Arrhythmias Flashcards
Atrial fibrillation
Most common arrhythmia
Risk increase with age, hypertension, CHF, and previous afib
Dilated atrium is more likely to afib
Characteristics:
- narrow ORS
- no clear P waves
- irregularly irregular rhythm, R-R peaks are not the same length consistently
3rd degree AVN conduction block
Complete uncoupling of atrial and ventricular rhythms
P-P interval is shorter than the R-R interval
Premature ventricular complex
Irregular rhythm
No P waves
No measurable PR interval
Wide QRS complex with large amplitude
INVERTED T-WAVE - meaning that the ventricular repolarization follows in same direction as ventricular depolarization, rather the opposite like its supposed to
Ventricular tachycardia (monomorphic)
Wide QRS
Fast rate (100-250bpm)
No p wave
No measurable PR interval
Ventricular tachycardia (polymorphic, Torsade de Pointes)
Irregularly irregular rhythym
Fast rate (200-250bpm)
No p wave
No measurable PR interval
Wide QRS
Appearance of neighboring complexes differ
Can be drug induced
(Looks like a bunch of squiggle lines with the amplitude close to a QRS complex)
Sinus tachycardia
P-wave is present
Just has a fast heart rate (>100)
Everything else is normal
Ventricular fibrillation
Irregularly irregular
No measurable p wave, PR interval, or QRS
Squiggle lines with amplitude of a P-wave
Atrial flutter
Flutter waves look like P-waves but at very high rates in between QRS complexes
See several flutter waves —> QRS —> more flutter —> QRS …
More common in neonates
There are P-waves…but not every P-wave corresponds to a QRS complex
What are the possible arrhymthmias?
(Is the PR interval changing?)
YES = 2nd degree AV block (Mobitz Type 1)
NO = 2nd degree AV block (Mobitz Type 2)
P-waves and R waves are completely out of sync = 3rd degree AV block = uncoupled atrial and ventricular rhythym
There is a P-wave AND every P-wave corresponds to a QRS
Possible arryhthymias?
Is the heart rate normal?
YES = possible 1st degree AV block (if abnormally long PR interval)
NO = (Is it too fast or too slow?)
—> too fast = sinus tachy
—> too slow = sinus brady
No P-waves
Normal QRS complex
What arrhythmia(s)?
Atrial flutter (if several successive flutter waves between QRS complexes)
No p-waves
Wids QRS complex
Possible arrhythmias?
Is the T-wave inverted?
YES (but can’t see it) = monomorphic ventricular tachycardia
YES = premature ventricular complex (PVC)
No p-waves
Narrow QRS
Possible arrhythmias?
Is the wave pattern irregularly irregular?
YES = afib
NO = possibly paroxysmal supraventricular tachycardia (PVST) = pwaves maby be absent or inverted from AVN retrograde conduction
No p-waves
Twisting QRS complex
Possible arrhythmias
Multifocal ventricular tachycardia
No p-waves or QRS
Possible arrhythmias?
Are there undulations?
NO = asystole
YES = ventricular fibrillation (undulation baseline with no consistent pattern of waves or complexes)
The two main mechanisms of arrhythmias?
- Issue with conductance
2. Impulse formation issue (automaticity)
The 3 types of conductance problems
- Membrane depolarization
- Reentry
- Conduction block
All three can lead to one another or occur at the same time
The 3 types of automaticity issues
- Early after depolarizations (EADs)
- Ectopic automaticity
- Delayed after-depolarizations (DADs)
These are not linked like the conduction issues
Conductance problem: membrane depolarization from myocardial ischemia
Lack of O2 and glucose —> fall in ATP…effects the tissue in 3 ways
- Fall in intracellular pH
- due to switch to anaerobic glycolysis and build up of lactic acid
- inhibits gap junctions between myocytes —> slows down conduction - ATP-mediated K+ channels are no longer inhibited
- normally blocked by ATP intracellularly
- increase in K permeability
- will lead to huge outflux of K+
- E-k will now be closer to zero (less-negative)…therefore so will the resting membrane potential - Na/K ATPase pump no longer functional
- without ATP, the Na/K pump will not be able to reestablish the normal concentration
**all of the these changes will lead to HYPERKALEMIA —> RMP now more depolarized
—> inactivates more Na cahnnels, leading to slower or blocked conduction
Effect of hyperkalemia to AP conduction
Slows them down
RMP will be more depolarized, since E-k will become less-negative
When this happens, more Na channels are inactivated…thus slowing down conduction
Conductance problem: Re-entry
Reentry involves a repetitive circular pattern of excitation…requires the 3 following things to occur
- Presence of more than one parallel conduction pathway…
—> meaning the excitation can flow along more than one route…if one route is blocked, excitation flowing down the others can come back around to flow along the original route in reverse direction - One pathway must have a unidirectional conduction block
—> one of the routes through which the excitation can flow is blocked in one direction…excitation from the other routes can come back around and flow in a retrograde direction along the blocked route - Conduction time around the circuit must be longer than the ERP of any cells within the circuit…
—> usually means the conduction is abnormally slow
—> the cells must be able to be activate when teh excitation comes around, or the circuit will be stoped when teh signal reaches cells in their refractory period
Re-entry can be a result of conduction disturbances (myocardial ischemia) or dispersion of refreatoriness
What is the normal mechanism of conduction when re-entry is not happening?
In normal sinus rhythm..
SAN —> AVN —> daughter branches —> muscles —> spread everywhere it can —> until runs into other routes of the signal —> stopped by other cells in ERPs —> one contraction takes place
What events would lead to re-entry?
- An unidirectional block can occure from an atherosclerotic plaque in a coronary artery
- blood flow will stop in the subendocardial region of the heart
- closer to the endocardial surface, will be somewhat ischemic - slows conduction
The other branch of conduction can go through the partially ischemic zones in a salutatory manner and summate, slowly conducting back up into the normal tissue, and forming a reentrant circuit
What disease states does reentry occur
Dilated cardiomyopathy
Myocardial infarction
Acute atrial dilation with heart failure
Exposure to ion channel blockers that produce unequal effects in different cells
Arrhythmias caused by re-entry
- premature ventricular contrations (or atrial)
- Sustained atrial or ventricular tachycardia - caused by a sustained reentrant circuit
- Afib or vent-fib = can be the result of many reentrant circuits, causing loss of synchronization of stimulation
- Atrial flutter = one large reentrant loop around the right atrium, moving clockwise or counter-clock wise
Conductance problem: conductance block
Types?
- His bundle conduction block
- R or L bundle block
- AV conduction block
His bundle block
Atrial-ventricular uncoupling —> results in bradycardia if distal purkinje fibers starts to pace the ventricle
Can lead to asystole
Right or left bundle block
Asynchronization —> loss of synced contraction leading to reduction of CO
AV conduction block (all types)
- 1st degree = prolonged PR interval, with a QRS complex after it like normal
- 2nd degree
- Mobitz Type 1 = progressive lengthening of the PR interval until the QRS complex drops out…repeat this (like EDM music)
- Type 2 = PR interval is fixed and there is a periodic drop out of QRS without preceding changes to PR - 3rd degree = no AV impulse conduction, p-waves are totally out of sync with QRS, p-waves are cycling at a different cycle length than the QRS
Automaticity problem: ectopic pacemaker
If cardiac arrhythmias develop as a result of increased automaticity in a site outside the SAN (or decreased)…
An ectopic pacemaker can establish an abnormal heart rate or rhythm
= enhanced depolarization of phase 4 outside the SAN
What can cause ectopic pacemakers
- Hypokalemia…can result of diuretics taken for congestive heart failure
—> leads to decreased K+ conductance in purkinje fibers
—> leads to a steeper slope of phase 4 depolarization
(Does not affect SAN, because purkinjes are way more sensitive to K+) - Localized sensitivity to catecholamines after ischemia
—> MIs can lead to a disruption in sympathetic innervation or an area of the endcardium —> increased sensitivity as a result of denervation —> cells increase expression of beta1-receptors and/or decrease in catecholamine reuptake —> sympathetic stimulation enhanced - Myocardial stretch —> stretched due to abnormal wall motion —> activates stretch-activated channels —> increases automaticity
Automaticity problem: EADs
Phase 3 event
Slowed repolarization rate leads to extra depolarizations before the repolarization finishes
Can be caused by:
- drugs that block repolarization currents
—> K channel blockers, quinidine, sotalol, ibutilide, erthyromycin
- congenital ion channel mutations
Worsened by brady, hypokalemia, and low Mg
Automaticity problem: DADs
phase 4 event
Extra AP develops
Ca2+ released by the SER spontaneously —> excess Ca influx —> Na/Ca exchange will occur during diastole —> Na/Ca depolarizing current produced —> extra beats can occur
Involves intracellular Ca2+ overload
- due to drug digoxin, catecholamine excess, or cardiomyopathy
Worsened by tachycadia
