What is the difference between vfib and vtach

Ventricular Tachycardia and Ventricular Fibrillation are both a group of conditions where the heartbeat is irregular, too slow, or too fast. Such conditions are known as Heart arrhythmia. Ventricular Tachycardia is a medical condition wherein the electrical impulses produced in the SA node are substituted by an ectopic pacemaker.

This condition can also result due to intake of recreation medical drugs. Vfib is the most serious arrhythmia and is an uncontrolled, irregular heartbeat. Instead of one missed heart beat from the ventricles, individual experiences several impulses that start simultaneously from different places — all commanding the heart to beat.

Ventricular Fibrillation is a condition where the electrical impulse conducting system functions in a haphazard manner. There is no coordination between the contraction activity, that triggers irregular rhythms in irregular time intervals. Here, rate and rhythm both get impacted unlike in tachycardia. Ventricular Fibrillation is a serious medical disease which if not treated immediately after it is diagnosed, leads to death.

Ventricular Tachycardia is a medical condition which is associated with the hearts irregular electrical impulses. Such a condition arises mostly in people having valvular hear disease. Ventricular fibrillation VFib is a medical condition in which the heart beats in an abnormal rhythm. The lower heart chambers show quivering activity and the heart is unable to pump any blood, leading to cardiac arrest.

Vfib is an emergency condition that is triggered by a heart attack. In both of these medical conditions, it is essential to examine the causes and symptoms seriously so that accurate and most suitable treatment and medication should be taken. Skip to content Vtach and Vfib are quite similar conditions that arise when the heartbeat or the heart count of a person gets irregular or unusual. Vtach is a medical term that is used to define irregular heart impulses and it mostly arises in those individuals having valvular heart disease.

Vfib is an emergency medical condition in which the lower heart chamber shudder, and the heart would not be able to pump blood which consequently leads to heart failure. The major causes are not particularly known but it is usually triggered by congestive heart failure, cardiomyopathy, structural heart disorder, etc. Vfib is caused by aortic stenosis, electrical shock , LQTS, Brugada syndrome, cardiomyopathies, heart failure, etc.

Risk factors include extreme electrolyte deformities, heart disorders, etc. A person with heart issues or a family history of vtach has a higher risk of this condition. Defibrillation, CPR, coronary angioplasty , and stent placement, etc. Is pulseless electrical activity a reason to refuse cardiopulmonary resuscitation with ECMO support? Am J Emerg Med. Herlitz, J. Nov Your Privacy Rights. To change or withdraw your consent choices for VerywellHealth.

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Side effects are slurred speech, altered levels of consciousness, seizures and bradycardia. Magnesium can be used for polymorphic Vtach associated with QT prolongation, also called torsades de pointes.

Dose is mg IV over 15 minutes. Side effects are hypotension, CNS toxicity, respiratory depression. Follow levels and watch closely with concomitant renal dysfunction. Vtach response to therapy depends on underlying etiology.

Key to treatment past antiarrhythmics and electricity will be identifying possible causes defined in pathophysiology section. If front-line arrhythmia therapy fails or clinical situation deteriorates, reconsider diagnosis. Reevaluate EKG, clinical history and presentation.

Seek expert help. The vast majority of adult cardiac arrests from Vfib and pulseless Vtach are secondary to myocardial ischemia, around , people per year. These arrhythmias are the most common cause of death in acute myocardial infarction. Primary Vfib not associated with an MI needs evaluation by an electrophysiologist.

Vtach occurs in areas of scar from prior MI, the risk of development depending on severity of myocardial necrosis, LV dysfunction and the degree of septal involvement.

Thus stable Vtach is more likely from an arrhythmogenic focus in an old scar. Therapy should be focused on underlying hypoxia, electrolytes, etc. Other possible causes of monomorphic Vtach include: dilated cardiomyopathy, hypertrophic cardiomyopathy, myocarditis, RV dysplasia, drug toxicity and electrolyte abnormalities. Polymorphic Vtach in the setting of a normal QT is usually secondary to acute coronary ischemia or myocardial infarction.

Outside of congenital syndromes such as long QT syndrome, polymorphic Vtach from prolonged QT occurs most frequently following exposure to a QT-prolonging drug.

Risk factors for torsades are female gender, hypokalemia, bradycardia, recent conversion from atrial fibrillation especially with a QT0prolonging drug, CHF, digitalis, baseline QT prolongation, subclinical QT syndrome or severe hypomagnesemia.

For Vfib arrest, high-quality CPR and defibrillation have been proven to increase survival to hospital disharge. Vascular access, drug delivery, advanced airway should not cause significant disruptions in CPR or delay defrbrillation.

Amiodarone is the first-line antiarrhythmic during cardiac arrest, as it has been shown to improve return to circulation.

Two observational studies have shown that magnesium can terminate torsades de pointes, it is not likely to be effective in terminating irregular or polymorphic Vtach with a normal QT interval. For stable Vtach, IV antiarrhythmic drugs or elective cardioversion is recommended. Lidocaine has been found to be less effective than amiodarone, sotalol or procainamide. Procainamide and sotalol should be avoided with QT prolongation. Procainamide should be avoided in CHF. At this time there is no conclusive evidence that one drug is better for termination of monomorphic Vtach.