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incorporat ing the BSE NEWSLETTER

NOVEMBER 2013ISSUE 84

Aff i l iated to the Br i t ish Cardiovascular Society

CONTENTS include:Tricuspid Valve Leaflet Recognition5 - 7Atrial Septal Aneurysms8 - 9Late Diastolic Signal10 - 12Front Cover12Circulation not as we know it13 - 14New Guidelines: Diastolic Dysfunction15 - 20Critical Care Echocardiography21 - 24European Cardiovascular Imaging25FEEL-UK28

BSE_ECHO_No84 V1:BSE_FEB_No58 18/11/13 17:30

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CONTENTSNOVEMBER 2013ISSUE 84

ECHO 2012/13 BSE COUNCIL MEMBERSOFFICERSPresident: Dr Guy Lloyd Eastbourne DGHImmediate Past President:Dr Navroz Masani University Hospital of WalesVice President:Jane Allen York Teaching HospitalHonorary Secretary:Jude Skipper Queen’s Hospital, EssexHonorary Treasurer:Tracy Ryan Walsall Manor DGH

ELECTED MEMBERS Gurpal Bhogal Russells Hall Hospital, DudleyDr Adelle Dawson Ninewells Hospital, DundeeDr P Rachael James Royal Sussex County HospitalJane Lynch Wythenshawe Hospital, ManchesterDr Jamil Mayet St Mary’s Hospital, LondonDr Thomas Mathew Nottingham City HospitalDr Jim Newton John Radcliffe Hospital, OxfordKeith Pearce Wythenshawe Hospital, ManchesterDr Bushra Rana Papworth HospitalDr Rick Steeds University Hospital, Birmingham

CO-OPTED MEMBERS (1 year term)Dr Chris Eggett SCST Representative, Freeman Hospital

NewcastleDr Nick Fletcher ACTA Representative, St.

George’s Hospital, LondonDr Mark Monaghan Kings College Hospital, LondonDr Muttucumarasamy Mahendran Primary Care

Representative, Milton Keynes Helen Rimington Academy of Healthcare Science

RepresentativeNicky Mills Industry Representative, Bracco UKDr Rizwan Sarwar Jr Dr Representative, John Radcliffe

Hospital, OxfordGill Wharton Academy CVRSGUI Professional Group

Representative

Dr Gordon Williams ECHO Editor York Teaching Hospital

INSTRUCTIONS TO AUTHORSECHO is published four times per year. It is the official publication of the British Society of Echocardiography the contact addressis: BSE Administration, Docklands Business Centre, 10-16 Tiller Road, Docklands, London E14 8PX, Tel. 020 7345 5185, Fax 0207345 5186 Email [email protected]. Members of the society are invited to submit articles, case reports or letter correspondence.

Submissions should be to ‘The Editor’, ECHO and forwarded by email to: [email protected] and copied to [email protected] .The format should be text as a normal word document and images supplied as high resolution jpeg, tiff, eps or pdf files. Otherformats including powerpoint or of web image construction may result in reduced resolution and may be unacceptable.

Articles should contain appropriate references. References to be constructed with the first two authors, thereafter abbreviate to ‘etal’, then article title, followed by journal reference.

Submissions to ECHO are currently not peer reviewed but may soon become so, changes will be advised. The Editor has discretionon acceptance. Patient consent is required for case reports.

It should be noted that opinions expressed in articles or letters are the opinions of the author(s) and not of the council of the BritishSociety of Echocardiography (BSE). Official BSE council views or statements will be identified as such.

Information in respect of advertisements can be obtained from [email protected].

Editor

Page 4 Presidents MessagePage 5 - 7 Tricuspid Valve Leaflet Recognition. Not what You May ThinkPage 8 - 9 Atrial Septal Aneurysms. Benign or Otherwise?Page 10 - 12 A Late Diastolic Signal in the Left Ventricular Outflow

Tract Augmented by Valsalva ManoeuvrePage 12 Front CoverPage 13 - 14 The Circulation but not as we know itPage 15 - 20 New Guidelines: A Guideline Protocol for the

Echocardiographic assessment of Diastolic DysfunctionPage 21 - 24 Critical Care EchocardiographyPage 25 European Association of Cardiovascular Imaging (EACVI)Page 26 - 27 BSE Annual Clinical and Scientific Meeting Liverpool

2013 - Delegate ReviewPage 28 Focused Echocardiography in Emergency Life Support

(FEEL-UK) - Could you be a Mentor?Page 29 - 31 Case Reports 1 BSE Accreditation Process UpdatePage 32 BSE Clinical Practice ForumPage 33 BSE Departmental AccreditationPage 34 Scrambled EchoesPage 35 Recently Accredited MembersPage 36 Dates for your Diary

BSE_ECHO_No84 V1:BSE_FEB_No58 18/11/13 17:30 Page 3

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PRESIDENT’SMESSAGE

Portable ultrasound devices, electronicstethoscopes or an invitation to mayhem?

When the facts change, I change my mind;what do you do? - Attributed to JohnMaynard- Keynes

The fact in question is that the hand held ultrasound device has

been invented, produced and sold at a relatively affordable

price, which is likely to drop further. We, in the echo

community, can do nothing about this. The question now turns

to how we respond to it! Everyone will have noticed that

interested parties are going out into the marketplace and simply

buying them with no reference to the echo department. In my

own institution one of my interventional colleagues turned up

with one. "What do you want with that?", I asked. He replied

"I want to look for pericardial effusions". "Oh no you don't", I

thought, "that is the job of the echo department". But actually

he was quite right and I was wrong, defensive and not acting in

the best interest of patients. To use a hand held device is a

wholly sensible thing to do because it rules in (or out) an

extreme pathology so much better than any other available test,

even in relatively inexpert hands.

There is a large literature to support the observation that doctors

are very bad at eliciting physical signs at all grades. This may

be as a result of shorter training and less clinical exposure, or

perhaps they were never up to much, but there was no way of

checking. Recent publications on hand held devices have

clearly shown that when they are used the chance of getting the

diagnosis right is much higher than using a stethoscope. So

they should be used, not as a replacement for a full echo, which

will always be required, but rather at the point of first contact,

to ensure the examining doctor is on the right track.

There is a fine philosophical line between this type of use and a

screening echo, to which I and BSE has always been opposed,

outside of certain specified areas. The electronic stethoscope

should be solely used to make sure the treatment is directed on

the right lines pending confirmatory tests, exactly like the

stethoscope. Take two examples that occur relatively

commonly; firstly the patient admitted with breathlessness the

admitting doctor, using his or her ears, cannot decide whether

this is heart failure, asthma or infection (a very common

scenario). The electronic stethoscope is deployed which

demonstrates a hyperdynamic heart with normal right and left

ventricles and no valve problems. The patient is then saved the

incorrect initial treatment of frusicillin (the imprecise cocktail

of antibiotics and diuretics) and it can be questioned whether an

echo is required if nothing else points to heart disease. This

patient hasn't had a screening echo, just a better diagnosis.

Likewise the patient who presents breathlessness and is noted to

have a loud systolic murmur. The house officer and registrar do

not agree whether it is mitral regurgitation or aortic stenosis, the

consultant wades in concerned about a VSD. This debate

simply need not occur, just have a look and see, get the patient

on treatment and then organise an echo to confirm and grade the

pathology. A screening echo approach on the other hand would

take a patient presenting with suspected heart failure and aim to

exclude or confirm the diagnosis. This position is fraught with

potential pitfalls of which we are all aware (the case of amyloid

or severe AS). So the key difference is that screening echo is

designed to make a diagnosis and divert people away from a

perceived unnecessary echo, while the ultrasound stethoscope is

simply there to firm up a clinical diagnosis before a definitive

test.

To see every health care professional examining the heart with

an ultrasound seems to run contrary to everything we stand for

in terms of quality and consistency. But the echo community is

going to have to face some difficult facts here. Hand held

ultrasonography is now entering the curriculum for medical

students, our own collaboration with the Intensive Care Society,

FICE, is heading for the core curriculum for ITU trainees. I

believe (and this is a personal belief and not the official position

of BSE) that if we as a society and a profession are to remain

relevant we need to keep engaged and indeed lead the process.

Defining simple patterns which help the clinicians to recognise

major heart pathologies, making them achievable, ensuring that

they have been achieved, and perhaps most important

continuing to emphasise the limitations of the technique, is

something that we can do. Nobody knows more about cardiac

ultrasound than we do.

Patients will always need an echo, it is the definitive test for

structural heart disease, the ultrasound stethoscope does not

change this in anyway. It may however over the next decade,

overturn the way a doctor makes a diagnosis at the bedside and

perhaps patients will get to us in better shape. Our choice now

lies between engaging and making the running or raising the

drawbridge; unfortunately they are already over the castle walls!

Guy Lloyd, President


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TRICUSPID VALVE LEAFLET RECOGNITIONNot what You May Think

Introduction

When training our students in transthoracic echocardiography,

we expect them to learn to identify normal and abnormal

cardiac structure and function as seen in the various imaging

planes. Usual questions put to the student are to name the aortic

valve cusps in the parasternal long and short axis, or the mitral

leaflets from apical four chamber view. How often do we ask

which tricuspid leaflets are visible in the various transthoracic

planes? How much can we remember about tricuspid valve

structure and function? This is a just a little refresher for those

that need it as I did when quizzed by a student on this subject

recently.

Anatomy of the Tricuspid Valve

The tricuspid valve is normally situated between the atrium and

the ventricle of the right side of the heart. It is usually the most

apically placed valve with the largest orifice (valve area is

usually 4-6 cm2 (1, 2)) and with a thickness of less than 3mm 3.

The tricuspid valve apparatus includes leaflets, chordae,

papillary muscles and a fibrous annulus. The three leaflets are

called anterior, posterior and septal. The anterior leaflet is the

largest of the three, and usually semicircular (may be

quadrangular). The posterior leaflet is of intermediate size and

is usually semi-circular and has a scalloped appearance (number

of scallops vary) 4, 5. The septal leaflet is semi-oval. It is usually

the smallest 1, 6 although there are differences of opinion where

some maintain the posterior is smallest 7, 8. Silver et al (1971)

performed a study involving dissecting normal hearts, and

reading their data on leaflet size, the posterior leaflet can be

smaller (on average) than the septal leaflet when it consists of a

single scallop, otherwise (when it is made up of several

scallops) it is larger than the septal leaflet 1.

The tricuspid annulus is oval in shape and becomes circular

when dilated. It expands in diastole and constricts in mid-

systole 9. The septal leaflet has part of its basal attachment to

the posterior wall of the RV, but mostly to the septal wall with

its base inserted obliquely across the membranous

interventricular septum, slightly more apically placed relative to

the septal insertion of the anterior mitral leaflet. The anterior

and posterior leaflets arise from their respective aspects of the

annulus 4.

The leaflets are attached by chordae to papillary muscles.

Usually there are three sets, each composed of up to three

muscles. The variability of the papillary muscles is a normal

characteristic of the tricuspid valve where usually two or three

can be seen, but can be up to as many as nine 10.

The chordae tendinae arising from each set are inserted into two

adjacent leaflets. There is disagreement as to which muscles

insert chordae into which leaflets. The anterior papillary muscle

is claimed to insert chordae into the septal and anterior leaflets9, alternately it is claimed that its attachments are to the anterior

and posterior leaflets (1). If the latter is true, then the medial

papillary muscle set inserts chordae into the posterior and septal

leaflets. The septal wall (and it is notable that there is no true

papillary muscle associated with the septal wall) inserts chordae

into the anterior and septal leaflets.

2D Echocardiography

When imaging the tricuspid valve, there are several views that

demonstrate the leaflets. These are the parasternal long axis

view of RV inflow (obtained through medial and posterior

angulation of the transducer probe), the parasternal short axis

view at the level of the aortic valve and the apical four chamber

view. There are also the subcostal four chamber and short axis

views which display the same leaflets as their respective apical

and parasternal counterparts 9.

Using 2D echocardiography usually only two of the three

leaflets can be seen in any one view. Over the years there has

been disagreement in the identification of leaflets seen in each

2D view, but the development of three-dimensional imaging has

provided the ability to image all three leaflets, their attachments

to the annulus and placements with regard to 2D scanning

planes. Recent studies have recreated these standard 2D views

using three-dimensional imaging 2.

Fig. 1. Apical 4 Chamber view. Tricuspid leaflets highlightedin this and all subsequent images. See text for explanations.

The consensus opinion of tricuspid leaflet nomenclature from

the apical 4 chamber view is that it shows the septal leaflet


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adjacent to the septum, and the anterior leaflet adjacent to the

RV free wall 2, 5, 6, 9, 11. However, Otto describes the leaflet

adjacent to the RV free wall in this view as either anterior or

posterior depending on the angle and rotation of image ..

Figure 2. Parasternal Short Axis View.

In the parasternal short axis view (when visualized) it is the

posterior leaflet seen adjacent to the RV free wall. The leaflet

adjacent to the aorta is roughly split 50/50 between septal and

anterior leaflet 2, 13.

Conversely, in both the Feigenbaum and Anderson textbooks,

and according to the ASE guidelines 11, the leaflet adjacent to

the RV free wall in this view is labeled as anterior, with the

septal leaflet visualized medially 6, 14. Interestingly, the EAE

textbook 9 agreed with this in the text, however this may be a

typo as the figure shown was contradictory and also the

reference used (and chapter written by) was from Anwar 2 .

Figure 3. Parasternal Long Axis View of RV inflow(posterior/inferior free wall)

In the parasternal long axis right ventricular inflow view the

anterior and posterior leaflets are seen 5, 6, 11, 14. However, Anwar

and the EAE claim that it is the septal leaflet seen associated

with the inferior wall and the anterior leaflet associated with the

anterior RV free wall 2, 9.

Figure 4. Parasternal Long Axis View of RV inflow (septalwall)

However, it is worth noting that when obtaining this view it is

sometimes the case that the septum is seen, and may not show

the RV posterior/inferior free wall and hence the septal leaflet

rather than posterior may be seen 8.

Unusually, in the parasternal short axis view midway between

the papillary muscle and mitral valve level all three leaflets may

be seen (more often in a dilated RV) 9.

Concluding Summary

In conclusion, the literature remains confusing and complex.

What at first sight may appear straight forward is confounded

by differing opinions in tricuspid leaflet nomenclature

particularly between the recent guidelines published by the

American Society of Echocardiography (Rudski et al 2010) 11

and the official textbook of the European Association of

Echocardiography (Galiuto et al 2011) 9.

It is interesting that the tricuspid valve has been visualised on

real-time Echocardiography for nearly 40 years and yet there

are still some disagreements with regard to leaflet recognition

and nomenclature. The following set of images (fig. 5) may

provide some help in both the present state of disagreement and

possible ways of clarification. The parasternal long axis RV

inflow views could depict either the posterior or septal leaflet

but by slightly modifying the imaging plane it very probably

depicts the septal leaflet. This may be one practical way of

resolving that issue. In the apical 4 chamber and sub costal long

axis views there is agreement that it is the anterior and septal

leaflets visualised with no dispute. However, the subcostal short

axis view depicts leaflets which are not agreed. As indicated, a

slight change to a parasternal short axis view may depict the

anterior and septal or possibly the posterior and anterior or

septal. It clearly is an issue which one would expect to be

clarified. We await definitive agreement and clarity but in the

meantime it highlights again the complexities of nature.


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Stuart Self, York teaching Hospitals

References

1. Rogers, JH and Bolling, SF. The tricuspid valve: current

perspective and evolving management of tricuspid

regurgitation. Circulation. May 26 2009;119(20):2718-25

2. Anwar, AM, Geleijnse ML, Soliman OII et al. 2007,

Assessment of the Tricuspid valve anatomy in adults by real-

time three-dimensional echocardiography, Int J Cardiovasc

Imaging 23:717-724

3. Crawford MH, Roldan CA. Quantitative assessment of valve

thickness in normal subjects by transesophageal

echocardiography. Am J Cardiol 2001; 87:1419

4. Silver et al, 1971 Morphology of the Human Tricuspid valve,

Circulation, 43-333-348

5. Brown, A and Anderson, V. 1983 Two dimensional

echocardiography and the tricuspid valve: leaflet definition

and prolapse, Br Heart J 49:495-500

6. Feigenbaum H, Armstrong WF, Ryan T. Tricuspid and

Pulmonary Valves. In: Feigenbaum H, ed. Feigenbaum's

Echocardiography. 6th ed. Philadelphia, PA: Lippincott

Williams and Wilkins; 2005; 362.

7. Ports TA, Silverman NH, Schiller NB. Two-dimensional

echocardiographic assessment of Ebstein's anomaly.

Circulation 1978:58:336-43.

8. Wigers SE, PlappertT, St John Sutton M; Echocardiography in

practice- a case oriented approach; 2001, Martin Dunitz Ltd

9. Galiuto L, Badano L, Fox K, Sicari R and Zamorano JL. The

EAE Textbook of Echocardiography; Oxford Medicine, Mar

2011.

The European Society of Cardiology Textbooks

10. Aktas EO, Govsa F, Kocak A, Boydak B, Yavuz IC.

Variations in the papillary muscles of normal tricuspid valve

and their clinical relevance in medicolegal autopsies. SaudiMed J. Sep 2004;25(9):1176-85.

11. Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher

MD, Chandrasekaran K, Solomon SD, Louie EK, Schiller

NB. Guidelines for the echocardiographic assessment of the

right heart in adults: a report from the American Society of

Echocardiography endorsed by the European Association of

Echocardiography, a registered branch of the European

Society of Cardiology, and the Canadian Society of

Echocardiography. J Am Soc Echocardiogr. 2010; 23(7):685-

713.

12. Otto C. Textbook of clinical echocardiography. 3rd ed.

Philadelphia: WB Saunders; 2004

13. Tei C, Shah PM, Cherian G, et al. Echocardiographic

evaluation of normal and prolapsed tricuspid valve leaflets.

Am J Cardiol. 1983; 52(7):796.

14. Anderson, B. Echocardiography: The normal examination

and echocardiographic measurements; 2000, 1st edn; MGA

Graphics, Australia)

Figure 5. Examples of various views with different scenarios of leaflet identification (see text)


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ATRIAL SEPTAL ANEURYSMSBENIGN OR OTHERWISE ?An atrial septal aneurysm (ASA) is best described as a localisedsaccular deformity of the atrial septum, predominantly central,involving the area of the fossa ovalis. The central septumbecomes hypermobile, protruding either towards the left atrium(LA or right atrium RA) or oscillating between both.

An ASA is generally considered to be due to redundant atrialseptal tissue, and that in turn possibly related to an inherent,inherited connective tissue deficiency. ASA’s have beendetected in foetal cardiac ultrasound scans and in new borninfants although the majority are detected in adulthood.Thatthere is a possible connective tissue relationship gains supportfrom the association of ASA’s with other connective tissueconditions, principally Marfan’s syndrome or mitral valveprolapse and occasionally sinus venosus aortic aneurysms, allconditions where an ASA is occasionally seen. Theseassociations suggest a possible causal link with an ASA but theyare not at present definitive relationships.

Similar, rather vague but possible relationships with otherpathologies have been postulated as explanations for why anASA may bulge predominantly to the left or the right.Principal examples of this are right heart overload states, e.g.pulmonary hypertension where the ASA bulges to the leftatrium and conditions in which the left atrial pressure iselevated e.g. mitral regurgitation where the ASA may bulgepredominantly to the right. The question of whether an atrialseptum is hypermobile or not and whether it is sufficiemtlyabnormal to be described as an aneurysm requires somediagnostic criteria.The initial requirement was for the centralatrial septum to bulge to 10 mm either to the left or the right ofthe central line of the atrial septum in an apical 4 chamber viewor if it exceeded 10 mm with a bi-directional excursion.Confirmation of the bulging may be obtained in sub-costal andparasternal views. The movements or oscillations of the atrialseptum should occur throughout the cardio-respiratory cycle.This basic approach has been taken to a more detailed andarguably too complex list of diagnostic catagories published inthe Journal of American Society of Echo in 1997 I

That definition labelled an ASA as follows:

Type 1 R where the ASA protrudes to the right throughout thecardiorespiratory cycle.

Type 2 L where the ASA protrudes to the left throughout thecardiac cycle

Type 3 R L where the maximum excursion of the ASA istowards the right atrium with the lesser movement towardsthe left atrium.

Type 4 L R the opposite of the above

Type 5 the ASA movement is bi-directional and equidistant tothe right and the left during the cardiorespiratory cycle.

It may not always be practical to allocate a patient specificallyto one of these categories but even if it is, there is a question ofrelevance in that association with other pathologies and specificpatient management may not vary regardless of the category ofASA movement.

Regardless of any accompanying pathology, which may or maynot be present or recognizable, the ASA itself may be associatedwith an atrial septal defect. This may be in the form of apotential atrial communication a patent foramen ovale (PFO) oran overt atrial defect either of the secundum type or multipleatrial defects. The reason for requesting an Echo in a patientwith an ASA may have originated due to the patient suffering acerebrovascular accident or transient cerebral ischaemic episodeor some subtle probable cerebral presentation. The frequency ofsuch requests has been such that it is generally accepted that anASA is causally related to cerebral embolic events. If an ASA isdetected, confirmation of the atrial septum being intact orotherwise is required and this usually is confirmed by a bubblecontrast Echo study. Should a cerebral event have occurred andthe presence of an ASA is debatable, the diagnostic accuracy ofa TOE study is significantly greater than transthoracic imagingin ASA detection. A TOE may be indicated as part of theinvestigation of a cerebral episode to exclude a left atrialthrombus and in the same study attention can be directed to thestatus of the atrial septum in respect of aneurysmal movement.If the atrial septum is intact and no pathology detected otherthan an ASA, the ASA may still be relevant with clinicalpractice being to treat with anti-platelet therapy if a cerebralincident has occurred.

Given the difficulty of recognising an ASA at Post Mortem(unless it is overt) in that it requires dynamic movement to berecognised and given the diagnostic capability of real timeechocardiography, the question of incidence arises. There areseveral studies addressing this question. That of Olivares-Reyes1

is being one of the larger in that 22,224 consecutive adult echostudies were reviewed for the presence of an ASA which wasdetected in 500 patients giving a prevalence of 2.2%. Theauthors also report the incidence of associated medical conditions.There was a predominance of ASA’s in females (63%).

Fig. 1. A4C views with a mobile ASA bulging alternately intothe RA and LA

Fig. 2. A 3-D image of an ASA bulging into the RA (leftimage) and a post mortem specimen of an ASA bulgingsimilarly.


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The vast majority of ASA’s are of the type described withhypermobility of the central atrial septum, there are reportedexceptions and rare presentations. The medical literature ispeppered with case reports of unusual presentations andchallenging Echo findings.

An aneurysm, if large enough, can occasionally if its neck isrelatively small encase slow moving blood. As such an ASA cancontain spontaneous contrast reflecting the slow bloodmovement but this containment of spontaneous contrast movingbetween the atria may not be readily recognizable, at leasttransthoracically and require a TOE study for clarification. Afurther development of this is for an ASA to contain blood clot.Such a mobile thrombus oscillating in either or both atria beingEcho reflective may readily give the impression of a tumourwith the commonest mis-diagnosis being a myxoma

There are other variations where a very large ASA, so calledgiant septal aneurysm may mimic a left atrial mass andsimilarly such a large ASA if bulging to the right may mimic aright atrial tumour. Given that the aneurysm may not containblood or may not contain thrombus these giant atrial septalaneurysms may mimic a cystic tumour in that they areencapsulated, the capsule being the thin aneurysmal atrial septaltissue. There are isolated reports of these giant atrial aneurysmsprolapsing and causing intermittent obstruction to flow througheither the mitral or tricuspid valves.

Reference has been made to patients with an ASA presentingwith a cerebral embolic or ischaemic episode and whilstcerebral events are the commonest as a consequence of acardiac source of emboli, embolization can occur in other partsand there are case reports of acute renal pain when after

thorough investigation no other explanation was forthcomingother than the presence of an atrial septal aneurysm which waspresumed to the source of embolus. There are other reports ofabdominal or distal limb embolic events where again only anASA was found as the probable explanation.

Atrial arrhythmias are known to be associated with the presenceof ASA’s and this association has been noted, even in foetal lifeRice 2 reported a high incidence of ASA’s detected on foetalstudies in foetus’s with atrial arrhythmias. In the adult, ASA’sare recognised to have an association with atrial fibrillationraising another intriguing situation of whether a cerebralembolic event in someone with atrial fibrillation in respect ofwhether the source was related purely to the AF or the ASA.

Although not aneurysmal there are other pathologies which canaffect the atrial septum and may be either recognisableparticularly on TOE study or be related to thrombotic events. Irefer to the fact that the atrial septum can undergo dissection.This is relatively rare and not a spontaneous event but can beassociated with mitral valve surgery. A rare congenital atrialseptal abnormality is an atrial septal pouch where there isincomplete fusion of the lower part of the atrial septum( theseptum primum) and the septum secundum resulting in aninverted pouch like structure the base opening either into theleft or the right atrium. This atrial septal pouch, rare though itis, has been recognised to be a source of intra-cardiac thrombus.

There is minimal literature in respect of the long-term follow-upof atrial septal aneurysms once recognised but Shinohara (ref 3)does report the follow-up of an ASA which later developedspontaneous contrast and later still developed the appearancesof a mobile thrombus within the aneurysm. This raises thequestion in respect of whether an ASA is a benign finding.There has been an attitude that it is benign and little noticetaken of an ASA other than perhaps the recognition of beingassociated with embolization and treatment with anti-plateletdrugs but there is a growing body of literature, mainly fromisolated case reports, of ASA’s progressing in terms of structuraland functional abnormalities such that it is I believe reasonablenow to consider that an ASA is not a benign incidental finding.

Gordon WilliamsEditor

References1. Olivares-Reyes A et al. J Am Soc Echocardiography 1997;

10(6): 644

2. Rice MJ. J Am Col Cardiology 1988; 12 (5):1292

3. Shinohara T et al Ann. Thoracic Surgery 2001:71(5): 1672Fig. 4. PLAX view with what appears to a LA mass. It turnedout to be thrombus in an ASA .

Fig. 5. An ASA bulging into the right atrium and obstructingtricuspid flow.

Fig. 3. A post Mortem histology slide of thrombus within anASA.

Right Atrium

Left Atrium


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A LATE DIASTOLIC SIGNALIN THE LEFT VENTRICULAROUTFLOW TRACTAUGMENTED BY VALSALVAMANOEUVREThe Doppler images presented were obtained from a standardtransthoracic echocardiogram (TTE) requested as part of apatients work up prior to urgent non-cardiac surgery. The mainfindings were severe asymmetrical left ventricular hypertrophywith sparing of the posterior wall. No outflow tract obstructionwas detected at rest or with valsalva. Incidentally a fairlydramatic increase in the velocity of the pre-ejection signal wasnoted during the strain phase of valsalva (Fig 1 A & B redarrow). With the sweep speed increased and scale reduced twoclear pre-ejection signals were apparent (Fig 1 C & D red &blue arrows). A Valsalva manoeuvre was also performed toassess the mitral inflow pattern. This demonstrated clear E Areversal (Fig 1 E & F).

In an interesting recent article in Echo Dr Williams describedhow in a non-compliant left ventricle (LV) the left atrialcontraction ‘pushes’ blood towards the outflow region creating alate diastolic signal1. The scant literature available on the originof such signals supports this hypothesis. One study found thelate diastolic signal correlated well with peak A wave velocityand inversely related to LV cavity size2. In this study the signal

was termed a ‘J wave’. Pulsed Doppler interrogation at multipleLV sites found the origin of the J wave to be in the LV outflowtract (LVOT) closer to the apex, the signal amplitude increasedas it was mapped towards the aortic valve, maximal signalamplitude was found approximately 2.6cm below the aorticannulus2. These findings are very similar to the findings ofPanayiotou & Byrd3 who also demonstrated an increase invelocities (confusingly termed A’ in this study) as they werefollowed back from apex to LVOT. In their study maximal A’velocity was noted 1.5-2.0cm below the aortic annulus3.

With regards to the images we present the timing of the firstaugmented signal (fig B & D red arrow), soon after the P waveand before the onset of systole is consistent with a J wave. Inthe studies we have cited above peak A wave velocity wasshown to correlate with peak J wave velocity. In our images theJ wave velocity increases as peak A wave actually decreasesduring the valsalva manoeuvre. We feel this is easily explainedby the fact that during the strain phase of valsalva preload isreduced4. The pressure difference between the LA and LV istherefore lower, which is manifest on the trans-mitral Doppleras a reduction in the maximal velocities of the E and A waves.We believe the factor which has augmented the signal duringvalsalva in this case is the increase in the proportion of LVfilling from the left atrium since, in the absence of increasedpreload, the now unmasked abnormal LV relaxation has notallowed for adequate early filling (Figure 1 E&F). The LV ishypertrophied and has reduced compliance therefore theincreased atrial ‘push’ is noted on the outflow Dopplers.

The timing of the second component (Figure 1 D blue arrow) isconsistent with isovolumic contraction. On the resting imagesthe pre-ejection signal appears to be merged as one component.On valsalva as the atrial component increases in velocity it

Fig. 1. A. CW Doppler throughthe aortic valve atrest, sweep speed25mm/s

Fig. 1. B. CW Doppler throughthe aortic valveduring strain phase ofvalsalvademonstrating a cleardiastolic signal priorto ejection (redarrow).


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becomes better defined from the isovolumic signal (the PRinterval also increased slightly from ~236ms-~250ms duringvalsalva allowing more time for the atrial component, althoughthis was measured only on the limited rhythm strip).

We would like to note that ideally this signal would have beenassessed with PW Doppler. The reason CW Doppler images arepresented is that the valsalva was performed to asses for LVOTobstruction. The late diastolic signal was an incidental finding,which was not further assessed as a part of this routine scan.

Late diastolic signals in the LVOT are often incidentally notedon Doppler. Surprisingly little information exists in theliterature on the origins of such signals. To the best of ourknowledge the clinical significance of such signals has not yetbeen studied however it is accepted that their presence isconsistent with a degree of diastolic dysfunction.

Paul Russhard, Dr Alamgir Kabir

Basildon and Thurrock University Hospital

Fig. 1. C. CW Doppler throughthe aortic valve at restsweep speed increasedto 75mm/s.

Fig. 1. D. CW Doppler throughthe aortic valveduring strain withsweep speedincreased, red arrowindicates the J wave,blue arrow indicatesisovolumiccontraction signal.

Fig. 1. E. Pulsed wave Dopplershowing trans-mitralfilling pattern at rest.

Fig. 1. F. Pulsed wave Dopplershowing reversedtrans-mitral fillingpattern during thestrain phase ofvalsalva.


The development of an aortic root “abscess” signifies a serious

situation in the progression of a patient’s endocarditis process.

Such a dilatation of the aortic root may in itself cause

complications by developing a fistulous connection into other

cardiac chambers or cause pressure on a coronary artery, or

rupture. Although the majority of patients require early

surgery, some survive the endocarditis process by medical

treatment leaving a long-term sacular aneurysmal like space in

the aortic root (similar to Fig 1). In other words they can

become a chronic feature such that when imaged they do not

necessarily reflect an acute episode of endocarditis. Hence,

access to and reviewing of patients previous Echo images are

important and should be sought, even if time consuming.

Infection from an infected aortic valve can spread down into the

intraventricular septum where it becomes encapsulated in the

septal myocardium, not washed by blood flow and then

becoming a true intra-myocardial abscess.

Gordon Williams

Editor

Fig. 1 despite being a still frame should be sufficient to raise the

possibility of an aortic root abscess cavity. Indeed that is

what it was. The image on the front cover of this issue is the

same patient with colour flow highlighting blood flow filling

and washing through the cavity space. This is also shown and

highlighted in fig. 2 on this page.

What exactly is an aortic root abscess? Basically it is an area

of thinned aortic root wall secondary to inflammation

consequent upon endocarditis of the aortic valve. The

terminology is strictly incorrect in that the definition of an

abscess is “an area containing pus”, pus being the material

produced by infection and containing inflammatory cells,

organising proteinaceous material, inflammatory organisms and

fluid. Abscesses are usually closed, containing the “pus” . In

the aortic root, the area is a sacular dilatation of the aortic wall,

the wall being acutely inflamed, but the area is “washed”

continuously by the blood flow during each systole (and during

diastole if the aortic regurgitation co-exists). The area

therefore contains no pus. An aortic root abscess therefore is

not strictly an abscess in the true definition of the term.

However, the phraseology has been applied for years and there

would be little point in anyone trying to change the terminology

now.

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Fig. 1. Apical 4 chamber view with an abscess cavity at thelevel of the aortic valve easily visible.

Fig. 2. The same view as Fig 1. with the addition of colourflow imaging helping to outline the space as an abscess cavity.Such cavities are usually acute but may be chronic signifyinga previous endocarditis episode.

FRONT COVER

References

1. Williams. G. An interesting Signal. Echo. 2013; 80: 15-16.

2. Jaeger. KM & Rahko. PS. Doppler Characteristics of Late-diastolic Flow in the Left Ventricular Outflow Tract. Journalof the American Society of Echocardiography. 1990 3(3)179-86.

3. Panayiotou. H & Byrd. BF. Origin and Significance ofDiastolic Doppler Flow Signals in the Left VentricularOutflow Tract. Journal of the American College ofCardiology. 1990. 16(7) 1625-31.

4. Nagueh. SF, Appleton. CP et al. Recommendations for theEvaluation of Left Ventricular Diastolic Function byEchocardiography. JASE 2009; 22(2) 107-33.


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THE CIRCULATION BUTNOT AS WE KNOW IT …IntroductionFor many of us, our daily occupations involve performingechocardiographic examinations to study the structure andfunction of the heart. Integral to this is an almost subconsciousappreciation of the pulsatile nature of the circulation wherebycardiac activity can be defined by clear contraction (systolic)and relaxation (diastolic) phases. Although one is usuallyaccustomed to this fundamental property of the circulation, itcan be insightful and fascinating to occasionally explore theorigins of our current knowledge.

BackgroundIn the 4th century B.C., the Greek philosopher Aristotleidentified the heart as being one of the most important organs inthe body. This was based on his study of chick embryos wherethe heart was seen to form first as a three-chambered organ.Aristotle described the heart as being a hot dry organ that wasthe centre of vitality in the body. It was the centre of emotion,intelligence and also heat. The remaining organs in the bodywere on the other hand described as being secondary andserving purely to cool the heart.

These teachings remained largely unchallenged for almost 600years until the 2nd century A.D. At this time the Greekphysician and philosopher, Galen of Pergamum, challengedAristotle in the importance of the heart as the primary organ.Galen believed that the liver served a greater function bydistributing essential nutrients around the body via the veins

and portalcirculation. Theheart in Galen’sopinion waslargely a generatorof heat andresponsible for thecirculation ofemotions via thearteries. It couldnot possibly be asimportant as theliver since it wasnot responsible forthe generation ofany of the fourbodily fluids(humors) that werebelieved to affecthuman behaviouraland personalitytraits (Figure 1).

Aristotle’s andGalen’s theoriespredominated theunderstanding ofthe circulation foralmost 2000 yearsthrough medievalIslam and the

Renaissance period. Whereas philosophers largely supportedAristotelian views, academic physicians supported Galen. Bythe middle of the 16th century a handful of physicians begun toquestion a number of key aspects of the traditional circulation.In 1559 Professor Matteo Colombo, (the first Professor ofanatomy at Pisa) postulated that blood passed from the venacava to the aorta via the heart and during this passage wastempered by air from the lungs. He also proposed that theheartbeat had two phases. These were initially termed“constriction” for what we term systole today and “systole” forwhat we call diastole. In 1628, at the age of 50 years and alifetime of dedication to anatomy and the circulation, WilliamHarvey published the book entitled “De Motu Cordis” (Figure2). This text represents one of the most substantial contributionsto cardiac physiology. It is the first complete description of thecirculation as a pulsatile system and the heart as a mechanicalpump. As a result of Harvey’s work he is widely recognised asone of the most important physicians in the history of medicine.A brief biography of his life and work is given below.

The life of Dr William Harvey William Harvey was born in Folkestone, Kent in 1578 and camefrom a family of merchants. After attending King’s School inCanterbury, he studied Arts and Medicine at Gonville and CaiusCollege, Cambridge. In 1600 Harvey attended one of theleading European medical schools in Padua, famous for itsanatomical and clinical teaching. He worked closely withHieronymus Fabricius (the most eminent anatomist in Europe atthe time) who recognised that veins had one-way valves but wasunsure as to their function. It was Harvey who took thesefoundations to solve the riddle of what part the valves played in

Fig. 1. Galen’s spirit system - Galenintroduced the spirit system with thenatural spirit located within the liver, thevital spirit within the heart and the animalspirit in the nervous system.

Fig. 2. A portrait of William Harvey


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the circulation of blood through the body. Early in his career,Harvey was recognized as an exceptional man and was electedby his peers a Consilarius in Padua in 1600, and again in thefollowing two years. In 1602 he received his doctor of medicinealthough was refused entry to the Royal College Physicians inspite of being ‘entirely satisfactory’ and it wasn’t until 1604 thathe gained the approval of the examiners, allowing him to befree to practice medicine under the jurisdiction of the RCP.

By 1607 he became a Physician to St Bartholomew’s hospitalearning £33 a year, a position he held for 36 years. In 1627 hebecame one of the eight Elect of the College responsible fordeciding who should practice medicine and in 1628 Treasurer tothe College. By 1630 William Harvey was appointed the royalphysician serving first James I and then to Charles I. It isreported that he was close to Charles I and spent time with himin Scotland and Oxford, where he became warden of MertonCollege. Following the beheading of Charles I for tyranny in1649, Harvey returned back to London to continue his medicalpractice. He was offered the position of President of the RCP in1654, however declined owing to his advancing age. In 1657Harvey died from a stroke after establishing an endowment fora librarian’s salary encouraging fellows to study and search outthe secrets of nature by way of experiment.

The work of William HarveyMuch of what we know about William Harvey’s work has beenobtained from his lecture notes that were started in 1616,shortly after he began his long tenure as the Lumleian Lecturerof Surgery and Anatomy. From these it is clear Harvey hadbegun early on to study the motions of the heart, respiration andcomparative and pathological anatomy in insects and up to 60mammals. Unfortunately over the years, many of Harvey’snotes, books and manuscripts were lost with only his lecture

notes and his two works in print surviving.

One of the publications that did survive was ‘Exercitationanatomica de motu cordis et sanguis in animalium’ (AnAnatomical Study of the Motion of the Heart and of the Bloodin Animals). This was published in 1628 and represents the firstdescription of how the heart propels the blood in a circularcourse through the body. Harvey waited for nine years beforepublishing this 72-page book whilst he spent timedemonstrating his experiments and expressing his views to hispeers (Table 1). The book opened with a simple but cleardedication to the King and gave a clear and connected accountof the action of the heart and movement of blood around thebody in a circuit. In his preface Harvey remarked:

“" these views, as usual, pleased some more, others less:some chid and calumniated me and laid it to me a crimethat I had dared to depart from the precepts and opinionsof all anatomists: others desired further explanation of thenovelties which they said were both worthy ofconsideration, and might perchance be found of signaluse."

Following the publication of “De motu cordis”, the contentswere discussed at length amongst scholars over the next 20years before being widely accepted in the later half of the 17thcentury. As a consequence of his achievements WilliamHarvey’s is recognised as being one of the most famousphysicians in the history of medicine. His work not onlychallenged the 2000-year-old theories of Aristotle and Galen onthe nature of the circulation, but also his own fundamentalbeliefs.

AcknowledgmentsFigures obtained from the public science photo library

Jessica Webb, Ronak Rajani St Thomas’ Hospital

Fig. 3. The title page of William Harvey’s De Motu Cordispublished in 1628. The first account of the circulation of theblood.

• Puncturing the aorta and draining the blood results inemptying of the veins – arteries and veins must beconnected.

• Pinching the vena cava causes the heart to drain.Pinching the aorta causes the heart to swell – blood flowmust be unidirectional.

• The septum is too tough and dense for blood to pass fromthe vena cava directly via pores in the septum to the aorta –blood flow from the inferior vena cava must pass to thelungs first.

• Using tourniquets veins would swell up with reducedtension – differential pressure within veins and arteries.

• Circulating blood explains why snake bite venom canspread through the entire body so quickly.

• The heartbeat has two phases – systole (contraction) anddiastole (relaxation).

• The heart is for contracting and expelling blood and withcontraction arteries dilate.

• Blood must have a circular motion and a continualpulsatile physiology

Table 1. Key deductions by William Harvey


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NEW GUIDELINESA Guideline Protocol for the Echocardiographic assessment of Diastolic Dysfunction

Echocardiography plays a central role in the non-invasive evaluation of diastole and should be interpreted in the clinical context.Multiple echocardiographic measurements have been proposed to assess diastolic function but no single parameter should be used inisolation. This document gives recommendations for the image and analysis dataset required for the assessment of diastolicdysfunction (DD) using established indices acquired as part of the minimum dataset. Due to the variable sensitivity and specificityof the available parameters in different clinical settings, contradictory data can occur and in a proportion of patients a final diagnosismay not be achieved. In these situations the conventional echo data should be supplemented with information from other forms ofassessment including haemodynamic measurement.

In this document, the parameters assessed are first set out systematically, with the key measurements highlighted in bold. For ease ofreference they are also listed below. A simplified flow chart follows to assist in diastolic dysfunction grading. Appendix 1summarises normal values. Appendix 2 provides recommendations on assessing diastolic function in specific clinical situations.

Dr Thomas Mathew (lead author)Dr Rick Steeds, ChairDr Richard JonesDr Prathap KanagalaDr Guy LloydDr Daniel Knight Dr Kevin O'GallagherDr David OxboroughDr Bushra RanaDr Liam RingJulie SandovalGill WhartonDr Richard Wheeler

Abbreviations:

E Vmax Mitral valve early filling on PW Doppler (m/s)

A Vmax Mitral valve atrial filling (m/s)

A dur Duration of atrial filling wave on PW Doppler (ms)

E/A ratio Ratio of E Vmax/A Vmax

DT Deceleration time (ms)

PV s Pulmonary vein systolic wave peak velocity (m/s)

PV d Pulmonary vein diastolic wave peak velocity (m/s)

PV s/d Ratio of pulmonary vein peak systolic velocity/peak diastolic velocity

PV a dur Duration of atrial reversal from PW Doppler of pulmonary vein flow (ms)

LAi Left atrial volume indexed to body surface area (mls/m2)

e’ Velocity of early myocardial relaxation measured on tissue Doopler imaging (cm/s)

E/e’ Ratio of MV E Vmax/ tissue Doppler early myocardial relaxation velocity

Mitral Vp: Propagation velocity of early filling wave into the LV (cm/s)

NOTE: key parameters are highlighted in bold. The remaining parameters are useful adjuncts when the diagnosis of diastolicdysfunction severity remains unclear

Published November 2013


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Measurements

E Vmax,A Vmax, E/A ratioDTA dur

Change in Mitral E/Aratio from baseline

Explanatory note for ARVC

Sample volume is placed at the level ofmitral leaflets tips (colour flow can be help-ful for optimal alignment, particularly whenLV is dilated)

Optimise spectral gain/wall filters to ensureclear crisp signal of onset and cessation ofLV inflow

Measurements are obtained over 3 cardiaccycles at end expiration

See appendix 1 for normal values

Decrease in 20cm/s in E wave velocity gen-erally indicates a good Valsalva technique

Decrease in mitral E/A ratio of >_ 50% ishighly specific of raised LV filling pressure.

Useful when differentiating grade 2 fromnormal.

Modality

PWDoppler

PWDopplerwithValsalva

VIEW

A 4C

Image

Normal

Grade 1

Grade 2

Grade 3

Grade 2 before valsalva


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PVs PDd s/d ratio

a-dur

Calculate: a dur - Adur

Superior angulation of the transducer in the4C view and colour flow is often required tolocate the right upper pulmonary vein (seenclose to atrial septum).

Sample volume is placed >0.5cm into thepulmonary vein

Wall filter settings should be lowered with afaster sweep speed (50-100mm/s) to opti-mise recording; aim to include clear visuali-sation of atrial reversal velocity waveform

Measurements are obtained over 3 cardiaccycles at end expiration.

If there are 2 systolic peaks (S1 and S2),peak S2 should be used to compute S/Dratio


a dur-A dur of more than 30ms indicatesraised LV filling pressure

PWDoppler

Above patient during valsalva

Normal PV flow

PV flow with S/D reversal


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e’

Calculate: E/e’ ratio

(Vp)

Calculate : Mitral E/Vpratio

TR V max

LA volume

Calculate : LAi

Velocities are recorded using PW TDI andnot colour coded TDI

Sample volume is placed at or within 1cm ofthe insertion site of mitral valve leaflets

Optimise the velocity scale and baseline todemonstrate full signal. Gain settingsshould be adjusted to display high ampli-tude annular velocities.

Measurements are obtained over 3 cardiaccycles at end expiration

e’ is unreliable in the presence of mitralannular calcification, mitral prosthetic valvesand annuloplasty rings and severe mitralvalve disease


e’ - average from 2 sites (lateral and septal)is used for the ratio.

Acquisition is performed in the 4c view with colour flow imaging (narrow colour sector) across the mitral valve and an M mode line placed through the centre of the LV inflow blood column (MV to LV apex).

Nyquist limit is adjusted to display the cen-tral highest velocity jet as blue.

Flow propagation velocity (Vp) is measuredas the slope of the first aliasing velocitymeasured from mitral valve plane to 4 cmdistally in to the LV cavity.

Mitral E/Vp ratio can be used to predict LApressure. E/Vp >2.5 indicates elevated LApressure (>15mmHg).

In the absence of lung or mitral valve dis-ease, raised PA pressure may indicate DD.

Average volume measured at ventricular endsystole (LA largest) using Modified Simpsonsor Area Length method and indexed to BSA

See minimum dataset and chamber quantifi-cation guidelines

TissueDopplerimaging(TDI)

ColourM-Mode

CWDoppler

2D

A 4C

A 4C

A 4C& A 2C

Normal Vp


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Measurement 16-20 years 21-40 years 41-60 years >60Mitral E/A ratio 1.88 ± 0.45 (0.98-2.78) 1.53 ± 0.40 (0.73-2.33) 1.28 ± 0.25 (0.78-1.78) 0.96 ± 0.18 (0.6-1.32)

Mitral DT (ms) 142 ± 19 (104-180) 166 ± 14 (138-194) 181 ± 19 (143-219) 200 ± 29 (142-258)

PV S/D ratio 0.82 ± 0.18 (0.46-1.18) 0.98 ± 0.32 (0.34-1.62) 1.21 ± 0.2 (0.81-1.61) 1.39 ± 0.47 (0.45-2.33)

Septal e’ (cm/s) 14.9 ± 2.4 (10.1-19.7) 15.5 ± 2.7 (10.1-20.9) 12.2 ± 2.3 (7.6-16.8) 10.4 ± 2.1 (6.2-14.6)

Lateral e’(cm/s) 20.6 ± 3.8 (13-28.2) 19.8 ± 2.9 (14-25.6) 16.1 ± 2.3 (11.5-20.7) 12.9 ± 3.5 (5.9-19.9)

Table 1. Normal values for age related Doppler derived diastolic measurements. Data are expressed as Mean ± SD (95% confi-dence interval) except those marked with asterisk. Adapted from reference 1.

Appendix 1

Appendix 2In certain clinical situations, conventional echo indices cannot be readily applied to assess diastolic dysfunction. The following

section provides recommendations on assessing diastolic function in this group of patients. In these patients, grading of DD is not

always possible and the aim is to estimate the filling pressures as a marker of diastolic dysfunction.

a. Left ventricular hypertrophy: In patients with heart failure symptoms and normal EF, evidence of concentric remodelling or raised

LV mass index is itself indicative of diastolic dysfunction. In this group of patients, assessment of other markers of diastolic

dysfunction does not provide additional diagnostic information

b. Sinus tachycardia: E A fusion occurs rendering E/A ratio and deceleration time unreliable in assessing DD. E/e’ ratio using fused

peak mitral inflow velocity and peak fused mitral annular velocity can still be used to predict LV filling pressures in this situation.

*E/A < 1 without any additional evidence of diastolic dysfunction can be normal above 60 years of age.

**E/A >2 and/or increased LA size without structural heart disease can be seen in young subjects and athletes.

***Combined with one or more parameters from below. Confidence of categorisation increases with increasing number of corroborative parameters.

# If E/e’ is between 9 and 12, additional measurements should be used (see text).

Figure 1: Practical approach to assessment and grading of Diastolic Dysfunction

E/A, DT, s/d, e’, LA volume

E/A < 1*DT > 230

E/A 1-2DT 130-230

e’normal

*** ***

e’ reduced

*** ***

Grade I Normal Grade II Grade III

• e’ - reduced• LA – normal or ↑• s/d >1• E/e’ – usually <_ 8

• LA – normal** • s/d > 1• E/e’ <8#

• LA – ↑• s/d <1• E/e’ usually >_13#

• e’ – reduced• LA – ↑• s/d <1• E/e’ – > 13

E/A >2**DT <130

Flow chart


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c. Atrial Fibrillation: Loss of atrial contraction, variable cycle length and the frequent occurrence of atrial dilatation limit the

usefulness of conventional indices in the assessment of DD. DT and E/e’ ratio averaged over 5-10 cardiac cycles (recorded from

cycle lengths equivalent to a heart rate between 60-80 beats/minute) can be used to assess LV filling pressures in this group.

d. Constrictive pericarditis: Constrictive pericarditis can present with heart failure symptoms and restrictive filling pattern (Grade

III) in the absence of diastolic dysfunction. Normal or increased e’ velocity can differentiate this condition from DD.

e. Mitral valve disease: Mitral E Vmax and PVs are affected by significant primary MR. a dur- A dur is the strongest predictor of

LV filling pressure in this situation.

f. Systolic dysfunction: Grading of DD and estimation of filling pressures provide additional prognostic information in patients with

established systolic dysfunction. Mitral inflow pattern (E/A ratio and DT) alone can be used to estimate filling pressure in this

population and no further evaluation is necessary except in borderline cases. Accordingly E/A ratio < 1 in this population often

indicates normal filling pressures and E/A ratio of 1-2 or > 2 strongly suggest raised pressures.

References:

1. Nagueh S, Appleton C, Gillebert T, Marino P, Oh J, Smiseth O, Waggoner A, Flachskampf F, Pellikka PA, Evangelista A.Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr.2009;22:107–133.

2. Appleton C, Hatle L. The natural history of left ventricular filling abnormalities: assessment of two-dimensional and Dopplerechocardiography. Echocardiography1992;9:437–47.

3. Poulsen S H, Jensen S E, Gøtzsche O, et al. Evaluation and prognostic significance of left ventricular diastolic function assessedby Doppler echocardiography in the early phase of a first acute myocardial infarction. Eur Heart J 1997. 1882–1889.188.

4. Temporelli PL, Scapellato F, Corrà U, Eleuteri E, Imparato A, Giannuzzi P. Estimation of pulmonary wedge pressure bytransmitral Doppler in patients with chronic heart failure and atrial fibrillation. Am J Cardiol. 1999;83:724–727.

5. Garcia MJ, Ares MA, Asher C, Rodriguez L, Vandervoort P, Thomas JD. An index of early left ventricular filling combined withpulsed Doppler peak E velocity may estimate capillary wedge pressure. J Am Coll Cardiol 1997; 29: 448-54.

6. Ommen SR, Nishimura RA, Appleton CP, Miller FA, Oh JK, Redfield MM, Tajik AJ. Clinical utility of Dopplerechocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneousDoppler-catheterization study. Circulation. 2000; 102: 1788–1794.

7. Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward JB. Left atrial volume as a morphophysiological expression of leftventricular diastolic dysfunction and relation to cardiovascular risk burden. Am J Cardiol. 2002;11:1284–1289.

8. Ommen SR, Nishimura RA. A clinical approach to the assessment of left ventricular diastolic function by Dopplerechocardiography: update 2003. Heart 2003;89(suppl 3):iii18e23.

9. Zile MR, Gaasch WH, Carroll JD, Feldman MD, Aurigemma GP, Schaer GL, Ghali JK, Liebson PR. Heart failure with a normalejection fraction: is measurement of diastolic function necessary to make the diagnosis of diastolic heart failure? Circulation2001;104:779–782.

10. Paulus WJ, Tschöpe C, Sanderson JE, et al. How to diagnose diastolic heart failure: a consensus statement on the diagnosis ofheart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of theEuropean Society of Cardiology. Eur Heart J. 2007;28:2539–2550.

11. Nagueh SF, Mikati I, Kopelen HA, Middleton KJ, Quiñones MA et al. (1998) Doppler estimation of left ventricular fillingpressure in sinus tachycardia. A new application of tissue doppler imaging. Circulation 1998: 1644-1650

12. Al-Omari MA, Finstuen J, Appleton CP, Barnes ME, Tsang TS. Echocardiographic assessment of left ventricular diastolicfunction and filling pressure in atrial fibrillation. Am J Cardiol. 2008;101:1759–1765.

13. Rossi A, Cicoira M, Golia G, Anselmi M, Zardini P. Mitral regurgitation and left ventricular diastolic dysfunction similarlyaffect mitral and pulmonary vein flow Doppler parameters: the advantage of end-diastolic markers. J Am Soc Echocardiogr.2001;14:562–568.

14. Redfield MM, Jacobsen SJ, Burnett JC, Jr, et al. Burden of systolic and diastolic ventricular dysfunction in the community:appreciating the scope of the heart failure epidemic. JAMA. 2003;289:194–202.


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CRITICAL CARE ECHOCARDIOGRAPHYIntroduction The benefits of echocardiography in the critically ill patient have become increasingly apparent over the last twenty years. Theability to visualise cardiac anatomy and obtain objective and reproducible measurements of cardiopulmonary function, without therisk of invasive intervention, has led transthoracic echo to be embraced at local1, 2, national3-5 and international6 level. In this articlewe review the evolution of critical care echocardiography as a unique area of practice, compare and contrast critical careechocardiography with traditional cardiology imaging, and stress the importance of inter-specialty collaboration in maximising thebenefit for patients of this growing sub-specialty.

Case 1A 54 year old lady was admitted to the intensive care unit of a university teaching hospital with multi-organ failure secondary to adeep pelvic infection. Laparotomy and hysterectomy were performed in an attempt to eliminate the source of infection. On returnfrom the operating theatre, increasing haemodynamic instability developed and there was a rapid increase in cardiovascularsupport requirements. Invasive haemodynamic monitoring revealed a low cardiac output state, which did not respond to fluidresuscitation. An Intensive Care Specialist Registrar, undergoing training and accreditation in Focused Intensive CareEchocardiography (FICE), performed a limited 2 dimensional scan. This demonstrated normal size left ventricle with visually goodsystolic function, adequate fluid volume and an unexpected anterior pericardial effusion. Immediate assistance was sought from aCardiac Physiologist who confirmed the presence of pericardial effusion and sought to determine haemodynamic significance. Thepatient and echo images were reviewed and discussed at the bedside by the echocardiographer, intensive care consultant andcardiology registrar. The effusion was associated with right ventricular collapse and greater than 25% variation in left ventricularinflow. It was therefore deemed to be haemodynamically significant and emergency pericardiocentesis was performed.• Echocardiography in the unstable critically ill patient often reveals unexpected pathology and significantly alters management. • Focused echocardiography is a limited, goal directed, 2D-scan intended to identify gross pathology with potential to cause

instability; subsequent formal scan is necessary to confirm findings, quantify abnormalities and exclude the presence of othermore subtle problems. The follow up scan is also a key form of education and governance for the focused operator.

• Interpretation of echo findings in the dynamic critical care environment and determination of their significance requires thecombination of technical expertise with understanding of critical illness. This usually involves input from the multi-disciplinaryteam. We believe this to work best if conducted in real time at the bedside.

History of Critical Care EchoThe use of ultrasound to visualise the heart was first described nearly sixty years ago7, yet the widespread use of echocardiographyin intensive care is a relatively recent development. A handful of pioneers recognised its potential as a determinant ofhaemodynamic status8 in the 1980’s: authors describe an instrument capable of providing real-time information on complex heart-lung dynamics and instantaneous feedback on the effects of pharmacological or mechanical intervention. Routine use at this timewas however uncommon. The introduction of transoesophageal echocardiography (TOE) to cardiac anaesthesia practice in the1990’s increased the anaesthetic community’s exposure to echo technology, undoubtedly accelerating uptake in general intensivecare settings. This experience gradually diffused from cardiac care to more general practice and by the 21st century,echocardiography is firmly established as a key facet of intensive care medicine patient assessment and monitoring in manyinstitutions9, 10.

Education and Critical Care EchoIn response to the increasing role of echocardiography within intensive care11, a consensus approach to training and accreditation hasbeen developed12. The UK, like many other healthcare systems13-15, introduced a two tier system of training16: a basic level attainableby the majority of practitioners aimed at providing rapid answers to binary clinical questions (e.g. is there tamponade? yes/no); andan advanced level suitable for the minority of doctors seeking diagnostic level skills and aiming to lead or develop local services. Amajor driver for this education programme was the recognition that echocardiography may be required on the intensive care unit atany time of day or night17, yet the majority of hospitals do not fund an echocardiography service out of hours. Development of basicechocardiography skills in appropriate doctors practicing within a structured governance framework could potentially provideanswers to out of hours clinical questions2.

Numerous studies have examined the effectiveness of basic level echocardiography18-21. On the whole these purport to demonstratethat a novice can attain sufficient skills in the course of a brief training programme to reliably identify ‘simple’ life threateningpathologies (e.g. tamponade; severe hypovolaemia; severe left ventricular failure). Whether the demonstration of these basic skills ina controlled, educational environment translates into meaningful change in practice as yet remains unclear. There is however generalacceptance that this rudimentary level of skill provides information of sufficient depth and quality to allow safe patient managementuntil a more skilled echocardiographer is available2.

The British Society of Echocardiography (BSE) Critical Care Echocardiography Accreditation 5, 22 provides opportunity for critical


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care doctors to develop and demonstrate competence in more advanced imaging. It aims to develop doctors with comparable levelsof expertise to accredited echocardiographers within cardiology services. As such most of the curriculum is drawn from the originalBSE accreditation. Candidates are expected to demonstrate similar understanding of anatomy, physiology and physics; they mustsubmit and log the same numbers of cases. The major difference between the standard and critical care accreditation is the range ofpathologies to which candidates must demonstrate exposure, the critical care accreditation having a more acute theme. It has beensuggested that advanced critical care echocardiographers should also be competent in TOE23: it providing superior image quality inthe difficult to scan critical care population and being a reasonably practical option in a patient group who are frequentlyanaesthetised. At present however, TOE familiarity is a not a mandatory component of critical care accreditation.

Despite the enthusiasm within critical care for developing an echocardiography skill base, cardiology services will continue to be theprimary provider of cardiac imaging in the intensive care, particularly for more complex cases. It is important therefore to considerhow the critical care environment differs from the cardiology department in which the vast majority of echocardiographers train andoperate.

Comparing Critical Care Echo to Traditional EchoThe differences between the patient population attending cardiology outpatient and those on intensive can be vast. The outpatientecho identifies cardiac pathology and tracks its evolution or response to therapy over months or years. The outpatient is usuallyphysiologically stable and no peri -procedural changes to management are made. The intensive care patient is, by definition,physiologically unstable. The inappropriate vasodilation associated with overwhelming infection is often profound and results inhyperdynamic physiology, subject to change minute by minute. As a result cardiac contractility and loading are unpredictable andcontinuously manipulated by titration of fluids and drugs. The interaction between heart and lung is rendered more complex andmore haemodynamically significant by the use of positive pressure ventilation; ventilatory parameters having marked impact onboth right and left heart performance. Critical illness or injury may impact upon the cardiovascular system in a myriad of ways;differentiating primary cardiac pathology from a multisystem effect requires both familiarity with echocardiography andunderstanding of critical illness pathophysiology. This complexity is confounded by the technical difficulty of acquiring adequateecho windows in the intubated supine patient, with multiple vascular lines and drains, on a large intensive care bed, in anenvironment with suboptimal lighting conditions and significant time-pressures. Furthermore, measurements and calculationscommonly used in standard echo protocols (e.g. valve areas, pulmonary artery pressure, diastolic function) may be subject toinaccuracy and uncertain significance in the intensive care patient9.

Case 2A 36 year old man with a background of acute myeloid leukaemia was admitted to the intensive care unit with Acute RespiratoryDistress Syndrome (ARDS) secondary to neutropaenic sepsis. His severe respiratory failure necessitated intubation and ventilation.Mechanical ventilation proved difficult and plasma oxygen and carbon dioxide remained abnormal despite maximal ventilatorysupport. Around twelve hours after ventilation, he displayed increasing haemodynamic instability with the dose of noradrenalinerequired to maintain an adequate blood pressure rising from 0.07 mcg/kg/min to a peak of 0.65mcg/kg/min. An Intensive CareSpecialist Registrar undertaking the BSE critical care accreditation performed a comprehensive scan. The right ventricle appearedvisually impaired and tissue Doppler suggested reduced longitudinal systolic function (s’ 9cms-1). A maximal tricuspid regurgitationjet velocity of 3ms-1 associated with absence of inferior vena caval variation suggested raised pulmonary artery pressure; the septumappeared flattened at end systole. No other abnormalities were identified. These findings were validated by the dutyechocardiographer and, on the basis of this information, the intensive care consultant introduced the inhaled pulmonary vasodilatornitric oxide. Cardiovascular stability improved and noradrenaline requirements fell to around 0.14mcg/kg/min. Repeat echoconfirmed marked improvement in right ventricular function and reduction in pulmonary artery pressure. • Heart-lung interaction is an important factor in critically ill patients; the use of positive pressure ventilation creates a unique

physiological environment. • Echocardiography provides an unparalleled means of assessing heart-lung interaction. • The use of inotropic and pressor drugs with potent effect on both loading and contractile performance • Repeat imaging, sometimes several times in a day, is often necessary due to the dynamic and rapidly changing nature of critical

illness.

Critical Care

Echocardiography

Suboptimal

Frequently multi-system

Seconds/minutes/hours

Highly significant in ventilated patients

Constantly titrated

Frequently applicable

Environmental Conditions

Site of pathology

Timescale for disease evolution

Heart-Lung interaction

Drug therapy

Mechanical interventions

‘Standard’ Outpatient

Echocardiography

Approaching optimal

Primarily cardiac in origin

Months to years

Of limited importance in most cases

Usually not altered immediately prior to echo

Not applicable


PAG E 23

Considering the complexity of the critically ill population - and the particular difficulty in obtaining and interpreting images in theintensive care – optimal use of echocardiography requires the combination of technical expertise with a sound understanding ofcritical illness. Whilst there are a handful of individuals who possess the necessary skills and knowledge, the majority of echoencounters on the intensive care require pooling of collective attributes and we believe critical care echocardiography to be mosteffective when contributing to a multidisciplinary clinical discussion.

Extended echocardiography in the intensive care unitHaving discussed the caveats of conducting and interpreting a standard echo study in the intensive care environment, it is worthconsidering how echocardiography technology and techniques may be extended to answer questions unique to the critically ill.Table 2 outlines some of the applications of echocardiography which are unique to intensive care and, resultantly, unlikely to befamiliar to those trained in a traditional, cardiology echocardiography.

Discussion

Focused (limited) echocardiography protocols are becoming a core aspect of intensive care training and practice. Many significantadvances in critical care echocardiography training and accreditation have occurred over the last decade. The enthusiasm and visionof the individuals driving this change has taken this area of practice from amateur observation to credible subspecialty and is to becommended. As critical care echocardiography comes of age we must however recognise it as a unique area of practice, distinctfrom the cardiological subspecialty from which it evolved. We must learn to negotiate its limitations, to interpret results in thecontext of critical illness and to extend the technology to develop unique applications which serve to improve the quality of criticalcare.

The difficulty lies in finding personnel with the appropriate skill mix to maximise the potential of critical care echocardiography.Whilst there exist individuals who are competent in comprehensive echo and have an in-depth understanding of critical illness theyare insufficient in number to provide ample cover across the health service. A more widely available alternative is the pooling ofexisting skills and knowledge: combining the technical expertise of the advanced echocardiographer with the experience of criticalillness possessed by intensive care clinicians. We believe these skills are best brought together at the bedside: critical careechocardiography cannot fulfil its potential if observations are simply recorded on a standard reporting form; findings should beinterpreted in light of the immediate physiology and this is best achieved when the study is a dynamic process involving real-timeinteraction between all relevant experts. Such bedside interaction is not solely beneficial to patient care; it is an opportunity forprofessional development. Intensive care clinicians undertaking focused echo studies greatly value opportunity to learn from expertsin the field and feedback forms an important part of governance. There has been no better time than now, for echocardiographers tohelp develop new skills and join forces with critical care colleagues eager to understand the opportunities and limitations of cardiacultrasound to improve outcomes for patients. With closer professional relationships there is an opportunity to improve outcomes forcritically ill patients with haemodynamic instability by the pooling complementary skills and encouraging timely bedsideinteractions.

Gillon Stuart, King's College Hospital, LondonAlejandro Rendon, Imperial College Trust, London

Pradeep Madhivathanan, Imperial College Trust, London David Walker, University College Hospital, London

Determination of ‘Haemodynamic State’

Titration of haemodynamic support

Titration of ventilatory support

Ventilator weaning studies

Cardiac arrest

Hypotension is commonly encountered on the ICU. Aetiology may be categorisedinto one of several ‘haemodynamic states’20: cardiogenic, hypovolaemic (i.e.preload dependent), vasodilatory (i.e. afterload reduction), obstructive. Echoprovides a rapid means of determining the state and directing management.

Pharmacological and mechanical support of the cardiovascular system is a dynamicprocess. Echo allows real-time visualisation of the effect of drugs and mechanicalinterventions (e.g. intra-aortic balloon pump, pacing, ventricular assist device) oncardiac function and permits optimisation.

Invasive ventilation may have profound impact on ventricular function. Real-timeassessment of cardiac function whilst ventilatory support is adjusted facilitatesoptimisation of heart-lung interaction.

Withdrawal of positive pressure ventilation can lead to worsening of cardiacfunction (e.g. deterioration in LV systolic function; increased severity of mitralregurgitation). This may prevent the liberation of patients from mechanicalventilation. Performance of echo studies on, and off, positive pressure ventilationidentifies dynamic cardiac factors impeding ventilatory wean.

The ability of echocardiography to identify reversible causes of cardiac arrest24 haveled to its inclusion in resuscitation guidelines25. Tamponade, massive pulmonaryembolism, hypovolaemia and potentially tension pneumothorax may be identified26.

Table 2 Critical Care specific applications of echocardiography


PAG E 24

References1. Colebourn C, Davies I, Becher H. Bridging the gap: training critical care clinician-echocardiographers through a collaborative

curriculum. Journal of the Intensive Care Society 2010; 11: 13-6.

2. Chambers J, Bruemmer-Smith S, Hindocha R,et al. Basic screening echocardiography: a training programme. J Intensive CareSoc 2011; 12: 293-4.

3. Fletcher SN, Grounds RM. III. Critical care echocardiography: cleared for take up. British Journal of Anaesthesia 2012; 109(4):490-2.

4. Douglas PS, Khandheria B, Stainback RF, et al. ACCF/ASE/ACEP/ASNC/SCAI/SCCT/SCMR 2007 Appropriateness Criteria forTransthoracic and Transesophageal Echocardiography_ A Report of the American College of Cardiology Foundation QualityStrategic Directions Committee Appropriateness Criteria Working Group, American Society of Echocardiography, AmericanCollege of Emergency Physicians, American Society of Nuclear Cardiology, Society for Cardiovascular Angiography andInterventions, Society of Cardiovascular Computed Tomography, and the Society for Cardiovascular Magnetic ResonanceEndorsed by the American College of Chest Physicians and the Society of Critical Care Medicine. Journal of the AmericanCollege of Cardiology 2007; 50(2): 187-204.

5. Bruemmer-Smith S, Colebourn C, Fletcher N. Accreditation for critical care echocardiography.

6. Price S, Via G, Sloth E, et al. Echocardiography practice, training and accreditation in the intensive care: document for the WorldInteractive Network Focused on Critical Ultrasound (WINFOCUS). Cardiovascular ultrasound 2008; 6(1): 49.

7. Edler I, Hertz CH. The Use of Ultrasonic Reflectoscope for the Continuous Recording of the Movements of Heart Walls.Clinical Physiology and Functional Imaging 2004; 24(3): 118-36.

8. Vieillard-Baron A, Slama M, Cholley B,et al. Echocardiography in the intensive care unit: from evolution to revolution?Intensive care medicine 2008; 34(2): 243-9.

9. Price S, Nicoll E, Gibson D, et al. Echocardiography in the critically ill: current and potential roles. Intensive care medicine2005; 32: 48-59.

10. Royse CF, Canty DJ, Faris J, et al. Core review: physician-performed ultrasound: the time has come for routine use in acute caremedicine. Anesthesia and analgesia 2012; 115(5): 1007-28.

11. Walker D. Echocardiography: time for an in-house national solution to an unmet clinical need? Journal of the Intensive CareSociety 2010; 11(2): 147.

12. Bruemmer-Smith S, Colebourn C, Fletcher N. Accreditation for critical care echocardiography. J Intensive Care Soc 2012; 13(3):196-7.

13. Popescu BA, Andrade MJ, Badano LP, et al. European Association of Echocardiography recommendations for training,competence, and quality improvement in echocardiography. European Journal of Echocardiography 2009; 10(8): 893-905.

14. McLean A, Yastrebov K. Echocardiography training for the intensivist. Crit Care Resusc 2007; 9(4): 319-22.

15. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of theAmerican Society of Echocardiography and American College of Emergency Physicians. Journal of the American Society ofEchocardiography 2010; 23(12): 1225-30.

16. Fletcher S, Grounds R. III. Critical care echocardiography: cleared for take up. British journal of anaesthesia 2012; 109(4): 490-2.

17. Orme RLE, Oram M, McKinstry C. Impact of echocardiography on patient management in the intensive care unit: an audit ofdistrict general hospital practice. British journal of anaesthesia 2009; 102(3): 340-4.

18. Vignon P, Dugard A, Abraham J, et al. Focused training for goal-oriented hand-held echocardiography performed bynoncardiologist residents in the intensive care unit. Intensive care medicine 2007; 33(10): 1795-9.

19. Manasia AR, Nagaraj HM, Kodali RB, et al. Feasibility and potential clinical utility of goal-directed transthoracicechocardiography performed by noncardiologist intensivists using a small hand-carried device (SonoHeart) in critically illpatients. Journal of cardiothoracic and vascular anesthesia 2005; 19(2): 155-9.

20. Royse C, Haji D, Faris JG, et al. Evaluation of the interpretative skills of participants of a limited transthoracic echocardiographytraining course (HART scan® course). Anaesthesia and intensive care 2012; 40(3): 498-504.

21. Melamed R, Sprenkle MD, Ulstad VK, et al. Assessment of left ventricular function by intensivists using hand-heldechocardiography. CHEST Journal 2009; 135(6): 1416-20.

22. Echocardiography BSo. http://www.bsecho.org/accreditation/types-of-accreditation/.

23. International expert statement on training standards for critical care ultrasonography. Intensive care medicine 2011; 37(7): 1077-83.

24. Price S, Uddin S, Quinn T. Echocardiography in cardiac arrest. Current opinion in critical care 2010; 16(3): 211-5.

25. (UK) RC. Advanced Life Support. 6th ed. London; 2011.

26. Zhang M, Liu ZH, Yang JX, et al. Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma.Critical care 2006; 10(4): R112.


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The European Association of Cardiovascular Imaging (EACVI)

was formed in 2012. The association aims to: “To promoteexcellence in clinical diagnosis, research, technicaldevelopment, and education in cardiovascular ultrasound andother imaging modalities in Europe”.

Club 35 is a branch of the association designed specifically for

the young echocardiographers. For a membership fee of just 35

Euro’s it offers a unrivalled range of educational, training and

research opportunities and the promotes collaboration of

echocardiographers across Europe.

Education

• 3D Echo box – an atlas designed to provide

echocardiographers with information on how to acquire,

derive and interpret 3D echocardiograms.

• Contrast Echo box – a tool designed provide a comprehensive

overview of practical acquisition and safety aspects of

contrast echocardiography.

• Valve Echo box is due to be added soon.

• Basic Online Echo Course – 16 chapters (containing both stills

and videos) covering the full range of topics from basic

physics to anatomy and assessment of valvular disease.

• EAE webinars – “live” web-based interactive lectures by

European Experts.

• Online Access to European Heart Journal Cardiovascular

Imaging

• Wikiecho – an online encyclopaedia of echocardiography

which is continually updated by users.

• Latest EACVI guidelines and protocols.

• Clinical Case portal

Research:

• 4 research grants are awarded annually by the EACVI. The

purpose of these awards is to provide an opportunity to obtain

research experience in an academic centre in an ESC country

other than their own. The grants are for the sum of 25,000

Euro over 1 year.

• A list of research echo labs who accept fellows together with

their area’s of expertise is designed to help prospective

fellows find a suitable project.

Networking:

Meet other echocardiographers with similar clinical and

research interests at the EACVI Club 35 sessions at EuroEcho.

Online discussion forum with your peers on LinkedIn “YoungNetwork of Cardiovascular Imaging Group”. Several

international leaders in echocardiography are active members of

this group which in less than 1 month has more than 135

members.

Club 35 Committee:

The Club 35 committee is composed of members from ESC

member states. A representative from each country has been

designated to represent the voice of their country within Club

35 and liaise with their peers and national echocardiography

societies about Club 35 initiatives.

Membership:

The cost of membership is 35 Euro for 1 year. You become a

full member of the EACVI. Membership is open to anyone with

an interest in echocardiography and under the age of 35. For

people over 35 other EACVI membership categories are

available.

To REGISTER ONLINE:

http://www.escardio.org/communities/EACVI

Dr Sanjeev Bhattacharyya

Cardiology Spr and EACVI Club 35 UK representative

E-mail: [email protected]

EUROPEAN ASSOCIATION OFCARDIOVASCULAR IMAGING (EACVI)


PAG E 26

BSE ANNUAL CLINICAL AND SCIENTIFIC MEETINGLIVERPOOL 2013 – DELEGATE REVIEWThis year’s meeting returned to Liverpool, and it was entirely appropriate for the location to be the “Liverpool ECHO Area”. Onceagain, Rick Steeds and the rest of the Education Committee had organised an impressive programme with a theme of“Echocardiography in Inherited and Acquired Structural Heart Disease.” As previously, there were 2 parallel sessions for just overhalf of the meeting, coming together for the keynote talks, and 4 international speakers.

Rick Steeds started the meeting off with a review of recent literature with “A Year in Echocardiography” grouping the publicationsinto LV function, valvular heart disease, focussed echocardiography and PFO closure. He followed this with an update on recentguidance released by the ASE on TOE and pericardial disease, and also by the EACVI on native valvular regurgitation andcardiovascular complications of radiotherapy – all of which can be downloaded from the ASE and EACVI websites.

The theme in the main auditorium was Congenital Heart Disease, which too often is daunting for those who do not get the chance toscan these patients in their routine practice. I was told by a reliable source that it started with an excellent presentation by Dr NavMasani which managed to demystify the approach to TTE, before other sessions on TOE and 3D echo. This was then followed bysessions on challenging cases in Adult Congenital valve disease, and then ASDs.

In the parallel session that I attended, there was an excellent presentation on 3D echocardiography, giving some useful practical tipson acquiring images for 3D analysis, before moving on to segmental analysis of the mitral valve and then LV assessment by 3D.This was then followed by a session on pitfalls in assessing valve disease, and started off with Low Flow Low Gradient (LFLG)aortic stenosis (AS), which was first described in 2001. Prof John Chambers clearly described a group of patients who haveimpaired LV function with a low stroke volume and low LVEF, and showed how dobutamine stress echocardiography (DSE) can beused in the decision making to classify patients as severe AS or pseudo-severe AS. Dr Jim Newton went on to talk on LFLG ASwith normal EF, which was only first described in 2007, and refers to a group of patients with a small LV cavity, concentric LVHwith normal LVEF, and low stoke volume with significant diastolic dysfunction, and he described how to calculate valvulo-arterialimpedance (Zva); this group of patients is sometimes not recognised without a full assessment, and because of this present late. Thiswas followed by excellent presentations on mitral stenosis in pregnancy by Dr Sara Thorne and then Dr Anita McNab on assessmentof mitral regurgitation (MR) in patients awaiting CABG, reinforcing the importance of the echocardiography in assessing both themechanism and severity of MR, as the echo will directly determine the surgical strategy.

The next session was a comprehensive overview of diastolic function, where Dr Thomas Mathew presented the new BSE guidelines,which appear to more practical and easier to follow than the comprehensive 27 page guidelines from the ASE in my opinion! Thiswas followed by further speakers presenting the difficult topics of assessing diastolic function in mitral valve disease, LVdysfunction and HCM.

This was followed by Prof Jeroen Bax (Leiden, Netherlands) who was asked to give the International BSE Invited Lecture on therole of echo before, during and after CRT. After the egress of a significant proportion of the audience, the AGM took place, wheremembers had the chance to quiz members of the BSE Council.

Attendance at the Saturday morning session was impressive, in view of the Social Event at Anfield Stadium (I was the one with theLuton Town scarf). I attended an excellent session on the pericarditis, LV non-compaction in the athlete and Tako-tsubocardiomyopathy (TTC). Dr Alexander Lyon explained that TTC, also called stress-induced cardiomyopathy, is classically caused by

emotional stress, where hormones such as adrenaline can cause apical-ballooning.Interestingly, it has been estimated that there are approximately 3000 cases in the UK per

year, and it has also been described in response to DSE!

After lunch, Dr Partho Sengupta (Mount Sinai, New York) gave an inspirationalInternational Lecture, covering the increased costs in healthcare in the USA, the

outreach programme that he is organising on behalf of the ASE on screening forRheumatic heart disease in India, LV fluid dynamics and “big data analytics”.For those that missed this lecture, there is a similar presentation which he gaveat the ASE on YouTube, though we did not get the 3D holograms inLiverpool.

The penultimate session was on the role of echocardiography inendocarditis and started off with Prof Jose Alberto San Román (Madrid)who talked on the role of TTE and TOE in right-sided endocarditis andhow this differs from left-sided endocarditis; he described how TTE isdiagnostic for endocarditis in the majority of IVDUs and the use of TOEis important in those with intracardiac/intravascular devices. This wasfollowed by Dr Jonathan Sandoe (Leeds) who was very brave as amicrobiologist to come to present guidelines from the British Society forAntimicrobial Chemotherapy on the appropriate use of echo in left-sidedendocarditis – underlying the importance of an appropriate triage systemfor echo requests in a stretched NHS. The last speaker was Prof CarlosMestres (Barcelona) who talked on surgery for infective endocarditis,


PAG E 27

and how the Barcelona multidisciplinary team manages patients.

The final session “Gems from the Presidents” is always my favourite, and worth staying for the entertainment, education as well asthe extra BSE Re-Accreditation point. Prof Mark Monaghan started off by presenting a case of a giant left atrium (135ml) that waslarger than the LV in a patient with a previous bioprosthetic mitral valve replacement. Dr Gordon Williams then gave a fascinatingpresentation on the ventricular myocardial band which divides the inter-ventricular septum (IVS). He started off showing one of aPolaroid photograph of an M-mode image with a line in the septum that was ignored as it was not understood. He went on to showhow this line is more obvious in a modern echo machine and visible by 2D. Interestingly, this feature can be explained by the doublehelical cardiac configuration and is due to the looping of the embryonic heart, first described by Francisco Torrent-Guasp as amedical student for which he was nominated for the 1978 Nobel Prize, and demonstrated by him in a video which is also availableon YouTube. Controversially, Gordon said that all the textbooks and guidelines are incorrect, as we should be measuring IVSthickness from this band rather than include the RV septum!

The meeting finished with the current President, Dr Guy Lloyd, showing how that even in the age of speckle trackingechocardiography, measuring MAPSE by M-mode can be used to calculate strain and strain rate with accuracy – though I suspect hedoes not perform this particular calculation daily!

In summary, I found the BSE meeting to be of excellent educational value and good fun, and the location was great. I am alreadylooking forward to next year’s meeting!

Dr Rizwan Sarwar, Cardiology Registrar, John Radcliffe Hospital

After an eventful train journey, I eventually arrived at the cosmopolitan city of Liverpool. The venue for our conference was theLiverpool Arena and Conference Centre.

I wanted to take the opportunity, not only to accrue valuable accreditation points but to feed back to our department as manydifferent aspects of the meeting as possible.

The conference covered a broad range of subjects including Adult Congenital Valve Disease using TTE, TOE and 3D, the pitfalls indetermining the severity of valve disease and the use of Strain Speckle Tracking. Lectures included the huge subject of DiastolicDysfunction, Tako-tsubo disease, RV assessment, Non- Compaction in the athlete and Stress Echo.

It is evident that 3D and Speckle Tracking is used more widely in echo, as it is in our department in Eastbourne; especially in ouradvancing research division. Dr Nik Abidin’s lecture, on ventricular function using 3D, explained how 90% of Simpson’s biplane EFcalculations were inaccurate compared with 3D which compares very well with CMR. Strain Speckle Tracking especially, however,still requires post processing which in the limited 45min session remains challenging. Staff limitations also restrict the trainingopportunities within a department to train in these new modalities.

The lectures by Dr Roxy Senior, Dr Jane Hancock and Dr Mark Monaghan, discussing the risk stratification by stress echo, wereparticularly interesting to me as I am involved in Stress echo in Eastbourne. The discussion of exercise verses stress and tissueDoppler and strain or perfusion being pertinent.

Professor John Chambers discussed the subject of low gradient, low flow aortic stenosis. I am one of a team of physiologists thatrun the Valve Clinic in Eastbourne, which is celebrating its 10th anniversary under Dr Guy Lloyd. Low flow AS is frequentlyinvestigated within the severe valve stress echo programme performed in conjunction with CPEX. Professor Chambers was keen topoint out as a caveat, the often mis-reporting of severe AS with perceived poor LV function. He reminded us that any mean gradient30-40mmHg indicates preserved contractility with visually reduced function.

The lecture by Dr Bushra Rana gave an insight into the 2D and 3D analysis of native and prosthetic mitral valves. The segmentalanalysis of the anatomy together prosthetic investigation of pannus formation, mis- match and paravalvular leaks was particularlyuseful in the valve clinic setting.

Mitral stenosis is a rare occurrence in the UK and new findings are generally from first generation immigrants. The lecture by DrJim Newton gave an insight into maternal mitral stenosis in Sri Lanka. With the aetiology of the valve often being rheumatic;frequently the mother develops pulmonary oedema by the end of the second trimester but with availability of echo, this has reducedmortality.

The grading of diastolic dysfunction and the sizing and quantifying of the RV were relevant to me as a QA lead. I am increasinglyaware of the need to clarify the grading of diastolic dysfunction and welcome the new BSE guidelines to be released soon tostandardise this. RV assessment with the comprehensive sizing at the three levels together with volume derivation is improvingwithin our department but appreciate from the lecture that that MRI is more accurate.

Dr Partho Sengupta presented an insightful and futuristic lecture about the massive amounts of information that is available withecho. He explained how it can be utilised using different modalities involving advanced echo holograms, with use of apps, in thescreening of the third world with valve lesions. He explained how handheld echoes have been performed in remote areas of theworld such as Delhi and how the data can be uploaded to a secure Cloud storage facility, then downloaded and interpreted byclinicians worldwide.

With the sudden increase for requests in our department for “echo ? endocarditis”, the series of presentations examining the role ofecho in decision making was useful, but still remains controversial. This is especially in view of a recent echo request based on apositive urine culture!

I would finally like to take this opportunity to thank BSE for sponsoring me to attend this meeting in Liverpool.

Lesley HartChief Clinical Physiologist, Eastbourne District General Hospital


PAG E 28

FOCUSED ECHOCARDIOGRAPHYIN EMERGENCY LIFE SUPPORT

(FEEL-UK) – COULD YOU BE A MENTOR?

Background

Successful resuscitation after cardiac arrest is dependent on 2 key factors - high quality CPR and identification and treatment of anyunderlying reversible cause(s).

Echocardiography is a powerful tool to detect causes such as pericardial effusion which can then be rapidly treated, but use ofEchocardiography in peri-resuscitation care is limited. This is due to numerous factors including the lack of availability andportability of machines and lack of personnel on the cardiac arrest team with the appropriate skills. Whilst the BSE regards fullAccreditation as the minimum standard to perform and interpret a full standard echo, it is not always feasible for an appropriatelytrained echocardiographer to attend in a timely manner. With the increasing availability of simpler, cheaper, more portable machineswith faster boot-up times, ultrasound use is becoming widespread in emergency and critical care medicine. It is used to aid vascularaccess and pleural imaging and FAST (focused ultrasound) is now considered a standard part of Advanced Trauma Life Support(ATLS).

The FEEL-UK training programme

FEEL-UK is a programme intended to train practitioners in the use of focused transthoracic echo in a standardised manner duringthe peri-resuscitation period, developed using experience from various international courses of focused echo in the critically ill.

The programme comprises a one-day course of lectures and small group (maximum 3 students) hands-on training sessions andsimulated resuscitation scenarios. It is run along the lines of the ALS/ATLS - highly standardised and regulated to ensure minimumstandards are achieved. Delegates are then required to continue their training locally by demonstrating competence in performingand interpreting focused studies on critically ill patients under the supervision of a local mentor (BSE Accredited or equivalent -usually a local Cardiologist, Cardiac Physiologist or Cardiology Registrar).

Focused echo differs from standard echo in a number of key ways – firstly, not all standard views are required – just the viewsnecessary to rule in or out some of the important causes of cardiac arrest. Secondly, potentially treatable findings in the peri-arrestsituation are expected to be gross and easily recognisable by eyeballing an echo study, for example a massive pericardial collectionor profound hypovolaemia. Measurements/Doppler studies are not part of the focused exam.

Thirdly, reporting follows a simple diagnostic approach answering yes or no to a series of questions applicable to the setting of peri-arrest and easily communicable to the resuscitation team.

The Mentor

The role of the mentor is crucial. The onus is on the student to identify and liaise with the mentor, who need not be present for allscans but ideally would observe the first ten or so to ensure correct technique and provide feedback on the study. Each studyrequires the student to obtain 4 standard views (parasternal long axis, parasternal short axis, apical 4 chamber and sub-costal),recording and reporting the scans systematically in accordance with the focused echo questions. A minimum of 50 scans is requiredto obtain FEEL-UK certification, these are reviewed at appropriate intervals and signed off by the mentor once satisfied the studentis performing and interpreting a FEEL examination adequately.

Echo departments are busy places, and finding the time to act as a mentor may seem difficult, but there are advantages. Input fromexperienced echocardiographers potentially results in raised standards, benefiting the patient, raising the profile of the mentor andimproving links between the department and Critical Care. After completing the process, enthusiastic students may even be inspiredto undertake full Accreditation!

For further information including course dates, go to www.FEEL-UK.com

Jane Lynch

BSE FEEL Representative


PAG E 29

CASE REPORTS1) Partial AnomalousPulmonary Venus Drainage(PAPVD)A 58 year old lady was referred for a transthoracicechocardiogram by her GP after an episode of atrial fibrillationto exclude cardiac structural abnormalities. The patient was afit, healthy person and did not have any complaints. At the timeof study she was in sinus rhythm.

The investigation identified a dilated coronary sinus andsignificantly enlarged right heart, which was unusually largeeven for severe pulmonary hypertension. In the apical 4chamber view, three engorged pulmonary veins were obvious.However, it was impossible to visualise the fourth vein. In thesubcostal views, the picture became clearer. The fourth (rightupper) pulmonary vein drained into the right atrium throughlarge sinus venosus atrial septal defect (2.1 cm). There wassuggestion of additional left sided superior vena cava causingthe dilated coronary sinus.

The patient underwent a cardiac MRI soon which confirmed alarge superior sinus venosus ASD with partial anomalouspulmonary venous drainage and a persistent left SVC. She iscurrently awaiting repair of her ASD and correction of partial

anomalous venous drainage.

Discussion:Partial anomalous pulmonary venous drainage (PAPVD) isdefined as a left-to-right shunt where one or more, but not all,pulmonary veins drain into a systemic vein or the right atrium.Anomalous right-sided pulmonary veins can drain into thesuperior vena cava (SVC), right atrium, inferior vena cava,azygos vein, hepatic vein or portal vein. The connecting sitesfor anomalous left-sided pulmonary veins can be the leftbrachiocephalic vein, coronary sinus and hemiazygos vein.PAPVD involving the right upper pulmonary vein can beassociated with a sinus venosus atrial septal defect (ASD)located near the SVC orifice [1].

All PAPVDs are left-to-right shunts, but unless more than 50%of the pulmonary flow drains to the right side of the heartclinical manifestations are rare. Dyspnoea, fatigue, exerciseintolerance, palpitations, syncope, atrial arrhythmias, right heartfailure, and pulmonary hypertension may occur.

PAPVD is usually diagnosed by transthoracic echocardiography(TTE) or transoesophageal echocar-diography (TOE) andcatheter based angiography. However, modern 128-slicemultidetector computed tomography (MDCT) scans are moreaccurate in defining ASDs and PAPVD.

Dr Otar Lazariashvili, Dr Tuan Peng ChuaRoyal Surrey County Hospital

Fig. 1. An image showing three pulmonary veins draininginto the left atrium (4 chamber view).

Fig. 4. The sinus venosus atrial septal defect (subcostal view).

Fig. 2. The right upper pulmonary vein (RUPV) can be seendraining into the right atrium (RA) through a sinus venosusatrial septal defect (ASD) in the subcostal view.

Fig. 3. Colour flow across the atrial septal defect.


PAG E 30

2) Cardiac Metastases ofMalignant MelanomaA 74 year old gentleman presented with a history of progressiveshortness of breath for the last 2 months and more so in the lastweek. He had had a malignant melanoma removed from his leftthigh 4 years previously. He was found to have recurrence ofthe disease in the gastric wall, spleen, retro cardio-oesophageallymph nodes and lymh nodes in gastro hepatic ligament in May2013 and was due to have anti-CTLA4 monoclonal antibody,Ipilimumab, as a part of a trial.

He had raised JVP and ankle oedema, but the chest was clear on

auscultation. An ECG showed right bundle branch block andatrial fibrillation with fast ventricular response. AnEchocardiogram showed a large mobile mass in the right atriumtraversing the tricuspid valve during diastole (Fig 1). RV wasdilated with pressure overload causing D shaped septum inparasternal short axis view (Fig 2). Pulmonary arterial pressurewas raised (Fig 3). The patient had a further CT scan of thechest, abdomen and pelvis which showed a mass in the rightmain pulmonary artery partially occluding the artery andextending onto the lobar and segmental branches of the rightlobe (Fig 4). Masses were also noted in the lobar and segmentalbranches of the lungs. Multiple metastases were also noted inthe liver and intra–abdominal lymph nodes (Fig 5). So this iscase of metastatic malignant melanoma with extensivemetastases to liver, lung, heart, lymph nodes and spleen. Due tothe extensive disease and poor performance status it wasdecided to manage the patient palliatively.

Discussion:Primary tumours of the heart are rare. In contrast, metastatic

Fig. 1. Apical 4 chamber view showing the mass in Rightatrium

Fig. 2. Short axis view showing D shaped septum suggestingRight ventricular pressure overload

Fig. 3. Increased TR velocity suggestive of raised pulmoanaryArtery systolic pressure

Fig. 4. CT scan showing mass in right pulmonary arterypartially obstructing the lumen

Fig. 5. CT scan showing multiple liver metastases


PAG E 31

involvement of the heart is relatively common. In one of thelargest autopsy series of over 1900 patients dying of cancer, 8%had metastatic disease to the heart 1. Cadiac involvement canhappen due to haematogenous metastases, direct invasion fromthe mediastinum, or tumour growth into the venacava andextension into the right atrium 2. Owing to their high propensityto haematogenous spread, malignant melanomas frequentlymetastasize to the heart, and represent the tumour with highestrate of cardiac metastasis 3. Other solid tumours commonlyassociated with cardiac involvement include leukaemia,lymphoma, lung cancer, breast cancer, soft tissue sarcomas,renal carcinoma, oesophageal cancer, hepatocellular carcinomaand thyroid cancer. Cardiac or pericardial metastases should beconsidered whenever a patient with known malignancydevelops cardiovascular symptoms particularly if this occurs inconjunction with cardiomegaly, a new or changing heartmurmur, electrocardiographic conduction delay, or arrhythmia.Emboli thought to originate in the heart should also raise thepossibility of cardiac involvement with tumour. The diagnosticevaluation relies upon echocardiography, MRI and CT to

ascertain the extent of cardiac involvement. In very selectivepatients, resection of cardiac metstases has been used to providesymptom palliation and prolong life. 4

Dr Kingsuk MukherjiWithybush Hospital

References :1. Silvestri F, Bussani R, Pavletic N, Mannone T. Metastases of

the heart and pericardium. G Ital Cardiol 1997; 27:1252.

2. Unusual sites of metastatic malignancy: case 1. Cardiacmetastasis in hepatocellular carcinoma.Longo R, Mocini D,Santini M, Giannantoni P, Carillio G, Torino F, Auriti A,Marcello R, Lanzi G, Cortese F, Gasparini G .J Clin Oncol.2004;22(24):5012.

3. Glancy DL,Roberts WC. The heart in malignant melanoma.A study of 70 autopsy cases.Am J Cardiol 1968; 21: 555-571

4. Surgical management of metastatic melanoma to theventricle. Messner G, Harting MT, Russo P, Gregoric ID,Mukhopadhyay M, Flamm SD, Frazier OH.Tex Heart Inst J.2003;30(3):218.

BSE ACCREDITATION PROCESS UPDATETo ensure that we are consistent in our processes, the following BSE Accreditationcategories must now be completed with a 24 month period around passing thewritten examination, including digital case collection and logbook submission. Thecategories are;

Transthoracic Echocardiography

Transoesophageal Echocardiography

Community Echocardiography

Critical Care Echocardiography

This means that you can decide during what period you will collect and submit yourlogbook cases as long as you have passed the written exam during this period.

For example; if you take the TTE Accreditation exam in April 2014 your logbook casesand digital cases could span 15th March 2014 - 14th March 2016 or 1st June 2012 to31st May 2014.

If you collect your cases in the 24 months prior to passing the exam, you must notsubmit before receiving confirmation that you have passed.

This is applicable to all candidates who passed the TTE and TOE Accreditationexaminations in Liverpool on 10th October 2013 and for all candidates who sit theabove accreditation examinations going forward.

Please see the most recent Accreditation packs for more information on obtainingBSE Accreditation.


PAG E 32

BRITISH SOCIETY OF ECHOCARDIOGRAPHYCLINICAL PRACTICE FORUMThe purpose of the BSE clinical practice forum is to identify areas of clinical echo practice where departments would like to

improve or introduce new techniques but face barriers which prevent them implementing change. We would then like to draw on the

experience of the whole BSE membership to provide practical solutions. We invite BSE members to submit their experiences of

these challenges, and importantly their solutions for how they were overcome. These will then be collated and published in a

forthcoming issue of Echo.

Integration of echocardiographic contrast agents into routine clinical practiceOne of the most common indications for an echocardiogram is the assessment of left ventricular (LV) function. In fact despite its

limitations, referrers will often specifically request quantification of LV ejection fraction. It is well recognised that up to 10% of

echocardiograms may be limited by sub-optimal visualisation of left ventricular cavity segments and thereby lead to inaccurate

assessment of LV function. The use of contrast agents for LV opacification has been shown to provide a cost effective, reproducible

and robust technique which improves our ability to assess LV ejection fraction in comparison to other imaging techniques. In 2012

the British Society of Echocardiography (BSE) undertook a nationwide survey to understand how the use of contrast enhanced

echocardiography has been implemented. The full results can be found in the published paper but some of the key findings are

discussed below. Overall less than 4% of echocardiographic studies were contrast enhanced despite the majority of the departments

being able to perform a contrast study if needed. The low use of contrast was deemed be due to the following factors: staff training

(access to i/v cannulation services and physician present as medical back-up for physiologists) (34.6%), extra time required for a

contrast study (29.9%) and the expense of contrast (18.7%).

The survey highlighted the barriers many echocardiographic units have faced when trying to integrate contrast into daily clinical

practice. Please write to us with any barriers you have found when trying to use contrast agents or if you have managed to solve

problems let us know how you did it.

Please e-mail: [email protected]

Questions:

• How can we train our physiologists to perform intra-venous cannulation independently?

• Can physiologists administer contrast agents independently within the echo lab? Does contrast need to be prescribed by a

doctor? Does a doctor need to be present?

• Who pays for the cost of contrast agents and how do we re-coup them? Are there any cost effective models we can use?

• Do the patients need to sign a consent form?

• Are there any risks we need to be aware of?

• Do physiologists require any extra insurance if they are administering contrast agents?

Future topics for the clinical practice forum include:

• Physiology led stress echo

• Supporting training and education

• Utilising 3d Echo effectively

• Implementing quality control processes

• Meeting the 7 day working week challenges

(and any others you suggest)


PAG E 33

BSE DEPARTMENTALACCREDITATIONI wish to share with you our experience of becoming the first BSE accrediteddepartment in Yorkshire back in December 2011. We are a large district general hospital trust, spread over 3 sites and performaround 11000 transthoracic echos a year and 150 trans-oesophageal echos. Across our 3 sites we have 13 Cardiac Physiologists and2 Consultant Cardiologists who perform echos regularly.

Having heard about BSE departmental accreditation, the first hurdle was to obtain funding for the £500 application fee. A case wassuccessfully made that the fee would be worthwhile in return for having accredited status of our echo service, particularly with AnyQualified Provider contracts being offered for other cardiac services in our area around that time. We therefore applied for the TTE,TOE and training parts of BSE departmental accreditation.

At first the criteria, paperwork and enormity of the task ahead seemed a mountain to climb but none the less, we began! On readingthe criteria there were some areas we needed to improve upon including devising a more detailed information leaflet for patients,running regular echo review meetings, increasing the number of echos reviewed for quality assurance and fulfilling the number ofsessions the clinical lead spends in echo. We did much of this work before arranging our formal visit so we felt we would besuccessful.

A physiologist and cardiologist from BSE Departmental Accreditation group then visited all 3 sites of our hospital. As well asreviewing documentation and gathering information from service leads, they talked informally to some of our physiologists involvedin echo and reviewed a selection of recently performed echos. They concluded that our clinical lead for echo spent enough time inecho as TOE and TTE sessions, echo meetings etc all counted towards this. Our visit report was helpful in helping us identify areasfor further improvement and confirmed that we had achieved accreditation in both TOE and TTE but further work was required toachieve the training accreditation.

Having an application process to follow benefitted our department by making us look critically at our practice. We improved ourquality control processes and the previously sporadic echo meetings at one site became a weekly cross-site meeting with regularclinical input that we feel improves quality. The process helped us secure funding for our older echo machines to be replaced, thisbeing one of the standards of departmental accreditation. We now have more physiologists with individual BSE accreditation andthis process has helped put the spotlight on improving and maintaining quality whilst dealing with the expanding service needs.

Above all, we feel that BSE department accreditation has given us local and national recognition for the high quality service wedeliver. Although attaining departmental accreditation requires hard work by the whole echo team, and management support, ourexperience is that this is well worthwhile and so we would advise any department considering this to go ahead and apply. Nodepartment is perfect but in the context of an increasingly competitive healthcare environment, a hallmark of quality cannot be a badthing for departments to attain.

Sarah RitzmannDoncaster & Bassetlaw Hospitals NHS Foundation Trust

COMMUNICATING WITH THE SOCIETYDawn Appleby [email protected] - 020 7345 5185

BSE, Docklands Business Centre, 10-16 Tiller Road, London, E14 8PXTel: 020 7345 5185 Fax: 020 7345 5186

We can also be contact via email to:

General and Post Accreditation (membership, re-accreditation, Distance Learning)Chris Grant at [email protected]

Accreditation (exams, logbook submissions) – Kemi Olanrewaju at [email protected]

Financial matters (payments, direct debits, duplicate receipts) – Ingrid Daniel at [email protected]

Meetings and Events – Dawn Appleby at [email protected] [email protected] - 020 7345 5185

For submission of educational articles or case reports for ECHO:Dr. Gordon Williams at [email protected] and/or [email protected]


PAG E 34

SCRAMBLED ECHOESUnscramble the clues, and then fit them in the

grid provided below to complete the puzzleClues

Scrambled Unscrambled3 letters

TEJIRMGEVURB

4 lettersLIMDBRISSEABSPULSPUCGEEDPOLO

5 lettersTIARACREALLAVVEROWEPDEGEWCARTHGASTESIPMRLABAS

6 lettersCROSTERALANPRALYNXRATICORALMITCALIPARATSIN

7 lettersSETDISCLIVEOLADOILAMYRODACHERASCOIDPRODLEP

8 lettersRASCLIVESUREPERSJETICONEBUSMROTHROPESLAP

9 lettersTROLSHHEDCLEEVRINTNONSEIDEA

Dr Jones had a hard time

delivering his speech,

what with the constant

murmur in the room

Stuart Self has provided us with another brain teaser.All correct entries will be put into a drawer to win £75 in vouchers.


PAG E 35

RECENTLY ACCREDITED MEMBERSCongratulations to the following members who have recently achieved BSE Accreditation

Transthoracic AccreditationRacquel Alicmas, Heatherwood and Wexham Park NHS TrustFoundationSiobhan Armstrong, St George's Cardiac InvestigationsDr Sajid Aslam, University Hospital of WalesMariam Batay, Queen Elizabeth HospitalSonia Batty, Royal Berkshire Hospital Michael BirdDr Louise Brown, Southampton General HospitalMaria Burnett

Howard Carter, Papworth HospitalVictoria Cavanagh-Craig, County Durham and DarlingtonNHS TrustJoyce Cervantes, Basildon and Thurrock university HospitalPaul Charlton, Great Western HospitalLindsay Coates-BradshawReuben Dane, Birmingham Heartlands HospitalDr Vijay Dhakshinamurthy, University Hospital of CoventryClaire Elliott, Morriston HospitalNaomi Farnon, University Hospitals South ManchesterSusan Geldard, Leeds General InfirmaryDr Mark Gilmore, Morriston Hospital, SwanseaMarcos Gonsalves, Buckinghamshire HealthcareCharlotte Guanlao, Poole Hospital NHS Foundation TrustSafia Hamid, Hammersmith Hospital Dr Alan Harkness, Colchester HospitalAmanda Hayden, Worcester Royal Hospital Lesley Jones, Warrington and Halton Hospitals NHSFoundation TrustCarys Jones, Glangwili General HospitalAllison Jones

Faye Jowsey, Leeds General InfirmarySatvinder Kahlon, Heart of England NHS FOUNDATIONTRUSTSteven Kane, Broomfield Cardiac Department ChelmsfordDr Afshin Khalatbari, Liverpool Heart and Chest HospitalDr Dipak Kotecha, University of BirminghamDaniel Lamb, Essex Cardiothoracic CentreRebecca Macrae, The Heart HospitalJayne Mahmoud, Lorn and Islands HospitalSheena Mathew, Addenbrook's NHS hospitalThomas McConnell, Royal Victoria HospitalLukshmi McCormick, Northwick Park Hospital

Bruno Mendes, King's College HospitalSarah Moon, Cardiff and Vale University Local HealthboardAsma Mullan, Queen Elizabeth Hospital, BirminghamFria Marie Nitura, West Middlesex University Hospital NHSTrustMaria Paton, Leeds General InfirmaryGemma Priest, New Cross HospitalDr Shouaib Qayyum, The Royal Wolverhampton NHS Trust Dr Hindocha Rakhee, Royal Sussex County HospitalDr Krishnaraj Sinhji Rathod, King George Hospital Simon Reece, Good Hope HospitalEmma Richardson, Portsmouth Hospitals NHS TrustJonathan Ritchie, University Hospital of North DurhamLaura Robinson, Sunderland Royal HospitalElaine Rogers, Ulster Hospital, BelfastJane Rogerson, Pinderfields HospitalLisa Romanis, Royal Infirmary of EdinburghIan Rose, Gateshead Health Dr Kulvinder SandhuDr Anshuman Sengupta, Bradford Royal InfirmaryEswararaj Sivaraj, Southampton General HospitalDenise Skedd, New Victoria HospitalChristopher Stanton, The Royal Liverpool and BroadgreenUniversity HospitalsLouise Stevenson, Sheffield Teaching HospitalJohn Stewart, Sunderland Royal HospitalDr Imran Sunderji, Castle Hill HospitalGarry Sykes, Leeds General Infirmary Charlotte Turner, Leeds General InfirmaryDewet van der Westhuizen, Homerton Hospital Dr Malgorzata Wamil, Milton Keynes HospitalNatasha Watchorn, Mid Yorkshire Hospitals NHS TrustDr John Whitaker, University Hospital LewishamDr John Whitaker, St Thomas' HospitalDr Kee Fui Wong, NHS TaysideDr Aaron Wong, Morriston HospitalDr Juqian Zhang, Queen's Hospital

Transoesophageal AccreditationDr Yasmin Ismail, University Hospitals BristolDr Douglas Atkinson, Manchester Royal InfirmaryDr Dipack Kotecha, University of Birmingham

Departmental AccreditationUniversity Hospital, Southampton


PAG E 36

4th December BJCA/BSE Day

Location: London

Contact: http://bsecho.org/general-

events/bjcabse-trainee-day/

6th December Mechanical Circulatory

Support Conference

Location: Newcastle

Contact: [email protected]

27th – 30th January Philips Hands On Echo Course

Location: Birmingham

Contact: [email protected] or

01954 200 018

DATES FOR YOUR DIARY 2013BSE members can also see up-to-date details via the

Events Calendar on the website www.bsecho.org

Full details and course descriptions for all these courses are availablefrom the BSE website.

2014

28th January Manchester TOE

Simulation Workshop

Location: Manchester


11th March Manchester TOE

Simulation Workshop



3rd & 4th April St Georges’ TOE Course

Location: London

Contact: [email protected] or

www.toe-courses.com

13th May Manchester TOE

Simulation Workshop



to the Editor

Letter

s

Submit articles, case reportsor letter correspondence to:[email protected]


PAG E 37

Advanced Imaging in Hypertrophic CardiomyopathySessions will include anatomy, diagnosis, the roles of multimodality imaging and pitfalls.

Presenters will include anatomists, surgeons and interventionists. The day is suitable to all involved in the care of patients with Hypertrophic Cardiomyopathy,

since it offers a holistic approach to their care with a focus on imaging such hearts.5 BSE reaccreditation points have been allocated to this meeting and

CPD points have been applied for.

For further details and to register please go to

www.bsecho.org/events-courses/advanced-imaging-2014/

Advanced Imaging Day 79th May 2014

Royal Society of Medicine, London

Advanced Imaging Day 79th May 2014

Royal Society of Medicine, London


PAG E 38

Core knowledge in Echocardiography 2014Post Graduate Centre, Nottingham University Hospitals, City Campus

Wednesday 21st and Thursday 22nd May 2014

Core knowledge in Echocardiography 2014Post Graduate Centre, Nottingham University Hospitals, City Campus

Wednesday 21st and Thursday 22nd May 2014C

ered by experts in the field of echocardiography and will cover the basics and current recommenda-tions for assessment of various conditions. In addition to didactic lectures, there will be interactive case discussions on various topics with tips and tricks for assessment. You can test your knowledge and improve confidence using self marking theory and video questions.

The course is aimed at anyone starting out in echocardiography or those wishing to refresh their knowledge. The course covers the majority of the syllabus for echocardiography accreditation examination and is ideal for those wishing to sit the BSE exam in the next 6-12 months.

Topics covered -Normal views and minimum data setPractical physics and image optimisation (how to make the best use of the ultrasound machine)Ischaemic heart disease and LV function – principals and methods of assessment;Right heart assessment including tricuspid and pulmonary valveAortic valve diseaseMitral valve diseaseCardiomyopathiesProsthetic valvesCardiac masses and endocarditisApproach to adult congenital heart disease (CHD)Echo in emergency medicineReporting a transthoracic studyHemodynamic assessment

Course fee includes handouts, refreshments and lunch. Local accommodation details available on request.

BSE members will need to register online. Non members will be able to print off a paper registration form.

ourse fee £250This is a 2 day course covering core topics in adult echocardiography. Course content will be deliv-

Course fee £250

Feedback from September 2013“Very useful and well run course. Good variety of topics covered - useful for refresher with measurements etc and very

useful for things that are not commonly done in every case.”“Very in-depth course covering a vast array of topics. Thoroughly enjoyed all lectures and look forward to putting all I have

learnt over the last 2 days into practice. Many thanks.”“Excellent course”

To register please go to www.bsecho.org For further details including sessionextracts please go to www.bsecho.org/events-courses/core-knowledge/


PAG E 39

e


Irish Cardiac Echo & Imaging Group

I.C.E.

Joint BSE & ICE MeetingSaturday 5th April 2014

Joint BSE & ICE MeetingSaturday 5th April 2014

Hilton Templepatrick, Belfast

This one day meeting will be held the day following the BSE spring accreditation exams taking place at the same location in Belfast.

Provisional Programme (subject to amendment)

• Surveillance of aortic regurgitation – just the LV?• Is low gradient low flow just moderate AS?

• Defining ischaemic MR on echocardiography• A systematic approach to ACHD on TTE

• Ventricular Septal Defects• Is TR enough in pulmonary hypertension?

• Echo in CRT – dead as a dodo?• Stress and Perfusion – now required reading

• Echo assessment of the RV – still a step too far?• DICE Cases: The Weird and the Wonderful

The day has been approved for 5 BSE re-accreditation points.CPD points have been applied for

To register to attend please go towww.bsecho.org/events-courses/bseice-meeting-2014/

The pre-registration fee is £65 per person.All registrations will be processed in GB£.

Onsite accommodation is available.


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