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Flashcards in Cardio Deck (145):
1

LAD supplies

anterior LV wall
atnerior septum
His purkinje

2

Left circumflex supplies

lateral LV wall

3

RCA (PDA) supplies

inferior LV wall
RV
posterior septum
AV, SA node

4

What typically increases isotropy?

catecholamines

5

during cardiac contraction, only ___ stays the same

A (H,I,Z all differ!)

6

4 things that decrease contractility and SV

B blockade
heart failure
acidosis
hypoxia/hypercapnia

7

4 things that increase contractility and SV

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

8

LV diastolic function determinants (5)

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

9

S3 represents

early diastole- dilated LV

10

S4 represents

late diastole-atrial kick to stiffened LV

11

paradoxical split

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

12

4 things that happen when you turn in symp NS

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

13

three types of shock

hypovolemic
distributive
cardiogenic

14

hypovolemic shock

too little blood
due to endothelial damage, excessive secretion, dehydration

15

distributive shock

enough blood but in wrong place (veins not arteries)
due to sepsis (vasodilator actions), reflex (vaso-vagal syncope)

16

cardiogenic shock

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

17

3 consequences of shock

multi-organ failure
neurohormonal response
death

18

2 differences between physiological and pathological hypertrophy

physiological- high ATPase myosin heavy chains and more SR

path- less ATPase myosin heavy chains and less SR

19

helpful and harmful of intropes

helpful- increase BP and SV
harmful- increase work (so worsen energy expenditure)

20

helpful and harmful of diuretics

helpful- decrease preload, EDV/P
harmful- decrease stroke volume

21

helpful and harmful vasodilators

helpful- decrease after load, so increase SV
harmful- decrease BP and tissue perfusion

22

helps systolic heart failure

inhibit neurohormonal signaling
modify mehcanical stress

23

eccentric hypertrophy compensates for

decreased shortening ability

24

treatment for eccentric hypetrophy

positive inotropic agents
diuretics
vasodilators
beta-blockers
aldosterone inhibitors
anticoagulants

25

louder subaortic murmur with

interventions that decrease left ventricular size or velocity of contraction

valsalva, standing, positive inotropic agents

26

treatment for dilated cardiomyopathy

ACEI, ARBS, Beta-blockers, diuretics, digitalis

27

treatment for hypertrophic cardiomyopathy

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

28

Beck's Triad of physical signs of pericardial tampnade

decreased arterial pressure
increased venous pressure
quiet heart

29

low serum K can be indicative of

primary hyperaldosteronism

30

how can you diagnose a phenochromocytoma

metanephirnes
vanillymandelic acid

31

hyper vs hypothyrodiism

hyper: thyroid stimulation of heart
hypo: increased TPR

32

2 phases of HTN

hyperkinetic phase
established or late essential HTN

33

polyarteriosis nodusa

medium vessel vasculitis

34

Wegenerg's polyangitis

smal vessel vasculitis

35

polyangiitis with granulomatosis

nose, lung kidney
PR3>>MPO

36

microscopic polyangitis

kidney
MPO>PR3
renal limited variant

37

churg straus angiitis

kidney 15%
MPO>>PR3

38

inferior leads

II, III, aVF

39

anterior septal leads

V1 V2 V3

40

anterior lateral leads

V4, V5, V6

41

lateral leads

I, avL

42

P wave

atrial depolarization (SA node-->ventricle)

43

QRS

ventricular depolarization

44

T wave

ventricular depolarization

45

LAE can be (3)

Left ventricular hyptrophy
LAFB- left anterior bundle branch block
IMI

II- 3 or more wide
V1- 1x1 box

46

each small block is

40 ms (0.04 s)
1 mm
0.1 mb amplitude

47

axis

postiive in lead I and avF

48

LAD

+ lead I, - avf

49

RAD

- lead I

50

5 reasons for RAD

RVH
Lateral MI
COPD
PE
L posterior bundle black

II- >2.5
V1- >1.5

51

PR interval should be

120-200 ms

52

short PR interval

WPW
**has to have a bypass tract**

53

widlong PR interval

1st 2nd 3rd degree av block

54

1st degree AV block

p for every QRS
Sanode-->purkinje

55

2nd degree AV block

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

56

3rd AV block- complete block

SA firing but AV doesn't work

57

wide QRS

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

(look at V1)

58

difference between NSTEMI and unstable angina

troponin - in unstable angina

59

4 aspects of myocardial oxygen demand

HR, BP, contractilibilty, preload/afterload

60

Inferiro MI

AV node, mobitz I

61

Anterior MI

His purkinje, Mobitz 2

62

if V1 is positive

RVH

63

respirophasic, positional

pericarditis

64

P waves come and go

V tach

65

lightheadedness

a fib, mobitz 1

66

hypertension

light headedness

67

definite angina in men and women

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

68

probable angina

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

69

nonanginal pain

men >50, 20 >50, 8
women >50 5, <50, 4

70

stagesof exercise ekg

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

71

MHR

220-age

72

2 factors that predispose patients to sudden cardiac death post MI

LV dysfunction
frequent ventricular ectopy (>10 per hr)

73

Amiodarine & Sotalol

most effective for Vt/vf
efect phase 3 in AP by increasing QT (prolonging repel)

74

genetic heterogenity

same phenotype can have multiple different genes
-->differential diagnosis

75

penetrance

effect of gene on population
--whole room has BRCA1, but only 70% get breast cancer

76

expression

same gene, diff phenotype- person to person

77

fibrillin

main component of extracellular microfibrils

78

marfaans gene

15q21
FBN1

79

platelet inhibitors

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

80

consider thrombolytics in patients

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

81

1/2-4 hrs after MI

sometimes waviness of boraders

82

4-12 hrs MI

occasional dark mottling

early coat necrosis, edema, hemorrhage

83

12-24 hrs

dark mottling

ongoing coag necrosis, early PMN infiltrate

84

1-3 days

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

85

3-7 days

central yellow-tan softening

dying neutrophils with dead eating by MOs

86

7-10 days

maximally yellow-tan and soft, red depressed margins

granulation

87

10-14 days

red-grey

well established granulation tissue and collagen

88

2-8 weeks

grey white scar progressive to core

increased collage, decreased cellularity

89

>2 months

scarring complete--white fibrous scar

dense collagenous scar

90

eisenmenger syndrome

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

91

R-->L shunts

cyanotic

92

5 R to L shunts

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

93

4 aspects of tet

VSD
pulmonary stenosis
overriding aorta
RVH

94

annular dilation

cardiomyopathy

95

leaflet perforation

endocarditis, trauma

96

prolapse

myomatous degeneration

97

chordial rupture

MVP, calcification

98

pap muscle rupture

ischemic heart disease

99

medication for MV issues

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

100

LVH on EKG

- in V1 and + in V5 >35

101

critical aortic stenosis associated with

>60 mmHg, flow >4 m/sec

102

Verapamil
Diltizem

Ca channel blockers

103

abnormal automaticity induced by

hypokalemia
hypoxia
ischemia
digitalis toxicity

104

automaticity/conduction is blocked by

quinidine
lidocaine

105

QRS complex

delays in intraventricular myocardium

106

Strain pattern

subendocardial hypoxia in hypertrophied ventricle

107

distolic depolarization

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

108

Pericarditis

nonprogressive ST elevation

109

when is the earliest you see q wave

hrs-days

110

q wave + t inversion

months

111

q wave + normal T

years

112

ST elevation and T inversion, no q waves

hrs

113

Mobitz 1 is

AV nodal block

114

Mobitz 1 channel

slow- calcium

115

Mobitz infarction

inferior MI

116

mobitz 1 drugs

digitlais
beta-blockers
Ca channel blockers

117

mobitz 1 therapy

atropine
sympathomimetics

118

Mobitz ii

his purkinje block

119

Mobitz II vs Mobitz I ORS

I- junctional-narrow QRS
II- idioventricular- wide ORS

120

M2 infarct

anterior MI

121

M2 drugs

type I anti-arry

122

M2 therapy

pacemaker

123

atrial rate of 250-350

a flutter

124

atria rate of >250

a fib

125

1st degree heart block

delay from atria-->ventricle

126

2nd degree heart block

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

occurs in settings of increased vagal tone, decreased sympaethtics

127

3rd degree heart block

persistent failure of conduction (all atria beats blocked)

128

failure of conductivity

heart block

129

decreased automaticity

sinus bradycardia

130

AV nodal/junctional tachycardia

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

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

131

abnormal automaticity of fast fibers is associated with

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

132

delta wave represents

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

133

three characteristics of re-entrant pathways

two anatomically or functionally distinct pathways

slow conduction

dispersion of refractoriness

134

superavent tachycardia vs vent tachy

supravent- narrow QRS
vent tach- wide QRS

135

prolonged QT usually due to

myocardial ion channel abnormalities
polymorphic Vtach-Torasades

136

digoxin and adenosine

av nodal blockers

137

Ca channels, av nodal blockers, b blockers

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

138

amidorone

blocks K channels
prevents reentrant Vtach

139

lidocaine

inhibits Na- only useful against Vtach

140

VSD causes LV

eccentric hypertrophy

141

O2 content=

O2 sat x [Hgb] x 1.34

142

LA pressure

6-12

143

RA pressure

6

144

Flow=

02 consumption/AV difference

145

SVR=

MAP-CVP/CO