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A/P > Lecture 11/1: EKG interpretations > Flashcards

Lecture 11/1: EKG interpretations Flashcards

End test 4

1
Q

What is an arrhythmia?

A

A problem with the conduction system or APs going through muscle of the heart

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2
Q

What are some causes of arrhythmias?

A
  1. Abnormal firing of pacemaker (faster or slower)
  2. Shift of pacemaker from sinus node
  3. Blocks at different points of transmission
  4. Abnormal pathway transmission
  5. Spontaneous generation of abnormal impulses
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3
Q

T/F: increasing Vrm closer to threshold potential, especially in pacemaker cells, increasesly the likelihood of firing a spontaneous AP from etopic pacemakers and cauing an arrhythmia.

A

T

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4
Q

______ K+ will decrease the concentration gradient. This will _______ the Vrm, which will increase HR.

A

Increasing

Increase

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5
Q

T/F: Things increase Vrm prevent the heart from reseting/repolaring correctly

A

T

Keep looking at this card

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6
Q

When will the AP fire if the Vrm is raised?

A

Early

This will cause an arrhythmia

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7
Q

T/F: in a healthy heart, the ventricles generates the AP

A

F

SA node does

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8
Q

What increases the likelihood of in arrhythmia?

A

Increasing Vrm

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9
Q

What are 2 things that can cause an increase in Vrm?

A
  1. Ischemia/Infarct
  2. Increase K+
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10
Q

Sinus Tachycardia: where does it originate?

A

SA node

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11
Q

Sinus Tachycardia: what is a characterized by?

A

Fast HR
P waves at a rate of greater than 100 bpm

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12
Q

Sinus Tachycardia: Causes:

A
  1. Increased body temp
  2. sympathetic stimulation
  3. loss of vagal stimulation of PNS
  4. Toxic conditions in heart
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13
Q

How does increased body temperature cause increase HR?

A

Increased body temp –> increase metabolic demands –> increased HR

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14
Q

Why does blood loss initially increase HR?

A

BP will drop –> info in fed to CNS –> ANS will tell heart to beat faster.

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15
Q

What compensatory mechanism do some arrhythmias have? What medication can you give to combat this?

A

Reflex activation of the SA node resulting in reflex sinus tachycardia

Beta blocker (-olol)

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16
Q

Sinus Tachycardia: describe the P & QRS complexes
RR intervals

A

There is a P for every QRS complex

Short RR intervals

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17
Q

What are toxic conditions in the heart that can increase Vrm?

A

Nicotine
Alcohol
Increased K+
Acidosis

NAKA

(create toxic conditions at SA node)

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18
Q

Sinus Bradycardia: where does it originate?

A

SA node

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19
Q

Sinus Bradycardia: what is a characterized

A

Slow HR
P waves at a rate of less than 60 bpm

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20
Q

Describe why Sinus Bradycardia is normal in athletes

A

D/t training, physiologically, they have a larger heart. Because of this, their SV is larger as well causing them to have a larger CO. The CNS senses this and the ANS slows down the heart rate so the body can have the proper CO needed (and not more than needed)

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21
Q

T/F: if you are healthy and have a lower resting heart rate, this is a problem

A

F

This is a good thing, unless dangerously low.

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22
Q

If your resting heart rate is _____, this is bad.

A

high

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23
Q

What are some common problems associated with high resting heart rate?

A

**Hyperthyroidism **
Valve problem

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24
Q

Sinus Bradycardia: Causes:

A
  1. Vagal stimulation (PNS)
  2. Decreases SNS tone
  3. Neural reflex to drugs (Ex. Lots of phenephrine –> vasoconstriction –> ANS decreases HR to decrease CO)
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25
Q

Sinus Bradycardia: describe the P & QRS complexes
RR intervals

A

There is a P for every QRS complex

Long RR intervals

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26
Q

What is another name for paroxysmal atrial tachycardia?

A

Supraventricular Tachycardia

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27
Q

What is a normal RR interval?

A

0.83 seconds

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28
Q

Atrial Tachycardia (SVT): Describe

A

SA node firing in an irregular way
RR intervals are regular then irregular

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29
Q

Atrial Tachycardia (SVT): Causes

A

Temporary decrease in vagal tone

When it stops, rhythm should go back to normal

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30
Q

Atrial Tachycardia (SVT): describe the P & T waves

A

May overlap and cant distingish them

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31
Q

Atrial Tachycardia (SVT): Treatments

A

Vagaling down
Beta blocker

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32
Q

SA node block: Causes:

A

Severe dysfunction
Ischemia

This causes the SA node to not be able to reset any VG L-type Ca++ channels

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33
Q

SA node block: what happens to the P wave?

A

May be inverted
may not have one

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34
Q

SA node block: where is the new pacemaker

A
  1. AV node
  2. then purkinje fibers
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35
Q

SA node block: describe how the p wave will look and why?

A
  1. No p wave: deep within the AV node or within the purkinje fibers (takes awhile to travel backwards through AV node, QRS is happening. P wave hidden within QRS)
  2. inverted p wave: at the beginning/front of AV node
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36
Q

Describe what happens in the heart when you move the pacemaker or have ectopic pacemakers (specifically SA node blocks)

A

Ventricles depolarizes early causing early closure of AV valves. Atria is contracting, while AV valves are closed –> pushing blood against close valves = blood turbulence –> damage the heart valves; generates blood clots; moves blood clots that are already there; calcified heart valves

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37
Q

What medication should you be on if you have a fib or a flutter? Why?

A

Anticoagulant

Syncytiums are not having coordinated contractions causing blood turbulence against heart valves causing increase risk of blood clots and calcified valves

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38
Q

What is the purpose of the delay at the AV node?

A

Coordinated contractions between syncytiums

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39
Q

What is the normal PR interval?

A

0.16

40
Q

AV node block: How does this present?

A

PR interval greater than 0.16

41
Q

AV node block: causes:

A
  1. Ischemia of AV node or bundle of His d/t increase in Vrm (increasing Vrm decrease ion channels involved in AP)
  2. Compression of AV bundle (by scar tissue or calcification)
  3. inflammation of AV bundle
  4. excessive vagal stimulation
  5. Excessive digitalis/beta blocker
42
Q

T/F: The more narrow an area is the faster it conducts an AP

A

F

Narrow = more resistance –> slower

43
Q

What is digitalis?

A

Na+/K+ ATPase inhibitor

Digoxin

44
Q

What does digitalis do in the heart?

A

Increases Vrm by inhibiting the Na/K ATPase pump. This causes more Na to be in the cell which decreases the rate of Ca++ removal from the cell during an AP. This can be helpful during HF as a last resort

45
Q

Why is digitalis dangerous?

A

It is non selective for Na+/K ATPase not just in the heart but everywhere

46
Q

What is a last resort effort for HF?

A

Digitalis
Digoxin

47
Q

Describe a 1st degree heart block

A

Regular rhythm with PR interval greater than 0.20 seconds

48
Q

Describe a 2nd degree type I heart block

A

Dropped QRS complexes
Atria has a faster rate than ventricles

PR intervals 0.25-0.45 seconds
PR intervals progressively increases until QRS is dropped

49
Q

What is the nickname for 2nd degree type I heart block?

A

Mobity Type I

Wenckebach periodicity

50
Q

Which 2nd degree HB is more dangerous?

A

Type II

51
Q

Describe 2nd degree type II heart block

A

Dropped QRS complexes
Atria has a faster rate than ventricles

PR intervals 0.25-0.45 seconds
Fixed PR interval with randomly dropped QRS complex

52
Q

What could be the ratio of P/QRS to dropped QRS complexes?

A

2:1
3:2
3:1

53
Q

What is the treatment for symptomatic 2nd degree type II heart block?

A

Pacemaker

54
Q

What is the nickname for 2nd degree type II heart block?

A

Motiz Type II

55
Q

Ventricular escape =

A

purkinje fibers

56
Q

Describe 3rd heart block

A

Total AV node/bundle block
Nothing is getting through the AV node

Sinus node doing 1 thing
Purkinje fibers doing another….
Complete dissociation of P waves from QRS

Relying on Ventricular escape for HR at 15-40bpm

Increased atria rate d/t decreased CO

57
Q

Describe A flutter

A

Circular reentery AP in atria completely separate from SA node (atria is contracting separate from SA node)

Somes AP able to hit during refractory period

High atria & ventricle rate

58
Q

Which atrial arrhythmia is worse? Why?

A

Afib

Circus movement

59
Q

What is circular reentry?

A

AP going around in a circle

Part of atria contracting & part is relaxed

Not effective priming for ventricles

60
Q

What causes circular and circus reentry movements?

A
  1. slow conduction rate
  2. hypertropy (stretched out atria/ventricle)
61
Q

Describe Afib

A

circus movement from etopic pacemakers in atria

Somes AP able to hit during refractory period

High ventricle rate

No p waves only “fibrillation”

61
Q

T/F: there are p waves in aflutter

A

F

62
Q

Afib is _______ movement while A flutter is _______ and has a defined pathway.

A

uncoordinated

coordinated

63
Q

What is circus movement?

A

A bunch of ectopic pacemakers firing AP in a bunch of different directions

64
Q

What is fibrillation?

A

Shaking his where parts of the heart are contracting while other parts are relaxing

results in no blood being pumped to that part of the heart

65
Q

Which atria gets stretched out easier? What does this mean?

A

R atria

Predisposes R atria to flutter and fibrillation easier

66
Q

Circus/circular movement causes ________ in the atria. Which increases the risk for clots in the ______ atria! This can cause the clot to go into that respective ventricle and go into the _________ and cause a ______

A

turbulence

Right

Pulmonary artery

Pulmonary embolism (PE)

67
Q

What is the treatment if you have some really bad etopic pacemakers?

A

Ablation for a few of them

68
Q

If you random faint, you may have what? Describe this

A

Stokes-Adam Syndrome

Random complete AV node block

Lag of about 30 seconds d/t purkinje fibers getting to threshold –> faints d/t low BP

69
Q

T/F: Stokes-Adam syndrome is a virus that you catch and never fully goes away

A

F

This is a hereditary condition that causes fainting

70
Q

Describe Alternans

A

Problem with conduction of the purkinje fibers

Irregular QRS every other heartbeat: ventricles cant depolarize like normal (larger&shorter every other)

Happens during tachy rhythms

71
Q

What causes alternans?

A

Ischemia of the purkinje fibers
Digitalis

72
Q

Describe Premature Atrial Contractions (PACs)

A

Ectopic tissue in atria fires AP early –> early depolarization of ventricles –> less filling –> decreased SV –> radial pulse deficit (sound)

73
Q

Causes of PACs

A

Ischemia
Irritation
Calcified plaques

74
Q

T/F: PACs cause Radial pulse deficits

A

T

75
Q

Describe Premature AV node contractions

A

Random AP generating from AV node

76
Q

Describe Premature Ventricular Contractions (PVCs)

A

Random AP happening in the ventricular muscle tissue!!! (not AV node or Purkinje but the muscle tissue baby!!!!!)

Prolonged QRS (Muscle tissue slow)
High voltage QRS (1 ventricle depolarizes while both depolarizing; they dont cancel out)

T-wave usually inverted

77
Q

T/F: PAC are worse than PVC

A

F

PVCs are dangerous and worse

78
Q

Causes of PVCs include:

A

CRNA school….

Caffeine
Nicotine
Stress
Lack of sleep

79
Q

What does Paroxysmal mean?

A

Brief & intermittent
temporary

80
Q

Describe Paroxysmal Ventricular Tachycardia

A

QRS originating within the venticular muscle tissue

Prolonged QRS
High voltage

Accelerated QRS complexes

no p waves

81
Q

Paroxysmal Ventricular Tachycardia can cause __________

A

V-fib

82
Q

Causes of Paroxysmal Ventricular Tachycardia include:

A

Infarction

83
Q

What drug can cause long QT syndrome?

A

Benadryl

84
Q

What is Early afterdepolarization?

A

AP hitting a cell before it had time to fully reset. We have less ion channels involved, so AP doesn’t look the same. Also less Ca++ coming in so heart wont contract as much –> decreased HR –> decreased CO

85
Q

What 2 drugs can increase EAD and DAD?

A

Atropine (antimuscarinic)
Epi (Beta agonist)

Both increase cAMP –> increase PKA –> increase phosphorylation of of L-type Ca++ channels –> increases their sensitivity –> increases likelihood of pacemaker cells in the ventricles wanting to fire AP early

86
Q

What does Early afterdepolarization look like? Why?

A

A long QT interval

Cells are not able to reset

87
Q

EAD can lead to ________ which can lead to ________

A

torsades de pointes

V-fib

88
Q

T/F: You can last in V-fib for a long time

A

F

It can kill quickly even with CPR and defibrillation….

89
Q

Describe Ventricular Fibrillation

A

Circus movement in ventricles

90
Q

What can cause V-fib?

A
  1. EAD/torsades
  2. Hyperkalemia
  3. Lidocaine
91
Q

Describe Lidocaine and its effects on the heart

A

It can slow conduction system in heart and cause circus movements –> increase risk for V fib

Generally lidocaine is safe, but if you dont need it, dont use it.

92
Q

What is the Bundles of Kent?

A

Connective tissue that allows for an extra pathway on the lateral walls between the L atria and L ventricles & vice versa

Bypasses the ventricular conduction system

93
Q

What percent of people have Bundles of Kent?

A

0.2%

94
Q

What is the treatmet for Bundles of Kent if they become problematic?

A

Ablation

A/P (24 decks)

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