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A&P 1 > Exam 4 Lecture 7 > Flashcards

Exam 4 Lecture 7 Flashcards

1
Q

What are the 3 Ratios of PR-Int to QRS Complexes in a 2nd Degree Type 2 HB

A

2:1
3:1
3:2

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2
Q

If P wave is Inverted, where is this source?

A

Retrograde AP from AV junction

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3
Q

Define PVC
*Why is the QRS duration longer?
*Why is the Amplitude of the QRS higher?
*Describe the T-Wave

A

Ventricle contraction before normal, as Ventricular muscle conduction is slower than the Purkinje System
*Longer b/c the AP starts in ventricular muscle, which takes longer to depolarize the Purkinje Fibers
*Higher b/c if the depolarization starts on the high lateral side of the L or R ventricle, this leads to increased magnitude
*T-Wave after PVC is usually inverted

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4
Q

List Pathway for Blood Clot in R atria to Lungs, per lecture

A

R atria, R ventricle, L ventricle, Pulmonary System

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5
Q

What is Cardiac Turbulence?
*What 2 things can this lead to

A

Blood swishing and hitting closed valves or walls, leading to increased blood clots and Ca++ deposits

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6
Q
A

Premature Ventricle Contraction

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7
Q

What is a normal CO?

A

5L/min

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8
Q

What are cranial nerves V and X

A

Trigeminal and Vagus

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9
Q
A

Atrial Flutter

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10
Q

Define Paroxysmal Ventricular Tachycardia
*Is this dangerous?
*What is this a precursor to?
*Talk about P waves, if any

A

Over active ventricle conduction system
*Yes, can lead to VFIB
*VFIB
*If any, probably inverted

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11
Q

What can cause Paroxysmal VTACH: 2 Things

A

Ischemia or Infarct

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12
Q

What are the Bundles of Kent
*What % of the population has this?
*How to treat if needed

A

Connections that bypass the normal connections such as the internodal system
*0.2%
*Cardiac Ablasion

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13
Q

Premature Contract: AV node Source: Talk about P wave

A

AV node ectopic issues, so missing P-Wave

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14
Q

3 Tx for SVT [Paroxysmal Atrial Tachycardia]

A

Vagal Reflex, BB, Digoxin

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15
Q
A

Sinus Tachycardia

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16
Q

SinoAtrial Block: Define what happens when the ventricles are depolarized early, in terms of creating “turbulence”

A

During contraction, AV valves are open. If you depolarize the ventricles early, the Atrium pushes blood against closed AV valves, leading to damage and more turbulence

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17
Q

Define PAC: Talk about SV
*What 3 things does this result from
*What is a Radial Pulse Deficit

A

Ectopic issues in atria fire early AP; Lower SV
*Ischemia, Irritation, Calcification
*Lower SV from less filling time in early depole = less noise when auscultating

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18
Q

Define Sinus Tachycardia
*How long is PR-Int
*BPM?

A

Abnormal SA node firing P-Waves faster than normal
*PR-Int<0.16 sec
*>100BPM

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19
Q

What does the Bundles of Kent do?

A

Connect R Atria with R vent or L atria with L vent

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20
Q

How to get out of VFIB, per lecture

A

Shocking

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21
Q

Define Paroxysmal Atrial Tachycardia[SVT]
*Talk about P and T waves
*Is this a permanent state of the Heart?

A

High HR driven by abnormal Atrial Excitation
*P waves and T waves may overlap
*No, usually this comes and goes

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22
Q
A

Atrial Flutter

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23
Q

Define Sinoatrial Block: Is this common?
*Talk about P-Waves, SV, and CO
*What becomes the New PM?
*PM if the new PM is blocked?

A

SA Node Blocked completely; Rare
*NO P waves, decreased SV and CO
*AV Node: 40-60 BPM
*Purkinje Fibers: 15-30 BPM

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24
Q

If P wave is late and Inverted, where is this source?
*can we see this?

A

Low AV Junction
*Mostly hidden by QRS complex, so probably not

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25
Q

If P wave is early and Inverted, where is this source?

A

HIGH AV Junction

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26
Q
A
  1. Premature Depolarization
  2. Repetitive Premature Depolarization
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27
Q
A

Sinus Bradycardia

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28
Q

What drug classes does Benadryl fall into?
*What heart arrhythmia can it cause

A

Antihistamine and Anticholinergic
*Tachycardia and PVC

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29
Q
A

Premature Contraction: Atrial Source

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30
Q

Predisposed to Afib: 2 Things

A

Age around 70 and Atrial Hypertrophy

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31
Q

Which is more dangerous: 2nd Degree Type 1 or Type 2?
*Tx for the more dangerous one?
*When do we usually “find” this Arrhythmia

A

Type 2
*Possible Pacemaker
*Preop EKG on Pt who hasn’t had one in a while

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32
Q
A

Ventricular Fibrillation

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33
Q
A

Torsades de Pointes

34
Q

How does Digoxin work

A

Block NaKATPase Pump, which increases Vrm by increased Na+ and Ca++ w/in the cell

35
Q
A

Sinoatrial Block

36
Q

What 3 things can cause a PAC

A

1.Ischemia
2. Irritation
3. Calcification

37
Q

Define Complete HB: 3rd degree
*What is the Ventricular Escape
*Is Atrial Rate faster or slower than normal? Why?

A

No correlation between P-Wave and QRS complex; total AV node or Bundle of His block
*15-30 BPM
*Faster than normal, as ANS tells heart to speed up Atrial contractions to compensate for poor CO

38
Q
A

Paroxysmal Atrial Tachycardia

39
Q

5 Causes of Cardiac Arrhythmias

A
  1. Abnormal Rhymic of PM [ectopic PM]
  2. Shift of PM from Sinus Node
  3. Blocks in cardiac transmission
  4. Abnormal Pathways of Transmission [hitting relative refract period]
  5. Spontaneous Generation of Abnormal Impulses
40
Q

What is a Cardiac Arrhythmia?

A

Problem with the Heart’s conduction system

41
Q
A

Ventricular Fibrillation

42
Q

2 Causes of Sinus Bradycardia

A

Vagal stimulation by PNS [can also decrease SNS, but not common]
Neural Reflex to Drugs [phenylephrine]

43
Q

Define A-Flutter: What type of Pathway
*Is this coordinated or uncoordinated
*Talk about P-Waves
*Is this a good or bad primer for the ventricles? Why

A

Circular reentry Pathway in Atria
*Coordinated
*NO P-Waves
*Bad Primer - leads to increased atrial and ventricle rates [cannot sync properly]

44
Q

Define a 2nd Degree Type 2 HB
*How long is the PR-Interval
*Which have fast rate: Atria or Ventricle?
*Describe the PR-Intervals

A

AV block that drops QRS complexes
*0.25-0.45 sec
*Atria rate is faster, as dropping QRS complexes
*PR-Intervals are FIXED RATIO

45
Q

Define a 1st degree HB

A

PR>0.20 seconds; longer time for atria to reach ventricles

46
Q
A

Incomplete Intraventricular Block: Alternans

47
Q
A

Atrial Fibrillation

48
Q

3 Causes of Sinus Tachycardia

A
  1. Hyperthermia [increased energy]
  2. Sympathetic Stimulation [loss of vagal tone, loss of blood, reflex stimulation]
  3. Toxic Conditions [Things that increase Vrm]
49
Q

If you have an increased resting HR, what could be 2 causes per lecture?

A

Hyperthyroidism or Valve issues

50
Q

Define Sinus Bradycardia
*What Pt. Pop is this commonly seen in? Why?
*BPM?

A

Abnormal SA nodal firing beats slower than normal
*Athletes who have a large SV; ANS tells Heart to slow down HR, as it has enough CO
*<60BPM

51
Q

6 Things that can cause Increased Vrm

A
  1. Hyperkalemia [decreased CG]
  2. Acidosis <7.4; Increased H, Increased Protons
  3. MI*
    4.Infarct*
  4. Ischemia*
  5. Drugs/Medications
52
Q

Define A-Fib
*What type of “movements”
*Is this coordinated or uncoordinated
*Talk about P-Waves
*Talk about Turbulence

A

Irregular “flutter” type electrical conductance in the Atria
*Ectopic PM and Circus Movements
*Uncoordinated
*No P-Waves
*Increased turbulence due to muscles contracting and relaxing in different “flutter” manner: Increased clot risk

53
Q
A

Complete Heart Block: 3rd Degree

54
Q
A

Incomplete Heart Block: 1st Degree

55
Q

What are PVC Precursors To?

A

Torsades, VFIB

56
Q

Overall, is having a higher or lower resting HR better?

A

Lower

57
Q

Define Stokes-Adams Syndrome
*Why do we pass out?
*What ventricular escape do we resume HR at?
*What is our seconds delay threshold until we pass out?

A

Fainting/Syncope due to an AV block that happens time to time
*We pass out due to the heart not pumping, so from hypotension
*15-30 BPM
*7-8 second threshold

58
Q
A

Incomplete Heart Block: 2nd Degree Type 2

59
Q

Which is worse: Afib or Aflutter? Why
*What medication type must the worst arrhythmia be “treated” with?

A

Afib, as it is uncoordinated, irregular electrical conductance
*Blood thinners

60
Q

How much longer does it take to depolarize the L ventricle compared to the R ventricle?
*Why

A

0.01 seconds
*More tissue

61
Q
A

Atrial Fibrillation

62
Q
A

Premature Contraction: AV Nodal/Bundle

63
Q

How do we end up in VFIB: No ventricular repolarization
*Talk about BP and BF

A

Atria BP low - Ventricle Output low - coronary BF low = No ventricular repolarization

64
Q

What are the 5 Things that can cause an AV Block
*Expand on Fibroblasts
*Expand on V and X reflex
*Expand on the meds listed

A
  1. Ischemia of AV node
  2. Compression of AV bundle [scar tissues from Fibroblasts in CHF/MI] = compression, which lowers AP conductance
  3. AV node inflammation
  4. Excessive Vagal Stimulation: V and X reflex
  5. Excess digitalis/BB: D - block NaKATPase Pump, leading to increased Vrm by Na+ and Ca++
    BB - inhibit cAMP, PKA
65
Q
A
  1. SA node
  2. Anterior Internodal System
  3. Middle Internodal System
  4. Posterior Internodal System
  5. AV node
  6. Interatrial Bundle [Bachman’s Bundle]
  7. Left Bundle Branch
  8. Right Bundle Branch
  9. Purkinje Fibers
66
Q
A

Incomplete Heart Block: 2nd Degree Type 1 Wenckebach

67
Q

Define IV Block: Alternans
*At which heartbeat does this occur
*What other arrhythmia will you most likely see this one?
*Causes of this?
*Talk a/b scar tissue and conduction speed in terms of QRS

A

Slowed conduction @ Purkinje System, as trouble repolarizing
*Every other HB
*VTACH
*Ischemia and Digitalis preventing the full repolarization of the Purkinje System
*Scar tissue/chronic depolarized = decreased conduction speed [longer QRS but less amplitude]

68
Q

Main difference between 2nd Degree Type 1 and Type 2 HB

A

Type 1: Variable PR-Int
Type 2: Fixed PR-Int

69
Q

Predisposed to AFlutter: 2 things

A

Slow conduction rate and Atrial Hypertrophy

70
Q

Ventricular Premature Depolarization:
*What does this look like on an EKG
*Talk about CO/SV
*3 Causes

A

Long QT syndrome
*Decreased CO/SV
*How sensitive Ca++ channels are [increased Beta agonist activity], mACh-R antagonists, Benadryl

71
Q

What are 4 Causes of PVCs

A

Caffeine, Nicotine, Stress, Lack of Sleep

72
Q

Any Increase in Vrm can cause what?
*What does this do to repolarization?

A

Risk of ectopic PM firing AP on its own
*delays it/prevents it

73
Q
A

Paroxysmal Ventricular Tachycardia

74
Q

Define a 2nd Degree Type 1 HB
*How long is the PR-Interval
*Which have fast rate: Atria or Ventricle?
*Describe the PR-Intervals
*Another Name for this?

A

AV block that drops QRS complexes
*0.25-0.45 sec
*Atria rate is faster, as dropping QRS complexes
*PR-Intervals are VARIABLE
*Wenckebach Periodicity

75
Q

Causes of R Axis Deviation

A
  1. Pulmonary Stenosis (R Vent Hypertrophy)
  2. RBBB
  3. Deep Breath (inspiration)
  4. R Vent Hypertrophy
  5. COPD
76
Q

Causes of L Axis Deviation

A
  1. LBBB
  2. L Vent Hypertrophy
  3. Decreased Lung Volume (expiration)
  4. Aortic Stenosis (L Vent Hypertrophy)
77
Q

Phrenic Nerve: Definition and Which Part of the Spine Involved

A

Bundle of Axons in the PNS
*C3, C4, C5

78
Q

Beta Agonist, in terms of inotropy, chrono, etc..

A

+ ino, chrono, dromo, luso

79
Q

Atenolol in terms of inotropy, chrono, etc..

A
  • ino, chrono, dromo, luso
80
Q

What 2 Main Things can Cause Circular Reentry, leading to VFIB

A

Slowed Conduction and Shorter Refractory Period

A&P 1 (24 decks)

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