Cardiac Arrhythmias pt 3 Flashcards Preview

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Flashcards in Cardiac Arrhythmias pt 3 Deck (52):

Most common form paroxysmal SVT • Reentry utilizing two AV nodal pathways, fast (rapid conduction and long refractory period) and slow (slow conduction and short refractory period)

SVT: AV nodal reentrant tachycardia

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SVT: AV nodal reentrant tachycardia relies on:

transient unidirectional block in one pathway and relatively slow conduction in the other


Young male comes in with palpitations, dizziness, chest pain and dyspnea. Your attending diagnoses him with SVT: AV nodal reentrant tachycardia and asks you to describe the conduction in this pts heart

Typically conduction antegrade from A to V occurs over slow pathway and retrograde limb of reentrant circuit is over fast pathway. (usually in young pts with symptoms listed)


Pt comes in with dyspnea, palpitations, and chest pain. She is 15 years old and doctor dx with AVNRT.... what is the acute tx recommendation?

Acute treatment aimed at termination: valsalva maneuvers, adenosine, beta blockers, calcium channel blockers.


What is the chronic tx recommendation for AV nodal reentrant tachycardia?

• Chronic treatment: observation, AV nodal blockade, catheter ablation targeting “slow” pathway of AV node and infrequently Class I, III antiarrhythmic drugs.


What pathways are utilized in AV reentrant tachycardias (NOT AV nodal reentrant!)

Reentry utilizing bypass tract or accessory pathway = an abnormal band of muscle cells 
crossing the AV groove to connect atrium and ventricle.

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Is conduction retrograde (V--> A) or antegrade (A--> V) in Atrioventricular reentrant tachycardia?

Can be either! If it's  tract conducts only retrograde can promote 
supraventricular tachycardia but is termed “concealed”.



A Atrioventricular reentrant tachycardia conducts antegrade (A-->V) will produce what findings on ECG?

Wolff-Parkinson-White or ventricular pre-excitation sydrome


Describe a delta wave

• conduction over AP beats AVN, short PR
• Slurred QRS due to slow ventricular activation by pathway other than HPS and fusion activation of ventricle by2 wavefronts, proceeding over AP and HPS

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You see a short PR with slurred QRS on an ECG, looks like this: Dx?

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Wolff Parkinson White syndrome; tract that conducts antegrade, produces this ventricular pre-excitation syndrome


No delta wave in orthodromic tachycardia(narrow QRS) because: 

antegrade depolarization of ventricles occurs exclusively over AV node

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compare and contrast WPW to orthodromic tachycardia

WPW we get angetgrade resulting in ventricular pre-excitation which gives us the delta wave ( short PR, slurred QRS) 

In orthodromic tachycardia, have a narrow QRS as antegrade depolarization of ventcles occurs exclusievely over AV node

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Therapy recommendation for pts with WPW:



• Acute therapy may require cardioversion if hemodynamically unstable.
• Definitive therapy with catheter ablation of accessory pathway is preferred in symptomatic and high risk patients.


What therapy should we avoid in pts with WPW?

 digoxin, beta blockers and calcium channel blockers may actually shorten the refractory period of 
accessory pathways, effectively speeding conduction

Instead use: IV amiodarone or procainamide may be used, slow accessory pathway conduction.


Premature ventricular beats or contractions ; includes V.tachycardia and V.fibrillation

ventricular arrythmias


What is more dangerous: SVT arrhthymias or ventricular arrhythmias?

Ventricular arrhythmias ; responsible for many cases of sudden death


Produced by firing of ectopic ventricular focus and produces a widened QRS because impulse originates from ectopic ventricular site and depolarizes ventricles not through the normal rapidly 
conducting His Purkinje system but via slow cell-to-cell connections.

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Ventricular Premature Beats or Contractions


In PVC, we will see inverted P wave in leads __, ___ and ___ due to ventricular origin with no relationship to P wave or retrograde V---> A conduciton

P wave inverted in II, III, and aVF


Do we see PVCs in normal hearts or hearts with cardiac disorders?



Pt comes in with high density PVCs ( > 20% of QRS complexes) , what do we worry about this pt forming?

may produce left ventricular systolic dysfunction which may be reversible with suppression of PVCs, 
medically or with ablation.


Primary therapy for PVC is 

observation and at times, beta blockers.



Series of 3 or more PVCs
• Sustained VT: > 30 seconds
• Non-sustained VT: < 30 seconds


parameters for Ventricular Tachycardia

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What do we expect to see in pt with ventricular tachycardia in regards to:


heart rate:

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QRS typically wide (> 120 ms)

 rate > 100 bpm.


Ventricular tachycardia is usually seen in patients with structural heart disease 
but can be present with normal heart; what predisposing conditions correlate with V.tachycardia?

 Predisposing conditions: coronary disease with ischemia or infarction, congestive heart failure,  ventricular hypertrophy, primary electrical disorders (long QT syndrome), valvular disease, congenital heart disease


In monomorphic ventricular tachycardia, QRS are: 

QRS complexes are identical from beat to beat and rate is regular.

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Sustained monomorphic VT typically results from________ and indicates underlying 
structural heart disease or myocardial scar.

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When can a pt without structual heart disease have a monomorphic VT?

Occasionally occurs as a triggered arrhythmia originating from an ectopic focus in a patient


 In Polymorphic VT, QRS complex : 

continually changes shape and rate varies from beat to beat.

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Mech of polymorphic VT

Mechanism is either multiple ectopic foci or changing reentrant circuit.



Causes of polymorphic VT include:

long QT with Torsades de pointes, acute ischemia or infarction, other rare inherited abnormalities of cardiac ion channels or calcium handling 


What do we worry about if polymorphic VT is sustained?

may cause syncope with cardiac arrest


_______ QRS



 In SMMVT: If wide complex tachycardia occurs in setting or prior infarct, CHF or acute ischemia, 
more likely ___________

Ventricular tachycardia


In SMMVT: we see AV dissociation which means

 no relationship between P waves and QRS complexes.


In SVT usually______ QRS



In SVT, we usually see narrow QRS.... we can have wide QRS if conducts with aberrant conduction, which means

 with preferential activation of ventricles over either right or left bundle branch resulting in right 
bundle branch block aberrancy or left bundle branch block aberrancy.


In SVT if pre-existing bundle branch block in sinus rhythm, QRS 
complexes should ______

should match.


SVT may respond to

vagal maneuvers


Torsades de Pointes is seen in patients with 

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QT prolongation (prolonged action potential duration), either due to drugs, bradycardia, electrolyte/metabolic disturbances or hereditary abnormality of ion 
channels (congenital long QT).


Specific form polymorphic VT presenting with varying amplitudes of QRS as though complexes were “twisting” about the baseline.

Torsades de Pointes (Twisting of Points)


Mech of Torsades de Pointes

• Mechanism is triggered activity, early afterdepolarizations.


Acute treatement of Torsades de Pointes

 cardiovert sustained VT to restore sinus rhythm, IV magnesium, correct underlying abnormalities (stop offending drugs), elevate heart rate and thus shorten QT either with beta agonists (isoproterenol) or pacing.


Chronic tx of Torsades de pointe

correct underlying triggers. If congenital long QT consider beta blocker and ICD.


Congenital Long QT Syndrome: Mutations Alter Ion Channel function to Enhance__________ 
or Impair___________ Prolonging Action Potential 

 Depolarizing Na+ Current

 Repolarizing K+ Current,


Sustained VT is potentially life-threatening and may degenerate to 

ventricular fibrillation or be associated with hemodynamic collapse.


Acute therapy in UNSTABLE patient with Ventricular tachycardia: ________
• Acute therapy STABLE patient: ________

unstable: electrical cardioversion.

stable: antiarrhythmic drugs (amiodarone, lidocaine) or sedate/cardiovert


in pt with VT, long term consider need for

 implantable cardioverterdefibrillator (ICD) for secondary prevention and potentially 
need for antiarrhythmic drugs or VT ablation.


Immediately life-threatening
• Disordered rapid activation of ventricles
• Does not produce coordinated ventricular contraction
• Occurs typically in setting of severe underlying heart disease or acute ischemia
• Untreated leads to death

Ventricular fibrillation

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What do we need to do for patient in V-fib? 

immediate electrical defibrillation, then look for cause, consider IV amiodarone



Survivors of V fib will usually receive 

ICD unless reversible cause identified (such as acute myocardial infarctions).