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Cardio Flashcards

1
Q

LAD supplies

A

anterior LV wall
atnerior septum
His purkinje

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2
Q

Left circumflex supplies

A

lateral LV wall

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3
Q

RCA (PDA) supplies

A

inferior LV wall
RV
posterior septum
AV, SA node

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4
Q

What typically increases isotropy?

A

catecholamines

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5
Q

during cardiac contraction, only ___ stays the same

A

A (H,I,Z all differ!)

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6
Q

4 things that decrease contractility and SV

A

B blockade
heart failure
acidosis
hypoxia/hypercapnia

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7
Q

4 things that increase contractility and SV

A

catecholamines
increase in intracellular Ca
decrease in extracellular Na
digitalis–>increases intracel Na and therefore increases intracellular Ca

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8
Q

LV diastolic function determinants (5)

A 
Lusitrophy
LA pressure (aka LV filling pressure)
LV compliance
Heart rate (diastolic filling time) (dec in HR= increase in diastolic fx)
atrial kick
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9
Q

S3 represents

A

early diastole- dilated LV

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10
Q

S4 represents

A

late diastole-atrial kick to stiffened LV

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11
Q

paradoxical split

A

normally A2, P2 (because pressure greater in aorta), but in aortic stenosis P2 actually goes before A2 (breathing will make this go away)

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12
Q

4 things that happen when you turn in symp NS

A

1 increase Hr
2- increase iontropy
3- increase arteriole constriction
4- increase venous constriction

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13
Q

three types of shock

A

hypovolemic
distributive
cardiogenic

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14
Q

hypovolemic shock

A

too little blood

due to endothelial damage, excessive secretion, dehydration

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15
Q

distributive shock

A

enough blood but in wrong place (veins not arteries)

due to sepsis (vasodilator actions), reflex (vaso-vagal syncope)

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16
Q

cardiogenic shock

A

inadequate filling of arteries caused by failure of cardiac pump
due to acute MI, pericardial tamponade, valve rupture PE, myocarditis

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17
Q

3 consequences of shock

A

multi-organ failure
neurohormonal response
death

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18
Q

2 differences between physiological and pathological hypertrophy

A

physiological- high ATPase myosin heavy chains and more SR

path- less ATPase myosin heavy chains and less SR

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19
Q

helpful and harmful of intropes

A

helpful- increase BP and SV

harmful- increase work (so worsen energy expenditure)

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20
Q

helpful and harmful of diuretics

A

helpful- decrease preload, EDV/P

harmful- decrease stroke volume

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21
Q

helpful and harmful vasodilators

A

helpful- decrease after load, so increase SV

harmful- decrease BP and tissue perfusion

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22
Q

helps systolic heart failure

A

inhibit neurohormonal signaling

modify mehcanical stress

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23
Q

eccentric hypertrophy compensates for

A

decreased shortening ability

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24
Q

treatment for eccentric hypetrophy

A 
positive inotropic agents
diuretics
vasodilators
beta-blockers
aldosterone inhibitors
anticoagulants
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25
Q

louder subaortic murmur with

A

interventions that decrease left ventricular size or velocity of contraction

valsalva, standing, positive inotropic agents

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26
Q

treatment for dilated cardiomyopathy

A

ACEI, ARBS, Beta-blockers, diuretics, digitalis

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27
Q

treatment for hypertrophic cardiomyopathy

A

diuretics with caution, treat htn, treat Mischemia, decrease HR

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28
Q

Beck’s Triad of physical signs of pericardial tampnade

A

decreased arterial pressure
increased venous pressure
quiet heart

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29
Q

low serum K can be indicative of

A

primary hyperaldosteronism

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30
Q

how can you diagnose a phenochromocytoma

A

metanephirnes

vanillymandelic acid

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31
Q

hyper vs hypothyrodiism

A

hyper: thyroid stimulation of heart
hypo: increased TPR

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32
Q

2 phases of HTN

A

hyperkinetic phase

established or late essential HTN

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33
Q

polyarteriosis nodusa

A

medium vessel vasculitis

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34
Q

Wegenerg’s polyangitis

A

smal vessel vasculitis

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35
Q

polyangiitis with granulomatosis

A

nose, lung kidney

PR3»MPO

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36
Q

microscopic polyangitis

A

kidney
MPO>PR3
renal limited variant

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37
Q

churg straus angiitis

A

kidney 15%

MPO»PR3

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38
Q

inferior leads

A

II, III, aVF

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39
Q

anterior septal leads

A

V1 V2 V3

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40
Q

anterior lateral leads

A

V4, V5, V6

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41
Q

lateral leads

A

I, avL

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42
Q

P wave

A

atrial depolarization (SA node–>ventricle)

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43
Q

QRS

A

ventricular depolarization

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44
Q

T wave

A

ventricular depolarization

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45
Q

LAE can be (3)

A

Left ventricular hyptrophy
LAFB- left anterior bundle branch block
IMI

II- 3 or more wide
V1- 1x1 box

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46
Q

each small block is

A

40 ms (0.04 s)
1 mm
0.1 mb amplitude

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47
Q

axis

A

postiive in lead I and avF

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48
Q

LAD

A

+ lead I, - avf

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49
Q

RAD

A
  • lead I
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50
Q

5 reasons for RAD

A 
RVH
Lateral MI
COPD
PE
L posterior bundle black

II- >2.5
V1- >1.5

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51
Q

PR interval should be

A

120-200 ms

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52
Q

short PR interval

A

WPW

has to have a bypass tract

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53
Q

widlong PR interval

A

1st 2nd 3rd degree av block

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54
Q

1st degree AV block

A

p for every QRS

Sanode–>purkinje

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55
Q

2nd degree AV block

A

2:1 Av block
I- wenkebach- lengthened PR
II- Mobitz I

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56
Q

3rd AV block- complete block

A

SA firing but AV doesn’t work

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57
Q

wide QRS

A

LBBB (q)
RBB (rabbit ears)
WPW (short PR)
ICVD- when nothing else fits

(look at V1)

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58
Q

difference between NSTEMI and unstable angina

A

troponin - in unstable angina

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59
Q

4 aspects of myocardial oxygen demand

A

HR, BP, contractilibilty, preload/afterload

60
Q

Inferiro MI

A

AV node, mobitz I

61
Q

Anterior MI

A

His purkinje, Mobitz 2

62
Q

if V1 is positive

63
Q

respirophasic, positional

A

pericarditis

64
Q

P waves come and go

65
Q

lightheadedness

A

a fib, mobitz 1

66
Q

hypertension

A

light headedness

67
Q

definite angina in men and women

A

men > 50: 95, 50 74, <50 59

68
Q

probable angina

A

men >50, 73 50, 37 <50, 30

69
Q

nonanginal pain

A

men >50, 20 >50, 8

women >50 5, <50, 4

70
Q

stagesof exercise ekg

A

I- 10, 4 mets
II- 12, 7 mets
III-14, 10 mets
IV- 16, 16 mets

71
Q

MHR

72
Q

2 factors that predispose patients to sudden cardiac death post MI

A

LV dysfunction

frequent ventricular ectopy (>10 per hr)

73
Q

Amiodarine & Sotalol

A

most effective for Vt/vf

efect phase 3 in AP by increasing QT (prolonging repel)

74
Q

genetic heterogenity

A

same phenotype can have multiple different genes

–>differential diagnosis

75
Q

penetrance

A

effect of gene on population

–whole room has BRCA1, but only 70% get breast cancer

76
Q

expression

A

same gene, diff phenotype- person to person

77
Q

fibrillin

A

main component of extracellular microfibrils

78
Q

marfaans gene

A

15q21

FBN1

79
Q

platelet inhibitors

A

ASAK- decreases Thromb A2
Plavix- inhibit P2y12 receptors
Eptifibatide- inhibit IIb/IIIa receptors

80
Q

consider thrombolytics in patients

A

<65 years old
presenting within 2 hrs of symptom onset
anterior MI

81
Q

1/2-4 hrs after MI

A

sometimes waviness of boraders

82
Q

4-12 hrs MI

A

occasional dark mottling

early coat necrosis, edema, hemorrhage

83
Q

12-24 hrs

A

dark mottling

ongoing coag necrosis, early PMN infiltrate

84
Q

1-3 days

A

mottling with yellow-tan infarct center, more PMNs, can get pericarditis

85
Q

3-7 days

A

central yellow-tan softening

dying neutrophils with dead eating by MOs

86
Q

7-10 days

A

maximally yellow-tan and soft, red depressed margins

granulation

87
Q

10-14 days

A

red-grey

well established granulation tissue and collagen

88
Q

2-8 weeks

A

grey white scar progressive to core

increased collage, decreased cellularity

89
Q

> 2 months

A

scarring complete–white fibrous scar

dense collagenous scar

90
Q

eisenmenger syndrome

A

pulmonary arteries constrict and after 5 years this becomes permanent
due to VSD

91
Q

R–>L shunts

92
Q

5 R to L shunts

A 
metrology of fallout
transposition of great arteries
tricuspid atresia
truncus arteriosus
total anomalous PVR
93
Q

4 aspects of tet

A

VSD
pulmonary stenosis
overriding aorta
RVH

94
Q

annular dilation

A

cardiomyopathy

95
Q

leaflet perforation

A

endocarditis, trauma

96
Q

prolapse

A

myomatous degeneration

97
Q

chordial rupture

A

MVP, calcification

98
Q

pap muscle rupture

A

ischemic heart disease

99
Q

medication for MV issues

A

ditizaem (ca blocker affecting AV node)
metoprolol (b blocker) to slow heart rate in Afib
and lengthen diastolic time

100
Q

LVH on EKG

A
  • in V1 and + in V5 >35
101
Q

critical aortic stenosis associated with

A

> 60 mmHg, flow >4 m/sec

102
Q

Verapamil

Diltizem

A

Ca channel blockers

103
Q

abnormal automaticity induced by

A

hypokalemia
hypoxia
ischemia
digitalis toxicity

104
Q

automaticity/conduction is blocked by

A

quinidine

lidocaine

105
Q

QRS complex

A

delays in intraventricular myocardium

106
Q

Strain pattern

A

subendocardial hypoxia in hypertrophied ventricle

107
Q

distolic depolarization

A

ischemic shifts ST segment because ischemic tissue injury–>increase in extracellular K concentration–>depolarizes cells–>current directed towards

108
Q

Pericarditis

A

nonprogressive ST elevation

109
Q

when is the earliest you see q wave

110
Q

q wave + t inversion

111
Q

q wave + normal T

112
Q

ST elevation and T inversion, no q waves

113
Q

Mobitz 1 is

A

AV nodal block

114
Q

Mobitz 1 channel

A

slow- calcium

115
Q

Mobitz infarction

A

inferior MI

116
Q

mobitz 1 drugs

A

digitlais
beta-blockers
Ca channel blockers

117
Q

mobitz 1 therapy

A

atropine

sympathomimetics

118
Q

Mobitz ii

A

his purkinje block

119
Q

Mobitz II vs Mobitz I ORS

A

I- junctional-narrow QRS

II- idioventricular- wide ORS

120
Q

M2 infarct

A

anterior MI

121
Q

M2 drugs

A

type I anti-arry

122
Q

M2 therapy

123
Q

atrial rate of 250-350

124
Q

atria rate of >250

125
Q

1st degree heart block

A

delay from atria–>ventricle

126
Q

2nd degree heart block

A

intermittent failure of conduction (some atrial beats conducted, some blocked)

occurs in settings of increased vagal tone, decreased sympaethtics

127
Q

3rd degree heart block

A

persistent failure of conduction (all atria beats blocked)

128
Q

failure of conductivity

A

heart block

129
Q

decreased automaticity

A

sinus bradycardia

130
Q

AV nodal/junctional tachycardia

A

AV node goes to a rate that is faster than sinus rate

seen with exercise hypotnesion, anxiety,hyperthyroidism, hypoglycemia, congestive heart failure

131
Q

abnormal automaticity of fast fibers is associated with

A 
increase sump tone (drugs, anxiety, hyperthyroidism)
hypokalemia
hypoxia/ischemia
digitalis toxicity
atrial enlargement
132
Q

delta wave represents

A

pre-excitation of ventricle via abnormal bypass tract between atrium and ventricle called bundle of kent

133
Q

three characteristics of re-entrant pathways

A

two anatomically or functionally distinct pathways

slow conduction

dispersion of refractoriness

134
Q

superavent tachycardia vs vent tachy

A

supravent- narrow QRS

vent tach- wide QRS

135
Q

prolonged QT usually due to

A

myocardial ion channel abnormalities

polymorphic Vtach-Torasades

136
Q

digoxin and adenosine

A

av nodal blockers

137
Q

Ca channels, av nodal blockers, b blockers

A

decrease how many beats can go through AV node so therefore decreasing HR

138
Q

amidorone

A

blocks K channels

prevents reentrant Vtach

139
Q

lidocaine

A

inhibits Na- only useful against Vtach

140
Q

VSD causes LV

A

eccentric hypertrophy

141
Q

O2 content=

A

O2 sat x [Hgb] x 1.34

142
Q

LA pressure

143
Q

RA pressure

144
Q

Flow=

A

02 consumption/AV difference

145
Q

SVR=

A

MAP-CVP/CO

SBM (18 decks)

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