SVT vs VT ECG

SVT and VT are fast heartbeats experienced as fluttering, pounding, or racing of the heart, a heart arrhythmia. The heart may have too too-fast or too-slow pattern of beat. Heart arrhythmias are classified based on odd speed. When the heart rate becomes greater than 100 beats a minute, tachycardia occurs.

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A heart rate of less than 60 beats a minute is bradycardia. Both arrhythmias are identifiable on the ECG. The SVT and VT differ in their origin. Ventricles, the heart's lower chamber, are the starting point for VT, and SVT starts from the atria, the upper chamber. Reading the blog will help us know the difference between SVT and VT and their clinical significance.

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Types of Arrhythmias

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1. Tachycardia

• Atrial Fibrillation (AFib): Rapid, uncoordinated heartbeat.

• Atrial Flutter: Is similar to a fib but more organised.

• Supra ventricular tachycardia, SVT: irregular heartbeat that starts in the atria, a pounding heartbeat that stops suddenly.

• Ventricular fibrillation: ventricles make an incomplete attempt to contract and quiver, causing a rapid and chaotic heartbeat.

• Ventricular tachycardia: Rapid, regular heart rate from the ventricles, which prevents the blood from being properly filled into the ventricles and then being pumped from the ventricles.

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2. Bradycardia

• Six sinus syndrome: When the sinoatrial node works too fast or too slow, it is common in older adults.

• Conduction block: When the electrical signals are blocked along the pathway, the heartbeat slows or stops.

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3. Premature beats: They are extra beats that are felt as skipped beats.

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Symptoms of Arrhythmia

Arrhythmias come to notice accidentally during a health checkup and remain symptomless in many patients.
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The symptoms are:

• Fluttering, pounding, or racing feeling in the chest.

• A fast or slow heartbeat.

• Chest pain.

• Shortness of breath.

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Some other symptoms may be:

• Anxiety.

• Tiredness.

• Lightheadedness or dizziness.

• Sweating.

• Fainting.

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How Does the Heart Work?

The two upper chambers are the atria and the two lower chambers are the ventricles in the four chambers of the human heart. Blood from all parts of the body collects in the right atrium, pumping it to the lungs for oxygenation through the right ventricle. The left atrium gets oxygenated blood from the lungs. From the left atrium, it is pumped to the left ventricle, and then to the entire body.

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Supraventricular Tachycardia (SVT)

It is a fast, erratic heartbeat affecting the atria and is also known as paroxysmal supraventricular tachycardia. The heartbeat is 150 to 220 times a minute. Most patients do not require any treatment for it sometimes other measures may be required.

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Types

Common SVT types are:

• Atrioventricular nodal reentrant tachycardia (AVNRT).

• Atrioventricular reciprocating tachycardia (AVRT) is the next most common type, and young people are more prone to it.

• People with heart disease have Atrial tachycardia, SVT.

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Other Supraventricular tachycardias are:

• Sinus nodal reentrant tachycardia.

• Inappropriate sinus tachycardia.

• Multifocal atrial tachycardia.

• Junctional ectopic tachycardia.

• Non-paroxysmal junctional tachycardia.

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Causes

It is not usually serious and occurs due to a fault in the electrical system of the heart. It is triggered in people who are on.

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• Medications.

• Caffeine.

• alcohol.

• cigarette smoking.

• physical or emotional stress.

• Congenital heart disease in children.

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Diagnosis

An ECG helps to diagnose SVT an ambulatory Holter monitor is given to people who experience SVT episodes regularly. The device is worn around the neck or waist, and electrodes attached to the chest record the heart's activity rhythm continuously for over 24 to 48 hours.

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A cardiac event monitor is for people who experience SVT not very regularly. The device is attached to a person’s wrist, and with the press of the button, he can record his heart rhythm when symptoms appear.

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Ventricular Tachycardia

Ventricular tachycardia occurs when the heart races to over 100 beats per minute. The heartbeat is so rapid that it prevents the ventricles from filling and pumping blood properly, leading to shortness of breath or lightheadedness.

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VT episodes have a short span, and the episodes that last longer than a few seconds can be life-threatening. Ventricular tachycardia causes sudden cardiac arrest, bringing to a halt all heart functions.

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Types

They are classified according to the length of the episode.

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• Non-sustained VT: lasts for 30 seconds without any symptoms.

• Sustained VT: lasts longer than 30 seconds and can cause serious health problems.

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Causes

A signal in the heart makes it beat too fast or too slow, causing inadequate filling and contracting of the ventricles.

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The causes of ventricular tachycardia are:

• Previous heart attack.

• Structural heart disease.

• Coronary artery disease.

• Congenital heart diseases.

• Electrolyte imbalances.

• Side effects of medicines.

• Using stimulants such as cocaine or methamphetamine.

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Diagnosis

VT requires evaluation of the following parameters.

• Medical history to assess the underlying risk factors for VT.

• History of symptoms before and during the VT episode.

• Family history of inherited cardiac conditions.

• ECG to assess the heart's rhythm.

• Non-invasive imaging test.  
  
  • Echocardiogram 
  • CT scan, 
  • Heart MRI

• A coronary angiogram for coronary artery disease.

• Genetic testing for people with a family history of heart disease.

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Differences Between SVT and VT

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Characteristics of SVT on ECG

SVT presents with specific patterns on ECG that distinguish it from other arrhythmias.

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1. Rapid heart rate: The heart rate is greater than 100 beats per minute and ranges from 150 to 250 bpm due to the high and rapid electrical signals originating from the atria or the AV node. The heart rate throughout the episode is faster and normal than normal sinus rhythm.

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2. Regular rhythm: The rhythm in SVT is regular, it is due to the abnormal electrical activity of short circuits that drive the heart rapidly.

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3. Absent or abnormal P waves:

• P waves are unidentifiable or abnormal in shape as the electrical impulses originate from areas outside the sinus node.

• P waves may be hidden within the preceding T Wave.

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4. Narrow QRS complex: The QRS complex is narrow, less than 120 milliseconds, because electrical impulses are transmitted through the normal conduction pathways.

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5. No visible PR Interval: PR interval is shortened or absent, which is due to the rapid conduction of impulses as electrical signals bypass the delay in the AV node. Sometimes P wave may form after the QRS complex, complicating the interpretation of the ECG.

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Characteristics of VT on ECG

Ventricular tachycardia VT can be life-threatening, so it must be diagnosed as early as possible.

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1. Heart rate

• VT heart rate is more than 100 bpm and can reach up to 200 bpm.

• The higher heart rate in VT originates from the ventricles.

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2. Wide QRS complexes

VT presents wide QRS complexes greater than 120 milliseconds, as the electrical impulses originate from the ventricles. They bypass the normal conduction pathway, and a slow ventricular depolarization causes the QRS complex to widen.

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3. Monomorphic QRS complexes in monomorphic VT. The QRS complexes are identical in shape and size. The consistency in QRS morphology suggests ventricular tachycardia.

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• originating from a single site in the ventricle.

• It is stable and has a better prognosis.

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The polymorphic VT has a variable QRS complex.

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4. Absence of P waves

P waves are usually absent, which indicates arrhythmia originates from the ventricles and not from the atria. The normal atrial impulses cannot trigger the electrical activity of the ventricles.

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5. Irregular rhythm and polymorphic VT

An irregular, erratic rhythm with varying QRS complexes shows polymorphic VT. It has multiple QRS patterns due to different sites of ventricular depolarization, making polymorphic VT harder to diagnose.

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SVT vs VT ECG

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Important to remember in SVT vs VT ECG

Not a single ECG feature is diagnostic of VT.

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ECG features are highly specific for VT.

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• A-     Axis

An axis deviation to the NW axis minus 90 to minus 180 degrees.

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• B-     Broad Complexes

More than 200 ms.

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• C-     Concordance

Concordance (a lack of RS complex in V1-6) in Precordial leads is specific for VT.

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• D-     Dissociation

It is specific for VT.

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• P and QRS complexes at different rates.

• Capture beats the SA node controls the ventricles, causing an isolated normal QRS complex.

• Fusion beats occur as a sinus and ventricular beat coincide to produce a hybrid complex.

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• E-      Early part of QRS

If it is slow, it is VT.

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Other differences between SVT and VT

Clinical presentations may be similar for both, yet they have important differences.

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• SVT presents with palpitations, dizziness, and shortness of breath.

• VT  causes more severe symptoms as chest pain, syncope, or sudden collapse.

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Response to treatment

• SVT responds well to adenosine, temporarily blocking AV node conduction and stopping the arrhythmia.

• VT requires more aggressive treatments, such as anti-arrhythmic drugs or even electrical cardioversion.

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The absence of response to these treatments suggests VT when the patient has a rapid heart rate and wide QRS complexes.

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Treatment for SVT and VT

SVT and VT require optimal patient outcomes.

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Treatment for SVT

Treatment restores the normal sinus rhythm and slows the heart rate.

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• Vagal manoeuvres like the Valsalva slow the heart rate by stimulating the parasympathetic nervous system.

• Medications block the AV node temporarily, allowing the sinus rhythm to resume.

• Beta-blockers control the rate and prevent recurrence.

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Treatment for VT

It is more aggressive due to life-threatening consequences.

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• Medications like Amiodarone stabilise the heart's electrical activity.

• Defibrillation prevents cardiac arrest in a  pulseless VT.

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Conclusion

Understanding SVT vs VT ECG is necessary for patient management. A quick diagnosis ensures timely treatment to prevent life-threatening complications. Gauze supports doctors by timely interpreting ECGs and making precise diagnoses. Continued education and practice improve patient outcomes and ensure optimal management of these arrhythmias.