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110 Cards in this Set

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describe X and Y axis of ECG
- X-axis: time
* Small box = 1 mm width = 0.04 seconds
* Large box = 5 mm width = 0.2 seconds
- Y-axis: electrical cardiac voltage
* Small box = 1 mm height = 0.1 mV
* Large box = 5 mm height = 0.5 mV
how do you calculate ventricular rate?
1500/small squares in RR interval
300/large squares in RR interval
how does ventricular size change with age
birth: RV > LV
1 mo: RV = LV
6 mo: LV:RV = 2:1
adult: LV:RV = 2.5:1
what is the juvenile T wave variant?
inverted T waves in right to middle chest leads in first decade of life
ecg of neonate, findings?
tall right precordial R waves
Right axis deviation
normal in a neonate with physiologic predominance of RV during fetal development
where is the SA node located?
junction of SVC and right atrium in area of sulcus terminalis
what does the p wave reflect?
phase 0, leading edge of atrial muscle depolarisation, complete when enters phase 2 plateau
can atrial repolarisation be seen on ecg?
yes, as Ta wave, usually obscured by QRS, but can be seen e.g. in heart block (downward deflection immediately after p wave)
describe the location of the AV node
The AV node lies within the triangle of Koch. The apex of this triangle lies at the membranous septum, with its long sides marked by the tendon of Todaro and the rim of the tricuspid valve; its base is at the coronary sinus
how can AV node conduction be evaluated on ECG?
PR interval = rough estimate, but also includes atrial conduction and His-Purkinje conduction
describe the process of ventricular depolarisation
excitation wavefront goes from AV node --> His-Purkinje system --> left-to-right septal activation --> left and right apex --> LV and RV endocardium --> epicardium --> base of LV --> RV outflow tract
what does the ST segment show?
phase 2 plateau of ventricular cells, before repolarisation
why is T wave usually longer than QRS?
repolarisation is less homogenous than depolarisation, hence protracted duration of T wave, also follows reverse path (epicardium --> endocardium)
what does the ECG show during depolarisation?
atrial depolarisation - usually not seen but can cause Ta wave
ventricular - T wave
U wave is ventricular + His-Purkinje depolarisation (the last area to depolarise)
describe ventricular depolarisation
AV node --> His-Purkinje --> left-to-right septum --> apices --> LV and RV endocardium --> epicardium --> base of LV --> RV outflow tract
describe ventricular depolarisation with reference to ECG
can have Q wave in left leads due to L-->R septal depolarisation, then positive R in left lead (assuming normal heart with dominant LV), negative in R leads, then left base and right outflow tract depolarisation generates a superior/rightward vector, leading to negative S in left leads, positive S in right arm lead
why does the T wave usually have the same vector as the QRS complex?
because ventricular repolarisation occurs from epicardium to endocardium (unlike atrial muscle)
correlate normal ECG to events
describe limb lead placement in a normal ECG
describe paediatric praecordial lead placement
what is the usual paper speed & amplitude response of an ECG?
rate 25mm/sec
amplitude 1mV/10mm, but can be reduced to 1mV/5mm or even 1mV/2.5mm
how does the cardiac axis change with age?
P wave axis should be 0 to +90 regardless of age. QRS is rightwardly deviated in newborns (~120degrees), then shifts towards +60 by 6 months & remains between 0 and 90 thereafter
DDx of abnormal QRS axis?
ventricular hypetrophy
intraventricular conduction disturbance
DDx of abnormal T wave axis?
should not differ from QRS axis by more than 60 degrees
hypertrophy + ventricular strain
conduction disturbance
describe morphology/rate of normal P wave and PR interval
P wave should be max 0.3mV (3mm in normal ECG), and max 0.12s (3 small squares)

PR interval should be < 0.16s (4 small squares) in children, up to 0.18s in adolescents
DDx of prolonged PR interval
enhanced vagal tone
cardiac meds e.g. digoxin, antiarrhythmics
conduction disease involving AV node or His-Purkinje system
cause of short PR interval? (<0.08s)
WPW syndrome
describe normal QRS morphology in L vs R leads
L leads: small Q, large R, small S
R leads: small R, deep S
L leads = I, II, aVl, V3-V6
R leads = aVR, III, V1-V2
normal QRS duration?
< 0.08s in infants
< 0.10s in older children
DDx of prolonged QRS?
Conduction block (e.g. BBB)
Slow myocyte conduction e.g. muscle injury, drugs, electrolyte disturbance
Severe ventricular hypertrophy
Some cases of preexcitation
What is the normal amplitude of the J point?
J point marks termination of S and beginning of ST and should be <1mm within isoelectric line. Can be elevated in healthy adolescents up to 2-3mm, usually in lateral (V4-V6) & inferior (II, III, aVF) leads, accompanied by tall T waves
Dx = benign early repolarisation, but this should not be made if J point is elevated >4mm, or if T wave amplitude is low
describe T wave normal morphology over time
birth - 7 days: upright in all precordial leads
7 days - adolescence: negative over right side (V1-V2), positive on left
adulthood: upright in all leads again
what is the formula for QTc? why should it be corrected?
QT(secs)/square root RR(secs). Corrected because normal QT is longer with slow heart rates, shorter with fast heart rates.
DDx of long QT
hereditary long QT syndromes
antiarrhythmics & other drugs
electrolye imbalances
describe the U wave
not always present, reflects LV and His-Purkinje repolarisation, usually <1/4 amplitude of T wave & same polarity, if >1/2 T wave amplitude, then include this in QT
describe ECG findings of RA enlargement
Look at lead II and V1.
Lead II: peaked p wave > 0.3mV
Lead V1: biphasic p wave with deep negative early deflection
describe findings of LA enlargement
Look at lead II and V1.
II: broad, notched p wave > 0.10s
V1: biphasic p wave in V1 with deep slurred terminal portion
difference between RA enlargement and LA enlargement on ECG?
Lead II: RA enlargement shows peaked P wave > 0.3mV, LA enlargement shows broad notched P wave > 0.10s

V1: both show biphasic p wave, RA enlargement has early deep negative deflection (or tall P wave), LA enlargement shows deep slurred terminal portion of p wave
of RVH and LVH, which is easier to pick up on an ECG?
what are the components of the innate immune system?
neutrophils, monocytes, macrophages, dendritic cells, NK cells, complement proteins, cytokines
what are the components of the adaptive immune system?
T lymphocytes, B lymphocytes
how does the innate immune system detect pathogens?
toll-like receptors detect pathogen-associated molecular patterns (PAMPs)
how do dendritic cells work?
recognise pathogenic products and migraine to lymph nodes, then mature and start to express molecules including MHC to present antigen to T cells.
presentations for paediatric heart disease
- cyanosis
- murmur (innocent, organic)
- palpitations, CCF, syncope - for arrhythmias
- inherited or dysmorphic syndromes
maternal GDM is associated with?
macrosomia with macrosomic heart, can have such thick muscle that they have failure, but it usually resolves
T1DM in early pregnancy is associated with which cardiac complication in the infant?
transposition of the great arteries
what cardiac complications are associated with TORCH infections?
pulmonary stenosis, septal defects, and with rubella - pulmonary artery narrowing
what congenital cardiac condition is associated with SLE?
congenital heart block
common causes of heart failure in children?
1. left to right shunts (VSDs, ducts, AVSDs, truncus)
2. severe left heart obstructions (not right heart), e.g. critical AS, hypoplastic left heart, critical coarctation
3. complex conditions with both shunt and l-r components
less common causes of heart failure in children?
1. valvular regurg e.g. rheumatic heart disease, important in rural Australia (MR, AR)
2. myocardial disease
e.g. idiopathic cardiomyopathy, myocarditis, Kawasaki
3. high output conditions are rare, e.g. severe anaemia, thyrotoxicosis, cerebral/hepatic AVMs
4. Arrhythmias e.g. SVTs, VT secondary to abnormal tumours
SVT in utero can cause?
Ventricular Purkinje cell hamartoma can cause?
persistent VT and cardiomyopathy
PJRT: permanent junctional reciprocating tachycardia causes?
permanent SVT, failure due to inadequate filling time, presents like a cardiomyopathy
what are some ablation methods?
cryoablation, cold probe, radiofrequency
symptoms of heart failure?
- slow feeds, poor oral intake
- dyspnoea
- sweating profusely, esp with feeding, crying, due to sympathetic overdrive
- failure to thrive
- occasionally excessive weight gain
How to mease cardiothoracic ratio on CXR.
1. cardiac width: take vertical line through middle of sternal shadow, take perpendicular lengths to cardiac edges
2. chest width is from inner margin of ribs above diaphragm
3. cardiac width > 50% of chest width = cardiomeguly
- Should be taken in mid-inspiration
- N.B. Infants can have horizontal lying hearts, confounding findings, & thymus can obscure heart
- Can also be affected by short AP diameter e.g. due to pectus excavatum
- therefore look @ lateral film to assess AP diameter + thymus
In what weeks of gestation is the heart most susceptible to adverse external influences e.g. rubella, teratogens
Causes of prolonged PR interval
Myocardial dysfunction e.g. myocarditis
Certain congenital heart disease (Ebsteins, ECD, ASD)
Causes of short PR
- Pre-excitation e.g. WPW syndrome
- Glycogen storage disease
Causes of variable PR
- wandering pacemaker
- Wenkebach type block
Bazett's dormula for QTc
QT / (root of the RR)
Normal QTc
Infants less than 6 months = < 0.49 seconds.
Older than 6 months = < 0.44 seconds.
Causes of long QTc
- drugs
- congenital e.g. Romano-Ward
- hypocalcaemia
- myocarditis
- head injury
Causes of short QTc
- hypercalcaemia
- digitalis
- congenital short QT syndrome
Causes of low amplitude QRS
- myocarditis
- pericarditis
- hypothyroidism
- normal in neonate
Why do right precordial T waves go from positive to negative in the first 48 hours of life?
pulmonary vascular resistance decreases, so right ventricular strain decreases
What is the significance of upright T waves in right precordial leads in childhood?
suggests RVH or strain even without RVH voltage criteria
definition of long QT?
Roughly, QTc > 44s
Use Bazett formula to work out QTc: QT/rootRR
There are better formulas..
complications of long QT?
ventricular tachycardia - torsades, leading to VF
sudden death
syncope, due to short episodes of torsades
causes of prolonged QT
1. electrolyte e.g. low C, low K, low Mg
2. familiial, can be autosomal dominant or recessive, assoc. with sensorineural hearing loss
3. macrolides e.g. erythromycin, cisapride, non-sedating antihistamines, sotalol, antipsychotics, cocaine, amphetamines, methadone,
4. anorexia
ASD with secundum - progress over time
Causes a L --> R shunt that grows bigger with time
ASD with secundum - examination findings
pink patient, normal pulses
right parasternal heave
no thrill
may have flow murmus e.g. diastolic tricuspid flow murmur, ejection systolic pulmonary flow mumur i.e. right sided murmurs because blood is going L --> R
What does a wide second heart sound indicate?
Delay on right side e.g. increased RV stroke volume, RBBB, ?pulm stenosis
What does fixed spilling of the heart sounds indicate?
Free communication between atria, compensates for different volumes in respiration
What would be the CXR findings of an ASD?
- cardiomegaly esp. RVH (see lat view)
- plethoric lung fields due to L --> R shunt
- prominent pulmonary artery at upper left heart border
what would be the ECG findings of ASD with secundum?
- RBBB (cause unknown)
- RV hypertrophy if delayed presentation
ASD with secundum - presentation
Asymptomatic initially
Later, risk of heart failure, arrhythmias
Pulmonary stenosis - clinical findings
Pulmonary stenosis - examination findings
Ejection systolic murmur
Ejection click = sound of valve opening
Soft and delayed S2 (eventually disappears and can only hear AV close)
RV impulse
Pulmonary stenosis CXR findings
Normal heart size (unless RHF is present)
Normal lungs
Prominent pulmonary artery segment - poststenotic dilatation
Pulmonary stenosis - ECG findings
RV hypertrophy in keeping with degree of stenosis
How do you calculate the pressure gradient of flow across a cardiac valve?
Peak velocity squared x 4
e.g. velocity 4m/s, flow = 64
When should pulmonary stenosis be treated?
Heart failure
RV systolic pressure > 60
Management of pulmonary stenosis
Balloon catheter dilatation, using balloon 30% bigger than valve diameter
Features of an innocent murmur
- No other signs (normal postductal sats, normal pulses, no heaves, no cyanosis)
- Short mid systolic murmur
- Louder while lying down
- Loudest in lower left sternal edge, NOT pulm/aortic areas
- Soft
- Louder on inspiration
which patients should recieve prophylaxis for endocarditis?
valve replacement
previous endocarditis
moderate sized VSD
Risks of prostaglandin E2
Apnoeas, altered breathing --> should be ventilated
describe normal splitting of S2
widens with inspiration
narrows with expiration
describe S3
rapid LV filling in early diastole
diminishes when sitting/standing
if persistent, can indicate dilated LV or L-->R shunt
"sloshing IN"
describe S4
atrial contraction into noncompliant ventricle e.g. HOCM, restrictive cardiomyopathy
occurs just before S1
"A stiff wall"
describe ejection clicks
early click at left sternal border = pulmonic valve (vary with respiration, louder on inspiration)
click at apex = aortic
mid-late ejection click at apex = MVP
incidence of innocent murmurs
what causes a wide split S2?
when it takes longer for the pulmonary valve to close, e.g. in RV volume overload (ASD, TAPVR, pulmonary regurg) or pressure overload (PS), or delayed conduction (RBBB)
what causes a narrow split S2?
when the pulmonary valve closes quickly (pulm HTN), or when there's only one semilunar valve (aortic or pulmonary atresia or truncus arteriosus)
DDx of ejection systolic murmur
truncal stenosis
DDx of pansystolic murmur
DDx of diastolic murmur
DDx of continuous murmur
aortopulmonary collaterals
runoff lesions
innocent systolic murmurs
- newborn murmur? (disappears by 2-3 wks)
- peripheral arterial pulmonary stenosis (due to normal branching of pulmonary artery, disappears by age 2)
- still murmur (between 2 and 7 yo)
- pulmonary ejection murmur (usually from age 3+)
- innominate/carotid bruit
innocent continuous murmur
venous hum (after age 2, infraclav area on right, obliterated by compressing jugular, caused by turbulence at confluence of subclavian and jugular veins)
what is pulsus paradoxus?
reduction in pulse amplitude or BP (by >10mmHg) with INSPIRATION
- sign of pericardial tamponade (reduced venous return to heart therefore reduced CO on inspiration)
causes of right axis deviation
normal in neonate
causes of left axis deviation
AVSD (LV working really hard)
pulmonary atresia, intact ventricular septum (??)
tricuspid atresia
meds that can cause QT prolongation
Class IA antiarrhythmics (procainamide), Class III (amiodarone, sotalol)
Inotropes (dobutamine, dopamine, adrenaline)
ABx (azithromycin, clarithromycin)
Antipsychotics (risperidone, lithium, haloperidol)
Sedatives (chloral hydrate, methadone)
Other: ondansetron, phenytoin, pseudoephedrine
Electrolytes: hypocalcaemia, hypokalaemia, hypomagnesaemia (MCK)
what's the normal QTc
</= 0.44s
normal cardiothoracic ratios
>50% in newborn
<50% after age 1
classic CXR finding for TGA
egg on string sign - narrow mediastinum, globular heart
classic CXR finding for tetralogy of Fallot
boot shaped heart (upturned apex, concave/straight right heart border)
classic CXR finding for unobstructed TAPVR
Snowman sign (dilated SVC, RA is body)
classic CXR findings for coarctation
"figure of 3" and rib notching (collaterals)