Cardiac Arrhythmias (Coromilas) - 11/7/16 Flashcards
Action potential of a pacemaker cell (e.g. the sinus node)
- Slow phase 4 depolarization:
- Largely caused by the If (pacemaker) inward current, which drives the cell to threshold (approximately −40 mV).
- If channels begin to open when membrane voltage becomes more negative than approx -50 mV (different entities than fast sodium channels responsible for rapid phase 0 depolarization in ventricular and atrial myocytes)
- Upstroke of the AP
- Caused by the slow inward current of Ca++ ions.
- Repolarization
- Reduction of the Ca++ current (due to inactivation of calcium channels) and progressive K+ efflux through voltage-gated potassium channels
- MDP, maximum negative diastolic potential
- TP, threshold potential
Organization of arrhythmias
How are arrhythmias caused?
Native pacemakers and latent pacemakers
Native pacemaker: SA node
- Normally sets HR (60-100 bpm)
Latent pacemakers: AV node / bundle of His / Purkinje fibers
- Have potential to act as pacemakers if necessary
- AV node / bundle of His (50-60 bpm)
- Purkinje fibers (30-40 bpm)
- AV
Overdrive Suppression
Not only does cell population w fastest intrinsic rhythm prevent all other automatic cells from spontaneously firing…. but it also directly suppresses their automaticity
OS: decreases a cell’s automaticity when cell is driven to depolarize faster than its instrinsic discharge rate
Cells maintain their transsarcolemmal ion distributions b/c of continuously active Na+K+-ATPase (3 Na+ ions out, 2 K+ ions in)
- Net effect creates hyperpolarizing current (inside cell is more negative)
- As cell potential becomes more negative, more time is required for spontaneous phase 4 depolarization to reach threshold voltage
- Result: rate of spontaneous firing is decreased
Hyperpolarizing current inc. when cell is caused to fire more frequently than its intrinsic pacemaker rate
- the more often cell is depolarized, the greater tha quantity of Na+ ions that enter cell
- Result of inc intracellular Na+ content –> Na+K+-ATPase becomes more active to restore normal gradient
- Inc. pump activity provides larger hyperpolarizing current to oppose the depolarizing current If to decrease rate of spontaneous depolarization
Electrotonic interaction between pacemaker (e.g. AV node) and myocardial cells
What happens in a diseased state?
Altered impulse formation (3)
- Altered automaticity (of SA node or latent pacemakers)
- Abnormal automaticity in atrial or ventricular myocytes
- Triggered activity
Altered Impulse Formation:
Increased SA node automaticity
What is the most important modulator of normal SA node automaticity?
Autonomic nervous system
- Sympathetic stimulation (B1-adrenergic receptors)
- Inc. rate of pacemaker depolarization via If
- Cause AP threshold to become more negative
- Examples:
- Exercise/stress when SNS inc. HR
Altered Impulse Formation:
Decreased SA Node Automaticity
Parasympathetic NS
- Major controller of HR at rest
- Cholinergic stimulation via vagus nerve acts at SA node
- Reduce If
- More negative MDP
- Less negative threshold level
Escape Rhythms
Occurs if SA node becomes persistently suppressed
Latent pacemaker initiates the escape beat ultimately producing escape rhythm
Enhanced automaticity of latent pacemakers
What can cause this?
If a latent pacemaker develops an intrinsic rate of depolarization faster than the SA node
ectopic beat - impulse is premature relative to normal rhythm whereas escape beat is late
Ectopic beats caused by:
- High catecholamine concentrations
- Hypoxemia
- Ischemia
- Electrolyte disturbances
- Certain drug toxicities (i.e. digitalis)
Altered impulse formation:
Abnormal automaticity
Myocardial cells outside specialized conduction system acquire automaticity + spontaneously depolarize
Cause: cardiac tissue injury
Also show ectopic beats but not from cells that usually possess automaticity
Altered Impulse formation:
Triggered Activity
Under certain conditions, an AP can “trigger” abnormal depolarizations that result in extra heart beats or tachyarrhythmias
- Early afterdepolarziation
- Delayed afterdepolarization
Induced by:
- Digitalis induced tachycardias
- Catecholaminergic polymorphic ventricular tachycardia
- RV outflow tract tachycardias
Altered Impulse Conduction
Alterations in impulse conduction also lead to arrhythmias.
Conduction blocks generally slow the heart rate (bradyarrhythmias);
however, under certain circumstances, the process of reentry can ensue and produce abnormal fast rhythms (tachyarrhythmias).
Altered Impulse Conduction:
Conduction Block
Propagating impulse is blocked when it encounters a region of the heart that is electrically unexcitable
When conduction block is within specialized conducting system of AV node or His-Purkinje system… the normal overdrive suppression that keeps latent pacemakers in His-Purkinje system in check is removed
Result: emergence of escape beats or escape rhythms
Altered Impulse Conduction:
Unidirectional Block and Reentry
Electric impulse circulates repeatedly around a reentry path, recurrently depolarizing a region of cardiac tissue
When an AP can conduct in a retrograde direction –> unidirectional block
Wolff-Parkinson-White Syndrome
In the normal heart, an impulse generated by SA node propagates through atrial tissue to the AV node, where expected slower conduction causes a short delay before continuing on to the ventricles.
However, approximately 1 in 1,500 people have WPW Syndrome –> born with additional connection between an atrium and ventricle.
- Accessory pathway (bypass tract)
- Connection allows conduction b/w atria and ventricles to bypass AV node
- Accessory pathway tissue conducts impulses faster than AV node
- Stimulation of ventricles during sinus rhythm begins earlier than normal
- PR interval is shortened (usually <0.12 sec), or <3 small boxes)
- VEntricles are “pre-excited”
HOWEVER, accessory pathway connects to ventricular myocardium rather than to purkinje system –> subsequent spread of impulse through ventricles from that site is slower than usual
In addition, b/c normal conduction over AV node proceeds concurrently, ventricular depolarization presents a combo of electric impulse traveling via accessory tract and that conducted through normal Purkinje system
Result: QRS complex is wider in WPW patients than normal
Mechanisms and Examples of Arrhythmia Development
