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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
Define Wolff-parkinson- white syndrome
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
Which type of AV nodal arrhythmia includes wolff-parkinson-white syndrome
Atrioventricular reciprocating tachycardia
27
Define Afib (3 classifications) What is the cause of it?
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
How does Afib occur?
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
What does lone Afib mean
When there is no apparent cause of afib
30
What are risk factors for Afib (7)
- 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
What is the highest prevalent age group in Afib
75-79
32
Why are Afib incidence expected to increase?
Due to reduced HF mortality
33
What happens to the ECG in Afib
- Loss of P wave - Irregular irregularity QRS complex
34
What is the difference between Afib and atrial flutter (2)
- caused by a single dominant reentrant loop (1 competing pacemaker) - Pattern is regular irregularity
35
What is the ventricular response (bpm) if Transduces every beat Transduces every 1/2 beat Transduces every 1/3 beat
- 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
What does ECG show for atrial flutter
"Saw-teeth" - P wave absent - QRS complex will be regular irregularity (show a pattern)
37
Define the classifications of Afib Paroxysmal Persistent Permenant
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
Define non-valvular afib
Afib with the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair
39
Define the classification of Afib on the CCS SAF score based on QOL Class 0 Class 1 Class 2 Class 3 Class 4
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
What are symptoms of Afib?
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
When does Afib become a medical emergency?
If CO is reduced by a lot OR if Afib happened in the context of ACS
42
Complications of AFib (4)
1. Thromboembolism 2. Atrial remodelling 3. Hemodynamic 4. Rapid ventricular rate
43
Why is thromboembolism the biggest complication? Where does it happen
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
T/F Afib patients have 5 times greater risk for ischemic stroke than regular patients
True
45
What is the atrial remodelling complication What are the electrohysiological changes? Patho-anatomical changes?
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
What are the hemodynamic consequences of Afib Due to?
Due to reduced atrial contraction - CO will be reduced Much worse in patients with CV disease (HF, mitral valve stenosis etc..)
47
What is the rapid ventricular rate complication
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
What is the clinical history to take for diagnosis of Afib (6)
- 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
What blood tests should you do for Afib diagnosis (3)
Thyroid Renal Hepatic function
50
What does the 6 minute walk test and exercise testing evaluate
Success of rate control - Holter monitor/event recording also does this
51
When is the holter monitor or event recording used?
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
Goals of therapy for Afib in terms of importance (3)
Prevention of thromboembolism Rate control Rhythm control

IPFC 4 Final (6 decks)

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