Afib Pathophysiology Flashcards
What is the normal conduction process
Where does it start?
What allows moves the right atrium’s electricity?
Where does it travel?
(5)
- Starts at SA node
- Travels through internodal tracts
- Bachman’s bundle allows right atrium’s electricity to move to the left atrium. - AV node (only conducting area between atria/ventricles)
- also insulates to make sure impulses only pass through the AV node - Impulse travels through Bundle of His
- Purkinje fibers
Properties of SA nodes (4)
- has automaticity (generate own impulses)
- Sets the rate of contraction of the heart
- fastest rate
- Affected by autonomic nervous system (cholinergic and sympathetic)
What does the following show:
Pwave
QRS complex
S-T wave
P-wave: atrial depolarization (contraction)
QRS complex: ventricular depolarization (contraction)
S-T wave: ventricular repolarization (relaxation)
What are the phases of an action potential
What occurs in each phase
What does each phase correspond to on the EKG
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)
What is the Action potential duration?
Time from phase 0 to end of phase 3
What is the effective refractory period:
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
Define automaticity
Which nodes have this
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
Define conduction
Impulse travels from SA to AV node through intranodal pathways
How many electrodes does the ECG have, where?
9 electrodes
- 2 on hands
- 1 foot
- 6 chest
How many leads are are there on ECG
12 leads
In ECG paper what does each represent in seconds
Small square
Large square
5 large squares
Small box: 0.04 sec
Large square: 0.20 sec
5 large squares: 1 sec
What is the easy rule for rate calculation in reading ECG papers
What does each box represent in bpm (1 box - 6 boxes)
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
Reasons for abnormal heart electrophysiology
Ischemia –> hypoxia (ACS)
Fiber stretch (cardiac dilation) (HF)
Hypokalemia
Excess catecholamine activity
Digoxin
What are 2 abnormalities in electrophysiology
- Abnormality in impulse GENERATION
- Abnormality in impulse CONDUCTION
Explain abnormality in impulse GENERATION (2)
- abnormal automaticity arrhythmia (aka ectopic foci)
- If other cells (which have automaticity) produce impulses faster than SA node -> Arrythmia due to generation abnormality - Triggered activity
- cells that should not be producing impulse start producing impulse
What are the 2 types of triggered activity
What phase does it occur?
What drugs/events cause this?
- Early afterdepolarization (EAD)
- Occurs in phase 2 or phase 3
- Caused by sotalol and Erythromycin
- Hypokalemia can cause this
- Torsade de Point - Delayed afterdepolarization DAD
- Occurs in phase 4
- caused Digoxin toxicity
Explain abnormality in impulse CONDUCTION
Bi-directional block without reentry or unidirectional block with reentry arrhythmia
Define “block” in conduction
When impulse is held longer than it should be
- cannot conduct the impulses
Define first-degree block AV block
Symptoms
drugs that can cause this
ECG
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)
Define 2nd degree AV block
MOA
Symptoms
ECG
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
Define 3rd degree AV block
MOA
Example
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
Define Ventricular fibrillation
occurs when a block occurs and the Purkinje fibres (downstream to the AV node) then “lead” the impulse
What are requirements for reentry of impulse (3)
What condition is it a major contributor to?
- 2 original pathways for impulse conduction
- One of the branches has a UNIdirectional block (prolonged refractoriness)
- Slow conduction in the other branch
This will activate the original site prematurely without the normal pacemaker
Contribute to afib
How can a unidirectional block and reentry happen?
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”
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
Which type of AV nodal arrhythmia includes wolff-parkinson-white syndrome
Atrioventricular reciprocating tachycardia
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
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)
What does lone Afib mean
When there is no apparent cause of afib
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
What is the highest prevalent age group in Afib
75-79
Why are Afib incidence expected to increase?
Due to reduced HF mortality
What happens to the ECG in Afib
- Loss of P wave
- Irregular irregularity QRS complex
What is the difference between Afib and atrial flutter (2)
- caused by a single dominant reentrant loop (1 competing pacemaker)
- Pattern is regular irregularity
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
What does ECG show for atrial flutter
“Saw-teeth”
- P wave absent
- QRS complex will be regular irregularity (show a pattern)
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)
Define non-valvular afib
Afib with the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair
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
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
When does Afib become a medical emergency?
If CO is reduced by a lot
OR
if Afib happened in the context of ACS
Complications of AFib (4)
- Thromboembolism
- Atrial remodelling
- Hemodynamic
- Rapid ventricular rate
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
T/F Afib patients have 5 times greater risk for ischemic stroke than regular patients
True
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
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..)
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
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)
What blood tests should you do for Afib diagnosis (3)
Thyroid
Renal
Hepatic function
What does the 6 minute walk test and exercise testing evaluate
Success of rate control
- Holter monitor/event recording also does this
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
Goals of therapy for Afib in terms of importance (3)
Prevention of thromboembolism
Rate control
Rhythm control
