Ventricular arrhythmia

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Ventricular arrhythmia

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Ventricular arrhythmia

• Wider QRS complex / opposite direction of T and
  QRS / absent P.
• ?30 cardiac output
• Premature ventricular contraction
• Idioventricular rhythm
• Ventricular tachycardia
• Torsades De Pointes
• Ventricular fibrillation
• Asystole

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Premature ventricular contraction

• Ectopic beat originate in the ventricles and
  earlier than expected
• herald the development of lethal ventriular
  arrhythmia(VT, VF)
• Uniform single ectopic ventricular pacemaker
  site
• Multiform single pacemaker but having different
  QRS complex(size, shape or direction)
• Unifocal from the same ventricular ectopic
  pacemaker
• Multiple focal different ectopic pacemaker sites
  
• Cause enhanced automaticity in the ventricular
  conduction or muscle tissue
• Electrolyte imbalance(K?or?, Mg ?, Ca ?)
• Metabolic acidosis
• Hypoxia
• Drug intoxication(coccaine, amphetamines,
  tricyclic antidepressants)
• Enlargement or hypertrophy of ventricular chamber
• Increased sympathetic stimulation
• Myocarditis
• Caffeine or alcohol ingestion
• Tobacco use
• Irritation of ventricles by pacemaker or
  pulmonary artery catheter
• Sympathomimetic drug(epi, isoproterenol)

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EKG

• Opposite T wave
• R-on-T phenomenona PVC strikes on the down slope
  of the preceding normal T wave
• Followed by a compensatory pause

• How often? Pattern? Really PVC?
• Absent p wave or after QRS complex
• Earlier QRS and durationgt0.12 sec with bizarre
  and wide configuration,

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• R-on-T phenomenona PVC strikes on the down slope
  of the preceding normal T wave

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S/S and intervention

• Sign and symptoms
• A weaker pulse after the premature beat and a
  longer pause between pulse waves
• Auscultation early heart sound with each PVC
• Maybe asymptomatic or palpitation or other S/S
  due to decrease of cardiac output
• Intervention
• A cardiac origindrug to suppress ventricular
  irritability( procainamide, amiodarone and
  lidocaine)
• Recently PVC underlying heart disease or complex
  medical condition
• Chronic PVC frequent PVC or dangerous pattern

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Idioventricular rhythm

• Ventricular escape rhythm, originates in an
  escape pacemaker site
• Inherent firing rate of ectopic pacemaker 30-40
  beat/minute?prevent ventricular standstill or
  asystole
• lt3 QRS complex from the escape pacemaker ? called
  ventricular escape beats or complex
• Accelerated idioventricular rhythm(AIVR) HRlt100
  beat/min but gt 30-40 beat/min? related to
  enhanced automaticity of ventricular tissue.
• DDx
• AIVR 100 gt AIVR gt 30-40 beat/min
• Idioventricular rhythm 30-40 beat/min

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Cause and significance

• When all of the hearts higher pacemakers fail to
  function or supraventricular impulse was blocked
• Idioventricular rhythm may accompany 3rd-degree
  heart block
• Cause
• Myocardial ischemia
• Myocardial infarction(MI)
• Digoxin toxicity, beta-adrenergic blockers,
  calcium antagonist, tricyclic antidepressant
• Pacemaker failure
• Metabolic imbalances
• Transient ventricular escape rhythm
  ?parasympathetic effect on higher pacemaker site
• Continuous idioventricular rhythm serious
  situation
• Slow rate and loss of atrial kick? ?cardiac
  output? death

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EKG

• Ventricular rate 20-40 beat/min
• QRS complex longer duration than 0.12 sec, wide
  and bizarre configuration

• T wave opposite to last part of QRS
• Prolonged QT interval
• Often occurs with 3rd-degree AV block
• Absent P

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S/S and intervention

• Continuous idioventricular rhythm due to
  ?cardiac output? dizziness, light-headedness,
  syncope or loss of consiousness
• Tx increase HR, improve cardiac output and
  establish normal rhythm
• Atropine increase HR
• If hypotension or clinical instability? pacemaker
• Transcutaneous pacemaker in an emergency
• Not to suppress the idioventricular rhythm?
  never use lidocaine or other antiarrhythmia to
  suppress the escape beat
• ECG monitor until restore hemodymamic stability
• Bed rest
• Education

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AIVR 100 gt AIVR gt 30-40 beat/minIdioventricular
rhythm 30-40 beat/min
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Ventricular tachycardia

• VT? V-tach?three or more PVC strike in a row and
  the ventricular rate gt100 beat/min
• Usually precedes ventricular fibrillation and
  sudden cardiac death.
• lt30 sec? few or no symptoms
• Sustained? immediate Tx to maintain cardiac
  output
• Cause
• Myocardial ischemia
• MI
• Coronary artery disease
• Valvular heart disease
• Heart failure
• Cardiomyopathy
• Electrolyte imbalance(?K)
• Drug intoxication procainamide, quinidine or
  cocaine
• ?ventricular refilling time and drop of cardiac
  output? carcdiovascular collapse

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ECG

• Rhythm ventricular rate 100250 beat/min
• Absent P wave or obscured or retrograde
• QRS duration gt 0.12 sec, bizarre and increased
  amplitude

• Opposite T wave if visible
• Two variation
• Ventricular flutter
• Torsades de pointes(polymorphic VT)

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S/S and intervention

• Weak or absent pulses
• Low cardiac output? hypotension, conscious
  change, angina, heart failure or organ perfusion?
• Intervention
• Evaluation of consciousness, respiration and
  circulation
• If pulseless? immediate defibrillation
• Unstable Pt ventricular rate gt 150 beat/min
  with S/S hypotension, SOB, chest pain or
  alternated consciousness? immediate synchronized
  cardioversion
• Stable Pt with wide-complex VT and no signs of
  heart failure
• Monomorphic
• Polymorphic
• Chronic, recurrent episodes of VT unresponsive to
  drug therapy? implantation cardioversion-defibrill
  ator (ICD)
• Education

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Torsades De Pointes

• Rapid ventricular rate 250350 beat/min
• Character QRS complex change back and forth,
  with amplitude of each successive complex
  gradually increasing and decreasing
• DDx ventricular flutter rapid, regular,
  repetitive beating of ventricle? single
  ventricular focus firing at a rapid rate of
  250350 beat/min? smooth and sine-waveappearance

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Torsades De Pointes

• French term meaning "twisting of the points
• torsade de pointes occurs in the setting of
  delayed ventricular repolarization, evidenced by
  prolongation of the QT intervals or the presence
  of prominent U waves.
• Drugs
• Quinidine and related antiarrhythmic agents
  (disopyramide and procainamide),
• Sotalol, amiodarone (less commonly),
• Psychotropic agents (phenothiazines and tricyclic
  antidepressants)
• Terfenadine, and others
• Electrolyte imbalances, including hypokalemia,
  hypomagnesemia, and less commonly, hypocalcemia,
  which prolong repolarization
• Miscellaneous factors such as severe
  bradyarrhythmias, liquid protein diets, and
  hereditary long-QT syndromes

From Goldberger Clinical Electrocardiography A
Simplified Approach, 6th ed.
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Torsades De Pointes

• This ventricular tachycardia is often caused by
  drugs conventionally recommended for the
  treatment of arrhythmias.
• Tx
• Removing or correcting causative factors such as
  drug toxicity, electrolyte imbalance, or
  underlying bradycardia.
• In emergency settings a temporary pacemaker may
  be inserted to accomplish "overdrive" suppression
  of the arrhythmia by increasing the underlying
  heart rate and thereby decreasing ventricular
  repolarization time.
• Intravenous magnesium sulfate has proved highly
  useful for suppressing this arrhythmia.
• Drug therapy with isoproterenol or bretylium has
  been used in selected cases.
• Sustained episodes of torsade de pointes?
  attempted cardioversion

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What is QTc?

• The QT interval varies with the heart rate
• Longer when the heart is beating slower and
  shorter when the heart beats faster
• The QT interval is "corrected" through the use of
  a mathematical formula to what it would be if the
  heart rate was 60 beats per minute (bpm).
• Many correction formulas have been proposed and
  tested however, the formulas most commonly in
  use are the Bazett, the Fridericia, and the
  Hodges correction formulas.
• Bazett?(QTcQT/RR1/2).
• Fridericia? QTcQT/RR0.33
• Hodges? QT (QTc) QT 1.75 (rate - 60)
• The Bazett Formula is usually programmed into the
  machine that measures your ECG and the QTc value
  is part of the information printed on the ECG.
• For men the QTc lt 420 msec and for women the QTc
  lt 440 msec.
• QTc values higher than normal are associated with
  increased risk of serious heart rhythm
  abnormalities (Torsades de Pointes).

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Ventricular fibrillation

• VF?chaotic, disorganized pattern of electrical
  activity? multiple ectopic pacemaker? no cardiac
  output? sudden cardiac death
• Cause
• CAD
• Myocardial ischemia
• MI
• Untreated VT
• Underlying heart disease
• Acid-base imbalance
• Electric shock
• Severe hypothermia
• Drug toxicity (digoxin, quinidine and
  procainamide)
• Electrolyte imbalance (??K, ?Ca)
• Completely ineffective contraction, cardiac
  output0 ? ventricular standstill and death

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ECG

• Ventricular rhythm no pattern or regularity
• P wave, QRS complex, PR interval, T wave cant
  be determined

• Coarse fibrillatory wave greater chance of
  successful electrical cardioversion than small
  amplitude

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S/S and intervention

• Full cardiac arrest, unresponsive, undetectable
  BP
• Intervention
• Access VF, confirm
• Immediate defibrillation is the most effective Tx
• CPR until defibrillator arrives
• Drug epi or vasopressin (for persistent VF)
• Antiarrhythmia agent amiodarone,lidocaine and Mg
• AED- automated external defibrillator?
  out-of-hospital setting
• Rapid recognition of the problem and
  defibrillation
• Education, CPR

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Asystole

• AKA ventricular standstill
• Result from a prolonged period of cardiac arrest
  without effective resuscitation
• DDx with VF
• Cause
• Hypovolemia
• MI(coronary thrombosis)
• Severe electrolyte imbalance(??K)
• Massive pulmonary embolism
• Hypoxia
• Drug overdose
• Hypothermia
• Cardiac tamponade
• Tension pneumothorax
• No electrical activity, no contraction? cardiac
  output0? no perfusion for vital organ

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ECG

• No electrical activity

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Intervention

• Immediate Tx CPR, oxygen and advanced airway
  control with intubation
• Check more than one ECG lead to confirm asystole
• IV Epi and atropine,vasopressin
• Consider terminating resuscitation if persist
  asystole.

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From Surg Clin N Am 85 (2005) 11031114