Ventricular Tachycardia (VT) is defined as three or more consecutive PVCs in a row at a rate greater than 100 beats per minute. VT is generally caused by single foci in either ventricle that fire at a rapid rate to override the SA node and thereby take control of the heart’s rhythm. A short run of consecutive PVCs is often called a “burst” of VT. ECG characteristics include a rapid,regular rhythm with a wide QRS. The QRS is wide since the origin of the rhythm is outside the bundle branches, thereby taking a longer time to conduct cell to cell within the ventricle.
Definitions used to classify ventricular arrhythmias:
• sustained: > 30 second duration or requiring intervention for termination
• non-sustained: 6 beats – 29 second
• monomorphic: regular rate and consistent beat-to-beat QRS morphology
• polymorphic: frequent changes of QRS morphology and/or axis. If sustained changes must occur at least every 1–2 second
• repetitive ventricular beats: 1–5 ventricular beats
Atrioventricular dissociation is present, but not always noticeable. This means that the sinus node is depolarizing the atria in a normal manner at a rate either equal to or slower than the ventricular rate. Thus sinus P-waves sometimes can be recognized between QRS complexes but do not conduct down into the ventricles. AV Dissociation strongly suggests ventricular tachycardia.Unfortunately AV dissociation only occurs in approximately 50 per cent of ventricular tachycardias (the other 50 per cent have retrograde atrial capture or “VA association”). Of the patients with AV dissociation, it is only easily recognized if the rate of tachycardia is <150 bpm.Faster heart rates make it difficult to visualize dissociated P-waves. This arrhythmia may be either well tolerated or associated with life-threatening hemodynamic compromise. The hemodynamic consequences of VT depend largely on the presence or absence of myocardial dysfunction (such as might result from ischaemia or infarction) and on the rate of VT (the faster the rate, the less well tolerated).
Possible Causes
• Myocardial irritability
• Acute MI
• CAD
• Drug toxicity
• Electrolyte imbalance
• Heart failure
ECG Criteria
1) Heart Rate: 100-250 bpm.
2) Rhythm: Ventricular rhythm regular.
3) P-waves: P-waves may or may not be seen. If present, they are not associated with the QRS complex. (AV disassociation occurs with this rhythm, but P-waves are not always seen).
4) PR Interval: Not applicable.
5) QRS Width: > 0.12 seconds, wide and bizarre in appearance.
6) Fusion beats or captures often occur when there is AV dissociation and this also strongly suggests a ventricular origin for the wide QRS tachycardia.
7) QRS morphology in V1 to V6: consider a few other morphology clues:
• Bizarre frontal plane QRS axis (i.e. from +150 degrees to –90 degrees or NW quadrant) suggests ventricular tachycardia.
• QRS morphology similar to previously seen PVCs suggests ventricular tachycardia.
• If all the QRS complexes from V1 to V6 are in the same direction (positive or negative),ventricular tachycardia is likely.
• Especially wide QRS complexes (>0.16s) suggests ventricular tachycardia.
• Also consider the following Four-step Algorithm reported by Brugada et al.,
Circulation 1991; 83:1649.
Step 1: Absence of RS complex in all leads V1-V6?
Yes: Diagnosis is ventricular tachycardia!
Step 2: No: Is interval from beginning of R-wave to nadir of S-wave > 0.1s in any RS lead?
Yes: Diagnosis is ventricular tachycardia!
Step 3: No: Are AV dissociation, fusions, or captures seen?
Yes: Diagnosis is ventricular tachycardia!
Step 4: No: Are there morphologic criteria for VT present both in leads V1 and V6?
Yes: Diagnosis is ventricular tachycardia!
8) Pre-existing complete BBB, if present is very helpful in diagnosis. For example, in a patient with complete RBBB during sinus rhythm, it is highly likely that wide complex tachycardia with LBBB pattern is VT.
9) Narrow complex tachycardia. Very rarely VT may be narrow complex. This may be the case, for example, if, in a patient with an anterior wall aneurysm the site of origin of the VT is in the basal portion of the intraventricular septum. Arrhythmia may then
spread over both ventricles in a similar fashion to the spread of intraventricular beats thereby causing a narrow QRS VT.
10) If in doubt, in patients with structural heart disease it is safer to diagnose VT and this usually proves to be correct. The ECG below shows a regular wide QRS tachycardia which was diagnosed as VT. Two examples of VT.
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| Ventricular Tachycardia |
Ventricular Fibrillation (VF)
Ventricular Fibrillation (VF) is the result of highly irritable ventricle(s), which begin to send out rapid electrical stimuli. The stimuli are chaotic resulting in no organized ventricular depolarization. The ventricles do not contract because they never depolarize. Because the ventricles are fibrillating and never contracting, the patient does not have a pulse, cardiacoutput, or blood pressure. The terms coarse and fine have been used to describe the amplitude of the waveforms in VF. With Coarse VF, the fibrillatory waves are more easily seen and are usually greater than 3mm in height (3 small boxes tall). Coarse VF usually indicates a more recent onset of VF, which could be more easily converted by prompt defibrillation. The presence of fine VF (which looks a bit like asystole and is less than 3mm in height) often means there has been a considerable delay since collapse, and successful resuscitation is more difficult.
Possible Causes
• Acute MI
• Untreated ventricular tachycardia
• Underlying heart disease
• Acid-base imbalance
• Electrolyte imbalances such as hypokalemia, hyperkalemia, and hypercalcemia
ECG Criteria
1) Heart Rate: None. No discernable P-waves or QRS complexes
2) Rhythm: Chaotic wavy recording. No discernable rhythm.
3) P-waves: None
4) PR Interval: Not applicable
5) QRS Width: Not applicable
ECG strip shows ventricular fibrillation.
 |
| Ventricular Fibrillation |
Torsades de Pointes
Definition
• VT characterized by QRS complexes of progressively changing amplitude and contour that seem to revolve about the isoelectric line.
• diagnosis based on characteristic VT and prolonged ventricular repolarisation time with QT intervals usually > 500 msec.
• additional ECG features that may be present include prominent U-wave, abnormal contour of T or TU-waves, T-wave alternans, subnormal spontaneous sinus rate (especially in children) and sinus pauses.
• Standard ECG recordings and analysis of QTc duration and T-wave morphology are the most useful tests in diagnosing LQTS. The prolongation of the QTc interval is defined based on age-specific and sex-specific criteria. The QTc, corrected for heart rate, is calculated by dividing the measured QT by the square root of the R-R interval, both of which are measured in seconds. QTc prolongation greater than 0.46 seconds indicates a high likelihood of LQTS diagnosis. However, approximately 10-15 per cent of gene-positive patients with LQTS present with QTc duration within the reference range.
Definition of the QTc Interval Based on Age-Specific and Sex-Specific Criteria.
• In patients with suggested LQTS with borderline QTc values (or even values within the reference range) in standard ECG, the analysis of dynamic behavior of QTc duration during exercise ECG testing or long-term Holter monitoring may reveal maladaptation of the QT interval duration to the changing heart rate, with evident QTc prolongation at a faster heart rate. Ventricular arrhythmias rarely are observed during exercise testing or Holter recordings in patients with LQTS.
• Invasive electrophysiology testing with attempts to induce ventricular tachycardia do not facilitates diagnosis.
• Detection of visible T-wave alternans in patients with LQTS indicates increased risk of cardiac arrhythmias (i.e, torsade de pointes and ventricular fibrillation).
• Detection of microvolt T-wave alternans has low sensitivity and high specificity in diagnosing LQTS. The prognostic value of microvolt T-wave alternans has not been studied systematically.
Causes of Long QT
Congenital
• Jervell-Lange-Nielsen syndrome. Autosomal recessive. Long QT and neural deafness
• Romano-Ward. Autosomal dominant. Normal hearing
• Sporadic form. Normal hearing
• Acquired: largely iatrogenic disease with most cases being due to drugs
• Antiarrhythmics
— type 1a and type 3 drugs associated with torsades
— of the type 1a drugs quinidine appears to have the greatest potential for causing it and is estimated to cause syncope in 0.5-4 per cent of patients as a result of this tachyarrythmia.
Prolongs QT interval in most patients, whether or not ventricular arrhythmias occur, but significant QT prolongation (500-600 ms) more often a characteristic of patients with quinidine syncope
— class Ic drugs may also prolong QT interval
• Non-cardiac drugs. Following have been associated with long QT and torsades:
— phenothiazines especially thioridazine
— tricyclic and occasionally tetracyclic antidepressants
— H1 blockers (e.g. terfenadine and astemizole; former particularly in association with erythromycin)
• Metabolic and electrolyte disorders
— hypokalaemia
— hypomagnesemia
— appears to be synergistic effect between these electrolyte disorders and type 1a drugs
• Bradycardia. VT is a complication of severe bradycardia
• CNS lesions
— intracranial disease, especially subarachnoid haemorrhage, occasionally produces torsades. Probably due to the influence of autonomic nervous system on ventricular repolarisation
• Cardiac lesions
— mitral valve prolapse and cardiac ganglionitis may be associated with long QT
Clinical Features
Congenital long QT syndrome
• may present in childhood with syncope due to torsades. Often precipitated by heightened sympathetic tone
• sudden death may occur but frequency of this complication seems to vary considerably from family to family (< 5% to 80 per cent)
• VT may evolve into VF but unlike VF associated with coronary or structural heart disease often resolves spontaneously to sinus rhythm
Definition
• VT characterized by QRS complexes of progressively changing amplitude and contour that seem to revolve about the isoelectric line.
• diagnosis based on characteristic VT and prolonged ventricular repolarisation time with QT intervals usually > 500 msec.
• additional ECG features that may be present include prominent U-wave, abnormal contour of T or TU-waves, T-wave alternans, subnormal spontaneous sinus rate (especially in children) and sinus pauses.
• Standard ECG recordings and analysis of QTc duration and T-wave morphology are the most useful tests in diagnosing LQTS. The prolongation of the QTc interval is defined based on age-specific and sex-specific criteria. The QTc, corrected for heart rate, is calculated by dividing the measured QT by the square root of the R-R interval, both of which are measured in seconds. QTc prolongation greater than 0.46 seconds indicates a high likelihood of LQTS diagnosis. However, approximately 10-15 per cent of gene-positive patients with LQTS present with QTc duration within the reference range.
Definition of the QTc Interval Based on Age-Specific and Sex-Specific Criteria.
• In patients with suggested LQTS with borderline QTc values (or even values within the reference range) in standard ECG, the analysis of dynamic behavior of QTc duration during exercise ECG testing or long-term Holter monitoring may reveal maladaptation of the QT interval duration to the changing heart rate, with evident QTc prolongation at a faster heart rate. Ventricular arrhythmias rarely are observed during exercise testing or Holter recordings in patients with LQTS.
• Invasive electrophysiology testing with attempts to induce ventricular tachycardia do not facilitates diagnosis.
• Detection of visible T-wave alternans in patients with LQTS indicates increased risk of cardiac arrhythmias (i.e, torsade de pointes and ventricular fibrillation).
• Detection of microvolt T-wave alternans has low sensitivity and high specificity in diagnosing LQTS. The prognostic value of microvolt T-wave alternans has not been studied systematically.
Causes of Long QT
Congenital
• Jervell-Lange-Nielsen syndrome. Autosomal recessive. Long QT and neural deafness
• Romano-Ward. Autosomal dominant. Normal hearing
• Sporadic form. Normal hearing
• Acquired: largely iatrogenic disease with most cases being due to drugs
• Antiarrhythmics
— type 1a and type 3 drugs associated with torsades
— of the type 1a drugs quinidine appears to have the greatest potential for causing it and is estimated to cause syncope in 0.5-4 per cent of patients as a result of this tachyarrythmia.
Prolongs QT interval in most patients, whether or not ventricular arrhythmias occur, but significant QT prolongation (500-600 ms) more often a characteristic of patients with quinidine syncope
— class Ic drugs may also prolong QT interval
• Non-cardiac drugs. Following have been associated with long QT and torsades:
— phenothiazines especially thioridazine
— tricyclic and occasionally tetracyclic antidepressants
— H1 blockers (e.g. terfenadine and astemizole; former particularly in association with erythromycin)
• Metabolic and electrolyte disorders
— hypokalaemia
— hypomagnesemia
— appears to be synergistic effect between these electrolyte disorders and type 1a drugs
• Bradycardia. VT is a complication of severe bradycardia
• CNS lesions
— intracranial disease, especially subarachnoid haemorrhage, occasionally produces torsades. Probably due to the influence of autonomic nervous system on ventricular repolarisation
• Cardiac lesions
— mitral valve prolapse and cardiac ganglionitis may be associated with long QT
Clinical Features
Congenital long QT syndrome
• may present in childhood with syncope due to torsades. Often precipitated by heightened sympathetic tone
• sudden death may occur but frequency of this complication seems to vary considerably from family to family (< 5% to 80 per cent)
• VT may evolve into VF but unlike VF associated with coronary or structural heart disease often resolves spontaneously to sinus rhythm
Acquired long QT
• principal clinical features are syncope and pre-syncope, often accompanied by palpitations
• sudden death may occur
• principal clinical features are syncope and pre-syncope, often accompanied by palpitations
• sudden death may occur
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