateral wall

I, avL

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38
Q

RCA

A

inferior wall

II, III, aVF

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39
Q

Causes of Dialted Cardiomyopathy

A

Alcohol, wet Beriberi, Coxsackie B, Cocaine, Chagas, Doxorubicin
hemochromatosis, peripartum

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40
Q

Causes of Hypertrophic Cardiomyopathy

A

AD/B myosin heavy chain mutation

Friedreich’s ataxia

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41
Q

Restricture Cardiomyopathy causes

A

sarcoidosis, amyloidosis, radiation, hemochromatosis,
endocardial fibroelastosis
Loffler’s syndrome

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42
Q

Loffler’s syndrome

A

eosinophilic infiltrate

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43
Q

Hypertrophic Cardiomyopathy treatment

A

B blocker

Non -DHP Ca Channel Blocker

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44
Q

CHF - systolic

A

decrease in contractility

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45
Q

CHF - diastolic

A

inability of heart to relax to accomodate incoming blood during diastole

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46
Q

CHF ultimately causes

A

decrease CO

inadequate O2 tissue delivery

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47
Q

Cellular Responses to CHF

A

increase RAS

increase Sympathetic output

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48
Q

increase RAS

A 
Na retention
Aldosterone
Vasoconstriction (increase afterload)
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49
Q

cardiac cath

A

advance right to left

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50
Q

A fib ventricular rate determined by

A

AV node refractory period

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51
Q

Chronic AV fistula

A

increase CO

decrease TPR

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52
Q

V Wave

A

Mitral regurg

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53
Q

Biventricular pacemaker

A

RA, RV, LV

LV – soronary sinus/AV groove

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54
Q

fibrinous pericarditis

A

dressler’s syndrome
uremia
radiation

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55
Q

serous pericarditis

A

viral

non infections – RA, SLE

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56
Q

purlent/suppurative pericarditis

A

bactieral infections (Pneumococcus, Streptocccus)

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57
Q

Cardiac Tamponade

A

increased JVD
distant heart sounds
pulsus paradoxus

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58
Q

scattered cells within a mucopolysacchride strome

A

myxoma

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59
Q

polyarteritis nodosa association

A

Hep B

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60
Q

Kawaski dz treatment

A

IV immunoglobulin and aspirin

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61
Q

Time after MI: 0-4 hrs

A

no change

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62
Q

Time after MI: 4-12 hrs

A

early coag necrosis
edema/hemorrhage
wavy fibers

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63
Q

Time after MI: 12-24 hrs

A

coag nec

marginal contraction band necrosis

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64
Q

Time after MI: 1-5 d

A

coag nec

neutrophilic infiltrate

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65
Q

Time after MI: 5-10d

A

macrophage phagocytosis of dead cells

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66
Q

Time after MI: 10-14 days

A

granulation tissue

neovascularization

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67
Q

Time after MI: 2 wks - 2 months

A

collagen deposition

scar formation

68
Q

a

A

right atrial contraction

69
Q

c

A

tricuspid valve during RV contraction

70
Q

x

A

right atrial relaxation

71
Q

v

A

inflow of venous blood

72
Q

y

A

emptying of RA after TC valve opening

73
Q

purpose of manuvers for PSVT

A

increase cardiac parasympathetic tone

74
Q

cartoid sinus massage

A

prolong AV node refractory period

75
Q

thiazide diuretics - side effects

A

hyper: uric, calcium, glycemia, lipidemia

hypokalemia, hypotension

76
Q

diet drugs

A

secondary pulmonary hypertension

77
Q

supine hypotension

A

compressing IVC
decrease venous return
decrease preload
decrease CO

78
Q

Ca and muscle types

A

skeletal is intracellular only

79
Q

AcH, adenosine

A

during phase 4, decrease hr

80
Q

golden yellow/brown cytoplasmic granules

A

think lipofuscin or hemosiderin

hemosidern will stain blue/black

81
Q

alveolar macrophages containing hemosidering

A

LSHF (heart failure cells)

82
Q

Sotalol mofa

A

also has K channel blocking effects (increase QT interval)

83
Q

Dobutamine

A

B adrenergic agonist (B1>B2)

increases mycoardial oxygen consuption

84
Q

increased myocardial oxygen consumption

A

+ chronotropic effect

85
Q

electrical speed of heart

A

purkinje > atria > ventricle > AV node

86
Q

coagulative necrosis

A

ischemic injury

87
Q

liquefactive necrosis

A

bacterial infection

cns infarcts

88
Q

fat necrosis

A

acute pancreatitis

89
Q

caseous necrosis

A

tb infection

90
Q

Ebstein’s anomaly

A

atrial displacement of tricuspid valve leaflets

lithium in utero

91
Q

Verpamil side effects

A

2nd and 3rd degree heart block

contraindicated in pts with CHF

92
Q

BAV associated with

A

Turners

93
Q

Daptomycin

A

treatment for MRSA
depolarization of cellular membrane
myopathy/CPK elevation
inactivated by pulmonary surfactant

94
Q

localized amyloidosis

A

due to natriuretic peptides

95
Q

prostacyclin

A

inhibits platelet aggregation

96
Q

Hibernating myocardium

A

decreasing energy metabolism but enough ATP to prevent contracture
also expression of TNF alpha, NOS
reverse with CABG or balloon angioplasty

97
Q

plaque

A

lipid core

fibromuscular cap

98
Q

foam cells

A

oxidized lipids consumed by macrophages

99
Q

prinzmetal angina

A

coronary artery vasospasm

100
Q

primzmetal angina treatment

A

ng or CCB

101
Q

aspirin/heparin after MI

A

limit thrombosis

102
Q

supllemental O2 after MI

A

minimize ischemia

103
Q

nitrates after MI

A

vasodilate veins and coronary arteries

104
Q

B blocker after MI

A

slows HR
decrease O2 demand
decrease risk for arrythmia

105
Q

ACEI after MI

A

decrease LV dilation

106
Q

fibrinolysis/angioplasty after MI

A

opens blocked vessel

107
Q

risk 4-24 hrs after MI

A

arrythmia

108
Q

risk 1-3 days after MI

A

fibrinous pericarditis

109
Q

risk months after MI

A

aneurysm
mural thrombosis
dresslers

110
Q

Anitschkow cells

A

reactive histiocytes with slender, wavy nuclei

111
Q

microangiopathic hemolytic anemia

A

aortic stenosis

112
Q

s. viridans

A

previously damaged valves

113
Q

s. aureus

A

iv drug use

114
Q

s. epidermis

A

prostheitc valves

115
Q

s. bovis

A

coldon cancer

116
Q

negative blood cultures

A

haemophilius, actinobacillus, cardiobacterium, eikenella, kingella

117
Q

metastasis to heart

A

breast and lung carcinoma
melanoma
lymphoma

118
Q

TEE (anatomy)

A

anterior - LA

posterior - descending aorta

119
Q

Class IA

A

Disopyramide, Quinidine, Procainamide
Na
increase AP duration, Qt interval

120
Q

Class IA Side Effects

A

thrombocytopenia, torsades

121
Q

quinidine toxicity

A

tinnuitis

122
Q

Class IB

A

Lidocaine, Tocainide, Mexiletine
decrese AP duration
best post MI

123
Q

Class IC

A

flecainide, propafenone
contraindicated post MI and structural heart disease
signifcantly prolong refractory period in AV node

124
Q

Class III

A

amodiarone, ibutilide, dofetilide, sotalol

increase AP duration, increase QT interval

125
Q

Amodiarone

A

has Class I, II, III, IV effects

least chance of torsades

126
Q

Class IV

A

verpamil, diltiazem

increase PR interval

127
Q

adenosine

A

increases K out of cells

128
Q

adenosine can be blocked by

A

theophylline, caffine

129
Q

Mg2+

A

effective in torsades

digoxin toxicityc

130
Q

carvedilol and HF

A

decreases mortality

131
Q

patent foramen ovale

A

normal

RAP&raquo_space; LAP, paradoxical emboli

132
Q

carcinoid heart disease

A

endocardial fibrosis, usually right sided

5HIAA in urine

133
Q

Neseritide

A

form of BNP

134
Q

paradoxical emboli

A

venous system –> arterial
(DVT –> stroke)
example: ASD

135
Q

Coronary Steal Syndrome

A

coronary arteriolar vasodilation exacerbates ischemia by decreasing collateral blood flow
examples: adenosine, dipyramide

136
Q

midsystolic click

A

MVP

137
Q

indicator of severity of MR

A

S3 gallop

138
Q

to maintain CO in AR…

A

increase LV preload

139
Q

Beta blockers work on what type sof tissue

A

cardiac

renal juxtaglomerular cells

140
Q

atenolol

A

selective B1 antagonist

141
Q

A fib treatment

A

1 - CCB, BB

2 - digoxin

142
Q

Dopaminergic Receptor types

A

D1 - S

D2 - i

143
Q

saline for hypovolemic shock

A

increase intravascular volume and preload

144
Q

Ergonovine test

A

prinzmetal angina/provokes chest pain

145
Q

causes of acute LV failure

A

MI, severe htn, arrythmia, drug use

146
Q

nitroprusside

A

balanced venous and arterial vasodilator

decrease preload and afterload

147
Q

beta blocker overdose

A

glucagona (increases cAMP)

148
Q

ANP produced by ventricles

A

due to hypertrophy

149
Q

CO calculation with O2

A

O2 consumption/ AV O2 difference

150
Q

dystrophic calcification

A

cell necrosis

151
Q

ASD consequences

A

pulmonary htn

152
Q

diastolic hf and ef

A

normal ef
decrease ventricular compliance
increased LV EDP

153
Q

increase in O2 sat from R atrium to ventricle

A

VSD

154
Q

Class I Sodium Binding Strength

A

IC > A > B

155
Q

arterial vasodilation leads to activation of

A

SNS

156
Q

HCM LV outflow obstruction due to

A

mitral valve cusps and IV septum

157
Q

ACE comes from

A

lung endothelium

158
Q

irreversible myocardial cell injury path

A

mitochondrial vaculozation

159
Q

drugs that act on proximal tubule

A

acetazolamide

160
Q

drugs that act on descending limb

A

mannitol

161
Q

drugs that act on thick ascending limb

A

loop diuretics/furesomide

162
Q

drugs that act on DCT

A

thiazide

163
Q

drugs that act on CT

A

na channel blockers/amiloride

aldosterone receptor antagonists

164
Q

Concentric LV hypertrophic

A

pressure

AS, chronic HTN

165
Q

Eccentric LV hypertrophy

A

volume overload

AR, MR, MI, DCM

166
Q

Kussmaul sign

A

paradoxical rise in JVP

due to constrictive pericarditis

167
Q

cyanosis in LE only

A

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First Aid Sections (25 decks)

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