neonatal ecg part2

Neonatal EKGDr.Vinayak Vijay Kodur

3rd year DM Neonatology ResidentL.T.Municipal Medical College,Mumbai

Atrial Hypertrophy• As the impulse begins in

RA, initial part of “p” wave is formed by RA and later by LA.

• RA= p pulmonale LA= p mitrale

• LA is posteriorly placed structure as compared to RA so p wave is biphasic in V1. LAH more negative than positive deflection in V1.

Atrial Hypertrophy• RAH

1. P wave amplitude > 2.5mm in Lead 2

2. p wave(initial part) >1.5mm in V1

3. P wave axis >60

• ASD, TAPVC, PAPVC, Tricuspid atresia, TR, Ebstein`s anomaly, PPHN, Pulmonary stenosis.

• LAH

• P wave duration >2.5mm (0.10sec) lead 2

• Lead 2 inter peak distance >o.o4sec.

• L to R shunt VSD, PDA, MR, MS.

LV and RV forces

• LV versus RV forces in hexaxial and precordial leads system.

Ventricular Hypertrophy Versus Ventricular Conduction Disturbances

• Are not always easy to distinguish; both present with increased QRS amplitudes.

• An accurate measurement of the QRS duration is essential.

RBBB Vs RVH

Volume vs Pressure overload: RVH

RVH criteria

• QR complex in V1

• An upright T wave in V1(normal in the first week of life),

• Increased R wave amplitude in V1, and increased S wave amplitude in V6 for the babies age.(according to the Davignon criteria).

• Sensitivity and specificity has not been tested in the neonate.

LVH criteria

• The performance of the ECG in recognition of left ventricular hypertrophy is poorer than generally recognised and has not been specifically tested in neonates.

• Left ventricular hypertrophy is expected to produce increased left sided voltages.

• Garson described the most helpful ECG signs in children as being T wave abnormalities in leads V5 and V6, increased R wave amplitude in V1, increased S wave amplitude in V6 (according to the Davignon criteria), and a combination of these last two variables.

LVH

• Left to right shunt lesions may result in left ventricular hypertrophy, but this may be in association with right ventricular hypertrophy and manifested as biventricular hypertrophy.

• Left ventricular hypertrophy in the newborn may be attenuated by the normal right-sided predominance of the newborn.

• The normal premature heart may not have developed the right-sided predominance, especially if <28 weeks gestation, and left ventricular predominance may be present.

LVH

Ventricular Conduction Disturbances

• Conditions that are grouped together as ventricular conduction disturbances have abnormal prolongation of the QRS duration in common. Ventricular conduction disturbances include the following:

1. BBB, right and left

2. Preexcitation (e.g., WPW-type preexcitation)

3. Intraventricular block

Ventricular Conduction Disturbances

• In BBBs (and ventricular rhythms), the prolongation is in the terminal portion of the QRS complex (i.e., “terminal slurring”).

• In preexcitation, the prolongation is in the initial portion of the QRS complex (i.e., “initial slurring”), producing “delta” waves.

• In intraventricular block, the prolongation is throughout the duration of the QRS complex.

• Normal QRS duration varies with age; it is shorter in infants than in older children or adults.

• Prolonged QRS duration >0.10 sec in adults and infants >0.08 sec.

Ventricular Conduction Disturbances

• By far the most commonly encountered form of ventricular conduction disturbance is RBBB.

• WPW preexcitation is uncommon, but it is a well-defined entity that deserves a brief description.

• LBBB is extremely rare in children, although it is common in adults with ischemic and hypertensive heart disease.

Ventricular Conduction Disturbances

• A= Normal

• B= BBB

• C= WPW

• D= Intra-ventricular block

BBB• The classical ECG in Ebstein’s anomaly of the tricuspid valve

displays a prolonged PR interval and a wide RBBB.

• Left anterior fascicular block is found atrio-ventricular canal defects and tricuspid atresia.

• In severe cardiomyopathy, interruption of the left bundle, which results from the involvement of the left ventricle and/or its conduction system, has been reported and carries a poor prognosis.

• Hereditary bundle branch block is an autosomal dominant (chromosome 19q). Affected individuals can have RBBB, left or right QRS axis deviation or AV block.

RBBB

• In RBBB, delayed conduction through the right bundle branch prolongs the time required for a depolarization of the RV.

• When the LV is completely depolarized, RV depolarization is still in progress. This produces prolongation of the QRS duration, involving the terminal portion of the QRS complex, called “terminal slurring” , and the slurring is directed to the right and anteriorly because the RV is located rightward and anteriorly in relation to the LV.

RBBB

• In a normal heart, synchronous depolarisation of the opposing electromotive forces of the RV and LV cancels out the forces to some extent, with the resulting voltages that we call normal.

• In RBBB (and other ventricular conduction disturbances), asynchronous depolarisation of the opposing electromotive forces may produce a lesser degree of cancellation of the opposing forces and thus results in greater manifest potentials for both ventricles.

• Consequently, abnormally large voltages for both RV and LV may result even in the absence of ventricular hypertrophy.

• Therefore, the diagnosis of ventricular hypertrophy in the presence of BBB (or WPW preexcitation or intraventricular block) is insecure.

RBBB

• In adults, when the QRS duration is longer than 0.12 second it is called complete RBBB, and when the QRS duration is between 0.10 and 0.12 second, it is called incomplete right bundle branch block (IRBBB).

• Normal QRS duration is shorter in infants and children.

• Therefore, dividing RBBB into complete and incomplete is generally arbitrary and is particularly meaningless in children.

Criteria for Right Bundle Branch Block

1. RAD, at least for the terminal portion of the QRS complex. (The initial QRS force is normal.)

2. The QRS duration clearly longer than the upper limit of normal for the patient’s age. When the prolongation of the QRS duration is only mild, it could be called incomplete RBBB.

3. Terminal slurring of the QRS complex that is directed to the right and usually, but not always, anteriorly:

A. Wide and slurred S waves in leads I, V5, and V6

B. Terminal, slurred R′ in aVR and the right precordial leads (V4R, V1, and V2).

4. ST-segment shift and T-wave inversion are common in adults but not in infants

Right Bundle Branch Block

RBBB

• Two paediatric conditions commonly associated with RBBB are ASD and conduction disturbances after open heart surgery involving right ventriculotomy.

• Ebstein’s anomaly, coarctation of the aorta in infants younger than 6 months of age, endocardial cushion defect, and partial anomalous pulmonary venous return; it is also occasionally seen in normal children. Rarely, RBBB is seen in myocardial diseases (cardiomyopathy, myocarditis).

• The significance of RBBB in children is different from that in adults. In several paediatric examples of RBBB, the right bundle is intact. In ASD, the prolonged QRS duration is the result of a longer pathway through a dilated RV rather than an actual block in the right bundle.

RBBB

• Right ventriculotomy for repair of VSD or tetralogy of Fallot disrupts the RV subendocardial Purkinje network and causes prolongation of the QRS duration without necessarily injuring the main right bundle, although the latter may occasionally be disrupted.

RBBB

• Although the RSR′ (or rSr′ ) pattern in V1 is unusual in adults, this pattern is a normal finding in infants, toddlers, and children.

• From vectorcardiographic points of view, in order for a newborn ECG pattern to change to the adult pattern, it has to go through a stage in which rSr′ or RsR′ pattern appears. It is almost impossible for a newborn ECG to change to an adult pattern without going through the rSr′ (or rsR′ ) stage. 1. An rsR′ pattern in V1 is normal if it is associated with

normal QRS duration and normal QRS voltage.

RBBB

2. If the rSr′ pattern is associated with only slightly prolonged QRS duration (not to satisfy the criterion of RBBB), it is then incomplete RBBB. The QRS voltage may be slightly increased in some cases for the same reason as discussed under RBBB.

3. If the rsR′ pattern is associated with slightly prolonged QRS duration and an abnormal QRS voltage, it is still IRBBB, not ventricular hypertrophy.

4. RVH is justified only if an abnormal QRS voltage is present in the presence of normal QRS duration.

LBBB

• LBBB is extremely rare in children.

• In LBBB, the duration of the QRS is prolonged for age, and the slurred terminal portion of the QRS is directed leftward and posteriorly.

• A Q wave is absent in V6. A prominent QS pattern is seen in V1, and a tall R wave is seen in V6.

• Associated with cardiac disease or surgery in the LV outflow tract, septal myomectomy, and replacement of the aortic valve.

• Rarely associated with LBBB include LVH, myocarditis, cardiomyopathy, MI, aortic valve endocarditis, and premature ventricular contractions (or ventricluar tachycardia [VT]) originating in the RV outflow tract.

LBBB

Intraventricular Block

• In, the prolongation is throughout the duration of the QRS complex.

• This usually suggests serious conditions such as metabolic disorders (e.g., hyperkalemia), diffuse myocardial diseases (e.g., myocardial fibrosis, systemic diseases with myocardial involvement), severe hypoxia, myocardial ischemia, or drug toxicity (quinidine or procainamide).

Wolf–Parkinson–White syndrome• Normally impulse

generated in SA node can only pass down to ventricles is via the conduction system as atria and ventricles are separated electrochemically by the fibrous tissue in between them.

• If there is some pathway of conduction intact then can result in WPW syndrome.

Wolf–Parkinson–White syndrome

• The anatomical substrate of preexcitation in Wolff–Parkinson–White (WPW) syndrome is a direct muscular connection between the atria and ventricles.

• Since accessory pathways rarely show decremental conduction, the electrical impulse is conducted prematurely to the ventricles resulting in a short PR interval.

• Conduction through the atrioventricular node and the accessory pathway results in collision of two electrical wavefronts at the ventricular level causing a delta wave and a fusion QRS complex with prolonged duration.

Wolf–Parkinson–White syndrome• Intermittent pre excitation is not uncommon in newborns and

infants.

• High prevalence of WPW syndrome is seen in newborns when two of the four following characteristics are noted:

1. PR interval <0.10s, 2. QRS complex duration >0.08s, 3. lack of a Q wave in V6 4. left axis deviation

Wolf–Parkinson–White syndrome

Wolf–Parkinson–White syndrome

• Depending on the location of the accessory pathway as well as the conduction properties of the atrioventricular node, even continuous preexcitation may be subtle and only detected in the mid-precordial leads.

• A common cause of a short PR interval in a normal heart is a low right atrial pacemaker. The P wave is negative in lead aVF and positive or isoelectric in lead I. The intraatrial conduction time from the high to low right atrium is eliminated and therefore the PR interval may be up to 40 ms less than normal.

• Ebstein`s anomaly, l-TGA, hypertrophic cardiomyopathy and cardiac tumours - increased prevalence.

Wolf–Parkinson–White syndrome

Complete (third degree) atrioventricular block

• Complete AV block implies complete absence of conduction from atrium to ventricle.

• ECG shows normal atrial activation and slower dissociated regular QRS complexes.

• 1: 15 000 to 20 000 live births

• maternal connective tissue disease anti Ro/SSA and La-SSB antibodies.

• However, only 2 to 5% of women with known antibodies will have a first child with AV block.

Complete (third degree) atrioventricular block

• Acquired complete AV block is rare in neonates. It is mainly infective (viral myocarditis, HIV infection) or may be related to tumours.

• Recurrence rate in SLE / Sjogren`s syndrome is 18%.

• Mortality rate in patients with neonatal AV block is still high, especially during the first 3 months of life.

• In spite of different treatment modes including the use of high doses of betablockers and pacing, there is still significant mortality.

Complete (third degree) atrioventricular block

First and second degree atrioventricular block

• Heart block associated with prolonged QT interval has been described in neonates and infants receiving cisapride.

• Second degree AV block due to QT interval prolongation has been also reported with the use of other agents such as doxapram in premature infants.

• Neonates may present with first or second degree AV block and rare reports exist demonstrating progression to complete AV block after birth in children with and without antibody mediated conduction disorders.

First and second degree atrioventricular block

• First degree: Prolonged PR interval but each p wave is followed by a QRS complex.

• Second degree

• Mobitz Type 1: Wenckebach periodicity, is almost always a disease of the AV node.

• With each p is followed by a QRS with progressively increasing PR interval until a beat is dropped, After the dropped QRS complex, the PR interval resets and the cycle repeats.

First and second degree atrioventricular block

• Is almost always a disease of the distal conduction system (His-Purkinje System).

• Mobitz II heart block is characterized on a surface ECG by intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening.

• There is usually a fixed number of non-conducted P waves for every successfully conducted QRS complex, and this ratio is often specified in describing Mobitz II blocks.

• For example, Mobitz II block in which there are two P waves for every one QRS complex may be referred to as "2:1 Mobitz II block"

2nd Degree Heart Block Mobitz type 1

P wave not followed by QRS

P wave followed by QRS with increasing PR interval

2nd degree block Mobitz type 2

Long QT syndrome

Long QT syndrome

• Prevalence 1:3000–5000

• Characterized by the occurrence of syncopal episodes due to torsades de points ventricular tachycardia (VT) and by a high risk for sudden cardiac death among untreated patients.

• 12% - sudden death is the first manifestation (4% infancy)

• Mutations of genes encoding ionic (potassium or sodium) channels involved in the control of ventricular repolarization.

• Approximately 30% of cases are due to ‘de novo’ mutations.

Long QT syndrome

• Several members of the same family are gene-carriers. Disease has low penetrance (gene-carriers may not show the clinical phenotype and may have a normal QT interval.)

• Therefore a normal QT in the parents does not rule out familial LQTS.

• Beta-blockers are the first choice therapy in LQTS and are effective in preventing recurrences in 80% of already symptomatic patients.

Long QT syndrome

Wondering Pacemaker

Sinus Arrhythmias

Premature atrial beats.

• Premature atrial beats usually have a different morphology and mean vector from sinus P waves.

• In regular sinus rhythm at a normal rate, a P wave that occurs before the next expected P wave is a premature atrial beat.

• A premature atrial beat may be conducted to the ventricles normally, or with ventricular aberration or not conducted or ‘blocked’.

• In infants, since the refractory periods of the bundle branches are similar, premature atrial beats may be conducted with either RBBB or left bundle branch.

Premature atrial beats.

• Blocked premature atrial beats occur in a bigeminal sequence, so-called ‘blocked atrial bigeminy’.

• This rhythm simulates sinus bradycardia; it is important to examine the T waves carefully for blocked P waves.

• The distinction is important since blocked atrial bigeminy is most often benign while severe sinus bradycardia may accompany systemic illness.

Premature atrial beats.

Tachyarrthymias

Supraventricular tachycardia.

• A rapid regular tachyarrhythmia, which results from an abnormal mechanism originating proximal to the bifurcation of the bundle of His and does not have the morphology of atrial flutter.

• The usual infant with SVT has an extremely regular R-R interval after the first 10–20 beats, most often at rates greater than 230 beats/min and usually 260–300 / min.

• In 60% of cases, the P waves are visible, but the P waves almost always have a different morphology from sinus.

• In over 90% of infants and children with SVT, the QRS complex is narrow.

SVT paper speed of 25mm/sec• Rapid narrow complex tachycardia at around 300 bpm.

SVT paper speed of 50mm/sec• Same patient. There are no visible P waves this is an AVNRT.

SVT reverted back to normal• Same patient, after reverting SVT back to sinus rhythm.

Supraventricular tachycardia.

• It is important to document SVT with a 12-lead ECG before attempting conversion of the rhythm unless the infant is critically ill.

• After sinus rhythm is achieved, the WPW pattern should be sought on a 12-lead ECG.

• An echocardiogram is indicated to determine ventricular function or the presence of congenital heart disease.

• Adenosine (0.1mg/kg) can be both diagnostic and therapeutic in SVT.

SVT- Adenosine

• Half life: <1.5 seconds: transient AV nodal block as well as sinus node block, negative chronotrope, ionotope.

• Side effects: flushing, nausea, dyspnea, bronchospasm are short lived.

• Give 0.1/kg rapidly into a large vein. Repeat after 2 minutes with 0.25mg/kg.

• Maximum total dose 12mg.

Supraventricular tachycardia.

Atrial Flutter

• Characterized by a rapid,regular form of atrial depolarization: the ‘flutter wave’.

• The picket fence morphology is similar to adults. However, the flutter wave durations are generally 0·09 to 0·18 s with atrial rates in infants between 300–500 beats/min.

• There is variable AV conduction from 1:1 to 4:1 yielding an irregular ventricular rate.

• The QRS complex is usually the same as in sinus rhythm although there may be occasional aberrancy.

Atrial Flutter

• Flutter waves, sawtooth p waves in lead 2, 3 avF (inferior leads)

• In neonate classic flutter waves might be absent.

• Positive and more discrete p waves in lead V1.

• Atrial rates of 300-600 with various degrees of aberrancy (BBB) and physiological AV block.

• After conversion to sinus rhythm, recurrence of flutter is rare in neonates with structurally normal heart.

Other Tachyarrhythmias

• Other types of supraventricular arrhythmias such as atrial fibrillation or multifocal tachycardia are extremely rare in the neonate.

Premature ventricular beats• A premature abnormal QRS (not similar to the sinus QRS complex) that

is not preceded by a premature P wave.

• In infants, the QRS duration may be normal or slightly prolonged but if the complex has a different morphology from the sinus, and is not preceded by a premature P wave, the diagnosis is a premature ventricular beat.

• The relationship between morphology and the site of origin is not exact enough to be able to predict which ventricle is causing the arrhythmia.

• The QT interval should be measured carefully.

• 24-h Holter monitoring may be worthwhile.

Premature ventricular beats

Ventricular tachycardia

• It is a series of three or more repetitive complexes that originate from the ventricles.

• The complexes are therefore different from the patient’s normal QRS; usually, the QRS duration is prolonged for the age of the patient (0·09 s or more in infants).

• ‘wide QRS’ tachycardia, the rate of VT 200–500 bpm.

• There may be a slight variation in the R-R interval over several beats. There may be sinus P waves continuing unrelated to VT (AV dissociation), retrograde P waves or no visible P waves.

Ventricular tachycardia

Potassium

• Potassium levels and changes in ECG:

Hyperkalemia• Serum potassium > 5.5 mEq/L is associated with repolarization

abnormalities:

• Peaked T waves (usually the earliest sign of hyperkalaemia)

• Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:

• P wave widens and flattens

• PR segment lengthens

• P waves eventually disappear

Hyperkalemia• Serum potassium > 7.0  mEq/L is associated with conduction

abnormalities and bradycardia:

• Prolonged QRS interval with bizarre QRS morphology

• High-grade AV block with slow junctional and ventricular escape rhythms

• Any kind of conduction block (bundle branch blocks, fascicular blocks)

• Sinus bradycardia or slow AF

• Development of a sine wave appearance (a pre-terminal rhythm)

Hyperkalemia• Serum potassium level of > 9.0 mEq/L causes cardiac

arrest due to:

• Asystole

• Ventricular fibrillation

• Pulseless Electrical Activity with bizarre, wide complex rhythm.

Hypokalemia• Hypokalaemia is defined as a potassium level < 3.5 mmol/L

• Moderate hypokalaemia is a serum level of < 3.0 mmol/L

• Severe hypokalaemia is defined as a level < 2.5 mmol/L

• Changes appear when K+ falls below about 2.7 mmol/l

Hypokalemia• Increased amplitude and width of the P wave

• Prolongation of the PR interval

• T wave flattening and inversion

• ST depression

• Prominent U waves (best seen in the precordial leads)

• Apparent long QT interval due to fusion of the T and U waves (= long QU interval)

Hypokalemia• On worsening of Hypokalemia.

• Frequent supraventricular and ventricular ectopics

• Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia

• Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes

Calcium• Calcium disorders and changes in ECG:

Hypercalcemia• The main ECG abnormality seen with hypercalcaemia

is shortening of the QT interval

• In severe hypercalcaemia, Osborn waves (J waves) may be seen

• Ventricular irritability and VF arrest has been reported with extreme hypercalcaemia

Hypocalcemia• Hypocalcaemia causes QTc prolongation primarily by

prolonging the ST segment.

• The T wave is typically left unchanged.

• Dysrhythmias are uncommon, although atrial fibrillation has been reported.

• Torsades de pointes may occur, but is much less common than with hypokalaemia or hypomagnesaemia.

Thank You