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A&P > Test 4 🩷 > Flashcards

Test 4 🩷 Flashcards

Cardiac

1
Q

How does cardiac muscle contract?

A

As a unit–similar to smooth muscle

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2
Q

How are cardiac cells connected to eachother?

A

Intercalated discs

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3
Q

What provides a pathway for neighboring cells to communicate?

A

Gap junctions

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4
Q

Where are gap junctions located in each cardiac cell?

A

the border of each cell–curvy/ jagged (intercalated discs)

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5
Q

How do intercalated discs allow for more gap junctions?

A

The cells fit together with the next cell creating more surface area for gap junctions

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6
Q

What is the pattern of cardiac muscle?

A

Striated

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7
Q

What does the cardiac muscle pattern correspond with?

A

alignment of actin and myosin

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8
Q

What type of sarcomeres are similar to cardiac sarcomeres?

A

Heart sarcomeres look similar to skeletal sarcomeres

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9
Q

How many nuclei per cardiac muscle cell?

A

one nucleus per cardiac cell

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10
Q

What is the function of stem cells?

A

slow process to generate new cardiac cells and patch areas where cells have died

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11
Q

Why wouldnt you be able to generate cardiac cells to replace tissue after MI?

A

Stem cells wouldnt be able to produce new cells fast enough

injury overwhelms the replacement system

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12
Q

What are fibroblasts?

A

Cells in the heart that deposit scar tissue

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13
Q

When do fibroblasts lay scar tissue in the heart?

A

usually at a controlled rate

can be uncontrolled in setting of disease processes (CHF)

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14
Q

What is an example of a disease where fibroblasts are overactive?

A

CHF–excessive scar tissue

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15
Q

What drug can be used to slow down fibroblast activity and prevent unnecessary scar tissure deposition?

A

ACE inhibitors

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16
Q

How do ACE inhibitors prevent unnecessary scare tissue deposition?

A

ACE inhibitors block RAAS-prevent growth factor from angiotensin II and prevent excess scar tissue in the heart

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17
Q

Which group should not be prescribed ACE inhibitors?

A

Pregnant women–angiotensin II is important for development of fetus and ACE inhibitors would block that growth/development

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18
Q

How does scar tissue mess with transduction system in the heart?

A

Scar tissue doesnt contract or conduct action potentials

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19
Q

What is the arrangement of cardiac ventricular muscle?

A

Syncytial connections

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20
Q

How many layers does ventricular muscle have?

A

2

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21
Q

How are the cells oriented in ventricular muscle layers?

A

The layers have cells oriented in different directions (perpendicular)

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22
Q

How do the ventricle contract?

A

They squeeze and rotate in opposite directions

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23
Q

What analogy was used in lecture to compare to ventricular contraction?

A

Wringing water out of a wet towel

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24
Q

What is meant by “top part of heart”?

A

Atria

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25
Q

What is meant by “lower half of heart”?

A

ventricles- everything below AV node

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26
Q

What makes up the vast majority of heart cells?

A

muscle tissue–can produce lots of force

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27
Q

What in the muscle cell is responsible for producing force when stimulated by an action potential?

A

Myofibrils–lots of myofibrils in each cardiac muscle cell

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28
Q

How is specialized conduction tissue different from muscle tissue?

A

conduction tissue does not produce force like muscle tissue

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29
Q

What is the main job of specialized conduction tissue?

A

Send action potentials quickly

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30
Q

How does conduction tissue send action potential quicker than other tissues?

A

Conduction tissue doesnt have myofibrils inside–less stuff inside so action potential can travel quicker

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31
Q

What is the deepest layer of cardiac muscle?

A

Sub-Endocardium

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32
Q

In which cardiac muscle layer do most MIs occur and why?

A

Sub-endocardium
wall pressure are highest in the deep parts of the heart muscle

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33
Q

Where are cardiac wall pressures the highest?

A

The deeper in the heart= higher wall pressure

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34
Q

Why is high wall pressure a bad thing?

A

makes it more difficult to perfuse

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35
Q

What are 2 thing that increases chances of cardiac ischemia?

A

Clogged vessels and really high wall pressures

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36
Q

Where is the endocardium and what is it composed of?

A

I cell layer thick endothelial layer

deep cardiac muscle

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37
Q

What makes up the bulk of the cardiac muscle wall?

A

Myocardium

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38
Q

What is the most superficial layer of the heart chambers?

A

Epicardium

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39
Q

Where do the major blood vessels sit in the heart?

A

All major BVs sit on top of the epicardium

some penetrate deep in some areas

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40
Q

What is the area directly outside of the epicardium?

A

Pericardiac space

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41
Q

What is contained in the pericardial space?

A

filled with a small amount of fluid and decent amount of mucus

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42
Q

what is the function of the pericardial space?

A

Mucus decreases friction with cardiac movement

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43
Q

What happens if there is friction in the pericardium?

A

It is very painful

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44
Q

What causes friction in the pericardium?

A

inflammation of pericardial space or loss of fluid/mucus in this area

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45
Q

What is the name of the connective tissue sack that encloses the heart?

A

Pericardium

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46
Q

What are the 2 layers of the pericardium?

A

Parietal pericardium
Fibrous pericardium

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47
Q

What is the difference between the parietal pericardium and the fibrous pericardium?

A

Parietal pericardium is the inner layer–stretchy

Fibrous pericardium is the outer layer–stiff and difficult to expand

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48
Q

How does the cardiac sarcomere look when the heart is relaxed?

A

under stretched–no H band because actin filaments are overlapping with each other

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49
Q

How does the cardiac sarcomere look when contracting?

A

myosin moves to z discs–provides good EF/SV

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50
Q

What is the purpose of the Purkinje fibers?

A

Conduct action potentials–no contraction

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51
Q

What is Vrm of purkinje fibers?

A

-90mV

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52
Q

How does the typical action potential of purkinje fiber look?

A

Extended action potential with plateau phase

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53
Q

What are both purkinje fibers and ventricles permeable to at rest?

A

slight permeability to Na+–not constantly permeable to Na+

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54
Q

Are purkinje fibers able to self depolarize?

A

Yes, but it takes them a long time since Vrm is -90mV and threshold is -70mV

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55
Q

Do purkinje fibers usually fire their own action potentials?

A

they can, but self depolarization rate is very slow

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56
Q

T or F: If things are working normally in the heart, purkinje fibers rely on APs generated from neighbor cells to depolarize

A

True–neighbor cell generates action potential and spreads to purkinje fibers

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57
Q

What is the threshold of purkinje fibers and ventricular muscle?

A

-70mV

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58
Q

What happens if there is no action potential from upstream neighbor cell?

A

Cell would eventually conduct own action potential but there would be a lag time (maybe 30 seconds before 1st AP)

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59
Q

What is Vrm for ventricular muscle?

A

-80mV

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60
Q

What causes ventricle to contract?

A

Action potential passing through

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61
Q

If there is a complete heart block at the AV node, would it take 30 second for every beat?

A

No, It takes a lot longer for the 1st beat to come back but once its gets going it will beat more regular just at a slower rate

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62
Q

What type of surgical manipulation can generate a complete heart block?

A

eye manipulation–sensors in the eye orbit and body doesnt like when they are messed with

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63
Q

What is V + X (5 and dime) reflex?

A

pressure in the eye socket sent to cranial nerve V (trigeminal) and eye socket pressure sensors send info to brainstem which sends message to vagus nerve (X) causing massive vagal output (heart rate drop)

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64
Q

What is cranial nerve V and what does it do?

A

Trigeminal nerve–in control of sensory perception in the eye socket

big nerve on side of face

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65
Q

What happens in response to massive vagal output from the CNS?

A

Prevents transmission of action potentials at the AV node–HR may go to 0 but come back in 30 seconds

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66
Q

What is necessary for heart cells to spontaneously depolarize?

A

Time

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67
Q

What does the slight slope in the resting phase between heart beats indicate?

A

Increased sodium permeability of the cell at rest (sodium leakiness)

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68
Q

Describe phase 4 of the cardiac action potential:

A

Resting membrane potential

slowly getting more positive with Na+ leakiness

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69
Q

Describe phase 0 in ventricular cardiac action potential:

A

Action potential is set off by Na+ coming into cell from gap junctions of neighbor cell

fast Na+ channels open briefly

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70
Q

Describe phase 1 of purkinje cardiac action potential:

A

K+ channels close during action potential

fast T-type Ca2+ channels open

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71
Q

When do K+ channels close during cardiac action potential?

A

End of phase 0 through phase 1 and 2 for duration of action potential

K+ channels start to open back up at very end of phase 2

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72
Q

What is happening during phase 2 of cardiac action potential?

A

Plateau phase–L-type Ca2+ channels open for extended period then close

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73
Q

What is happening at phase 3 of ventricular action potential?

A

K+ channels open back up and reset cell back to phase 4 (Vrm)

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74
Q

How long is the typical cardiac action potential and why is it necessary?

A

200ms–allows for coordinated contraction

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75
Q

What phase correlates with when the heart is contracting?

A

Phase 2–longer plateau means longer contraction

Shorter plateau is shorter contraction

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76
Q

Why do we need coordination between superficial and interior parts of the heart?

A

Allows heart to produce a lot of force and eject a lot of blood

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77
Q

What is the only outward current during a heartbeat?

A

K+

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78
Q

What is meant by inward rectifying K+ channels?

A

Current of K+ is still outward, but it is in response to something else coming in (like Ca2+ or Na+)

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79
Q

When is K+ current the highest during cardiac action potential?

A

K+ current is high at rest and during repolarization

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80
Q

When is K+ current depressed during cardiac action potential?

A

During duration of action potential

makes sense because K+ channels close

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81
Q

What is the sodium permeability compared to calcium permeability in cardiac action potential?

A

Large increase in Na+ permeability compared to less significant increase in Ca2+ current

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82
Q

Why is there not as much Ca2+ current compared to Na+ current in cardiac AP?

A

Not as much Ca2+ coming in because not very many Ca2+ channels in the cell wall

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83
Q

What is Ohms law?

A

V=iR

Voltage= current x resistance

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84
Q

What does “i” represent?

A

ionic current

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85
Q

What 2 things does ionic current depend on?

A

Number of channels open

electrochemical gradient of the ion

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86
Q

What par of the nervous system primarily controls nodal tissue?

A

Parasympathetic

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87
Q

What innervates the SA node?

A

Right vagus nerve

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88
Q

What innervates the AV node?

A

Tips of the left Vagus nerve

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89
Q

What is the main function of the parasympathetic nervous system at the heart?

A

suppressed activity of pacemaker cells in the nodal areas of the heart

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90
Q

What is the function of sympathetic innervation at the heart?

A

Wide spread Innervation to the heart primarily the atria and ventricles

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91
Q

Where does the sympathetic chain connect at the heart?

A

Sympathetic chain has thick connections with atrial and ventricular muscle tissue

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92
Q

What is the primary catecholamine released from sympathetic nerves at the heart?

A

Norepinephrine

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93
Q

What receptors does norepinephrine interact with in the heart?

A

Beta receptors

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94
Q

Which areas of the heart have fast action potentials?

A

Ventricular conduction system (purkinje) and ventricular muscle cells

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95
Q

What is another term for ventricular muscle cell?

A

Ventricular myocyte

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96
Q

What is the peak of action potentials in ventricular myocyte?

A

+20mV

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97
Q

What amount of depolarization is happening in the ventricle muscle and ventricular conduction system?

A

100mV

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98
Q

How is the amount of depolarization in a ventricle determined?

A

Difference in charge between Vrm and peak of action potential

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99
Q

What does the EKG measure?

A

Sum of all current flowing between electrodes placed on the body

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100
Q

Which current does the EKG show?

A

All mV that is making its way around the heart

looking at depolarization or repolarization that is spreading through the heart

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101
Q

What is normal amplitude for QRS deflection?

A

1.5mV (a little over 3 boxes in amplitude)

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102
Q

How many mV is each small box on an EKG?

A

+0.5mV

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103
Q

What is the voltage on an EKG like compared to voltage generated with ventricle action potential?

A

Lower voltage on EKG compared to action potential

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104
Q

Why is the voltage so much lower on EKG compared to action potential?

A

A lot of the voltage is lost from the action potential in high resistance tissues

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105
Q

What is meant by high resistance tissues in the body?

A

Parts of the body that impede the flow of electrical current

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106
Q

What are examples of high resistance areas in the body?

A

Fat and air

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107
Q

What would you expect an EKG for someone with COPD to look like?

A

Lower QRS complex due to increased air which increases voltage lost

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108
Q

What happens to a tissue as it depolarizes or repolarizes?

A

There is a charge gradient between the part that has depolarized and the part that is repolarized

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109
Q

What would be the voltage if measured with a voltage meter of a resting cell?

A

0mV

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110
Q

What would be the voltage of a completely depolarized cell?

A

0mV

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111
Q

What would be the measured voltage of cell that is half way depolarized starting from the left?

A

High positive # voltage

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112
Q

What would be the measured voltage of a tissue that is halfway repolarized from left to right?

A

High negative # voltage

electrodes are traveling toward the anode

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113
Q

At what point is electrical current the highest in depolarization and repolarization?

A

When the cell has reached the 1/2 way point between depolarized and repolarized

biggest charge difference

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114
Q

If repolarization occurs from right to left, what would you expect the voltage meter to read when the repolarization if half way through?

A

Very positive #

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115
Q

Where is conduction system?

A

Conduction system is very deep in the heart wall

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116
Q

How does depolarization travel in the heart?

A

from inside to outside

Action potential starts in deep areas of the heart then makes its way to the surface of the heart as time passes

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117
Q

What is the first thing in the heart to depolarize?

A

Inside of ventricles

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118
Q

What depolarizes second to the inside of ventricles?

A

Outer layer of ventricular muscle depolarizes

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119
Q

How does repolarization in ventricular muscle start and spread in the heart?

A

Repolarization starts in superficial layers and travels to deeper layers of ventricular wall

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120
Q

Compare depolarization pattern and repolarization patter in the heart:

A

Repolarization is happening opposite order of depolarization

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121
Q

Explain how repolarization of ventricles is still positive deflection:

A

Epicardium is repolarizing before endocardium (spreads from outside to inside)

electrons are still coming towards positive electrode

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122
Q

If electrons are traveling toward positive electrode what would you expect on a voltage graph?

A

Positive deflection

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123
Q

If electrons are traveling away from the positive electrode what would you expect on a voltage graph?

A

Negative deflection

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124
Q

What electrical event is represented by the P wave?

A

atrial depolarization

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125
Q

What electrical event is represented by the T wave?

A

Ventricular repolarization

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126
Q

What electrical event is represented by QRS complex?

A

depolarization of ventricles

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127
Q

How does current travel through the ventricle?

A

electrons come from area of depolarization to areas of the heart that are still resting or that have repolarized

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127
Q

What is the first thing to completely depolarize in the heart?

A

interventricular septum

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128
Q

What happens to electrical current in a cell that has area of injury (ie ischemia)?

A

Ischemic area cant repolarize

little spot of depolarization creates current at rest when there shouldnt be

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128
Q

What type of current is there when the tissue resets after action potential?

A

there should be no current

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129
Q

What are examples that can cause and area of the cell to be chronically depolarized?

A

lack of nutrients–oxygen, glucose

obstruction like a blood clot

anything that leads to ischemia

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130
Q

What happens if part of a tissue cant get the nutrients it needs?

A

Tissue without enough energy will not be able to repolarize

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131
Q

What types of currents result from infarcted issues that do not electrically reset?

A

Currents of injury

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132
Q

What are currents of injury?

A

Current from a sick part of the cell at rest that should not be happening

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133
Q

How are currents of injury/ electrical abnormalities diagnosed?

A

12 lead EKG

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134
Q

What is the pacemaker of the heart?

A

SA node

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135
Q

What is the MOA of the SA node being the pacemaker?

A

Tissue at SA node depolarizes and reaches threshold faster than any other cell in the heart

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136
Q

What does SA nodal cell depolarization rate correspond with?

A

depolarizes decently fast to produce our normal heart rate of 72bpm

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137
Q

What is a normal heart rate in a health adult?

A

72bpm

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138
Q

What is the resting membrane potential of SA nodal cell?

A

-55mV

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139
Q

What is threshold potential in SA nodal cells?

A

-40mV

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140
Q

What causes the large increase in membrane potential at phase 4 in SA nodal cells?

A

HCN channels
NA+/Ca2+ leak channels

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141
Q

What allows the SA node to reach threshold quickly

A

large increase in membrane potential at phase 4 (at rest) so it doesnt take long to go from resting to threshold

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142
Q

What does HCN channel stand for?

A

Hyperpolarization and cyclic nucleotide channel

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143
Q

What do HCN channels do?

A

when open, they are non specific cation channels

allow Na+ and Ca2+ through

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144
Q

What is the majority of current through HCN channels?

A

Na+ primarily then Ca2+

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145
Q

Why is Na+ the primary current for HCN channels?

A

Na+ is smaller and fits through channel easier than Ca2+

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146
Q

Why doesnt K+ come out through HCN channels?

A

In theory the channel would allow it out, but there is so much Na+ and Ca2+ coming through it that K+ doesnt really move through it

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147
Q

Why are HCN channels called hyperpolarization?

A

HCN channels open when the cell reaches Vrm

Vrm in the heart is comparable to hyperpolarization

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148
Q

When do HCN channels open?

A

When the heart cell reaches Vrm
With increase cAMP/ Increased Beta activity

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149
Q

What does the cyclic nucleotide portion of HCN channels correlate with?

A

HCN channels can be controlled with cyclic nucleotides like cAMP

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150
Q

How does beta activity influence HCN channels?

A

Norepinephrine binding to to beta receptors in heart increases adenylyl cyclase which produces cAMP

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151
Q

What does the “A” in cAMP stand for?

A

Adenosine

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152
Q

With normal amounts of beta receptor activity, what can we expect in regards to HCN channels?

A

Normal amount of HCN channels operating during phase 4

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153
Q

What phase of the action potential do HCN channels open?

A

phase 4

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154
Q

What happens to HCN channels when a beta agonist is given?

A

increases cAMP and opens more HCN channels

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155
Q

What happens to the slope of phase 4 when a beta agonist is given?

A

more HCN channels open would increase the slope of phase 4 and decrease the time of phase 4

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156
Q

How does a beta agonist increase HR on a molecular level?

A

-stimulates adenylyl cyclase
-increases cAMP
-opens more HCN channels
-Vrm goes to threshold faster
-earlier AP
-increased HR

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157
Q

What happens to HCN channels with a beta blocker?

A

Less HCN channels open with phase 4

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158
Q

What happens to heart rate when atenolol is given on a molecular level?

A

-Less HCN channels open
-Reduced slope during phae 4
-Longer to reach threshold and generate AP
-Slower HR

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159
Q

What happens to the slope in phase 4 when a beta agonist is given?

A

Slope is steeper and less time in phase 4 leads to earlier APs

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160
Q

How does cholinergic and adrenergic signaling occur in the heart?

A

They antagonize eachother

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161
Q

What happens to membrane potential with activation of mACh-receptors?

A

The receptors provide a conduit for K+ to leave the cell so membrane potential is more negative

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162
Q

What happens to membrane potential with increased levels of acetylcholine?

A

More K+ channels are open so membrane potential decreases

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163
Q

What happens to the slope during phase 4 with increased acetylcholine?

A

the slope of the line is the same, it will just be a lower starting point and take longer to get to threshold

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164
Q

What does acetylcholine do to the heart?

A

Decreases HR by increasing K+ leaving the cell

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165
Q

What does beta adrenergic activity do to K+ channels?

A

increases cAMP and Shuts down K+

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166
Q

What do mACh-receptors do in regards to cAMP?

A

Decrease cAMP

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167
Q

How do mAch-receptors agonists decrease cAMP?

A

Inhibitor alpha subunit on adenylyl cyclase

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168
Q

What determines how many K+ channels are open in the heart?

A

Acetylcholine at the nodal tissue

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169
Q

What would happen in the cell if K+ permeability is reduced?

A

Vrm would be more positive and would hit threshold faster

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170
Q

What cardiac effects would be seen with slight hyperkalemia?

A

Increase in HR by increasing Vrm

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171
Q

What does hyperkalemia do to K+ gradient?

A

Reduces the gradient so less K+ movement and increased Vrm

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172
Q

What is a normal K+ concentration gradient?

A

30:1

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173
Q

What effect does blood calcium level have on membrane potential in the heart?

A

Blood calcium levels can change threshold potential in heart tissue

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174
Q

What happens in reasonable hypercalcemia in reference to cardiac cells?

A

Increases threshold potential (more positive) and lowers HR

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175
Q

What happens to cardiac cells if a patient is hypocalcemic?

A

Makes threshold potential more negative and increases HR

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176
Q

How does calcium cause changes in threshold potential of myocytes?

A

unknown how calcium does this

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177
Q

What does the sub-endocardium usually refer to?

A

Left ventricle

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178
Q

How would depolarization from left to right look?

A

Positive deflection–moving toward positive electrode

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179
Q

How is the amplitude of the deflections for cardiac action potentials determined?

A

By how much current

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180
Q

How does repolarization from left to right look?

A

Negative deflection

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181
Q

How would repolarization that is opposite of original depolarization look?

A

Positive deflection (double negative)

reason why T wave is positive deflection on EKG

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182
Q

Why do ventricular action potentials have a smaller phase 4 slope?

A

There are not very many HCN channels or leaky Na+/Ca2+ channels

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183
Q

Are there HCN channels present in ventricular action potentials?

A

Yes, just not as many

know there are still some because of the slight increase at phase 4

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184
Q

Compare phase 4 slope in ventricular fast APs and slow SA APs:

A

Slope of phase 4 is much steeper/greater than in ventricular action potentials

more HCN channels

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185
Q

What does phase 0 represent in fast APs and slow APs?

A

The upstroke of the action potential

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186
Q

How does phase 0 in fast AP look compared to phase 0 in slow AP?

A

In fast AP–phase 0 is almost straight up and down

slow AP has less slope to phase 0 with longer duration

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187
Q

What causes the steep slope of phase 0 in ventricular AP?

A

VG Na+ channels are creating fast increase

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188
Q

Are there VG Na+ channels involved in nodal tissue AP?

A

No, phase 0 is due to L-type Ca2+ channels

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189
Q

What causes the slope in phase 0 of nodal areas in the heart?

A

L-type slow Ca2+ channels

slower to open and stay open longer

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190
Q

What determines how fast APs move around in the heart?

A

Slope of phase 0

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191
Q

How would an action potential be traveling that has a steep/ fast phase 0?

A

AP is starting off fast and is propagated to the next cell very quickly

this is what happens with ventricular current

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192
Q

What is usually involved in action potential propagation?

A

sodium current

lots of VG Na+ channels opening in fast action potentials that can move Na+ through gap junctions to neighbor cells to fire AP there

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193
Q

How does the action potential travel in nodal tissue if there are not VG Na+ channels?

A

phase 0 slope is lower so it takes longer to move action potential from one cell to another

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194
Q

Do the atria use VG Na+ channels to propagate action potentials?

A

Atria do not have many VG Na+ channels–slow for AP to generate and spread to next cell

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195
Q

Why does it take longer for the atria to conduct action potentials and for the action potentials to spread?

A

Not as many VG Na+ channels

primary current is Ca2+(more difficult for Ca2+ to travel through the gap junctions)

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196
Q

What happens in phase 3 of nodal cells?

A

L-type Ca2+ channels close and VG K+ channels open to reset the cell

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197
Q

Some people include a phase 2 in nodal cells, where would this be?

A

Phase 2 would be a “plateau” phase from L-type Ca2+ channels

Dr Schmidt doesnt agree with phase 2

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198
Q

What phase is missing from nodal cells that is present in ventricular cells?

A

Phase 1

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199
Q

What phases do slow action potentials include?

A

Phase 4,0, sometimes 2, and 3

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200
Q

Why is the AV node a slower pacemaker than the SA node?

A

The cells in AV node are not leaky to Na+ and Ca2+ during phase 4

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201
Q
A
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202
Q

What is vrm of AV node compared to SA node?

A

AV node vrm is more negative (lower than SA)

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203
Q

What does a lower vrm in AV nodes indicate?

A

In the AV node it takes longer to generate its own AP

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204
Q

Are there HCN channels in the AV node?

A

Yes, but not as many as SA node

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205
Q

Which cells have the most HCN channels?

A

SA nodal cells

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206
Q

Compare the shape of SA and AV node APs:

A

SA and AV nodal AP have similar shape

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207
Q

Compare Purkinje and ventricular APs:

A

Both are fast and both have similar shape

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208
Q

What is the duration of ventricular action potentials?

A

Ventricular action potentials vary in length

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209
Q

Which ventricular tissue correlates with the longest action potential duration in the ventricle?

A

Deep interior ventricular action potentials are longer

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210
Q

Where would you expect to see the longest duration of ventricular action potential?

A

Deep–in the sub endocardium

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211
Q

How do action potentials in the deep layers of the heart fire?

A

Action potentials in the deep parts of the heart get start earlier and repolarize later than superficial tissue

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212
Q

How do action potentials conduct in the superficial ventricular myocyte?

A

action potential get started a little bit later in the superficial levels because it takes time for AP to move from inside ventricle to outside

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213
Q

What is the duration of AP in superficial ventricular myocyte?

A

Decreased duration

will depolarize last and repolarize first

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214
Q

What is an example of superficial tissue in the heart?

A

Epicardium

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215
Q

How does repolarization in epicardial tissue compare to repolarization in sub endocardium?

A

Repolarization in epicardial tissue is over sooner than in sub endocardium

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216
Q

What is the order of ventricular repolarization?

A

repolarization travels from outside to inside ventricle

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217
Q

How does ventricular AP length vary based on the layer of ventricular tissue?

A

superficial ventricular tissue has a shorter AP than deeper tissue

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218
Q

Why do deep tissues in the ventricle have a longer action potential?

A

It is important to get all of the muscle to squeeze at the same time to get enough force to eject blood

makes sure there is overlap in contracting time so heart muscles contract together

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219
Q

How do atrial action potentials look?

A

in between ventricular AP and SA nodal AP

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220
Q

What does phase 0 in atrial AP look like?

A

Straight up and down, similar to ventricular AP

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221
Q

Is there a plateau phase in atria AP?

A

small plateau phase but doesnt need plateau because atria are only contracting for short period of time and not pumping against a lot of resistance

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222
Q

Is it important to coordinate inner atria muscle contraction with outer like in the ventricles?

A

Not an issue in the atria because the atria walls are thin

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223
Q

How frequently does SA node generate AP with normal vagal stimulation?

A

AP every 0.83 seconds

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224
Q

How fast would SA node generate AP without any nervous system influence?

A

110bpm

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225
Q

How fast would SA Node generate AP if only influenced by sympathetic nervous system (not parasympathetic)?

A

120 bpm

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226
Q

How many beats does the SNS increase heart rate?

A

10 bpm

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227
Q

Which nervous system has the greater effect on heart rate?

A

Parasympathetic

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228
Q

How frequently does SA node generate AP with only simulation from Parasympathetic nervous system?

A

60-62bpm

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229
Q

Self depolarization at the SA node produces and action potential every _________ seconds.

A

0.83 seconds

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230
Q

How can we calculate HR from normal self depolarizing rate of SA node?

A

60 seconds per minute/0.83 seconds= 72bpm

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231
Q

What works as the “breaks” in the resting heart?

A

Parasympathetic–vagal system

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232
Q

What is the secondary pacemaker cell?

A

AV node

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233
Q

If AV node becomes primary pacemaker of the heart, how fast would it generate APs?

A

40-60bpm

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234
Q

What are the purkinje fibers and where is it located?

A

ventricular conduction system

buried in ventricular muscle mass

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235
Q

What rate would purkinje fibers generate AP if they take over as pacemaker of the heart?

A

15-30bpm

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236
Q

If the purkinje fibers take over as primary pacemaker, would you be able to survive?

A

Would be enough to keep us going for a little bit (like to get to hospital)

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237
Q

What does the conduction system of the heart allow for?

A

coordinated timing of all muscle mass

orderly process where signals get sent on defined pathways and tale defined amount of time

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238
Q

What happens if there is a timing issue in the cardiac muscle?

A

the muscle tissue is active or inactive at wrong period of time–causes issues with function

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239
Q

If the atria aren’t working, would the ventricles still work?

A

Technically we dont need the atria to fill the ventricles with blood, but if they aren’t helping then the ventricle wont be as full as normal and output will decrease leading to low BP

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240
Q

What is a crucial element to having a functional heart pump?

A

Coordinated timing

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241
Q

What makes sure AP can travel from SA to AV?

A

Conduction tissue

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242
Q

What is the conduction system of the ventricles?

A

Purkinje fibers

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243
Q

What is the conduction system of the atria?

A

3 pathways in the right

one to the left atria

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244
Q

Where are the 3 conduction pathways for the RA?

A

Between SA and AV node

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245
Q

What are the 3 conduction pathways in the RA?

A

Internodal pathways:
-anterior
-middle
-posterior

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246
Q

Which internodal pathway branched off to conduct the LA?

A

conduction tissue from anterior internodal pathway

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247
Q

What is the conduction tissue in the LA called than branched from the anterior internodal pathway?

A

Interatrial bundle

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248
Q

Where does the interatrial bundle create?

A

pathway for AP between right atria and left atria

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249
Q

What is another term for interatrial bundle?

A

Bachmans bundle

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250
Q

What is the function of bachmans bundle?

A

Conduct electrical signals to the left atria and propagate signals from SA to AV node

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251
Q

What is the time it take for AP to move from SA to AV node?

A

0.03 seconds–now the AP is at the AV node

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252
Q

How long does it take for entire RA to depolarize?

A

0.07 seconds

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253
Q

Why does it take longer for left atrium to depolarize than right?

A

AP has to travel further to LA

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254
Q

At what time does the last part of the LA depolarize?

A

0.09 seconds

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255
Q

What is the point when both atria are fully depolarized?

A

0.09 seconds

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256
Q

What does atrial depolarization correspond with?

A

P wave should be 0.09 seconds long

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257
Q

When does the P wave start and end?

A

P wave starts when AP starts and ends when all atrial tissue is depolarized

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258
Q

Regions in the LA that are closer to the RA depolarize _________.

A

quicker (0.04 seconds)

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259
Q

What part of LA is furthest away from conduction tissue?

A

lower lateral part of LA

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260
Q

Why does it take longer for the LA to fully depolarize?

A

Further away from conduction tissue

AP has to travel through muscle in atria with myofibrils that do not conduct AP very fast

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261
Q

What causes the delay in AP traveling from upper left atria to lower left atria?

A

AP is traveling through muscle and myofibrils that do not conduct electricity very fast and there is not specialized conduction tissue in this area

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262
Q

What does the top half of the heart include?

A

Atria, SA, AV

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263
Q

What is the path for AP to take to fully depolarize ventricles

A

AP moves from SA through right atrium to AV through bundle branches and purkinje to all of the ventricle

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264
Q

How long does it take for action potential to travel from SA to all of the ventricle?

A

0.22 seconds

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265
Q

Why is delay at AV node a good thing?

A

Gives atria time to contract before ventricles

Allows AV to function as a filter

allows ventricles to contract

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266
Q

What happens with AP conduction with older hearts?

A

Older hearts have more tissue–takes longer for AP to travel through all the tissue

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267
Q

How does AV node function as a filter?

A

AV node can filter out extraneous AP in the atria so we dont end up with fast ventricular rhythms

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268
Q

What happens if there is crazy electrical activity in the atria (ex afib)?

A

AP in the top half of the heart are not coordinated with the lower half of the heart because AV node is filtering

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269
Q

What is the absolute refractory period of the AP?

A

point in time if another AP hits before the cell is fully reset from the previous AP–there will not be a new AP

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270
Q

How does AV node filter through extraneous AP?

A

If AP hits the node during its refractory period there will not be a new AP generated

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271
Q

How is the AV node structured?

A

Has an area that is Big and fat

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272
Q

What does the fat area of the AV node allow for?

A

Low conduction–Fat doesnt conduct AP

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273
Q

What makes the conduction in the AV node delayed/slower?

A

Fat tissue

Low number of gap junctions between conduction cells

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274
Q

How much time does it take for AP to travel from internodal pathway to AV?

A

0.03 seconds after SA fires

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275
Q

What is the time of the delay for the AP to get through AV node?

A

0.12 seconds–this is when the AP is traveling through the fat tissue

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276
Q

What is the delay in the AP at the bundle of His (penetrating bundle)?

A

0.01 seconds

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277
Q

What is another name for the bundle of His?

A

Penetrating bundle

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278
Q

What area allows for crossover of AP from atria to ventricular septum?

A

Area just above left and right bundle branch

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279
Q

What is the amount of time it takes AP to get from SA to main bundle branches?

A

0.03 + 0.13= 0.16 seconds

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280
Q

How long does it take AP to get from AV through bundle of his?

A

0.12 delay at AV + 0.01 delay at bundle of His= 0.13 seconds

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281
Q

After SA fires, how long until main bundle branches get AP and what does this correspond with?

A

0.16 second–corresponds with PR interval

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282
Q

What triggers the QRS complex?

A

initiation of AP in the main bundle branches in the interventricular septum

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283
Q

What happens if there is an abnormal pathway in the atria causing AP that aren’t suppose to be there?

A

If AP hits AV node during refractory period it will not propagate action potential to ventricles

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284
Q

How does the AV node protect against ventricular tachycardia rhythms?

A

AV node will not propagate action potential to the ventricle if it is hit with AP during refractory period

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285
Q

What part of the heart depolarized first and why?

A

ventricular septum–where bundle branches are located

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286
Q

Where are the bundle branches located?

A

ventricular septum

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287
Q

How does depolarization spread after after hitting the septum?

A

2 different directions:
-toward left ventricle
-toward right ventricle

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288
Q

What pattern does depolarization of the heart follow?

A

Pattern where electrical signals are sent toward the left foot

289
Q

What is the degree of average electrical movement during typical heart beat?

A

59 degrees

290
Q

What does EKG show in regards to current?

A

EKG shows all electrical activity in the heart

291
Q

What is a typical magnitude of depolarization for ventricular AP?

A

100mV or more

292
Q

What would EKG look like if we moved the leads closer to the heart?

A

Voltage (deflection) to be a lot higher–less tissue getting in the way

293
Q

What would be expected for QRS deflection if the electrodes are places closer to the heart?

A

3-4mV instead of 1.5mV

294
Q

Which leads would we see a larger deflection in?

A

V1-V6 chest leads–closer to the heart in a 12 lead

295
Q

What happens to the voltage in a 3 lead EKG?

A

increased loss of voltage because there is a lot of tissue/structures in the way

is: air in lungs, fat

296
Q

What does the QT interval correspond with?

A

length of longest ventricular AP (endocardial)

length of time for ventricular depolarization

297
Q

Which parts of the heart are depolarized for the duration of the QT interval?

A

The deeper parts of the heart (endocardium)

298
Q
A
299
Q

Where does the EKG start when the cell is at rest?

A

0

300
Q

How big is a normal P wave deflection?

A

positive deflection–2.5 small boxes long and 2.5 small boxes tall

301
Q

Why does the P wave show up as a positive deflection?

A

because movement from SA to AV–AP is traveling toward the foot–toward positive lead

302
Q

If P wave originates at SA node what deflection do we expect to see?

A

Positive

303
Q

If P wave originates in AV node–what deflection do we expect to see

A

action potential would travel retrograde back to SA node

P wave would be inverted because traveling toward negative electrode

304
Q

What causes a P wave to be high?

A

Problem with RA (hypertrophy)

305
Q

What size on EKG correlates with a high P wave?

A

greater than 3 boxes high

306
Q

Why does RA hypertrophy cause increase in height of p wave?

A

more tissue= larger magnitude of deflection

more tissue= more electrical current for the positive electrode to see

307
Q

What is happening if the P wave is too long?

A

Conduction problem with the LA

308
Q

What happens to the P wave if the left atrium is stretched out?

A

takes longer for the entire LA to be repolarized (so its depolarized longer) causing longer P wave

309
Q

What is happening if p wave has a double hump?

A

electrical block in LA–preventing AP from spreading to LA correctly

310
Q

What deflection is seen with Q wave?

A

Negative deflection

311
Q

Do all leads have Q waves?

A

No

312
Q

What does the R wave indicate?

A

Positive deflection

corresponds with depolarization of ventricles

313
Q

What does the PR interval measure?

A

Period from start of atria depolarization to initiation of electrical activity in the ventricle

314
Q

Why is the PR interval not called PQ?

A

We do not always have a Q wave

would technically be PQ is Q wave always existed

315
Q

What is the ideal time for PR interval?

A

0.16 seconds–time from SA to bundle branches in ventricular septum

316
Q

What is the time between R waves? (RR interval)

A

0.83 seconds

317
Q

What can RR interval be used for?

A

Reliable way to calculate heart rate

318
Q

What deflection does the S wave have?

A

Negative deflection

319
Q

What does the QRS show us on an EKG?

A

time source of the AP working through the ventricular conduction system and ventricular muscle

320
Q

When does QRS complex end?

A

When all ventricular muscle has been depolarized

321
Q

How is the end of ventricular depolarization depicted on an EKG?

A

Point after QRS where entire lower half of heart is depolarized (back to 0 on EKG)

322
Q

What is the resting point after the QRS called?

A

J-point

323
Q

What is the J-point used for?

A

reference point for currents of injury

324
Q

How long does it take to get the last part of ventricle fully depolarized

A

0.22 seconds

325
Q

How long should the ideal QRS complex be?

A

0.22 (heart is completely depolarized) - 0.16 (atrial depolarization to bundle branches) = 0.06 seconds

326
Q

How long is the QRS in most people?

A

longer than 0.06 seconds

people usually have more heart tissue than what is ideal

327
Q

Why do ideal number for EKG recording measurements not work for normal people?

A

Most people have more heart tissue than what is ideal–creating longer time for depolarization wave to spread

328
Q

What are examples that could increase the size of ventricles?

A

High blood pressure

drinking too much caffeine over long period of time

329
Q

What is the typical QRS deflection amplitude?

A

magnitude of deflection of 1.5mV

positive 1mV and 0.3 mV negative added together for total

330
Q

How to calculate magnitude of deflection for QRS:

A

How far above baseline added to how far below baseline= magnitude of deflection

331
Q

What does magnitude of deflection measure?

A

total amount of electrical current during QRS

332
Q

What can cause a high voltage QRS?

A

Electrodes closer to the heart

heart tissue bigger than normal

333
Q

What does increased ventricular tissue do to electrical activity in the heart?

A

extra ventricular tissue will allow for more electrical activity causing enlargement of QRS complex

334
Q

What do enlarged ventricles do to QRS complex?

A

widens QRS
increases magnitude of QRS

335
Q

What does dilated cardiomyopathy do to QRS complex?

A

ventricle walls are stretched out

widen/prolong qrs complex

336
Q

When does atrial repolarization occur on an EKG?

A

Toward the end of R wave

hidden in QRS

337
Q

What is another term for J-point?

A

Isoelectric point

338
Q

What does the J-point show on the EKG?

A

point where entire ventricles are depolarized

339
Q

How is the J-point used to identify currents of injury?

A

look at j-point and compare that to different point in EKG where heart should be completely repolarized

340
Q

What part of the EKG should the heart be completely repolarized?

A

right side of T wave

341
Q

What is J-point useful in determining?

A

ST elevation and ST depression by comparing to TP interval

342
Q

T orF: The j point is useful because it shows when ALL tissue is depolarized–including areas of injury

A

T

343
Q

Why do we look at area after T wave to compare to J point?

A

All healthy tissue should be resting after T wave–unhealthy tissue would still be depolarized causing current

344
Q

What does QT interval show on EKG?

A

Includes start of depolarization in the septum up until all tissue in ventricle is repolarized

345
Q

What is typical time period for QT interval?

A

0.25 to 0.35 seconds

duration of fast action potential in endocardial heart tissue

346
Q

Where is the ST segment measured?

A

End of S wave to start of T wave

347
Q

What is ST segment beneficial for?

A

useful to look at for areas of injury and ischemia

348
Q

What is happening that results in the T wave on EKG?

A

repolarization of the ventricles

349
Q

Why is the T wave an upward deflction?

A

repolarization is spreading from superficial to deep layers and repolarization is opposite of depolarization and is moving in an opposite way of depolarization

350
Q

How does the heart cause a physiologic increase in heart rate?

A

reduces time before SA node fires
Heart will shorten ST segment and QT segment

351
Q

What happens to ventricular repolarization if ST and QT segments are shortened?

A

ventricle repolarizes earlier and body would be able to fire AP sooner–increasing HR

352
Q

What is Lusitropy?

A

How fast the resetting of ventricles occurs during an AP

353
Q

What is meant by positive lusitropy agent?

A

repolarizes the ventricles faster than normal causing increase in HR

354
Q

Inotropy

A

Stronger heart beat (more Ca2+ in heart)

355
Q

chronotropy

A

increased heart rate

356
Q

Dromotropy

A

speed of conduction of action potential

357
Q

What is dromotropy dependent on?

A

Dependent on Na+ current coming in

the more Na+ the faster the AP conduction can be

358
Q

What is the voltage of each big box on EKG?

A

0.5mV

359
Q

What is the voltage of each small box on ekg?

A

0.1mV
smaller boxes divide larger box up 5 times

360
Q

Why are the EKG measurements set up how they are?

A

From the old school paper machines

paper was fed through machine at 25mm/sec

361
Q

How many big boxes per second?

A

5 big boxes in one second

362
Q

How much time is measured by each big box?

A

1/5 of a second–0.2 seconds

363
Q

How much time is measured by each small box?

A

each small box =1/5 of big box

0.04 seconds for each small box

364
Q

What is a premature action potential?

A

Smaller than normal AP

365
Q

What causes premature action potentials?

A

If the cell is mostly reset but not entirely and an AP is generated

366
Q

What is the period called when a cell is mostly reset but not entirely?

A

Relative refractory period

367
Q

Why dont we want these premature action potentials (early heart beats)?

A

uncoordinated electrical system with mechanical pumping leads to uncoordinated contraction and decreased pumping performance

368
Q

How does a relative refractory period AP correspond with heart pumping?

A

Heart will not pump efficiently

369
Q

What is a later premature action potential?

A

Heart has been able to fully reset–generates AP a little early

370
Q

What is the absolute refractory period?

A

toward the peak of AP

371
Q

Can an AP be generated during absolute refractory period?

A

No, AP would not be generated even if cell was stimulated with outside current

372
Q

What is the serous visceral pericardium?

A

Very thin/ clear membrane that sits between parietal pericardium and the heart

373
Q

How are action potentials propagated in the heart?

A

Gap junctions

374
Q

What would cause slower propagation through gap junctions?

A

Ca2+ will be slower transmission because its bigger–can still generate AP

375
Q

What is a downside to gap junctions?

A

Bidirectional current/ synapse

376
Q

Why would it be safer to have synaptic connections in the heart opposed to gap junctions?

A

Chemical synapses do not allow for current to back travel

would take much longer

377
Q

What is the primary thing protecting us from retrograde movement in cardiac cells?

A

absolute refractory period

378
Q

How does the heart guard against re-entry rhythms?

A

By having a refractory period

379
Q

What plane does a 3 lead EKG display?

A

frontal/ coronal

380
Q

What plane do augmented leads use to display EKG?

A

Frontal/ coronal

381
Q

How can you tell augmented leads?

A

Have an “a” in front

382
Q

Where is aVR located?

A

augmented right lead

383
Q

What is the 3 lead EKG measuring?

A

Electrical movement and direction of movement in the frontal plane

384
Q

How is lead II set up in a 3 lead EKG?

A

Positive electrode on left foot
Negative electrode on right arm

384
Q

What deflection does lead II see with atrial depolarization?

A

Large positive–SA to AV moved toward left foot

385
Q

What deflection is seen in lead II with ventricular depolarization?

A

large positive deflection: current moving toward left foot

385
Q

Where are the positive and negative connection for lead I for 3 leak EKG?

A

Positive connection on left arm
Negative connection on right arm

386
Q

How does lead I view electrical current?

A

Horizontal plane: left and right movement

387
Q

Where are the positive and negative connections for lead III on 3 lead EKG?

A

Positive on left foot
Negative on left arm

388
Q

How many electrodes on the left foot for a 3 lead EKG?

A

2 positive electrodes

389
Q

How many electrodes on the right arm for a 3 lead EKG?

A

2 negative electrodes

390
Q

How many electrodes on left arm for 3 lead EKG?

A

One positive electrode and one negative electrode

391
Q

Who is the dutch scientist who theorized the electrical triangle for the heart?

A

Einthoven: theorized Einthoven’s triangle

392
Q

What equipment is needed to look at electrical activity in the heart?

A

Recorder and amplifier to turn signals into something that can be processes

393
Q

What is the typical mean electrical axis for depolarization of the ventricles and the direction?

A

59 degrees pointed toward left foot

394
Q

At what degree is lead II oriented in?

A

60 degree angle from horizontal

395
Q

What is the term when mean electrical axis is less than 59 degrees (textbook less than 0)?

A

Left axis deviation

396
Q

Which direction would the heart rotate for a left axis deviation?

A

Counter clockwise

397
Q

How would the mean electrical axis look for a left axis deviation?

A

Up and towards the left arm from right to left

398
Q

What is it called when heart is rotated clockwise?

A

Right axis deviation

399
Q

How is net electrical axis pointed for a right axis deviation?

A

Pointed toward right side of the body

400
Q

What degree is classified as a right axis deviation?

A

Anything greater than 59 degrees

400
Q

What are some things in the heart that would cause the electrical axis to change from one way to another?

A

Bundle branch blocks–depending on which branch is blocked

401
Q

What type of axis deviation might a person with COPD have?

A

Lunger are hyperinflated–shifts heart to the right (oriented straight up and down)

right axis deviation

402
Q

How can ventilation change heart orientation?

A

When exhaling- heart is oriented more on left side (left axis deviation)

when taking a deep breath in- shifts heart to the right (right axis deviation)

403
Q

How is electrical activity changed if one side of the heart is much larger than the other?

A

The larger side has more electrical activity going to that area

404
Q

What degree of axis does lead II have?

A

60 degree from horizontal

405
Q

What would be another way to say mean electrical axis of 300 degrees?

A

-60 degrees

406
Q

If mean electrical axis is negative, what direction does it rotate from horizontal?

A

Counter clockwise

407
Q

If mean electrical axis is positive, what direction does it rotate from horizontal?

A

clockwise

408
Q

Why does it take less time for AP to travel through right ventricle?

A

Right heart walls are thinner–only pumping against resistance of pulmonary circulation

409
Q

What happens with AP travel in the left ventricle?

A

Left ventricle walls are thicker
Takes longer for last sliver of ventricle to depolarize

410
Q

Why does the left lateral section of the ventricle take longer to depolarize?

A

It is furthest from the AV node

411
Q

Where is the first place to depolarize in the ventricles?

A

Main bundle branch at the inter ventricular septum

412
Q

Why do we see positive deflection with the p wave?

A

depolarization in the atria is moving from SA to AV–toward left foot

413
Q

What would we expect to see if we could see atrial repolarization?

A

Repolarization of the atria would be a negative deflection heading toward left foot

414
Q

Why do we not see the repolarization wave of the atria?

A

Hidden by QRS–atria walls area thin so not a ton of muscle tissue to rise above qrs

415
Q

What deflection would atrial T wave be?

A

Negative deflection

416
Q

Why would the atrial T wave be more spread out than the P wave?

A

When the conduction system is working in retrograde it doesnt have the same properties as when moving forward

417
Q

What is the electrical axis for lead I?

A

0 degrees–horizontal

418
Q

How can we determine how much current is measures at lead I?

A

draw a triangle: the amount of current picked up in lead I corresponds with how long the side of the triangle is that is moving on horizontal axis

419
Q

How would lead I amplitude look compared to lead II during depolarization?

A

Lead I would be smaller amplitude positive deflection

420
Q

What would lead I show if mean electrical axis is 90 degrees?

A

Lead I would show 0—wouldnt see any current moving toward it

421
Q

What would lead I show if mean electrical axis is toward the right side of the body?

A

Lead I would be negative deflection–current moving from left to right (toward negative electrode)

422
Q

What would Lead I show if mean electrical axis is along the same horizontal plane moving left to right?

A

Very negative deflection

423
Q

What type of deflection should all electrical events have in lead II during ventricular depolarization?

A

Large and positive deflection for all events

424
Q

What would lead II show if mean electrical axis is 90 degrees?

A

large positive deflection in lead II–still close in line with lead II

425
Q

What is the normal electrical axis of lead III?

A

120 degrees from horizontal

426
Q

What can be accomplished with a 3 lead EKG?

A

Diagnose any conduction and arrhythmia problems using 3 lead axis

427
Q

How can a 3 lead EKG be used to figure out what the mean electrical axis is?

A

Look at how positive or how negative the deflections are in the 3 different leads

428
Q

What is a benefit of 12 lead EKG compared to 3 lead EKG?

A

3 lead EKG can figure out what the problem is

12 lead is better for figuring out where the problem is (more eyes on the problem with chest leads)

429
Q

How does einthovens law look at the heart leads?

A

As an equilateral triangle

430
Q

What is Einthoven’s Law?

A

Net deflection in Lead I + net deflection in Lead III = Net deflection in Lead II

431
Q

How to find net deflection?

A

Positive deflection of QRS minus negative deflection of QRS

432
Q

Does Einthovens law always work?

A

Yes, works in every situation in the 3 standard leads

433
Q

If mean electrical axis is 60 degrees, what would be expected in lead I, lead II, and Lead III?

A

Lead I and Lead II would have similar size that would add up to size of lead II positive deflections

434
Q
A
435
Q

What is expected on 3 lead EKG when only the septum is depolarized?

A

LI: small positive deflection
L2: a little more positive deflection
L3: small positive deflection

436
Q

What is expected on EKG when the heart is half way depolarized?

A

LI: increased positive deflection
L2: Very positive deflection
L3: increased positive deflection

437
Q

If a vector is draw for lead II what can be said about lead I and lead III?

A

Vector for lead I and lead III equals lead II

438
Q

What is expected on EKG when MORE than half of the heart is depolarized?

A

Current slows down
LI, L2, and L3: still positive but less positive than last plot

439
Q

What happens to net electrical axis when only superior lateral wall of left ventricle is left to depolarize?

A

Net electrical axis is shifted and pointing up and to left arm (toward last sliver of resting tissue)

440
Q

What is expected on EKG when only the upper lateral wall of the left ventricle is resting?

A

L1: would be slightly positive
L2: Slightly negative
L3: Very negative

441
Q

What movement shows up as positive deflection in Lead I?

A

Right to left movement

442
Q

What creates the S wave during electrical depolarization of the ventricles?

A

When there is only a little bit of tissue on the left ventricle waiting to be depolarized

Electrical axis shift to the left causes negative deflections in lead 2 and lead 3 (s wave)

443
Q

During the last stage of depolarization, how does the negative deflection in lead II compare to lead III?

A

Lead III has more negative deflection

Lead II is only slightly negative

444
Q

What would the current in the 3 lead EKG look like when the entire heart is depolarized?

A

No current

445
Q

Which lead is least likely to have an S wave?

A

Lead I–never had a negative deflection during depolarization

446
Q

What is the origin or the Q wave?

A

The first thing to depolarize in the bundle branches is a part of the septum to the left side of the inter ventricular septum

447
Q

Where does the depolarization head after the initial part of the septum is depolarized?

A

To the right

448
Q

What would the 3 leads on the EKG see during initial spread of depolarization from the septum?

A

L1: negative
L2: Slight negative
L3: slight positive

449
Q

What does a big vector indicate?

A

a lot of electrical activity

450
Q

What does a smaller vector indicate?

A

Less electrical current

451
Q

What angle would be the most electrical activity in regards to each lead?

A

Parallel with the plane

452
Q

What do the 3 lead electrodes looks like for the R wave?

A

Current is pointing down to the left

Large positive deflection in LII
positive deflection in LI
positive deflection in LIII

453
Q

How is the net electrical axis pointed for a normal S wave in a 3 lead EKG?

A

Current is up to the left

454
Q

How would the 3 lead EKG leads look for the S wave?

A

LI: positive
LII: slightly negative
LIII: more negative than LII

455
Q

What electrical activity is happening at the ST segment?

A

should have no electrical activity

Entire heart is depolarized–same charge in all the tissue

456
Q

Where are the augmented leads located?

A

Half way between the standard leads

457
Q

What does the V stand for in the augmented leads?

A

voltage

458
Q

What does the last letter in the augmented leads indicated?

A

Location on the body

459
Q

How many electrodes do the augmented leads us?

A

1 positive
average of 2 negative

460
Q

Where is the positive electrode for aVR?

A

Right arm

461
Q

Where does the negative electrode come from for aVR?

A

between left arm and left leg–average between those 2 electrodes

462
Q

How are most of the deflection in aVR oriented?

A

Usually current is heading away from right arm–negative deflections

463
Q

Which augmented lead is the least used?

A

aVR

464
Q

What degree is aVR at?

A

210 degree from horizontal

465
Q

Where is the positive electrode in aVL?

A

left arm

466
Q

Where is the negative electrode in aVL?

A

average of right arm and left leg

467
Q

What is the degree for aVL?

A

150 degrees

468
Q

What are normal deflections in a healthy heart for aVL?

A

everything that is positive in lead II is the same in aVL (P, T, QRS)

469
Q

What size should the qrs be in aVL?

A

Same as standard: 1.5mV

470
Q

Where is the positive electrode in aVF?

A

left foot

471
Q

Where is the negative electrode coming from in aVF?

A

negative electrode is average from left arm and right arm

472
Q

What orientation is aVF looking?

A

straight up

473
Q

What is the purpose of aVF?

A

resolution to see problems–especially between LII and LIII

474
Q

What degree is aVF at?

A

90 degrees

475
Q

What deflections would we see for depolarization from aVF?

A

positive deflections for QRS, P, and T wave

476
Q

What is another name for precordial leads?

A

Chest leads

477
Q

How many leads make up the precordial leads?

A

6 extra leads around the chest

478
Q

Where are the positive leads located for the precordial leads?

A

V1-V6 around the heart are positive precordial leads

479
Q

Where are the negative electrodes for 12 lead ekg?

A

Negative electrodes are a combination of electrodes on right arm, left arm, and left foot

uses standard leads as the negative leads

480
Q

Where is V1 placed?

A

right side of sternum–4th intercostal space

481
Q

Where is V2 placed?

A

Left side of sternum–4th intercostal space

482
Q

What is another name for V1 and V2 leads?

A

Septal leads

483
Q

How does QRS look in the V1?

A

QRS downward deflection

484
Q

How do the P and T wave look in V1

A

Inverted

485
Q

Why is there not alot of electrical current toward V1?

A

current normally heads toward left foot and off to the side–misses V1

486
Q

Which precordial lead is the most useful to figure out where a problem in the heart is?

A

V2

487
Q

How does the QRS look in V2?

A

Negative deflection

488
Q

What is V2 used for?

A

Figure out anterior and posterior injuries

489
Q

Why is V2 used to see anterior and posterior issues?

A

It is situated so it points directly at the front of the heart

490
Q

How would current move with a posterior infarct?

A

from back of the heart to the front of the heart

491
Q

How would V2 read electrical current from posterior infarct?

A

current coming toward V2–positive electrode

492
Q

How would current move if an anterior part of the heart is ischemic?

A

Electrons from anterior part of the heart would move toward positive charged area in posterior part of the heart

493
Q

How would V2 read electrical current from an anterior infarct?

A

negative current of injury–current going away from V2

494
Q

Where is V3 located?

A

Sandwiched between V4 and V2

495
Q

What is another term for V3 and V4 leads?

A

Anterior leads

496
Q

How does V4 see electrical activity heading toward it?

A

all electrical activity heading toward V4 is a big positive deflection

497
Q

Why is V4 a positive deflection?

A

Situated in line with normal electrical axis of the heart

498
Q

which precordial lead should have the largest positive deflection in QRS?

A

V4

499
Q

What is another name for V5 and V6?

A

Lateral leads

500
Q

How does QRS look in V5 and V6?

A

QRS is smaller because the leads are over on lateral side of the thorax and not as inline with normal cardiac electrical axis

501
Q

Where are lead V4, V5, and V6 located?

A

5th intercostal space on left side

502
Q

How does the electrical activity in the precordial leads compare to electrical activity in a 3 lead EKG?

A

Precordial electrical activity is larger (bigger deflections) because electrodes are placed closer to the heart

503
Q

What is happening electrically that shows up as an inverted T wave?

A

Repolarization is happening in the same way as depolarization

When inside of the heart is resetting before the outside

504
Q

What happens when ventricular repolarization is happening in the same direction as depolarization?

A

Positive QRS and inverted T wave

505
Q

What is a biphasic T wave?

A

Half up half down

tissue is repolarizing in abnormal way

506
Q

How can yo figure out mean electrical axis from LI, LII, and LIII?

A

plot LI and LIII based of net magnitude of QRS

507
Q

What does a mean electrical axis down to the right indicate?

A

Potentially right ventricular hypertrophy along with large QRS in lead I and lead III

508
Q

How does depolarization differ in someone with right ventricular hypertrophy?

A

Left ventricle would depolarize first then current would shift to the right side of the body

509
Q

How does ventricular depolarization typically look?

A

Both ventricles depolarize at the same time

510
Q

What happens if there is an occlusion in one of the bundle branches?

A

Higher resistance in that bundle branch–unaffected side would depolarize faster then shift current to resting portion

causes wonky electrical activity

511
Q

How can we figure out which bundle branch is blocked?

A

Determine the electrical axis of the heart
up to the left would be LBBB

512
Q

Why is repolarization hard for the heart compared to depolarization?

A

To repolarize have to have Na/K pump working to get Na+ out after AP, and other things that require energy for the cell to repolarize

513
Q

What happens to the heart if there is an energy deficiet?

A

EX: blocked vessel–some of the tissue isnt getting enough energy and it will be stuck in depolarized state

514
Q

What is it called if an area in the heart is stuck in a depolarized state?

A

area of injury

515
Q

How would current flow around the area of injury?

A

Current would be from injury toward are of reset heart tissue

516
Q

When would current of injury be seen?

A

When the rest of the heart it resting

517
Q

What type of EKG change would be expected in Lead II from a small area of ischemia in the left ventricle?

A

TP segment elevated–looks like ST depression

518
Q

What part of the heart wall is usually impacted by an infarction?

A

usually the entire wall

519
Q

How does the electrical current typically look when part of the left ventricle is infarcted?

A

Large vector up and to the right

520
Q

What would you expect in Lead II if part of the left ventricle is infarcted?

A

TP segment dropped down–would make ST look elevated

521
Q

What type of current is associated with J-point that is higher than TP segment in LI, LII, or LIII?

A

Negative current of injury

522
Q

What type of current is associated with J-point that is lower than TP segment?

A

Positive current of injury

523
Q

After plotting the the vectorcardiogram for the current of injury, how is the area of injury in the heart determined?

A

Arrow of mean electrical activity for currents of injury is pointing AWAY from the where the injury is

524
Q

Which part of the heart is ischemic if the mean electrical current of injury is pointed down to the right?

A

Left heart issue

525
Q

What is indicated by J-point that is higher than TP segment in V2?

A

Negative current of injury

-current would be flowing away from V2–would be an anterior infarct

526
Q

What is indicated by a mean electrical current of injury that is pointed straight up?

A

issue in apex of the heart

527
Q

Why cant computers calculate these different vectors accurately?

A

Zero point is very difficult for a computer to figure out

Computer cant figure out J point

528
Q

What has to happen to close M gate and re open H gate on VG Na+ channels?

A

Cell has to repolarize

529
Q

What happens to VG Na+ channels if unable to repolarize?

A

They are stuck in inactive form- cant be used for action potential

530
Q

What are the 2 gates on the L-type Ca2+ channels?

A

Activation gate (D gate)
Inactivation gate (F gate)

531
Q

Where are the 2 gates for the L-type Ca2+ channels located?

A

D gate: outside
F gate: inside

532
Q

What has to happen in order for the D gate to open?

A

Voltage dependent. Has to have enough of a depolarization to open

533
Q

Compare D gate to M gate:

A

D gate takes longer to open and is open for a longer amount of time compared to M gate

D gate: CA2+
M gate: Na+

534
Q

What is the order for resetting L-type calcium channels during repolarization?

A

activation gate (D) closes then inactivation gate (F) opens

535
Q

What is the resting state for L-type Ca2+ channels?

A

D gate is closed
F gate is open

536
Q

How is Vrm different for L-type Ca2+ channels compared to VG Na+ channels?

A

Vrm for L-type calcium channels is more positive than VG Na+ channels

537
Q

Which pacemaker cells has the fastest diastolic depolarization rate?

A

SA nodal cell: Phase 4 is the steepest

538
Q

Why are there no VG Na+ channels in nodal tissue? (2 reasons)

A

1) There might not be any VG channels in that tissue

2) The VG Na+ channels do not function because Vrm in nodal tissue is too positive for them to reset

539
Q

What is the slope of phase 0 in purkinje tissue related to?

A

VG Na+ channels

540
Q

What happens to ventricular action potentials if Vrm is more positive?

A

Will start to lose VG Na+ channels and slope of Phase 0 decrease

541
Q

What happens to phase 1 if Vrm in ventricular AP is increased?

A

Peak of phase 1 might not be as high as normal

542
Q

What happens to the action potential if vrm in ventricular AP is super positive that there are no VG na+ channels involved?

A

AP would look like slow nodal AP

Ca2+ would be able to generate decent AP

543
Q

What issues occur when the VG Na+ channels are not repolarizing?

A

Conduction issues–sodium is usually required for fast propagation through gap junctions

544
Q

Why are there conduction issues in the heart when Na+ influx is decreased?

A

AP is more reliant on Ca2+ to spread AP to other cells

Ca2+ doesnt fit through gap junctions as well as Na+

545
Q

If Vrm is more positive than -55 what will happen to AP?

A

Lose VG Na+ and L-type Ca2+ channels–wouldnt have any action potential

546
Q

What determines the slope if phase 0?

A

Which ions are involved and how many ions are coming in

547
Q

What issues cause vrm to be more positive than normal?

A

elevated K+
Acidosis
Ischemia/ infarction

548
Q

How does acidosis increase resting membrane potential?

A

enzymes arent able to function outside pH of 7.4 and cant catalyze chemical reactions needed to reset the cell and provide energy

ultimately the cell can not repolarize

549
Q

What type of drugs block VG Na+ channels?

A

-CAINE drugs

550
Q

How does lidocaine affect ventricular action potentials?

A

reduced slope of phase 0

551
Q

Which cells are the most leaky to Ca2+ at rest?

A

Nodal tissue

552
Q

Which cells are the least permeable to Ca2+ at rest?

A

Purkinje

553
Q

What are the 2 mACh-receptors at the heart?

A

-mACh-R is associated with potassium channels

-mACh-R with inhibitory alpha subunit

554
Q

What is the primary way nodal tissue maintains or adjusts Vrm?

A

Through mACh-r that are linked to potassium channels

555
Q

What happens when an agonist binds to mACh-r in nodal tissue?

A

increased K+ permeability reduces vrm and reduces heart rate

556
Q

What happens if mACh-R in nodal tissue are blocked?

A

K+ permeability decreases so membrane potential is more positive and heart rate increases

557
Q

Do mACh-R have beta antagonism?

A

No, works as a stand alone system

558
Q

What does the alpha subunit on mACh-R inhibit?

A

Inhibits adenylyl cyclase

559
Q

Where is adenylyl cyclase located in the heart?

A

tethered to the cell wall in the heart

560
Q

What is the function of adenylyl cyclase?

A

Turn ATP into cAMP

561
Q

What does an agonist at mACh-R do to adenylyl cyclase?

A

Slows down adenylyl cyclase through inhibitory alpha subunit that is activated when the agonist binds to the receptor

562
Q

What happens with the alpha subunit at the beta receptors in the heart?

A

alpha subunit is stimulatory at the beta receptors

stimulated adenylyl cyclase causing increase cAMP

563
Q

What other channels are activated by certain beta receptors?

A

Some beta receptor cause direct activation of HCN channels

564
Q

How do beta receptors cause HCN channels to open?

A

increase cAMP by increasing speed of adenylyl cyclase causes HCN channels to open

565
Q

What happens when more HCN channels are open?

A

More Na+ and Ca2+ coming into any pacemaker cell during phase 4

566
Q

What does cAMP further increase activity of?

A

Protein kinase A

567
Q

What are targets for PKA?

A

L-type Ca2+ channels
Troponin I
Phospholamban

568
Q

What does PKA do to L-type Ca2+ channels?

A

Phosphorylates them to make them more sensitive and easier to open

Increases amount of Ca2+ coming in from outside during AP

569
Q

Why is phosphorylation of L-type Ca2+ channels dangerous?

A

too much beta adrenergic activity–Ca2+ channels are too sensitive they may open at the wrong time causing EAD or DAD

increase risk for heart attacks with increased activity level

570
Q

What happens when PKA phosphorylated troponin I?

A

increases contractile protein sensitivity to calcium and increases cycling rate of cross bridge generating filaments

571
Q

What effect does PKA have on phospholamban?

A

increases speed of the SERCA pump increases HR

phospholamban usually inhibits SERCA so by phosphorylating it allows SERCA to reset cell faster

572
Q

What breaks down cAMP in the heart?

A

Phosphodiesterase–breaks it down into AMP

573
Q

What is the outcome of a PDE inhibitor?

A

increased cAMP and increased PKA

574
Q

What causes arrhythmias?

A

Problem with conduction system or the action potential is gong through the muscle outside the conduction system

575
Q

What usually generates abnormal rhythmicity in arrhythmias?

A

Abnormal pacemaker in the heart

576
Q

What happens if a random tissue starts generating action potentials on its own?

A

Action potentials would probably be out of sequence from normal and can spread through gap junctions

577
Q

Why do gap junctions allows for inappropriate current to travel through them?

A

Gap junctions do not filter, they dont care about which way the signal is moving

They are just a pathway for action potentials to spread

578
Q

What is an ectopic pacemaker?

A

Area in the heart that is generating action potentials other than the SA node

579
Q

What happens if ventricular muscle starts generating action potentials?

A

An arrhythmia will be generated

580
Q

What happens to areas in the heart that have been blocked from action potentials moving through?

A

Sometimes the the tissue that is blocked will generate its own action potential

581
Q

How do normal action potentials differ from arrhythmia action potentials?

A

Normal action potentials have a defined pathway and speed

Arrhythmia pathways are abnormal

582
Q

What makes arrhythmia pathways abnormal?

A

AP from these pathways could hit a tissue causing an AP to fire during relative refractory period or fire early than its suppose to

583
Q

What can cause ectopic pacemakers in the heart?

A

Increased VRM
Increased serum K+
Ischemia

584
Q

How does increase VRM help generate arrhythmias?

A

If resting membrane potential is closer to threshold potential in the pacemaker cell an AP can be fired earlier

Increased VRM Increases probability of having an action potential generated on its own

585
Q

What happens if the AV node is ischemic?

A

If bad enough may halt all AP through AV node

If VRM increases in AV node it may fire AP earlier than normal causing an arrhythmia

586
Q

What is the issue in abnormal sinus rhythms?

A

Abnormal firing of SA node

587
Q

What is happening in sinus tachycardia?

A

SA node is firing faster than normal

588
Q

At what rate is sinus tachycardia officially called sinus tachycardia?

A

> 100bpm

589
Q

What are some reasons for sinus tachycardia?

A

-Moderate increase in body temp
-Reflex sympathetic stimulation
-Loss of vagal stimulation

590
Q

How does increased body temp cause sinus tachycardia?

A

Increased body temp increases the energy demands of the body

591
Q

What happens to heart rate initially with massive blood loss?

A

sympathetic nervous system is trying to pump more blood to replace what is being lost

–increasing heart rate to try to compensate

592
Q

What happens to hear rate with low blood pressure?

A

Nervous system can sense low BP if ventricles arent working right–feeds into back to SA node to increase rate to try to improve BP

593
Q

Why are beta blockers sometimes administered with anti-arrhythmics?

A

Beta blocker helps to prevent compensatory sinus tachycardia through reflex activation of SA node

594
Q

What are toxic conditions of the heart that can result in sinus tachycardia?

A

Conditions that increase VRM
-hyperkalemia
-acidosis
-nicotine
-alcohol

595
Q

What is the definition of sinus bradycardia?

A

<60 bpm

596
Q

Where does sinus bradycardia originate?

A

SA Node–generating slower rate than normal

597
Q

What happens to RR interval with sinus bradycardia?

A

prolonged RR interval

598
Q

Why do athletes or very healthy/active people have lower resting heart rates (sinus brady)?

A

Heart is physiologically bigger which increases stroke volume with each beat

nervous system will tell heart to slow down because there is a lot of SV with each beat and we only need 5L/min

599
Q

What is associated with a higher resting heart rate?

A

decreased stroke volume

600
Q

If heart rate is elevated at rest and there is no other reasons why it would be, what could be the reason for this?

A

Overactive thyroid

601
Q

What happens to heart rate with increased vagal stimulation?

A

Bradycardia

602
Q

Why doesnt taking away sympathetic nervous system drastically decrease HR?

A

There is only a small amount of SNS input during a resting heart rate so taking it away doesnt do much since there isnt alot to start with

603
Q

Explain the neural reflexive bradycardia with drugs:

A

Phenylephrine–arteries squeezing increases BP which baroreceptors sense and respond by feeding back to the heart to reduce heart rate to maintain homeostasis

604
Q

What does the paroxysmal aspect of paroxysmal atrial tachycardia indicate?

A

Atrial tachycardia that comes and goes

605
Q

Where is the problem originating from in paroxysmal atrial tachycardia?

A

SA node: firing at increased rate

606
Q

What do P and T waves look like in paroxysmal atrial tachycardia?

A

rate is sped up so P and T waves are overlapped and hard to distinguish from each other –looks like one notch

combo of atrial P wave and ventricular T wave

607
Q

What could cause paroxysmal atrial tachycardia?

A

A drug that block vagal tone in the heart

608
Q

What is it called when SA impulses are completely blocked?

A

Sinoatrial Block

609
Q

What causes sinoatrial blocks?

A

Severe dysfunction at the SA node

If SA node is ischemic and cant reset any of its ion channels to produce action potentials

610
Q

What do P waves look like in sinoatrial block?

A

P waves are either inverted or hidden

611
Q

Which region of the heart becomes the pacemaker if there is a sinoatrial block?

A

AV would be next in line if it is healthy

612
Q

What takes over as pacemaker if SA and AV node are messed up?

A

Purkinje system–15-30bpm so very compromised output

613
Q

What determines if we can see an inverted P wave in a sinoatrial block?

A

Depends on which part of the AV node is generating the action potentials

We can see inverted P wave if pacemaker is set up in early parts of AV node

614
Q

What causes the inverted P wave?

A

Retrograde movement from AV to SA

615
Q

If pacemaker is set up in later parts of the AV node–what happens to P wave?

A

P wave would still be inverted we just wouldnt see it–would take time to travel backwards through AV node and ventricular electrical activity would mask it

616
Q

What is decreased with all arrhythmias?

A

Stroke volume

617
Q

Under normal circumstances, the atria should contract when the AV valves are __________?

A

Open

618
Q

What causes early closure of AV valves?

A

If something causes the ventricles to depolarize early–causes early closure of the AV valves

619
Q

Why is early closure of AV valves a bad thing?

A

Atria are trying to contract and push blood through a closed valve–creates turbulence

620
Q

What happens with turbulence in the heart?

A

Creates blood clots and calcifications of the valves

621
Q

What is categorized as enhanced delay at AV node?

A

PR interval beyond 0.16

the more increased delay= more abnormal block

622
Q

What causes an enhances delay at the AV node?

A

-AV nodal ischemia
-Compression of AV node
-AV bundle inflammation
-Excessive vagal stimulation
-Excess beta blockers

623
Q

What is occurring with AV node ischemia?

A

raises Vrm and less VG ion channels participating in AP

624
Q

How does compression of AV node cause an enhanced delay?

A

Cells are pressed down and have a smaller diameter–decreased rate of action potential propagation with smaller diameter (increased resistance)

625
Q

What causes compression of AV node?

A

Caused by remodeling of heart by fibroblasts

626
Q

What is blocked with excessive vagal stimulation?

A

SA and AV nodes are blocked–reliant on ventricular escape to kick in

627
Q

What is the MOA of digitalis?

A

Inhibits Na/K ATPase pump

increases vrm–used for extreme heart failure

628
Q

What happens if Na/K pump is inhibited like with Dig?

A

-More sodium in the cell
-More calcium in the cell since its usually pumped out by Na/Ca exchanger

629
Q

Why is dig usually the last med to try for heart failure?

A

Very dangerous by inhibiting cells ability to reset itself–not completely specific to heart

630
Q

How do beta blockers enhance delay at AV node?

A

Reduce speed of conduction at AV node

631
Q

PR interval greater than 0.2 seconds:

A

incomplete 1st degree heart block

632
Q

Characteristics of 2nd degree heart block?

A

-Dropping QRS
-PR interval increases to >.25 seconds
-P wave doesnt always correspond to QRS

633
Q

Which part of the heart has a faster rate during second degree heart block?

A

Atria has a faster rate than the ventricles (losing QRS)

634
Q

What is another name for Mobitz type 1?

A

Wenckebach periodicity

635
Q

What are the characteristics of a wenckebach?

A

Irregular PR interval

635
Q

Which mobitz block is more dangerous?

A

Mobitz type 2

636
Q

What are the characteristics of Mobitz type 2?

A

-Fixed P wave to QRS ratios
-regular/fixed PR interval on p and qrs that we have

637
Q

What is the typical ratio seen of p waves to QRS complexes with mobitz type 2?

A

2:1
3:2
3:1

638
Q

Which heart block would need a pacemaker?

A

Second degree mobitz type 2
complete heart block

639
Q

What is happening in a complete heart block?

A

Total AV node block and bundle of His

640
Q

What does the heart rely on for its pacemaker in a complete heart block?

A

Ventricular escape–purkinje system (15-30bpm)

641
Q

What happens to atrial rate during complete heart block?

A

Cardiac output if reduced–nervous system sees low BP and feed back to heart to increase atrial rate

nervous system telling SA node to fire faster

642
Q

What do the P waves look like in complete heart block?

A

-Random P waves all over the place
-no correlation of timing between P waves and QRS complexes because no action potentials are getting through AV node

643
Q

What is a genetic syndrome that involves complete block of the AV node at random times associated with fainting spells?

A

Stokes-Adams Syndrome

644
Q

What happens to ventricular escape rhythm in Stokes-Adams Syndrome?

A

Delayed ventricular escape 5-30 seconds
-reason why lose consciousness–if ventricular escape was faster wouldnt pass out

645
Q

What causes a person with Stokes-Adam Syndrome to faint?

A

Delayed ventricular escape–period of time with no electrical activity in the heart

646
Q

What arrhythmia causes circular reentry that is separate from SA node?

A

A flutter

647
Q

What part of the atria is involved in Aflutter?

A

The entire atria

648
Q

How is the atria contracting in a person with a flutter?

A

Atria are contracting in a way that is separate from SA Node

649
Q

What predisposes people to a flutter?

A

Slower conduction rate and atrial hypertrophy

650
Q

Why does aflutter only occur at a slower conduction rate?

A

If faster the AP would run into tissue in the refractory period that would stop the circular movement in the atria

651
Q

How does atrial hypertrophy assist with development of aflutter?

A

Atria is stretched out there is more space for electricity to travel and less likely for circular movement to hit and area of the atria in refractory period

652
Q

What can cause refractory period to not be as effective in preventing arrhythmias?

A

Slow conduction rate and increased distance (atria hypertrophy)

653
Q

Why is Aflutter not an effective primer for the ventricles?

A

Part of the atria is contracting and part of the atria is relaxed–net result would be a high atrial rate

654
Q

Why is atrial rate higher in aflutter?

A

Not waiting for SA node to fire an action potential

655
Q

Can there be elevated ventricular rates in a flutter?

A

Sometimes a few AP pass into ventricles so some elevated ventricular rates

656
Q

Which is worse: Afib or Aflutter?

A

Afib

657
Q

How is afib different from a flutter?

A

Afib doesnt have a defined pathway that electrical current is taking

658
Q

Where is the ectopic pacemaker in afib?

A

There are lots of ectopic pacemakers firing on their own and no coordinated at all

659
Q

What predisposes someone to afib?

A

When the atria are stretched out–increases surface area for weird electrical activity

660
Q

How are the atria contracting in afib?

A

small bits of the atria have little contraction–shaky muscle that causes turbulence

661
Q

What is generated in afib that increases risk for blood clots?

A

Lots of turbulence is generated from all the ectopic pacemakers

662
Q

What could happen if clots are forming in the right atria?

A

Could be pushed into pulmonary system–PE

663
Q

What is the main predisposing factor for afib?

A

Increased age–atria stretched out over time

664
Q

Can afib be treated with ablations?

A

No, since there are multiple sources of pacemaker activity

could ablate a few if they are super problematic

665
Q

What is the movement in the atria called that is associated with afib?

A

Circus movement–going nuts

666
Q

What is shown on ECG in place of p wave for someone in afib?

A

No pave just fibrillations–no blood being pumped

667
Q

Would a patient feel if they are in afib?

A

Depends, but probably would be uncomfortable feeling heart beating at wrong time

668
Q

What is the main issue in afib and aflutter?

A

Atria are not coordinated with the ventricles

669
Q

Why should people with afib/flutter be on an anticoagulant?

A

Since atria arent coordinated with ventricles at certain points atria are contracting and trying to push blood against closed valves–increases risk for clotting and valve calcification

670
Q

What type of issue is Alternans?

A

Incomplete interventricular block

671
Q

What is the primary issue with alternans?

A

Problem with resetting in the purkinje conduction system

672
Q

What could cause increase risk for alternans?

A

-Ischemic purkinje system
-compressed with scar tissue
-inflammation of purkinje

673
Q

What does the pattern for alternans look like on an EKG?

A

irregular QRS that occurs every other beat

alternating between normal QRS and prolonged/low QRS

674
Q

What is happening to the irregular QRS in alternans?

A

Conduction speed of irregular QRS is lower than normal because cell wasnt fully reset and takes longer for AP to get through the tissue (wider)

675
Q

What is the ratio for normal to irregular QRS complexes in alternans?

A

1:1

676
Q

What happens if there is an area in the purkinje system that is chronically depolarized?

A

Slows down purkinje system–can cause Alternans

677
Q

When is alternans more likely to occur?

A

with high ventricular heart rate–slower heart rate would allow more time for repolarization and QRS would look normal

678
Q

What causes premature atrial contractions?

A

Ectopic tissue in atria that fires action potentials early

679
Q

What causes premature atrial contractions?

A

Ischemia, irritation, or calcified plaques

680
Q

What happens in the ventricle as a result of PACs?

A

Creates abnormal filling in the ventricles–not as much time for filling and reduces priming ability of the atria

681
Q

What happens as a result of PACs?

A

Atria beat is not timed right and not in coordinated manner–lower stroke volume in these premature beats

682
Q

What happens to the stroke volume with PACs?

A

Stroke volume is lower

683
Q

What occurs with PACs as a result of lower stroke volume?

A

Radial pulse deficit if listening (less noise generated during PAC)

684
Q

What happens when there are premature contractions originating from AV node or bundle?

A

Obscure P wave depending on timing when AP moves forward into ventricle

685
Q

Where does an early and inverted P wave originate?

A

Originates in high AV

686
Q

Where does a late and inverted P wave originate?

A

Low AV source (probably wont see P wave because its hidden by QRS)

687
Q

What are some things that can cause premature ventricular complexes?

A

Caffeine, Stress, lack of sleep, nicotine

688
Q

What is happening at a PVC?

A

Bigger than normal QRS complex that is happening too quickly

689
Q

Why are normal qrs complexes smaller than PVCs?

A

In normal QRS, the ventricles are depolarizing at about the same time–some of the electrical activity cancels out when depolarizations are coordinated

690
Q

Where does the pacemaker usually start for PVCs?

A

Ectopic pacemaker in the ventricular muscle tissue–takes longer to get into purkinje system (reason why PVC is longer)

691
Q

What happens during ventricular depolarization that produces PVCs?

A

Ventricles are depolarizing independent of each other–not cancelling out any of the current–large deflection in PVCs

692
Q

How does the T wave look after a PVC?

A

If depolarization is abnormal would expect repolarization to be abnormal–usually causes inverted T waves

693
Q

What can PVCs be a precursor to?

A

Paroxysmal Ventricular tachycardia

694
Q

Where does paroxysmal ventricular tachycardia originate?

A

Purkinje system

695
Q

What is happening in paroxysmal ventricular tachycardia?

A

Purkinje conduction system is overactive–high voltage prolonged QRS

696
Q

What causes paroxysmal ventricular tachycardia?

A

Severe ischemia

697
Q

What is paroxysmal ventricular tachycardia a precursor to?

A

V fib

698
Q

What is happening with ventricular rate in paroxysmal ventricular tachycardia?

A

Ventricles are firing at a faster rate than AV or SA node

699
Q

What are early after depolarizations?

A

When an action potential is fired a little early but before it is fully reset

700
Q

How do EAD compare to regular action potentials?

A

EAD are smaller and do not allow for good pumping

701
Q

Why are contractions from EAD weaker than normal?

A

Not very much Ca2+ coming in leads to a decreased force of contraction

702
Q

Why is there a decrease in Ca2+ coming in with EAD?

A

Less ion channel involvement because cell hasnt fully reset

703
Q

How do EAD look on an EKG strip?

A

Look like prolonged QT interval

704
Q

What predisposes someone to early after depolarizations?

A

Sensitivity to L-type calcium channels

705
Q

What can cause and increased sensitivity/ overactive L-type Ca2+ channels?

A

Increased beta adrenergic activity increases sensitivity of l-type ca2+ channels and they are more prone to fire AP

706
Q

What do mACh-R antagonists do in the heart?

A

sensitize L type calcium channels making them more sensitive to firing

707
Q

How does increased amount of Benadryl affect the heart?

A

anticholinergic–presents as long QT syndrome because cells are not resetting themselves before the next AP

708
Q

What are EADs precursors to?

A

Torsades de pointe

709
Q

What is torsades de point a precursor to?

A

Vfib

710
Q

What happens to coronary blood flow if ventricular output is low?

A

eventually coronary blood flow is impacted and none of the tissues can repolarize–leads to vfib

711
Q

What can be attempted to correct vfib?

A

Shock–direct current to reset the heart

712
Q

What would prevent the heart from resetting from a shock to correct vfib?

A

If the ischemia is too severe

713
Q

What are the abnormal accessory bundles that some people have genetically?

A

Bundles of kent

714
Q

What are the bundles of kent and where could they be located?

A

Electrical connections that bypass the normal

extra tissue that connects High lateral wall of left ventricle to left atria or right ventricle to right atria

715
Q

What percent of the population has bundles of kent?

A

0.2%

716
Q

What is a solution if the extra pathway from the bundles of kent becomes an issue?

A

ablation–get rid of the tissue to break the electrical pathway

717
Q

What is an example of a reentry source?

A

Bundles of Kent

A&P (5 decks)

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