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IPFC 4 Final > Afib Pathophysiology > Flashcards

Afib Pathophysiology Flashcards

1
Q

What is the normal conduction process
Where does it start?
What allows moves the right atrium’s electricity?
Where does it travel?
(5)

A
  1. Starts at SA node
  2. Travels through internodal tracts
    - Bachman’s bundle allows right atrium’s electricity to move to the left atrium.
  3. AV node (only conducting area between atria/ventricles)
    - also insulates to make sure impulses only pass through the AV node
  4. Impulse travels through Bundle of His
  5. Purkinje fibers
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2
Q

Properties of SA nodes (4)

A
  • has automaticity (generate own impulses)
  • Sets the rate of contraction of the heart
  • fastest rate
  • Affected by autonomic nervous system (cholinergic and sympathetic)
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3
Q

What does the following show:
Pwave
QRS complex
S-T wave

A

P-wave: atrial depolarization (contraction)
QRS complex: ventricular depolarization (contraction)
S-T wave: ventricular repolarization (relaxation)

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4
Q

What are the phases of an action potential
What occurs in each phase
What does each phase correspond to on the EKG

A

Phase 0: Na entry through Na channels
ECG: QRS complex (depolarization)

Phase 1: Ca entry –> contraction starts
ECG: QRS complex (overshoot phase, notch)

Phase 2: Slow Na entry + Ca entry + K exit
ECG: between S-T (plateau)

Phase 3: Ca channels close + K exit continues
ECG: T-wave (repolarization)

Phase 4: Na exit + K entry (priming for next contraction) (resting membrane potential)
ECG: between T-P (plateau)

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5
Q

What is the Action potential duration?

A

Time from phase 0 to end of phase 3

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6
Q

What is the effective refractory period:

A

Time where the heart cell cannot propagate any further impulses
- If this time changes, then the heart might be propagating more impulses (arrythmia)
- Phase 0-3

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7
Q

Define automaticity
Which nodes have this

A

The ability of the pace-maker cells to depolarize spontaneously (due to the pace-maker current)
- Available in SA node, AV node, and His-Purkinji system

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8
Q

Define conduction

A

Impulse travels from SA to AV node through intranodal pathways

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9
Q

How many electrodes does the ECG have, where?

A

9 electrodes
- 2 on hands
- 1 foot
- 6 chest

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10
Q

How many leads are are there on ECG

A

12 leads

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11
Q

In ECG paper what does each represent in seconds
Small square
Large square
5 large squares

A

Small box: 0.04 sec
Large square: 0.20 sec
5 large squares: 1 sec

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12
Q

What is the easy rule for rate calculation in reading ECG papers
What does each box represent in bpm (1 box - 6 boxes)

A

Easy rule: count how many boxes between 2 QRS intervals (if intervals are regular) ->
* 1 box: 300 bpm
* 2 box: 150 bpm
* 3 box: 100 bpm
* 4 box: 75 bpm
* 5 box: 60 bpm
6 box: 50 bpm

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13
Q

Reasons for abnormal heart electrophysiology

A

Ischemia –> hypoxia (ACS)
Fiber stretch (cardiac dilation) (HF)
Hypokalemia
Excess catecholamine activity
Digoxin

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14
Q

What are 2 abnormalities in electrophysiology

A
  1. Abnormality in impulse GENERATION
  2. Abnormality in impulse CONDUCTION
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15
Q

Explain abnormality in impulse GENERATION (2)

A
  1. abnormal automaticity arrhythmia (aka ectopic foci)
    - If other cells (which have automaticity) produce impulses faster than SA node -> Arrythmia due to generation abnormality
  2. Triggered activity
    - cells that should not be producing impulse start producing impulse
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16
Q

What are the 2 types of triggered activity
What phase does it occur?
What drugs/events cause this?

A
  1. Early afterdepolarization (EAD)
    - Occurs in phase 2 or phase 3
    - Caused by sotalol and Erythromycin
    - Hypokalemia can cause this
    - Torsade de Point
  2. Delayed afterdepolarization DAD
    - Occurs in phase 4
    - caused Digoxin toxicity
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17
Q

Explain abnormality in impulse CONDUCTION

A

Bi-directional block without reentry or unidirectional block with reentry arrhythmia

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18
Q

Define “block” in conduction

A

When impulse is held longer than it should be
- cannot conduct the impulses

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19
Q

Define first-degree block AV block
Symptoms
drugs that can cause this
ECG

A

Beat is taking longer time to travel through AV node
- no beat is dropped, slower transduction

Symptoms
- light-headedness and dizziness

Drugs
- Beta blockers
- NDHPs CCB (verapamil, diltiazem)

ECG
- slower HR (bradycardia)

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20
Q

Define 2nd degree AV block
MOA
Symptoms
ECG

A

Conduction held long AND some beats do not make through
- Reduction in O2 supply
- Atrium contracting faster than ventricle

Symptoms
- Chest pain
- dec HR
- SOB

ECG
- Some P-waves with no corresponding QRS complex

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21
Q

Define 3rd degree AV block
MOA
Example

A

All beats are dropped and another automaticity foci (like AV-junctional foci) will take over as the pace-maker
- Heart’s ability to pump blood is significantly reduced

Ex. Ventricular fibrillation

22
Q

Define Ventricular fibrillation

A

occurs when a block occurs and the Purkinje fibres (downstream to the AV node) then “lead” the impulse

23
Q

What are requirements for reentry of impulse (3)
What condition is it a major contributor to?

A
  1. 2 original pathways for impulse conduction
  2. One of the branches has a UNIdirectional block (prolonged refractoriness)
  3. Slow conduction in the other branch

This will activate the original site prematurely without the normal pacemaker

Contribute to afib

24
Q

How can a unidirectional block and reentry happen?

A

A unidirectional block can happen when cells have a longer-than-normal refractory period, so conduction in one section cannot proceed (but it will travel down other branches normally).
- However, once those “blocked” cells exit the refractory period, they receive the impulse from neighbouring cells, causing “re-entry”

25
Q

Define Wolff-parkinson- white syndrome

A

There is additional pathway for impulse to travel BACK to atrium from ventricle
- Insulation is lost

Atria/ventricles should be insulated from each other
- The AV node should be insulated from each other

26
Q

Which type of AV nodal arrhythmia includes wolff-parkinson-white syndrome

A

Atrioventricular reciprocating tachycardia

27
Q

Define Afib (3 classifications)
What is the cause of it?

A

Impulse generation/conduction dysfunction (caused by ectopic foci, triggered activity and/or AV block) and/or
multiple atrial re-entrant loops/wavelets
- both cause loss of ordered conduction/proper contraction

  • non-synchronized
  • Supraventricular
  • Tachyarrhythmia
28
Q

How does Afib occur?

A

Structural heart disease state (MI, HTN, valvular disorders, mitral stenosis, HF) that causes
- left atrial distension
- acute PE
- high adrenergic tone (thyrotoxicosis (inc thyroid), surgery, alcohol withdrawal, sepsis)

29
Q

What does lone Afib mean

A

When there is no apparent cause of afib

30
Q

What are risk factors for Afib (7)

A
  • CV risk factors: HTN, DM, obesity
  • CVD disease: IHD, LV dysfunction, Valvular heart disease, HF
  • Sleep apnea
  • hyperthyroidism
  • Post CV surgery (damage to the heart)
  • Heavy alcohol drinking (cardiotoxic -> “holiday heart”)
  • Genetic factors
31
Q

What is the highest prevalent age group in Afib

A

75-79

32
Q

Why are Afib incidence expected to increase?

A

Due to reduced HF mortality

33
Q

What happens to the ECG in Afib

A
  • Loss of P wave
  • Irregular irregularity QRS complex
34
Q

What is the difference between Afib and atrial flutter (2)

A
  • caused by a single dominant reentrant loop (1 competing pacemaker)
  • Pattern is regular irregularity
35
Q

What is the ventricular response (bpm) if
Transduces every beat
Transduces every 1/2 beat
Transduces every 1/3 beat

A
  • If it transduces every beat: 300bpm ventricular rate
  • If it transduces 1/2 beats: 150bpm ventricular rate
  • If it transduces 1/3 beats: 100bpm ventricular rate
36
Q

What does ECG show for atrial flutter

A

“Saw-teeth”
- P wave absent
- QRS complex will be regular irregularity (show a pattern)

37
Q

Define the classifications of Afib
Paroxysmal
Persistent
Permenant

A

Paroxysmal: lasting less than 7 days and will return to sinus rhythm ALONE (self-limiting)

Persistent: Episodes lasting more than 7 days and can return to sinus rhythm alone or by cardioversion

Permanent: Will not return to sinus rhythm (Cardioversion failed or not attempted/planned)

38
Q

Define non-valvular afib

A

Afib with the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair

39
Q

Define the classification of Afib on the CCS SAF score based on QOL
Class 0
Class 1
Class 2
Class 3
Class 4

A

Class 0: Asymptomatic

Class 1:
* Minimal effect
* Minimal, infrequent
* 1 episode

Class 2:
* Minor effect
* Mild awareness
* Rare episodes (a few a year)

Class 3:
* Moderate effect
* Moderate awareness
* More common episodes (every few months) OR more severe symptoms

Class 4
* Severe effect
* Very unpleasant symptoms
* Frequent, highly symptomatic
* Syncope
* CHF

40
Q

What are symptoms of Afib?

A

heart is racing (palpitations)
- can be without a reason or exercise

Chest and Neck pressure
- if both atrium and ventricle are contracting at the same time
- Right atrium contracting against a closed tricuspid valve

Severe: syncope and hemodynamic collapse

41
Q

When does Afib become a medical emergency?

A

If CO is reduced by a lot
OR
if Afib happened in the context of ACS

42
Q

Complications of AFib (4)

A
  1. Thromboembolism
  2. Atrial remodelling
  3. Hemodynamic
  4. Rapid ventricular rate
43
Q

Why is thromboembolism the biggest complication?
Where does it happen

A

Because blood is not being ejected properly from the heart -> stasis can lead to clot formation
- can go to left ventricle –> brain –> lead to stroke

Where?
- Left Atrial Appendage secondary to atrial stasis

44
Q

T/F Afib patients have 5 times greater risk for ischemic stroke than regular patients

A

True

45
Q

What is the atrial remodelling complication
What are the electrohysiological changes?
Patho-anatomical changes?

A

Changes in the atrial tissue
- the longer the heart remains in Afib (persistent), the more difficult it will be for the heart to return to normal electrical/contractile functions

Electrophysiological
- dec of effective refractory periods
- mediated by intracellular Ca2+ overload

Patho-anatomical
- Atrial fibrosis
- Loss of atrial muscle mass

46
Q

What are the hemodynamic consequences of Afib
Due to?

A

Due to reduced atrial contraction
- CO will be reduced

Much worse in patients with CV disease (HF, mitral valve stenosis etc..)

47
Q

What is the rapid ventricular rate complication

A

Because of a lot of areas generating impulses, a lot of impulses die in the AV node
- However, many reach the ventricles and increase rate up to 180 bpm
- if happens a long time, ventricles can develop cardiomyopathy and maybe HF

48
Q

What is the clinical history to take for diagnosis of Afib (6)

A
  • Symptoms
  • Clinical type (paroxysmal, persistent, permanent)
  • Onset of first symptom
  • Frequency, duration, precipitating factors
  • Response to any medications used
  • presence of any underlying heart disease (hyperthyroidism, alcohol consumption)
49
Q

What blood tests should you do for Afib diagnosis (3)

A

Thyroid
Renal
Hepatic function

50
Q

What does the 6 minute walk test and exercise testing evaluate

A

Success of rate control
- Holter monitor/event recording also does this

51
Q

When is the holter monitor or event recording used?

A

Used in paroxysmal AF (if ECG shows no problems)
- patient presses button when they feel symptoms
- Also used to evaluate success of rate control

52
Q

Goals of therapy for Afib in terms of importance (3)

A

Prevention of thromboembolism
Rate control
Rhythm control

IPFC 4 Final (6 decks)

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