Cardiac Arrhythmias pt 3

Question 1

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)

Answer 1

SVT: AV nodal reentrant tachycardia

Question 2

SVT: AV nodal reentrant tachycardia relies on:

Answer 2

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

Question 3

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

Answer 3

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)

Question 4

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?

Answer 4

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

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

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

Answer 7

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

Question 8

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

Answer 8

Wolff-Parkinson-White or ventricular pre-excitation sydrome

Question 9

Describe a delta wave

Answer 9

• 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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

antegrade depolarization of ventricles occurs exclusively over AV node

Question 12

compare and contrast WPW to orthodromic tachycardia

Answer 12

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

Question 13

Therapy recommendation for pts with WPW:

Acute

Definitive

Answer 13

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

Question 14

What therapy should we avoid in pts with WPW?

Answer 14

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.

Question 15

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

Answer 15

ventricular arrythmias

Question 16

What is more dangerous: SVT arrhthymias or ventricular arrhythmias?

Answer 16

Ventricular arrhythmias ; responsible for many cases of sudden death

Question 17

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.

Answer 17

Ventricular Premature Beats or Contractions

Question 18

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

Answer 18

P wave inverted in II, III, and aVF

Question 19

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

Answer 19

Both

Question 20

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

Answer 20

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

Question 21

Primary therapy for PVC is

Answer 21

observation and at times, beta blockers.

Question 23

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

Answer 23

parameters for Ventricular Tachycardia

Question 24

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

QRS:

heart rate:

Answer 24

QRS typically wide (> 120 ms)

rate > 100 bpm.

Question 25

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?

Answer 25

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

Question 26

In monomorphic ventricular tachycardia, QRS are:

Answer 26

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

Question 27

Sustained monomorphic VT typically results from\_\_\_\_\_\_\_\_ and indicates underlying structural heart disease or myocardial scar.

Answer 27

reentry

Question 29

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

Answer 29

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

Question 30

In Polymorphic VT, QRS complex :

Answer 30

continually changes shape and rate varies from beat to beat.

Question 31

Mech of polymorphic VT

Answer 31

Mechanism is either multiple ectopic foci or changing reentrant circuit.

Question 32

Causes of polymorphic VT include:

Answer 32

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

Question 33

What do we worry about if polymorphic VT is sustained?

Answer 33

may cause syncope with cardiac arrest

Question 34

SMMVT \_\_\_\_\_\_\_ QRS

Answer 34

WIDE

Question 35

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

Answer 35

Ventricular tachycardia

Question 36

In SMMVT: we see AV dissociation which means

Answer 36

no relationship between P waves and QRS complexes.

Question 37

In SVT usually\_\_\_\_\_\_ QRS

Answer 37

narrow

Question 38

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

Answer 38

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.

Question 39

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

Answer 39

should match.

Question 40

SVT may respond to

Answer 40

vagal maneuvers

Question 41

Torsades de Pointes is seen in patients with

Answer 41

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

Question 42

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

Answer 42

Torsades de Pointes (Twisting of Points)

Question 43

Mech of Torsades de Pointes

Answer 43

• Mechanism is triggered activity, early afterdepolarizations.

Question 44

Acute treatement of Torsades de Pointes

Answer 44

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.

Question 45

Chronic tx of Torsades de pointe

Answer 45

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

Question 46

Congenital Long QT Syndrome: Mutations Alter Ion Channel function to Enhance\_\_\_\_\_\_\_\_\_\_ or Impair\_\_\_\_\_\_\_\_\_\_\_ Prolonging Action Potential Duration

Answer 46

Depolarizing Na+ Current Repolarizing K+ Current,

Question 47

Sustained VT is potentially life-threatening and may degenerate to

Answer 47

ventricular fibrillation or be associated with hemodynamic collapse.

Question 48

Acute therapy in UNSTABLE patient with Ventricular tachycardia: \_\_\_\_\_\_\_\_ • Acute therapy STABLE patient: \_\_\_\_\_\_\_\_

Answer 48

unstable: electrical cardioversion. stable: antiarrhythmic drugs (amiodarone, lidocaine) or sedate/cardiovert

Question 49

in pt with VT, long term consider need for

Answer 49

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

Question 50

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

Answer 50

Ventricular fibrillation

Question 51

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

Answer 51

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

Question 52

Survivors of V fib will usually receive

Answer 52

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