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ecg Flashcards

0
Q

what plane is the precordial aka chest leads in

A

transverse plane

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1
Q

what plane is the six limb lead in

A

frontal plane

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2
Q

Lead 1 and avL

A

high lateral wall LV

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3
Q

II and III and AVF

A

inferior wall of LV

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4
Q

AVR

A

looks toward RA

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5
Q

V1 and V2

A

anterior and septal

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6
Q

V3 and V4

A

anterior view of LV

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7
Q

V4-V6

A

lateral view of LV

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8
Q

how long is a regular p wave

A

.06-.12

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9
Q

how long is the PRI

A

3-5 boxes aka .12-.20

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10
Q

how long is the QRS

A

1-2.5 boxes

.04-.10

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11
Q

order of the av node

A 
atrial depolarization
atrial systole
ventricular depolarization & atrial repolarization
ventricular diastole
ventricular repolarization
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12
Q

what does sinus bradycardia look like

A

everything normal except HR less than 60

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13
Q

Causes of bradycardia (4)

A

training
beta blockers
decreased automaticity of SA node
Vagal response (suctioning, ICH)

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14
Q

Symptoms of bradycardia

A 
pacemaker
atropine
syncope
dizzy
angina 
diaphoresis
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15
Q

what is sinus tachycardia

A

everything normal except HR is more than 100

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16
Q

Causes of sinus tachycardia

A 
increased sympathetic NS
pain
exercise
emotion
caffeine
cigarettes
amphetamines
fever
infection
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17
Q

what is sinus dysrhythmia

A

P- normal
QRS- normal
RR- VARIES MORE THAN ONE SMALL BOX
rate: 40-100

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18
Q

Causes of sinus dysrhythmia

A

infection
digoxin toxicity
fever

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19
Q

sinus dysrthymia affect on HR and inspiration/expiration

A

HR increases with inspiration

HR decreases with expiration

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20
Q

Wandering atrial pacemaker

impulses arise from areas other than SA node

A

P- vary in appearance
RR intervals vary
HR <100

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21
Q

PT implications for wandering atrial pacemaker

A

ischemia
injury to SA node (right coronary artery)
can progress to A fib

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22
Q

Premature atrial complex

ectopic focus initiates impulse

A

P wave of early beat has a different appearance

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23
Q

PT implications of premature atrial complex

A 
emotional distress
caffeine
nicotine
alcohol
MI
can progress to a-fib
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24
Q

A flutter

repeated atrial depolarization from one foci
repeated firing

A

P waves: sawtooth pattern
more than one P wave before QRS
RR interval vary
HR- 250-350

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25
Q

what does the AV node do in A flutter

A

AV node blocks some impulses from being conducted to ventricles

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26
Q

What causes A flutter

A

beta blockers

cardioversion

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27
Q

PT implications for A flutter

A 
mitral valve disease
CAD
MI
stress
hypoxemia 
pericarditis
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28
Q

A fib

quivering of atria due to MULTIPLE ectopic foci

A

P waves absent (wavy baseline)

RR irregular

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29
Q

causes of A fib

A 
old age
CHF
MI
digoxin toxicity
drug use (heroine)
stress
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30
Q

controlled A fib

A

HR <100

little impact on CO

31
Q

Uncontrolled a fib

A

HR >100

impact on CO

32
Q

Symptoms of A fib

A

dizzy/light headed
diaphoresis
palpitations

33
Q

A fib characteristics

A

turbulent blood flow: likes to clot: high risk of stroke

anti-arrthymic meds
cardioversion

34
Q

Junctional Rhythm

Av junction becomes primary pacemaker

aka ESCAPE rhythm

A

NO P wave

rate: 40-60 (intrinsic rate of AV node)

35
Q

Causes/ symptoms of Junctional Rhythm

A 
SA pathology
increased vagal tone
digoxin toxicity
MI
drop in CO

atropine
pacemaker

36
Q

1st degree heart block

impulse begins in SA node
impulse delayed on the way to AV node or AV conduction time is prolonged

A

PRI is PROLONGED

HR may be slow

37
Q

causes of 1st degree heart block

A

CAD
infarction
beta blockers

38
Q

2nd degree AV block type 1

-wekenbach or mobitz 1

progressive prolongation of PRI until 1 impulse doesnt get through

A

p wave before every QRS until P STANDS ALONE (conduction blocked)

RR irregular

RARELY PROGRESSES TO OTHER BLOCKS

39
Q

2nd degree type 1 block seen with

A

RCA disease/infarction

beta blockers

40
Q

2nd degree type 2 block

blocked conduction of one impulse to ventricles

A

RR interval varies
no change in PRI

more than one P stands alone

41
Q

2nd degree type 2 block characteristics

A

MI (LAD)
infarction of AV node (RCA)
digoxin toxicity

drop in CO
pacemaker
atropine
can progress to complete heart block

42
Q

3rd degree AV block

-complete heart block

no impulses from above the ventricle are conducted through AV node

NO communication between atria & ventricles

A

P waves have NO relation to QRS
QRS is WIDE

HR- 30-50

43
Q

characteristics of complete heart block

A

MI
dioxin toxicity

drop in CO (dizzy, SOB, chest pain, diaphoresis)
permanent pacemaker
atropine

MEDICAL emergency

44
Q

Premature ventricular complex

ectopic focus from a ventricle

ventricular depolarization occurs before SA node fires

A

QRS is WIDE

no P wave

followed by compensatory pause

45
Q

bigeminey

A

every other beat is a PVC

46
Q

trigeminy

A

every 3rd beat is a PVC

47
Q

couplet

A

2 PVCs paired together

48
Q

triplet

A

3 PVCs in a row

49
Q

unifocal

A

if PVCs appear the same

50
Q

multifocal

A

if PVCs appear different

51
Q

Causes of PVC

A 
caffeine
nicotine
stress
overexertion
hypo/hyperkalemia
ischemia
cardiomyopathy
cardiac irritation
52
Q

characteristics of PVC

A

increased frequency of PVCs leads to

  1. decreased filling time
  2. decreased preload
  3. decreased SV

drop in CO
may progress to V tach or V fib

53
Q

PVC is more dangerous when

A 
couplets
multifocal
more than 6 a minute
triplets
anti-arrthymia
54
Q

Ventricular tachycardia

V-tach

A

3 or more PVCs in a row

absent P wave
wide QRS
V rate: 100-250

55
Q

V tach characteristics

A 
ischemia/infarction
CAD
HTN
Digoxin
electrolyte imbalance

CO GREATLY AFFECTED
light head, syncope, chest pain
weak pulse
disorientation

cardioverion, defib, pharm therapy

56
Q

torsades de pointes

A

twists around isoelectric line

occurs during v tach
significant drop in CO

57
Q

ventricular fibrillation

quivering of ventricles
multiple ectopic foci = no synchronous contraction

A

NO CO
zig zag
progression of v tach

58
Q

V fib comes from:

A

infarction
ischemia
MI
digoxin toxicity

59
Q

V fib needs:

A

defibrillation
oxygen
CPR
cardiac meds

60
Q

MI

A

altered electrical conduction during angina

t wave inversion
t wave flat or peak
ST segment: elevate or depressed at least 1 mm

61
Q

MI zone of ischemia

A

T wave inversion of flattening

62
Q

MI zone of infarction

A

Q wave: transmural MI
Non Q wave: sub endocardial
bundle branch blocks

63
Q

MI: transmural

Q wave

A

all 3 layers affected

more than .04 sec in duration
at least one quarter the height of R wave

64
Q

MI: subendocardial

non Q wave

A

inner half of myocardium

more likely to re-infarct

65
Q

location of ischemia/infarction

V1, V2, V3, V4

A

anterior left ventricle

66
Q

location of ischemia/infarction

V1, V2

A

septal infarction

67
Q

location of ischemia/infarction

II, III, AVF

A

inferior infarction, RCA

68
Q

location of ischemia/infarction

I, avL

A

lateral infarction

circumflex artery

69
Q

A fib

goals of therapy

A

Control ventricular rate: block AV node

Convert a fib or flutter to NSR

70
Q

How do you control rate of a fib

A

Beta blockers
CCBAs
Digoxin

71
Q

How to convert a fib to NSR

A

Amiodarone

72
Q

Ventricular arrhythmia

Goals of chronic therapy

A

Treat underlying condition
Prevent v fib
Reduce PVCs

73
Q

Ventricular arrhythmia

Common meds

A 
Beta blockers
Amiodarone
Flecanide
Quinidine
Procainamaide
74
Q

Pacemaker

A

Estim of myocardium to depolarize

Appears as vertical line on ecg

ECG (1 decks)

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