Cardio 27 : Supraventricular Tachyarrhythmias Flashcards
Supraventricular
Rhythm generated above the ventricles
Tachyarrhythmia
Atrial complexes greater than 100 bpm
Supraventricular Tachyarrhythmia
Abnormal action potential (impulse) formation by SA node, atria or junction/AV node
OR
Abnormal conduction of impulses through normal or abnormal pathways
What part of the conduction system is mostly responsible for ventricular responses in SVT ?
AV node
What drugs can be given to help slow AV nodal conduction ?
Adenosine
BB’s
CCB’s (Non DHP’s -Verapamil and Diltiazem)
Dihydropyridines have vasodilatory effect. Little
effect on chronotropy
Digoxin
3 Electrophysical etiologies for SVT
Tissue automaticity
Triggered Activity
Re-entry
Tissue automaticity (etiology)
Foci in cardiac tissues become more “irritable”-more likely to cause their own action potential
Usually seen in setting of systemic stress or from a biochemical effect on tissues
What is the state of the ANS in increased tissue automaticity ?
Increased Sympathetics
Decreased PS.
Other factors leading to automaticity include: Increased systemic catecholamines Hypoxemia Hyperthyroidism Chemical stimulants, including caffeine Drugs-excess Digoxin, toxins (ethanol) Stretch of myocardium
Re-entry SVT is due to …
two adjacent areas of conducting tissue with differing conduction velocities and refractory periods. Abnormal conduction between them sets off a circuit that rapidly paces the atria and/or the ventricles.
The timing of Re-entry SVT tends to be
paroxysmal and short lived
Triggered SVT
An action potential (depolarization) that occurs during the repolarization period of a preceding AP
paroxysmal
term applied to several types of tachycardias, essentially means rapid onset, and often rapid termination.
NOT GRADUAL
Symptoms of SVT
Palpitations Fatigue Lightheadedness Chest discomfort Dyspnea Presyncope
What symptom rarely occurs with SVT
syncope
More associated with :
Abrupt termination of SVT
Other structural abnormalities
Aortic stenosis, hypertrophic cardiomyopathy,
etc.
palpitations that are Nonparoxysmal with gradual onset and termination are indicative of …
Physiologic Sinus Tachycardia
palpatations that are Irregular are associated with..
Premature complexes, Atrial Fibrillation, or Multifocal Atrial Tachycardia
Palpitations that are Recurrent with abrupt onset and termination are indicative of
paroxysmal (very likely re-entry SVT)
Palpitation that can be terminated by vagal maneuvers likely involve
Re-entry involving AV node
Persistant tachycardia of weeks- months duration can cause what dangerous morbidity to occur ?
cardiomyopathy and subsequent heart failure if not treated
List the different types of SVT
Sinus tachycardia AV Nodal Re-entry Junctional tachycardia Atrial Tachycardia Multifocal Atrial Tachycardia Atrial Fibrillation Atrial Flutter
sinus tachycardia
Tachycardia with impulses originating from the sinus node.
Can be due to increased automaticity of sinus node, can also be re-entrant.
Types of sinus Tachycardia
Physiologic Sinus Tachycardia
Inappropriate Sinus Tachycardia
Postural Orthostatic Sinus Tachycardia (POTS)
Sinus Re-entry
An expected increase in sinus rate above 100 BPM due to a given level of physical, emotional, pathological or pharmocologic stress.
Physilogic stress
Causes of physiologic stress
Physical/Emotional: Exercise, fear, anger, stress, etc.
Pathologic: fever, anemia, MI, hypoxia, hypovolemia, CHF, pulmonary embolism, infection, shock, thyrotoxicosis, pheochromocytoma
Pharmocologic:
1.Stimulants: caffeine, nicotine, alcohol, amphetamines, cocaine, ectasy, other recreational drugs
2.Prescribed medications: Beta agonists, atropine, aminophylline, catecholamines, some anti-cancer drugs
EKG findings of Physiologic Sinus tach
(+) P-waves in I, II, aVF (Left sided leads), (-) in aVR
Normal PR interval
P waves may become peaked, have large amplitude
Every P-wave associated with a QRS complex, except in setting of AV block
What is the main goal of treating physiologic sinus tach ?
Treat the underlying cause !
Beta Blockers are used to treat physiologic sinus tach. under what conditions
emotion/anxiety related disorders
MI, CHF
Thyrotoxicosis (diltiazem or verapamil if beta blocker is C/I)
Inappropriate sinus tach
Persistent increase in sinus rate out of proportion to or without physical, emotional, pathological or pharmocologic stress.
What is likely the cause of Inappropriate sinus tach
Mechanism likely due to enhanced automaticity or abnormal excess sympathetic or reduced parasympathetic tone.
Criteria for diagnosing sinus tach
Persistent sinus tach during the day with excessive increase in rate in response to activity, with normalization of heart rate at night
Tachycardia and symptoms are not paroxysmal
P-wave morphology identical with sinus
Exclusion of other causes (anemia, hyperthyroidism, etc.)
Beta blockers are first line for symptomatic pts with Innapropriate Sinus tach. What can be done if patient is refractory to this ?
Ablation therapy
POTS
Syndrome of excessive tachycardia that is induced by standing up and relieved by lying down.
Mechanism for POTS formation
Central beta-hypersensitivity of baroreflex that does not terminate tachycardia induced by standing upright
Mild peripheral autonomic neuropathy that impairs appropriate vasoconstriction o standing.
Presence of autoantibodies to autonomic neurotransmitter receptors-one half of POTS cases are seen in setting of preceding viral illness
Others, not all mechanisms are known or understood
DIagnosis of POTS
1) EKG showing sinus tachycardia
2) Head upright tilt table test showing increase in at least 30 bpm, or rate greater than 120 after 5-10 minutes upright
3) Absence of orthostatic hypotension
4) Absence of known autonomic neuropathy
5) Symptoms provoked by standing upright, relieved by lying down
Non-pharmacologic tx includes :
Volume expansion is mainstay-copious fluid and salt intake
Thigh high compression stockings
Sleeping with head of bed elevated (increases vasopressin secretion)
Sinus Node Re-entry Tachycardia
Paroxysmal episodes of sinus tach, usually triggered by and terminated by an ectopic atrial beat
Unknown whether re-entry circuit is confined to sinus node or includes near-by tissue, but usually responds to vagal maneuvers and adenosine, so likely that sinus node is involved in a re-entry circuit
Sinus Node Re-entry Tachycardia Diagnosis:
1) Tachycardia and symptoms are paroxysmal
2) P-wave morphology identical to sinus
3) Rhythm induced and/or activated by premature atrial stimuli
4) Termination occurs with vagal maneuvers or adenosine
5) Induction of rhythm does not depend on atrial or AV nodal conduction time
6) EP Study is definitive
Treatment of SNRET
adenosine, vagal maneuvers, amiodarone, beta-blockers, verapamil, diltiazem or digoxin.
Refractory cases may need EP study with ablation.
Atrioventricular Nodal Reciprocating Tachycardia
Most common cause of paroxysmal SVT
May involve AV nodal tissue only or AV node and nearby atrial tissue.
Re-Entry mechanism
A re-entry circuit is set up in the setting of a ectopic beat occurring after a normally conducted impulse-one pathway is refractory and therefore blocked, while the other conducts the beat. The blocked pathway then repolarizes and “catches” the returning depolarization, sending it back up the circuit and causing a re-entry circuit.
Typical AVNRT
The slow pathway conducts the impulse from the atria to the ventricles, therefore the slow pathway is the antegrade pathway.
results in a p-wave that is during or close to the QRS. This is called a short RP interval (≤ 70 msec,short). The P-wave is also short (40 msec). The p-wave sometimes produces a pseudo-r’.
Atypical AVNRT
Fast pathway is antegrade, producing a long RP interval.
Dx of AVNRT
Dx is best ascertained by intra-cardiac EP.
EKG of Typical AVNRT
HR 140-250 BPM
short RP interval (less than 70 msec), short p-wave (40 msec) pseudo-r’ in lead V1.
EKG of Atypical AVNRT
long RP interval, p-wave negative in leads III, aVF and is inscribed before the QRS complex.
Inverted p-wave (junctional)
treatment of acute ustable AVNRT
Direct current CVN
Treatment of acute stable AVNRT
adenosine, vagal maneuvers
Long Term treatment of AVNRT
either pharm or ablation
Ablation of slow conduction is definitely more effective in the long run
Risk of ablation includes heart block and subsequent need for pacemaker implantation.
Junctional Tach.
Tachycardia originating in junctional region between AV node and His-Purkinjie system
Focal Junctional Tach
Very uncommon
Paroxysmal
Originates from AV node or Bundle of His
Due to increased automaticity or triggered phenomena
Usually presents in pediatric ages or young adulthood**
Pts quite symptomatic, can go into heart failure if tachycardia is incessant**
Diagnosis of Focal Junctional Tach.
HR 110-250 bpm Narrow complex or BBB pattern AV dissociation often present Rhythm may sometimes be erratic, like Atrial fibrillation Best demonstrated by EP study
Tx of Focal junctional block
Beta Blockers are good pharmcologics.
Ablation may be needed but may have risk of AV block
Non Paroxysmal Junctional Tach.
Benign arrhythmia**
Due to enhanced automaticity or triggered mechanism
Gradual onset and termination-”warm up and cool down”
Can not be terminated by pacing maneuvers**
HR usually 70-120 bpm
What may Non Paroxysmal Junctional Tach. be a marker for ?
Digitalis Toxicity Hypokalemia Myocardial Ischemia After cardiac surgery COPD Hypoxia Inflammatory conditions
Tx of COPD Non Paroxysmal Junctional Tach.
BB’s
Mainly just treat the underlying cause !
AVRT differs from AVNRT in that …
Tachycardia reciprocating between atria and ventricles by using extranodal accessory pathways
Accessory pathways are conductive tissue bridges that cross the insulating fibrous valvular annulus
What is unusual of accessory pathways ?
Accessory pathways can be capable of antegrade or retrograde conduction of APs
What occurs if accessory pathway is anterograde
If accessory pathway conduction is antegrade, the QRS will be skewed slightly at the beginning, the so-called Delta wave. This phenomenon is called “pre-excitation”
If accessory pathway conduction is retrograde
then the pathway is called “concealed”, because the initial impulse conducts normally down the AV node and is not evident on EKG tracing.
Pre-excitation (delta wave + normal rhythm) + tachyarrhythmia =
Wolff-Parkinson-White Syndrome
Orthodromic AVRT
the impulse travels antegrade down AV node and retrograde up accessory pathway
Majority of AVRT
Antidromic AVRT
impulse travels antegrade down accessory pathway and retrograde up AV node
QRS complex of orthodromic AVRT ?
Orthodromic AVRT will usually yield a narrow complex tachycardia, outside of the setting of aberrancy or bundle branch block
QRS complex of antidromic AVRT
Anti-dromic AVRT usually results in a wide complex tachycardia
Most common arrhythmia with Wolff Parkinson White ?
AVRT is most common arrhythmia (95%)
In patients with WPW and A-Fib, accessory pathways seem to play a role in causing the A-Fib. What can be done to correct this ?
Abblation !
Of note, A-Fib in the setting of young, healthy people is strongly associated with
pre-excitation. That is to say,
what is the recommended treatment for WPW
for WPW that is diagnosed, catheter ablation is strongly recommended due to the risk for degeneration to A-Fib and sudden death.
What is the treatment of choice for a patient with hemodynamically stable AVRT
Ibutilide, procainamide, or flecainide are the treatments of choice medically due to their conduction slowing properties.
Adenosine must be given judiciously
atrial tach.
Tachycardia resulting from impulse formation in atrial focus not related to sinus node or AV node
Focal atrial Tach.
Paroxysmal OR Gradual onset/termination
HR 100-250, rarely 300
Benign except in incessant forms
Can be caused by increased automaticity, re-entry, or triggered mechanisms. **
Drug induced focal atrial tachy.
Digitalis toxicity can induce a focal atrial tachycardia with a slow ventricular response (due to digoxin induced AV block)
Treatment is holding digoxin, administration of digoxin antibodies if heart block continues
why is it important to figure out the direct cause of FAT (re-entry, automaticity, triggered)
*Specific medicinal therapy depends on whether FAT is due automaticity, re-entry, etc.
TOC for unstable FAT
: Cardioversion
TOC for Acute, hemodynamically stable pt with FAT
adenosine, beta blockers, central calcium channel blockers, flecainide, propafenone, amiodarone, sotalol
TOC for Recurrent Symptomatic/incessant FAT
catheter ablation
Multifocal Atrial Tachycardia
Atrial Tachycardia with three or more sites of impulse generation
P waves will have multiple shapes Irregular rhythm!
Irregular sensation of palpitations
Almost always associated with pulmonary disease, metabolic disease, or electrolyte imbalance *****
treatment of MFAT
Treat the underlying disease state!
Almost always associated with pulmonary
disease, metabolic disease, or electrolyte
imbalance *****
Rate control usually with calcium channel blockers, Beta blockers often C/I due to lung disease
Atrial flutter
Also called “macro-re-entrant atrial tachycardia”
Organized atrial rate between 250-350 bpm
Ventricular rates may be 2:1, 3:1, etc, or variable
Atrial rhythm shows regular, frequent p-waves on EKG called “flutter waves”
Etiology of atrial flutter
Due to re-entry circuits set up around: Cavotricuspid isthmus (CTI) Area of prior scarring in atria
Cavotricuspid isthmus (CTI) dependant Atrial Flutter
Most common cause for Atrial Flutter
Re-entry circuit most often propagates counterclockwise around tricuspid valve
Can also be clockwise, or involve other patterns around cavotricuspid isthmus, but these are rare
Cavotricuspid isthmus independant Atrial Flutter
Most atrial flutter not involving the cavotricuspid isthmus is found involving areas of prior scarring of the atria, usually from cardiac surgery
Also called “lesion related macro-re-entrant atrial tachycardia”
Usually flutter waves on EKG are less well demonstrated
Unstable atrial flutter
Cardioversion (CVN) and/or rate control with BBs, Verap, Dilt, Dig, Amio
Stable atrial flutter
Atrial overdrive pacing, DC CVN, ibutilide, flecainide, propafenone, sotalol, procainamide, amio
Treatment of long term atrial flutter
Overall direct current cardioversion of first episode and catheter ablation of recurring atrial flutter are very successful. Pharmacologic cardioversion is not, and carries inherant risks of anti-arrhythmic drugs.
why will you not cardiovert a patient with Atrial flutter ?
Studies have shown a risk for thrombo-embolism after DC CVN of Atrial flutter. Attempts to convert to sinus rhythm should only occur if:
Patient is anti-coagulated to INR of 2-3
Arrhythmia is less than 48 hours old
TEE shows no clots (anti-coagulate anyway)
waht is a major danger associated with atrial fibrillation ?
As atria have no organized contractile ability, blood movement is poor. Static blood may form clots that can embolize
unstable atrial fibrillation
Cardioversion !
Stable
Rate control with BB’s etc
