Ch276 Supraventricular Tachyarrhythmias Flashcards
T or F: Most supraventricular tachyarrhythmias produce wide QRS complex tachycardia (QRS duration >120 ms)
False
mostly narrow QRS-complex <120 ms
2 types of supraventricular tachyarrhythmia
- Physiologic sinus tachycardia
2. Pathologic tachycardia
T or F: Supraventricular arrhythmia usually precipitates cardiac arrest in patients with Wolff-Parkinson-White syndrome or severe heart disease such as hypertrophic cardiomyopathy
False
Rarely
Diagnostic of supraventricular arrhythmia
ECG
Normal sinus rhythm rate
60-100 beats/min
Sinus tachycardia rate
> 100 beats/min
Difference of sinus tachycardia vs atrial tachycardia
Sinus tach: GRADUAL increase and decrease in rate
Atrial tach: ABRUPT onset and offset
Treatment for physiologic sinus tachycardia
Treat the underlying condition
Uncommon condition in which sinus rate increases spontaneously at rest or out of proportion to physiologic stress or exertion
Inappropriate sinus tachycardia
Common: women, 3rd-4th decade
Defining feature of physiologic sinus tachycardia
Normal sinus mechanism precipitated by exertion, stress, concurrent illness
Drug that blocks the funny current (If) causing sinus node depolarization
Ivabradine
Syndrome wherein symptomatic sinus tachycardia occurs with postural hypotension
Postural orthostatic tachycardia syndrome (POTS)
Condition due to autonomic dysfunction following a viral illness and resolve spontaneously over 3-12 months
Postural orthostatic tachycardia syndrome (POTS)
Treatment for POTS that can be helpful
Volume expansion with salt supplementation Oral Fludrocortisone Compression stockings a-agonist midodrine Exercise training
Condition due to abnormal automaticity, triggered automaticity, or a small reentry circuit confined to the atrium or atrial tissue extending into a pulmonary vein, the coronary sinus, or vena cava
Focal atrial tachycardia (AT)
Sustained, nonsustained, paroxysmal, incessant
Type of focal atrial tachycardia that can cause tachycardia-induced cardiomyopathy
Incessant AT
Difference of AT from AV nodal-dependent SVTs
AT will not terminate with AV block and atrial rate will not be affected
Defining feature of Inappropriate sinus tachycardia
Tachycardia from normal sinus node area that occurs without an identifiable precipitating factor as a result of the dysfunctional autonomic regulation
Defining feature of Focal atrial tachycardia
Regular atrial tachycardia with defined P wave
In AT, P wave may fall on top of the T wave or coincident with QRS. What maneuvers can be done to expose the P wave?
Carotid sinus massage
Valsalva maneuver
Administration of AV nodal-blocking agents (Adenosine)
Maneuvers that increase AV block
Common causes of physiologic sinus tachycardia
- Exercise
- Acute illness with fever, infection, pain
- Hypovolemia, anemia
- Hyperthyroidism
- Pulmonary insufficiency
- Drugs that have sympathomimetic, vagolytic, or vasodilator properties
- Pheochromocytoma
Treatment for AT with recurrent episodes
- Beta blockers
- Calcium ch blockers (Diltiazem, Verapamil)
- Flecainide
- Propafenone
- Disopyramide
- Sotalol
- Amiodarone
Recommended treatment for recurrent symptomatic AT if unresponsive to drugs OR Incessant AT causing tachycardia-induced cardiomyopathy
Catheter ablation
The most common form of PSVT
AV nodal reentry tachycardia (AVNRT)
women>men, 2nd-4th decade
T or F: AVNRT is usually associated with structural heart disease.
False
NOT usually associated
T or F: In AVNRT, P wave can be difficult to discern
True
Is AVNRT responsive to Valsalva manuever?
Yes
Recommended treatment for recurrent or severe episodes or when drug therapy is ineffective, not tolerated, or not desired in patients with AVNRT
Catheter ablation of the slow AV nodal pathway
Condition due to automaticity within the AV node; Rare in adults and more frequently encountered as incessant tachycardia in children usually in perioperative period surgery for congenital heart disease
Junctional Ectopic Tachycardia (JET)
Is JET, a narrow or wide QRS tachycardia?
Narrow QRS tachycardia
A junctional automatic rhythm between 50 and 100 beats/min
Accelerated junctional rhythm
Defining feature of AV nodal reentry tachycardia
- Paroxysmal regular tachycardia with P waves visible at the end of the QRS complex or not visible at all
- Most common paroxysmal sustained tachycardia in healthy young adults
- More common in women
Conditions associated with accessory pathways
- Ebstein’s anomaly of tricuspid valve
- Forms of hypertrophic cardiomyopathy (PRKAG2 mutations)
- Danon’s disease (LAMP2, lysosomal membrane disorder)
- Fabry’s disease (lysosomal storage disease)
Location of accessory pathways
Across either an AV valve annulus or septum, most frequently between the left atrium and free wall of the left ventricle, followed by posteroseptal, right free wall, and anteroseptal locations
ECG findings associated with accessory pathways
- Short P-R interval (<0.12s)
- Slurred initial portion of the QRS (delta wave)
- Prolonged QRS duration (widened QRS complex)
Defined as preexcited QRS during sinus rhythm and episodes of PSVT
Wolff-Parkinson-White (WPW) syndrome
The most common tachycardia caused by an AP
PSVT (Orthodromic AV reentry)
Pathway of orthodromic AV reentry
Reentry wavefront propagates from atrium anterogradely over the AV node and His-Purkinje system to ventricles and then re enters atria via retrograde conduction over the AP
Most common preexcited tachycardia in which activation propagates from atrium to ventricle via the AP and then conducts retrogradely to the atria via the His-Purkinje system and the AV node
Antidromic AV reentry
T or F: Preexcitated tachycardia is associated with ventricular fibrillation and sudden death.
True
AV nodal-blocking agents that are contraindicated in preexcitated tachycardia
Oral or IV verapamil Diltiazem Beta blockers IV adenosine IV amiodarone
Treatment for preexcited tachycardia
Electrical cardioversion
IV procainamide
Ibutilide
*slow ventricular rate
In focal atrial tachycardia, P wave morphology can be used to estimate the location of the ectopic focus
- Right atrium - positive P wave in lead I and biphasic in V1
- Atrial septum - narrower P wave duration than sinus rhythm
- Left atrium - monophasic, positive P wave in V1
- Superior atrial location (Superior vena cava/superior pulmo veins) - positive in inferior limb leads II, III, aVF
- Inferior location (Ostium of coronary sinus) - negative P waves in limb leads II, III, aVF
Relationship of Focal Atrial Tachycardia on structural heart disease
Can occur in the absence of structural heart disease OR can be associated with any form of heart disease that affects the atrium
Possible causes of Focal Atrial Tachycardia
- Sympathetic stimulation which can be a sign of an underlying illness
- Digitalis toxicity
Frequent sites of origin of Focal Atrial Tachycardia
- valve annuli of left or right atrium
- pulmonary veins
- coronary sinus musculature
- superior vena cava
P wave in Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- No discernible P-waves (inscribed during the QRS) (80-90%*)
- Slightly after the QRS (10%*)
- Slightly before the QRS (1-5%*)
*accdg to life in the fast lane ;)
Condition causing incessant tachycardia and tachycardia-induced cardiomyopathy due to slow conduction that facilitates reentry associated with accessory pathways
Paroxysmal junctional reciprocating tachycardia (PJRT)
In a patient presenting narrow QRS PSVT together with hypotension, what is your next step?
QRS-synchronous direct current cardioversion
In a patient presenting with narrow QRS PSVT and hemodynamically stable, what is the next step?
Vagal manuevers
IV adenosine
IV verapamil/diltiazem
Figure 276-9, p. 1483
In a narrow QRS PSVT, hemodynamically stable patient, however did not respond to sympatholytic and vagotonic maneuvers and drugs, what is the next step?
IV ibutilide + AV nodal-blocking agent
IV procainamide + AV nodal-blocking agent
Cardioversion
Figure 276-9, p. 1483
Defining feature of Atrial Flutter
Organized reentry creates organized atrial activity commonly seen as sawtooth flutter waves at rates typically faster than 200 beats/min
Table 276-1, p. 1477
Condition due to a large reentry circuit and is often associated with areas of scar in the atria
Macroreentrant atrial tachycardia
Condition due to a circuit that revolves around the tricuspid valve annulus, bounded anteriorly by the annulus and posteriorly by functional conduction block in the crista terminalis
Common or typical right atrial flutter
Pathway of wavefront of common atrial flutter
Through an isthmus between the inferior vena cava and the tricuspid valve annulus (sub-Eustachian or cavotricuspid isthmus)
Circuit most commonly revolves in a counterclockwise direction and produces negative sawtooth flutter waves in leads II, III, aVF and positive P waves in lead V1
Common atrial flutter
Rate: 240-300 beats/min
T or F: Atrial flutter will respond to maneuvers that increase AV nodal block
True
Common right atrial flutter often occur in association with what conditions?
Atrial fibrillation
Atrial scar from senescence or prior cardiac surgery
Macroreentrant atrial tachycardia that are not dependent on conduction through the cavotricuspid isthmus
Atypical atrial flutters
What condition does left atrial flutter and perimitral left atrial flutter more commonly seen?
After extensive left atrial ablation for atrial fibrillation or atrial surgery
In a patient with atrial flutter and hemodynamically unstable, what is your next step?
Electrical cardioversion
In a patient with atrial flutter and hemodynamically stable, what is the next step?
Administer AV nodal-blocking agents
For patients with atrial flutter more than 48h or for patients at increased risk of thromboembolic stroke based on CHA2DS2-VASc scoring system, what should be given prior to conversion?
Anticoagulation
Components of CHA2DS2-VASc scoring system
Congestive heart failure Hypertension Age>/= 75 y/o Diabetes mellitus Stroke or TIA, embolus Vascular disease Age 65-75 y Sex - female
Give the mechanism for each anticoagulant: Warfarin Dabigatran Rivaroxaban Apixaban
Warfarin - Vitamin K antagonist
Dabigatran - Thrombin inhibitor
Rivaroxaban - Xa inhibitor
Apixaban - Xa inhibitor
Table 276-6, p. 1485
Treatment for recurrent episodes of common atrial flutter that abolishes arrhythmia in over 90% of patients
Catheter ablation of cavotricuspid isthmus
Anti arrhythmic drug therapy for atrial flutter
Sotalol
Dofetilide
Disopyramide
Amiodarone
> 70% have recurrence
T or F: 50% of patients with atrial flutter will develop atrial fibrillation within the next 5 years
True
Characterized by atleast three distinct P-wave morphologies with rates typically between 100 and 150 beats/min
Multifocal Atrial Tachycardia (MAT)
What conditions do multifocal atrial tachycardia usually encountered?
- Chronic pulmonary disease
2. Acute illness
Treatment for MAT
Treat the underlying disease and correct any metabolic abnormalities
T or F: Electrical cardioversion if effective for MAT
False.
No effect.
Drug therapy for MAT that can be considered
Verapamil or Diltiazem - may slow atrial and ventricular rate
Amiodarone - long term therapy avoided due to pulmonary fibrosis
Beta blocker - not tolerated in severe pulmonary disease
Characterized by disorganized, rapid, and irregular atrial activation with loss of atrial contraction and with an irregular ventricular rate that is determined by AV nodal conduction
Atrial fibrillation (AF)
Most common sustained arrhythmia
Atrial fibrillation
Men>women, white>black
T or F: Prevalence of AF increases with age
True
Risk factors for developing atrial fibrillation
- Age
- Hypertension
- Diabetes mellitus
- Cardiac disease
- Sleep apnea
AF increases the risk of developing these conditions
- Heart failure
- Stroke (5x)
- Dementia
Acute precipitating factors associated with AF
- Hyperthyroidism
- Acute alcohol intoxication
- Acute illness (MI, pulmo embolism, cardiac surgery)
Clinical types of AF
- Paroxysmal AF (start and stop spontaneously)
- Persistent AF (>7 days)
- Long-standing persistent AF (>1 year)
Treatment for paroxysmal AF
Catheter ablation that isolates these foci
T or F: In high risk patients with AF, antiplatelets have equal effects as anticoagulants
False
Less effect
New onset AF producing severe hypotension, pulmonary edema or angina : What is your next step?
Cardioversion with QRS synchronous shock of 200J
In new onset AF that reinitiated after cardioversion : what is your next step?
Administer antiarrhythmic drug (Ibutilide)
Repeat cardioversion can be considered
Goals of therapy for AF in a stable patient
- Rate control to alleviate or prevent symptoms
- Anticoagulation if appropriate
- Cardioversion to restore sinus rhythm if AF is persistent
In the absence of contraindications, what systemic anticoagulation can you give in new onset AF?
Heparin (immediately)
Patient at the ER came within 48h of the onset of AF and anticoagulation was never given. Upon probing, he is low risk for stroke. What should be done?
- Cardioversion
2. Anticoagulate based on CHA2DS2-VASc score
Two approaches that can mitigate the risk of thromboemolism related to cardioversion in patients with AF exceeding 48h or with unknown duration
- Anticoagulate continously for 3 weeks before and minimum of 4 weeks after cardioversion
- Start anticoagulation and perform transesophageal echocardiogram to determine if thrombus is present in left atrial appendage. If absent, cardioversion can be performed and anticoagulation continued for a minimum of 4 weeks
Drug therapy for acute rate control in patients with AF
- Beta blockers and/or
- Calcium channel blockers (Verapamil/Diltiazem, IV or PO)
- Digoxin may be added (esp in heart failure)
Goal: Reduce ventricular rate to less than 100/min or guided by clinical situation
Goal of therapy for chronic AF
Rate control - to alleviate and prevent symptoms, prevent deterioration of ventricular function (beta adrenergic blockers, calcium ch blockers, digoxin)
Goal: Heart rate <80beats/min to less than 100 beats/min with light exertion
Next step for chronic AF that can’t be controlled by medications:
Catheter ablation and permanent pacemaker
Anticoagulation for patients with AF who have rheumatic mitral stenosis or mechanical heart valves
Vitamin K antagonist
Patients that can be given vitamin K antagonist (warfarin) OR newer oral anticoagulants
- Had more than 48h of AF and are undergoing cardioversion
- Have prior history of stroke
- CHA2DS2-VASc score >/=2, but may be considered in patients with a risk score of 1
Risk factors for bleeding as a major risk of anticoagulation
- Age >65-75 y/o
- Heart failure
- History of anemia
- Excessive alcohol
- NSAID use
- With coronary stents who require antiplatelet with aspirin and thienopyridine
T or F: Newer anticoagulants are noninferior to warfarin but superior by 0.4-0.7% in reduction of mortality, stroke, major bleeding and intracranial hemorrhage.
True
Reversing agents for warfarin anticoagulation
FFP
Vitamin K
Time limit for newer anticoagulants to improve clotting once it is excreted
12 hours
T or F: Antiplatelet agents aspirin and clopidogrel are noninferior to warfarin for stroke prevention in AF and do not reduce the risk of bleeding
False
ASA and clopidogrel are inferior to warfarin
T or F: Aspirin alone is better than Clopidogrel combined with aspirin for stroke prevention in patients with AF
False
Clopidogrel combined with aspirin is better than aspirin alone
T or F: Clopidogrel combined with aspirin is inferior to warfarin and has greater bleeding risk than aspirin alone for stroke prevention in patients with AF
True
Goal of pharmacologic therapy in AF
Maintain sinus rhythm
Reduce episodes of AF
Drugs that help control ventricular rate, improve symptoms and possess a low-risk profile, but have low efficacy for preventing AF episodes
Beta adrenergic blockers
Calcium channel blockers
Indication and contraindication for Class I sodium channel-blocking agents (flecainide, propafenone, disopyramide)
For:
Subjects without significant structural heart disease
Against:
- Negative inotropic and proarrhythmic effects
- Avoided in patients with coronary artery disease or heart failure
Indication and contraindication for Class III agents (Sotalol, Dofetilide, Dronedarone, Amiodarone)
For:
With coronary artery disease or structural heart disease
Amiodarone more effective in 2/3 of patients
Against:
- 3% risk of inducing excessive QT prolongation and torsades des pointes
- Dronedarone increases mortality in patients with heart failure
- 20% of patients on long-term amiodarone experience toxicities
This procedure involves cardiac catheterization, transatrial septal puncture, and radiofrequency ablation or cryoablation
Catheter ablation
Major complications of catheter ablation
2-7% risk
Stroke (0.5-1%)
Cardiac tamponade (1%)
Phrenic nerve paralysis
Bleeding from femoral access sites
Fluid overload with heart failure 1-3 days after procedure
Sinus node injury requiring pacemaker implantation
T or F: Catheter ablation is less effective for persistent AF.
True
More extensive ablation is often required