AFIB PATHO Flashcards
Normal conduction of the heart
- 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
What is P wave, QRS complex and S–>T wave?
P wave - atria depolarization, QRS complex –> ventricular depolarization, S–> T wave is ventricular repolarization
What are the 5 phases of AP?
- Phase 0 -> depolarization, Na entry through NA channels –> QRS complex on ECG
- Phase 1 -> Overshoot phase, Ca enters the cell and contracting starts –> QRS complex on ECG
- Phase 2 –> Plateau phase –> Inward slow Na, Inward Ca+, Outward K continues
4.Phase 3 –> repolarization, Ca2+ channels inactivate and outward K continues - Outward NA and inward K through active pumping
What is automaticity and conduction?
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
How do you interpret rhythm?
Shape of waves, consistency, intervals, irregular (regular or irregular irregularity)
What are the reasons for abnormal heart cardiac electrophysiology?
Ischemia–> Hypoxia, Fiber stretch, Hypokalemia, Excess catecholamine activity, Digoxin (IFHED)
What is abnormality in impulse generation?
- Abnormal automaticity arrhythmia –> normal automaticity cells escapes the dominance of the SA node
- Triggered activity arrhythmia –> where a cell that is normally not a pacemaker becomes a pacemaker due to preceding action potential
What is abnormality in impulse conduction?
Bidirectional block without reentry or unidirectional block with reentry arrhythmia
What is triggered activity arrhythmia?
- 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
What are the three degrees of block in the AV node?
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
What is a major contributor to afib patho?
Abnormality in impulse conduction –> reentry
What are the sites, rate and mechanisms of arrhythmia?
Site
- Supraventricular tachycardia
*Atrial arrhythmia
*AV nodal arrhythmia
-Ventricular tachycardia or fibrillation
Mechanisms
- Enhanced automaticity
-Triggered activity
-Reentry
What is AFib?
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
How AF occurs?
- Disease state such as structural heart disease that causes left atrial distension, acute pulmonary embolism
- High adrenergic tone (thyrotoxicosis, surgery, alcohol withdrawal, sepsis, etc)
Lone AF –> No apparent cause
What are the risk factors for Afib?
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
What causes AF?
Multiple reentrant atrial loops
Atrial flutter
Caused by single, dominant, reentrant loop
Rapid atrial impulses (270-330 bpm) but regular atrial activation (regular irregularity)
Classification of AFib
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
CCS SAF SCORE (QOL)
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
Symptoms of AF
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
Complications of AF
- Thromboembolism
- Atrial remodeling
- Hemodynamic consequences
- Rapid ventricular rate
What is thromboembolism?
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
Atrial remodelling
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
Hemodynamic consequences
CO reduces –> bad for HF pts, mitral valve stenosis or cardiomyopathies with baseline reduced CO
Rapid ventricular rate
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
Clinical evaluation
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
Goals of therapy
Prevention of thromboembolism, rate and rhythm control
