Congenital Heart Disease
This is a deliberately brief description of CHD. Echo assessment of anything more complicated than this requires zen master expertise.
Secundum commonest where fossa ovalis absent.
Primum in inferior septum.
L to R shunt with pulmonary hypertension and R heart failure.
Best seen in subcostal window.
Colour shows flow across.
Assess flow across with PW also.
Look for R sided dilatation and RV volume overload (paradoxical septal motion in diastole).
Assess for pulmonary hypertension.
Perform shunt calculation.
ratio of RV SV to LV SV
For RV SV measure RVOT diameter and PW same spot for VTI.
For LV SV measure LVOT diameter (PLAX) and PW same spot in A5C for VTI.
For PFO get patient to do valsalva and look for right to left flow in A4C and subcostal views.
Perform contrast study (agitated saline) if not sure if ASD or PFO present. If no shunt, micro-bubbles dissipate within the lung vessels and so are not seen the left heart. If the shunt is myocardial will get contrast appearing in the LA within 3 cardiac cycles of RA opacification. An intrapulmonary shunt (eg AV malformation) takes 5 cycles or longer.
Atrial septal aneurysm looks like bulging IAS protruding or moving at least 10mm with a base of at least 15mm.
Located in thin fibrous membranous septum just below AV.
PLAX (hole below AV).
In the muscular septum. Will be here if the result of an MI. May be multiple.
Inlet (canal, posterior)
Posterior to TV septal leaflet.
Subpulmonary (outlet, doubly committed)
In between the outflow tracts just below AV and PV.
PSAX and A5C
Associated AR from RCC prolapse.
Same principles as for ASD.
Small holes will have higher velocities – restrictive VSD.
Velocity of the jet related to pressure by Bernoulli so can calculate ventricular pressure difference.
Look for R heart and LA dilatation.
TTE 1st line in all suspected IE except in prosthetic valves or to assess IE complicationswhere TOE 1st line.
Near zero risk (so no need for echo) if absence of:
- Prosthetic valve
- IVDA (drug abuser)
- Embolic signs
- Central line (so most ICU patients will have an indication if signs after admission)
- Positive blood cultures
Irregular mass attached to upstream side of valve leaflet (atrial side for MV and TV).
Can be attached to any part of valve but most often at coaptation line.
Move with the leaflet but oscillate.
May prolapse through valve.
Fungal vegetations bigger than bacterial.
TTE has a sensitivity of 50% for detecting vegetations down to 2mm (misses 75% below 5mm).
Overall sensitivity TTE about 75% (absence does not exclude).
Specificity 95% (seeing vegetations with clinical suspicion means highly likely have IE).
High negative predictive value if completely normal study (IE very unlikely).
Describe by MELTS
Motion (independent of valve), Effects (regurg, abscess), Location (upstream, on prosthetic material), Texture, Shape.
- Prolonged tachycardia
Ischaemia, valvular disease and hypertension cause LV dilatation and impairment but are not usually classified as DCM.
Dilatation and systolic impairment of LV.
Often accompanied by pulmonary hypertension and dilatation of other chambers with MR and TR.
Wall thickness normal.
LV more spherical.
Spontaneous echo contrast and thrombus (slow turbulent flow).
Early closure of AV and delayed closure MV.
As LVEDP rises then will get evidence of diastolic dysfunction.
65% asymmetrical (mostly septal but can be apical).
35% symmetrical (need to make sure no other cause like AS or hypertension).
Obstructive or non obstructive.
Systolic function preserved. LV non-dilated with small cavity. EF normal or increased.
Diastolic function impaired.
LVOT increased velocity (significant gradient and turbulent flow – can distinguish AS from HOCM by using PW to see where velocity highest).
Obstructive if gradient >30mmHg (including with exercise).
Sabre shaped LVOT trace (rate of rise in velocity increases throughout systole as the LVOT narrows).
Increased LVOT velocity causes a Venturi effect causing systolic anterior motion (SAM) of the anterior MV leaflet. The leaflet will touch the septum in systole. This may cause a posteriorly directed jet of MR.
Fluttering/early closure of AV.
Velocity increased with valsalva.
Hypertrophied LV (?RV too)
Normal atrial size
Infiltration or deposition.
Amyloid, haemochromatosis, endocardial fibrosis, sarcoid, glycogen storage disease.
Systolic function preserved. LV non-dilated. (EF preserved but systolic function not normal).
Diastolic function impaired – stiff LV.
LV and RV may be hypertrophied.
Dilated atria and IVC.
Myocardium echo-bright and speckled in amyloid.
Arrhythmogenic RV cardiomyopathy
Dilated RV with dysfunction
Aneurysms of RV free wall.
Echo-bright moderator band and myocardium.
Constrictive Pericarditis vs restrictive cardiomyopathy.