Ventricular

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Ventricular arrhythmia

Ventricular ectopics	Classification of VT	Diagnosis of VT
Non-sustained VT	Sustained VT	Torsades de pointes
Further reading

Ventricular ectopics

in immediate post-MI period of no prognostic significance
in post acute phase of MI VEBs associated with poor long-term outcome but there is no evidence that their suppression with anti-arrhythmics improves prognosis. Further investigation of underlying ischaemic heart disease indicated
common in heart failure. Associated with adverse prognosis but again suppression with anti-arrhythmics does not improve outcome. ACE inhibitors improve prognosis and decrease frequency of VEBs but former not due to latter
in otherwise apparently normal individuals very frequent VEBs (> 200/hr) seems to be associated with increased prevalence of IHD and should prompt some non-invasive cardiovascular investigations

Ventricular tachycardia

Classification

can be classified by morphology, duration, underlying mechanisms or underlying "substrate"
mechanisms, prognostic significance and management of sustained VT may differ according to underlying "substrate" (eg coronary artery disease, mitral valve prolapse, dilated cardiomyopathy)
definitions used to classify ventricular arrhythmias:
- sustained: > 30 sec duration or requiring intervention for termination
- non-sustained: 6 beats - 29 sec
- 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 sec
- repetitive ventricular beats: 1-5 ventricular beats

Diagnosis of VT

Clinical

symptoms largely depend on haemodynamic effects of arrhythmia
history of previous MI and first appearance of tachycardia after infarction strongly suggest VT
conversely long history of recurrent tachycardia dating back to childhood and absence of organic heart disease or the presence of ventricular pre-excitation suggest SVT
on examination changes in intensity of 1st heart sound may be detected during VT and there may be cannon waves in neck due to AV dissociation

ECG criteria

(ECG)

Is a RS complex present in any precordial lead? If not then diagnosis is VT
If RS present measure duration of R to S nadir. If >100 ms in any V lead then diagnosis is VT
If RS not > 100 ms look for AV dissociation (independent p waves, fusion beats or capture beats)
If AV dissociation not present decide whether QRS complexes have a right or left BBB pattern. If pattern is typical in both V1 and V6 the rhythm is SVT. If any atypical features rhythm is VT
Pre-existing complete BBB. Very helpful in diagnosis. eg in patient with complete RBBB during sinus rhythm, it is highly likely that wide complex tachycardia with LBBB pattern is VT
Narrow complex tachycardia. Very rarely VT may be narrow complex. This may be the case, for example, if, in 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
If in doubt, in patients with structural heart disease it is safer to diagnose VT and this usually proves to be correct

Non-sustained VT

Definition

poorly defined
not a distinct clinical entity
VT that persists for an arbitrary period of time in the absence of intervention.
most usual definition requires minimum of 4 consecutive VEBs and a maximum duration of 30s

Symptoms

very variable as it is a poorly defined category
range from none to syncope

Mechanism

often polymorphic: this morphology compatible with both re-entry and triggered automaticity as underlying mechanisms
monomorphic VT usually due to re-entry
triggered automaticity not reliably examined by programmed stimulation
in clinical practice EPS offers assistance in treating some patients: mainly those in whom the technique can provoke a tachycardia similar to spontaneous arrhythmia. Sensitivity and specificity modest

Clinical situations

Myocardial infarction

occurs in as many as 35% of patients in acute phase of MI. Has neither immediate nor late prognostic significance
5-10% in post-acute phase. Probably does have prognostic significance; may be a marker of susceptibility to sustained VT
treat symptomatic patients

Reperfusion VT

usually well tolerated
may be a marker of good prognosis as may signify recovery of electrically deranged cells
no indication for prophylactic anti-arrhythmics

Heart failure

occurs in many patients with heart failure
only modest proportion symptomatic
associated with adverse prognosis. No benefit from treatment with amiodarone in CHFSTAT study. Amelioration of heart failure may be best strategy
subgroup analysis of CHFSTAT and GESICA studies suggests that those patients with heart failure due to idiopathic cardiomyopathy may benefit from amiodarone

Right ventricular dysplasia

increasingly recognized as aetiological factor for VT in young patients who initially do not seem to have structural heart disease
VT characteristically provoked by exercise
rate may be very rapid and VT usually symptomatic
very little known about natural history but in some there is a progressive cardiomyopathic deterioration of the RV with islands of fatty infiltration and fibrosis that provide ideal conditions for re-entrant VT
several patterns of VT may occur in each patient
treat symptomatic patients

Normal individuals

nothing known of true prevalence or implications

Treatment

treat symptomatic patients only
innocuous forms: reassurance may be all that is necessary
first line: beta blockade. Sotalol 0.5-1.5 mg/kg IV over 5-20 min
if these fail try other drugs known to be effective against VT. No scientific way to choose agent but selection should take account of risk/benefit ratio

Sustained VT

Needs to be considered with reference to specific underlying disease

Coronary artery disease

monomorphic VT most common form of sustained VT
usually occurs after MI
arrhythmias originate within or at border zone of damaged myocardium
underlying mechanism probably re-entry
ischaemia seems to be less frequently involved in initiation of monomorphic VT. Tends to present with polymorphic VT or VF instead

Dilated cardiomyopathy

underlying mechanism less well understood
prognostic significance of spontaneous VT uncertain
no evidence that empirical antiarrhythmic therapy is useful for preventing arrhythmias or for improving survival
value of programmed ventricular stimulation for assessment of drug efficacy controversial

Mitral valve prolapse

sustained VT in patients with clinically significant mitral valve prolapse rare
mechanism poorly understood
response to treatment variable
some patients respond well to beta-blockers or calcium antagonists while others do better with class I or III drugs
programmed stimulation of little clinical value

Hypertrophic cardiomyopathy

non-sustained VT associated with high risk of sudden death
occasionally sustained VT recorded
cellular mechanisms not well understood

Right ventricular cardiomyopathy

response rate to treatment varies from report to report
? sotalol most effective drug

Apparently normal hearts

patients virtually always < 50 yrs
usually single VT morphology, typically RBBB and LAD
ECG during sinus rhythm normal or shows minor ST or T abnormalities
most patients symptom-free or only have palpitations
probably does not involve re-entry
may be initiated during exercise
may be terminated by verapamil, beta-blockers, or adenosine

Monitoring effectiveness of treatment

can be difficult to determine efficacy of treatment and first indication of treatment failure may be sudden death
relative merits of programmed stimulation and ambulatory monitoring unclear. Latter only of value in patients with frequent episodes of VT

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

ECG

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% 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 (eg terfenadine and astemizole; former particularly in association with erythromycin)
- Metabolic and electrolyte disorders
  - hypokalaemia
  - hypomagnesaemia
  - 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%)
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

Management

Acute

correct underlying cause if possible
avoid precipitating drugs
IV magnesium and temporary atrial or ventricular pacing are initial therapy
pacing suppresses VT which often does not recur even after cessation of pacing
isoproterenol (isoprenaline) to increase heart rate can be tried cautiously until pacing instituted
prevention of recurrence: beta blockade at maximum tolerated dose, perhaps in combination with class 1b drug

Ventricular arrhythmia

Ventricular ectopics

Ventricular tachycardia

Classification

Diagnosis of VT

Clinical

ECG criteria

Non-sustained VT

Definition

Symptoms

Mechanism

Clinical situations

Treatment

Sustained VT

Coronary artery disease

Dilated cardiomyopathy

Mitral valve prolapse

Hypertrophic cardiomyopathy

Right ventricular cardiomyopathy

Apparently normal hearts

Monitoring effectiveness of treatment

Torsades de pointes

Definition

Causes of long QT

Clinical features

Management

Further reading