Download Paediatric Cardiology for General Paediatrics

Paediatric Cardiology for
General Paediatricians
Dr Talal Farha
Consultant Paediatrician
SpR Regional Teaching
Taunton 22 Jan 2008
Essentials in looking at an ECG
Rhythm (sinus….nonsinus)
Rate, Atrial and ventricular rates.
QRS axis, T axis, QRS-T angle
Intervals: PR. QRS, and QT
P wave amplitude and duration
QRS amplitude and R/S ratio
Q wave
St- Segment and T wave abnormalities
ECG tips

How do you determine Sinus rhythm?

What is T axis?

What is QRS/T angle?
Rhythm


P before every QRS
P axis (0-90). P inverted in aVR
P wave axis

The location of the P-wave axis determines the origin of
an atrial-derived rhythm:

0 to 90
degrees = a high right (normal sinus rhythm)

90 to 180
degrees = a high left

180 to 270 degrees = a low left

270 to 0
degrees = a low right
T wave

In most leads, the T wave is positive.

A negative T wave is normal in lead aVR.

Lead V1 may have a positive, negative, or biphasic T
wave. In addition

It is not uncommon to have an isolated negative T wave
in lead III, aVL, or aVF.
Inverted (or negative) T waves can be a sign of


Coronary ischemia
Left ventricular hypertrophy
T axis

Determined by the same methods as QRS

0 to + 90 is normal

T Axis out side the normal quadrant could suggest
conditions with Myocardial dysfunction.
QRS-T Angle

Formed by the QRS axis and the T axis

QRS-T angle >60 degrees is unusual but if > 90
degrees, it is abnormal.

Abnormally wide angle, with T axis outside the normal
quadrant is seen in
- severe ventricular hypertrophy with starin
- Ventricular conduction disturbances
- Myocardial dysfunction of a metabolic or ischemic nature.
Top Tip For ECG
 Read
more ECGs
Do not forget, nothing replaces good traditional
clinical examination and detailed history
Syncope

How often related to the heart?

What are the related cardiac conditions?

How do we approach it?
Definition

Syncope is a transient loss of consciousness and muscle
tone.

Near syncope:
premonitory signs and symptoms of imminent syncope
occur; dizziness with or without blackout, pallor,
diaphoresis, thready pulse and low BP
Cause

Brain function depends on Oxygen and glucose.

Circulatory, metabolic, or neuropsychiatric causes.

Adults syncope mostly cardiac.

Children’s mostly benign.
Causes of Syncope in Children

Extra cardiac causes
 Vasovagal
 Orthostatic
 Failure of systemic venous return
 Cerebrovascular occlusive disease
 Hyperventilation
 Breath holding
1- Vasovagal Syncope
Neurocardiogenic
Common Syncope

Predrome for few seconds; dizziness, light-headedness,
pallor, palpitation, nausea, hyperventilation then Loss of
consciousness and muscle tone

Falls without injury

Lasts about a minute, awake gradually
Vasovagal Syncope








Anxiety
Fright
Pain
Blood
Fasting
Hot and humid conditions
Crowded places
Prolonged motionless standing
Vasovagal Syncope
Pathophysiology

Standing posture without movement shifts blood to the
lower extremities

Decrease venous return, stroke volume, BP

Less stretching of vent muscle and mechanoreceptors
(mrcpts), decline in neural traffic form mrcpts, decreased
arterial pressure, increase sympathetic output with

Higher HR, vasoconstriction (higher diastolic pressure)
Vasovagal Syncope Patients

Decreased venous return produces large increase in
ventricular contraction force

Activation of LV mechanoreceptors (normally only
responds to stretch)

Increase neural traffic mimicking high BP condition

Paradoxical withdrawal of sympathetic activity,
vasodilatation, hypotension and bradycardia

Reduction of brain perfusion
Diagnoses

ECG, Holter, EEG, glucose tolerance test all are
normally negative in V V E

Tilt test
Management


Supine +/- feet up
Prevention
 Pseudoephedrine
 Metoprolol
 Fludrocortisone
 Disopyramide
 Scopolamine
2- Orthostatic Hypotension

What happen when we stand up?
HR, vasoconstriction
Absent or inadequate upright position response,
Hypotension without increased HR
Diagnoses

BP and HR supine and standing up.

BP drop after 5-10 minutes up still by 10-15 mmHG

Positive tilt test without autonomic signs
Management




Elastic stockings
High salt diet
Corticosteroids
Slow upright position
Micturition Syncope

Rare form of orthostatic

Rapid bladder decompression associated with
degreased total peripheral vascular resistance.
3- Failure of systemic venous return

Increased intrathoracic pressure

Decreased venous tone (drugs; nitroglycerin)

Decreased volume (bleed…)
4- Cerebrovascular occlusive disease

Mainly adult
Cardiac causes of Syncope

Structural heart disease

Arrhythmia
Why Cardiac ?





Syncope at rest
Provoked by exercise
Chest pain
Heart disease
FH of sudden death
What Cardiac

Obstructive lesions

Myocardial dysfunction

Arrhythmias
Obstructive lesions

AS, PS, HOCM, PHTX

Precipitated by exercise, no increase in cardiac output to
accommodate increased demand.
Examination, CXR, ECG, Echo
Myocardial Dysfunction

Ischemia, infarction secondary to CHD, Kawasaki’s..

Myocarditis
Arrhythmia
Arrhythmia
Lack of output
(Fast or slow heart)
SVT, VT, SSS, CHB,
Normal
heart structure
Long QT, WPW
Abnormal Heart
Structure
Ebstein's, MS, MR,
CCTGA
Post op, TOF, TGA
MVP VT
Cmpthy SVT, VT,
s brady
Long QT



Syncope, seizures, palpitation during exercise or with
emotion
ECG
Ventricular arrhythmias (Tachy) with risk of sudden
death
Long QT
Defective ion
channels
Congenital
Over 50 mutations in
4 sites
Jarvell-lange-nielson
Deafness AR
Romano-ward
no deafness AD
Sporadic no FH
no Deafness
Acquired
Drugs, illnesses,
Autoimmune
Neurological
Nutritional
Electrolytes
clinically

FH 60%

Deafness 5%

Presentation with Syncope 26%, seizure 10%, cardiac arrest 9%,
presyncope palpitation 6%

Symptoms during exercise or emotion

Normally symptoms related to ventricular arrhythmias, mostly end of
second decade of life.

Syncope in adrenergic arousal, exercise (swimming is a
particular trigger)

Abrupt noises (Alarm, doorbell, phone..)
Tests

ECG with QTc >0.46 seconds
 Frequently finding abnormal T wave
 Bradycardia (20%)

Exercise test, maximum prolongation after 2 minutes of
recovery, ventricular arrhythmia in 30% during exercise
Holter monitoring may show longer QTc

Diagnoses Criteria

Electrophysiological society
- QTc >0.44 with no other causes (0.46 sec)
- Positive family history plus unexplained syncope,
seizure or cardiac arrest proceeded by trigger such as
exercise, emotion
Treatment






Discuss with cardiologist
Avoid drugs associated with long QT
Avoid swimming, competitive sports
Beta blockers
Demand cardiac pacing (Pacemaker and defib)
Left cardiac sympathetic denervation
Prognoses

Untreated 75-80% mortality

Beta blockers reduce mortality to some extent

The adjusted annual mortality rate on treatment is 4.5%
(10 year mortality of 50%)
Advise related to CHD

If one child has CHD, what are the chances of the
second?

One parent has CHD, can offspring be affected? What
are the chances?
See Handouts, statistical list of potential risks
Pathophysiology of congenital heart lesions
Pathophysiology of left to right shunt lesions ASD
Pathophysiology of left to right shunt
lesions VSD
Pathophysiology of left to right shunt
lesions PDA
Pathophysiology of left to right shunt
lesions AVSD
Pathophysiology of Obstructive and valvular
regurgitation lesions MR
Pathophysiology of Obstructive and valvular
regurgitation lesions AR
Pathophysiology of Obstructive and valvular
regurgitation lesions PR
Pathophysiology Cyanotic lesions
TGA with good mixing
65%
LA 90%
RV 80%
LV 90%
Pathophysiology
TGA with poor mixing
30%
45%
100%
LA 92%
RV 45%
45%
LV 92%
Pathophysiology
TGA with poor mixing
30%
45%
100%
LA 92%
RV 45%
45%
LV 92%
Tips
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
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Read ECGs, easy to loose ECG skills.
Ask for help
As all specialties, it is only common sense.