Cardiac Arrhythmias pt 3 Flashcards
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
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.
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
You see a short PR with slurred QRS on an ECG, looks like this: Dx?
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
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
Therapy recommendation for pts with WPW:
Acute
Definitive
- 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.
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?
Both
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
What do we expect to see in pt with ventricular tachycardia in regards to:
QRS:
heart rate:
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.
Sustained monomorphic VT typically results from________ and indicates underlying
structural heart disease or myocardial scar.
reentry
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.
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
SMMVT
_______ QRS
WIDE
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
narrow
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
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
Duration
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
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).
