Tachyarrythmias Flashcards
What is tachyarrythmia?
Tachy-arrhythmia = Tachycardia = heart rate >100 beats / min. for 3 beats in a row
1) Narrow QRS complex QRS <120ms
2) Wide QRS complex QRS >120ms
What are the 3 mechanisms for tachyarrythmias?
increased Automaticity
Re-entry
After-depolarizations = ‘Triggered activity’
How can cells become a dominant pacemaker?
any cell with Phase 4 slow depolarization can in theory become the dominant pacemaker.
in theory any badly damaged cell can become the dominant pacemaker even if NO normal phase 4
What is the 2 critical criteria for re-entry?
electrically isolated tissue with uni-directional block (–> can’t be depolarized in usual way)
AND
slowed retrograde conduction
_____________________________
two adjacent pathways with different electrophysiological (ie. conduction, velocity, refractory period) are connected proximally and distally
BUT one of the pathways are blocked because it is in prolonged refractory or repolarization period
AND
the unblocked pathway with slow conduction receives premature AP that then gives enough time for the blocked pathway to recover and get excited retrogradely
At what stages of the action potential does Early After-depolarizations occur?
Occur in either stage 2 or 3
More likely to occur in conditions that increase AP duration and therefore ↑ QT
What is an example of early after-depolarization?
Torsades de pointes
What can cause early after-depolarization?
Low blood K+
Low blood Mg++
genetically abnormal K+ (Na+) channels = congenital long QT syndromes
K+-channel blocking drugs (e.g. anti-arrhythmics, many other drug classes)
What may result in response to long repetitive sequence of early after depolarizations?
other surrounding cells might no longer be refractory (able to be re-fired)
fire off (since connected to depolarized cell)
premature firing of patchy areas of heart
Ventricular Tachycardia +/- death!
How do Late After-Depolarizations occur?
cells with too much Ca++ left over
- stimulates Ca/Na+ exchanger leading to a inward current.
- depolarizes cell partially again
- if long enough / high enough depolarization
- fires whole heart off again –> tachycardia
What causes Late After-Depolarizations?
high levels of catecholamines / sympathetic drive drug toxicity (e.g. Digoxin)
T or F: Tachyarrhythmias include premature beats & tachycardias
T
What are Atrial Premature beats?
different P-waves compared with sinus, earlier than expected sinus P
What causes APBs?
caused by similar conditions that cause sinus to fire faster, = increased atrial automaticity
What ECG features are observed in premature ventricular beats?
bizarre, wide QRS with ST / T segments opposite to QRS (abnormal depolarization –> abnormal repolarization)
If every 2nd beat is a PVC, then rhythm called ventricular….
bigeminy
If PVC every 4th beat…
quadrigeminy
if two PVC in a row ….
couplet
What cause VPBs?
increased Ventricular automaticity:
- irritation / injury / inflammation (for non-pacemaker cells)
- catecholamines / drugs
- Electrolyte abnormalities , hypokalemina or hypomagnesenia
- hypoxia
When is VPBs benign?
not unusual in normal hearts (~5/ hour)
usually benign IF no structural heart disease, if needed, can use beta-blockers
What does Narrow Complex Tachycardia imply?
Implies rhythm not arising from ventricles
= SUPRA-VENTRICULAR TACHYCARDIA (SVT)
T or F: Narrow Complex Tachycardia is concerning
F:
usually not immediately life-threatening
can be a marker of underlying serious conditions
often sudden onset, sudden offset
What are the seven SVTs from most normal to abnormal?
- Sinus tachycardia (most normal)
- Ectopic atrial tachycardia
- AV nodal re-entry
- Atrio-Ventricular re-entry
- Multi-focal atrial tachycardia*
- Atrial flutter
- Atrial fibrillation
What is sinus tachycardia?
Sinus P waves >100bpm
What causes sinus tachycardia?
anything that normally should cause heart to increase output –> sinus tachycardia:
exercise, fear, emotions, pain
fever, severe infections
low blood count, low oxygen
Enhanced automaticity
How to treat sinus tachycardia?
Need to treat underlying cause
What is atrial tachycardia?
Ectopic non-sinus P’s >100bpm
What causes atrial tachycardia?
anything that normally can cause sinus tachycardia, can also cause atrial tach
rarely due to structural problem in atria
How to treat atrial tachycardia?
need to treat underlying cause, some may respond to beta blockers (like sinus tachycardia)
What is another name for atrial tachy?
Ectopic Atrial Rhythm
What are the two part to AV node re-entry (AVNRT)?
Slow pathway = slow conduction, faster recovery
Fast pathway = fast conduction, but slower recovery
How does AVNRT occur?
Premature atrial beat might find fast pathway refractory:
- conduct down slow pathway - fires ventricle - now fast pathway recovered - retrograde conduction back up - fires atrium retrograde (hidden P’s) - repetitive ‘short circuit’
What does Atrio-Ventricular Reciprocating Tachycardia (AVRTach) require?
Requires an accessory pathway = bypass tract = Wolff-Parkinson White Syndrome = WPW
AV node and bypass tract have different conduction speeds / refractoriness –> set up for re-entry
- Bypass tract = abnormal, extra A-V connection, that forms a loop with AV-node*
- -> Orthodromic AVRT
- -> Antedromic AVRT
How does AVRT occur?
Premature atrial beat might find accessory pathway refractory
- conduct down AVN - fires ventricle - now accessory pathway recovered - retrograde conduction back up - fires atrium retrograde (ectopic P’s) - repetitive ‘short circuit’
T or F: in Antedromic AVRT QRS generated = wide (cell-to-cell spread in ventricles), even though Supraventricular
T
What is multi-focal atrial tachy?
rate >100bpm
> 3 different P-waves, with different PR’s
due to abnormal atrial automaticity
usually very irregular, unpredictable where / when next atrial P will arise
no dominant P morphology (ie. lots of different P wave morphologies)
rhythm is irregular irregular
What usually is an association with MFAT?
classic association with severe chronic lung disease, or low Mg++
What is atrial flutter?
re-entry ‘short circuit’ in (Right) Atrium
typical atrial rate is 300bpm (250-350)
typically AVN conducts in integer ratios:
2:1 –> heart rate 150bpm
3:1 –> heart rate 100bpm
4:1 –> heart rate 75bpm
can be regular, irregular regular, irr irregular
What kind of ECG is expected for atrial flutter?
typically see ‘saw tooth’ pattern inferiorly
Where is the short circuit found in atrial flutters?
re-entry ‘short circuit’ in (Right) Atrium
What is atrial flutter an indication of?
often a sign of structurally abnormal RA
T or F: RA size dictates the severity of atrial flutter
T:
increased RA size –> longer circuit –> decrease flutter rate
What are risks of atrial flutter?
carries risk of clots in heart –> increase stroke risk
often deteriorates into Atrial fibrillation
What is the trestment for atrial flutter?
Treatment: initially try rate-slowing drugs
may have to ‘shock’ heart back to sinus
What is atrial fibrillation?
totally chaotic atrial depolarizations, no single pacemaker any more
5-30 wavefronts of electrical depolarization randomly winding through atria, colliding / competing to fire any recently repolarized tissue
atrial rate 350-600bpm
Multiple wondering reentrant circuits within the atrium
AV Node filters out most –> average heart rates ~120-180bpm
What kind of pulse is expected in AFib?
Irregularly irregular pulse
What are some risks in AFib?
- no organized atrial pump
- risk of developing clots inside atria (especially appendages)
- risk of clot dislodging
- catastrophic sudden artery blockages (strokes / heart attacks / etc.)
- loss of atrial ‘kick’ filling ventricles
T or F: atrial fib is not common
F:
commonest major arrhythmia
lifetime risk Afib ~1 / 6 adults > 40y !!
What usually causes aFib?
anything that causes sinus tachy can also –> risk of Atrial fib.
any major structural heart disease –> risk of Atrial fib.
most common cause in N. America = high blood pressure
What is treatment for aFib?
Acute Afib –> consider shock, or rate-slowing drugs
if initially comes &goes, might consider anti-arrhythmia drugs, after rate slowing drugs
if persistent / permanent, rate controlling drugs (B-blockers, Ca-channel blockers, digoxin)
Always estimate risk of clots –>blood thinners when:
CHADS score ≥ 1
What are three possibilities resulting to wide complex tachycardia?
1) SVT with bundle branch refractory –> bundle block
= ‘SVT with aberrancy’
(rarely SVT with WPW bypass tract aberrancy)
OR
2) more likely, Ventricular origin = venticular arrythmia (VFib, Torsades, VT)
Or
artifact
What ECG features you would see with SVT with aberrancy?
usually see P-waves 1:1 with QRS
should show typical RBBB or LBBB
QRS usually <140-160ms
What ECG features you would see with ventricular arrythmia?
usually bizarre, often >160ms
if >30s = sustained VT
What are 5 clues for VT?
1) see dissociated P-waves ‘marching through’ the tachycardia = VT
OR
- occasionally a sinus (partly) ‘captures’ the ventricle –> narrow(er) QRS = capture / fusion beats
3) QRS usually bizarre:
not LBBB or RBBB like
>160ms if ‘LBBB’ like
>140ms if ‘RBBB’ like
- all QRS’s in V1-6 either up- or down-going = CONCORDANCE
- extreme QRS axis (-90 to 180°)
What is VT usually due to?
most of VT is NOT from automaticity
mostly due to re-entry, usually from scar tissue (from MI)
–> monomorphic VT (QRS look the same throughout)
T or F: VT can lead to cardiac arrest
VT can often be too fast –> cardiac arrest, especially if poor heart function
What is the treatment for VT?
arrhythmia drugs usually ok if good heart
If any concern patient’s not fully stable, shock heart using external pads on chest, synchronize shock with QRS = Electrical CARDIOVERSION
if very unstable or heart stops electrical shock without any synchronization = DEFIBRILLATION
What is a rare type of VT?
Torsades-de-Pointes
rare type of VT, often short bursts
(polymorphic VT –> different QRS morphorlogy throughout)
What causes TdP?
due to early after-depolarizations, usually from long QT
What ECG features are present in TDP?
VT changes morphology over time, like sine waves ‘twisting of points’
Often starts by alternating slow / premature beats (short – long QT) e.g. ventricular bigeminy
How to treat TdP?
- correct K+ / Mg++ deficits (large i.v. Mg++ dose often immediately helpful)
- stop drugs causing long QT
- can use drugs or temporary pacemaker to speed up HR (shorten QT)
- in some congenital long QT, beta blockers actually help!
- Sometimes need defibrillator
What happens in ventricular fibrillation?
Ventricles no longer one electrical unit
chaotic, random, colliding wave fronts of electrical activity –> CARDIAC ARREST
T or F: vFib is lethal
T:
100% lethal, brain dead in ~5min.
What is the treatment for Vfib?
Only treatment = immediate electrical DEFIBRILLATION
What is the principle behind electrical shocks?
If deliver large voltage / current via chest or via internal wire –> all of heart cells depolarize, no matter what state they were in hope then sinus rhythm resumes
How to administer shock?
If still have a pulse, deliver shock in middle of QRS = synchronized cardioversion
If no pulse, shock ASAP! = defibrillation
T or F: atrial dilation is a risk factor aFib and atrial flutter
T:
