Tachyarrhythmias
Tachyarrhythmias
Tachyarrhythmias are abnormal rhythms with fast heart rates that have impulses coming from either the atria or ventricles. Tachyarrhythmias can occur without any untoward symptoms, or they can be symptomatic. Sinus tachycardia can be a normal response to exercise, play, stress, or fever.
Symptomatic tachycardia is indicative of hemodynamic compromise concerning for shock or cardiac arrest. If the cardiac function is significantly affected by tachyarrhythmias, then patients can rapidly deteriorate. Patients with symptomatic tachycardia show signs and symptoms, including:
- Hypotension
- Altered mental status
- Shock
- Sudden collapse
- Respiratory distress and failure
- Decreased cardiac output
- Decreased coronary perfusion
Tachycardias and tachyarrhythmias are classified by the QRS period. QRS complexes < 0.09 seconds are narrow complex tachycardias such as sinus tachycardias, supraventricular tachycardias, and atrial flutter. QRS complexes > 0.09 seconds are wide complex tachycardias such as ventricular tachycardias and supraventricular tachycardias with aberrant intraventricular conduction.
Sinus Tachycardia
During sinus tachycardia, impulses originate from the sinus node as a compensatory response to physiologic conditions that demand an increase in cardiac output or oxygen delivery. These conditions include exercise, pain, anxiety, hypoxia, hypovolemia, shock, fever, metabolic stress, injury, toxins, drugs, and anemia.
Sinus tachycardia has a relatively short R-R interval with a rate < 220 bpm in infants and < 180 bpm in children. The presence of the P wave indicates the rhythm is sinus. The PR interval is constant and normal in duration, and the QRS complex is narrow (< 0.09 seconds).
Related Video – ECG Rhythm Review – Sinus Tachycardia
Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is caused by aberrant impulses originating anywhere above the ventricles. A common cause is the reentry of impulses within the AV node or through an accessory pathway. SVT in infants and children commonly causes cardiovascular compromise.
Key Takeaway
If the patient has no recorded history of heart disease that has caused aberrant conduction, then wide QRS tachycardias are assumed to be secondary to VT and not SVT.
Infants with SVT frequently present with congestive heart failure (CHF). Often, children with SVT are asymptomatic until the child develops CHF. Patients will be irritable, present with poor feeding, increased sleepiness, vomiting, and skin changes such as paleness, mottling, or cyanosis. Older children may complain of palpitations, shortness of breath, chest pain, lightheadedness, and syncope. The result of untreated SVT is cardiovascular collapse.
Initial Assessment in Symptomatic SVT
Initial Assessment in Symptomatic SVT
The child’s heart rate helps the clinician to quickly distinguish SVT from sinus tachycardia. In SVT, the heart rate will be > 220 bpm in infants and > 180 bpm in children. A heart rate that is elevated but lower than that is likely sinus tachycardia.
Other ECG findings in SVT include:
- abnormal appearance of P waves or absent P waves (to the point that the provider may not be able to assess a PR interval)
- a constant R-R interval
- a narrow QRS complex (rarely, a wide QRS)
Related Video – ECG Rhythm Review – Supraventricular Tachycardia (SVT)
Wide QRS complex SVT occurs in only 10% of children in SVT. Wide QRS complexes are caused by aberrant intraventricular conduction. A rate-related bundle branch block likely causes the impulses.
Wide QRS complex SVT can also result from impulses that travel via an accessory pathway from the atria to the ventricles bypassing the AV node and then returning to the AV node via a different pathway.
SVT and VT have similar ECG characteristics. If the patient has no recorded history of heart disease that has caused aberrant conduction, then wide QRS tachycardias are assumed to be secondary to VT and not SVT.
Related Video -One Quick Question: What are the Differences Between ST (sinus tachycardia) and SVT?
Atrial Flutter
Atrial flutter is another narrow QRS complex tachycardia. It can occur in children with congenital heart disease as well as infants with a normal heart. Cardiac surgery can precipitate atrial flutter due to iatrogenic causes.
Atrial flutter is caused by a reentrant mechanism that allows impulses to occur only within the atria. Since the AV node is located below the atria, there may be no signs of AV conduction in the atrial pathway. This reentrant conduction of impulses within the atria can exceed 300 bpm, but since the ventricles are not involved, the ventricular rate is slower. Because of that phenomenon, atrial flutter produces a “saw-tooth” pattern of P waves.
Related Video – ECG Rhythm Review – Atrial Flutter
Ventricular Tachycardia
Ventricular tachycardia is a wide QRS complex tachycardia that has impulses originating within the ventricles. It is not a common tachyarrhythmia in children. VT can exceed 200 bpm. At this rate, ventricular filling, stroke volume, and cardiac output are inadequate and can rapidly deteriorate into pulseless VT or ventricular fibrillation.
Characteristic ECG changes in VT:
- Ventricular rate of 120 bpm or greater and regular
- Wide QRS complex (> 0.09 seconds)
- P waves are absent or unidentifiable
- T waves are opposite in deflection from the QRS complex
Related Video – ECG Rhythm Review – Ventricular Tachycardia
When a child develops VT, they usually have underlying heart disease and may have undergone cardiac surgery. They may have long QT syndrome or have acquired myocarditis and cardiomyopathy. These children often have family members with a history of sudden, unexplained death, cardiomyopathy, or an inherited cardiac ion “channelopathy.” Children with electrolyte imbalances such as hyperkalemia, hypocalcemia, and hypomagnesemia or drug toxicities may develop VT.
When the QRS complexes occurring during VT appear uniform, the rhythm is described as monomorphic. Polymorphic VT is present when the QRS complexes vary in appearance. In general, patients in VT deteriorate quickly. Patients in polymorphic VT decompensate very quickly.
Torsades de pointes is a specific type of wide complex polymorphic VT in which the QRS complex seems to twist along the isoelectric line. The ventricular rate can be 150–250 bpm. This condition is associated with prolonged QT intervals precipitated by long QT syndrome and drug toxicity.
Torsades de pointes can occur in bursts and then spontaneously resolve. The provider may see a prolonged QT interval during episodes of sinus rhythm but be unable to evaluate the QT interval.
Other conditions that cause torsades de pointes include hypomagnesemia, hypokalemia, and antiarrhythmic drug therapies (Class IA: quinidine, procainamide, dipyridamole; Class IC: encainide, flecainide; Class III: sotalol, amiodarone).
VT and polymorphic VT can rapidly deteriorate into VF, which is associated with sudden death. Likewise, prolonged QT syndrome and channelopathies can also cause VF and torsades de pointes that can elicit VF and sudden death.