AFIB PATHO

Question 1

Normal conduction of the heart

Answer 1

• Electrical signal starts in SA node
• Automaticity (spontaneous impulse generation) affected by ANS (cholinergic and sympathetic)
• Other parts have automatic properties too but rate is less than SA node
• AV node is the only conducting port of the ventricles

Question 2

What is P wave, QRS complex and S–>T wave?

Answer 2

P wave - atria depolarization, QRS complex –> ventricular depolarization, S–> T wave is ventricular repolarization

Question 3

What are the 5 phases of AP?

Answer 3

1. Phase 0 -> depolarization, Na entry through NA channels –> QRS complex on ECG
2. Phase 1 -> Overshoot phase, Ca enters the cell and contracting starts –> QRS complex on ECG
3. Phase 2 –> Plateau phase –> Inward slow Na, Inward Ca+, Outward K continues
   4.Phase 3 –> repolarization, Ca2+ channels inactivate and outward K continues
4. Outward NA and inward K through active pumping

Question 4

What is automaticity and conduction?

Answer 4

Automaticity –> ability of pace maker cells to depolarize spontaneously (available in SA, AV node and His-Purkinhi system)

Conduction –> Impulse travels from SA to AV node through intranodal pathways, AV holds pulse briefly then releases through the His-Purkinji system, Impulse then travels to all ventricular cells through terminal filaments

Question 5

How do you interpret rhythm?

Answer 5

Shape of waves, consistency, intervals, irregular (regular or irregular irregularity)

Question 6

What are the reasons for abnormal heart cardiac electrophysiology?

Answer 6

Ischemia–> Hypoxia, Fiber stretch, Hypokalemia, Excess catecholamine activity, Digoxin (IFHED)

Question 7

What is abnormality in impulse generation?

Answer 7

1. Abnormal automaticity arrhythmia –> normal automaticity cells escapes the dominance of the SA node
2. Triggered activity arrhythmia –> where a cell that is normally not a pacemaker becomes a pacemaker due to preceding action potential

Question 8

What is abnormality in impulse conduction?

Answer 8

Bidirectional block without reentry or unidirectional block with reentry arrhythmia

Question 9

What is triggered activity arrhythmia?

Answer 9

• Initiated by afterdepolarization because of abnormal calcium and sodium influx during or just after full cellular repolarization (previous AP triggers new activity)

Early afterdepolarization
- Phase 2 (type 1) or phase 3 (type II)
- Caused by drugs such as sotalol and Erythromycin or hypokalemia
- Underlying cause of TdP

Delayed afterdepolarization
- Phase 4
- Seen in digoxin toxicity

Question 10

What are the three degrees of block in the AV node?

Answer 10

First degree –> When the beat is taking longer time to travel through the AV node

Sx: Light headedness and dizziness
Meds: BBs, and CCBs cause this block

Second degree –> When some beats do not make it through the AV node –> sig reduction in O2 supply

Sx: Chest pain, increased HR and SOB

Third degree –> No pulse being conducted and another automaticity foci will take over as the pacemaker –> heart’s ability to pump blood reduced

Question 11

What is a major contributor to afib patho?

Answer 11

Abnormality in impulse conduction –> reentry

Question 12

What are the sites, rate and mechanisms of arrhythmia?

Answer 12

Site
- Supraventricular tachycardia
*Atrial arrhythmia
*AV nodal arrhythmia
-Ventricular tachycardia or fibrillation

Mechanisms
- Enhanced automaticity
-Triggered activity
-Reentry

Question 13

What is AFib?

Answer 13

Supraventricular Arrhythmia that is distinguished by non-synchronized atrial activation with a resulting worsening of atrial mechanical function
- More prevalent among elderly popn
-Associated with HF sx
-With reduced mortality of pts with HF, AF incidence will increase

Question 14

How AF occurs?

Answer 14

1. Disease state such as structural heart disease that causes left atrial distension, acute pulmonary embolism
2. High adrenergic tone (thyrotoxicosis, surgery, alcohol withdrawal, sepsis, etc)

Lone AF –> No apparent cause

Question 15

What are the risk factors for Afib?

Answer 15

CVD risk factors: HTN, DM, Obesity
CVD disease: ischemic heart disease, LV dysfunction, valvular heart disease, and HF
Sleep apnea
Hyperthyroidism
After CV surgery
Heavy alcohol drinking
Genetic factors

Question 16

What causes AF?

Answer 16

Multiple reentrant atrial loops

Question 17

Atrial flutter

Answer 17

Caused by single, dominant, reentrant loop

Rapid atrial impulses (270-330 bpm) but regular atrial activation (regular irregularity)

Question 18

Classification of AFib

Answer 18

Paroxysmal –> Recurrent self-limiting episodes (less than 7 days)

Persistent –> Episodes lasting more than 7 days and sinus rhythm achievable (spontaneously or by cardioversion)

Permanent –> Cardioversion failed or not attempted/planned

Question 19

CCS SAF SCORE (QOL)

Answer 19

Class 0 –> Asymptomatic
Class 1 –> Minimal effect on patient’s general QOL
Class 2 –> Minor effect on QOL
Class 3 –> Moderate effect on QOL
Class 4 –> Severe effect on QOL

Question 20

Symptoms of AF

Answer 20

Intermittent episodes of palpitations (rapid HR)
- sometimes AF is asymptomatic

Chest pressure or neck sensation if both atrium and ventricle contracting at same time

Syncope and hemodynamic collapse

Medical emergency if CO reduces or if AF happened in the context of ACS

Question 21

Complications of AF

Answer 21

1. Thromboembolism
2. Atrial remodeling
3. Hemodynamic consequences
4. Rapid ventricular rate

Question 22

What is thromboembolism?

Answer 22

Stall blood within the left atrium may cause thrombus formation

Happens in left atrial appendage secondary to atrial stasis –> clot may move to left ventricle and cause stroke in the brain

Individuals with AF have 5x greater risk for ischemic stroke

Question 23

Atrial remodelling

Answer 23

Changes in atrial tissue that can contribute to the progression of AF
–> Longer time of AF (such as with persistent AF) may cause difficulty of returning to normal electrical and contractile functions

Electrophysiological changes of the atrial tissues –> decrease of effective refractory periods, mediated by intracellular calcium overload

Pathoanatomical changes –> atrial fibrosis, loss of atrial muscle mass

Question 24

Hemodynamic consequences

Answer 24

CO reduces –> bad for HF pts, mitral valve stenosis or cardiomyopathies with baseline reduced CO

Question 25

Rapid ventricular rate

Answer 25

High number of generating impulses –> sig no of impulses die in the AV node

Lots of impulses still sent to the ventricles –> ventricular rates increase (180 bpm)

If it happens for long time –> ventricles may then develop cardiomyopathy and potentially HF

Question 26

Clinical evaluation

Answer 26

Clinical history and physical exam
- presence and nature of sx associated with AF
-Clinical type of AF
-Onset of the first symptomatic attack or date of discovery of AF
-Frequency, duration, precipitating factors and modes of termination of AF
- Response to any pharm agents
-Presence of underlying heart disease or other reversible conditions

ECG
Transthoracic echocardiography
Blood tests – thyroid, renal and hepatic
Six min walk test to evaluate success of rate control
Exercise testing for rate control
Holter monitor or event recording –> 24 hr ambulatory ECG (machine produces ECG when sx appear), if diagnosis unclear, evaluate success of rate control

Question 27

Goals of therapy

Answer 27

Prevention of thromboembolism, rate and rhythm control