Cardiac Arrhythmias

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pediatric Cardiac Arrhythmias

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بسم الله الرحمن الرحيم

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Cardiac Arrhythmias

Bradyarrhythmias:

Bradyarrhythmias

Sinus Bradycardia:

Definition: Slow heart rate due to physiologic slowing of the sinus node. The lower limit of normal for heart rate varies with age (first year of life <100 bpm , 1–4 years <90 bpm , >5 years <60 bpm ) Recognition clues: A P wave precedes every QRS. A QRS follows every P wave. Normal P waves axis and morphology (upright in leads I and AVF). The PR interval is generally less than 200 ms. Causes: Factors influencing the sinus node, such as vagal stimulation, hypothyroidism, sedative medications, etc. Almost every antiarrhythmic medication causes sinus bradycardia to some degree. Management: Diagnose and treat the underlying cause of sinus bradycardia . In the case of symptomatic sinus bradycardia due to sinus node dysfunction with or without sinus pauses, atropine or epinephrine can be given to increase the sinus rate. Sinus Bradycardia

Sinus bradycardia:

Sinus bradycardia

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Ectopic Atrial Rhythm Definition: A rhythm originating from a nonsinus source in the atrium. This can often be an escape rhythm seen when the sinus rhythm becomes very slow, or an accelerated ectopic atrial rhythm in the range of 70–90 bpm that is “outrunning” the sinus rate. Recognition clues: The P wave morphology is abnormal (often inverted in AVF). A P wave precedes each QRS. A QRS follows each P wave . Causes: This rhythm is usually idiopathic. Rhythms originating from low in the atrium near the coronary sinus are not uncommon. Management: Ectopic atrial rhythms are generally benign and require no treatment . They are often seen as escape rhythms in patients with injury to the sinus node following surgery for congenital heart disease.

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Ectopic atrial rhythm

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Wandering Atrial Pacemaker Definition: The term “wandering atrial pacemaker” is used when the rhythm is seen to oscillate between sinus rhythm and an ectopic atrial rhythm or between two ectopic atrial rhythms. Recognition clues: The P wave morphology is abnormal and variable. A P wave precedes each QRS. A QRS follows each P wave. Causes: Idiopathic. Management: This is generally a benign finding that does not require treatment.

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Wandering atrial pacemaker

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Junctional Rhythm Definition: A rhythm originating from the AV junction with a slow or low-normal heart rate. Recognition clues: P waves are absent or appear after the QRS in the T wave. QRS is narrow or identical to baseline sinus QRS morphology. Causes: Slow junctional rhythms are usually escape rhythms that are seen with slowing of the sinus node rate. Junctional rhythms that slightly exceed the sinus rate (70–90 bpm range) are referred to as “accelerated junctional rhythms.” Management: Generally benign and require no treatment. Very slow junctional rhythms (<50 bpm ) may indicate sinus node dysfunction or hypervagal tone.

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Junctional rhythm Escape junctional rhythm

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First Degree AV Block Definition: Sinus rhythm with a prolonged PR interval (typically greater than 200 ms ). The term “First Degree AV Block” is somewhat of a misnomer because every atrial beat conducts to the ventricle, and hence there is delayed AV conduction, but no real AV “block.” Regardless, the term is commonly used and accepted . Recognition clues: A P wave precedes every QRS and a QRS follows every P wave. The PR interval is greater than 200 ms. Causes: Anything producing conduction delay between the atrium and the ventricle will prolong the PR interval. Increased vagal tone will prolong conduction through the AV node. Conduction delay in the His–Purkinje system after heart surgery may prolong the PR interval as well. The PR interval is sometimes prolonged in rheumatic fever or Kawasaki disease. Management: Generally benign and requires no treatment.

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First degree AV block

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Second Degree AV Block In first degree heart block all of the P waves conduct, and in third degree heart block none of the P waves conduct. Second degree block, therefore, describes the various bradyarrhythmias that display AV conduction on some of the beats, but not all of the beats. There are four types of second degree AV block, described below: Mobitz I Mobitz II 2:1 AV block. High Grade AV block

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Second Degree AV Block: Type I or Mobitz I ( Wenckebach ) Definition: In Wenckebach conduction, the PR interval gradually prolongs until finally there is a P wave that is not followed by a QRS. The PR interval shortens on the beat following AV block, gradually prolonging again on subsequent beats as the cycle repeats. This can be a normal finding, and is often observed in athletes during sleep. Recognition clues: This is an irregular rhythm. Gradual prolonging of the PR interval until finally a P wave does not conduct . The R–R interval between subsequent beats shortens as the PR interval prolongs.

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Causes: Increased vagal tone, antiarrhythmic drugs or digoxin, and secondary to injury to the AV node after surgery for congenital heart disease. Management: This is generally a benign finding that does not required intervention in the absence of symptoms. It is particularly common in well-trained endurance athletes. In symptomatic individuals temporary or permanent pacing may be required. Second degree AV block: Type I or Mobitz I ( Wenckebach )

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Second Degree AV Block: Type II or Mobitz II Definition: Type II AV block does not display any gradual prolonging of the PR interval prior to AV block, rather, the PR interval remains the same and intermittently sinus beats are not conducted. Mobitz II, in contrast with Wenckebach conduction, is considered an abnormal finding. Recognition clues: This is an irregular rhythm. The PR interval on conducted beats remains constant. Causes: Mobitz II block is often related to conduction system disease below the level of the AV node in the His bundle or the bundle branches. Management: Symptomatic bradycardia with second degree heart block is an indication for temporary or permanent pacing. In asymptomatic infants who have undergone surgery for congenital heart disease, second degree heart block is an indication for pacing.

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Second degree AV block: Type II or Mobitz II

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Second Degree AV Block: 2:1 AV Block Definition: In two-to-one AV block, every other atrial beat does not conduct. Since there is never more than one conducted beat in a row, there is no opportunity to look for gradual prolongation vs. fixed PR intervals and hence, 2:1 AV block may represent Mobitz I or Mobitz II block . Recognition clues: This is a regular rhythm. The PR interval on conducted beats usually remains constant. Causes: 2:1 AV block has the same etiology as Mobitz I or Mobitz II block. Management: This arrhythmia is treated similarly to other types of second degree AV block.

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Second degree AV block: 2:1 AV block

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Second Degree AV Block: High Grade AV Block Definition: The term “high-grade AV block” applies to the patient with near complete heart block, but clear evidence of occasional conduction. Recognition clues: Two or more P waves in a row are not followed by a QRS. Appears similar to complete heart block except occasional atrial beats have AV conduction. Management: Temporary or permanent pacing is indicated in symptomatic individuals .

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Second degree AV block: high-grade AV block

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Third Degree AV Block Definition: Complete heart block is when atrial depolarization is not followed by ventricular depolarization due to block of conduction at the AV node. The P wave in these cases are not followed by QRS complexes throughout the rhythm strip . Recognition clues : The QRS rate should be regular in complete heart block. The atrial rate is also usually regular. Any irregularity in the ventricular rate should raise suspicion for intermittent AV conduction (second degree block). It is impossible to diagnose complete heart block unless there are more P waves than QRS complexes. For example, in a patient with a sinus rate of 60 bpm and accelerated junctional rhythm at 80 bpm , AV conduction cannot be evaluated because the ventricular rate is “outrunning” the atrial rate. QRS morphology depends on the escape rhythm in complete heart block. Most patients will have a junctional escape rhythm with regular, narrow QRS complexes . Patients with a ventricular escape rhythm will have wide QRS morphology .

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Causes: Complete heart block can be congenital or acquired and is caused by conduction block at the level of the AV node, His bundle, or Purkinje conduction system . In some instances congenital complete heart block is caused by maternal lupus , although many mothers of infants with congenital heart block have no evidence of autoimmune disease. Complete heart block in children is often the unintended consequence of surgery to repair congenital heart disease, particularly after repair of large ventricular septal defects, tetralogy of Fallot , or AV canal defects. Other acquired causes of heart block include lyme disease (first, second, or third degree heart block are possible), cardiomyopathy, and antiarrhythmic drug overdose. Myocardial infarction can cause heart block in adults because of ischemia to the AV node or His–Purkinje system .

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Management: Atropine and/or epinephrine are often effective in increasing the rate of the escape rhythm, particularly in patients who present with complete heart block and slow junctional rhythms. Transcutaneous pacing can be performed with most bedside external defibrillators, although this maneuver is quite painful. While permanent pacemaker implantation is the standard of care for adults with complete heart block, the decision to implant a pacemaker in a small child or infant is more difficult because procedural complication rates are higher. Many infants with congenital \ complete heart block will have good escape rates and pacemaker implantation can be deferred until they have grown in size.

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Third degree AV block

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Normal Sinus Rhythm Definition: The normal cardiac rhythm originates from a collection of cells in the high lateral right atrium knows as the sinus node. Normal sinus rhythm is defined as a rhythm originating from the sinus node with a normal rate and normal AV conduction . Recognition clues: P wave axis is normal. A P wave precedes every QRS. A QRS follows every P wave. The PR interval is normal.

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Normal sinus rhythm (NSR)

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Tachyarrhythmias

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Sinus Tachycardia Definition: Sinus tachycardia is the most common “arrhythmia” encountered in children , and is defined as normal tachycardia originating from the sinus node. The sinus node is sensitive to catecholamines and achieves maximal rates just above 200 bpm in most children. A rate of 220 bpm is a useful benchmark for differentiating sinus tachycardia from true arrhythmias, although some children (particularly newborns) can achieve sinus rates as high as 230 bpm . Recognition clues : “Warms up and cools down.” Normal P wave morphology. Normal PR interval. Usually a regular narrow complex rhythm. Patients who have a preexisting wide QRS (i.e. s/p repaired congenital heart disease ) will have a wide QRS during sinus tachycardia.

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Causes: Pain, agitation, fever, beta agonist medications (such as albuterol), distress, dehydration, etc. Management: Sinus tachycardia should be considered a normal response to stressors and stimulation rather than an arrhythmia. Once the diagnosis of sinus tachycardia has been confirmed, efforts should be made to diagnose and treat the secondary cause of tachycardia. Antiarrhythmic medications should not be used in patients with sinus tachycardia because they will blunt the body’s compensatory response and will decrease cardiac output. Sinus tachycardia

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Supraventricular Tachycardia Second to sinus tachycardia, supraventricular tachycardia (SVT) is by far the most common tachyarrhythmia seen in infants and children. The term “supraventricular tachycardia” describes any arrhythmia that originates from above the ventricles or AV junction. AV nodal reentrant tachycardia ( AVNRT) and orthodromic reciprocating tachycardia (ORT) account for about 90% of SVT encountered in children. These two arrhythmias have a similar clinical course and are often described with the term “paroxysmal SVT” (PSVT). Less common causes of SVT in children include atrial fibrillation, atrial flutter, ectopic atrial tachycardia, multifocal atrial tachycardia, and others

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Supraventricular tachycardia (SVT)

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Paroxysmal SVT: WPW and Tachycardia Mediated by an Accessory Pathway Definition: Circus movement tachycardia (CMT), orthodromic reciprocating tachycardia (ORT ), and AV reentrant tachycardia (AVRT) are all synonyms used to describe the most common type of SVT mediated by an accessory pathway. This type of paroxysmal SVT is usually initiated by a critically timed premature atrial or ventricular beat. The tachycardia loop propagates down the AV node and returns to the atrium via an accessory connection, before returning back down the AV node. The majority of accessory pathways will only conduct in a single direction from the ventricle to the atrium. However, in about 25% of patients with this type of tachycardia the accessory pathway is capable of conduction in both directions. In those cases , pathway conduction is manifest on the resting ECG during sinus rhythm as a delta wave or “ preexcitation ”. Individuals with both SVT and manifest preexcitation on their baseline ECG are said to have Wolff–Parkinson–White syndrome (WPW).

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Paroxysmal SVT: AV Node Reentrant Tachycardia Definition: In terms of its clinical presentation, AVNRT is nearly indistinguishable from accessory pathway mediated tachycardia. Electrophysiologically , it is a reentrant arrhythmia that circles within the AV node or peri -AV nodal tissue. This arrhythmia is thought to occur when there are two extensions on the AV node (often referred to as “dual AV node pathways” or “dual AV node physiology ”). The tachycardia loop travels down one extension and up the other, completing the reentrant loop. recognition clues: Classically present as palpitations that start and stop abruptly. Usually 200–300 bpm . Always regular, usually narrow QRS tachycardia. Wide QRS (bundle branch block or SVT with aberrancy) is sometimes observed . Bimodal age distribution: most commonly encountered in infants or adolescents, but can be seen in any age group. Rarely associated with syncope. Patients with WPW syndrome will demonstrate a short PR interval and wide QRS during sinus rhythm ( preexcitation ). Shortness of breath and heart failure symptoms will develop after 12–24 h of continuous SVT.

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Causes: Although accessory pathway connections and/or dual AV node physiology are anatomically present from the time of birth, tachycardia usually does not occur until it is initiated by a critically timed premature atrial contraction ( PAC) or premature ventricular contraction (PVC). Hence, episodes of tachycardia tend to be relatively infrequent, but are often provoked by exercise or anxiety. Stimulant drugs like caffeine can provoke SVT episodes. Fever and respiratory infections can also provoke episodes, particularly when high doses of beta-agonist inhalants are required to manage the respiratory symptoms. Management of acute SVT episodes: If given properly, adenosine should terminate any episode of paroxysmal SVT. Once sinus rhythm is restored, the patient is usually started on antiarrhythmic medication to prevent future episodes. While electrical cardioversion will also terminate SVT, it should be remembered that the vast majority of SVT episodes are relatively well tolerated. Cardioversion is only indicated as a first line therapy in the patient who is truly pulseless and appears lifeless.

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Long-term management of paroxysmal SVT: Beta-blockers and digoxin are the most commonly used first line drugs for SVT. Verapamil could also be considered for first line therapy in an older patient. Drugs like Sotalol , Propafenone , Flecainide , and Amiodarone are considered when first line agents fail. The majority of infants with SVT will “outgrow” the arrhythmia by 1 year of age and antiarrhythmic medications can be discontinued. In about one-third of cases, the arrhythmia will return later in life, usually in adolescence . Catheter ablation is the definitive cure for SVT, and is equally effective for both AVNRT and pathway-mediated SVT. In general, success rates are over 95% with this procedure. Serious complications occur in less than 1% of procedures. Ablation can be considered as a first-line therapy for adolescents with SVT. In younger children (5–10 years old) ablation is also safe and effective, but is generally reserved for children who have frequent tachycardia or have failed medical therapy. While ablation is sometimes performed in infants and toddlers, the risk of complications like vascular compromise and heart block increases. Ablation in very young children is therefore reserved for patients with incessant refractory tachycardia that has not responded to maximal medical therapy.

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Supraventricular tachycardia (SVT)

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Ectopic Atrial Tachycardia Definition: Just as an Ectopic pregnancy occurs outside the normal intrauterine location, ectopic atrial tachycardia is similar to sinus tachycardia except that it occurs in an abnormal atrial location away from the sinus node. It differs from the previously mentioned forms of SVT because the mechanism is abnormal automaticity rather than reentry. Ectopic atrial tachycardia often occurs in short bursts. The rate can accelerate and decelerate (similar to sinus tachycardia) in a “warm up” or “cool down” fashion. Recognition clues: A P wave usually precedes every QRS. The PR interval is slightly prolonged (160–200 ms ). P wave morphology in tachycardia is distinctly different from P wave morphology in sinus rhythm .

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Causes: Ectopic atrial tachycardias can originate from anywhere in the atria, but most commonly originate near the pulmonary veins in the left atrium, or around the right atrial appendage or crista terminalis in the right atrium . EAT can be provoked by systemic infections, particularly respiratory infectionswith fever. Inotropic medications like epinephrine can exacerbate EAT. Management: Beta-blockers are first line therapy, although they are not as effective in EAT as in the more typical forms of reentrant PSVT. Second line agents like flecainide or amiodarone may be required. Nonsustained tachycardia may persist despite treatment. In refractory cases catheter ablation is an option.

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Ectopic atrial tachycardia

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Atrial Flutter Definition: Atrial flutter is a reentrant arrhythmia confined to the atrium. In adults and older children, the most typical form has atrial rates of about 300 bpm . In infants, atrial rates can be 400 bpm and above. Ventricular rates will vary, and while 2:1 conduction is the most commonly observed finding in adults (atrial rate of 300 bpm and ventricular rate of 150 bpm ), variable conduction can sometimes make this rhythm look irregular. Ultimately, the pulse rate during atrial flutter depends on the robustness of AV nodal conduction. Scars left in the atrium after surgery to repair congenital heart disease can serve as a substrate for unusual types of atrial flutter. In this setting, the arrhythmia is referred to as “intra atrial reentrant tachycardia” (IART), and the atrial rates may be much slower than the 300 bpm seen in typical atrial flutter .

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Recognition clues: Classically sawtooth pattern, especially in inferior leads. Atrial rate is always regular. Ventricular rate is usually regular, but may be irregular if there is variable AV conduction . Abnormal P wave morphology. Incessant behavior, unlike the paroxysmal or episodic types of SVT. Atrial rate is unaffected by adenosine . Causes: In children, “typical” atrial flutter is much less common than other forms of SVT. It is more common in neonates and is often encountered in the newborn nursery . The key electrophysiologic substrate in “typical” atrial flutter is a zone of slow atrial conduction between the tricuspid valve and the inferior vena cava (“the cavotricuspid isthmus”). Conduction travels across this gap and through the atrium in a counterclockwise, or less commonly a clockwise direction. In the patient with repaired congenital heart disease, atriotomy scars may create other areas of slow conduction that serve as a substrate for the arrhythmia.

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Management: Atrial flutter in infants is often managed with synchronized cardioversion . If available, transesophageal pacing can sometimes be successful in terminating atrial flutter and avoids the need for cardioversion . Atrial flutter will spontaneously resolve without cardioversion in many cases and often within 24 h. If the patient is tolerating the rhythm, it is reasonable to give digoxin or diltiazem and wait for spontaneous conversion. While adenosine will not terminate atrial flutter , a single dose is often given as a diagnostic maneuver to produce temporary AV block and reveal flutter waves. Once the rhythm is converted to sinus, the vast majority of infants will never experience another episode of atrial flutter and prophylactic treatment with antiarrhythmic drugs is not necessary. Since the arrhythmia is usually well tolerated for the first few hours, cardioversion does not need to be done emergently, and is best performed in a controlled setting with conscious sedation or general anesthesia and under the supervision of an experienced pediatric cardiologist.

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Catheter ablation is offered to older children and adults with atrial flutter, and provides a definitive cure for the arrhythmia. In a “typical” flutter ablation, the goal is to block conduction across the cavotricuspid isthmus, and success rates are similar to those seen in patients with accessory pathways or AVNRT. Ablation in patients with repaired congenital heart disease is often more complex and associated with higher recurrence rates. Amiodarone and procainamide are occasionally used to convert atrial flutter in situations where cardioversion has failed or is contraindicated . One disadvantage of using drugs to treat atrial flutter with 2:1 conduction is that the atrial rate slows before terminating. A patient with 2:1 conduction at atrial rates of 300 bpm may have 1:1 conduction once the atrial rate has slowed to 240 bpm . Hence the antiarrhythmic drug may actually lead to an increased heart rate. AV nodal blocking agents like diltiazem or digoxin will not terminate atrial flutter, but are useful for controlling ventricular rates until cardioversion is performed.

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Atrial flutter Atrial flutter with variable atrioventricular conduction and irregular heart rhythm

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Management Overview of Tachyarrhythmias Tachyarrhythmias can be challenging to diagnose in children. The sinus node is capable of achieving rates in the low 200s and occasionally as high as 230 bpm . Sinus tachycardia at rates above 180 bpm is often seen in infants and young children with fever or agitation. Assessment of vital signs and overall condition is the first and most important step in arrhythmia diagnosis and management. Truly unstable or pulseless tachyarrhythmias should be treated with prompt cardioversion . Otherwise , a proper 12 lead ECG should be obtained prior to administration of adenosine or other antiarrhythmic drugs. Single lead rhythm strips and bedside monitors can be misleading and a 12 lead ECG is the most important tool in choosing the correct diagnosis and management plan. A fast tachyarrhythmia of any kind will eventually lead to congestive heart failure and decreased myocardial contractility. Patients who present 12–24 h after arrhythmia onset often complain of shortness of breath and fatigue and may have low blood pressure. As in other forms of cardiogenic shock, intravenous fluid boluses may worsen symptoms and should be avoided.

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Adenosine is an invaluable tool for the treatment and diagnosis of supraventricular arrhythmias . Adenosine is a safe medication due to its short half life. It is important to note the following issues when using adenosine: Adenosine should be administered through a large bore IV and followed immediately by a large saline flush (5–10 cc depending upon the length of the IV line to the patient). This is best accomplished with the use of a “T” connector that allows the adenosine and the flush to be attached simultaneously so the flush can be given immediately following the adenosine. In small infants, the volume of adenosine can be as small as 0.3 ml when only 1 mg is required. It may be helpful to dilute the medication to allow for a larger volume to ensure that all of the medication enters the circulatory system and remains in the IV line. Adenosine is rapidly metabolized in the bloodstream, so anything prolonging the transit time to the heart will potentially render the drug ineffective. Adenosine should always be injected into the most central vein that is available with the shortest external IV tubing possible. Despite this, adenosine can be effective when administered through a peripheral IV or even an intraosseous line if a large flush is given.

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Diminished cardiac output slows the velocity of blood through the veins, and hence prolongs adenosine’s transit time from the IV to the heart. In patients with heart failure or patients who have developed heart failure from a prolonged tachyarrhythmia , larger doses of adenosine may be required and longer times (up to 20 s) may be observed from the time of injection to the observed effect. Atrial fibrillation, sustained or nonsustained , may be observed after a dose of adenosine is given and this may occur in as many as 10% of patients. While this rhythm is relatively well tolerated in most patients, patients with WPW may have rapid AV conduction during atrial fibrillation resulting in rapid ventricular rate. Since hemodynamic compromise is an unusual, but possible complication of adenosine administration, a crash cart with an external defibrillator should always be readily available when adenosine is administered. Adenosine is a bronchoconstrictor and its administration may cause pain. Its use is cautioned in patients with acute asthma exacerbation. Patients almost always have sinus tachycardia for 1–2 min following adenosine administration, which is possible secondary to pain. Patient with atrial flutter and 2:1 conduction may experience 1:1 conduction during the 1–2 min post-adenosine catecholamine surge with a resulting doubling of the heart rate.

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Junctional Ectopic Tachycardia and Accelerated Junctional Rhythms Definition: Junctional tachycardias are automatic arrhythmias arising from the AV junction . Junctional rhythms that slightly exceed the sinus rate are relatively benign and are referred to as “Accelerated Junctional Rhythms”. For faster junctional tachycardias associated with hemodynamic compromise, the term “ junctional ectopic tachycardia ” (JET) is used. JET is frequently seen in the first 24 h following surgery for congenital heart disease. Patients undergoing extensive repair around the AV junction ( Tetraolgy of Fallot , VSD repair, AV Canal repair, etc.) are particularly susceptible to JET. Recognition clues: A narrow complex tachycardia with no visible P waves Usually regular, but may be irregular. Displays “warm-up” and “cool-down” phenomenon. Unaffected by adenosine.

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Causes: Accelerated junctional rhythms are idiopathic and for the most part benign . JET is most often seen in the postoperative period and may be related to inflammation or surgical trauma relating to the AV node or AV junction. In this setting , the arrhythmia may be exacerbated by fever, pain, inotropic infusions, or anything that provokes endogenous catecholamine release. Outside of the postoperative period , clinically significant JET is extremely rare. Management: When JET occurs after cardiac surgery, the rhythm can usually be controlled by weaning inotropic medications, controlling fever and pain, and waiting for the arrhythmia to resolve. In severe cases, amiodarone or procainamide are used, sometimes in combination with ice to cool the patient’s core temperature

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Junctional ectopic tachycardia (JET)

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Ventricular Tachycardia Definition: In the emergency department or EMS setting, ventricular tachycardia (VT ) is most often encountered in older adults with coronary artery disease and/or heart failure and is often thought to be a more malignant or poorly tolerated arrhythmia than SVT. In the pediatric population, ventricular tachycardia usually occurs in children without structural heart disease or ventricular dysfunction. Hence VT is often reasonably well tolerated and may be strikingly similar to SVT in terms of its clinical presentation. Furthermore, SVT in children is often associated with wide QRS or bundle branch block aberrancy which makes it challenging to differentiate VT from SVT with aberrancy. The most reasonable strategy is to treat all wide complex tachycardia as VT until proven otherwise. “ Monomorphic VT ” describes a regular wide complex tachycardia with identical QRS morphology in each beat. “Polymorphic VT” describes an irregular wide complex tachycardia with beat-to-beat variations in the QRS morphology. “Torsade de points” describes polymorphic VT that occurs in the setting of a long QT interval

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Recognition clues: Wide QRS tachycardia. History of structural heart disease. “ VA dissociation” is pathognomonic for VT and is seen when the P wave or atrial rate is slower than the ventricular rate during tachycardia. Sinus capture or “fusion beats” are also pathognomonic and are seen as occasional narrow QRS beats during wide complex tachycardia. QRS duration greater than 130 ms. Rates of 160–250 bpm . Causes: Ventricular tachycardia often occurs in the setting of underlying structural heart diseases, like hypertrophic cardiomyopathy, myocarditis, arrhythmogenic right ventricular dysplasia, cardiac tumors, and congenital heart disease (particularly tetralogy of Fallot or left sided obstructive lesions). Underlying electrical heart diseases like long QT syndrome, catecholaminergic polymorphic VT (CPVT ), and Brugada syndrome are all causes of polymorphic VT.

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Management: Cardioversion is the treatment of choice for patients who are pulseless or unstable. With rare exceptions, ventricular tachycardia will not respond to adenosine. However, adenosine is safe to give for the patient with VT, and is often given as a diagnostic maneuver to differentiate VT from SVT with aberrancy. Correction of electrolyte abnormalities, especially in patients with long QT syndrome, is essential. Cardiology consultation is recommended before starting antiarrhythmic drugs for VT in the stable patient. Intravenous procainamide or amiodarone are usually effective first line treatments for VT. Verapamil is generally contraindicated in VT, but is useful in certain situations. In older children with stable monomorphic VT, catheter ablation is the definitive cure for this arrhythmia. In patients with unstable VT or with underlying disease like hypertrophic cardiomyopathy, an implantable cardioverter defibrillator (ICD) is often indicated.

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Ventricular tachycardia (VT)

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Premature Atrial Contraction Definition: A single beat originating from a nonsinus location in the atrium that occurs prior to the next expected sinus beat, and is preceded by a premature P wave. Depending on how early the PAC occurs, the P wave will be followed by either a narrow QRS (conducted PAC), a wide QRS (aberrantly conducted PAC), or no QRS ( nonconducted PAC ). Recognition clues: A premature P wave is seen. The P wave morphology usually differs from the sinus morphology. Causes: Electrolyte disturbances Idiopathic Misplaced central venous lines or intracardiac devices with the tip in the atrium (typically right atrium) Common in newborns Inotropic infusions ( epinephrine , dopamine, etc.) Management: PACs are generally well tolerated and benign. Generally no treatment is required.

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Premature atrial contraction (PAC)

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Premature Ventricular Contraction Definition: A single wide QRS beat that occurs prior to the next expected sinus beat , and is not preceded by a premature P wave. Recognition clues: Always wide QRS Not preceded by a P wave Causes: Electrolyte disturbances Idiopathic Misplaced central venous lines or intracardiac devices with the tip in the ventricle (typically right ventricle) Digoxin toxicity Pericarditis and/or myocarditis Inotropic infusions ( epinephrine , dopamine, etc.) Cardiomyopathy .

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Management: PVCs are generally well tolerated and benign, especially if the QRS morphology is identical with each PVC (monomorphic) indicating that PVCs are originating from a single ventricular focus. Generally no treatment is required. A thorough workup for underlying electrolyte abnormalities or structural heart disease should be performed before deeming the problem benign. Antiarrhythmic drug ingestions should be considered, particularly in toddlers, and one should inquire about bottles of antiarrhythmic drugs in the household.

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Premature ventricular contraction (PVC)

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Thank you