Cardiology

Front 1

describe X and Y axis of ECG

Back 1

- 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

Front 2

how do you calculate ventricular rate?

Back 2

1500/small squares in RR interval
300/large squares in RR interval

Front 3

how does ventricular size change with age

Back 3

birth: RV > LV
1 mo: RV = LV
6 mo: LV:RV = 2:1
adult: LV:RV = 2.5:1

Front 4

what is the juvenile T wave variant?

Back 4

inverted T waves in right to middle chest leads in first decade of life

Front 5

ecg of neonate, findings?

Back 5

tall right precordial R waves
Right axis deviation
normal in a neonate with physiologic predominance of RV during fetal development

Front 6

where is the SA node located?

Back 6

junction of SVC and right atrium in area of sulcus terminalis

Front 7

what does the p wave reflect?

Back 7

phase 0, leading edge of atrial muscle depolarisation, complete when enters phase 2 plateau

Front 8

can atrial repolarisation be seen on ecg?

Back 8

yes, as Ta wave, usually obscured by QRS, but can be seen e.g. in heart block (downward deflection immediately after p wave)

Front 9

describe the location of the AV node

Back 9

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

Front 10

how can AV node conduction be evaluated on ECG?

Back 10

PR interval = rough estimate, but also includes atrial conduction and His-Purkinje conduction

Front 11

describe the process of ventricular depolarisation

Back 11

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

Front 12

what does the ST segment show?

Back 12

phase 2 plateau of ventricular cells, before repolarisation

Front 13

why is T wave usually longer than QRS?

Back 13

repolarisation is less homogenous than depolarisation, hence protracted duration of T wave, also follows reverse path (epicardium --> endocardium)

Front 14

what does the ECG show during depolarisation?

Back 14

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)

Front 15

describe ventricular depolarisation

Back 15

AV node --> His-Purkinje --> left-to-right septum --> apices --> LV and RV endocardium --> epicardium --> base of LV --> RV outflow tract

Front 16

describe ventricular depolarisation with reference to ECG

Back 16

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

Front 17

why does the T wave usually have the same vector as the QRS complex?

Back 17

because ventricular repolarisation occurs from epicardium to endocardium (unlike atrial muscle)

Front 18

correlate normal ECG to events

Back 18

Front 19

describe limb lead placement in a normal ECG

Back 19

Front 20

describe paediatric praecordial lead placement

Back 20

Front 21

what is the usual paper speed & amplitude response of an ECG?

Back 21

rate 25mm/sec
amplitude 1mV/10mm, but can be reduced to 1mV/5mm or even 1mV/2.5mm

Front 22

how does the cardiac axis change with age?

Back 22

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

Front 23

DDx of abnormal QRS axis?

Back 23

ventricular hypetrophy
malpositions
intraventricular conduction disturbance
infarction

Front 24

DDx of abnormal T wave axis?

Back 24

should not differ from QRS axis by more than 60 degrees
hypertrophy + ventricular strain
ischaemia
myopathy
conduction disturbance

Front 25

describe morphology/rate of normal P wave and PR interval

Back 25

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

Front 26

DDx of prolonged PR interval

Back 26

enhanced vagal tone
cardiac meds e.g. digoxin, antiarrhythmics
conduction disease involving AV node or His-Purkinje system

Front 27

cause of short PR interval? (<0.08s)

Back 27

WPW syndrome

Front 28

describe normal QRS morphology in L vs R leads

Back 28

L leads: small Q, large R, small S
R leads: small R, deep S

Hint 28

L leads = I, II, aVl, V3-V6
R leads = aVR, III, V1-V2

Front 29

normal QRS duration?

Back 29

< 0.08s in infants
< 0.10s in older children

Front 30

DDx of prolonged QRS?

Back 30

Conduction block (e.g. BBB)
Slow myocyte conduction e.g. muscle injury, drugs, electrolyte disturbance
Severe ventricular hypertrophy
Some cases of preexcitation

Front 31

What is the normal amplitude of the J point?

Back 31

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

Hint 31

Dx = benign early repolarisation, but this should not be made if J point is elevated >4mm, or if T wave amplitude is low

Front 32

describe T wave normal morphology over time

Back 32

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

Front 33

what is the formula for QTc? why should it be corrected?

Back 33

QT(secs)/square root RR(secs). Corrected because normal QT is longer with slow heart rates, shorter with fast heart rates.

Front 34

DDx of long QT

Back 34

hereditary long QT syndromes
antiarrhythmics & other drugs
electrolye imbalances

Front 35

describe the U wave

Back 35

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

Front 36

describe ECG findings of RA enlargement

Back 36

Look at lead II and V1.
Lead II: peaked p wave > 0.3mV
Lead V1: biphasic p wave with deep negative early deflection

Front 37

describe findings of LA enlargement

Back 37

Look at lead II and V1.
II: broad, notched p wave > 0.10s
V1: biphasic p wave in V1 with deep slurred terminal portion

Front 38

difference between RA enlargement and LA enlargement on ECG?

Back 38

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

Front 39

of RVH and LVH, which is easier to pick up on an ECG?

Back 39

RVH

Front 40

what are the components of the innate immune system?

Back 40

neutrophils, monocytes, macrophages, dendritic cells, NK cells, complement proteins, cytokines

Front 41

what are the components of the adaptive immune system?

Back 41

T lymphocytes, B lymphocytes

Front 42

how does the innate immune system detect pathogens?

Back 42

toll-like receptors detect pathogen-associated molecular patterns (PAMPs)

Front 43

how do dendritic cells work?

Back 43

recognise pathogenic products and migraine to lymph nodes, then mature and start to express molecules including MHC to present antigen to T cells.

Front 44

presentations for paediatric heart disease

Back 44

- CCF
- cyanosis
- murmur (innocent, organic)
- palpitations, CCF, syncope - for arrhythmias
- inherited or dysmorphic syndromes

Front 45

maternal GDM is associated with?

Back 45

macrosomia with macrosomic heart, can have such thick muscle that they have failure, but it usually resolves

Front 46

T1DM in early pregnancy is associated with which cardiac complication in the infant?

Back 46

transposition of the great arteries

Front 47

what cardiac complications are associated with TORCH infections?

Back 47

pulmonary stenosis, septal defects, and with rubella - pulmonary artery narrowing

Front 48

what congenital cardiac condition is associated with SLE?

Back 48

congenital heart block

Front 49

common causes of heart failure in children?

Back 49

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

Front 50

less common causes of heart failure in children?

Back 50

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

Front 51

SVT in utero can cause?

Back 51

hydrops

Front 52

Ventricular Purkinje cell hamartoma can cause?

Back 52

persistent VT and cardiomyopathy

Front 53

PJRT: permanent junctional reciprocating tachycardia causes?

Back 53

permanent SVT, failure due to inadequate filling time, presents like a cardiomyopathy

Front 54

what are some ablation methods?

Back 54

cryoablation, cold probe, radiofrequency

Front 55

symptoms of heart failure?

Back 55

- slow feeds, poor oral intake
- dyspnoea
- sweating profusely, esp with feeding, crying, due to sympathetic overdrive
- failure to thrive
- occasionally excessive weight gain

Front 56

How to mease cardiothoracic ratio on CXR.

Back 56

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

Front 57

In what weeks of gestation is the heart most susceptible to adverse external influences e.g. rubella, teratogens

Back 57

3-5

Front 58

Causes of prolonged PR interval

Back 58

Hyperkalaemia
Myocardial dysfunction e.g. myocarditis
Certain congenital heart disease (Ebsteins, ECD, ASD)

Front 59

Causes of short PR

Back 59

- Pre-excitation e.g. WPW syndrome
- Glycogen storage disease

Front 60

Causes of variable PR

Back 60

- wandering pacemaker
- Wenkebach type block

Front 61

Bazett's dormula for QTc

Back 61

QT / (root of the RR)

Front 62

Normal QTc

Back 62

Infants less than 6 months = < 0.49 seconds.
Older than 6 months = < 0.44 seconds.

Front 63

Causes of long QTc

Back 63

- drugs
- congenital e.g. Romano-Ward
- hypocalcaemia
- myocarditis
- head injury

Front 64

Causes of short QTc

Back 64

- hypercalcaemia
- digitalis
- congenital short QT syndrome

Front 65

Causes of low amplitude QRS

Back 65

- myocarditis
- pericarditis
- hypothyroidism
- normal in neonate

Front 66

Why do right precordial T waves go from positive to negative in the first 48 hours of life?

Back 66

pulmonary vascular resistance decreases, so right ventricular strain decreases

Front 67

What is the significance of upright T waves in right precordial leads in childhood?

Back 67

suggests RVH or strain even without RVH voltage criteria

Front 68

definition of long QT?

Back 68

Roughly, QTc > 44s
Use Bazett formula to work out QTc: QT/rootRR
There are better formulas..

Front 69

complications of long QT?

Back 69

ventricular tachycardia - torsades, leading to VF
sudden death
syncope, due to short episodes of torsades

Front 70

causes of prolonged QT

Back 70

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

Front 71

ASD with secundum - progress over time

Back 71

Causes a L --> R shunt that grows bigger with time

Front 72

ASD with secundum - examination findings

Back 72

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

Front 73

What does a wide second heart sound indicate?

Back 73

Delay on right side e.g. increased RV stroke volume, RBBB, ?pulm stenosis

Front 74

What does fixed spilling of the heart sounds indicate?

Back 74

Free communication between atria, compensates for different volumes in respiration

Front 75

What would be the CXR findings of an ASD?

Back 75

- cardiomegaly esp. RVH (see lat view)
- plethoric lung fields due to L --> R shunt
- prominent pulmonary artery at upper left heart border

Front 76

what would be the ECG findings of ASD with secundum?

Back 76

- RBBB (cause unknown)
- RV hypertrophy if delayed presentation

Front 77

ASD with secundum - presentation

Back 77

Asymptomatic initially
Later, risk of heart failure, arrhythmias

Front 78

Pulmonary stenosis - clinical findings

Back 78

Hepatomegaly,
Fatigue

Front 79

Pulmonary stenosis - examination findings

Back 79

Ejection systolic murmur
Ejection click = sound of valve opening
Soft and delayed S2 (eventually disappears and can only hear AV close)
RV impulse

Front 80

Pulmonary stenosis CXR findings

Back 80

Normal heart size (unless RHF is present)
Normal lungs
Prominent pulmonary artery segment - poststenotic dilatation

Front 81

Pulmonary stenosis - ECG findings

Back 81

RV hypertrophy in keeping with degree of stenosis

Front 82

How do you calculate the pressure gradient of flow across a cardiac valve?

Back 82

Peak velocity squared x 4
e.g. velocity 4m/s, flow = 64

Front 83

When should pulmonary stenosis be treated?

Back 83

Heart failure
RV systolic pressure > 60

Front 84

Management of pulmonary stenosis

Back 84

Balloon catheter dilatation, using balloon 30% bigger than valve diameter

Front 85

Features of an innocent murmur

Back 85

- 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

Front 86

which patients should recieve prophylaxis for endocarditis?

Back 86

valve replacement
previous endocarditis
moderate sized VSD

Front 87

Risks of prostaglandin E2

Back 87

Apnoeas, altered breathing --> should be ventilated

Front 88

describe normal splitting of S2

Back 88

widens with inspiration
narrows with expiration

Front 89

describe S3

Back 89

rapid LV filling in early diastole
diminishes when sitting/standing
if persistent, can indicate dilated LV or L-->R shunt
"sloshing IN"

Front 90

describe S4

Back 90

atrial contraction into noncompliant ventricle e.g. HOCM, restrictive cardiomyopathy
occurs just before S1
"A stiff wall"

Front 91

describe ejection clicks

Back 91

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

Front 92

incidence of innocent murmurs

Back 92

40-45%

Front 93

what causes a wide split S2?

Back 93

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)

Front 94

what causes a narrow split S2?

Back 94

when the pulmonary valve closes quickly (pulm HTN), or when there's only one semilunar valve (aortic or pulmonary atresia or truncus arteriosus)

Front 95

DDx of ejection systolic murmur

Back 95

AS
PS
truncal stenosis
ASD
coarctation

Front 96

DDx of pansystolic murmur

Back 96

MR
TR
VSD

Front 97

DDx of diastolic murmur

Back 97

AR
PR
MS
TS

Front 98

DDx of continuous murmur

Back 98

PDA
AVM
aortopulmonary collaterals
runoff lesions

Front 99

innocent systolic murmurs

Back 99

- 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

Front 100

innocent continuous murmur

Back 100

venous hum (after age 2, infraclav area on right, obliterated by compressing jugular, caused by turbulence at confluence of subclavian and jugular veins)

Front 101

what is pulsus paradoxus?

Back 101

reduction in pulse amplitude or BP (by >10mmHg) with INSPIRATION
- sign of pericardial tamponade (reduced venous return to heart therefore reduced CO on inspiration)

Front 102

causes of right axis deviation

Back 102

normal in neonate
ToF
TGA
TAPVR
ASD

Front 103

causes of left axis deviation

Back 103

AVSD (LV working really hard)
pulmonary atresia, intact ventricular septum (??)
tricuspid atresia

Front 104

meds that can cause QT prolongation

Back 104

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)

Front 105

what's the normal QTc

Back 105

</= 0.44s

Front 106

normal cardiothoracic ratios

Back 106

>50% in newborn
<50% after age 1

Front 107

classic CXR finding for TGA

Back 107

egg on string sign - narrow mediastinum, globular heart

Front 108

classic CXR finding for tetralogy of Fallot

Back 108

boot shaped heart (upturned apex, concave/straight right heart border)

Front 109

classic CXR finding for unobstructed TAPVR

Back 109

Snowman sign (dilated SVC, RA is body)

Front 110

classic CXR findings for coarctation

Back 110

"figure of 3" and rib notching (collaterals)