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RACP CARDIO > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Typical CXR finding of: Egg on a string/Egg on it’s side?

A

TGA

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2
Q

Typical CXR finding of: Box Shaped Heart

A

Ebstein’s Anomaly - Big RA, minimal bloodflow to main pulmonary artery

  • Relative oligemia, narrow upper mediastinum
    Marked cardiomegaly
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3
Q

Typical CXR finding of: Coeur En Sabot - Upturned Apex

A

RVH - Tetralogy of Fallot

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4
Q

Typical CXR finding of: Snowman Sign

A

TAPVD - Additional opacities in upper mediastinum but no typical thymic indenations

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5
Q

Most common ASD?

A

Ostium Secundum - Fossa Ovalis defect -75%

Ostium Primum (partial AVSD 15%)

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6
Q

When would you do a fontan?

A

Single ventricle pathology - can’t fix a ventricle

I.e. HLHS, Tricuspid atresia, unbalanced VSD (i.e. with LV/RV disparate size)

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7
Q

Fontan Complications

A 
Fontan heart failure - low output
Protein losing enteropathy - stool alpha 1 antitrypsin
Thromboembolic PE or Stroke
Arrythmia incl heart block req. PPM
Hypoxia
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8
Q

Reasons for prophylaxsis for infective endocarditis for dental procedures

A

Prosthetic valve
Cogenital repair within 6/12 or residual defect
Prev I.E.
Heart Transplant

And give amoxicillin to cover S. Viridans

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9
Q

Ebsteins Anomaly?

A

Thick failure to delaminate Tricuspid leaflet - RVOT, often also ASD w R-> L shunt

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10
Q

Pulmonary stenosis - syndromic associations?

A

Noonans - Valvular
Williams - Supravalvular
Alagille - Peripheral pulm stenosis

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11
Q

Heart defect carrying greatest risk transformation to eisenmengers?

A

Biggest L->R Shunt, so PDA, then VSD, then huge ASD

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12
Q

Most common location for VSD?

A

Membranous 80% (Near Aortic valve and tricuspid valve)

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13
Q

Mechanism for LV failure in VSD?

A

L->R shunt occurs in SYSTOLE, so LV “sees” the work, transmission of flow and pressure, then dilation on return to LA

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14
Q

Mechanism for RV failure in ASD?

A

L->R Shunt in diastole, big R Atrium then big R ventricle

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15
Q

Complications from PDA in older?

A

L->R Shunt and eisenmengers

Endocarditis

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16
Q

Calculate Qp:Qs?

A

(Systemic O2 difference)//(Pulmonary O2 Difference)

No shunt = 1
>2 significant L->R
Less than 1 R->L

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17
Q

“Step up” in O2 content intracardiac - what % is significant to suggest shunt?

A

7%

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18
Q

Calculate Pulmonary Vascular Resistance?

A

(MEAN Pulmonary Artery mmHg - MEAN Left Atrium mmHg) /Qp
In absence of shunt Qp is cardiac output

Normal is <3.5 woods units . M 2
Severe is >8 um2

Also test in 100% O2 and with +/- 20=80ppm iNO

RV Pressure should be 1/3rd LV Pressure
Mean PA pressure should be <20
PVR is 1/6 of SVR

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19
Q

Fick’s Method of cardiac output estimation?

A

VO2/difference in oxygen content of arterial vs. venous = CO

VO2 is estimated using LaFarge tables - baseline oxygen consumption is ~ 125ml/min/m2 and at 100% and 75% content of blood difference is about 50 ml/litre =

Adults are ~ 2m2 so cardiac output is 250/50 = 5L/min

Note Hb 150g/L x 1.34 ml o2/g of Hb = 200 ml/L of O2 at 100%, or 100ml/L at 50% , or 150ml/L at 75%

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20
Q

Clinical findings in Atrial Septal Defect

A

Females 3:1
Ostium Secundum

Subtle failure to thrive
Excercise intolerance in older child
Chance discovery of murmur - systolic ejection systolic (Left middle/upper sternal) border from increased RVOT blood flow, mid diastolic flow rumble from across TV (lower left sternal border), Fixed, widely split second heart sound (RV always volume loaded)
Qp:Qs in region of 2-4:1

ECG - Superior axis, incomplete RBBB

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21
Q

Why does respiration change 2nd heart sound?

A

Inspiration = -ve thoracic pressure, increase venous return
Increase venous return = increase RV pressure
Increase RV pressure is later closure of PV - widened 2nd heart sound in INSPIRATION

//
DDx - ASH/PAPVR - Increased RV volume
Slow RV contraction - i.e. RBBB
Pressur Overload - i.e. Pulmonary stenosis
Early aortic closure - i.e. mitral regurg

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22
Q

Fractional Shortening?

A

(ESD-EDD)//ESD

Normal is 27%

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23
Q

Ejection Fraction

A

(ESV-EDV)/ESV

Normal is 55%

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24
Q

Incidence of congenital cardiac defect?

A

0.5-1% of births

That is ~ 1/3rd of major congenital abnormalities

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25
Q

Heart Embroyology -

When does the heart beat?
When is semilunar valve complete?

A

Beats at 22days gestation

Semilunar valve done at day 65

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26
Q

What are some normal R Heart Pressures?

A 
RA 2-8mmHg
RV 2-32 mmHg
PA 25/10
Mean PA 19-29mmHg 
Pulmonary capillaries ~ 8mmHg

PVR = 2mmHg/L/min/M2

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27
Q

What are some normal L heart pressures?

A

Left atrium 8mm (2-12)
Left ventricle 8-100mmHg (Peak 90-140, end diastolic 5-12)
Aorta 100/60, mean 70-105mmHg

SVR ~ 16mmHg/L/min/m2

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28
Q

In a Qp:Qs calculation - how to handle all pulmonary blood flow coming from shunt - i.e. BT

A

Calculate using arterial oxygenation value as Pulmonary artery is filled by systemic artery

Similar to using ‘true’ mixed venous before level of shunt

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29
Q

AVSD ECG Clue?

A

Superior Axis

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30
Q

What happens to the AV valves in AVSD?

A

In a complete AVSD there is a common AV valve, with one mitral leaflet and one tricuspid leaflet being replaced by a superior and inferior leaflet.
So the “Right valve” has 4 leaflets and the “Left valve” has 3 leaflets due to the communication.

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31
Q

How much deoxygenated Hb to detect cyanosis?

A

50g/L

So therefore polycythaemic will look cyanotic at sats of 75% whilst anaemic patients will appear cyanotic at sats of 50%

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32
Q

What physiological variables influence pulmonary vascular resistance - WHAT STATES INCREASE PVR?

A 
Hypoxia
Hypercapnia
Ionotropes/Increased sympathetic tones
Polycythaemia
Pulmonary emboli
Pulmonary odema
Pulmonary effusion
33
Q

What physiological variables DECREASE pulmonary vascular resistance/PVR?

A

Oxygen
Adenosine
NO - inhaled and prolonged due to SILDENAFIL (inhibition of 5PDE -> increased cGMP)
Prostacyclin
Ca channel blockers
Endothelin receptor antagonist (BOSENTAN)

34
Q

Which Right to Left shunts cause increased Pulmonary Blood Flow?

A

Truncus arteriosus
TGA
TAPV

35
Q

Which Right to Left shunts cause decreased Pulmonary Blood Flow?

A

Tetralogy of fallot
Tricuspid atresia
Ebsteins anomaly

36
Q

Major criteria for rheumatic fever?

A

Migratory poly arthritis mostly affecting large joints
Carditis (Tachycardia, cardiac enlargement, new murmurs)
Choreiform limb movements (Sydenham chorea)
Transietn dmarcated skin rash on trunk (Erythema marginatum)
Nodules over bony prominences

Need two major in setting of recent streptococcal infection

37
Q

Minor Criteria for Rheumatic fever

A 
Fever
Arthralgia
Previous Hx of rheumatic fever
Raised ESR/CRP
Prolonged PR on ECG

Need two minor and one major in setting of streptococcal infection

38
Q

Rheumatic Heart Disease affects who and which structures?

A

80% of cases in Aus from ATSI population

Mitral valve > Aortic valve
Often asymptomatic until severe

39
Q

What determines direction and volume of ATRIAL level shunts?

A

The relative compliance of the ventricles
So in an ASD the blood goes L -> R then into compliant R ventricle
In a TAPVD the blood goes pulmonary veins -> R Atrium, then still mostly into R ventricle despite volume load, though enough to fill L Ventricle

40
Q

What determines shunt at VENTRICLE level?

A

In small/restrictive the PRESSURE difference across the shunt

In large/unrestrictive the relative RESISTANCE downstream in pulmonary and systemic circuits

41
Q

Continous murmur through back?

A

Aorto-pulmonary collaterals (As seen in pulmonary atresia, or tetralogy/pulmonary atresia variants)

42
Q

Describe a TET spell

A

Tetralogy of Fallot
Transient INCREASE in PVR leads to decreased PBF - Increased cyanosis (e.g. 20%!)
Clinically - Sudden drop in volume of murmur - because RVOT flow lessened, Hyperpnea - rapid deep breathing

Treat by dropping PVR to allow restoration of PBF or increasing SVR for same
Sleep
Morphine
Knees to chest
Oxygen
43
Q

Define OLIGOGENIC disease and give an example of cardiac disease with this pattern

A

Continuum of complexity in genetic architecture

Accumulation of SNP accumulations until reach threshold to exhibit BRUGADA syndrome, Early repolarisation, DCM

44
Q

2011 Criteria for “Class 1” genetic testing - i.e. when is it worthwhile?

A

Positive predicitive value >40% Signal to noise ratio >10%
Diagnosis relevance
Prognosis/managment relevance
Obliged to offer to relatives

45
Q

Regarding LQT Syndrome - what is the genetic causes?

A

SCN5A - Nav1.5 Channel - Gain of function LQT3 (Romano Ward) vs. Loss of function in same gene cause Brugada

LQT1 - KCNQ1 K channel - LOSS of function
LQT2 - KCNH2 (HERG) - LOSS of function

46
Q

Long QT syndrome prevalence?

Measure how?

A

1:2000

Tangent from downstroke vs. baseline, Lead II and Lead V5
From Q to T
QTc = QT / Sqroot RR interval

R on T phenomenon - Torsades into VF or resolution

Do gene testing if QTc > 480ms pre-pubertal, >500ms adult
consider if >460ms

47
Q

Long QT - which genotypes are most common?

A

QT1 - 40% Gene KCNQ1- KvLQT1 - decreased potassium
Symptoms on EXERTION/SWIMMING - Give beta blockers

QT2 - 40% Gene KCNH2 - HERG protein - decreased potassium
Symptoms on Auditory or postpartum - Give beta blockers

QT 3- 10% Gene SCN5A - Na v1.5 - increased sodium activitiy
The rest (Up to LTQ16)- uncommon
Give beta blockers and mexeletine

48
Q

Brugada Syndrome?

Gene
Provocative test

A

V2 - ST segment change
Flecanide - blocks sodium channel
Main gene is SCN5A - Protein NaV1.5 - 20-30% of brugada, LOSS of function

49
Q

What is CPVT?

A

Catecholaminergic Polymorphic ventricular tachycardia
Starts in childhood
Bidirectional VT deteoriates to VF
Excercise TEST - causes Ventricular ectopics, or bVT, or pVT

60% genetic positive RYR2 - RYANODINE RECEPTOR 2 - Calcium Channel - GAIN IN FUNCTION

50
Q

Hypertrophic Cardiomyopathy - ?Incidence, ?genetics

A

1:200-1:500
Cause of sudden cardiac death under sporting stress
Several hundred mutations across 35 genes
So Index case may
Mostly due to Sarcomeric genes
Cardiac Myosin binding protein C (MYBPC3) and beta-myosin heavy chain MYHB7 (together 70%)

51
Q

Acceptable cardiothoracic ratio on CXR?

A

In AP (i.e. neonate view) =60%

In PA (hugging the plate/adolescent view) =50%

52
Q

Clue to identify a R sided aortic arch?

A

Sometimes can’t deliniate aortic knuckle because structures are midline.
Search for a R-sided INDENTATION of trachea. No normal structure causes this.
It’s presence indicates a R-sided arch OR a mediastinal anomaly

53
Q

On a CXR - What is Plethora?

A

End on-arteries larger than adjacent bronchi

Need significant increased flow - i.e. Qp:Qs 2:1 or greater

54
Q

On a CXR - Pulmonary artery hypertension?

A

Big central arteries with peripheral pruning

55
Q

On a CXR - Pulmonary venous hypertension?

A 
Hyperinflation (As a compensatory mechanism for airway collapse in setting of interstial fluid) 
Pulmonary odema (alveolar)
Interstital opacities
Pleural effusions
Kerley B -septal lines
56
Q

On a CXR - DDx for Hyperinflation?

A

Viral infection
Bronchiolitis
Early pulmonary odema

How to distinguish?

Plethora alone won’t cause hyperinflation
Plethora and hyperinflation - CCF or viral

57
Q

Ivabradine

A

Selective sinus node blocker, used in HF in addition to beta blockade

58
Q

SGLE2 inhibitors

A

Heart failure

59
Q

Neprilysin inhibitors

A

Inhibit breakdown of naturetic peptides which Are beneficial in HF.

60
Q

Naturetic peptides?

A

Released from atrium and ventricle in setting of stretch
Prognostic, if 3x ULN - increased risk of death/transplant
Can use serially to measure function of therapy
Useful with skeletal muscle/heart my myopathy
N terminal or regular BNP
Useful in adults with unexplained breathlessness

61
Q

HCM

Incidence
Histology

Gene

A

1:500
Histology appearance of myocyte disarray - sarcomeres not lined up with each other

Autosomal dominant
Many proteins/genes

Sarcomeric HCM - any age - earliest/commonly cardiac beta-myosin - then troponin T and myosin binding

Inborn errors of metabolims -infancy
Malformation syndrome -infancy

62
Q

Role of Rx in paediatric HCM?

A

Propanolol
Verapamil/Diltiazem - Probs better than beta blockers
Disopyramide - negative inotorope

//
Low evidence
Relieve ischaemic chest pain or LVOTO
No impact on survival

63
Q

Normal HR in children?

A

1st week 125
1 month - 2 month 150

5 yr - 7yr = 100

64
Q

In Sinus rhythm - where to Ax the axis of P-waves?

A

Sinus node - axis 0-90, so that is upright in I and aVF (Just like normal QRS axis)

65
Q

What does LAD mean in paeds?

A

It doesn’t mean LVH - it means abnormal activation of LV muscle mass

EXAMPLES:

Abnormal distribution of conduction
Primum ASD
CAVSD (AV Canal) (Cos no muscle for conduction system to run through)
Tricuspid Atresia
Other single V
DORV
HCM
Noonan PS esp HCM
66
Q

Acceptable Axis for newborn?

A

0-160? - aka can be most positive in III

67
Q

PR Interval

A

<0.16 young children
<0.18 in adolescents

SHORTENS with excercise

68
Q

Wenckebach

A

Only need Preblock PR > Post block PR

Progressive widening of PR
Can be difficult to establish if 2:1 block

69
Q

MOBITZ type 2 ? Whats it look like, whats it from, any situations where difficult to distinguish from type 1?

A

Occasoinally drops beat
Difficult to work out in 2:1 block
Conducting system (i.,e. Type 2 more likely) if wide QRS

70
Q 
Bundle Branch Blocks
AV sits at bottom of R atrium
Splits into bundle of HIS
If blocked then myocardium has to propogate acrsoss
Then what does each block look like?
A

Widened QRS
In R-BBB in V1 - rsR’ - where the R’ is wider than the r - COMMONLY SEEN AFTER REPAIR OF Tetralogy of Fallot

Vs. incomplete RBBB (normal in 7% of kids, frequent ASD) RSR’ - same duration/amplitude

In RBBB the QRS is positive in V1
In LBBB the QRS is downwards in V1

71
Q

T-Wave Alternans

- T waves upright/downwards - P waves hidden in Twaves

A

Pathognomic for Long QT syndrome

72
Q

When calculating QTc - which RR?

A

The preceeding beat

In Sinus Arrythmia may give a longer QTc after a shorter RR - so must average over a selection in order to determine

73
Q

What cut-offs for QTc?

A

450 M, 460 F

Use Lead II or V5
QTc - QT Measured / Sqr root (Preceed RR in seconds)

But remember that the normal distributions of genetically affected and normal population OVERLAP

Can use QTCalculator to refine this further

74
Q

Regarding WPW - ? Intermittent excitatoin

Lead V6?

A

In Lead V6 Loss of Q wave, because Q wave in V6 is septal depolarisatio L-R normally

75
Q

Right Atrial Hypertrophy?

Left Atrial Hypertrophy on ECG?

A

P amplitude >3mm in any lead

R normally first, then L
If R is big it goes later, so sums onto L and becomes tall

Left Atrial Hypertrophy
Might be wide in II or bifid in V1 but actual definition is -ve deflection in V1 >1mm depth and > 0.04 length

76
Q

Inverted T wave in V1

A

Should be inverted in ALL R Precordial leads by > 8days

Accept up to V4 as normal throughout

Progressive change to upright T across precordium from L to R with growth - may persist until late teens in V1

If Upright T in V1 BEFORE 8 YEARS = RVH is PRESENT

77
Q

Criteria for RVH on ECG?

A

T wave UPRIGHT in V1/V3R/V4R between 8 days and 8 years

Q wave in V1/V3/V4R

R character +++ in V1 or S character —— in V6

78
Q

LVH - ECG voltage criteria

A

R in V6 + S in V1 > 60mm (use V5 if R > V6) ,
Or S in V1 > twice the R in V5
Abnormal R/S ratio
>95th centile S in V1 or R in V6

LATERAL LEADS - Strain in R wave and QRST angle is more than 90%, and T wave is opposite to QRS in lead of interest

79
Q

BVH - ECG?

A

> 65mm in equiphasic central lead

Or >45mm in 4x large euqiphasic chest leads

RACP CARDIO (1 decks)

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