Transcript
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Approach to Paediatric Conduction Disturbances.
Dr. Shreesh Bhat.2nd year PG, MD Paediatrics
Guided By – Asso. Prof. Dr. S S Mishra.SVPPGIP, Cuttack.
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ECG
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What is Arrhythmia?
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Mechanism of Arryhthmogensis1. Disorder of impulse formation.
a) Enhanced Automaticity/ Ectopic Pacemaker Activity.b) Triggered Activity.
1) Early after depolarization.2) Delayed after depolarization.
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1. Disorder of impulse conduction.a) Reentry.
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Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
Reentry Requires…
Electrical Impulse
Cardiac Conduction Tissue
1. 2 distinct pathways that come together at beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
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Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
Premature Beat Impulse
Cardiac Conduction Tissue
1. An arrhythmia is triggered by a premature beat 2. The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway
Repolarizing Tissue (long refractory period)
Reentry Mechanism
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3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
Cardiac Conduction Tissue
Reentry Mechanism
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4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit
Fast Conduction PathSlow Recovery
Slow Conduction PathFast Recovery
Cardiac Conduction Tissue
Reentry Mechanism
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Reentry Requires…
1. 2 distinct pathways that come together at beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
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Combined disorder.
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Arrhythmia PresentationPalpitation.Dizziness.Chest Pain.Dyspnea.Syncope.Sudden cardiac death.
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BRADYARRHYTHMIASTACHYARRHYTHMIAS
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CARDIAC OUTPUT=
HEART RATE STROKE VOLUME.
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BRADYCARDIAHeart rate less than what is normal for the child’s age
and level of activity
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Common causesPrimary-
Congenital conduction anamoly.Surgical injury to conduction system.Myocarditis.Cardiomyopathy.
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SecondaryMost common- HYPOXIA.Acidosis.Hypothermia.
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Sinus BradycardiaRate: 40-59 bpmP wave: sinusQRS: Normal.Conduction: P-R normal or slightly prolonged at
slower ratesRhythm: regular or slightly irregular
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This rhythm is often seen as a normal variation in athletes, during sleep, or in response to a vagal maneuver. If the bradycardia becomes slower than the SA node pacemaker, a junctional rhythm may occur. .
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Sick Sinus Syndrome
• Conduction problem with no junctional escape during sinus pause
• Diagnose with ECG or Holter. If inconclusive, need electrophysiologic testing.
• If asymptomatic, leave alone. If symptomatic, needs pacemaker.
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First Degree AV Block
• Delay at the AV node results in prolonged PR interval
• PR interval>0.2 sec.• Leave it alone
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Second Degree AV Block Type 1 (Wenckebach)
• Increasing delay at AV node until a P wave is not conducted.
• Often comes post inferior MI with AV node ischemia• Gradual prolongation of the PR interval before a
skipped QRS. QRS are normal!• No pacing as long as no bradycardia.
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Second Degree AV Block Type 2
• Diseased bundle of HIS with BBB. • Sudden loss of a QRS wave because P wave
was not transmitted beyond AV node. QRS are abnormal!
• May be precursor to complete heart block and needs pacing.
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Third Degree AV Block
• Complete heart block where atria and ventricles beat independently AND atria beat faster than ventricles.
• Must treat with pacemaker.
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BUNDLE BRANCH BLOCKRate: variableP wave: normal if the underlying rhythm is sinusQRS: wide (> 0.09 seconds)Conduction: This block occurs in the right or left
bundle branches or in both. The ventricle that is supplied by the blocked bundle is depolarized abnormally.
Rhythm: regular or irregular depending on the underlying rhythm.
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Left bundle branch block is more ominous than right bundle branch block because it usually is present in diseased hearts. Both may be caused by hypertension, MI, or cardiomyopathy. A bifasicular block may progress to third degree heart block.
Treatment is artificial pacing for a bifasicular block that is associated with an acute MI.
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EVALUATECARDIOPULMONARY COMPROMISE?
HYPOTENSIONPOOR SYSTEMIC PERFUSION ALTERED MENTAL STATUS
ALONG WITH RESPIRATORY DISTRESS OR FAILURE.
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ManagementTreat underlying cause in Stable patients.
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CPR
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EpinephrineIO/IV 0.01mg/kg (1:10000 dil, 0.1ml/kg). Repeat every
3-5 minutesET tube- 0.1mg/kg (1:1000 dil, 0.1ml/kg.)
Atropine0.02mg/kg. Repeat after 5min. (Min. 0.1mg Max. 0.5mg)
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CARDIAC PACINGINDICATIONS• Syncope, presyncope or exercise intolerance
that can be attributed to bradycardia• Symptomatic 2nd or 3rd degree AV block• Congenital 3rd degree AV block with wide QRS• Advanced AV block after cardiac surgery • Recurrent 2nd degree- type 2 AV block after MI • 3rd degree AV block with wide QRS or BBB.
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Tachyarrhythmias
• Sinus Tachycardia.• Atrial fibrillation.• Atrial flutter.• Supraventricular tachycardia.• Ventricular tachycardia.
» Monomorphic» Polymorphic (Torsades de pointe)
• Ventricular fibrillation.
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Always Evaluate QRS rhythm.BEST SEEN IN PRECORDIAL LEADS.=0.09second duration= 10mm height.Q wave present only in left sided leads (V4-6).R and S waves.
R in V1-2 < S in V1-2.S in V1-2 < 20 mm.R in V5-6 < 25mm.S in V5-6 < 5mm.
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<0.09 Second – Narrow complex tachycardia.>0.09 Second – Wide complex tachycardia.
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SINUS TACHYCARDIARate: Greater than normal for age.P wave: sinusQRS: normal(<0.09 second)Conduction: normalRhythm: regular or slightly irregular The clinical significance of this
dysrhythmia depends on the underlying cause. It may be normal.
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Underlying causes include: increased circulating catecholamines hypoxia .increased temperature stress response to pain.
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ATRIAL FIBRILLATIONRate: atrial rate usually between >400/bpm.P wave: not present; wavy baseline is seen instead. QRS: normalConduction: variable AV conduction; if untreated
the ventricular response is usually rapid. Rhythm: irregularly irregular. (This is the
hallmark of this dysrhythmia).
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Atrial Flutter
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Atrial Flutter
• Atrial activity of 250-400/bpm with sawtooth pattern. Usually a 2:1 conduction pattern; if it is 3:1 or higher, there is AV node damage
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Rate control© Beta-blockers
© Continuation after CABG may prevent a-fib© Good for hyperthyroid or post-MI patients with a-fib© Carvedilol decreases mortality in patients with CHF© Esmolol is good for acute management
© Digoxin actually increases vagal tone, thus indirectly slowing AV node conduction. But it is used essentially only in patients with LV dysfunction because it’s inotropic.
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Rate control© Calcium Channel Blockers
© Nondihydropyridines (verapamil or dilitiazem) block AV node conduction but also have negative inotropy, so don’t use in CHF.
© Dihydropyridines (nifedipine, amlodipine, felodipine) have no effect on AV node conduction
© Adenosine is too short acting to be of any use in a-fib
© Last choice is AV node ablation and permanent pacing
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Rhythm control© Rhythm control does not decrease
thromboembolic risk and may be proarrhythmic
© Class 1A (quinidine, procainamide, disopyramide) slows conduction through HIS can cause torsades de pointes during conversion. They also enhance AV node conduction, so they should be used only after rate is controlled
© Class 1C (propafenone, and flecainide) slow conduction through HIS are good first choice.
• Amiodarone is good if patient is post-MI or has systolic dysfunction.
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Cardioversion for A-Fib
• If symptomatic.• Patients with a-fib for more than 2 days
should be receive 3 weeks of anticoagulation before electrical cardioversion.
• Give coumadin for 4 weeks after cardioversion
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Anticoagulation Rules for Atrial-Fibrillation
© Everybody who has rheumatic heart disease should be anticoagulated
© If <65 yo and with h/o DM, HTN, CHF, CVA, prosthetic valves, thyrotoxicosis, LV dysfunction or LA enlargement, then give coumadin
© If no risk factors, do nothing. © 65-75 yo with any of above risk factors, give
coumadin; if no additional risk factors, give coumadin or aspirin
© >75 yo give coumadin but keep INR 2-2.5 due to increased risk of bleed
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The most common cause of this rhythm in healthy individuals is sinus bradycardia.
It may also be seen in the presence of a high degree or complete AV block. If the ventricular rate is slow, hemodynamic compromise may occur.
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Supraventricular TachycardiaHeart Rate - >220/min in infants >180/min in
children.P waves – absent/ abnormal.QRS Complex- Narrow (<0.09 second). Wide if
abberant pathway present.
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ST v/s SVTSinus Tachycardia. Supraventricular
Tachycardia.
Gradual Onset. Abrupt Onset.
Signs of underlying ST (eg. Fever, pain, anemia)
May be signs of CHF.
Heart Rate - <220/min in infants <180/min in children.
Heart Rate - >220/min in infants >180/min in children.
P wave-Normal P wave-Absent/Abnormal.
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PVC BigeminyRate: variableP wave: usually obscured by the QRS, PST or T
wave of the PVCQRS: (wide > 0.09 seconds); morphology is
bizarre with the ST segment and the T wave opposite in polarity. May be multifocal and exhibit different morphologies.
Conduction: the impulse originates below the branching portion of the Bundle of His; full compensatory pause is characteristic.
Rhythm: irregular. PVC's may occur in singles, couplets or triplets; or in bigeminy, trigeminy or quadrigeminy.
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PVC Bigeminy
PVCs can occur in healthy hearts. For example, an increase in circulating catecholamines can cause PVCs. They also occur in diseased hearts and from drug (such as digitalis) toxicities.
Treatment is required if they are:associated with an acute MI, occur as couplets, bigeminy or trigeminy, are multifocal, or are frequent (>6/min).
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Ventricular Tachycardia.Rate: usually between 100 to 220/bpm, but can
be as rapid as 250/bpm P wave: obscured if present and are unrelated
to the QRS complexes. QRS: wide(>0.09 second) and bizarre
morphologyConduction: as with PVCsRhythm: three or more PVCs in a row; may be
regular or irregular.
Ventricular tachycardia almost always occurs in diseased hearts.
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Ventricular Tachycardia.Some common causes are:
CAD acute MI digitalis toxicity CHF ventricular aneurysms.
Patients are often symptomatic with this dysrhythmia.
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TORSADE DE POINTESRate: usually between 150 to 220/bpm, P wave: obscured if presentQRS: wide (>0.09 second) and bizarre
morphologyConduction: as with PVCsRhythm: Irregular
Paroxysmal –starting and stopping suddenly
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Hallmark of this rhythm is the upward and downward deflection of the QRS complexes around the baseline. The term Torsade de Pointes means "twisting about the points.“
Caused by drugs which lengthen the QT interval.
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QTcLead II and Lead V5 QTc = QT interval/ RR.
Normal QTc Males = 0.45seconds. Females = 0.46seconds.
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Prolonged QT interval.Drugs-
Antibiotics- Erythromycin, Azithromycin, Cotrimoxazole.Antifungals- Ketoconazole, Itraconazole.Antidepressants-Tricyclic compounds(Imipramine)Antiarrhythmics- Class 1a and 3.Cisapride, Glibenclamide, Furosemide.Organophosphates.Hypocalemia, Hypocalcaemia, Hypomagnesemia
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VENTRICULAR FIBRILLATIONRate: unattainableP wave: may be present, but obscured by
ventricular wavesQRS: not apparentConduction: chaotic electrical activityRhythm: chaotic electrical activity
This dysrhythmia results in the absence of cardiac output. Almost always occurs with serious heart disease, especially acute MI.
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IDIOVENTRICULAR RHYTHMRate: 20 to 40 beats per minuteP wave: AbsentQRS: Wide (>0.09second)Conduction: Failure of primary pacemakerRhythm: Regular
Also called " dying heart" rhythmPacemaker will most likely be needed to re-establish a normal heart rate.
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Causes: Myocardial Infarction Pacemaker Failure Metabolic imbalance Myoardial Ischemia
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Management.
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If hemodynamically unstable..Immediately Cardiovert.
Initial dose – 0.5 J/kg.Subsequent dose – 2.0 J/kg.
If FAILURE, then start CPR.
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Hemodyanamically Stable..Check for Rhythm.
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Narrow Complex.Sinus Tachycardia – Treat underlying cause.SVT-Vagal Maneouvres.Medication-
Inj. Adenosine 0.1mg/kg (Max. 6mg) rapid iv bolus. 2nd dose 0.2mg/kg (Max. 12mg) both preferably in central vein by Rapid Flush technique.
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Wide Complex.Treat underlying cause.Medication-
Inj Amiodarone- LD 5mg/kg (max 300mg) over 20-60 min upto a maximum of 15mg/kg/day. Rapid dose associated with hypotension and bradycardia.
Inj. Procainamide- LD 15mg/kg over 30-60 minutes. Similar precautions. Prolongs QT interval like Amiodarone.
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Lidocaine- LD 1mg/kg followed by infusion of 20-50 mcg/kg/minute.Magnesium Sulphate- 25-50mg/kg iv over 10-15minutes.(For TORSADE DE POINTES)
>1year* age- Inj. Verapamil 0.1mg/kg over atleast 2minutes.
*<1 year age-Refractory Hypotension and cardiac arrest
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WPWDelta waves(Pre-excitation complex) in QRS complex.
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Brugada SyndromeST Segment elevation “Saddle type” RBBB type
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References-PALS guidelines.Nelson’s Textbook of Pediatrics.Nada’s Pediatric Cardiology.Recent Advances in Pediatrics, S. Dutta.Essentials of medical Pharmacology.
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THANK YOU.
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Classification of Anti-arrhythmicsClass Action Examples Side Effects1A Fast sodium channel blocker varies
depolarization and action potentialduration
Quinidine,procainamide,disopyramide
Class: nausea, vomitingQuinidine: hemolyticanemia, thrombocytopenia,tinnitusProcainamide: lupus
1B Lidocaine,Mexiletine
Lidocaine: dizziness,confusion, seizures, comaMexiletine: tremor, ataxia,rash
1C Flecainide,Propafenone
Flecainide: pro-arrhythmia,nausea, dizzyness
2 beta-blockers SA node & AV nodeconduction
Propranolol,metoprolol
Class: CHF, bronchospasm,bradycardia, hypotension
3 Prolong action potential by blockingK+ channels
Amiodarone,sotalol
Amiodarone: hepatitis,pulmonary fibrosis, thyroiddisorders, peripheralneuropathySotalol: bronchospasm
4 calcium channel blockers AV nodeconduction
Verapamil,dilitiazem
Class: AV block,hypotension, bradycardia,constipation
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ECG AxisNormal Axis in pediatrics – 0o to 110o
Use Lead I & II and AVF
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Quadrant Method.LEAD I LEAD AVF Quadrant Axis
Positive Positive Left Lower Normal (0 to +90 degree)
Positive Negative Left upper Possible LAD (0 to –90 degree)
Negative Positive Right lower RAD (+90 to 180 degree)
Negative Negative Right upper Extreme Axis deviation (-90 to 180 degree)
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Quadrant Method.LEAD I LEAD AVF Quadrant Axis
Positive Positive Left Lower Normal (0 to +90 degree)
Positive Negative Left upper Lead II-Positive-Normal(0 to -30 degree).Negative- LAD (-30 to –90 degree)
Negative Positive Right lower RAD (+90 to 180 degree)
Negative Negative Right upper Extreme Axis deviation (-90 to 180 degree)
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References-PALS guidelines.Nelson’s Textbook of Pediatrics.Nada’s Pediatric Cardiology.Recent Advances in Pediatrics, S. Dutta.Essentials of medical Pharmacology.
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