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Supra - ventricular Tachycardia (SVT)
Supra - ventricular Tachycardia (SVT)
Rapid rhythms originating from atria/AV node (above the ventricles)
Narrow complex - unless there is something messing with conduction down the normal path (bundle branches)
Episodic SVTs (abrupt onset & offset) = paroxysmal SVTs (PSVT)
Patho
Patho
Sinus origin: ↓ SV ➔ compensatory ↑ in HR (MI, HF), etOH/stimulants, hyperthyroid
Ectopic origin: Focus/foci fires fast enough to take control of rate
Reentry: electrical loop
SSX
SSX
Palpitations "I feel my heart pounding"/"I feel like my heart is racing", chest pain
↓ diastolic filling ➔ ↓ CO ➔ ↓ perfusion ➔ Dizzy/presyncope/syncope
Polyuria/urgency (atria contracting with closed valves ➔ ↑ pressure ➔ ↑ ANP)
DX
DX
What is the clinical picture? Gradual or sudden onset? Hx of?
How fast is it?
What does the P wave look like?
What is the relationship of the P and the QRS?
TX
TX
Sinus Tach (Not SVT)
Sinus Tach (Not SVT)
HR > 100
Regular
EKG
Normal P-wave and they all look the same
Narrow QRS
How fast is this? ~ Two big boxes in between
If regular: 300, 150, 100, 75, 60, 50
Multifocal atrial tachycardia
Multifocal atrial tachycardia
Multifocal: many origins in atria ➔ different looking P-waves
HR 100 - 180
Irregularly irregular
Patho
Pulmonary dz (COPD)/RAE↓ O2/ ↑ CO2 / ↑ H+, hypoK, HypoMg
EKG
> 3 different & distinct P-waves with variable PR
Isoelectric baseline (make sure it isn't a-flutter or a-fib)
A-fib has no distinct P-waves
TX
β-blockers, CCB if pulmonary DZ present
(β blockers bad in COPD/asthma)
Wandering atrial pacemaker: 3 different P-waves with HR < 100
Rapid AFIB
Rapid AFIB
HR 110 - 160
Irregularly irregular
EKG
No discernible P-waves
TX
β-blockers, non-dihydropyrdine CCB (diltiazem), digoxin
DC cardioversion if sick
Anticoagulation
Ablation is definitive
Vagal maneuvers/adenosine usually won't cardiovert a-fib
Can slow rate down enough to see fibrillatory waves but can also cause ↑ ventricular response and worsening rate
A-FLUTTER
A-FLUTTER
HR Atrial rate is 300
AV conduction ratio (how many impulses get through to ventricle) ➔ ventricular rate
1:1 - 300
2:1(MC) - 150
3:1 - 100
4:1 - 75
Regular
Regularly irregular if 2:1/4:1 in fixed pattern
Irregularly irregular if variable block
Patho
Reentry within right atrium, usually around tricuspid valve
EKG
Flutter waves (saw-tooth pattern) best seen in inferior leads
TX
β-blockers, CCB (non-dihydropyrdine)
DC cardioversion if sick
Anticoagulation
Ablation is definitive
Vagal maneuvers and adenosine will not cardiovert flutter to NS
But can slow the rate down enough to see flutter waves
A-flutter with 2:1 conduction
A-flutter with 4:1 conduction
Accelerated junctional Rhythm (AJR)/Junctional Tachycardia
Accelerated junctional Rhythm (AJR)/Junctional Tachycardia
HR 70-100 (AJR), > 100 (junctional tach)
Regular
Patho
AV junction puts out a higher rate than the SA node and takes over pace
Classic cause of AJR is digoxin toxicity
EKG
Inverted P-waves in inferior leads, absent, or buried in QRS
Short PR in junctional tachycardia
TX
Typically transient; IV β-blockers or CCB (non-dihydropyrdine) in acute
Junctional Tachycardia
Atrioventricular NODAL reentry (AVNRT)
Atrioventricular NODAL reentry (AVNRT)
Functional reentry circuit (within AV node)
Common cause of PSVT
HR 150 - 220
Regular
Patho
Reentrant loop through the two pathways within AV node (see picture)
Usually brought on by PAC
EKG
Typical (MC): P-wave usually buried in QRS. If present, likely after QRS and inverted (retrograde conduction) in inferior leads
Atypical: P-wave so long after QRS that it may appear as if it is before QRS
TX
Usually cardioverts with vagal maneuvers or adenosine
Two pathways within the AV node: a fast one and slow one
If an extra signal makes it to the AV node and the fast pathway is open it will take it
If the slow pathway comes out of refractory while the new signal makes its way down, the signal can go back up the slow pathway
Then back down the fast pathway when that comes out of refractory
Atrioventricular reentry (AVRT)
Atrioventricular reentry (AVRT)
Anatomical reentry (involving an accessory pathway)
Wolff-Parkinson-White (WPW) is a common cause of AVRT
HR 150 - 250
Regular
Patho
Reentrant loop:
one pathway AV node and other pathway is an accessory pathway
EKG
Orthodromic (MC): Orthodromic has narrow QRS
(because signal traveling down the septum)
P-wave typically buried or after QRS
Antidromic: Anti - going up the septum ➔ Wide QRS, Short PR
TX
Orthodromic (narrow)
Vagal maneuvers
Can give adenosine (or verapamil) but can ➔ rapid afib
"Second line" procainamide
Antidromic (wide)
Procainamide
Avoid adenosine unless positive AVRT dx
Telling the difference between a wide complex tachycardia of ventricular origin and antidromic AVRT is difficult
Adenosine shouldn't be given in ventricular tachycardias
Orthodromic (MC)
Atrium ➔ AV NODE ➔ ventricle (antegrade)
Ventricle ➔ accessory pathway ➔ atrium (retrograde)
Antidromic
Atrium ➔ accessory pathway ➔ ventricle (antegrade)
Ventricle ➔ AV node ➔ atrium (retrograde)
Wolff-Parkinson-White (WPW)
Wolff-Parkinson-White (WPW)
Congenital accessory pathway (bundle of Kent) ➔ ventricular preexcitation
Pre-excitation ➔ Delta wave (slurred upstroke at start of QRS)
Slurred upstroke ➔ short PR & wide QRS
Seen in sinus EKG (their baseline EKG)
Preexcitation can ➔ AVRT (Orthodromic MC), A-fib, A-flutter
TX
Stable
WPW ➔ orthodromic: Procainamide
Can give adenosine but can ➔ rapid afib
Antidromic (confirmed): can use adenosine, procainamide safer
AF with preexcitation: Procainamide
Definitely can not use av-nodal blockers (adenosine)
Unstable
**DC cardioversion if sick**
Ablation is definitive
The narrow complex in orthodromic AVRT means that the impulse coming from the atria is taking the AV node pathway
Since the signal is conducted up the accessory pathway (away from the ventricle) the ventricle is not pre-excited... and you don't see a ∆ wave
So, since orthodromic AVRT is MC in WPW... you won't see ∆ waves in WPW induced orthodromic AVRT
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