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LIFESCI 3AA3 > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Ecchymosis

A

bruise, discoloured spot resulting from an accumulation of blood under the skin surface caused by an injury

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2
Q

Ablation

A
  • when they try to calm the rhythm of the heart by burning of some nerve fibres inside the heart
  • they gain access to the heart by going through lungs and gaining access to pulmonary vessels
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3
Q

Heart Arrhythmia

A

abnormal heart rhythm

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4
Q

Three types of arrhythmias

A

bradycardia, tachycardia, and uncoordinated contractions

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5
Q

Bradycardia

A
  • slower than normal heart rate and is usually less than 60 bpm
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6
Q

Tachycardia

A
  • faster than normal heart rate and is usually more than 100 bpm
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7
Q

Uncoordinated contractions

A

causes fibrilation

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8
Q

list the two syndromes that can cause bradycardia

A

carotid sinus syndrome, and heart block

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9
Q

How does carotid sinus syndrome cause bradycardia?

A

baroreceptors on the carotid artery are excessively sensitive which triggers a response from the vagus nerve, causing a domination of the vagal-Ach effects on the heart which then causes a decrease in heart rate (i.e. bradycardia)

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10
Q

What are the two types of heart blocks that can lead to bradycardia?

A

SA block and AV block

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11
Q

How can SA block lead to bradycardia?

A
  • SA block is when impulses from the SA node to atrial muscle are blocked and so atrial contraction does not occur
  • atrial contraction is depolarization which means there is an ending of the P wave
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12
Q

How did AV block lead to bradycardia?

A
  • AV block is when impulses through the Bundle of His is blocked which slows down impulse travel from atria to ventricle
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13
Q

Where is electrical activity initiated in the heart?

A

SA node

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14
Q

How do contractions start?

A

Electrical activity initiated at SA node is sent to the AV node which then makes its way to the Bundle of His which then sends it to the Purkinje fibres to cause coordinated contraction.

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15
Q

Bachman’s bundle

A

responsible for coordinating the contraction of both the left and right atria, and the left and right ventricle

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16
Q

What are the three key stages of the cardiac cycle?

A

P, QRS complex and T.

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17
Q

What happens during P wave?

A

atria depolarization

- depolarization is the precursor to contracting of the heart

18
Q

What happens during the QRS complex?

A
  • two events need to occur in order for the QRS complex to be generated: ventricle depolarization, and atria repolarization
19
Q

What happens during the T wave?

A

ventricle repolarization

- repolarization is the precursor to relaxing of the heart

20
Q

Paroxysmal tachycardia

A

tachycardia that happens suddenly

21
Q

two types of fibrillation that occurs as a result of paroxysmal tachycardia

A

supraventricular fibrillation (rapid heart beat in the atria or AV node) and ventricular fibrillation (rapid heart beat in the ventricle)

22
Q

Postural orthostatic tachycardia syndrome (POTS)

A
  • difficulty adjusting to standing position from lying

- rapid heart beat (120bpm) within 10 minutes of standing

23
Q

Atrial fibrillation

A

chaotic electrical activity in the atria causing atria to quiver

24
Q

When is an individual diagnosed with Afib?

A

when AF duration is more than 30 seconds

25
Q

How does atrial fibrillation also lead to ventricular fibrillation?

A

it can lead to ventricular fibrillation as well because when atria contracts, blood flows from atria to ventricle and so irregular atrial contraction can affect blood flow

26
Q

two consequences of Afib

A

stroke (blood pools in your heart and forms clots which then travel to the brain) and heart attack (blood pools in your heart and forms clots)

27
Q

Atrial remodelling

A
  • occurs when Afib remains untreated for a very long time

- this remodelling decreases the heart’s ability to pump blood to the rest of the body

28
Q

What is the Virchow’s triad?

A

risks and consequences of Afib
- three parts: stasis (decreased blood flow), endothelial injury (damage to the inside of the blood vessel) and hypercoagulability (formation of more blood clots)

29
Q

difference between tachycardia and fibrilation

A

tachycardia is fast heart rate while fibrillation is chaotic heartbeat

30
Q

What happens during depolarization at the cardiomyocyte?

A

sodium channels open and sodium ions enter the cardiomyocyte

31
Q

What happens during the plateau stage at the cardiomyocyte?

A

sodium channels close, calcium channels open and calcium ions enter the cardiomyocyte. potassium channels open, potassium ions exit cardiomyocytes.

32
Q

What happens during repolarization at the cardiomyocyte?

A

calcium channels close. potassium channels stay open and potassium ions continue to exit cardiomyocyte

33
Q

Absolute refractory period

A

phase in which another action potential cannot be generated which is important because it allows for the heart to fully contract and fully pump blood

34
Q

Relative refractory period

A

phase in which another action potential can be generated if the stimulus is large enough

35
Q

What happens to the refractory period for people with atrial fibrillation?

A

the relative refractory period is altered. If we have activation of the sodium channels caused by maybe the presence of a hormone, this will cause another action potential to be generated. If this happens, the heart will not be able to fully relax, and expand before blood flows from atria to ventricles.

36
Q

Where is ablation treated?

A

left-atrium-pulmonary vein junction because this region has the highest autonomic nerve density

37
Q

Interatrial septum

A

Wall that allows for Bockman’s bundle to travel through in order to establish coordinated contraction between both atria’s and allows for communication between the sinoatrial node located in right atrium and left atrium of the heart

38
Q

Autonomic remodelling

A

when individuals experience increase in nerve growth factors (i.e. nerves start to grow) within one month of having a myocardial infarction

39
Q

How does autonomic remodelling link heart attack to atrial fibrillation?

A

Having a heart attack can decrease blood flow and eventually lead to cell death and tissue death of parts of the heart. In order to compensate for the tissue death, nerve endings will increase. The increase in nerve endings (i.e., nerve sprouting) can cause an increase in duration of atrial fibrillation.

40
Q

Hypertrophy

A

enlargement of the heart due to the increase in size of its cells (specifically enlarged interventricular septum and shrinking of the left ventricular space)

41
Q

Fibrosis

A

replacing healthy muscle cells with collagen and other matrix type proteins which decrease contractility and increase stiffness

LIFESCI 3AA3 (4 decks)

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