History and exam
Key diagnostic factors
common
coronary artery disease
Ventricular fibrillation is common during active ischaemia; chronic coronary disease leads to scar formation, which increases risk of ventricular tachycardia.
presence of other risk factors
Other risk factors include left ventricular systolic dysfunction, hypertrophic cardiomyopathy, long QT syndrome, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy, and family history of sudden death.
tachycardia
Essential to the diagnosis by definition.
hypotension
Degree of hypotension will depend on the rate and duration of the tachycardia and will be an indication of reduced cardiac output.
Other diagnostic factors
common
weak pulse
Palpation of the carotid or femoral pulse provides useful information regarding the heart rate (frequency of the pulse in bpm) and cardiac output (force of the pulse), which, if reduced, may be revealed by a weak pulse.
syncope
Frequently observed in patients with ventricular tachycardia, due to cerebral hypoperfusion from hypotension; however this is non-specific.
presyncope
Frequently progresses to syncope.
airway compromise
This may include stridor and/or apparent obstruction to breaths delivered during rescue breathing.
impaired consciousness
Unconsciousness is a sign of diminished cerebral perfusion in a haemodynamically unstable patient. An alert patient with a normal blood pressure would be considered haemodynamically stable.
light-headedness
Sign of diminished cerebral perfusion in a haemodynamically unstable patient.
dizziness
Sign of diminished cerebral perfusion in a haemodynamically unstable patient.
diminished responsiveness
Sign of diminished cerebral perfusion in a haemodynamically unstable patient.
chest discomfort
Symptom of inadequate coronary perfusion.
dyspnoea
Symptom of inadequate coronary perfusion, often with resultant left ventricular dysfunction or mitral regurgitation.
uncommon
asymptomatic
Ventricular tachycardia does not always cause symptoms.
Risk factors
strong
coronary artery disease
Coronary artery disease creates ischaemia in myocardial tissue. In the long term, myocardial infarction leads to ventricular scarring, with areas of delayed electrical conduction along the border zone of the scar, as well as within the scar, that are the substrate for re-entrant circuits.
acute myocardial infarction
Acute ischaemia facilitates arrhythmias due to three electrophysiological mechanisms: re-entry, triggered activity, and automaticity.
left ventricular systolic dysfunction
Systolic dysfunction, regardless of the cause, is strongly associated with ventricular arrhythmias. Scars in the ventricle create areas of slowed electrical conduction and set up the substrate necessary for re-entrant ventricular tachycardia/ventricular fibrillation. These scars can be created by prior myocardial infarction (ischaemic cardiomyopathy) or abnormal myocardial fibrosis (non-ischaemic cardiomyopathy).[7]
hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy (HCM), a genetic condition characterised by cellular disarray of the myocardium that results in asymmetrical thickening of the ventricle, has been linked to increased risk of developing ventricular arrhythmias. The phenotypic expression of this disorder is highly variable, and the risk of ventricular arrhythmia varies among individuals. In general, the following clinical risk factors are considered as high risk and merit consideration of prophylactic implantable cardioverter-defibrillator placement: 1) family history of sudden death from HCM; 2) massive left ventricular hypertrophy (wall thickness ≥30 mm); 3) unexplained syncope; 4) left ventricular systolic dysfunction; 5) left ventricular apical aneurysm; 6) extensive late gadolinium enhancement on cardiovascular magnetic resonance imaging; and 7) non-sustained ventricular tachycardia on ambulatory monitor.[8][9]
See Hypertrophic cardiomyopathy for more information.
long QT syndrome
Long QT syndrome (LQTS) represents a genetic disorder that manifests as a prolongation of the corrected QT interval on the ECG. The clinical prognosis varies according to the phenotypic manifestation of the genetic defect. Multiple subtypes of LQTS have been described; patients are at increased risk of experiencing a particular form of polymorphic ventricular tachycardia known as torsades de pointes (TdP). While there are over a dozen mutations that are known to cause LQTS, approximately 75% of patients with clinically certain LQTS diagnosis have one of three mutations (LQT1-3). Typically, patients with LQTS type 1 (LQT1) are at increased risk of developing TdP during periods of physical exertion. LQTS type 2 (LQT2) is often characterised by initiation of TdP following a startle reflex or a period of heightened emotional stress. Patients with LQTS type 3 (LQT3) tend to develop arrhythmias during sleep.[10] Beta-blocker medications have been shown to reduce the arrhythmia burden in LQTS, except with LQT3 patients. Implantable cardioverter defibrillators are recommended for patients with high-risk features.[11]
See Long QT syndrome for more information.
short QT syndrome
Syndrome manifested by a short QT interval (QTc generally 330 milliseconds or less, but can be diagnosed with QTc <360 milliseconds in presence of certain clinical features) and an increased risk of sudden death due to polymorphic ventricular tachycardia.
Brugada syndrome
Brugada syndrome is a disorder of myocardial sodium channels, which leads to a characteristic J-point elevation and downward-sloping ST segment elevation in the right precordial leads due to regional inhomogeneities in ventricular repolarisation, and results in an increased risk of sudden death due to polymorphic ventricular tachycardia and ventricular fibrillation. A mutation in the SCN5A (sodium channel) gene has been implicated, but is present in only a minority of patients. SCN10A has also been identified as a major susceptibility gene for Brugada syndrome.[12] Three patterns of ECG abnormalities have been described. Type I pattern consists of J point elevation with a 'coved' ST segment elevation of at least 2 mm, with negative T wave; type II pattern has ST segment elevation of at least 2 mm and 'saddleback' appearance, and type III pattern has features of either type I or II pattern, but ST elevation of under 2 mm. Only type I pattern is considered diagnostic. Risk factors for sudden death in patients with Brugada pattern include a history of unexplained syncope and spontaneous type I Brugada pattern on ECG. Use of electrophysiological testing to determine susceptibility to sudden death has been somewhat controversial. However, inducibility of ventricular fibrillation does not appear to help in risk stratification.[13]
Drug challenges with various anti-arrhythmic medications (procainamide, flecainide, or ajmaline) can be helpful to diagnose borderline cases of Brugada syndrome; positive response to the drug challenge results in increased ST elevation of the right precordial leads.[14]
ventricular pre-excitation
ECG abnormality notable for slurring of the initial portion of the R wave due to an abnormal AV conduction pathway, which activates ('pre-excites') a portion of the ventricular myocardium before the normal electrical impulse conducts down the AV node/His-Purkinje system. Pre-excitation is most commonly seen in patients with an accessory pathway due to Wolff-Parkinson-White (WPW) pattern or syndrome. Patients with WPW that are capable of rapid conduction down the accessory pathway (i.e., from atria to ventricles) are at risk of having atrial fibrillation with rapid conduction to the ventricles degenerating into ventricular fibrillation. This can manifest as an irregular rhythm with varying, but wide, QRS complexes. Importantly, patients with accessory pathways can have antidromic reciprocating tachycardia (ART), which is a macro-reentrant circuit involving antegrade conduction down the accessory pathway, and retrograde conduction up the AV node. This form of supraventricular tachycardia is indistinguishable from ventricular tachycardia arising from the base of the ventricles, since activation of the ventricles originates at the location of the accessory pathway in ART.
arrhythmogenic right ventricular cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disorder characterised by progressive heart failure, ventricular arrhythmias, and sudden death. In this disease, various regions of the right (and less commonly left) ventricular muscle are replaced by deposition of fat and fibrotic tissue. The disease may be transmitted in an autosomal-dominant fashion and in some families is related to mutations in the genes encoding desmosomal proteins (plakoglobin, desmoplakin, and plakophilin). Early symptoms include syncope and palpitations (especially during periods of heavy exertion); as the disease progresses, symptoms of right ventricular failure become more prominent. In advanced presentations, patients may develop biventricular failure. Patients with ARVC frequently manifest interventricular conduction delays on ECG; the finding of an epsilon wave in lead V1 is a specific sign for the disease, and represents late activation of a portion of the right ventricle. A Holter monitor typically reveals left bundle branch block-morphology premature ventricular contractions (often of more than one ECG morphology), or non-sustained ventricular tachycardia. Echocardiogram and/or right ventricular angiography may reveal right ventricular dilation, regional dyskinesis, and/or reduced systolic function. Cardiac magnetic resonance imaging may reveal fibro-fatty infiltration of the right ventricular myocardium.[4][18] Although the original descriptions characterised predominantly RV involvement, variants with earlier and/or greater left ventricular involvement have been reported, leading to the use of the term 'arrhythmogenic cardiomyopathy' as a broader term to include all phenotypes.
electrolyte imbalance
Electrolyte abnormalities (particularly hypokalaemia and hypomagnesaemia) may incite and/or contribute to ventricular tachycardia.
drug toxicity
Pharmacogenetic variants exist that result in prolongation of the QT interval with administration of certain drugs, including macrolide antibiotics, chlorpromazine, haloperidol, and domperidone. An up-to-date list of drugs is available through research centres. CredibleMeds: Arizona Center for Education and Research on Therapeutics Opens in new window
Chagas disease, and other cardiomyopathies
Across the developing world, infectious and other forms of non-ischaemic cardiomyopathy may also play a significant role in the aetiology of ventricular arrhythmias (e.g., Chagas disease in Central America).[3]
weak
sleep-disordered breathing (SDB)
Impaired baroreflex mechanisms in SDB may increase the incidence of VT and sudden cardiac death through increased sympathetic activation and parasympathetic withdrawal.[15]
family history of sudden death
A family history of sudden death should alert the physician to seek potential arrhythmogenic causes. Genetic testing is available for inherited cardiovascular diseases including long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy, and catecholaminergic polymorphic ventricular tachycardia.[16][17]
mental or physical stress
Catecholamine-sensitive ventricular tachycardia (VT) may only arise during periods of heightened mental or physical stress. Examples include torsade de pointes with certain gene mutations in long QT syndrome, catecholaminergic VT, VT associated with arrhythmogenic right ventricular cardiomyopathy, and even idiopathic VT (e.g., right ventricular outflow tract VT).
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