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Posts Tagged ‘left atrium’

We presume  ECG  fails miserably against echocardiography for assessing hemodynamics , while  echocardiogram  has  little value  when it comes to studying   electrophysiology .  Ironically ,  we often  ignore  the fact  ,   ECG can  provide  important long-term   hemodynamic  data . The pattern of  chamber enlargement  give us  vital clues to the prevailing hemodynamic  stress and loading conditions. While echo  can be termed as an  anatomical and  physiologic   modality  , ECG  apart from  its unique capacity to record cardiac  electrical finger prints ,  it  provides  useful ,  anatomical ,  hemodynamic information too !

While Doppler is a  fascinating modality to measure hemodynamic data in a moment to moment fashion it can never ever tell us  , what has been going around in the preceding months or years. This  is were chamber size helps which  give us chronic physiological information (Chronic  Doppler ?)

A simple E:A reversal  in  mitral inflow doppler can be a  innocuous  finding in isolation  . If it is associated with even   minimal grades of  LAE  it gains huge importance. That is why left atrial size is  funnily referred to as HB A1C of diastolic dysfunction ( A marker of chronicity  of  diastolic dysfunction)

If LAE is so important to diagnose diastolic dysfunction , why  we are so  obsessed  with doppler filling profiles  of mitral valve ,pulmonary veins, mitral annular tissue Doppler and what not ! .Many of these sophisticated doppler methods are extremely operator dependent  and are  subjected  to technical and mathematical errors. Especially , with  tissue doppler where we  magnify the errors as we  filter  extremely  slow tissue motion .

For  many  decades  we  have failed  to impress ourselves  , about the importance of subtle P wave abnormalities in the  ECGs   of  hypertensive patients.

In fact those  innocuous looking  slurs and notches   in P waves ,  suggest the left atrial  stress and a definite marker of underlying LV diastolic dysfunction .

P wave is the only electrical wave that occur in diastole .Hence there is no surprise  ,i  gives us enormous information about this phase of cardiac cycle .

If only we look  at them carefully, zoom it (Now it is made easy with so many softwares)  analyse critically we can find a wealth of information about the atrial behavior in hypertension.

Experience from our hypertension clinic  with periodic echocardiograms suggest ,  the following  ECG  findings   can be   good markers  of significant  diastolic dysfunction .

  1. Notched P wave
  2. Wide  P waves
  3. Slurred  P wave
  4. Bi-phasic P waves

* Surprisingly  , these abnormalities correlated with at least grade 1 diastolic dysfunction even in the absence of  for LAE or LVH by echocardiogram.

** In an  occasional patient  P waves  can widen due to inter atrial block or conduction delay. This a rare exception for wide P waves without LAE.

Final message

A well recorded and   analysed   ECG can  predict diastolic dysfunction  with fair  degree of accuracy .This fact need to be emphasized  by every one  .  Next to ECG ,  LA size and volume  by 2d echo are excellent parameters  to assess diastolic function in a long term fashion. Sophisticated  but  error prone ,  momentary doppler parameters are getting too much attention  at the cost of simple ,  shrewd ECG and 2D echo  !

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Even though it is a great vein , often the imaging pulmonary veins by echocardiography is a not a pleasant excercise.

This is due to the following facts

  • The pulmonary veins are posterior structures
  • They occupy the far field of echocardiographic window
  • The pulmonary veins often enter obliquely into the LA
  • The course of PVs are highly variable ( Like RCA origin !) especially in ASDs ,where identifying PVs becomes all the more important

Hence no fixed imaging angle can be advised . But generally a pattern is observed.

  • Right pulmonary veins are best viewed in apical 4 chamber or 5 chamber or in between (Especially RUPV is  seen best in 4.5 chamber view !)
  • Left pulmonary vein , can be seen in apical 4 chamber but best visualised in  Para sternal short axis view.

Other modalities for imaging pulmonary veins

TEE : Can be  very useful since it is brings the vein closer to the probe .But needs more expertice.

Contrast echo :Probably a simple and best modality often underutilised.

Very useful to clinch the diagnosis when PVs take abnormal course as in PAPVC .

MDCT , Spiral CT, MRI  are the new age modalities that can provide us  with dramatic  3d images of PVs.

The  echocardiogram will always prevail over these sophisticated gadgets for its simplicity and also it’s ability to give us the physiology of pulmonary venous flow which is vital in many diseases(Constriction, Diastolic function etc)

The following illustration is a gross attempt to simplify the imaging of PVs.Please note the rules may not be applicable in all.

Left upper and lower pulmonary veins in short axis view will be posted shortly .

Reference

The images are  based on  personal observations and  an  excellent insight  on the topic from  Department of Cardiovascular Medicine, Guangdong Provincial People’s Hospital, Guangzhou , China

http://ejechocard.oxfordjournals.org/content/9/5/655.full

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                                       Left atrium is the posterior most chamber of the heart.  It is almost a mid line structure.  The normal size of left atrium is about 4 / 4 cm. Normal left atrial volume is 46ml in men and 38 ml in women .(Atrial volume in a normal adult population by two-dimensional echocardiography Y Wang, Chest, Vol 86, 595-601.)  Left atrium  is not an easy chamber to identify in the  X ray chest as it does not form  the cardiac border.( Except a small circumference of left atrial appendage.(LAA)

Left atrium can enlarge in multiple directions.Generally it dilates in the path of least resistance.

 

  • It is believed left atrial appendage  enlargement occur early .  LAA enlargemnet seen as a fullness beneath the pulmonary artery shadow. It may be the earliest finding of LAE in X ray. ( This may appear as straight left heart border , as in classical  mitral stenosis where MPA is also enlarged). The LAA enlargement is not necessarily in  in proportion  with LAE.
  • LA could  also enlarge posteriorly by pushing the esophagus towards the spine.This is visible only in barium swallow.
  • Then LA can enlarge either to left or right ( Usually towards right) and  reach the right heart border or over shoot it and form the right heart border by itself.This occurs very late in the course.
  • The other direction  LA goes on to enlarge is superiorly. When LA enlarges superiorly it hits on the left main  bronchus and lifts it.This is measured by the widened subcarinal angle which is normally less than 75 degrees.
  • LA can enlarge anteriorly  sometimes , but it is resisted by right ventricle but rarely right ventricle yields to the LA push and produce a left parasternal lift which could be mistaken  for RV enlargement.
  • Inferior enlargement can not happen in a significant way as it is limited by the AV groove and strong fibrous skeleton. 

With the advent of echocardiography X ray assessment of LA is redundant .(Academic value and in fellows training programs).The upper limit of normal LA size is around 4.5cm.

LA enlargement is commonly seen in

  • Rheumatic mitral stenosis, regurgitation. Gross enlargement up to 10 cms are common.
  • Hypertensive heart disese.
  • Cardiomyopathy, especially restrictive where both atria enlarge.

In all these conditions if  atrial fibrillation occurs  LA size increases further.

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The left atrium always  dilate to pressure overload.And it almost never hypertophies even whne the mean LA pressure raises to high levels. Why ?

1.The atrium basically has little muscle cells to hypertrophy.The left atrial thickness is only 2mm.

They are basically designed to passively fill the ventricles. But this is not always true  physiologically.We

 call it as booster pump and 30% of LV filling is  contributed by active pumping of  left atrium. 

2. The second reason for left atium not gettting hypertrophied  is ,  there are four decompressing exits

(safety  valves) in left atrium  namely, pulmonary viens. In fact it’s a paradox the back pressure across

pulmonary circulationmay result in RV hypertrophy

Inference & potential research areas

If by some mechanism if we can induce hypertophy of left atrium will it be a mechanical advantage for left ventricle in failing hearts .By cell therapy we can convert inert atrial cells into activley contracting cells.

DR.S.Venkatesan, madras medical college,  Chennai, India .

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