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LIFESCI 3AA3 > TOPIC THREE: ARRHYTHMIAS > Flashcards

TOPIC THREE: ARRHYTHMIAS Flashcards

1
Q

What is tachycardia

A

Fast heart rate

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2
Q

What does IV metoprolol do

A

It is a beta blocker

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3
Q

What is ablation fro cardioversion

A

Serious treatment

Try to calm the heart rhythm by burning off some of the nerve fibres in the heart

Go through the lungs and pulmonary vessels

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4
Q

What is Wolff Parkinson White syndrome

A

Tachycardia and atrial reactivation

The atria become reactivated

Similar to atrial fibrillation (chaotic activity of the atria)

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5
Q

How do you use an ECG to diagnose

A

Measure the distance between different features on an ECG to make a diagnosis

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6
Q

What is the ECG diagnosis for Wolff-Parkinson-White syndrome

A

Long distance between the P and R peaks

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7
Q

What is a heart arrhythmia

A

An abnormal heart rhythm

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8
Q

What is bradycardia (bpm)

A

Slow heart rate

<60 bpm

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9
Q

What is tachycardia (bpm)

A

High heart rate

>100 bpm

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10
Q

What is fibrillation

A

Uncoordinated contractions

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11
Q

Where can fibrillation happen

A

In the atria or ventricles

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12
Q

What happens if fibrillation happens in the ventricles

A

It can be fatal

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13
Q

Are there many people living with atrial fibrillation

A

yes

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14
Q

Different types of bradycardia

A
  1. Carotid sinus syndrome

2. Heart block (SA block or AV block)

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15
Q

What is Carotid sinus syndrome and how does it work

A

Baroreceptors in the carotid artery are excessively sensitive meaning they are activated a lot. This activation tiggers a response from the vagus nerve. The vagus nerve releases Act which decreases HR

The heart can even stop for 5-10 seconds

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16
Q

What are baroreceptors

A

Pressure sensors in the heart that are really important for controlling BP and vasodilation of the carotid artery

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17
Q

What is the treatment for carotid sinus syndrome

A

Pacemaker

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18
Q

What is an SA block and how does it work

A

Sinal Atrial Block

Impulses from the SA node to the atrial muscle are blocked

Electrical activity does not travel to the atria and therefore there is absence of the P wave

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19
Q

When is the P wave caused

A

When the atria contract and there is depolarization

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20
Q

What is an AV block and how does it work

A

Impulses through the Bundle of His blocked

The impulse does not travel through the Bundle of His from the atria to the ventricles

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21
Q

What is the Bundle of His

A

Runs between the atria and the ventricles

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22
Q

Reasons an AV block can happen

A

Ischemia (lack of blood flow) or compression by scar tissue due to an MI

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23
Q

What is an AV block also called

A

Wenckebach block

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24
Q

What does the SA node do

A

It is an important pacemaker of the heart

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25
Q

How does the SA and AV node interact

A

The SA node sends a message to the AV node

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26
Q

What does the AV node do

A

The AV node sends the message to the atrial ventricular bundle (Bundle of His)

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27
Q

What happens when the signal reaches the Bundle of His

A

The right and left bundle branch down the inter-ventricular septum and then he message is sent to the Perkinje fibres that travel up the side of the ventricles to coordinate contraction

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28
Q

Do the left and right ventricles contract together?

A

Yes

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29
Q

What causes the coordinated contraction of the left and right atria

A

Bachman’s Bundle

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30
Q

The Cardiac Cycle

What is the P wave

A

Atrial Depolarization

Depolarization is the precursor to contraction of the heart

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31
Q

The Cardiac Cycle

What is the QRS complex

A

Ventricles are depolarizing and the atria are repolarizing

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32
Q

The Cardiac Cycle

What is the T wave

A

The ventricles are repolarizing

Repolarization is the precursor to relaxation

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33
Q

Do both atria and both ventricles contract at the same time

A

Yes to both

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34
Q

What is paroxysmal tachycardia

A

Tachycardia that happens suddenly

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35
Q

Types of paroxysmal tachycardia (3)

A

Supraventricular fibrillation

Ventricular fibrillation (V fib)

Postural orthostatic tachycardia syndrome (POTS)

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36
Q

What is Supraventricular fibrillation

A

Rapid heart heats in the atria or there is an issue with the AV node

This is an umbrella term that encompasses Afib

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37
Q

What is ventricular fibrillation (v fib)

A

Most serious

Unconscious within 4-5 seconds, death of tissue within minutes

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38
Q

What is postural orthostatic tachycardia syndrome (POTS)

A

Individuals have difficulty adjusting to standing positions from lying down

Results in rapid heart beat (120 bpm) within 10 mins of standing (not always instantaneous)

Sometimes due to medication (vasodilators, diuretic, antidepressants)

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39
Q

What is Afib

A

Chaotic electrical activity in the atria, causing the atria to quiver

This could lead to ventricular fibrillation

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40
Q

What is the diagnosis of Afib (time)

A

Afib duration >30s is used to diagnose

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41
Q

What will the ventricles do in Afib

A

Pump irregularly and fast (125 - 150 bmp) and have 20-30% reduction in blood flow

Recall that when the heart contracts, blood flow along the major coronary vessels reduces. When the heart relaxes, there is greater flow fo blood through the vessels

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42
Q

Can people be treated for Afib

A

Yes

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43
Q

An aside about coffee

A

Genetic variant that makes individuals less effective at metabolizing caffein which might increase CVD risk

There is a really big variability in the research on if coffee is good or bad for you

There might be some individual variation due to the genetic component based on the metabolism of caffeine

There is a U shaped distribution at the top
Greater than 6 cups of coffee a day is associated with a 22% increased risk of a CVD risk

The fast metabolizers tended to have an increase risk in CVD whereas the slow metabolizers did not (look at the CI that crosses 1)

Genetics may play a role, past 6 cups of coffee a day is associated with an increased risk of CVD

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44
Q

What category does afib fall under

A

super ventricular fibrillation or tachycardia syndrome

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45
Q

What is afib the most common type of

A

arrhythmia

46
Q

What is the prevalence of afib in Canada

Has it been increasing or decreasing

A

350 000

Rate has been increasing
1.68% in 2000, 2.36% in 2014

47
Q

Can afib be asymptomatic

A

yes

48
Q

What happens to the blood in the heart with afib

A

Blood can pool in the heart and form clots

49
Q

What happens to clots (afib)

A

Can move to the brain and cause an ischemic stroke
- increased risk by 4-5 times

Can move the the heart and cause a heart attach especially at the LAD node which leads to the left ventricle

Can lead to heart failure - inability for the heart to pump blood after a long period of time

50
Q

Is there remodelling during afib

A

Yes - there is remodelling the heart which may result in it not pumping properly

51
Q

What is Virchow’s triad

A

Stasis
Hypercoaguability
Endothelial injury

52
Q

What is stasis

A

Blood not moving - not leaving the heart as efficiently

53
Q

What is hypercoagulability

A

Greater risk of coagulation - blood clots

54
Q

What is endothelial injury

A

Damage to inside of the blood vessels

55
Q

What are cardiomyocytes

A

The cells that make up the heart

Contain different channels which contribute to heart contraction

56
Q

What is the depolarization phase of heart contraction

A

The Na channels open, Na enters the cardiomyocyte

The resting membrane potential increases towards +30

57
Q

What is the resting membrane potential of a cardiomyoctye

A

Around -90

58
Q

What happens during the plateau phase of heart contraction

A

The Na channels close, the Ca channels open, the K channels open.

Na stops flowing, however Ca starts to move into the cardiomyocyte which K leaves the cardiomyocyte. Eventually there is a balance leading to the plateau

The heart is fully contracting at this phase, the ventricles are empty and the blood is going to the body/lungs

It is impossible for another action potential to occur during this phase (refractory) - unless you have afib!

59
Q

Which channels are voltage gated

A

Ca and K channels

Their opening is triggered by the voltage hitting +30

60
Q

What happens during repolarization of heart contraction

A

Ca channels close, K channels stay open.

Losing more K than gaining +ive ions now. The membrane potential drops back towards resting

61
Q

What is the absolute refractory period

A

An action potential canon the generated - it is really important to allow the heart to fully contract

Happens during the depolarization and plateau phase

62
Q

What is the relative refractory period

A

Another action potential can be generated if the stimulus is high enough

Perhaps more Na channels open due to hormones

If the heart keeps having more Acton potentials at the stage, the heart is not able to fully relax and expand before the blood goes from the atria to the ventricles

Happens during repolarization

63
Q

Which channels are ligand gated

A

Na channels

64
Q

What system causes the heart to pump

A

The ANS

65
Q

Where are there innervations and what is responsible for the innervations

A

Inside and outside the heart

Ganglions of the ANS inside and outside the heart

66
Q

What is a ganglion

A

A group of neuron cell bodies in the PNS

67
Q

Where are the intrinsic nerves in the heart

A

Nerves in the atria

68
Q

Where are the extrinsic nerves in the heart

A

Extrinsic sympathetic nerves

Cervical
Cervicothoracic (stellate ganglion)
Thoracic

69
Q

What are the cervicothoracic (Stellate ganglion)

What stain shows SNS activity

What stain shows PNS activity

A

Really important for controlling the rhythm of the heart

The stellate ganglion contribute to the sympathetic and parasympathetic nerves. These are the most important.

When the stellate ganglion are activated they contribute to both PNS and SNS activity. We can see staining for:
• Adrenergic = SNS
• Cholinergic = PNS

70
Q

What coordinates the atria contracting together to push the blood to the ventricles

How does it communicate

A

Coordinated by Bachman’s bundle

Allows for communication between the SA node (in the right atria) and the left atria of the heart though the interatrial septum

71
Q

Where is the greatest intrinsic nerve density

A

Autonomic nerve density greatest 5mm from left atrium-pulmonary vein junction

The area that is treated with ablation is usually the left atrium-pulmonary vein junction

72
Q

Is Afib SNS or PNS related

A

Co-localization of adrenergic (SNS) and cholinergic (PNS) nerves

Atrial fibrillation is not just an issue with the SNS

There is an imbalance in SNS and PNS activity

73
Q

What are the main contributors to the extrinsic innervation

A

The vagus nerve (PNS)

Stellate Ganglion (SNS)

74
Q

How much of PNS action on the heart is from the vagus nerve

A

75%

75
Q

Where is the vagus nerve found

A

It is a cranial nerve

76
Q

Does the vagus nerve provide PNS, SNS or both nerves

A

Both, but it is majority PNS

77
Q

How do we know the vagus nerve is involved in PNS and SNS (what enzymes are seen)

A

The vagus nerve releases neurotransmitters that contribute to enzymes responsible for PNS and SNS activity

Tyrosine hydroxyls (TH) - SNS
Choline acyteltransferase (ChAT) - PNS
78
Q

What foes TH do

A

Enzyme involved in the synthesis of catecholamines (ie NE)

These contribute to SNS activity

79
Q

What does ChAT do

A

Enzyme involved in the synthesis of Ach

Contributes to PNS activity

80
Q

Are stellate ganglion more PNS or SNS

A

Major source of SNS innervation/ activity

81
Q

Is the stellate ganglion only SNS?

A

NO!

There are TH and ChAT enzymes found here as well

82
Q

What hormone does the SNS release that acts on the heart

A

Norepinephrine

83
Q

What does NE do on the heart

A

NE is the major hormone involved in afib

Binds to Beta receptor of the heart

84
Q

What happens when NE binds to beta receptors

A

There is increased permeability of Na and Ca to enter the cells - Na is responsible for depolarization therefore there is increased rate of SA node spontaneous depolarization

Since the SA node communicates with the AV node, there is increased conduction to the AV branched

There is therefore increased contractility and increased stroke volume

Max stimulation of SNS = 200 bpm

85
Q

What does the PNS release onto the heart

A

Ach

86
Q

What happens when the PNS releases Ach onto the heart

A

There is decreases SA node spontaneous depolarization

Therefore there is decreased conduction to the AV branches

There is increases permeability of K to leave the cell leading to hyper polarization (making it harder for the cardiomyocytes to contract and decreasing heart rate)

Does not significantly change contractility

Max stimulation = 25 bpm

87
Q

What is autonomic remodelling

A

The remodelling that occurs when there is a heart attack (cell death, necrosis)

88
Q

What happens to nerve growth after a heart attack

A

There is increases nerve growth factors within a month of a heart attack

The heart might be weaker due to ischemia or cell death, the heart is trying to compensate by increasing nerve endings that travel to the heart

89
Q

Canine experiment

A

Post MI - increase nerve growth factor levels within 1 month

Canines: inject nerve growth factor - increase in the enzyme that led to NE synthesis - the density of the nerves of the heart increases over time - increases innervation of the heart (stained for TH, proxy for studying the amount of hormone produced by the SNS)

They also used anti-growth associated protein 43 antibody (GAP43)
Stain the cells
- GAPS 43 protein expressed in the growth cone of sprouting axons is a marker for nerve sprouting (Like TH is)
- Increase of GAP43-positive nerves in dogs with AF suggest that nerve sprouting is responsible for the sympathetic hyperinnervation in these dogs
- Some of the GAP43-positive nerves may have been parasympathetic nerves
- We attempted to stain with the anti-cholinacetyletransferase (ACH precursor) antibody.

Although the parasympathetic nerve ganglion was well stained, no parasympathetic nerve twigs were identified

90
Q

What is the term for the nerve regrowth after a heart attack

A

Nerve sprouting at non-infracted areas

It is a compensation mechanism

91
Q

Why is nerve sprouting bad (afib)

A

Nerve sprouting can lead to increased duration of Afib and increased sympathetic innervation which can lead to irregular heart beat characteristics of people with afib

92
Q

How do we know that PNS and SNS are involved in afib

A

Recall that both the PNS and SNS are involved in atrial fibrillation

  • If it was just a fast heart rate, then the SNS would be the major contributor
  • Since it is so inconsistent in people with afib, we know that both parts of the nervous system are involved
93
Q

Neural control in Afib

Flow SNS

A

Excitation of sympathetic nerves in afib patients leads to the release of NE from the nerve endings.

NE binds to the beta-adrenergic receptor on the cardiomyocytes.
This leads to PKA being activated by cAMP (secondary messenger).

Ca is then released from the sarcoplasmic reticulum (calcium storage spot).

  • Calcium is important for muscle contraction
  • Calcium is involved in the cross-bridge cycle which leads to contraction

More Ca is also allowed into the cell by an L type calcium channel

All of these leads to prolong depolarization and greater contraction strength of the heart
- Longer depolarization will increase the length of the absolute refractory period

When this is coupled with excessive PNS activation (as it is with afib) there are issues

94
Q

Neural control in Afib

Flow PNS

A

Excitation of PNS nerves
When parasympathetic nerves are activated there is Ach release

Ach binds to an M2 Type 2 Muscarinic receptor on the cardiomyocyte

This will activate K channels allowing more K to exit the cell
This leads to repolarization and reduction in action potential duration

This makes the number of beats per minute very irregular

  • SNS is changing depolarization
  • Repolarization and the duration of the action potential are changing with the PNS
95
Q

What is a sarcolemma

A

Cell membrane of the cardiomyocyte

96
Q

What types of receptors are on the sarcolemma

A

beta-adrenergic receptor

97
Q

What happens when the beta-adrenergic receptor is activated (SNS)

A

cAMP and PKA involvement

98
Q

What channels does PKA open

A

L type Ca channels allowing more Ca into the cell

99
Q

Where else does Ca come from

A

The sarcoplasmic reticulum

100
Q

What are downstream, effects (besides heart contraction) of more Ca in the cell

A

Genetic activation of the hypertrophy and fibrosis programs of the heart

101
Q

What is hypertrophy

A

There is an enlargement of the interventricular septum after a heart attack

There is shrinking of the left ventricular space - less blood filled in this area and therefore less blood pumped to the body

102
Q

What is fibrosis

A

Replacing healthy muscle cells of the heart with collagen and other matrix proteins which increases stiffness and decreases contractility

103
Q

Summary effects

A

The SNS and PNS are not functioning properly

Norepinephrine

  • Fast depolarization, faster heart rate
  • Greater strength of contraction
  • Activation of hypertrophic and fibrotic gene programs

Ach

  • Shorter duration of depolarization
  • Faster repolarization
  • leads to irregular heartbeat, and decreased stroke volume

Overall leading to pathological heart remodelling

104
Q

What is lone afib

A

Afib in individuals without other heart conditions

105
Q

What is pathological afib

A

Afib coinciding with other heart conditions

106
Q

Ways to manage afib

A

There are different ways to manage afib
- One way is to manage the risk factors associated with afib
- Here we are managing risk factors after ablation
o There is a short-term efficacy of ablation, but then the nerve sprouting might reoccur – therefore managing other risk factors associated with CVD and afib development might help to limit the need for re-ablation

107
Q

What is the most common site for ablation

What is the goal

A

The target site for ablation is the left atrium around the junction of the pulmonary veins

The procedure is to burn off the nerve endings that have sprouted in the atrium to decrease the electrical activity in the left atrium

108
Q

Afib - remodelling of the heart - ablation

Study

A

The results of the study showed that the left atrium volume decreased in size

  • For someone with afib, the larger the heart size means the heart has undergone more remodelling
  • Shrinking the heart is bringing it back to what a more normal heart would look like
  • Reversing the heart remodelling
  • However, there is still some heart remodelling that will not be replaced (fibrosis), but changing the size of the heart can be done

Based on echocardiogram results the researchers determined that in the risk factor management group, there was a decrease in the left atrium volume as well as a decrease in the left ventricular septum size
- Maybe going back to pre afib heart measurement size
The afib severity score was also significantly different

There were also positive changes in the control group
- The control group had the ablation but not the risk factor management as part of the study

Some people also decreased their medications

In general, ablation + RFM was superior in this study

109
Q

Ablation vs. drugs

The Catheter Ablation vs Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial

What was the trial testing

A

Is ablation more effective than drug therapy

110
Q

Why is drug treatment a little more complicated

A

There are a lot of afib drugs, they may not be as effective, there might have to be some trial and error and see which one works well for the individual patient

111
Q

The Catheter Ablation vs Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial

Results

A

Primary outcome: death, stroke, serious bleeding or cardiac arrest

  • There was no significant difference between the two groups (ablation vs. drugs)
  • 8% in ablation group, 9.2% in drug group  NS

Looking at other outcomes like morality or CVD hospitalization, there was a 17% lower risk in the ablation group
People with ablation appeared to be a t lower risk for recurrent afib.

112
Q

The Catheter Ablation vs Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial

Take home messages

A

Based on death, stroke, serious bleeding or cardiac arrest - doesn’t matter if someone picked medication or ablation

Based on mortality, hospitalization and recurrence of afib - Ablation is better than medication

But, intention to treat analysis data for patients, regardless If they decide to switch groups (ie don’t want ablation and move to medication)

  • Intention to treat analysis analyses data from patients regardless if they decide to move to the different group
  • Someone who was assigned to the ablation group could switch to the medication if they were uncomfortable with the ablation, but their data would be analyzed as if they were in the ablation group still
  • Per protocol: the patients are analyzed by the treatment they received
  • Statisticians think that this might have some more bias in it

Absolute treatment differences do not warrant recommendation for ablation

  • The researchers talked about the absolute treatment differences vs. the relative #
  • The percent differences between the two groups that we were talking about above are relative differences
  • The absolute treatment differences did not warrant one over the other
  • The doctors cannot recommend someone picking one over the other for certain

LIFESCI 3AA3 (6 decks)

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