VENTRICULAR DYSRHYTHMIAS

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VENTRICULAR DYSRHYTHMIAS

• CHAPTER 6

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INTRODUCTION

• VENTRICLES PRODUCE CARDIAC OUTPUT
• INEFFECTIVE ATRIAL OUTPUT MAY CAUSE COMPROMISED
  VENTRICULAR OUTPUT
• INEFFECTIVE VENTRICULAR OUTPUT THERE IS NO
  CARDIAC OUTPUT
• VENTRICULAR DYSRHYTHMIA IS OFTEN A PRECEDENT TO
  LIFE-THREATENING CARDIORESPIRATORY ARREST
• CATEGORIZED AS VENTRICULAR OR SUPRAVENTRICULAR,
  INDICATING THE ORIGIN IN OR ABOVE THE VENTRICLES
• SVTS INCLUDE SINUS TACH, ATRIAL TACH, ATRIAL
  FLUTTER, ATRIAL FIB, AND JUNCTIONAL TACH

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SA NODE AND AV NODE FAILURE THE VENTRICLES CAN
INITIATE AN IMPULSE FROM THE BUNDLE BRANCHES,
PURKINJE FIBERS, OR VENTRICLE MUSCLE. THE
IMPULSE MUST TRAVEL IN A RETROGRADE DIRECTION TO
DEPOLARIZE THE ATRIA THEN TRAVEL FORWARD TO
DEPOLARIZE THE VENTRICLES. THE P WAVE IS
USUALLY HIDDEN IN THE QRS COMPLEX THE QRS IS
WIDE AND BIZZARE AND GREATER THAN 0.12
SECONDS USUALLY LIFE THREATENING
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PREMATURE VENTRICULAR CONTRACTION

• AN INDIVIDUAL COMPLEX THAT ORIGINATES FROM AN
  AREA BELOW THE BUNDLE OF HIS AND OCCURS EARLIER
  THAN THE NEXT EXPECTED COMPLEX.
• PVCS ARE COMMON, AND CAN OCCUR IN ANY UNDERLYING
  RHYTHM.
• P WAVES ARE ABSENT.
• THE QRS IS ALWAYS WIDE AN EQUAL OR GREATER THAN
  0.12 SECONDS.

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THE T WAVE IS USUALLY DEFLECTED IN THE
OPPOSITE OF THE QRS COMPLEX. A COMPENSATORY
PAUSE IS FOUND WITH PVCS PVCS ARE THE MOST
OMINOUS OF ALL ECTOPIC BEATS. INDICATES
INCREASED VENTRICULAR IRRITABILITY. CAUSES M.I.

GALL BLADDER DISEASE ISCHEMIA
( SYMPATHETIC
NERVOUS ELECTROLYTE IMBALANCE STIMULATION
) DRUG TOXICITY ACIDOSIS PAIN COPD
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SINCE PVCS ARE NOT RHYTHMS, THE UNDERLYING
RHYTHM MUST BE IDENTIFIED. THE RATE AND RHYTHM
VARY WITH THE UNDERLYING RHYTHM. PVCS ARE
COUNTED IN THE TOTAL NUMBER OF R WAVES
TO DETERMINE RATE.
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SITE OF ORIGIN

• UNIFOCAL- PVC ORIGINATES FROM ONE SITE WITHIN THE
  VENTRICLES.
• MULTIFOCAL- PVCS ORIGINATE FROM DIFFERENT SITES
  AND HAVE VARYING SIZES AND SHAPES.
• MULTIFOCAL PVCS ARE DANGEROUS BECAUSE THE
  VENTRICLES ARE INCREASED IN IRRITIBILITY.

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Unifocal PVCs
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FREQUENCY OF OCCURENCE

• BIGEMINY- EVERY OTHER COMPLEX IS A PVC. MOST
  SERIOUS SINCE THE VENTRICLES HAVE A HIGH DEGREE
  OF IRRITABILITY.
• TRIGEMINY EVERY THIRD COMPLEX IS A PVC
• QUADRIGEMINY EVERY FOURTH COMPLEX IS A PVC

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COUPLET- TWO PVCS IN A ROW THAT ARE
NOT SEPARATED BY A COMPLEX OF THE
UNDERLYING RHYTHM. RUN OF VT THREE OR MORE
PVCS EXIST IN A ROW, NOT SEPARATED BY A QRS
COMPLEX OF THE UNDERLYING RHYTHM. VT IS USUALLY
SHORT IN DURATION AND THE PVCS ARE
UNIFOCAL. BOTH COUPLETS AND VT CAN LEAD TO
LETHAL DYSRHYTHMIAS.
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R ON T

• ADDITIONAL TERM USED TO DESCRIBE PVCS.
• R WAVE OF THE PVC FALLS ON THE T WAVE OF THE
  PREVIOUS COMPLEX.
• VERY VULNERABLE PERIOD OF VENTRICULAR
  REPOLARIZATION.

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R on T Phenomenon
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CRITERIA FOR TREATMENT OF PVCS

• MORE THAN 6 IN A ONE MINUTE STRIP
• MULTIFOCAL
• COUPLETS
• RUN OF VT
• R ON T
• MEDICALLY UNSTABLE

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Couplets
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INTERPOLATED BEAT

• A PVC THAT OCCURS ABOUT HALFWAY BETWEEN TWO
  NORMAL BEATS.
• ALREADY COMPENSATORY IN THE OVERALL RHYTHM WITH
  NO PAUSE FOLLOWING IT.
• THE FIRST REGULAR BEAT AFTER THE INTERPOLATED
  BEAT USUALLY HAS A PROLONGED PR INTERVAL.

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Interpolated Beat
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FUSION BEAT

• OCCURS WHEN THE ATRIA ARE DEPOLARIZING AT THE
  SAME TIME A VENTRICULAR CONTRACTION OCCURS.
• THE RESULTING BEAT IS A FUSION OF THE NORMAL BEAT
  THAT SHOULD HAVE OCCURRED AND THE PVC.
• A KIND OF RARE PVC.

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DIFFERENTIATION OF PVC
P WAVE ABSENT QRS INTERVAL WIDE AND BIZARRE
(gt0.12 SECONDS) PAUSE COMPENSATORY T WAVE
OPPOSITE TO THE QRS COMPLEX FREQUENCY MOST
COMMON IN PATHOLOGY CAUSE CARDIAC IRRITABILITY
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VENTRICULAR TACHYCARDIA (VT)

• ORIGINATES FROM A SINGLE SITE IN THE VENTRICLES.
• 100 TO 250 IMPULSES PER MINUTE.
• RUN OF THREE OR MORE CONSECUTIVE PVCS.
• COMMONLY PERSISTS FOR AN EXTENDED PERIOD OF TIME.
• LIFE-THREATENING.
• MAY OCCUR WITH OR WITHOUT PULSES.
• A PATIENT WITH A PULSE IS USUALLY HYPOTENSIVE.

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VT IS OMINOUS BECAUSE OF ITS TENDENCY
TO DEGENERATE TO VENTRICULAR FIBRILLATION WITHOUT
A PULSE. THE PULSELESS CARDIAC ARREST PATIENT IS
APENIC AND/OR PULSELESS WILL REQUIRE BASIC
OR ADVANCED LIFE SUPPORT. P WAVES MAY EXIST
BETWEEN VENTRICULAR COMPLEXES IF THERE IS AN A-V
BLOCK. P WAVES WILL HAVE NO REGULAR
RELATIONSHIP TO THE QRS COMPLEXES. USUAL REGULAR
RHYTHM.
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SYMPTOMS OF VT

• RUN OF VT MAY ONLY FEEL SLIGHTLY WEAK OR
  COMPLAIN OCCASIONAL PALPITATION.
• SUSTAINED VT MAY BE UNSTABLE LEADING TO
  UNRESPONSIVENESS, LOSS OF PULSE

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ALGORHYTHM OF TREATMENT FOR VT
ASSESS THE PATIENT. IF STABLE PROVIDE
OXYGEN START IV, REASSESS LIDOCAINE, REASSESS IF
VT IS CONTROLLED,IV OF LIDOCAINE IF NOT
SUCCESSFUL WITH LIDOCAINE PROCAINAMIDE UNTIL ONE
OF THE FOLLOWING TOTAL OF 17MG/KG HAS BEEN
GIVEN PVCS HAVE STOPPED PATIENT HYPOTENSIVE QRS
BECOMES 50 WIDER THAN BEFORE THE
PROCAINAMIDE. IF VT CONTROLLED, IV OF
PROCAINAMIDE
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REASSESS THE PATIENT, IF THE VT IS NOT CONTROLLED
WITH LIDOCAINE OR PROCAINAMIDE,
ADMINISTER BRETYLIUM. IF BRETYLIUM CONTROLS THE
VT START A BRETYLIUM IV. MONITOR THE PATIENT IF
THE PATIENT HAS A PULSE BUT POOR CARDIAC
OUTPUT PERFORM SYNCHRONIZED CARDIOVERSION IF THE
HEART RATE IS gt150 LIDOCAINE IF MAX DOSE HAS NOT
BEEN GIVEN CONTINUE CARDIOVERSION LIDOCAINE 5-10
MIN. UNTIL 3 MG/KG GIVEN PULSELESS CPR
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TORSADE DE POINTES

• TRANSLATED IT MEANS TWISTING OF THE POINTS.
• LOOKS SIMILAR TO VT.
• UNKNOWN IF IT IS FROM SINGLE OR MULTIPLE SITES.
• BEGINS CLOSE TO THE BASELINE GRADUALLY INCREASING
  AND DECREASING IN A REPEATING PATTERN.

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THIS OCCURS IN A PERIOD OF 5 TO 20 BEATS. THE
RHYTHM RESEMBLES A TWISTING AND TURNING MOTION
ALONG THE BASELINE. TORSADE USUALLY HAS A RATE
OF 200 TO 250 BEATS PER MINUTE. AMPLITUDE
CONTINUALLY CHANGES FROM COMPLEX TO
COMPLEX. WARNING SIGNS PROLONGATION OF QT
INTERVAL PROMINENT U WAVES VERY LARGE T
WAVES VENTRICULAR BIGEMINY WITH R ON T
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CAUSES OF TORSADES

• HYPOKALEMIA AND QUINIDINE THERAPY.
• SEVERE BRADYCARDIA AS A MAJOR PREDISPOSING FACTOR.

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MANAGEMENT

• ELIMINATE DRUG TOXICITES
• ELIMINATE ELECTROLYTE IMBALANCES.
• QUINIDINE IS THE PRIMARY CULPRIT OF DRUG
  TOXICITY.
• THIS IS A LIFE-THREATENING DYSRHYTHMIA.
• CARDIAC OUTPUT IS NOT MAINTAINED, AND ADEQUATE
  OXYGEN IS NOT CIRCULATED.

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TREATMENT

• VAGAL STIMULATION
• INTRAVENOUS LIDOCAINE
• MECHANICAL PACEMAKERS
• CAUTIOUSLY ADMINISTERED IV ISOPROTERENOL.
• UNSYNCHRONIZED CARDIOVERSION
• CPR IF NO PULSE

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VENTRICULAR FIBRILLATION

• ONE OF FOUR FORMS OF CARDIAC ARREST ASYSTOLE,
  PULSELESS VENTRICUALR TACHYCARDIA,
  ELECTROMECHANICAL DISSOCIATION (EMD).
• EASIEST TO RECOGNIZE.
• V FIB IS A LETHAL DYSRHYTHMIA.

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IT ORGINATES FROM MANY DIFFERENT SITES WITHIN THE
VENTRICLES. THE CARDIAC CELLS DO NOT HAVE TIME
TO COMPLETELY DEPOLARIZE AND REPOLARIZE. THE
MYOCARDIUM LACKS EFFECTIVE MUSCULAR CONTRACTION.
THE MYOCARDIUM HAS A QUIVERING MUSCULAR ACTIVITY.
FIB REVEALS AN IRREGULAR WAVY BASELINE COARSE
VENTRICULAR FIBRILLATION THE WAVES HAVE A HIGHER
AMPLITUDE
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COARSE FIB WAVES INDICATE A GREATER NUMBER
OF CARDIAC CELLS ARE ABLE TO RESPOND TO
THE ELECTRICAL STIMULATION. FINE VENTRICULAR
FIBRILLATION HAVE LESS AMPLITUDE, INDICATING
FEWER CARDIAC CELLS ARE ABLE TO RESPOND TO
ELECTRICAL IMPULSE. FINE V FIB RESPONDS LESS
EASILY TO TREATMENT.
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WARNING DYSRHYTHMIAS

• VENTRICULAR TACHYCARDIA
• 5 OR MORE PVCS PER MINUTE
• MULTIFOCAL PVCS
• COUPLETS
• R ON T PHENOMENON

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V FIB THERAPY

• DEFIBRILLATION
• DEFIBRILLATION PRODUCES A STIMULUS MUCH STRONGER
  THAN THE NORMAL CARDIAC STIMULI.
• THE STIMULUS DEPOLARIZES ALL CELLS THAT ARE IN A
  REPOLARIZED REFRACTORY STATE.
• THE INTENT IS TO PRODUCE A UNIFORM STATE OF
  POLARIZATION.

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THE DEFIBRILLATION CAN ENABLE THE
NATURAL PACEMAKERS OF THE HEART TO REASSERT
THEIR INFLUENCE ON CARDIAC CONDUCTION. DEFIBRILLA
TION IS MORE SUCCESSFUL WHEN PERFORMED SHORTLY
AFTER THE ONSET OF THE DYSRHYTHMIA. DEFIBRILLATIO
N SHOULD NOT DELAY THE INITIATION OF BASIC LIFE
SUPPORT.
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BEGIN CPR IMMEDIATELY THREE ATTEMPTS OF 200
JOULES, 200 TO 300, AND 360 REASSESS AFTER EACH
ATTEMPT 100 OXYGEN WITH BAG-VALVE MASK INTUBATE
AS SOON AS POSSIBLE IV FLUIDS. REASSESS DEFIBRILLA
TE AT 360 JOULES. REASSESS EPINEPHRINE. REPEAT
EVERY 3 TO 5 MINUTES. REASSESS DEFIBRILLATE AT
360 JOULES AFTER ADMINISTRATION OF EPINEPHRINE
WITHIN 60 SECONDS. ADMINISTER LIDOCAINE. MAY
REPEAT 3 TO 5 MINUTES DEFIBRILLATE AT 360
JOULES IF NECESSARY ADMINISTER BRETYLIUM
TYSOLATE MAY REPEAT IN 5 MINUTES
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ADMINISTER PROCAINAMIDE IF BRETYLIUM IS
LESS EFFECTIVE. MAGNESIUM SULFATE IN SEVERE V-FIB
THAT DOES NOT RESPOND TO DEFIBRILLATION. START AN
INFUSION DRIP OF WHATEVER MEDICATION WAS
SUCCESSFUL IN ENDING THE V-FIB. ASSESS THE
PATIENT.
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IDIOVENTRICULAR RHYTHM

• ANY RHYTHM ORIGINATING IN THE VENTRICLES.
• REGULAR, SLOW RHYTHM WITH WIDE VENTRICULAR
  COMPLEXES WITHOUT P WAVES.
• 15 TO 40 BEATS PER MINUTE.

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AGONAL RHYTHM

• DYING HEART
• USUALLY ORIGINATES FROM A SINGLE SITE IN THE
  VENTRICLES.
• THE ATRIA, AV JUNCTION, BUNDLE OF HIS, AND BUNDLE
  BRANCHES CAN NO LONGER FUNCTION AS PACEMAKERS.
• lt20 BEATS PER MINUTE.

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VENTRICULAR ASYSTOLE

• ASYSTOLE LITERALLY MEANS WITHOUT CONTRACTIONS.
• NO WAVES, NO COMPLEXES
• RHYTHM IS FLATLINE ON THE EKG.
• PATIENT IS PULSELESS AND APNEIC.
• MANAGEMENT INCLUDES CHEMOTHERAPIES AND BASIC LIFE
  SUPPORT.

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Asystole
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ELECTROMECHANICAL DISSOCIATION

• THE FAILURE OF THE MYOCARDIUM TO MECHANICALLY
  RESPOND TO NORMAL ELECTICAL DEPOLARIZATION IS
  EMD.
• NOT GENERALLY A DYSRHYTHMIA, RATHER A CONDITION.
• THE ELECTRICAL RHYTHM IS FREQUENTLY NSR.

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MANAGEMENT INCLUDES IMMEDIATE BASIC LIFE SUPPORT
WITH ADVANCED LIFE SUPPORT. PERICARDIAL
TAMPONADE CAN MIMIC EMD. OCCURS WHEN THE HEART
CHAMBERS OR VESSELS BLEED INTO THE PERICARDIAL
SAC. BLOOD ACCUMULATES AND EVENTUALLY
COMPRESSES THE HEART. MARKED PROGRESSIVE
CARDIAC OUTPUT, NARROWING PULSE PRESSURE,
DISTENDED NECK VEINS, AND SHOCK
SYMPTOMS. DIMINISHED HEART SOUNDS.
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MANAGEMENT

• REQUIRES THE REMOVAL OF THE BLOOD IN THE
  PERICARDIAL SAC.
• PERICARDIOCENTESIS USUALLY RESULTS IN DRAMATIC
  IMPROVEMENT.
• CARDIAC TAMPONADE MUST BE CONSIDERED IN ANY
  PATIENT PRESENTING WITH EMD.