| Fact | Explanation |
|---|---|
| May have a congential etiology | When ventricles beat very fast (120 to 300 beats per minute), and neither coordinated with the atria it is called a ventricular tachycardia. Most commonly VT is seen in a weak cardiac musculature due to a cardiomyopathy, or when there's scarring of the heart due to prior myocardial infarction. But channelopathies,electrolyte imbalances, structural heart disease such as tetralogy of Fallot, systemic diseases such as rhematoid arthritis, certain drugs can also cause a VT. The pathophysiology of the arrhythmia is usually caused by electrical reentry or abnormal automaticity. Inherited channelopathies such as long/short QT syndromes, catecholaminergic polymorphic ventricular tachycardia and Brugada syndrome have a congenital etiology. When there's beat to beat variation of the QRS complex, it's called polymorphic VT and if similar it's called monomorphic VT [9] [10] [11] |
| Palpitations [1] [7] | Sensation of pounding of the heart is due to abnormal rhythm [1] [7] |
| Light-headedness/ Syncope [2] [7] | Due to cerebral hypo-perfusion due to extreme tachycardia [2] [7] |
| Chest pain [1] [7] | Can be due to ischaemia or palpitations it self [1] [7] |
| Anxiety [1] [7] | Due to palpitations [1] [7] |
| Sudden death [2] [6] [7] | In catecholaminergic polymorphic ventricular tachycardia (CPVT) there can be episodes of syncope, seizures, or sudden death [2] [6] [7] |
| Fact | Explanation |
|---|---|
| Tachycardia [1] [2] [3] | VT is usually caused by electrical reentry or abnormal automaticity and this results in tachycardia [1] [2] [3] |
| Hypotension [3] | Prolonged VT could result in hypotension due to incomplete filling and incoordinated contractions. [3] |
| Tachypnoea [3] | Prolonged VT could result in increased respiratory rate [3] |
| diaphoresis [3] | Sometimes patients may present with haemodynamic instability due to prolonged VT and reduced cardiac output due to tachycardia result in poor perfusion and resultant increased sweating [3] |
| Pallor [3] | Sometimes patients may present with haemodynamic instability due to prolonged VT and reduced cardiac output due to tachycardia result in poor perfusion and pallor [3] |
| Diminished level of consciousness [3] | Sometimes patients may present with haemodynamic instability due to prolonged VT and reduced cardiac output due to tachycardia result in poor perfusion to brain and diminished level of consciousness [3] |
| Elevated jugular venous pressure with cannon a waves [4] | This is observed if atria are in sinus rhythm [4] |
| Murmers [7] | When a valvular disease or hypertrophic obstructive cardiomyopathy causes the VT, murmurs may be heard. [7] |
| Displaced apex [7] | Due to cardiomegaly due to underlying ischaemic heart disease [7] |
| Rales on respiratory system examination [7] | If the arrhythmia leads to congestive cardiac failure, auscultation of lungs may reveal rales [7] |
| Varying intensity of the first heart sound [6] | Due to loss of atrioventricular (AV) synchrony. [6] |
| Fact | Explanation |
|---|---|
| Atrial Fibrillation [1] | This is the most common cardiac arrhythmia, and can lead to heart failure, stroke, and death and this can mimic VT [1] |
| Atrial Flutter [2] | This gives a sawtooth pattern on the electrocardiogram (ECG) and clinical presentation may mimic VT [2] |
| Ventricular Fibrillation (VF) [3] | Rapid, polymorphic VT may be difficult to distinguish from VF in which QRS complexes are very irregular and this condition is life threatening [3] |
| Pacemaker induced tachycardia [4] | Sometimes these can generate tachycardias and considered as a differential diagnosis [4] |
| Wolff-Parkinson-White syndrome [5] | There is an accessory pathway between the atrium and ventricle and patients with WPW syndrome have clinical symptoms that mimic VT [5] |
| Accelerated idioventricular rhythm [6] | This is slower than VT and considered as a good change in electrocardiogram which clinicians like to see after reperfusion therapy. [6] |
| Supraventricular tachycardia with abberant conduction [7] | This is clinically similar to VT and also produces a broad complex tachycardia in electrocardiogram[7] |
| Fact | Explanation |
|---|---|
| Electrocardiography (ECG [1] | Broad complex tachycardia (BCT) is seen. Some of ECG differential diagnosis are supraventricular tachycardia (SVT) with aberrant conduction and bundle branch block (BBB) [1] |
| Serum electrolytes [2] | As electrolyte disturbances commonly cause VT, it's important to screen for electrolyte abnormalities. Hypokalemia, hypomagnesemia, and hypocalcemia might cause VT or torsades de pointes. [2] |
| Serum drug levels and toxicology screen [3] | Overdose of Digoxin, Tri-cyclic antidepressants, cocaine drug levels as these may cause VT [3] |
| Serum cardiac markers [4] | Myocardial ischemia or infarction can lead to VT, therefore serum cardiac markers are measured. [4] |
| Echocardiography [5] | This is done to diagnose the underlying disease which could be hypertrophic, dilated, or right ventricular cardiomyopathy, segmental hypokinesia due to myocardial infarction [5] |
| Cardiac imaging studies [6] [9] | When echocardiography results are inconclusive, to detect structural heart diseases this is done. [6] [9] |
| Monitoring devices [7] [8] | Halter monitoring, implantation of a loop recorder are monitoring devices used to assess patients with history of syncope but when the resting ECG is normal [7] [8] |
| Myocardial biopsy [9] | This could be important to diagnose hypertrophic cardiomyopathy, arrhythmogenic right ventricular disease or sarcoidosis, amyloidosis [9] |
| Electrophysiological studies (EPS) [10] | When a patient has a history of myocardial infarction, or has clinical symptoms of VT rarely these tests are done. [10] |
| Fact | Explanation |
|---|---|
| Venography [1] | Obstruction of the access vein is a known complication of both permanent pacemaker and implantable cardioverter defibrillation implantation, therefore this could be done prior to implantation. [1] |
| Renal function tests including estimated glomerular filteration rate, serum creatinine, blood urea nitrogen [2] [3] | To assess fitness for anesthesia [2] |
| Full blood count [3] | To exclude anaemia. [3] |
| Coagulation studies [3] | To exclude any coagulopathy. [3] |
| Fact | Explanation |
|---|---|
| Electrocardiography (ECG) [1] | To assess for development of any other life threatening arrhythmias such as ventricular fibrillation, and to see the arrhythmias induced by drug therapy. [1] |
| Echocardiography [2] | To assess for ejection fraction, for the possibility of congestive cardiac failure as consequence later [2] |
| Liver function tests [3] | To see any amiodarone induced liver damage with long term amiodarone therapy [3] |
| Chest x ray [3] | To see any amiodarone induced lung changes with long term amiodarone therapy [3] |
| Thyroid profile [3] | To see any amiodarone induced hyper/hypothyroidism with long term amiodarone therapy [3] |
| Fact | Explanation |
|---|---|
| Genetic testing for familial disorders [2] [3] | Long QT syndrome, ARVD, or dilated or hypertrophic cardiomyopathy, Catecholaminergic Polymorphic Ventricular Tachycardia have inherited etiologies therefore, genetic testing is done. [2] [3] |
| Electrocardiography [1] | To see any features of long QT syndrome, Brugada syndrome in an asymptomatic patient who has a family history of VT or sudden death [1] |
| Echocardiography [4] | To carry out screening in families who might be affected with hypertrophic obstructive cardiomyopathy or dilated cardiomyopathy which may lead to VT [4] |
| Treadmill testing [1] | To see any features of exercise induced long QT syndrome, in an asymptomatic patient who has a family history of VT or sudden death [1] |
| Fact | Explanation |
|---|---|
| Acute management of ventricular tachycardia in an unstable patient. [1] [2] [3] | Synchronized direct current (DC) cardioversion is used in patients with unstable monomorphic VT and unstable polymorphic VT is treated with immediate defibrillation. [1] |
| Acute management with drugs in a stable patient [1] [2] [3] | Intravenous (IV) procainamide, sotalol, Lidocaine is used in a stable patient [1] |
| Correction of electrolyte abnormalities [4] | hypokalemia or hypomagnesemia from diuretic use should be corrected first [4] |
| Correction of drug toxicity [4] | Treatment with anti-digitalis antibody is required if Digitalis toxicity is suspected [4] |
| Dietary management [6] | low-cholesterol diets, low-salt diets, or both are recommended for patients with VT and caffeine which is a stimulant is also helpful. [6] |
| Activity [5] | Increased sympathetic tone during strenuous physical exertion can stimulate a VT. Therefore it's better avoided [5] |
| Patient education [7] | patient education regarding nature, course, prognosis of disease, the precautions after starting anti arrhythmic therapy, or ICD implantation is needed. [7] |
| Patient identification [7] | When a patient presents with syncope, cardiac arrest, patient identification with a bracelet/ diagnosis card is helpful for further management [7] |
| Fact | Explanation |
|---|---|
| Anti arrhythmic drug therapy [1] | ACC/AHA/ESC guidelines recommend combination of amiodarone and beta blockers when symptoms do not respond to beta blocker or when there's myocardial infarction resulting in ventricular dysfunction. In patients with heart failure beta receptor–blocking drugs (metoprolol, carvedilol, and bisoprolol), Angiotensin-converting enzyme inhibitors (ACEI), Aldosterone antagonists are used.[1] [7] |
| Radiofrequency catheter ablation [2] [3] | Cardiomyopathy, bundle-branch block, and and myocardial infarction causing a dysfunctional ventricles benefit from this [2] [3] |
| Implantable cardioverter defibrillator implantation [4] [5] [6] | When a patient has hemodynamically unstable VT, unexplained syncope, familial sudden death syndromes ICD implantation may be beneficial. [4] [5] [6] |