ECG Flashcards
Adult & Pediatric ECG
Heart rate > 100 . q Apparent right ventricular strain pattern:
Ø T wave inversions in V1-V3 ( juvenile T-wave pattern).
Ø Right axis deviation.
Ø Dominant R wave in V1.
Ø RSR’ pattern in V1. q Short PR intervals (<120 ms) and QRS duration (<80ms). q Slightly peaked P waves (< 3 mm in height is normal in first 6 months). q Slightly prolonged QTc (< 490 ms in first 6 months). q Q waves in inferior and left precordial leads (II, III, aVF, V5 and V6 ). q Marked Sinus arrhythmia.
ECG interpretation
S1 # Rhythm, Rate, Axis #s2 P wave, PR interval #s3 QRS complex #s4
QT, ST and T
Be fore you read the ECG, look for
Identification information
Calibration and paper speed
Calibration and paper speed
Standered ECG recording speed is : 25 mm/sec
Standered ECG
calibration is :
Am
10 mm/mV
Sinus
vThis requires:
1. P wave preceding each QRS complex, with a constant PR
interval. 2. Normal P wave axis (zero to +90 degrees), i.e. P wave is
upright in leads I and aVF.
Axis
The addition of Lead II can help determine
pathological LAD from normal axis/physiological
LAD.
Axis
The addition of Lead II can help determine
pathological LAD from normal axis/physiological
LAD.
P wave
v The P wave represents atrial depolarization. v The normal P wave morphology is upright in leads I, II, and aVF, but it is inverted in lead aVR. v The P wave is typically biphasic in lead V1 (positive-negative), but when the negative terminal
component of the P wave exceeds 0.04 seconds in duration (equivalent to one small box), it is
abnormal. v Normal P-wave amplitude is < 3 mm & normal P wave duration is < 0.09 seconds in children and < 0.07
seconds in infants.
Right atrial enlargement:
§ Tall, peaked waves.
Left atrial enlargement:
§ Broad M shaped.
§ Deep negative P wave in
The PR interval
The PR interval is measured from the start of the P wave to the start of the Q wave and is best seen in lead II. v It reflects the transit time through the AV node .
Usually < 200 ms in older children, < 130 ms in newborns
2nd Degree heart block Mobitz I.
v Progressive prolongation of PR interval until there is loss of AV conduction= loss of QRS . v Dx: 2nd Degree heart block Mobitz I.
AV Block management
Bradycardia (HR < 60) . Inadequate for clinical
v Mintain airway: assess breathing as needed. v Give oxygen. v Monitior ECG, BP, Pulse oxemitry. v Establish IV access.if impaired perfusion
## assess perfusion
If inadequate
v Prepare for Tr a n s c u t a n e o u s pacining. v Consider Atropine (0.5 mg IV) while waiting pacer. v Consider Epinephrine (2-10mcg/min) OR Dopamine(2- 10mcg/min) infusion while awaiting pacer or pacing is ineffective. بعدها
v Prepare for transvenous pacing. Inadequate for clinical v Treat contributaing causes. condition
v Consider expert consultaion.
Child of SLE mother
High risk for complete heart bock
R\s ratio
In V1 and V6
Long according to age = vent enlargement
Rs = v1v6 RVE
SR = v1v6 LVE
RBBB
More common in children particularly after open heart surgery. Ø Wide QRS (> 120 ms) > 3 tiny sq Ø RSR’ (rabbit ears) Ø Wide S wave in V6.
Premature Atrial Contractions (PACs)
Premature atrial contractions (PACs) are very
common in asymptomatic pediatric patients and
are benign.
Clinical presentation: Ø Feeling a “skipped beat” or “pause,” often followed by a strong beat. v Management: Ø No additional evaluation is necessary. Ø Inciting events should be avoided. Ø Refer if associated with dizziness, syncope, chest pain, or shortness of breath.
Premature Ventricular Contractions (PVCs)
Clinical presentation
Management
v Ectopic beats originating from the ventricle. v May occur in as many as 25% of healthy children. v Can be a presenting sign of myocarditis OR
cardiomyopathy. v Occurs more frequently in patients with structural heart
disease.
v Clinical presentation:
o Premature, wide QRS, no P waves. o May be normal if uniform and
decrease with exercise.
Ø Usually asymptomatic Ø Chest fullness Ø Dizziness Ø Feeling that the “heart skips” and
then resumes with a strong beat.
Management:
history of sudden death.
Ø No Tr e a t m e n t for PVCs if :
1. Single, uniform in appearance.
2. Suppressed or not aggravated by exercise.
3. No evidence of underlying heart disease or family
QT interval
The QT interval measures the depolarization and
repolarization of the ventricles. v QT prolongation is associated with development of
ventricular arrhythmias and sudden death. v It is commonly caused by various medications or can be a
manifestation of an underlying ion channelopathy.
QT interval
The QT interval is dependent on the heart rate. v A faster heart rate leads to a shorter QT interval, whereas a slower
heart rate leads to a longer QT interval. v A corrected QT interval (QTc) corrects for the variations in heart rate. v QTc is the QT interval divided by the square root of the RR interval in
seconds ( Bazett formula).
QT interval
Limits
Lower limit of the normal QTc range: 370 msec. v Upper limit of the normal QTc range:
Ø Prior to 15 years: 450 msec in boys and
460 msec in girls. Ø After 15 years: 440 msec in boys and 450
msec in girls.
v However, a definitely prolonged QTc interval is
considered beyond 480 msec. A QTc interval
that is within the upper normal limit and 480
msec is generally considered borderline. v A useful rule of thumb: Normal QT is less than
half the preceding RR interval. v A normal QTc interval does not exclude the
presence of a long QT syndrome. Up to 40% of
people with the genetic mutation have a QTc
interval within the normal limits.
Long QT Syndrome (LQTS) Schwartz score
EKG 1 QTc 2 ≥480 ms 3 =460-479 ms 2 =450-459 ms (in males) 1 ≥480 ms during 4th minute of recovery from exercise stress test 1 Torsade de pointes 2 T wave alternans 1 Notched T wave in 3 leads 1 Low heart rate for age 0.5 Clinical history Syncope W/stress 2 W/o stress 1 Family history Family member(s) w/definite LQTS 1 Unexplained sudden cardiac death at age <30 yrs in immediate family 0.5 Cngenital deafness 0.5 Total score @@@@
v Score <1, low probability of LQTS. v 2-3, intermediate probability of LQTS. v ≥4, high probability of LQTS. v The same family member cannot be
counted in both family history categories.
Long QT Syndrome (LQTS) presentation
v Family history of unexplained sudden death. v Congenital deafness in the family:
Ø Hereditary LQTS (Jervell and Lange – Nielsen syndrome). v Fainting spells while swimming, startling, or exercising. v Syncope, seizures, palpitations, cardiac arrest. v As many as 10% have episodes of sudden cardiac arrest.
Atrial Flutter
Atrial rates of 300-400 beats/min with variable conduction so that
the ventricular rate is slower then the atrial rate. v Clinical presentation:
Ø Infants may present with congestive heart failure. Ø Older children may have palpitations, dizziness, syncope,
chest pain, and shortness of breath. Ø Prolonged atrial fibrillation or flutter (usually > 24 h) can result
in clot development within the left atrium.
Diagnosis:
Ø EKG : Atrial flutter most
commonly conducts to the ventricles in a 2:1 fashion with a ventricular rate of 150-200 beats/min.
Ø Classic inverted “saw-tooth”
deflections that are best seen in leads II, III, aVF.
Urgent cardiac evaluation and treatment.
Ø Synchronized electrical cardioversion performed if no
thrombus. Ø Chronic atrial flutters > 2 wks, or if thrombi identified
ü Diltiazem, or beta-blocker can be used and anticoagulants
(2-4 wks) before direct cardioversion.
Ø Radiofrequency catheter ablation may cure most common
types of atrial flutter.
SVT cp
School-aged children Ø Palpitation, heart pounding,
“beeping in my chest”. Ø Chest pain or fulness,
shortness of breath. Ø Heart rate; 180 – 240 beats /
min.
Infants School-aged children Ø Palpitation, heart pounding, Ø Heart rates of 220 – 270 beats / min. Ø Poor feeding, pallor, irritability and lethargy if prolonged. Ø Congestive heart failure with hemodynamic decompensation.
SVT
Superaventricular Tachycardia (SVT)
v SVT is defined as a rapid tachycardia originating above the
bundle of His. v Pathogenesis :
Ø Reentrant tachycardia using an accessory pathway
(AP). Ø Reentrant atrioventricular nodal tachycardia (AVNRT),
typically seen in adolescents. Ø Ectopic atrial focus.
SVT)
v Management:
Stable:
Ø Vagal maneuvers; for example, place ice bag to the face 10-20s. Ø Adenosine (Avoid verapamil in infant < 1 year because of risks of hypotension and
shock).
Ø Avoid digoxin in WPW (pre-excited baseline ECG). Ø Beta blockers (e.g., propranolol).
q Unstable: Ø D/C cardioversion.
q Pe d i at r i c cardiology referral:
Ø Electrophysiological study with ablation procedure is the definitive treatment of
choice (older children).
Wolff-Parkinson White (WPW)
v A condition in which an aberrant accessory pathway causes pre-excitation of
the ventricles. v Associated conditions:
v Presentation is an incidental finding on an ECG or a tachyarrhythmia.
Ø Cardiomyopathy. Ø Ebstein’s anomaly. Ø Corrected transposition of the great arteries.
v Radiofrequency ablation of the accessory pathway. vAntiarrhythmic drugs to slow accessory pathway conduction. vTermination of acute episodes;
üVagal maneuvers (eg, Valsalva maneuver, carotid sinus massage,
splashing cold water or ice water on the face). üAdenosine and verapamil or diltiazem are dosed on the basis of
weight.
RVH
RVH is diagnosed on ECG in the presence
of a R/S ratio of greater than 1 in lead V1 in
the absence of other causes, or if the R
wave in lead V1 is greater than 7
millimeters tall. v The strain pattern occurs when the right
ventricular wall is quite thick, and the
pressure is high, as well. v Strain causes ST segment depression and
asymmetric T wave inversions in leads V1
to V3.
VT
Ventricular tachycardia (VT) in children is defined as a tachycardia of at least three successive ventricular beats. Ø Many patients are asymptomatic. Cardiomyopathy Electrolyte imbalance Cardiac disease Prior cardiac surgery Use of drugs, caffeine and decongestants
Ventricular Tachycardia (VT) v Clinical presentation
Ventricular Tachycardia (VT)
v Clinical presentation:
Ø Many patients are asymptomatic. Ø Pallor. Ø Fatigue. Ø Chest pain. Ø palpitation. Ø Syncope.
Ventricular Tachycardia (VT) v Management:
Ø Any patient identified as having VT should be assessed
immediately for hemodynamic instability.
Ø Once clinically stable, such patients require a cardiac
evaluation, including radiography, echocardiography, exercise
stress testing, and 24-h Holter monitoring.
Ventricular Fibrilation (Vfib)
Ventricular Fibrilation (Vfib)
v Ventricular fibrillation (VF) is a rare pediatric cardiac emergency.
v The heart tremors rather than
contracts and, therefore, pulses
are not palpable.
Management:
Ø Any patient suspected of having VF requires
advanced cardiac life support intervention because
circulation ceased within seconds of onset. Ø Asynchronous cardioversion (Defibrillation).
A fib
ECG
Atrial fibrilliation (AF) is the most
common arrhythmia seen in adult
BUT it is rare in children. v AF is charachterized by an
extremely fast atrial rate (P wave
at a rate of 350-600 beat / min)
irregular irregular
ECG showing atrial
fibrillation. vNote : 1. the absence of distinct
P wave. 2. chaotic activity of atria. 3. irregular R-R intervals
with narrow QRS
complex.
Atrial fib
In patients who are hemodynamically unstable:
Ø immediate evaluation and treatment are warranted,
including emergency cardioversion, if necessary.
vIn stable patients:
Ø treatment depends on the duration of atrial fibrillation
and the presence of underlying cardiac disease or other comorbidities.
vAtrial fibrillation treatment poses three main therapeutic
dilemmas.
T wave
The precordial T-wave configuration changes over time:
Ø For the first week of life, T waves are upright throughout the precordial leads.
Ø After the first week, the T waves become inverted in V1-3 (= the “juvenile T-
wave pattern”). Ø This T-wave inversion usually remains until ~ age 8; thereafter the T waves
become upright in V1-3. Ø However, the juvenile T-wave pattern can persist into adolescence and early
adulthood (= “persistent juvenile T waves”).
Tall, peaked T waves
1. Hyperkalemia 2. LVH (volume
overload) 3. Benign early
repolarisation
Flat T waves
1. Normal newborn 2. Hypothyrodism 3. Hypokalemia 4. Digitalis 5. Pe r i c a rd i t i s 6. Myocarditis 7. Myocardial ische
Large, deeply inverted T waves
Raised intracranial pressure (intracranial Haemorrhage, traumatic brain injury)
