Ventricular Arrhythmias Jayna Gardner-Gray - PowerPoint Presentation

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Ventricular Arrhythmias

Jayna Gardner-Gray

4/23/2020

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Abnormal rhythm

that originates in the ventricles

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Increased activity of automatic focus in ventriclesReentry circuit of fast and slow pathway is confined to ventricles

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TachyarrhythmiasIs my patient in sinus rhythm?Is my patient stable or unstable?Is my QRS complex narrow or wide?Is my rhythm regular or irregular?

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Common TypesJunctional RhythmIdioventricular RhythmPremature Ventricular ContractionsVentricular TachycardiaMonomorphic Polymorphic

Bidirectional LVOT RVOT Fasicular Annular

Ventricular FlutterVentricular Fibrillation

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Junctional Rhythm

The electrical activation originates near or within the AV node

Normal His-Purkinje is used, the QRS complex is usually narrowRate is 40-60 beats per minuteP wave is frequently not seen; it can be buried within the QRS complex

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Idioventricular rhythmOriginate in the ventricles “slow VT” All characteristics of VT applyHeart rate less than 60 bpm idioventricular rhythm Heart rate between 60 and 120 bpm accelerated idioventricular rhythm

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Accelerated Idioventricular rhythm

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Premature Ventricular ContractionsBroad QRS complex (≥ 120 ms) with abnormal morphology.

Caused by electrical irritabilityPremature — occurs earlier than would be expected for the next sinus impulse.

Usually followed by a full compensatory pause. Unifocal or MultifocalAnxiety, Sympathomimetics, Beta-agonists, Excess caffeine, hypokalemia, hypomagnesemia, digoxin toxicity, myocardial ischemia

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Isolated PVC: no repeating patternBigeminy: every sinus beat followed by a PVCTrigeminy: Every second sinus beat followed by PVC

Couplet: 2 consecutive PVCsTriplet: 3 consecutive PVCs

Nonsustained Ventricular Tachycardia: Three or more consecutive PVCs

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Ventricular TachycardiaMost common cause of wide complex tachycardia (80%)Life threatening arrhythmias that originates in the ventriclesOccurance of 3 or more ventricular beats (100-250 bpm)QRS >120msElectrical instability that can cause deterioration to ventricular fibrillation

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Ventricular TachycardiasUntil 1961 patients post MI were placed away doctors and nurses to avoid stress and possible arrhythmia30% of people with ventricular arrhythmias would die in the hospital post MI In 1961 the concept of electrical shock to terminate these rhythms was proposed

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BreakdownPulseless vs hemodynamically stableSustained (>30 sec) vs. non sustained (<30 sec)Monomorphic vs. polymorphic

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Risk of ventricular tachycardiaAcute MIElectrolyte abnormalitiesPost CABGDilated cardiomyopathyFamily history: HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia

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SVT vs. VTMajority (90%) of wide complex tachycardias are VTSVTs may display widened QRS (BBB, aberration, toxins, hyperkalemia)SVTs are rarely life threatening

Presence of stability should not be regarded as diagnostic of SVT ***If in doubt treat as VT

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SVT vs. VTThe likelihood of SVT with aberrancy is increased if:Previous ECGs show a bundle branch block patternPrevious ECGs show evidence of WPW (short PR < 120ms, broad QRS, delta wave)

The patient has a history of paroxysmal tachycardias that have been successfully terminated with adenosine or vagal maneuversYounger patient <35

yo

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Brugada CriteriaMost used algorithm If any of the 5 criteria are met the patient has VT

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Brugada Algorithm

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1.Is there concordance present in the precordial leads (leads V1-V6)?"Are all of the QRS complexes completely upright, or downward in the precordial leads?"

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Is the R to S interval > 100ms in any one precordial lead?

Use calibers to measure between the R and S waves in the precordial leads

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3.Is AV dissociation present?AV dissociation occurs when P waves are seen at different rates than the QRS complex.

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4. Examine QRS morphology (V1-2, V6)RBBB pattern (upright in V1)LBBB pattern (downward in V1).

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If upward in lead V1 (RBBB pattern)VT is present if:A monophasic R or biphasic qR complex in V1, V2

If an RSR' pattern “bunny-ear” is present in V1 or V2, with the R peak being higher than the R’ peak

Biphasic rS complex in V6

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Failed V1-2 Brugada criteria

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If downward in lead V1 (LBBB pattern)VT is present if:A wide R wave in lead V1 or V2 of >30msSlurred or notched downstroke

of the S wave in V1 or V2 Duration of onset of the QRS complex to peak of QS or S >70ms QS wave in

V6

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If none of the above criteria are met a diagnosis of SVT can be made

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Polymorphic Ventricular Tachycardia

Can cause hemodynamic instability

May degenerate into VFMore likely if HR >220

QT prolongation: Medications, electrolyte abnormalities and medical conditions Bigeminy in a patient with long QT syndrome PVC occurs during the preceding T wave, known as ‘

R on T’ phenomenon

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Abnormal giant T-U waves may precede polymorphic VT

 

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Bidirectional Ventricular Tachycardia

Axis: ? both …

QRS axis shifts 180 degrees

Also look like alternating left and right bundle-branch block 

Digoxin Toxicity

, Long QT syndromes, sarcoidosis, myocarditis, polymorphic VT

 

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Ventricular Flutter

Extreme form of ventricular tachycardia with loss of organized electrical activity

Short lived: swift progression to Ventricular fibrillation

>250bpm

Treat: standard ACLS

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Ventricular Fibrillation

Fatal arrhythmia

Ventricular Rate > 400 bpm

No forward cardiac output

Disorganized activity on ECG