TOPIC THREE: ARRHYTHMIAS Flashcards
1
Q
What is tachycardia
A
Fast heart rate
2
Q
What does IV metoprolol do
A
It is a beta blocker
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
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)
5
Q
How do you use an ECG to diagnose
A
Measure the distance between different features on an ECG to make a diagnosis
6
Q
What is the ECG diagnosis for Wolff-Parkinson-White syndrome
A
Long distance between the P and R peaks
7
Q
What is a heart arrhythmia
A
An abnormal heart rhythm
8
Q
What is bradycardia (bpm)
A
Slow heart rate
<60 bpm
9
Q
What is tachycardia (bpm)
A
High heart rate
>100 bpm
10
Q
What is fibrillation
A
Uncoordinated contractions
11
Q
Where can fibrillation happen
A
In the atria or ventricles
12
Q
What happens if fibrillation happens in the ventricles
A
It can be fatal
13
Q
Are there many people living with atrial fibrillation
A
yes
14
Q
Different types of bradycardia
A
- Carotid sinus syndrome
2. Heart block (SA block or AV block)
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
16
Q
What are baroreceptors
A
Pressure sensors in the heart that are really important for controlling BP and vasodilation of the carotid artery
17
Q
What is the treatment for carotid sinus syndrome
A
Pacemaker
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
19
Q
When is the P wave caused
A
When the atria contract and there is depolarization
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
21
Q
What is the Bundle of His
A
Runs between the atria and the ventricles
22
Q
Reasons an AV block can happen
A
Ischemia (lack of blood flow) or compression by scar tissue due to an MI
23
Q
What is an AV block also called
A
Wenckebach block
24
Q
What does the SA node do
A
It is an important pacemaker of the heart
25
How does the SA and AV node interact
The SA node sends a message to the AV node
26
What does the AV node do
The AV node sends the message to the atrial ventricular bundle (Bundle of His)
27
What happens when the signal reaches the Bundle of His
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
28
Do the left and right ventricles contract together?
Yes
29
What causes the coordinated contraction of the left and right atria
Bachman's Bundle
30
The Cardiac Cycle
What is the P wave
Atrial Depolarization
Depolarization is the precursor to contraction of the heart
31
The Cardiac Cycle
What is the QRS complex
Ventricles are depolarizing and the atria are repolarizing
32
The Cardiac Cycle
What is the T wave
The ventricles are repolarizing
Repolarization is the precursor to relaxation
33
Do both atria and both ventricles contract at the same time
Yes to both
34
What is paroxysmal tachycardia
Tachycardia that happens suddenly
35
Types of paroxysmal tachycardia (3)
Supraventricular fibrillation
Ventricular fibrillation (V fib)
Postural orthostatic tachycardia syndrome (POTS)
36
What is Supraventricular fibrillation
Rapid heart heats in the atria or there is an issue with the AV node
This is an umbrella term that encompasses Afib
37
What is ventricular fibrillation (v fib)
Most serious
Unconscious within 4-5 seconds, death of tissue within minutes
38
What is postural orthostatic tachycardia syndrome (POTS)
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)
39
What is Afib
Chaotic electrical activity in the atria, causing the atria to quiver
This could lead to ventricular fibrillation
40
What is the diagnosis of Afib (time)
Afib duration >30s is used to diagnose
41
What will the ventricles do in Afib
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
42
Can people be treated for Afib
Yes
43
An aside about coffee
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
44
What category does afib fall under
super ventricular fibrillation or tachycardia syndrome
45
What is afib the most common type of
arrhythmia
46
What is the prevalence of afib in Canada
Has it been increasing or decreasing
350 000
Rate has been increasing
1.68% in 2000, 2.36% in 2014
47
Can afib be asymptomatic
yes
48
What happens to the blood in the heart with afib
Blood can pool in the heart and form clots
49
What happens to clots (afib)
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
Is there remodelling during afib
Yes - there is remodelling the heart which may result in it not pumping properly
51
What is Virchow's triad
Stasis
Hypercoaguability
Endothelial injury
52
What is stasis
Blood not moving - not leaving the heart as efficiently
53
What is hypercoagulability
Greater risk of coagulation - blood clots
54
What is endothelial injury
Damage to inside of the blood vessels
55
What are cardiomyocytes
The cells that make up the heart
Contain different channels which contribute to heart contraction
56
What is the depolarization phase of heart contraction
The Na channels open, Na enters the cardiomyocyte
The resting membrane potential increases towards +30
57
What is the resting membrane potential of a cardiomyoctye
Around -90
58
What happens during the plateau phase of heart contraction
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
Which channels are voltage gated
Ca and K channels
Their opening is triggered by the voltage hitting +30
60
What happens during repolarization of heart contraction
Ca channels close, K channels stay open.
Losing more K than gaining +ive ions now. The membrane potential drops back towards resting
61
What is the absolute refractory period
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
What is the relative refractory period
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
Which channels are ligand gated
Na channels
64
What system causes the heart to pump
The ANS
65
Where are there innervations and what is responsible for the innervations
Inside and outside the heart
Ganglions of the ANS inside and outside the heart
66
What is a ganglion
A group of neuron cell bodies in the PNS
67
Where are the intrinsic nerves in the heart
Nerves in the atria
68
Where are the extrinsic nerves in the heart
Extrinsic sympathetic nerves
Cervical
Cervicothoracic (stellate ganglion)
Thoracic
69
What are the cervicothoracic (Stellate ganglion)
What stain shows SNS activity
What stain shows PNS activity
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
What coordinates the atria contracting together to push the blood to the ventricles
How does it communicate
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
Where is the greatest intrinsic nerve density
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
Is Afib SNS or PNS related
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
What are the main contributors to the extrinsic innervation
The vagus nerve (PNS)
Stellate Ganglion (SNS)
74
How much of PNS action on the heart is from the vagus nerve
75%
75
Where is the vagus nerve found
It is a cranial nerve
76
Does the vagus nerve provide PNS, SNS or both nerves
Both, but it is majority PNS
77
How do we know the vagus nerve is involved in PNS and SNS (what enzymes are seen)
The vagus nerve releases neurotransmitters that contribute to enzymes responsible for PNS and SNS activity
```
Tyrosine hydroxyls (TH) - SNS
Choline acyteltransferase (ChAT) - PNS
```
78
What foes TH do
Enzyme involved in the synthesis of catecholamines (ie NE)
| These contribute to SNS activity
79
What does ChAT do
Enzyme involved in the synthesis of Ach
| Contributes to PNS activity
80
Are stellate ganglion more PNS or SNS
Major source of SNS innervation/ activity
81
Is the stellate ganglion only SNS?
NO!
There are TH and ChAT enzymes found here as well
82
What hormone does the SNS release that acts on the heart
Norepinephrine
83
What does NE do on the heart
NE is the major hormone involved in afib
Binds to Beta receptor of the heart
84
What happens when NE binds to beta receptors
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
What does the PNS release onto the heart
Ach
86
What happens when the PNS releases Ach onto the heart
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
What is autonomic remodelling
The remodelling that occurs when there is a heart attack (cell death, necrosis)
88
What happens to nerve growth after a heart attack
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
Canine experiment
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
What is the term for the nerve regrowth after a heart attack
Nerve sprouting at non-infracted areas
It is a compensation mechanism
91
Why is nerve sprouting bad (afib)
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
How do we know that PNS and SNS are involved in afib
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
Neural control in Afib
Flow SNS
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
Neural control in Afib
Flow PNS
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
What is a sarcolemma
Cell membrane of the cardiomyocyte
96
What types of receptors are on the sarcolemma
beta-adrenergic receptor
97
What happens when the beta-adrenergic receptor is activated (SNS)
cAMP and PKA involvement
98
What channels does PKA open
L type Ca channels allowing more Ca into the cell
99
Where else does Ca come from
The sarcoplasmic reticulum
100
What are downstream, effects (besides heart contraction) of more Ca in the cell
Genetic activation of the hypertrophy and fibrosis programs of the heart
101
What is hypertrophy
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
What is fibrosis
Replacing healthy muscle cells of the heart with collagen and other matrix proteins which increases stiffness and decreases contractility
103
Summary effects
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
What is lone afib
Afib in individuals without other heart conditions
105
What is pathological afib
Afib coinciding with other heart conditions
106
Ways to manage afib
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
What is the most common site for ablation
What is the goal
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
Afib - remodelling of the heart - ablation
Study
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
Ablation vs. drugs
The Catheter Ablation vs Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial
What was the trial testing
Is ablation more effective than drug therapy
110
Why is drug treatment a little more complicated
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
The Catheter Ablation vs Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial
Results
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
The Catheter Ablation vs Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial
Take home messages
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
