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A & P > Exam 4 > Flashcards

Exam 4 Flashcards

Cardiac

1
Q

Is non-nodal cardiac muscle multi-unit or unitary?

A

Unitary (visceral)

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2
Q

How does non-nodal cardiac muscle communicate with one another?

A

Gap junctions

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3
Q

The “grooves” that allow for more placement of gap junctions between cardiac cells would be referred to as?

A

Intercalated discs

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4
Q

Are intercalated discs wide spread throughout all cells?

A

No, only found in the heart

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5
Q

Are cardiac cells multi-nucleated?

A

No, only one nucleus per cell

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6
Q

The sarcomere of Cardiac muscle is similar to that of?

A

Skeletal muscle

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7
Q

What are stem cells?

A

Cell regeneration (replaces old/dead cells)

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8
Q

Is stem cell replacement a fast or slow process in the heart? How would injury (MI) affect it?

A

Slow process
- Massive injury like an MI would be too great for stem cells to overcome

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9
Q

What are fibroblasts?

A

Cells that generate scar tissue

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10
Q

When do fibroblasts come into play?

A

When the stem cells are overwhelmed & can not repair injury

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11
Q

What are disadvantages of fibroblasts?

A

They dont contract or conduct APs (messes with conduction system)

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12
Q

What can excessive scar tissue lead to?

A

CHF

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13
Q

What type of drug is typically given to prevent scar tissue deposition?

A

ACE inhibitors

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14
Q

What is used as a growth factor for scar tissue placement?

A

Angiotensin II

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15
Q

What are benefits of ACE inhibitors?

A
  • afterload reducer
  • prevent growth factor of Angiotensin II on heart
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16
Q

Which population should stay away from ACE inhibitors & ARBs?

A

Pregnant women (angiotensin II used as growth factors - the babies need it)

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17
Q

Daddy compared the squeezing of the heart to what?

A

The ringing of a towel (Endocardial fibers & Epicardial fibers contract in different directions)

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18
Q

What is the syncytial connections as referred to in lecture?

A

Arrangement of heart muscle
- Top half –> Atria
- Bottom half –> ventricle (bellow AV)

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19
Q

What is the difference between Muscle tissue & Conduction tissue in the heart?

A

Muscle tissue:
- Can produce lots of force by having extra myofibrils

Conduction tissue:
- specialize in conducting APs
- no myofibrils (not used for contraction)

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20
Q

What is the deep cardiac muscle? (inner most) & what is also combined with this layer?

A

Endocardium
- endothelium combined with this layer

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21
Q

What muscle layer is the bulk of the muscle wall?

A

Myocardium

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22
Q

What is the outside layer of the heart? (superficial)

A

Epicardium

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23
Q

What layer of the heart are the major blood vessels sitting on top of?

A

Epicardium

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24
Q

What is the space just outside the epidcardium?

A

Pericardium

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25
Q

What is found in the Pericardium space?

A

Small amount of fluid & mucus

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26
Q

What role does mucus play in the Pericardium?

A

Allows for the heart to move around without causing friction (protective)

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27
Q

What can lead to friction in between the heart and the pericardium?

A

Inflammation or loss of fluid/mucus
- Friction is extremely painful

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28
Q

What are the 3 layers of the Pericardium & what are some characteristics?

A

Visceral Layer
- very thin, clear membrane
- allows heart to slide around Pericardium
connects to epicardium & parietal layer
- innermost

Parietal Pericardium
- Middle layer
- stretchy

Fibrous Pericardium
- outer layer
- Stiff, does not expand well (if fluid get in here it can cause issues as it does not expand well)

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29
Q

Which two layers of the Pericardium are apart of the Serous Pericardium?

A

Parietal Layer & Visceral layer

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30
Q

What is the muscle super deep in the muscle wall? (found in myocardium or endocardium)

A

Subendocardium

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31
Q

Where would an MI most likely take place?

A

Subendocardium

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32
Q

Where would our wall pressures be the highest?

A

Subendocardium (the deeper you go the harder it is to perfuse increasing pressure)

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33
Q

At rest the cardiac sarcomere is ___

A

under stretched (actin have a bit of overlap)

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34
Q

What are Purkinje fibers used for & what is their Vrm?

A

Conduction
-90 vrm

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35
Q

What is the ventricular muscle used for & what is its Vrm?

A

Contraction
-80 vrm

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36
Q

At rest both purkinje fibers & ventricular muscle are permeable to ..?

A

Na (not constant)

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37
Q

Most cardiac cells have the ability to __ if given enough time

A

Depolarize

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38
Q

What causes the resting membrane potential line to not be flat? (slight slope up)

A

Increased permeability of Na/Ca at rest (Vrm increases as time goes by)

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39
Q

What is the threshold for both Purkinje & Ventricular muscle?

A

-70

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40
Q

Purkinje fibers have the ability to generate their own AP, but what typically happens in a healthy heart?

A

The neighboring cell produced an action potential & caused the purkinje fiber to depolarize as normal purkinje fibers take a while to develop their own AP

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41
Q

If there is a complete atrial block, what will the purkinjes do? & how long will it take for generate?

A

The Purkinje fibers will generate their own APs, HOWEVER, there is a lag time for about 30secs to generate that first AP

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42
Q

What happens with repeated eye manipulation?

A

Vagal response –> drops HR
- pressure from manipulation sent to cranial nerve V (trigeminal) –> trigeminal sends message to brainstem cranial nerve X (Vagus) –> leads to massive vagal stimulation

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43
Q

How many phases are there in the ventrical electrical conduction?

A

5

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44
Q

What is phase 4 of a Ventricular muscle AP?

A

Vrm (has slight increasing slope caused by Na permeability)

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45
Q

What is phase 0 of a ventricular muscle AP?

A

Rapid up stroke dependent on fast sodium channels (dont stay open long) & we have K channels closing at this time (some stay open)

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46
Q

What is phase 1 ventricular muscle AP?

A

More upstroke - Fast calcium current through T-type channels

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47
Q

What is phase 2 of a ventricular muscle AP?

A

Plateau - caused by slow L-type calcium channels

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48
Q

What is phase 3 of a ventricular muscle AP?

A

Repolarization - slow L-type calcium channels close & K channels open back up

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49
Q

How long does a typical heart AP last?

A

200milisec

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50
Q

The duration of the AP in the heart is mainly determined by?

A

Calcium coming into the heart (phase 2)

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51
Q

Can K current ever be inward (into cell)?

A

DADDY SAID NO

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52
Q

What is Olms law?

A

Voltage = Current x Resistance

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53
Q

What is ionic current dependent on?

A

how many channel are open & electrochemical gradient

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54
Q

What does the right side of the vagus nerve connect to?

A

SA node

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55
Q

What does the left side of the vagus nerve connect to?

A

AV node

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56
Q

What is the main emphasize of the parasympathetic on the heart?

A

suppression of nodal areas of the heart through ACh on m-ACh-R

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57
Q

What is the role of the sympathetic nervous system on the heart and how?

A

It is more widespread on the heart & does have some affect on nodal areas through
- has thick connections with atrial & ventricular muscle releasing catecholamines (NE - is the main one) affecting B receptors

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58
Q

What is the high point (mV) of depolarization of ventricular muscle?

A

+20 mV

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59
Q

What is the difference in mV between vrm & the high point of a ventricular myocyte?

A

100mV

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60
Q

What does an EKG measure?

A

The sum of all the current flowing between 2 electrodes placed on the body

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61
Q

What is the total mV of healthy QRS complex?

A

about 1.5 mV (about 3 big boxes)

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62
Q

Where do we lose a lot of voltage?

A

Tissue (air, fat)

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63
Q

Why would we see a lower QRS complex in a pt with COPD?

A

pts lungs are hyperinflated & air does not conduct electricity –> reducing voltage –> smaller QRS

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64
Q

Angiotensin II is a growth factor similar to that of?

A

Vegetative endothelium growth factor (doubt we will need to know this but it was a response to a question someone asked)

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65
Q

Would we have reduced hound healing with ACE inhibitors?

A

No, there is enough growth factors to promote wound healing

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66
Q

What are the type of K channels that close in response to an influx of cations? & why do they close?

A

Inward rectifying Potassium channels
- close in response to influx of cations to increase length of contraction/AP/depolarization in the heart

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67
Q

Electrons moving towards a positive electrode would have a? (Away from a negative electrode)

A

Positive deflection

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68
Q

Electrons moving away from a positive electrode would have a? (towards a negative electrode)

A

Negative deflection

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69
Q

In a resting cell, if electrodes were placed, what would the meter read & why?

A

0
- there would be no charge difference between the two electrodes

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70
Q

If there was a slight change in polarity caused by depolarization going towards the positive electrode, what would the meter read & why?

A

The meter would read slightly positive as electrons would be moving towards the positive electrode making the inside of the tissue slightly positive & the outside slightly negative

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71
Q

If half of the tissue was depolarized going towards the positive electrode how would that read on a meter & why?

A

The meter would read the most positive/highest
- the electrons would have the most current & the most motive to spread

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72
Q

If majority of the tissue was depolarized going towards the positive electrode how would that read on a meter & why?

A

The meter would read slightly positive
- the electrons would still have current but the motive to spread would not be as great as majority of the tissue is depolarized

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73
Q

If the entire tissue is depolarized how would that read on a meter & why?

A

The meter would read 0
- there is no longer a charge difference between the two electrodes

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74
Q

If slight repolarization occurred away from the positive electrode what would the meter read & why?

A

The meter would read slightly negative
- the electrons would be moving away from the positive electrode but would not have a lot of current

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75
Q

If half of the tissue was repolarized away from the positive electrode what would the meter & why?

A

The meter would read the lowest/most negative (greatest negative deflection)
- the electrons would have the greatest current & motive moving away from the positive electrode

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76
Q

If majority of the tissue was repolarized away from the positive electrode what would the meter read & why?

A

The meter would read slightly negative
- the electrons would still have current away from the positive electrode but the motive would be diminished as majority of the cell is repolarized

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77
Q

If the entire tissue was repolarized (resting state) how would that read on a meter & why?

A

The meter would read zero
- there would no longer be a charge difference between the two electrodes

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78
Q

Depolarization occurring towards a positive electrode would have what type of deflection on an EKG?

A

Positive

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79
Q

Repolarization occurring towards a positive electrode would have what type of deflection on an EKG?

A

Negative

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80
Q

Repolarization occurring away from positive electrode would have what type of deflection on an EKG?

A

Positive

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81
Q

How does the slope of phase 4 in nodal tissue compare to that of a phase 4 slope in ventricular muscle?

A

The slope in Nodal is much greater in phase 4

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82
Q

What is another term used to describe phase 4 in nodal tissue?

A

Diastolic Depolarization (Depol.)

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83
Q

The faster the rate of Diastolic Depol. the faster the __?

A

HR
(if it depolarizes faster we should be able to reach threshold faster –> generate faster APs)

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84
Q

How does Phase 0 of nodal tissue compare to that of ventricular muscle?

A

Nodal tissue
- less drastic upstroke compared to ventricular muscle as nodal tissue does not use fast Na channels –> uses L-type calcium channels

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85
Q

What does the use of L-type calcium channels do to an AP in the heart?

A

Extends APs
- L-type calcium channels slow to open & slow to close

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86
Q

What is importance of the slope in phase 0?

A

Determines how fast AP will move to next cell
- steep slope –> Fast AP propagation
- low climbing slope –> Slow AP propagation

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87
Q

How does AP propagation differ in the Atria vs Ventricles?

A

Atria propagation is slower as it uses slow L-type channels

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88
Q

what occurs in Phase 3 of an AP in nodal tissue?

A

Repolarization
- L-type calcium channels close
- VG K channels open

(some books say phase 2 is a little plateau before phase 3 but daddy said no)

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89
Q

Why does the AV node not have as fast of automaticity as SA node?

A

AV node has a lower Vrm –> takes longer for it to generate its own APs

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90
Q

HCN channels can be found in SA, AV & ventricular muscle
List them in order from the most to least HCN channels

A

Highest in SA, then AV & very few in Ventricular muscle

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91
Q

Why do the APs in the deep muscle differ from the APs in the superficial muscle?

A

Depolarization begins in the deep muscle & works its way out
Repolarization begins superficially & works its way in

It also aids in contraction as the later start of the epicardium allows for unison

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92
Q

How does the Action potential differ from the deeper parts of the ventricular muscle (subendocardium) vs that of the superficial muscle (epicardium)

A

Deep ventricular AP
- depolarization starts sooner
- repolarization last longer

Superficial ventricular AP
- Depolarization starts later
- repolarization ends sooner

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93
Q

What are some characteristics of Atrial muscle APs?

A

Fast upstroke & fast repolarization
- only contract for a short period of time as they only need to pump into the ventricle with little resistance
- atrial walls are thin allow for APs to reach entire atria quickly

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94
Q

How long does it take the SA node to generate rate its own AP?

A

0.83 seconds

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95
Q

The SA on its own without any vagal stimulation will generate how many bpm?

A

110 bpm

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96
Q

If you add normal SNS activity to SA node how many BPMs with out vagal stimulation?

A

120 bpm

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97
Q

How many bpms if the SA is only stimulated by vagal & not SNS?

A

60-62 bpm

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98
Q

How many bpm does the AV node generate?

A

40-60 bpms

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99
Q

What allows for conduction between the SA node to the AV node? (What three pathways?)

A

Internodal Pathways (3 of them)
- Posterior (right side)
- Middle (middle duh)
- Anterior (left side)

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100
Q

How many APs can the Purkinje system generate?

A

15-30 bpm

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101
Q

What comes off the anterior nodal pathway?

A

Interatrial bundle (Bachmann’s)
- conducts APs to the left atria

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102
Q

How long does it take for an AP to reach the AV node from the SA node?

A

0.03 secs

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103
Q

How long does it take for the entire right atria to depolarize?

A

0.07 secs

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104
Q

How long does it take for the entire left atria to depolarize?

A

0.09 secs
- This is the Duration of the P-wave as at this point entire atria should be depolarized in normal heart

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105
Q

When Dr. J says “top half of heart” what is he referring to?

A

Atria

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106
Q

How long should it “ideally” take for AP to reach the entirety of the heart from the SA node?

A

0.22 secs

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107
Q

Where do ventricular depolarizations start? Where do they travel to?

A

Start in the deeper areas of the ventricle and travel superficially

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108
Q

Ventricular muscle depolarizes ____ to ____

A

Deep to Superficial

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109
Q

The P wave is the ___polarization of the ____

A

Depolarization of atria

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110
Q

The QRS wave is __polarization of the _____

A

Depolarization of ventricles

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111
Q

The T wave is ___polarization of the ______

A

Repolarization of the ventricles

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112
Q

Despite repolarization being the reverse of depolarization, the T wave is still ____. The reason is that the _____ repolarizes before the ____.

A

Positive; Epicardium repolarizes before endocardium

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113
Q

The conduction system is ____ in the heart wall.

A

Deep

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114
Q

Depolarization of the ventricles is a ____ deflection.

A

Positive

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115
Q

If electrons are going towards the positive electrode, it shows up as a ____ deflection. If they are going away from the electrode, it is a ____deflection.

A

Positive.

Negative.

Tylerism - if you add something, it’s +1, or positive (electron going to the electrode)
If you take something away, it’s -1, or negative. The electron is going away from the electrode.

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116
Q

What is a current of injury?

A

If the heart muscle has an area that is ischemic (i.e. infarct), it will not reset. It is chronically depolarized. There is a current present due to depolarization that should not be there. A current of injury refers to the area that is stuck depolarized.

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117
Q

What tool can we use to find current of injury, or any electrical abnormality in the heart?

A

12 lead EKG

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118
Q

What about the 12 lead EKG allows us to find where current of injury is?

A

Many different perspectives/views available from 12 leads, allows us to pinpoint the area.

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119
Q

What causes the delay at the AV node?

A

AV node has fat which doesnt conduct well & AV node does not have very many gap junctions leading to more delay

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120
Q

Which generates a faster action potential, the SA or AV node?

A

SA node - it is easier to depolarize, thus has a higher rate of depolarization.

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121
Q

What is the normal HR in a healthy individual?

A

72 BPM

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122
Q

What is the Vrm of the SA node?

A

-55mV

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123
Q

What is the threshold for the SA node?

A

-40mV

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124
Q

Can the purkinje system generate action potentials?

A

Yes, if we wait forever. It is reliant on slow Na/Ca channels (assuming SA/AV does not work)

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125
Q

How long is the delay at the AV node?

A

0.12 sec

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126
Q

The SA node is fairly permeable to __ and __. What kind of channels?

A

Na & Ca

Leak & HCN channels

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127
Q

What does HCN channel stand for? How does it work?

A

Hyperpolarization Cyclic Nucleotide mediated channel

A few open when reaching Vrm (phase 4). More and more open throughout phase 4, leading to a sloped line until threshold.

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128
Q

How long is the delay at the Bundle of His (penetrating bundles)?

A

0.01 sec

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129
Q

How long does it take for an AP to go from SA node to intraventricular septum (start of Bundle branches)?

A

0.16 sec

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130
Q

What does the current of HCN channels consist of? Which one has the strongest current?

A

Na, K, Ca (nonspecific to cations).

Sodium has the strongest current because it is small.
Calcium also flows through, but is clunky so not as much.

K does flow through, but mostly takes other routes to get in/out of the cell.

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131
Q

What is the angle of a typical heart beat?

A

59 degrees

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132
Q

Can HCN channels be controlled? If so, by what?

A

Yes, by beta receptors and mAch-R.

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133
Q

How do beta agonists control HCN channels? What does this lead to?

A

Beta agonists act on adenylyl cyclase, producing cAMP which is a cyclic nucleotide. Cyclic nucleotides work on HCN channels.

By increasing beta activity, cAMP increases, thus opening more HCN channels.

This leads to a steeper phase 4 slope –> less time in phase 4 –> Faster HR

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134
Q

How do beta antagonists control HCN channels? What does this lead to?

A

Decreased adenylyl cyclase activity –> Decreased cAMP –> Decreased phase 4 slope –> Longer time in phase 4 –> reduced HR

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135
Q

How do mACh-R control HCN channels?

A

MACh-R reduce activity of cAMP, which reduces PKA activity, which reduces HCN sensitivity. This decreases calcium influx and decreases heart rate.

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136
Q

What is physiologic antagonism in regard to the heart?

A

If beta agonistic activity is happening, we will have activation of mACh-R.

Beta adrenergic activity will close mACh-R K channels.

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137
Q

A small amount of hyperkalemia will result in ____. Why?

A

A faster heart rate; Higher K outside of the cell –> Less gradient –> Vrm is more positive

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138
Q

How do calcium levels change threshold potential?

A

Not even daddy knows; lots of excess Ca (within reason) increases threshold potential. It takes a longer period of time in phase 4 to reach threshold, which slows down HR in a healthy person.

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139
Q

A calcium deficiency would result in a ______ heart rate.

A

Faster; Reduced calcium in the blood makes the threshold more negative, leading to shorter phase 4 –> Faster HR

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140
Q

If the P wave is high, you have a problem with the ___ side of the heart.

A

Right

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141
Q

What is the average length & amplitude of a p-wave generated by the SA node?

A

2.5 long & 2.5 tall (positive deflection)

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142
Q

If an AP were to be generated by the AV node what kind of deflection would get on an EKG & why?

A

Negative Deflection
- depolarization is going up atria to SA node (away from positive electrode)

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143
Q

What would be the typical cause of a high P wave?

A

Atrial hypertrophy
(more tissue = the larger the deflection)

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144
Q

If we have a high P wave, which side of the atria is the probable cause for it?

A

Right atria

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145
Q

What would be the typical cause of a long P wave?

A

conduction issue –> typically Atrial dilation

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146
Q

If we have a long P wave, which side of the atria is the probable cause for it?

A

Left Atria

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147
Q

What is the typical cause of a P wave with a hump?

A

Conduction issue, an electrical block is preventing proper spread to left atria

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148
Q

If the P wave is long, you have a problem with the ___ side of the heart.

A

Left

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149
Q

The __ wave is a ____ deflection before a R wave.

A

Q wave; negative deflection

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150
Q

A ___ wave is a ____ deflection ____ the baseline that corresponds to the ____ of the ventricles.

A

R wave; positive deflection; above baseline; corresponds to the depolarization of the ventricles

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151
Q

Does every lead have a Q wave? Why is this important?

A

No; The period of time between the start of the P wave and initiation of ventricular activity is the PR interval. It is TECHNICALLY PQ, but we don’t always have PQ on every lead so we call it PR)

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152
Q

How long is the PR interval, and what does it represent?

A

0.16 seconds; time from SA to interventricular septum

153
Q

The ___ wave is a ___ deflection after the R wave.

A

S; negative

154
Q

How long does it take for the last bit of ventricular muscle to depolarize?

A

0.22 seconds

155
Q

How long is the QRS? What does it represent electrically? How do we get this number?

A

0.06 seconds = QRS

Represents ventricular depolarization

(Last ventricular muscle depolarization - time it takes to go from SA to ventricular septum = QRS)
0.22sec - 0.16 sec = 0.06 sec

156
Q

The QRS is 0.06 seconds. Is this the goal? Does it usually take longer or shorter?

A

While 0.06 seconds is ideal, it typically takes a bit longer.

157
Q

What causes the average person to have a longer QRS?

A

The average person has a little more heart tissue present. More heart tissue = more resistance.
This is caused by caffeine + HTN. Typically this leads to a QRS >0.08seconds.

158
Q

What is the normal height of the QRS? How high up from baseline, and how far below baseline?

A

1.5mV

Per Schmidt: +1mV up, -0.3mV down.

He also said 5 large boxes, but that doesn’t really check out.

159
Q

If we have a very tall QRS, what is it, and could be the cause?

A

High voltage

Electrodes could be really close to the heart (less tissue between the heart and the leads)

OR

There is more heart tissue present. More heart tissue = higher voltage.

160
Q

What would extend the QRS? Why?

A

Dilated cardiomyopathy (stretched ventricles without extra size)

More distance for AP to travel

161
Q

Where does the atria repolarize?

A

Somewhere between R and S –> obscured by the QRS complex

162
Q

Between the QRS and the T wave, the ventricles should be _____. Why is this important?

A

Depolarized (muscle + conduction system)

This is a reference area to find current of injury.

163
Q

What is the area immediately after the QRS called? What other name does it have? (after the upstroke of S)

A

J point; Isoelectric point

164
Q

If we have an ischemic area of the heart, will it be depolarized or repolarized?

A

Depolarized - injured tissue cannot repolarize.

165
Q

True/false = At the J point, healthy ventricular tissue is depolarized as well as ischemic/unhealthy tissue.

A

True.

166
Q

After repolarization of the ventricles (T wave), is ischemic tissue repolarized as well?

A

No; ischemic tissue is unable to repolarize.

167
Q

Ischemic, depolarized tissue will be the source of ___ _____ after the T wave on EKG.

A

Odd tracings

168
Q

Comparing the __ ____ and the point past the T wave allows us to identify ischemic areas of the heart.

A

J point

169
Q

Coronary arteries get blood during ____.

A

Diastole.

170
Q

What is the QT interval?

A

Time from the start of depolarization in the septum/ventricle until the point that all tissue is repolarized.

171
Q

How long is the QT interval? (Start of Q, end of T)

What else shares this time in the heart?

A

0.25-0.35 seconds

This is the duration of the action potential within ENDOcardial heart tissue. (Endocardial first to depolarize, last to repolarize in the ventricle)

172
Q

The T wave has an _____ deflection. It represents _____ of the ventricle, which spreads from the ____ layer to the ____ layer of ventricular muscle.

A

Upward (positive on normal EKGs)

Repolarization

Epicardial to endocardial

173
Q

When we have a physiologic increase in HR, what happens? What is this called?

A

Shortened RR interval (thus shortening QT) –> ventricle repolarizes sooner –> Fires AP sooner –> Faster HR

Lusitropy (How fast the resetting process is; usually shaves time off the ST segment as well)

174
Q

A positive Lusitropic drug would do what?

A

Make the heart reset faster, thus raising HR. It reduces the time before the P wave as well.

175
Q

What is Inotropy? What ion influences this?

A

Strength of contraction; Calcium (more in heart, more inotropy)

176
Q

What is Chronotropy?

A

HR

177
Q

What is Dromotropy? What is it dependent on?

A

Speed of conduction of action potentials.

Dependent on Na current (more Na = faster transmission)

178
Q

What is Lusitropy?

A

Resetting the heart after AP

179
Q

What is the RR interval?

A

Time between two QRS complexes

180
Q

How do you calculate HR based on RR interval?

A

(60 seconds in a minute) divided by RR interval (0.83 seconds) = HR (which is 72bpm on average)

181
Q

What is the typical RR interval?

A

0.83 seconds

182
Q

You are on the Planet X-71. One minute is 90 seconds on this planet. Assuming a human landed on this planet and had normal physiology, what is their HR on Planet X-71?

A

90 divided by 0.83 seconds (RR interval) = Roughly 108BPM on Planet X-71.

Doing this card just in case Daddy is mean

183
Q

On an EKG strip, what axis is mV found on?

A

y-axis (up and down)

184
Q

How many mV is a big box on an EKG?

A

0.5mV

185
Q

How many small boxes make up a big box on an EKG?

A

5

186
Q

How many mV is a small box on an EKG?

A

0.1mV

187
Q

How was modern EKG timing determined? Why don’t we use paper anymore; what was the logistical challenge?

A

Old EKG machines fed paper into the EKG machine at 25mm/sec.* The boxes were designed to work with the old EKG paper.

Storing massive amounts of paper was a logistical problem, as it needed to be stored as long as a facility was open.

188
Q

How many seconds is a big box on an EKG?

A

0.2 seconds

189
Q

How many small boxes are in a big box on the x-axis of an EKG?

A

5

190
Q

Time is on what axis of the EKG?

A

X-axis (left/right)

191
Q

How many seconds does a small box contain on an EKG?

A

0.04 seconds (1/5 of 0.2 seconds)

192
Q

When did Schmidt use the old EKG machines? What animal did he experiment on?

A

His lab at his old school. He experimented on goats.

193
Q

What is the refractory period?

A

After an action potential, the heart has to reset itself. That is this period.

194
Q

If you stimulate the heart during the absolute refractory period, what happens? Why?

A

Nothing. You can’t generate an action potential as the cell is not reset, even with outside electrical sources.

195
Q

What happens if you stimulate the heart during the relative refractory period? What is significant about this?

A

The cell is repolarized enough to give a small action potential, though the contraction will be considerably weaker.

This is why we want coordinated electrical activity - mechanical pumping is messed up if we have abnormal electrical activity.

196
Q

What is an early premature contraction?

A

The heart is completely reset, so an action potential is generated. The action potential starts during the relative refractory period - contraction will be weak/kind of suck.

197
Q

What is a later premature contraction?

A

The heart was stimulated after the refractory period. The heart was fully reset. An action potential is generated with a full force contraction.

198
Q

What is Einthoven’s Law? What must be subtracted?

A

Lead I + Lead III = Lead II

Subtract the negative deflection part of the QRS; only include the positive deflection.

199
Q

Which standard limb lead has the largest positive deflection in a healthy person?

A

Lead II

200
Q

Does Einthoven’s Law always work?

A

Yes - Adding the positive deflection of lead I & III will always equal the positive deflection of lead II at any given time.

201
Q

Which standard leads have a negative Q wave deflection, & which one has the greatest negative deflection?

A

Lead I & Lead II
- lead 1 had the greatest negative Q wave deflection

202
Q

Which Standard limb lead a positive Q wave?

A

Lead III

203
Q

What is the mean electrical axis of the ventricular septum?

A

59 degrees (right shoulder to left foot)

204
Q

The net deflection will be roughly the same for what two standard limb leads?

A

Lead I & III.

205
Q

In leads such as aVR, aVF, or aVL, what does the lowercase a stand for?

A

Augmented

206
Q

What is the first part of the ventricular septum to depolarize? Which direction is the current flowing at the very start of this? Why is this significant?

A

The left side of the septum.

Towards the right; this is what causes a Q wave.

Source: CV physiology book Ch 4. page 89

207
Q

Which ventricle is thinner? Why?

A

Right; only has to pump against pulmonary circulation.

208
Q

Which ventricle is thicker? Why? What does this imply with electrical activity?

A

Pumping against SVR; It takes a longer time (0.22 seconds) for the action potential to reach the last area of ventricular muscle. This is because it is the furthest from the AV node and has lots of tissue to travel through.

209
Q

What area of the ventricle is the last to depolarize?

A

LEFT top part of the left ventricle (think: end of purkinje fibers)

210
Q

Where is the main bundle branch?

A

Interventricular septum

211
Q

During depolarization, what direction is charge going? (negative vs positive)

A

Negative is going to the outer portion of the heart, positive is inside the heart.

212
Q

What direction does the mean electrical axis of atrial P waves go? Positive or deflection? Why?

A

Left foot; Positive; electrical axis is going to left POSITIVE lead (left foot)

213
Q

The electrical axis from the SA to AV node would be to the

A

left foot

214
Q

If we had aberrant electrical activity from the AV node that happened to fire backwards through gap junctions, what would be the net deflection of the atria?

A

Negative

215
Q

In the atria, does repolarization happen in the same sequence/direction as depolarization?

A

Yes

216
Q

Is repolarization of the atria a positive or a negative deflection? Why? Can we see this?

A

Negative deflection; heading away from the left foot for repolarization (toward negative lead in right arm)

No - p wave repolarization is obscured within QRS complex

217
Q

What is the advantage & disadvantage of Gap junctions?

A

Advantage
- Fast (no need to wait for neurotransmitter)

Disadvantage
- AP can travel either way (so if a part of the heart is generating an AP when it shouldnt - Rogue AP will travel with relative ease in wrong direction)

218
Q

What is a safe guard that helps prevent unwanted APs?

A

The refractory period
(helps prevent unwanted APs by not being able to fire another AP until a certain time)m

219
Q

What are other terms used for the view of the 3 lead setup?

A

Frontal plane & Coronal plane

220
Q

Are the atria thin or thick compared to the ventricles? Why? What is the implication in regard to voltage?

A

Think; much less muscle than the ventricles;

Less muscle mass = less voltage. AKA, does not have

221
Q

Right to left movement on the axis will increase amplitude of which lead? What determines this axis?

A

Lead I

Direction of the heart (changes with inspiration, COPD, etc)

222
Q

When the ventricles are 50% depolarized, is it a positive or a negative deflection on EKG?

A

Positive - strongest positive current at this point. The current is flowing toward the positive lead II (left foot).

223
Q

When more than 50% of the ventricle is depolarized, will the QRS be in an upstroke or downstroke? Why?

A

Downstroke, but still positive;

Not as much real estate for electrons to move to –> less current

224
Q

When more than 50% of the ventricle is depolarized, will each lead look different? Why?

A

Yes;

Different parts of the ventricle are depolarized. Each lead gives a different view. It would follow that the tracings may be a little different.

225
Q

When nearly all of the ventricle is depolarized, will it show as a positive or negative deflection on EKG? Why?

A

Lead I - will show positive as current is still moving left to right
Lead II - will show negative as current away from the positive electrode
Lead III - will show negative as current is moving the opposite direction

226
Q

When nearly all of the heart is depolarized, what happens to the axis? What happens in each lead as a result?

A

The axis is shifted to the left arm, as it is trying to depolarize the last bit of the left ventricle.

Lead I - Positive deflection (right to left)
Lead II - Small negative deflection (S wave)
Lead III - Negative deflection (moving away from positive lead)

227
Q

When nearly all of the heart is depolarized, what is unique about lead I? How about lead III?

A

Lead I - There is no Q wave; there is a positive deflection.

(NEED TO EDIT THIS**^^ I think I mistyped, will fix over the weekend) did he ever fix it? the world may never know

Lead III - Significantly more negative deflection than the other leads, as current is headed the opposite direction as the positive lead.

228
Q

Which lead is least likely to have an S wave in a healthy person?

A

Lead I

229
Q

When the heart is fully depolarized, is there a negative or a positive deflection?

A

Neither - net 0mV in a healthy heart. The mV is at the isoelectric line in this case until repolarization (T wave)

230
Q
A
231
Q

Which lead would give you the best view of depolarization in a healthy heart & why?

A

Lead II
- depolarization of a healthy heart travels at a 59 degree angle which almost parallels the angle view of lead II

232
Q

What is the angle view lead II gives us?

A

60 degree angle
- Diagonal view n

233
Q

Where is the lead placement for lead II in a 3 lead setup?

A

Negative lead goes on right arm/shoulder
Positive lead goes on left hip

234
Q

Where is the lead placement for lead I in a 3 lead setup & what is the angle view?

A

Positive electrode goes on left arm/shoulder
Negative electrode goes on right arm/shoulder
- angle is 0 (or 360) horizontal view going left to right

235
Q

Where is the lead placement for lead III in a 3 lead setup & what is the angle view?

A

Positive electrode goes on left hip
Negative electrode goes on left am/shoulder
- angle view is 120 –> diagonal reading from left shoulder/arm to left hip

236
Q

What is Einthoven’s triangle?

A

The triangular view that is formed with the 3 lead setup

237
Q

In lead I, what would be described as a left axis deviation (counterclockwise) ?

A

Anything that causes the axis to change less than 0

238
Q

In lead I, what would be described as a right axis deviation (clockwise) ?

A

Anything that causes the axis to change greater than 0

239
Q

What are somethings that can change the orientation of the heart?

A

Bundle branch block, COPD, ventilation, changes in position of the heart

240
Q

A large inhale can change the orientation of the heart in which direction?

A

To the right
- (right axis deviation)

241
Q

A large exhale can change the orientation of the heart in which direction?

A

To the left
- (left axis deviation)

242
Q

If the normal mean axis of the heart (59 degrees) is shifted counterclockwise, what can of deviation is this?

A

Left axis deviation

243
Q

If the normal mean axis of the heart (59 degrees) is shifted clockwise, what can of deviation is this?

A

Right axis deviation

244
Q

What is the clinically accepted deviation range?

A
  • Greater than 90 degrees (right axis deviation)
  • Less than 0 degrees (left axis deviation)
245
Q

For daddy’s class, what is the accepted deviation range?

A

Anything greater or less than 59 degrees
(mean axis)

246
Q

A positive degree axis means the rotation is moving which direction?

A

Clockwise

247
Q

A negative degree axis means the rotation is moving which direction?

A

Counter clockwise

248
Q

Why does the left ventricle take longer to depolarize compared to the right ventricle?

A

The left ventricle is thicker & has more muscle

249
Q

Why does the left lateral portion of the ventricle take the longest to depolarize?

A

It is the furthest away from the SA node
- depolarization moves down septum then up laterally & goes from deep to superficial

250
Q

Repolarization of the P wave happens towards the positive electrode resulting in a ___ deflection

A

Negative

251
Q

Depolarization of the atria caused by the AV node travels in which direction?

A

Both Directions
- travels down Septum & back up atria

252
Q

Which lead has the Largest deflections (P wave, QRS, & T wave)

A

Lead II

253
Q

Why is the deflection in Lead I smaller than that in lead II?

A

The normal axis deviation is 59 degrees moving diagonally & slight to the left
- the right to left movement is picked up by lead I but the current is much less resulting is small deflections

254
Q

How could we determine how much current is moving from right to left? (positive deflection)

A

You could use the mean axis of lead II (60 degrees) to connect to the mean axis of lead I (0 degrees) & form a triangle & using Pythagoreans theorem to find the lengths of each side of the triangle which would give you the voltage

255
Q

How could we determine how much current is moving from left to right? (negative deflection)

A

Again using Pythagoreans theorem except use lead III (120 degrees) to connect to lead I (0 degrees) & find the lengths of the triangles which would give you the voltage

256
Q

If the mean axis orientation was pointed straight down (90 degrees) what should we see in leads II & I?

A

Lead I should read nothing/0 –> no deflection as there is no right to left movement
Lead II should still have deflection as the current is still picked up by Lead II & III

257
Q

If the net electrical axis was pointed to the left what would we see on lead I?

A

Lead I would have a larger deflection as there would be more right to left current moving towards the positive electrode

258
Q

Where are leads V1 and V2 placed?

A

4th intercostal space

259
Q

Where are leads V4-6 placed?

A

5th intercostal space

260
Q

Where is lead V3 placed?

A

Between leads 2 & 4

261
Q

What is a vectorcardiogram? Do we use this anymore?

A

Oldschool way to see electrical activity of the heart - worked by vectors of electrical activity in real time. The pattern went in an oval shape.

No, it’s old

262
Q

Is the T wave a positive or negative deflection?

A

Positive normally

263
Q

What is the first part of the ventricle to reset?

A

Epicardium

264
Q

The general tendency of electrical current of the heart goes to the

A

Left foot

265
Q

Within the epicardium, what part of the ventricle resets first?

A

The very tip of the bottom of the heart

266
Q

The T wave will show ______ in leads I, II, and III.

A

A small positive deflection

267
Q

What does an inverted T wave mean in terms of electrical activity of the ventricles? Is this efficient? Why?

A

Normally, depolarization and repolarization goes the opposite way in the ventricles (endocardium to epicardium, epicardium to endocardium).

When the ventricles depolarize and repolarize in the same direction, you would have an inverted T wave. This is due to current going the opposite way of the positive lead on the left foot.

Not efficient - problem with timing, thus problem with optimal blood flow in the heart.

268
Q

What is a biphasic T wave?

A

T wave is half up, half down. Daddy says don’t bother knowing why - just know something is messed up, and we would like for it to go away.

269
Q

When taking an abnormal EKG and plotting it out to determine axis deviation, what leads do we use?

A

Leads I and III determine mean electrical axis

270
Q

When plotting out axis deviation on a given set of EKG strips, what are we looking for other than deviation?

A

Conduction problems; ischemia problems

271
Q

When drawing vectors, does size matter?

A

Yes; bigger the size, bigger the current.

272
Q

What axis deviation would right ventricular hypertrophy cause? Why? What lead will this be especially apparent in? Would this lead have a smaller or larger deflection?

A

Right axis deviation; More tissue on the right side of the heart –> longer time to depolarize. This means that the left ventricle will finish depolarizing before the right, and the mean electrical axis will shift to the right.

Lead I - lead I views right to left movement. Changing the axis directly impacts the magnitude of lead I. It will have a larger positive deflection.

273
Q

What does it mean when you see “rabbit ears” in your QRS complex?

A

Bundle branch block

274
Q

If you have a left axis deviation with abnormal electrical activity in lead III, what would this imply?

A

Left bundle branch block

275
Q

How do our bundle branches work? What is a bundle branch block?

A

Action potentials are propagated through bundle branch blocks and depolarize the right and left ventricle at nearly the same time. The left ventricle takes slightly more time due to increased tissue mass.

A bundle branch block has some sort of resistance/blockage of action potential within one of the bundle branches, leading to unequal depolarization of the ventricular walls. This shifts the mean axis to whatever side the block is on, which will manifest as EKG changes in mV.

276
Q

A right axis shift would do what to lead III? What could be the likely cause?

A

Large QRS

Ventricular hypertrophy

277
Q

A right axis deviation would mean what in regard to depolarization of ventricles?

A

Right ventricle is taking longer to depolarize

278
Q

A current of injury would show up in what way on an EKG?

A

ST depression or elevation.

279
Q

What area do we look at on an EKG to diagnose electrical abnormalities such as ST elevation/depression?

A

j-point

280
Q

The heart has to do what to conduct an action potential to get another heart beat/contraction?

A

Repolarize (remove sodium from the cell)

281
Q

Repolarization requires _____. When is this a problem?

A

Energy (Na/K/ATPase pump, Ca channels, etc)

Ischemic injuries. If we have an energy deficit such as a MI, the tissue is not getting needed energy. It then stays depolarized. This is referred to as the area of injury.

282
Q

What happens to the electrical current of the heart with an area of injury/current of injury?

A

Current flows from injured area to the resting areas; occurs at a time when the ventricles should be reset. This shows up funny on EKG; especially after the T wave and before the P wave. This is called a current of injury.

283
Q

Where do we expect to see no current on a normal EKG?

A

Between the end of the T wave and the beginning of the P wave.

284
Q

What should be happening between the end of the T wave and the beginning of the P wave?

A

Nothing. The atria and ventricles should be resting. There should be no current in a healthy heart until depolarization of the atria.

285
Q

What are the two important components of the vector (Arrow)?

A
  • Angle of the arrow
  • Size of the arrow
286
Q

Arrow pointed towards a positive lead would read as a?

A

Positive deflection

287
Q

Arrow pointed towards a negative lead would read as a?

A

Negative deflection

288
Q

An arrow that is perpendicular to the positive/negative electrode would read as?

A

Nothing, no deflection

289
Q

What does the Q wave represent on the EKG

A

The initial depolarization of the bundles branches of the left lateral ventricular side of the intraventricular septum
- initial depolarization heads toward right arm

290
Q

What would the Q wave look like in each of the three leads?

A

Lead I - Negative deflection (largest negative deflection)
Lead II - slightly negative deflection
Lead III - positive deflection (no Q wave)

(NEED TO EDIT THIS ONE) - no u dont its perfect bb

291
Q

Which lead will have the largest R wave in a healthy heart?

A

Lead II

292
Q

In the augmented leads what does a, V & the last part stand for?

A

a - augmented
V - voltage being used
third part tells us what part of the body has the positive electrode

293
Q

Where the leads position for aVR? what angle view does it give us? What do the deflections typically look like?

A
  • positive electrode – right arm
  • negative electrode – combination of left arm/left leg
  • 210 degree angle view
  • Majority of current moving away from positive lead – negative deflections
  • sees between leads I & II
294
Q

Where the leads position for aVL? what angle view does it give us?

A
  • positive electrode – left arm
  • negative electrode – combination of right arm/left leg
  • Gives us 150 degree angle view
  • sees between leads I & III
295
Q

Where the leads position for aVF? what angle view does it give us?

A
  • Positive electrode – Left foot
  • negative electrode – combination of left arm/right arm
  • 90 degree angle view (stares straight up)
  • sees between leads II & III
296
Q

What type of deflections would you see in aVR, aVF, aVL?

A
  • aVR – Negative
  • aVL & aVF – Positive
297
Q

How precordial leads are there & are they positive or negative?

A
  • 6 precordial leads
  • all positive
298
Q

Where ae the precordial leads placed?

A
  • Septal leads – V1 & V2 (4th intercostal space)

V3 is between 2 and 4
V4-6 are in the 5th intercostal space

  • Anterior leads – V3 & V4
  • Lateral leads – V5 & V6
299
Q

Which precordial leads will most likely have negative deflections?

A

V1 & V2

300
Q

Which precordial lead is used to determine if the area of injury is anterior or posterior?

A

V2

301
Q

If the current of injury is posterior (remains depolarized) what would V2 read?

A

Positive deflection
- current is moving from back of heart to front of heart where V2 is

302
Q

If the current of injury is Anterior (remains depolarized) what would V2 read?

A

Negative deflection
- current is moving from front to back away from V2

303
Q

Which precordial lead will have the greatest deflection?

A

V4
- closest lead to the heart placed near the normal electrical axis giving us a large positive deflection

304
Q

Ischemia is most likely to occur in which part of the heart?

A

Subendocardium of the left lateral ventricle

305
Q

Which way would the ischemic area of the left lateral subendocardium layers current of injury travel towards?

A

Towards positive electrode of Lead II – positive deflection on lead II
- towards left foot

306
Q

In a large infarct of the left ventricle, which way would the current of injury travel & how would this be seen on lead II?

A

Current of injury would travel away from positive electrode of lead II
- Negative deflection

307
Q

What is the reference point used when determining current of injury?

A

J point

308
Q

If the J point is depressed compared to the T/P wave, what is the most likely cause? & what kind of deflection would this look like?

A

Ischemia
- Positive deflection –> P/T wave are elevated compared to J point

309
Q

If the J point is elevated compared to the T/P wave, what is the most likely cause? & what kind of deflection would this look like?

A

Infarct
- Negative deflection –> P/T wave are depressed compared to J point

310
Q

When comparing where the current of injury is, you compare the J point to what?

A

End of T wave/beginning of P wave
- there should be no current during this time

311
Q

Why do we only use leads I & III for the vectogram

A

Einthoven’s Law
- leads I & III should equal lead II

312
Q

In V2, if the J point is higher than the T/P wave, what kind of deflection is that & where is the current coming from?

A

Negative deflection
- Current is coming from the Anterior

313
Q

In V2, if the J point is lower than the T/P wave, what kind of deflection is that & where is the current coming from?

A

Positive deflection
- Current is coming from the posterior

314
Q

When we have a slow conduction rate of the atria, what could happen?

A

Circular reentry pathways can occur. This is completely separate from what is happening at the SA node.

315
Q

What happens to circular reentry pattern if the SA node conducts faster than the reentry pattern?

A

If the SA node was conducted at a faster rate, the circular reentry patterns would run into cells recently depolarized from the SA node during the refractory period and would be shut down.

To clarify, circular reentry does not exist with an adequately performing SA node + atria usually

316
Q

What are two causes for the circular reentry pathways found in atrial flutter?

A

Slow conduction + atrial dilation

317
Q

If someone has a dilated atria, what happens to conduction speed? What does this imply with circular reentry pathways?

A

Atrial stretching/dilation predisposes people to Atrial flutter.

The distance of tissue that needs to depolarize is greater in someone with atrial dilation, meaning that it takes longer for action potentials to propagate. Circular reentry pathways will occur here.

318
Q

Muscle wise, what is the atria doing during circular reentry pathways? Is this good, or bad? Why? What happens with the ventricles?

A

Part of the atria is contracting, part of it is relaxed at any given time since depolarization is happening in a circular motion. This is not an effective primer for ventricular preload. This is bad.

The P wave will be abnormal.

319
Q

What defines atrial flutter?

A

Circular reentry pathways within atria

Atria muscle is coordinated (in a circle, not coordinated in a fantastic way)

P waves may or may not be visible, but in any case will be abnormal

High atrial/ventricular rates

320
Q

What is the difference between atrial flutter and atrial fibrillation in regard to electrical activity? Which one is “worse?”

A

Flutter = coordinated; circle
Fibrillation = uncoordinated; scattered, CIRCUS MOVEMENT

321
Q

What predisposes someone to atrial fibrillation? What population is more at risk?

A

Stretched out atria.

Older people (70+) more predisposed to afib

322
Q

Given that the cardiac muscle in atrial fibrillation is “shaky,” what happens to the blood flow? Why is this bad? If someone lives with A-fib, what will they need to take?

A

Blood will be turbulent. Turbulence –> emboli in right atria –> right ventricle –> Pulmonary circulation –> Pulmonary embolism –> bad day

They need blood thinners if they will remain in this rhythm.

323
Q

Aside from age and atrial stretch, what else causes atrial fibrillation? Can anything be done?

A

Ectopic pacemakers. You can ablate a few of these, but some ectopic pacemakers may not be able to be “zapped,” meaning that you may have some degree of afib afterwards necessitating blood thinners.

324
Q

On an EKG strip, the “squiggles” between the T wave and QRS complex in atrial fibrillation represent ____.

A

The atria muscles shaking/fibrillating.

325
Q

Can the circus movement within the atria during a-fib travel anywhere else? Are patients aware of this?

A

They can generate QRS complexes/ventricular depolarization at an irregular rate. This is uncomfortable, patients can feel it.

326
Q

When do people typically get diagnosed with Atrial Fibrillation?

A

During doctor check ins, especially in the aging populations. As people get older, the atria are more stretched out. Older people are more likely to be diagnosed with Atrial Fibrillation for this reason. If diagnosed, the patient will need blood thinners.

327
Q

What are premature atrial contractions a result of?

A

Ectopic pacemaking tissue. We should only get action potentials from the SA node normally, but if the SA node is not functioning properly we can get ectopic tissue firing off.

328
Q

In premature atrial contractions, what happens to the majority of the ectopic current? What about the rest of it?

A

Majority of current will die out, but sometimes will result in a QRS complex (resulting in a PAC)

329
Q

What are the three specific causes daddy mentioned about premature atrial contractions?

A

Ischemia, irritation, calcified plaques

330
Q

Why are premature atrial contractions bad?

A

Abnormal filling of the ventricle. Since the action potential is coming from ectopic tissue, depolarization is not following the predefined path of the SA->AV node. This leads to reduced priming ability of the atria. This then reduced stroke volume of that beat, resulting in a radial pulse deficit.

331
Q

Premature contractions from an AV nodal/bundle source originate in the _____. What does this mean for the P wave?

A

Middle of AV junction

Atria is depolarizing from AV to SA node in this case, which would result in a negative deflection. While this is true, the P wave will often be obscured by the QRS complex since we do not have the delay of the AV node in this case between the AV/ventricles.

Conversely, if the action potential originated just north of the AV node, we would have the AV delay between the P wave and QRS. This would be a negative deflection, as the AV node would depolarize inferior to superior.

332
Q

With premature ventricular contractions, does the normal QRS or the premature QRS have a larger deflection? Why?

A

Premature QRS has a larger deflection. Normally the ventricles depolarize fully within 0.01 seconds of one another. This effectively cancels out some of the voltage shown on EKG.

When there is a PVC (ectopic area within one of the two ventricles), the ventricles depolarize at different times from one another. All of the collective voltage is shown on EKG (think 50% + 50% = 100%) resulting in a larger deflection.

333
Q

Why is the QRS prolonged in premature ventricular contractions?

A

The action potential is taking longer to make it through the ventricles (instead of moving equally through both ventricles with near equal time, it is depolarizing one ventricle before the other, extending the duration of the QRS. The depolarization doesn’t always make it to the purkinje fibers. Muscle tissue conducts slower than the purkinje fibers.

334
Q

Myocardial infarction can lead to which rhythm? Is this dangerous? Furthermore, what rhythm can that rhythm lead to?

A

Paroxysmal Ventricular Tachycardia; yes it’s dangerous, you’re going to have a bad day

Leads to V-Fib

335
Q

Where does paroxysmal ventricular tachycardia come from in the heart?

A

Either purkinje fibers or ventricular muscle

336
Q

Would the accelerated QRS complexes in paroxysmal ventricular tachycardia be a positive or a negative deflection? Would they be small or large?

A

Large and positive

337
Q

Why is there high voltage in paroxysmal ventricular tachycardia?

A

Daddy doesn’t know, but he says it’s fact no cap frfr

338
Q

In paroxysmal ventricular tachycardia, are P waves visible? If they are, are they positive or negative?

A

Not really, but if they are then we would expect a negative deflection. (depolarizing inferior to superior)

339
Q

What does paroxysmal mean?

A

We don’t have an idea why it happens, it just does

340
Q

True/false Paroxysmal ventricular tachycardia has prolonged QRS

A

True

341
Q

A ventricular depolarization during the absolute refractory period would result in what?

A

Nothing; cells aren’t reset

342
Q

A ventricular depolarization during the relative refractory period (early after depolarization), would result in what?

A

A small crappy contraction, would not have many calcium ion channels reset so will not have a great pumping performance and likely won’t have great filling either.

343
Q

What happens if we repetitive premature depolarizations?

A

Severely compromised cardiac output; the cells would not be fully reset, resulting in a lot of garbage contractions

344
Q

If we don’t fully reset the cardiac cells before depolarizing again, what will show on the EKG?

A

A long QT interval

345
Q

Calcium influx determines what in the cardiac muscle cell?

A

How much force can be generated.

346
Q

What can predispose us to ventricular premature depolarization? (Hint: Long QT); What impact does the SNS/PNS have on this?

A

Calcium channel sensitivity

SNS: Beta agonist –> Increased phosphorylation of L type Ca channels –> Leads to sensitivity –> Early after depolarization –> Crappy pumping

PNS: mACh-R antagonist –> Same problem as beta agonist

347
Q

What common OTC drug can cause long QT syndrome? Why?

A

Benadryl (high dose/OD)

Benadryl is an anticholinergic; cross reactivity on mACh-R, leads to long QT

348
Q

Long QT syndrome is the precursor to what? What can this lead to?

A

Long QT syndrome is synonymous with ventricular premature depolarization. Long QT –> Torsades de pointes –> V-Fib

349
Q

Why does torsades de pointes lead to v-fib?

A

If pumping capacity is diminished enough, aortic blood pressure will drop. The coronary arteries are perfused directly from the aorta during diastole. Decreased aortic blood pressure will result in decreased coronary blood flow, which will lead to ischemia. Ischemic tissue cannot repolarize. The end result is V-Fib.

350
Q

What are the two types of fibrillation? Which one is going to kill you faster? Can they both kill you? How?

A

Atrial and ventricular fibrillation

Ventricular fibrillation will kill you faster - BP is dead/dead.

Atrial fibrillation can still kill you. A-fib –> Blood clot in atria –> clot goes to pulmonary circulation -> PE

351
Q

How can you fix V-Fib? Is it ever too late?

A

If you pump enough current (defibrillate) through the entire heart, you may be able to get the heart to reset if you are early.

If the heart has been ischemic for more than a few minutes, it may have been damaged to the point where it will not be able to repolarize, meaning the patient will die.

352
Q

What does the electrical activity of the ventricle look like during v-fib? What happens with the muscle?

A

There is a blocked impulse from somewhere in the heart, as well as an ectopic stimulus point. This stimulus point sends action potentials in every direction randomly, leading to uncoordinated quivering of the heart - very little if any cardiac output with this rhythm.

353
Q

What are a couple things mentioned in class that increase Vrm & cause arrhythmias?

A
  • Ischemia (need energy to repolarize)
  • Hyper K
354
Q

If the SA node is firing APs faster than normal, what would be the arrythmia be called?

A

Sinus Tachycardia

355
Q

What are some characteristics of Sinus Tach?

A
  • P wave before every QRS
  • Rate faster than 100 bpms
  • Short PR
356
Q

What could cause sinus tach?

A
  • Increased body temp
  • Sympathetic stimulation or loss of stimulation from vagal
  • Toxic conditions – anything that increases VRM (Nicotine, alcohol, ischemia)
357
Q

What is the arrhythmia called when the SA fires APs at a slower rate than normal?

A

Bradycardia

358
Q

What are some characteristics of bradycardia?

A
  • less than 60 bpms
  • P wave before every QRS
  • Long R to R intervals
359
Q

What can cause Brady?

A
  • Athletes with large strong physiologic heart (Have a large stroke volume)
  • increased Vagal stimulation & decreased SNS stimulation
  • Reflex brady – response to increased BP caused by a medication
360
Q

The SA node firing normally then rapidly, then normally again caused by classified as what type of arrhythmia?

A

Paroxysmal Atrial Tachycardia

361
Q

What are characteristics of Atrial Tachycaridia?

A
  • normal RR interval then rapid RR interval then back to normal RR interval caused by SA node
  • P & T waves may over lap d/t timing
  • comes & goes
362
Q

What can cause Paroxysmal Atrial Tachycardia?

A
  • Vagal reflex – something blocks vagal then vagal returns to normal
  • Medications – Beta blockers & Digoxin
363
Q

If the SA node becomes dysfunctional & a new pacemaker takes over, what arrhythmia would this be classified as?

A

Sinoatrial Block

364
Q

What are come characteristics of Sinoatrial block?

A
  • SA node impulses are blocked
  • New pacemaker takes over – AV node first then Purkinje if both SA & AV are messed up
  • Long RR intervals
365
Q

If the AV node takes over for the SA node, how will this affect the P wave?

A

AP moves retrograde (Down to up) & takes a while
- Early AV node – inverted P wave
- Late AV node – No visible P wave

366
Q

What is turbulence & what does it cause?

A

Sloshing of blood against closed valves/arteries
- can cause calcification & blood clots

367
Q

Impulses through AV node & AV bundles that are slowed or blocked would be referred to as what kind of arrhythmia?

A

Atrioventricular block

368
Q

What can cause an AV block?

A
  • Ischemia of AV nodal or AV bundle fibers (caused by coronary ischemia)
  • Compression of AV bundle (scar tissue or calcified tissue)
  • AV nodal or AV bundle inflammation
  • Excessive Vagal stimulation
  • Excessive Digitalis/Beta blockers
369
Q

How does Ischemia effect the AV node impulse transmission?

A

Ischemia increases Vrm –> less VG ion channels involved in APs –> reduced transmission

370
Q

How does compression of the AV bundle slow impulses of AV node?

A

Remodeling of the heart –> fibroblasts lay scar tissue near AV node & compresses it –> decreases diameter of axons —> increases resistance –> decreases speed of propagation
- Calcification has the same effect

371
Q

How does Excessive vagal stimulation slow or block impulses through AV node?

A

SA & AV node are blocked –> no APs will get through as vagal stimulation is too great to overcome with SNS (ventricle will eventually generate its own AP)

372
Q

How does Digitalis impair impulses through AV node?

A

Stops ATPase pump –> increases vrm –> increases Na intracellularly & slows Ca removal
(Dangerous as it increases Vrm & stops ATPase pump not only in the heart but other areas)

373
Q

What is 1st degree heart block?

A

Increase in PR interval greater than 0.20 sec
- delay – no loss of QRS
- Still have P wave in front of every QRS

374
Q

What is 2nd degree Type 1 heart block?

A
  • PR interval increases to 0.25 to 0.35 secs
  • some impulses get through AV node & some dont – dropped QRS
    Atria rate is faster than ventricles – due to dropped QRS
  • Irregular PR interval – gets longer than drops
375
Q

What is another name for 2nd degree Type 1 heart block?

A

Mobitz Type 1: Wenckebach

376
Q

What is 2nd degree Mobitz type II block?

A
  • PR interval increased to 0.25-0.45 sec
  • some impulses make it through other dont
  • atria has faster rate than ventricles – due to dropped QRS
  • Fixed Ratio & PR – dropped QRSs will typically follow a pattern
377
Q

Which Type of 2nd degree block is more dangerous? & what kind of treatment can be done?

A

Type II
- Pacemaker – reduces amount of dropped QRS complexes

378
Q

What is Third degree heart block?

A

Complete dissociation of P waves & QRS complexes – nothing gets through AV node/Bundle of His
- R to R interval is similar – ventricular escape 15-40 bpms
- Random P waves – elevated atrial rate

A & P (6 decks)

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