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RACP CARDIO > CARDIO > Flashcards

CARDIO Flashcards

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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
Heart Embroyology - When does the heart beat? When is semilunar valve complete?
Beats at 22days gestation Semilunar valve done at day 65
26
What are some normal R Heart Pressures?
``` RA 2-8mmHg RV 2-32 mmHg PA 25/10 Mean PA 19-29mmHg Pulmonary capillaries ~ 8mmHg ``` PVR = 2mmHg/L/min/M2
27
What are some normal L heart pressures?
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
28
In a Qp:Qs calculation - how to handle all pulmonary blood flow coming from shunt - i.e. BT
Calculate using arterial oxygenation value as Pulmonary artery is filled by systemic artery Similar to using ‘true’ mixed venous before level of shunt
29
AVSD ECG Clue?
Superior Axis
30
What happens to the AV valves in AVSD?
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.
31
How much deoxygenated Hb to detect cyanosis?
50g/L | So therefore polycythaemic will look cyanotic at sats of 75% whilst anaemic patients will appear cyanotic at sats of 50%
32
What physiological variables influence pulmonary vascular resistance - WHAT STATES INCREASE PVR?
``` Hypoxia Hypercapnia Ionotropes/Increased sympathetic tones Polycythaemia Pulmonary emboli Pulmonary odema Pulmonary effusion ```
33
What physiological variables DECREASE pulmonary vascular resistance/PVR?
Oxygen Adenosine NO - inhaled and prolonged due to SILDENAFIL (inhibition of 5PDE -> increased cGMP) Prostacyclin Ca channel blockers Endothelin receptor antagonist (BOSENTAN)
34
Which Right to Left shunts cause increased Pulmonary Blood Flow?
Truncus arteriosus TGA TAPV
35
Which Right to Left shunts cause decreased Pulmonary Blood Flow?
Tetralogy of fallot Tricuspid atresia Ebsteins anomaly
36
Major criteria for rheumatic fever?
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
Minor Criteria for Rheumatic fever
``` 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
Rheumatic Heart Disease affects who and which structures?
80% of cases in Aus from ATSI population Mitral valve > Aortic valve Often asymptomatic until severe
39
What determines direction and volume of ATRIAL level shunts?
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
What determines shunt at VENTRICLE level?
In small/restrictive the PRESSURE difference across the shunt In large/unrestrictive the relative RESISTANCE downstream in pulmonary and systemic circuits
41
Continous murmur through back?
Aorto-pulmonary collaterals (As seen in pulmonary atresia, or tetralogy/pulmonary atresia variants)
42
Describe a TET spell
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
Define OLIGOGENIC disease and give an example of cardiac disease with this pattern
Continuum of complexity in genetic architecture | Accumulation of SNP accumulations until reach threshold to exhibit BRUGADA syndrome, Early repolarisation, DCM
44
2011 Criteria for “Class 1” genetic testing - i.e. when is it worthwhile?
Positive predicitive value >40% Signal to noise ratio >10% Diagnosis relevance Prognosis/managment relevance Obliged to offer to relatives
45
Regarding LQT Syndrome - what is the genetic causes?
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
Long QT syndrome prevalence? | Measure how?
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
Long QT - which genotypes are most common?
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
Brugada Syndrome? Gene Provocative test
V2 - ST segment change Flecanide - blocks sodium channel Main gene is SCN5A - Protein NaV1.5 - 20-30% of brugada, LOSS of function
49
What is CPVT?
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
Hypertrophic Cardiomyopathy - ?Incidence, ?genetics
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
Acceptable cardiothoracic ratio on CXR?
In AP (i.e. neonate view) =60% In PA (hugging the plate/adolescent view) =50%
52
Clue to identify a R sided aortic arch?
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
On a CXR - What is Plethora?
End on-arteries larger than adjacent bronchi | Need significant increased flow - i.e. Qp:Qs 2:1 or greater
54
On a CXR - Pulmonary artery hypertension?
Big central arteries with peripheral pruning
55
On a CXR - Pulmonary venous hypertension?
``` 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
On a CXR - DDx for Hyperinflation?
Viral infection Bronchiolitis Early pulmonary odema How to distinguish? Plethora alone won’t cause hyperinflation Plethora and hyperinflation - CCF or viral
57
Ivabradine
Selective sinus node blocker, used in HF in addition to beta blockade
58
SGLE2 inhibitors
Heart failure
59
Neprilysin inhibitors
Inhibit breakdown of naturetic peptides which Are beneficial in HF.
60
Naturetic peptides?
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
HCM Incidence Histology Gene
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
Role of Rx in paediatric HCM?
Propanolol Verapamil/Diltiazem - Probs better than beta blockers Disopyramide - negative inotorope // Low evidence Relieve ischaemic chest pain or LVOTO No impact on survival
63
Normal HR in children?
1st week 125 1 month - 2 month 150 5 yr - 7yr = 100
64
In Sinus rhythm - where to Ax the axis of P-waves?
Sinus node - axis 0-90, so that is upright in I and aVF (Just like normal QRS axis)
65
What does LAD mean in paeds?
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
Acceptable Axis for newborn?
0-160? - aka can be most positive in III
67
PR Interval
<0.16 young children <0.18 in adolescents SHORTENS with excercise
68
Wenckebach
Only need Preblock PR > Post block PR Progressive widening of PR Can be difficult to establish if 2:1 block
69
MOBITZ type 2 ? Whats it look like, whats it from, any situations where difficult to distinguish from type 1?
Occasoinally drops beat Difficult to work out in 2:1 block Conducting system (i.,e. Type 2 more likely) if wide QRS
70
``` 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? ```
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
T-Wave Alternans | - T waves upright/downwards - P waves hidden in Twaves
Pathognomic for Long QT syndrome
72
When calculating QTc - which RR?
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
What cut-offs for QTc?
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
Regarding WPW - ? Intermittent excitatoin Lead V6?
In Lead V6 Loss of Q wave, because Q wave in V6 is septal depolarisatio L-R normally
75
Right Atrial Hypertrophy? Left Atrial Hypertrophy on ECG?
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
Inverted T wave in V1
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
Criteria for RVH on ECG?
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
LVH - ECG voltage criteria
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
BVH - ECG?
>65mm in equiphasic central lead Or >45mm in 4x large euqiphasic chest leads

RACP CARDIO (1 decks)

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