ECG in Ventricular

arrhythmiasDr Mostafa Hekmat

Cardiologist

Electrophysiologist

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A look at ventricular arrhythmias

•Ventricular arrhythmias originate in the ventricles below the bundle of His.

•They occur when electrical impulsesdepolarize the myocardium using a different pathway from normal impulses

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A look at ventricular arrhythmias

•Ventricular arrhythmias appear on an ECG in characteristic ways.

•The QRS complex is wider than normal because of the prolonged conduction time through the ventricles

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A look at ventricular arrhythmias

• The T wave and the QRS complex deflect in opposite directions because of the difference in the action potential during ventricular depolarization and repolarization.

• P wave is absent because atrial depolarization doesn’t occur

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No kick from the atria• When electrical impulses are generated

from the ventricles instead of the atria, atrial kick is lost

• Cardiac output decreases by as much as 30%.

• Patients with ventricular arrhythmias mayshow signs and symptoms of cardiac decompensation, including hypotension, angina, syncope, and respiratory distress.

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Potential to kill•Although ventricular arrhythmias

may be benign, they’re potentially deadly because the ventricles are ultimately responsible for cardiac output.

•Rapid recognition and treatment of ventricular arrhythmias increases the chance for successful resuscitation

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Premature ventricular contraction

• A PVC is an ectopic beat that may occur in healthy people without causing problems.

• PVCs may occur singly, in clusters of two or more, or in repeating patterns, such as bigeminy or trigeminy

• When PVCs occur in patients with underlying heart disease, they may indicate impending lethal ventricular arrhythmias

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Premature ventricular contraction•PVCs are usually caused by electrical irritability in the ventricular conduction system or muscle tissue.

•This irritability may be provoked by anything that disrupts normal electrolyte shifts duringcell depolarization and repolarization

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Premature ventricular contraction• Electrolyte imbalances, such as hypokalemia, hyperkalemia,

hypomagnesemia, and hypocalcemia

• Metabolic acidosis

• Hypoxia

• Myocardial ischemia and infarction

• Drug intoxication, particularly cocaine, amphetamines, and tricyclic antidepressants

• Enlargement of the ventricular chambers

• Increased sympathetic stimulation

• Myocarditis

• Caffeine or alcohol ingestion

• Proarrhythmic effects of some antiarrhythmics

• Tobacco use.

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Premature ventricular contraction• PVCs are significant for two reasons.

• 1, they can lead to more serious arrhythmias, such as ventricular tachycardia or ventricular fibrillation.

• The risk of developing a more serious arrhythmia increases in patients with ischemic or damaged hearts.

• 2,PVCs also decrease cardiac output, especially if the ectopic beats are frequent or sustained.

• Decreased cardiac output is caused by reduced ventricular diastolic filling time and a loss of atrial kick

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PVC• PVCs look wide and bizarre and appear as early

beats causing atrial and ventricular irregularity.

• The P wave is usually absent.

• Retrograde P waves may be stimulated by the PVC and cause distortion of the ST segment.

• The PR interval and QT interval aren’t measurable on a premature beat,

• QRS complex in the premature beat exceeds 0.12 second.

• The T wave in the premature beat has a deflection opposite that of the QRS complex.

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R-on-T•When a PVC strikes on the downslope

of the preceding normal T wave it can trigger more serious rhythm disturbances

• Because the cells haven’t fully repolarized, VT or VF can result

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The pause that compensates

•Interval between two normal sinus beats containing a PVC equals two normal sinus intervals.

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An interpolated PVC

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Multiform

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Couplet

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Bigeminy

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CLINICAL FEATURES• The prevalence of premature complexes

increases with

• Age

• Male gender

• Hypokalemia

• PVCs are more frequent in the morning in patients after MI

• This circadian variation is absent in patients with severe left ventricular dysfunction.

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The importance of PVCs

•Depends on the clinical setting

• In the absence of underlying heart disease, the presence of PVCs usually has no impact on longevity or limitation of activity

•Antiarrhythmic drugs are not indicated

• Patients should be reassured if they are symptomatic

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Identifying idioventricular rhythm

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Accelerated idioventricular rhythm

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Torsades de pointes

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Torsades de pointes

• Is a special form of polymorphic ventricular tachycardia

•The rate is 150 to 250 beats/minute, usually with an irregular rhythm, and the QRS complexes are wide with changing amplitude.

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Torsades de pointes• This arrhythmia may be

paroxysmal, starting and stopping suddenly, and may deteriorate into ventricular fibrillation

• Reversible causes

• Amiodarone, ibutilide, erythromycin, haloperidol, droperidol, and sotalol

• Myocardial ischemia and electrolyte abnormalities, such as hypokalemia, hypomagnesemia, and hypocalcemia

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Ventricular fibrillation•Electrical activity in the ventricles

•Electrical impulses arise from many different foci.

•It produces no effective muscular contraction and no cardiac output.

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Ventricular tachycardia• Three or more PVCs occur in a row and the

ventricular rate exceeds 100 beats/minute

• VT is an extremely unstable rhythm.

• It can occur in short, paroxysmal bursts lastingfewer than 30 seconds and causing few or no symptoms.

• Alternatively, it can be sustained, requiring immediate treatment to prevent death, even in patients initially able to maintain adequate cardiac output

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Ventricular tachycardia• Conditions that can cause ventricular tachycardia

include:

• MI

• Coronary artery disease

• Valvular heart disease

• Heart failure

• Cardiomyopathy

• Electrolyte imbalances such as hypokalemia

• Drug intoxication from digoxin (Lanoxin), procainamide, Quinidine, or Cocaine

• Proarrhythmic effects of some antiarrhythmics

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Unpredictable V-tach• A patient may be stable with a normal

pulse and adequate hemodynamics or unstable withhypotension and no detectable pulse.

• Because of reduced ventricular filling time and the drop in cardiac output, the patient’s condition can quickly deteriorate to ventricular fibrillation and complete cardiac collapse

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Ventricular tachycardia

• The ventricular rate is usually rapid—100 to 250 beats/minute.

• The P wave is usually absent but may be obscured by the QRS complex.

• Retrograde P waves may be present.

• The QRS complex is wide and bizarre, usually with an increased amplitude and a duration of longer than 0.12 second.

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VT + RBBB• (1) the QRS complex is monophasic or biphasic in V1, with an initial deflection different from that of the sinus-initiated QRS complex

• (2) the amplitude of the R wave in V1 exceeds the R′

• (3) a small R and large S wave or a QS pattern in V6 may be present.

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Left Septal VT

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VT + LBBB• (1) the axis can be rightward, with negative deflections deeper in V1 than in V6,

• (2) a broad prolonged (more than 40 milliseconds) R wave in V1

• (3) a small Q–large R wave or QS pattern in V6 can exist

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RVOT VT

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VT• QRS duration exceeding 140 milliseconds

• In precordial leads with an RS pattern, the duration of the onset of the R to the nadir of the S exceeding 100

• Fusion beat

• Capture beat

• AV dissociation has long been considered a hallmark of VT

• Retrograde VA conduction to the atria from ventricular beats occurs in at least 25% of patients

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Supraventricular arrhythmiawith aberrancy

• (1) consistent onset of the tachycardia with a premature P wave

• (2) very short RP interval (0.1 sec)

• (3) QRS configuration the same as that occurring from known supraventricular conduction at similar rates

• (4) P wave and QRS rate and rhythm linked to suggest that ventricular activation depends on atrial discharge (an AV Wenckebach block)

• (5) slowing or termination of the tachycardia by vagal maneuvers

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• A QRS complex in V1 - V6, either all negative or all positive favors a VT

• The presence of a 2 : 1 VA block VT

• Positive QRS complex in V1 - V6

• Can also occur from conduction over a left-sided accessory pathway.

• Supraventricular beats with aberration

• Triphasic pattern in V1

• An initial vector of the abnormal complex similar to that of the normally conducted beats

• Wide QRS complex with long-short cycle sequence

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Treatment

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Treatment

•PVCs, even in the setting of an acute MI, need not be treated unless they directly contribute to hemodynamic compromise

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Treatment

•Any wide QRS complex tachycardia should be treated as ventricular tachycardia until definitive evidence is found to establish another diagnosis

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Treatment• Beta blockers are often the first line of therapy.

• If they are ineffective, class IC drugs seem particularly successful in suppressing PVCs,

• Flecainide and Moricizine have been shown to increase mortality in patients treated after MI

• Should be reserved for patients without coronary artery disease or LV dysfunction

• Amiodarone

• Should be reserved for highly symptomatic patients and those with structural heart disease.

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