Klein TTE Q book Flashcards
How can you differentiate linear aortic artifacts (which are caused by reverberation) from aortic dissection?
1) These artifacts typically occur when the aortic diameter is > than the LA diameter
2) Dissection flaps, unlike linear artifacts, have independent motion the posterior aortic wall (artifacts move in parallel to the posterior aortic wall)
3) Dissection flaps, unlike artifacts, have rapid oscillatory movements
4) Artifacts are usually created at the posterior aortic wall interace with the LA, not the anterior aortic wall
What type of artifact does a mechanical valve create?
Reverberation artifact
What type of artifact is a double image aortic valve?
Refraction
What type of artifact is a mitral valve below diaphragm?
Mirror image
What type of artifact is distortion of ball and cage valve?
Propagation speed
How can you tell the difference between a side lobe artifact and a refraction artifact, when both appear adjacent to the original structures?
- Echo Intensity:
Side Lobe Artifact:
The artifact is usually fainter and less well-defined compared to the actual structure since it originates from secondary energy (side lobes).
Refraction Artifact:
The artifact can appear nearly as bright and well-defined as the actual structure because it is part of the primary beam, albeit redirected.
- Behavior with Probe Manipulation:
Side Lobe Artifact:
Does not move significantly with changes in probe angle or position.
Persistently aligns with the original reflective structure producing the side lobe.
Refraction Artifact:
Shifts position depending on the angle of insonation because refraction follows Snell’s Law.
Moving the probe can make the artifact disappear or change its displacement.
When does a mirror image artifact occurs, and how can you reduce it?
It occurs when the doppler gains are set too high and it can be reduced by decreasing the power output or gain and optimising the angle between the ultrasound beam and doppler flow.
How can you differentiate from a LV thrombus and near field clutter?
1) Change from fundamental to harmonic imaging (this also helps with reduce side lobe / grating lobes / reverberation artifacts)
2) Increasing transducer frequency
3) Decreasing the depth
4) Using multiple views
5) Contrast agents (decrease the MI)
What are the artifacts that could mimic LV thrombus?
1) Reverberation (near-field clutter, comet tail)
2) Range ambiguity
3) Attenuation (shadowing)
What is a ghosting artifact
Colour doppler that is distorted beyond anatomic borders due to multiple reflections
What is refraction?
Bending of the ultrasound beam that results in side-to-side images
How can you tell AR on a M-mode tracing of the LV?
Fluttering of the mitral valve leaflets
What, on an M-mode of the LV, suggest high LVEDP?
The “b-bump” which is at the end of the leaflet
What is the formula for relative wall thickness?
(2 x PWTd)/LVIDd
The UL is 0.42
What is the UL for LV mass index
115 g/m2 in men
95 g/m2 in women
Do you need to have a holodiastolic murmur for severe AR?
In acute severe AR, the LV diastolic pressure rises rapidly because the LV is non-compliant (stiff). This can cause early equalization of aortic and LV pressures, truncating the murmur (it may only be early diastolic).
Similarly, in chronic severe AR with very low systemic vascular resistance or hypotension, the aortic diastolic pressure may fall, reducing the pressure gradient and shortening the murmur.
If you put a pulse wave in the RVOT just prior to the pulmonary valve in a patient in NSR with severe PAH, what will you see?
Small or absent A wave (atria cannot contract sufficiently against the high RVEDP seen, therefore v little blood flow so small or absent A wave)
A mid-systolic notch (flying “W” sign)
In an acute PE, are pulmonary pressures significantly raised?
typically not >50 mmHg
What findings do you see on M mode for a subaortic membrane?
Fluttering of the RCC (top) cusp
Abrupt, very early posterior motion of the right cusp of the aortic valve
Talk about chamber collapse assessment in tamponade assessment:
Normal Chamber Dynamics:
The RV and RA naturally collapse during parts of the cardiac cycle due to physiologic variations in pressures.
RA collapse: Occurs briefly during atrial systole (end-diastole).
RV collapse: May occur during early systole due to contraction.
Pathologic Chamber Collapse in Tamponade:
In tamponade, pericardial pressure exceeds the chamber pressures (RA and RV diastolic pressures), leading to prolonged, abnormal chamber collapse.
RA collapse: Abnormal if it persists for more than one-third of the cardiac cycle.
RV collapse: Significant if it occurs during diastole, when the RV is supposed to be filling.
RA collapse in tamponade occurs in late diastole, when the RA should be filling.
RV collapse in tamponade occurs in early diastole, when the RV is supposed to be filling.
Is hypertension related to dilatation of the sinuses of Valsalva?
No - just the distal aortic segments
When should the aortic annulus be measured?
Mid-systole
When should all the other aortic measurements be made e.g. STJ, Asc aorta
End-diastole
An IVC diameter <1cm with spontaneous collapse indicates
intravascular volume depletion
Is IVC dilation in athletes suggestive of raised RA pressure?
No - they have normal collapsibility
When should IVC diameters be measured?
End-expiration and end diastole using M mode - correlates better with RA pressure
Are 2D methods of RV function i.e. TAPSE, S’ reliable post cardiac surgery?
No, but 3D RVEF is more reliable
What are the abnormal cutoffs for RV size and function
RV base > 41mm
RVEF < 45%
RV FAC <35%
TAPSE <17mm
RV S’ <9.5 cm/s
RV strain >- 20%
RIMP by PW >0.43
RIMP by TDI >0.54
Should you index your RV dimensions to BSA?
According to ASE, only if a patient is at the extremes of BSA
When should the continuity equation not be used when assessing stenosis severity?
If there’s concomitant regurgitation
What are the absolute contraindications to TOE?
- Oesophageal or pharyngeal obstruction
- Oesophageal diverticulum
- GI bleeding from an unknown source
- Perforated viscus
What are the relative contraindications to TOE?
- Oesophageal varicies
- History of radiation to the neck
- Barrett’s oesophagus
- Coagulopathy
Do fibroelastomas have stalks?
Half do, half don’t.
Most commonly found on the aortic valve followed by the mitral.
What is the most reliable visual guide to the presence of hypovolaemia?
Small LVESV
How do you manage acute SAM?
This can occur in aortic (decreased LV cavity size from relief of increased afterload) or mitral valve repair (redundant posterior mitral valve leaflet) or replacement
Avoid catecholamines (beta 1 agonists e.g. dobutamine, norad, isoprenaline, levo), make sure patient is intravascularly replete, and if BP support is needed than use phenylephrine.
How can you differentiate CW of AS versus MR?
By looking at the positive deflection - in AS there’s a gap (lasting about 80 ms) during isovolumetric relaxation that starts immediately at the cessation of the AS signal, at the time of aortic valve closure, and ends at mitral valve opening, the beginning of the mitral valve antegrade flow signal.
This is unlike an MR signal where there is no gap between the MR jet and the EA like signal on top.
What is a high risk atheroma on echo?
If it protrudes into the lumen by 4mm or more, and/or shows mobility, that atheroma is considered severe and associated with increased perioperative mortality (mostly from atheroembolic events that shower cholesterol plaques to the liver, kidneys, brain and skin).
What is the formula for MVA
MVA = 220 / PHT
Alternatively MVA = 759 / DT
What is the formula for PHT (ms)
PHT = 0.29 x deceleration time
What’s the formula for SV
SV = MVA x VTI
What is Qs and Qp in a patient with a PDA?
Unlike an ASD or VSD, Qp represents flow across the LVOT and Qs represents flow across the RVOT.
And the shunt flow is Qp - Qs (of you can do SV LVOT - SV RVOT)
And depending on the Qp Qs you can say which part of the heart will dilate. If the Qp:Qs > 1, then the left sided will dilate first as it’s accommodating more blood
What is normal PADP and how is it calculated?
5 to 16 mmHg
PADP = 4 x [Pulmonary artery end diastolic velocity]squared + RAP
(RAP can be estimated based on IVC size and response to inspiration unless there is significant tricuspid stenosis)
Define severe MR quantitatively
EROA 0.4cm2 or more
RF 50% or more
RV 60ml or more
VC 0.7cm or more
The formula for EROA
EROA = [2πr² x V aliasing]/V max
The formula for instantaneous flow rate [IFR]
=2πr² x V aliasing
Regurgitant volume formula
Rvol = EROA x VTI
Regurgitant fraction formula
Rfrac = Rvol/SV x100
Pulmonary artery wedge pressure (PAWP) formula
PAWP = 4.6 + 5.27 x [E / Vp]
Where E = peak blood flow velocity of the mitral inflow in cm/s
Vp = flow propagation velocity of the mitral inflow (in cm/s) obtained by colour M-mode.
Vp measures the rate which red blood cells reach the LV apex from the mitral valve level during early diastole.
The rate of blood flow from the mitral valve to the LV apex is determined by the rate of LV relaxation during early diastole.
Therefore, Vp is an indirect measure of the rate of LV relaxation, the lower the Vp, the slower the LV relaxation and higher the LVEDVP.
The normal PAWP is 12mmHg or less.
What is the pseudonormal filling pattern?
E/A 1-2, E wave deceleration time >160 ms or more
What is a restrictive filling pattern?
E/A >2, E wave decel time <160 ms
What are the normal flow propagation velocity values?
In young individuals, Vp > 55cm/s
In middle aged and elderly individuals, Vp>45 cm/s
What are the criteria for severe AR
Regurgitant orifice ≥ 0.3 cm2
Regurgitant fraction ≥ 50%
Regurgitant volume ≥60 ml
Vena contracta (cm) >0.6
Is the VC strongly influenced by the Nyquist limit?
No
By lowering the colour Doppler Nyquist limit, one lowers the velocity filter allowing for inclusion of lower velocities and an increase in the colour area.
VC contains predominantly high velocities, but PISA radius becomes progressively larger with lower Nyquist limits.
What is E/e’ a sign of?
Left atrial pressure
What does an E/e’ >15 mean?
LAP is elevated
> 12 means LAP is elevated if the lateral e’ is used
> 15 means LAP is elevated if the medial e’ is used
Formula for LAP
LAP = 1.9 + 1.24 x (E/e’)
A simplified version of the above is 4 + (E/e’)
A normal LAP is <12 mmHg
What’s the formula for LVSP
LVSP = Peak systolic gradient of the MR jet (i.e. 4V² + LAP)
What’s the formula for the peak to peak gradient of e.g. AS
P2P = LVSP - SBP
P2P is lower than the peak instantaneous gradient obtained by CW doppler across the aortic valve
What is the formula for pressure gradient
Pressure gradient (4V²) = DBP - LVEDP
where V = end-diastolic velocity of AR
Is the peak LVSP higher or lower than SBP in patients with AS?
Always higher
Does AR affecting calculating the AVA using the continuity equation?
No - both the VTI LVOT and VTI AV are equally affected by AR
What is the continuity equation for AVA
AVA = CSA LVOT x [VTI LVOT/VTI AV]
What’s the formula for PVR
PVR = [MPP - LAP] / Qp
When MPP is mean pulmonary artery pressure = 1/3 [PASP - PADP]
LAP = Left atrial pressure
Qp = pulmonary blood flow (litres/min)
The normal PVR is 1-2 Wood units
ASD closure should not be performed if the PVR is 2/3 or more of the systemic vascular resistance (SVR)
Normal SVR is 11-16 Wood units
A PVR ≥ 9 wood units usually precludes ASD closure
RVSP in a patient with VSD and no LVOTO can be calculated as
RVSP = SBP - Peak systolic VSD gradient (4V²)
Normally PASP = RVSP however in the presence of pulmonic stenosis,
PASP = RVSP - Peak PS gradient
In the presence of a VSD, what is RVEDP
RVEDP = LVEDP - end diastolic VSD gradient (4V²)
What’s the formula for dP/dT
Change in pressure / RTI
Where RTI (in seconds!) is the relative time interval measured in seconds, between MR jet velocities of 1 m/s and 3 m/s.
and change in pressure represents the difference between the LV to LAP gradients at V2 and V1.
The normal dP/dT is >1200 mmHg/s (although the book says 1661 + 323 mmHg/s)
How do you calculate LAP
In the absence of LVOTO or significant AS, SBP = LVSP
and if you know the peak velocity of an MR jet, then you can calculate the pressure gradient between LA and LV by 4V²
then do SBP (i.e. LVSP) - 4V² = LAP
if LAP ≥ 12 mmHg, it’s elevated
In MS, is the peak velocity of the mitral E wave expected to be low, normal or high
High
velocity (V) across an orifice is inversely related to the cross sectional area (CSA) of the orifice
therefore the smaller the CSA or MVA, the higher the peak velocity of the mitral E wave
What assumption does PHT make?
That LV pressure and compliance are normal, and therefore that the deceleration slope of the mitral E wave on spectral Doppler tracings in diastole is the function of the MVA alone
The reason why PHT is unreliable immediately post BMV is because with the increase in valve area, as LV compliance cannot change acutely, LVEDP increases, the diastolic LA/LV gradient decreases, and the mitral PHT shortens above and beyond what would be expected by an increase in MVA alone after BMV.
How can you calculate AVA
AVA = [CSA LVOT (πr²) x TVI LVOT]/TVI Aortic valve
OR
AVA = [CSA LVOT (πr²) x Peak LVOT velocity]/Peak aortic valve velocity
What is the dimensionless index?
Peak LVOT velocity / peak Aortic valve velocity
In AS, is the SBP higher or lower than the LVSP?
Lower
To calculate pressure gradients the formula is
4V²
Don’t confuse with πr² !!!!
How can you calculate the mean aortic valve gradient form a peak aortic velocity and LVOT diameter?
Mean gradient = 0.6 x the peak gradient
Peak gradient = 4V²
Can pregnancy / high cardiac output or severe AR be responsible for a peak LVOT 1 m/s but peak AV of 5 m/s?
No, both conditions would result in a significant increase in both velocities not just one.
Can the subvalvular LVOT velocity i.e. by PW be normal in obstructive HCM with a significant gradient at rest?
No
In an uncomplicated PDA, what do you expect to see on the CW trace?
Antegrade flow in both systole and diastole
In severe PR, will the PASP be higher than RVSP?
No. RVSP will be higher as regurg leads to reduced pressure in the PA in systole (less volume!)
Does regurg lead to increase forward flow velocities?
Yes. velocity = Q/PVA
Where Q is the volumetric flow across the pulmonic valve in systole
(Q = SV x HR)
When PVA remains constant, any increase in stroke volume leads to increase transvalvular velocity
What does a lack of measurable of end-diastolic gradient mean on e.g. PR CW Trace suggestive of severe PR?
It means that there is a large regurgitant orifice which results in the pressure gradient between the pulmonary artery and the RV equalising rapidly, being achieved by mid-diastole.
What effect does Valsalva have on the mitral E wave velocity?
Valsalva reduces preload, leading to a lower early diastolic pressure gradient between the LA and LV. This leads to a lower peak velocity of the mitral E wave and a lower mitral E/A ratio.
A peak of AR velocity ≥ 35 ms indicates
elevated LVEDVP
AR is the atrial reversal wave seen on PV CW doppler (the negative deflection reflecting blood going back into the PVs during systole / QRS complex on ECG)
Also if the duration of the AR wave is ≥ 30 m/s more than the duration of the mitral inflow A wave, this suggest an elevated LVEDP
As LAP increases, what do you expect of the ratio of the S wave (systolic) to D (diastolic) wave in the PV CW doppler tracings to be?
The higher the LAP, the lower the S/D ratio is (i.e. the S wave decreases more than the D wave)
Explain interventricular dependence
Normal Mechanism: Inspiration and Intrathoracic Pressure
During inspiration, the intrathoracic pressure drops (becomes more negative), which:
Increases venous return to the right side of the heart (right atrium and right ventricle).
Reduces the pressure inside the pulmonary veins (the vessels bringing oxygenated blood from the lungs to the left atrium).
Why the Drop in Intrathoracic Pressure Decreases LA and LV Filling
Pulmonary Veins Are Also in the Thoracic Cavity:
The pulmonary veins are exposed to the same intrathoracic pressure changes as the lungs and other thoracic structures.
When intrathoracic pressure decreases (during inspiration), it reduces the pressure in the pulmonary veins.
Pressure Gradient Between Pulmonary Veins and LA:
Blood flows from the pulmonary veins into the left atrium due to a pressure gradient.
Normally, the pressure in the pulmonary veins is slightly higher than the pressure in the left atrium, which drives blood flow into the LA.
Effect of the Pressure Drop:
During inspiration, the pressure in the pulmonary veins decreases due to the drop in intrathoracic pressure.
If the pressure in the pulmonary veins decreases, the pressure gradient between the pulmonary veins and the left atrium also decreases.
A smaller pressure gradient means less blood flows into the left atrium during diastole, reducing LA filling and, consequently, LV filling.
Analogy to Understand This
Think of blood flow as water flowing downhill due to gravity:
The steepness of the hill represents the pressure gradient.
A larger gradient (steeper hill) means faster flow.
When the hill flattens (smaller gradient), the flow slows down.
During inspiration:
The drop in intrathoracic pressure flattens the “hill” (reduces the pulmonary vein-to-LA pressure gradient), leading to reduced flow into the left atrium.
Additional Factors in Constrictive Pericarditis
In constrictive pericarditis, the effect is exaggerated because:
The rigid pericardium prevents the left atrium and ventricle from expanding fully to compensate for this reduced pressure gradient.
This further impairs LV filling during inspiration.
The SVC and IVC are veins that carry systemic venous blood back to the right atrium.
These veins are located primarily in the thoracic cavity but originate from outside the thorax. During inspiration:
The intra-abdominal pressure increases (due to diaphragmatic contraction).
The intrathoracic pressure decreases.
This combination creates a favorable pressure gradient for blood flow from the IVC (abdomen) and SVC (upper body) into the right atrium.
Thus:
Blood flow in the SVC and IVC increases during inspiration, and pressures in these vessels do not drop significantly because the increase in flow offsets any reduction in intrathoracic pressure.
- Overview of Expiration
During expiration, the intrathoracic pressure increases (becomes less negative or even slightly positive in some conditions).
This rise in intrathoracic pressure affects the flow dynamics of:
Systemic veins (SVC/IVC): Blood returning to the right atrium (RA).
Pulmonary veins: Blood returning to the left atrium (LA).
Expiration reverses many of the changes seen during inspiration. - Systemic Venous Return (SVC/IVC)
Key Effect: Reduced systemic venous return.
During expiration:
The rise in intrathoracic pressure compresses the SVC and IVC, increasing their internal pressure and partially reducing the pressure gradient driving blood into the right atrium.
At the same time, intra-abdominal pressure decreases (as the diaphragm relaxes), further reducing venous return through the IVC.
This results in less blood flow into the right atrium and a subsequent reduction in right ventricular (RV) filling. - Pulmonary Venous Return
Key Effect: Increased pulmonary venous return.
During expiration:
The increased intrathoracic pressure is transmitted to the pulmonary veins, which slightly increases their pressure.
The pressure in the left atrium also increases (because it’s in the thoracic cavity), but the rise in pulmonary venous pressure is greater than the rise in left atrial pressure, improving the pressure gradient.
This leads to improved left atrial (LA) filling and subsequent left ventricular (LV) filling. - Interventricular Dynamics
Inspiration vs. Expiration:
During inspiration, the right ventricle (RV) fills at the expense of the left ventricle (LV) (due to septal shift and ventricular interdependence).
During expiration, the opposite happens: LV filling improves at the expense of the RV.
In conditions like constrictive pericarditis, this interplay is exaggerated:
The interventricular septum shifts toward the RV during expiration (because RV filling is reduced), allowing more space for the LV to fill. - Hepatic Vein Flow
During expiration, when RV diastolic pressure rises (due to reduced RV filling), there may be retrograde flow into the hepatic veins. This is a hallmark finding in conditions like constrictive pericarditis, where RV filling is severely restricted.
During inspiration, hepatic vein anterograde flow significantly increases.
What does aortic coarctation look like on PW doppler?
Anterograde flow throughout the cardiac cycle i.e. including diastole, with a large peak systolic gradient (this indicates severe coarctation)
What does a normal PW look like in the descending aorta
There is systolic anterograde flow but no diastolic anterograde flow.
There is a small amount and duration of flow reversal in early diastole but it’s not throughout diastole which is what’s seen in severe AR
If you see a significant peak systolic gradient on PW in the desc aorta, why is this not significant AS?
Because significant AS would be above the baseline if the PW was in the asc aorta.
Also severe AS is not characterised by an antegrade diastolic gradient across the aortic valve
Is BP higher in the legs or arms in coarctation?
Coarctation usually occurs distal to the origin of the neck arteries
BP in the arms is higher that that in the legs
How can I differentiate between a TR and AS jet on CW?
AS flow does not occur during the short period of isovolumetric contraction straight after the QRS onset. It only occurs in the subsequent ejection period.
In contrast, the TR jet extends throughout systole.
The AS flow is therefore of a shorter duration and has a later onset compared to the TR jet.
What’s the difference between the EA pattern in tamponade and constrictive pericarditis?
In tamponade, LV filling is impaired from the onset of diastole therefore the peak velocity of the mitral E wave is lower than that of the A wave (i.e. impaired relaxation pattern), and the deceleration time is prolonged.
In constrictive pericarditis, early diastolic filling is rapid and then abruptly decreases in late diastole when the expanding myocardium reaches the rigid pericardium. Therefore there is a restrictive filling pattern (E/A>2, deceleration time of E wave <160 ms)
What is the formula for calculating respiratory variation to identify tamponade?
E expiration - E inspiration / E expiration
(this is measured from the EA trace taken at the tips of the mitral valve leaflets)
≥25% inspiratory drop is suggestive of tamponade, constrictive pericarditis
However, marked respiratory variations also occur with laboured breathing, asthma, COPD, PE and obesity
How can you differentiate restrictive cardiomyopathy vs constrictive pericarditis?
There are no significant respiratory variations in mitral inflow in patients with restrictive cardiomyopathy
e’ velocity is also significantly decreased in restrictive cardiomyopathy but normal or raised in constrictive pericarditis
How can you tell if TR is severe based on CW?
There will be a sharp upstroke of the TR jet, followed by a rapid deceleration slope.
The sharp upstroke also indicates a normal dP/dT and thus normal RV function.
When the TR orifice is large, there is ventricularisation of the RAPs, which results in a very rapid pressure equilibration between RVP and RAP.
The rapid rise in RAP results in a rapid deceleration slope.
The peak velocity in very severe TR is often low, and just because its low, doesn’t mean there isn’t significant pulmonary hypertension.
In severe TR, the jet peaks in early systole, but if there was a midcavitary RV gradient, the peak would be in late systole.
In an uncomplicated VSD, to calculate the LVEDP what is the formula
In the absence of TS or AS,
LVEDP = VSD end-diastolic gradient + RA end-diastolic pressure
and RV peak systolic pressure
= SBP - VSD peak systolic gradient
What are the signs of constrictive pericarditis on mitral annular tissue doppler tracings?
Annulus reversus
Peak E’ velocity is normally higher in the lateral compared to the medial annulus i.e. E’ lateral / E’ medial > 1
Eventhough E’ values are reduced in restrictive cardiomyopathies, this ratio is maintained
unlike in constrictive pericarditis where the lateral E’ is significantly reduced compared to the medial E’ which is often normal or increased
How do you measure LA pressure in someone with an ASD?
Peak LA pressure = peak trans-ASD gradient + RA pressure
What’s the formula for regurgitant volume?
R volume = EROA x VTI
How can you calculate SBP knowing the Vmax of a MR jet and LA pressure
Peak LV to LA gradient is 4Vmax²
Peak LVSP = 4Vmax² + LA pressure
In the absence of AS
Peak LVSP = SBP
Is MR typically holosytolic?
Yes and in these cases both EROA and regurgitant volume are accurate measures of MR severity
However when MR is only late systolic (e.g often in MVP), the VTI is often small, therefore the calculated regurgitant volume will be small as R vol = EROA x VTI
he EROA isn’t a good measure and you should use other measures i.e. regurgitant volume, fraction
What’s the formula for regurgitant fraction
RF = R vol / R vol + forward stroke volume
What does Cor triatriatum look like on CW doppler?
Clinically, it presents like MS
On doppler, unlike MS (supra, valvular or subvalvular), it has a triphasic flow which consists of a systolic (S) wave and two diastolic waves: early diastolic (E) wave and late diastolic (A) wave.
There is elevated transmitral pressure gradient in systole and diasotle. MS (whatever form) only has an elevated transmitral gradient in diastole.
In Cor triatriatum you have a perforated membrane that divides the LA into two: the posterior LA which receives the PVs, and the anterior LA which is connected to the LA appendage and is bound by the MV.
What’s the formula for PAWP
PAWP = 1.24 x (E/e’) + 1.9
Septal e’ is often used
Normal PAWP is 6-12 mmHg
Is the pulmonary artery system a higher pressure system than the aorta in the presence of an uncomplicated PDA?
No
with a PDA, more blood flows through the pulmonary valve than the aortic valve because of the recirculation of blood from the systemic circulation into the pulmonary circulation.
However, this does not mean pulmonary pressures immediately increase; the pulmonary vascular system absorbs this extra flow efficiently, at least initially.
Therefore to calculate pulmonary artery pressure (systolic or diastolic), subtract the systolic or diastolic pressure of the PDA from the systolic or diastolic blood pressure and you will get the pulmonary artery systolic or diastolic blood pressure
Which nyquist limit should you use when calculating EROA
the one in the direction of the flow
When does diastolic MR occur?
It may occur in severe LVSD or CHB
How is LAVI calculated?
LAV = 0.85 x [(A1 x A2)/L] and then divide the result by BSA
How do you differentiate normal from pseudonormal diastolic function pattern
pseudonormal e’ <8 cm/s, normal e’ >8 cm/s
Or PW doppler of PV will show systolic wave blunting / S <D
How does the septum move in LBBB
Septum moves posteriorly in the preejection period and then moves anteriorly (away from the posterior LV wall) during the ejection phase of systole
In cardiac surgery, the IVS moves towards the RV rather than the LV in systole, with normal thickening
E>A in …?
Constrictive pericarditis !
in tamponade, E < A !
Does standard doppler exclude high velocities?
No
Standard doppler excludes low velocities and
tissue doppler (as tissue moves at a slower velocity) excludes high velocities
Strain rate can be defined as
the change in velocity between two points divided by their distance
What is the most powerful diastolic predictor of mortality post MI?
E/e’
What is the best strain predictor of cardiac events in a patient with acute HF?
Global circumferential strain
What is a contraindication to Optison contrast?
Allergy to blood products
Contraindication to all contrast agents except Optison is?
Right to left shunt (except in a PFO)
This is because although contrast agents normally pass into the LV - when they pass through the normal route of the lungs, they lose energy and are diluted.
When they pass directly into the LA from the RA, the bubbles are undiluted, and of a higher concentration, increasing the likelihood of microvascular obstruction.
This is not the case with saline bubbles, which are bigger, air filled and therefore less stable / quickly reabsorbed.
Are contrast agents (not saline) used for the detection of intracardiac shunts including PDA?
No
Delay in replenishment on myocardial perfusion imaging (beyond 3 seconds during stress imaging) should be considered abnormal and can be confined to just the subendocardial layers?
During rest 4-5 seconds
During stress within 2 seconds
What will be seen in an unroofed coronary sinus with a left sided injection?
LA then RA enhancement
What is a low MI
<0.3
What is a very low MI
<0.2
should be combined with pulse sequences to get the nonlinear responses from microbubbles
What’s the formula for LVM
=1.04[(LVDD + IVS + PW)³ - LVDD³] - 13.6
the diameters are in cm
The answer can be indexed to BSA
what GLS is associated with an EF of 35%
about -13%
Ischaemic MR tends to occur in which part of the cardiac cycle
Early systole (mainly)
What is definitive of constrictive pericaridits?
Hepatic vein end diastolic flow reversal velocity / forward flow velocity >0.8
What medial e’ velocity suggests constriction as opposed to restrictive cardiomyopathy
≥ 8 cm/s
What other findings suggest restrictive cardiomyopathy?
LAVI > 48 ml/m2
E/e’ >15
How do you estimate LV filling pressures in patients with Afib
Peak acceleration rate of mitral E velocity ≥1900 cm/s2
IVRT less than or equal to 65 ms
DT of pulmonary venous diastolic velocity less than or equal to 220 ms
E/Vp ratio ≥ 1.4
Septal E/e’ ratio ≥ 11
Assessing LV filling pressures in sinus tachy?
Lateral E/e’ > 10 (or even better >12)
What makes PH likely to be non-cardiac?
If the E/e’ is <8
Raised LV filling pressures in restrictive cardiomyopathy?
EA > 2.5
Raised LV filling pressures in MS?
Mitral A velocity >1.5 m/s
Raised LV filling pressures in MR?
E/e’ >15 (only in the setting of decreased LVEF)
Diastolic stress test reveals what?
E/e’ remains normal in healthy individuals, but e’ significantly drops in those with diastolic dysfunction causing the E/e’ to significantly increase
What are the criteria used in diastolic function assessment
E/e’ >14
Septal e’ <7 or lateral e’ <10
TR > 2.8 m/s
LAVI > 34 ml/m2
How does Valsalva differentiate pseudonormal relaxation from impaired relaxation?
A decrease of 50% or more in E/A with Valsalva is highly specific for increased LV filling pressures in cardiac patients
Physiology of the Valsalva Maneuver
During the strain phase of the Valsalva maneuver:
Preload decreases due to increased intrathoracic pressure reducing venous return to the heart.
This causes a temporary reduction in left atrial (LA) pressure and subsequently decreases LV filling pressure.
Diastolic Patterns on Mitral Doppler
Normal Filling:
E/A ratio: Normal.
Valsalva: A small reduction in both E and A wave velocities without a significant change in the E/A ratio.
Impaired Relaxation (Grade I Diastolic Dysfunction):
E/A ratio: <1 (reduced E wave and increased A wave).
Valsalva: E and A velocities decrease slightly, but the pattern remains consistent (E/A ratio stays <1).
Pseudonormal Pattern (Grade II Diastolic Dysfunction):
E/A ratio: Appears normal (1–1.5) due to elevated LA pressure “masking” impaired relaxation.
With Valsalva:
Reduced preload unmasking the true pattern of diastolic dysfunction.
E wave decreases disproportionately, causing the E/A ratio to fall to <1 (revealing an underlying impaired relaxation pattern).
Restrictive Filling (Grade III/IV Diastolic Dysfunction):
E/A ratio: >2, with a short deceleration time (<160 ms) due to markedly elevated LA pressure and severely reduced LV compliance.
With Valsalva:
Minimal change in the E/A ratio.
E velocity may decrease slightly, but the restrictive pattern persists because of fixed, high LV filling pressures.
Why the Valsalva Maneuver Works
In pseudonormal diastolic dysfunction, the normal-looking E/A ratio at rest is due to elevated LA pressure artificially boosting the E velocity.
The Valsalva maneuver reduces LA pressure transiently, unmasking the impaired relaxation (true E/A <1).
In restrictive filling, the elevated LA pressure and stiff LV prevent significant changes in the mitral inflow pattern, even with preload reduction.
Summary
Pseudonormal Pattern: Valsalva causes E/A to decrease to <1.
Impaired Relaxation: E/A remains <1 (no change).
Restrictive Filling: Minimal or no change in E/A, remains >2.
How can you calculate LVEDP from AR?
4V² from the AR end diastolic velocity and then DBP - this result = LVEDP in the absence of any significant AS or LVOTO
Similarly, for LAP, it is the SBP - 4V² (from MR)
What are the hallmarks of restrictive cardiomyopathy
Advanced diastolic dysfunction and atrial dilatation in spite of a normal LV size and function
If one wave is present on the mitral valve inflow doppler, how can you tell if it’s an E or an A
There’s a positive relationship between the mitral E wave and pulmonary vein D wave and a negative relationship between the mitral A wave and pulmonary venous D wave.
How do you differentiate hibernating myocardium from non-viable myocardium on stress TTE
Non-Viable (Scarred) Myocardium:
No improvement in wall motion at any dose of dobutamine.
Remains akinetic or hypokinetic throughout stress testing.
Hibernating Myocardium:
Demonstrates improved motion at low doses (viability).
May worsen or plateau at higher doses (ischemia).
How much infarction of a wall will result in RWMA?
20%
Does Q wave mean non-viable?
Up to 40% are still viable in that territory
What does GLS do in a patient with flow limited CAD in a stress TTE
Reduced at baseline
Increases at low-dose
Decreases below baseline at peak stress
If you see LV dilatation on stress TTE, what does that suggest?
Severe, extensive CAD
A lack of distal collateral circulation
What assumptions does the bernouli equation make?
The number 4 in the simplified formula is the approximation of the 1/2p , it assumes a blood mass density of 1060 kg/m3,
however blood mass density is lower when significant anaemia is present which would lead to overestimation of the pressure gradient if the same formula is applied
conditions that increase cardiac output e.g. anaemia, fever, subvalvular AS, significant valvular regurgitation, will increase the inflow velocity V1, which is usually considered negligible, leading to overestimation of pressure gradients
if the LVOT velocity is >1 m/s, can you use 4V²
NO!
You have to use 4 (V2² - V1²)
What are associations with a subaortic membrane?
PDA
PS
Coarctation
VSD
A non calcified with moderate AR - what is the treatment?
Repair, not replacement
The criteria (quantification) for severe AR are
EROA ≥ 0.3 cm2
RF ≥ 50 %
RVol ≥60 ml
VC ≥0.6 cm (best analysed in PLAX)
Jet-to-LVOT width ratio >65%
PHT <200ms
Diastolic flow reversal in the desc aorta
LVEDD>65mm (indexed >31)
What is the calcium score cut off for severe AS
Men ≥2000
Women ≥ 1200
How do you calculate the projected aortic valve area when you can’t achieve a normal flow rate / stroke volume
Formula for Projected AVA
The formula to calculate projected AVA is:
ProjectedAVA = MeasuredAVA + [dAVA/dFlow × (250−ActualFlowRate)]
Where:
Measured AVA: Aortic valve area at the patient’s current flow rate.
dAVA/dFlow: Slope of the relationship between AVA and flow rate, determined during low-dose dobutamine stress echocardiography.
250: Standardized normal flow rate in mL/s.
Actual Flow Rate: Current stroke volume index (SVI) / ejection time.
Steps to Calculate Projected AVA
Measure AVA and Flow Rate:
Use the continuity equation to calculate AVA at baseline and different stages of low-dose dobutamine stress echocardiography.
Flow rate is determined as:
FlowRate(mL/s)
=
StrokeVolume
EjectionTime
FlowRate(mL/s)=
EjectionTime
StrokeVolume
Determine dAVA/dFlow:
Plot AVA against flow rate at multiple stages of stress testing.
Calculate the slope (dAVA/dFlow
dAVA/dFlow) of this relationship.
Normalize to a Flow Rate of 250 mL/s:
Using the formula above, adjust the AVA to what it would be at a flow rate of 250 mL/s.
Interpreting Projected AVA
Severe AS: Projected AVA ≤ 1.0 cm² at a normalized flow rate.
Pseudo-Severe AS: Projected AVA > 1.0 cm², suggesting the low measured AVA was due to low flow rather than true stenosis.
Clinical Use
This method is primarily used in:
Low-flow, low-gradient AS with preserved or reduced LVEF.
Distinguishing pseudo-severe AS from true severe AS when baseline data are ambiguous.
By normalizing flow, the projected AVA helps provide a more accurate assessment of AS severity.
Define LV contractile reserve
Increase in SV by ≥ 20% during dobutamine stress
Just double check that the LV isn’t better during stress because of worsening MR!
Can you calculate SV from Simpson’s biplane?
Yes but better with 3D as 2D has limitations due to foreshortening
SV = [(7 x LVEDD³) / (2.4 + LVEDD)] x LVEF
Make sure you measure below the septal bulge that is frequently seen in AS
You can’t use this method if moderate or more MR is present
What’s another way to calculate projected AVA
Projected AVA = AVA rest + [(AVA peak - AVA rest)/(Q peak - Q rest)] x (250 - Q rest)
Q = SV / ejection time
What are the different groups in patients with normal flow low gradient AS (often labelled as moderate AS)
(1) Patients with moderate AS and measurement error in the SV and thus in the AVA
(2) Patients with moderate AS and a small body surface area therefore while the AVA is small, the indexed AVA is >0.6 cm2/m2, suggesting mod AS
(3) Patients with severe AS with discordant grading due to consistencies in the AVA gradient cut-point values used in the guidelines e.g. AVA of 1cm2 corresponds to a value of 30-35 mmHg not 40 mmHg.
How do you approach someone with moderate AS
(1) exclude measurement error esp LVOT diameter
(2) If patient is symptomatic and SV is low then stress TTE
if SV is normal then CT calcium score
What Nyquist limit should be used in severe AR assessment
50-60 cm/s
In the presence of severe AR, what will the mean AV gradient be?
Overestimated
You can correct the gradient by 4 (V² peak - V² LVOT)
What is the formula for PHT
PHT = 0.29 x deceleration time
What does the Wilkins score take into consideration for, for BMV favourability?
Leaflet mobility
Leaflet thickening
Leaflet calcification
Subvalvular thickening
but NOT subvalvular calcification
How do you calculate the MR regurgitant volume?
MR volume = Mitral stroke volume - Aortic stroke volume
(in the absence of significant AR)
This is because mitral stroke volume = forward flow + regurgitant flow
and the aortic stroke volume = only forward flow
If you dont have the MR velocity when calculating PISA, what can you assume
it is 500 cm/s
You can also assume that the aliasing velocity is set at 30 cm/s or 40 cm/s
What’s a simplified calculation to assess R volume
R Vol = 1.9 x R² x aliasing velocity
(assuming that the ratio between MR TVI and velocity is relatively constant i.e. 1/3.25)
Is PHT reliable in elderly patients with severe degenerative calcific MS?
No
it is influenced by several other factors including diastolic dysfunction, AR (if present)
Coronary spasm can induce
acute severe MR, resulting in flash pulmonary oedema
Acute transient severe MR is also described with DC cardioversion and stress cardiomyopathy
Coronary vasospasm can be induced with metergine infusion
What’s a contraindication to Mitraclip?
Leaflet calcification at the device landing zone (e.g. A2 and P2 scallop calcifications at the valve tip)
What are the optimal aliasing velocity for PISA
30-40 cm/s
What direction is the MR jet in SAM?
Posteriorly
If you see an anteriorly directed jet, think of another MV pathology e.g. flail leaflet
How does heart rate impact transmitral gradients in MS assessment?
Impact of Heart Rate on Gradients
Tachycardia (Increased Heart Rate):
Shortened diastole: Less time for blood to flow through the stenotic mitral valve.
Higher flow velocity: To maintain stroke volume in a reduced filling time, blood must flow faster, increasing the transvalvular gradient.
Effect on Mean Gradient: The mean gradient increases disproportionately, leading to overestimation of the severity of MS.
Bradycardia (Decreased Heart Rate):
Prolonged diastole: More time for blood to flow through the stenotic mitral valve.
Lower flow velocity: Flow rate decreases, reducing the pressure gradient.
Effect on Mean Gradient: The mean gradient decreases, potentially underestimating the severity of MS.
Clinical Implications
Heart Rate Normalization in MS Assessment:
To accurately assess mitral stenosis severity, gradients should be interpreted in the context of the patient’s heart rate.
Ideally, measurements should be performed at a heart rate close to normal physiological rates (~60–80 bpm).
Role of Heart Rate in Exercise or Tachycardia:
During exercise or tachycardia, gradients may increase substantially, reflecting the hemodynamic burden of MS during stress.
Stress echocardiography can reveal latent hemodynamic significance of MS, even if resting gradients appear mild.
Mean Gradient vs. Valve Area:
Unlike the gradient, the calculated mitral valve area (MVA) (via the pressure half-time or continuity equation) is less sensitive to changes in heart rate.
MVA is a more reliable indicator of MS severity, particularly in patients with tachycardia or atrial fibrillation.
BMV cannot be used in patients who
underwent mitral valve repair
What is the formula for R vol
R vol = EROA x VTI
Severe MR due to SAM can occur in
HCM
Hypertensive heart disease with prominent basal septum
Acute anterior infarcts with hyperdynamic compensatory function
Acute ballooning syndrome with hyperdynamic base
The optimal treatment for ischaemic MR is
controversial
repair mod or severe MR at the time of CABG
EROA > 0.25 and or a R vol > 30 ml are associated with a poor outcome
An LVEF <60% is an indication for severe MR intervention
True
The chance of mitral valve repair is higher with which mitral valve leaflet
the posterior mitral valve leaflet
Can you use the bernouli equation to estimate RVSP in severe TR with a flail leaflet?
Not if there’s laminar flow and not turbulent flow as then the RA and RV are just one common chamber really
If you want RVSP, you can try mean and diastolic pulmonary pressures using CW doppler or a cath
What is a gerbode defect
communication between RA and LV
Can be iatrogenic post AV surgery
or post endocarditis
occurs because TV is normally more apical than MV
How do you calculate TVA in TS?
190/PHT
In rheumatic TS, when does doming of the valve occur
in diastole
Doming in systole is reflective of stenosis
Pulmonary artery systolic pressures can be estimated using
TR velocity (4V² + RAP)
or VSD (SBP - 4V²)
or RVOT jet = 79 - (0.45 x RVOT AT)
Mean pulmonary artery systolic pressure can be calculated
by PR jet (4Vmax² + RAP)
What is RVH
> 0.4 cm wall thickness
Is the PA normal in severe PS
Post stenotic dilatation is common altho the PaSP is usually normal
The most common mobile mass on the TV is
A fibroelastoma
myxoma and sarcoma are much less common
Chiari network rarely prolapses through the TV
When does infundibular stenosis occur?
In Fallots,
HCM
RVOT tumours
its high velocity jet can damage the PV resulting in PR
best seen in the parasternal SAX or subcostal views
PV at the infundibulum is accurate but if infundibular stenosis + PS present, difficult to distinguish which one is more important
Are right sided metallic valves implanted?
They are avoided as the RV is a low pressure system so the risk of valve thrombosis is much higher
A homograft is usually the valve of choice
When is Kussmaul’s sign seen? (increase in venous pressure with inspiration)
Constrictive pericarditis
When are giant V waves seen?
TR
When is pulsus paradoxus seen?
≥10 mmHg drop in SBP with inspiration
doesnt occur if hypotensive or regional tamponade
What is pulsus alternans?
alternating strong and weak pulse - seen in end stage LVSD
Upside down W sign is seen when
PH
(mid systolic closure of the PV, about 50% of the cases)
sometimes severe TR with a dilated PA
Fibromas are often in which chamber?
Ventricles
Frequently in the ventricular septum
Often with central calcification (unlike rhabdomyomas)
Usually single
Is bicuspid PS common?
No, dysplastic unicuspid or trileaflet PS is more common
Chest pain can occur (due to coronary ischaemia or RVH)
BPV should be performed in asymptomatic with PG / MG > 60/40 or symptomatic with PG / MG > 50/30
Look at the PV trace and you can see what the RVOT trace is like
The smaller the size of the functional RV in an Ebstein’s anomaly, the
less likely TV repair will be successful.
The septal leaflet is often tethered and can float into the RVOT causing obstruction in some.
ASDs are associated.
If the TR jet is central, what should be the Nyquist limit
50-60 cm/s
What are the criteria for TR severity
> 10 cm² jet area
EROA ≥ 0.4
Rvol ≥ 45
VC > 0.7
PISA radius >9mm (Nyquist 28 cm/s)
Systolic flow reversal in hepatic vein
E wave ≥ 1 cm/s
Definition of aortic valve patient prosthesis mismatch (PPM)
BSA indexed EOA ≤ 0.85 cm2 / m2
Pressure recovery phenomenon tends to occur in
Prosthetic valves (specifically ball and cage and bileaflet valves)
Small aortas (<3cm)
can occur in native valves but mild, and not common
PPM should be suspeced when Vmax is
> 3 m/s
Mitral valve PPM definition
BSA indexed EOA < 1.2 cm2/m2
Check what when assessing for mitral stenosis
Heart rate
Mean gradient of 10 mmHg is v abnormal at HR of 60 bpm
but at a HR of 120 bpm, MG of 10 mmHg can be “normal”
Check BP in MR
Criteria for significant prosthetic aortic valve stenosis:
Peak velocity >4
MG >35
DVI <0.25
EOA <0.8
Rounded, symmetrical contour of the jet velocity
AT > 100
AT is measured - time from base to peak velocity
Criteria for possible prosthetic aortic valve stenosis
Peak velocity >3 m/s
MG >20
DVI <0.29
EOA <1.2
Triangular to intermediate jet
AT >80
What does haemotocrit have to do with high prosthetic valve gradients
Low HCT = anaemia
which can cause high output and thus elevated gradients
Can the PHT be used to calculate the effective orifice area in patients with prosthetic valves?
No - except for serial studies to detect any changes but not by itself.
Suspected prosthetic tricusipid valve stenosis when MG is
> 6 mmHg
What are the criteria for significant prosthetic mitral valve stenosis
Vmax ≥ 2.5
MG > 10
VTI Prosthetic mitral valve / VTI LVO > 2.5
EOA <1
PHT >200
Criteria for possible prosthetic mitral valve stenosis
Vmax >1.9
MG > 5
VTI Pr Mv / VTI LVO >2.1
EOA <2
PHT >129
Vegetations less than what size can easily be missed by TTE
5mm
Unlike TOE which can detect 1mm size vegetations
What’s the differential of a mitral annular abscess?
Caseous calcification - echolucent space within the calcification of the mitral annulus
Other features such as perforation, vegetation, valve dysfunction could point towards it being an abscess than caseous calcification
Define abnormal aortic root thickening that is suspicious of aortic root abscess
> 10 mm
What is the normal thickness of the eustachian valve
3mm
So if it’s >5mm, suspect a vegetation (occurs in 3% of cases)
Use the RV inflow / parasternal short axis views to evaluate
How can you differentiate antiphospholipid syndrome valvular masses from IE?
While the former can be mobile, pedunculated, immobile or broad-based in the setting of leaflet thickening, with heterogenous echogenicity, presenting as multiple lesions at any location on the leaflet (base to tip)
BUT tissue destruction is usually absent in APLA and when present should raise the suspicion of IE
What are the cardiac manifestations of Behcet’s disease
Valvular insufficiency (mostly aortic)
Intracardiac thrombi (in 19%) affecting the right side
MI
EMF
In the setting of acute severe MR
Peak MR gradient increases much higher than the mean MR gradient
When will systolic flow reveral in the PVs not be present in the context of severe MR
Severely dilated LA which is highly complaint and able to accomodate the increased pressure
Or very eccentric jet that is directed away from the PVs
What are the RFs for paravalvular regurg in TAVIs
Too low or high implantation
Low cover index
Greater calcium burden
Self expanding valve
What’s a risk factor for coronary obstruction in TAVI?
Female sex
What factor favours SAVR over TAVI
Severe LVOT calcification
What factors favour TAVI over SAVR
Female sex
Small annulus
Inclusion criteria for the original Mitraclip trial
- Regurgitant jet origin associated with the A2 to P2 segments of the mitral valve
For functional MR
- coaptation length of at least 2mm and a coaptation depth of no more than 11mm
For leaflet flail
- A flail gap <10mm
- Flail width <15mm
What needs to be confirmed prior to release of the Mitraclip
- adequate capture of the anterior and posterior leaflets
- absence of a high (typically >6mm) gradient
- Adequate mitral valve area (>2cm2)
- The MR severity reduced
What is a contraindication to LAA closure
Valvular Afib
What’s the most common complication of Watchman device?
Significant / serious pericardial effusion
Percutaneous closure of prosthetic paravalvular regurg is contraindicated in
active endocarditis
dehiscence involving more than 25% of the valve ring
How soon after BMW can you use PHT to calculate MVA
1-2 days
What is a successful BMW
≥50% increase in MWA
Final area ≥1.5 cm2
no more than Grade 1 MR
often a >50% decrease in MG
What are factors which predict a greater likelihood of improvement in LV function in DCM
Improvement in LV sphericity index in response to dobutamine
RWMA as opposed to global hypokinesis
Increased LV mass
Cardiac sarcoidosis is associated with
Basal septal thinning
LV and RV aneurysms (basal inferolateral and LV apical segments are the most common)
What are very specific signs of previous radiotherapy
Aorto-mitral curtain thickening or calcification
Calcification in the aortic sinuses
Radiotherapy adverse effects typically occur 15-20 years after radiotherapy
Recovery of LV function with dobutamine in peripartum cardiomyopathy (and maintenance of normal LV function while on dobutamine) suggests
low risk of reoccurrence of peripartum cardiomyopathy with subsequent pregnancies
Define apical HCM
LV apex >15mm
Apical to posterior wall thickness ratio >1.5
In apical HCM, it can either be the isolated or the mixed form.
In the isolated form, LVIDD is usually normal, as is the LVEF.
What RWT is consistent with athletic heart
<0.6 (or <0.5 in some studies)
What’s the cut off for RWT concentric
> 0.42
How can you assess severity of AR in an LVAD heart?
VC
Jet width
Regurg duration e.g. holosystolic and holodiastolic
You can’t use PHT or flow reversal in the desc aorta
Which of the nutritional deficiencies causes high output HF
Thiamine deficiency
Selenium deficiency can cause
DCM
Seen in TPN patients
It’s reversible by giving selenium
RWMAs are typically seen in
infiltrative conditions such as GPA or sarcoidosis
Amyloid frequently causes
Non dilated HFrEF
What are the common cardiac manifestations of RA
CAD (showing as RWMA)
Diastolic dysfunction
What factors should make you think of constrictive pericarditis
Previous cardiac surgery
Prior radiation therapy
What type of diastolic flow reversal in the hepatic veins are seen in constrictive pericarditis
expiratory
in restrictive cardiomyopathy, inspiratory diastolic flow reversal is seen
Hypereosinophilic syndrome is associated with
restricted posterior mitral leaflet motion from inferobasal endocardial thickening
Is septal bounce unique to constrictive pericarditis?
No, it can occur post cardiac surgery, in severe RV volume overload ..
Are septal bounce and respiratory variation of the IVS the same?
No, septal bounce is respiration independent, and reflects the rapid equilibration of ventricular pressures during early diastole - septum suddenly shifts
Differentiate constrictive pericarditis from COPD
COPD doesnt have restrictive diastology on mitral inflow
Also inspiration causes a significant increase in SVC systolic flow velocity in COPD, but not in constrictive pericarditis
The mitral and tricuspid flow variation with respiration in CP is not as intense as tamponade
true
A lack of typical respiratory flow velocity changes should not exclude the diagnosis of constrictive pericarditis because up to 50% of patients with it may not meet these criteria
You can do things like head up tilt, sitting or diuresis to reduce preload to unmask any doppler velocity changes
Is GLS reduced in CP
Not really
but GCS usually is
What part of the cardiac cycle are aortic measurements taken in?
End-diastole
with the exception of the aortic annulus, which is measured in mid systole
How do you distinguish true from false lumen in aortic dissection?
True lumen is generally the smaller lumen that receives brisk systolic antegrade flow and expands during systole
The false lumen is generally the larger lumen but is compressed during systole and receives reduced systolic antegrade flow which is delayed and lower in velocity
What’s the definition of aortic aneurysm
At least 1.5 times greater than the normal expected size
less than this is ectasia
The diameter of the sinus of Valsalva is about 0.2 cm in men and 0.1 cm in women greater in size than the tubular ascending aortic diameter.
If the tubular ascending aortic diameter is significantly greater in size than the sinus than that is a pathological process.
What is the shone complex
4 obstructive lesions
(1) Supravalvular mitral ring
(2) Parachute like mitral valve
(3) Subaortic stenosis
(4) Aortic coarctation
Valvular AS and bicuspid aortic valve may also occur
What’s the most common cardiac defect in Noonan’s
PS
HCM
Are quadricuspid valves commonly associated with dissection, aneurysms, coarctation
No just severe AR
Altho unicuspid valves are commonly associated with aneurysms
In the AF population, at least moderate mitral regurgitation has been shown to be protective for clinical stroke
true
Spontaneous echo contrast is more common in AFib than Aflutter
True
How do you differentiate cor triatriatrium vs supravalvular mitral ring?
LAA is in the distal (mitral valve) atrial chamber but it’s in the proximal (PV) atrial chamber in supravalvular mitral ring
Eustachian valve vs Chiari network
Eustachian valve (remnant of the valve of IVC to direct flow into LA) is usually immobile (occasionally can show independent motion)
Chiari network (valve of the coronary sinus) is highly mobile, membranous structure arising near the orifice of the IVC
When does PV stenosis occur
IF it occurs, 2-5 months post PVI
PW doppler at the ostium of the PV shows elevated velocities and spectral broadening both in systole and diastole
Can hepatic vein systolic flow reversal occur in settings other than severe TR?
Yes, significant RV dysfunction by itself.
Also in severe TR, you can just get systolic blunting - don’t always get systolic flow reversal which is typically late peaking
What are the features of mechanical tricuspid stenosis
PHT ≥ 230 ms (although cant always measure PHT e.g. rounded contour )
In the absence of high output state e.g. sepsis, anaemia, hyperthyroidism, a MG ≥ 6 mmHg and/or velocity > 1.7 m/s are supportive of mTVRs
What is suggestive of raised RVEDP
Tricupsid E/A ratio >2.1, deceleration <120ms
Late diastolic antegrade flow in the PA
(I’m not sure if the first two are cut-offs)
Hepatic veins cannot be used to predict RAP in
TS or TR
Pericardial compression syndromes
high grade AV block
Heart transplants
but not restrictive cardiomyopathy
What are the RV features of advanced restrictive cardiomyopathy
RVH >7mm
Tricuspid inflow shows a restrictive filling pattern
Hepatic vein flow shows reduced forward systolic flow / increased diastolic flow and inspiratory diastolic atrial flow reversal
What does 1cm JVP correspond to ?
0.7 mmHg
therefore 15cm JVP corresponds to 10 mmHg in the RA
What’s the formula for PVR
PVR = [TR velocity / RVOT VTI] * 10
Formula for mean PA pressure
Mean PA pressure = PA diastolic pressure + 1/3 x pulse pressure
or
(PA systolic pressure + 2 x PA diastolic pressure)/3
How else can calculate mean PA pressure
80 - 0.5 (acceleration time)
What does hepatic vein show in PR
Predominant diastolic forward flow
(not systolic reversal)
In severe PS you will see
A prominent A reversal signal in the hepatic veins, after RA contraction
These patients will have a D shaped septum in systole and diastole
Severe PR does not lead to increased RVSP because
it increases diastolic pressure
overtime maybe through RV systolic dysfunction
Fibroelastomas…
Valve dysfunction is rare
Can occur on any valve
Rarely, they can occur on papillary muscle, chordae, atria
Largest reported is 40mm
Median size 8mm
Short pedicle is seen 50% of the time
Myxomas
can occassionally be found on the posterior wall of the LA altho
this should raise suspicion of a malignant tumour (think of the v malignant and poor outcome leiomyosarcomas which originate from the PVs, and present in patients in their 30s)
Leiomyosarcomas have a preference for LA
Angiosarcomas prefer RA (most cardiac tumours prefer the R heart)
Mechanical valves were, for some time, favoured in right sided carcinoid heart disease
because there were concerns that the vasoactive substances would wreck the bioprosthetic valve
but with better carcinoid treatment this of less concern
also with the liver problems, and subsequent coagulation issues, bioprosthetic valves may be favoured
Cardiac melanoma is involved in more than
50% of cases with metastatic melanoma
Ventricular compliance (i.e. RV being more compliant than the LV) is the most important factor in dictating the direction of an ASD shunt
true
In a septum primum ASD, the AV valves insert at the same level
true
Primum ASD is associated with a cleft mitral valve
Pressure gradient =
Pressure gradient = flow x resistance
Nyquist limit
Nyquist limit = PRF/2
PRF =
PRF = 77,000 (cm/s) / imaging depth (cm)
PRP =
PRP = (micros) = imaging depth (cm) x 13 (micros/cm)
Duty factor (%) =
Duty factor (%) = pulse duration / pulse repetition period x 100
Impedance =
Impedance = density x propagation
Pulse duration =
Pulse duration = cycles / frequency
Intensity =
Intensity = power/beam area
Wavelength =
Wavelength = 1.54 (mm/micros) / frequency (MHz)
Propagation speed =
Propagation speed = frequency x wavelength
MI =
MI = peak (-) pressure / square root of frequency
Flow =
Flow = CSA x velocity
Use the modified Bernouli equation if V1 is
> 1.5 m/s
LVSP =
LVSP = 4V² (MR Vmax) + LAP
LVEDP =
LVEDP = DBP - 4V² (AR end diastolic velocity)
LV mass =
LVM = 0.8 x 1.04[(LVIDD + IVS + PWD)³ - LVIDD³)] + 0.6 g
LAP =
LAP = E/e’ + 4
LAP=
LAP = 1.24 x E/e’ + 1.9
RVSP = 4V² (TR Vmax) + RAP
true
RVSP =
RVSP = SBP - 4V² (VSD Vmax)
RVEDP =
RVEDP = LVEDP - 4V² (VSD diastolic velocity)
RV fractional change =
RV FAC = ED area - ES area / ED area x 100 (normal is 35% or more)
PASP =
PASP = 4V² (TR V max) + RAP
PAEDP =
PAEDP = 4V² (PR end diastolic velocity) + RAP
Mean PAP =
Mean PAP = PASP + 2/3 x PADP
Mean PAP =
Mean PAP = Pulmonary artery pulse pressure/3 + PADP
Mean PAP =
Mean PAP = 80 - (0.5 x RVOT acceleration time)
Mean PAP =
Mean PAP = 4V² (PR peak diastolic velocity) + RAP
Mean PAP =
Mean PAP = VTI mean gradient TR + RAP
Mean PAP =
Mean PAP = 0.6 x PASP
PVR =
PVR = (TR V max / VTI RVOT) x 10 = 0.16
PVR =
PVR = (mPAP - mPCWP)/CO
AV mean systolic gradient =
0.6 x Peak gradient
EROA =
EROA = Regurgitant flow / V (AR max)
EROA =
EROA = Regurgitant volume / VTI (AR)
Regurgitant volume =
Rvol = EROA x VTI AR
Regurgitant vol =
Rvol = SV LVOT - SV mitral (if competent)
R fraction =
R fraction = SV LVOT - SV mitral (if competent) / SV LVOT
MVA =
MVA = PHT/220 or 759/DT
PISA: MVA =
PISA: MVA = 2π² x V aliasing / Vmax MS
MVA =
MVA = CSA x VTI LVOT / VTI mitral
