CARDIO Flashcards
Typical CXR finding of: Egg on a string/Egg on it’s side?
TGA
Typical CXR finding of: Box Shaped Heart
Ebstein’s Anomaly - Big RA, minimal bloodflow to main pulmonary artery
- Relative oligemia, narrow upper mediastinum
Marked cardiomegaly
Typical CXR finding of: Coeur En Sabot - Upturned Apex
RVH - Tetralogy of Fallot
Typical CXR finding of: Snowman Sign
TAPVD - Additional opacities in upper mediastinum but no typical thymic indenations
Most common ASD?
Ostium Secundum - Fossa Ovalis defect -75%
Ostium Primum (partial AVSD 15%)
When would you do a fontan?
Single ventricle pathology - can’t fix a ventricle
I.e. HLHS, Tricuspid atresia, unbalanced VSD (i.e. with LV/RV disparate size)
Fontan Complications
Fontan heart failure - low output Protein losing enteropathy - stool alpha 1 antitrypsin Thromboembolic PE or Stroke Arrythmia incl heart block req. PPM Hypoxia
Reasons for prophylaxsis for infective endocarditis for dental procedures
Prosthetic valve
Cogenital repair within 6/12 or residual defect
Prev I.E.
Heart Transplant
And give amoxicillin to cover S. Viridans
Ebsteins Anomaly?
Thick failure to delaminate Tricuspid leaflet - RVOT, often also ASD w R-> L shunt
Pulmonary stenosis - syndromic associations?
Noonans - Valvular
Williams - Supravalvular
Alagille - Peripheral pulm stenosis
Heart defect carrying greatest risk transformation to eisenmengers?
Biggest L->R Shunt, so PDA, then VSD, then huge ASD
Most common location for VSD?
Membranous 80% (Near Aortic valve and tricuspid valve)
Mechanism for LV failure in VSD?
L->R shunt occurs in SYSTOLE, so LV “sees” the work, transmission of flow and pressure, then dilation on return to LA
Mechanism for RV failure in ASD?
L->R Shunt in diastole, big R Atrium then big R ventricle
Complications from PDA in older?
L->R Shunt and eisenmengers
Endocarditis
Calculate Qp:Qs?
(Systemic O2 difference)//(Pulmonary O2 Difference)
No shunt = 1
>2 significant L->R
Less than 1 R->L
“Step up” in O2 content intracardiac - what % is significant to suggest shunt?
7%
Calculate Pulmonary Vascular Resistance?
(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
Fick’s Method of cardiac output estimation?
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%
Clinical findings in Atrial Septal Defect
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
Why does respiration change 2nd heart sound?
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
Fractional Shortening?
(ESD-EDD)//ESD
Normal is 27%
Ejection Fraction
(ESV-EDV)/ESV
Normal is 55%
Incidence of congenital cardiac defect?
0.5-1% of births
That is ~ 1/3rd of major congenital abnormalities
Heart Embroyology -
When does the heart beat?
When is semilunar valve complete?
Beats at 22days gestation
Semilunar valve done at day 65
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
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
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
AVSD ECG Clue?
Superior Axis
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.
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%
What physiological variables influence pulmonary vascular resistance - WHAT STATES INCREASE PVR?
Hypoxia Hypercapnia Ionotropes/Increased sympathetic tones Polycythaemia Pulmonary emboli Pulmonary odema Pulmonary effusion
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)
Which Right to Left shunts cause increased Pulmonary Blood Flow?
Truncus arteriosus
TGA
TAPV
Which Right to Left shunts cause decreased Pulmonary Blood Flow?
Tetralogy of fallot
Tricuspid atresia
Ebsteins anomaly
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
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
Rheumatic Heart Disease affects who and which structures?
80% of cases in Aus from ATSI population
Mitral valve > Aortic valve
Often asymptomatic until severe
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
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
Continous murmur through back?
Aorto-pulmonary collaterals (As seen in pulmonary atresia, or tetralogy/pulmonary atresia variants)
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
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
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
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
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
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
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
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
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%)
Acceptable cardiothoracic ratio on CXR?
In AP (i.e. neonate view) =60%
In PA (hugging the plate/adolescent view) =50%
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
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
On a CXR - Pulmonary artery hypertension?
Big central arteries with peripheral pruning
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
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
Ivabradine
Selective sinus node blocker, used in HF in addition to beta blockade
SGLE2 inhibitors
Heart failure
Neprilysin inhibitors
Inhibit breakdown of naturetic peptides which Are beneficial in HF.
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
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
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
Normal HR in children?
1st week 125
1 month - 2 month 150
5 yr - 7yr = 100
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)
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
Acceptable Axis for newborn?
0-160? - aka can be most positive in III
PR Interval
<0.16 young children
<0.18 in adolescents
SHORTENS with excercise
Wenckebach
Only need Preblock PR > Post block PR
Progressive widening of PR
Can be difficult to establish if 2:1 block
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
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
T-Wave Alternans
- T waves upright/downwards - P waves hidden in Twaves
Pathognomic for Long QT syndrome
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
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
Regarding WPW - ? Intermittent excitatoin
Lead V6?
In Lead V6 Loss of Q wave, because Q wave in V6 is septal depolarisatio L-R normally
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
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
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
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
BVH - ECG?
> 65mm in equiphasic central lead
Or >45mm in 4x large euqiphasic chest leads
