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Posts Tagged ‘rvh’

RVH is  traditionally  categorized into three types . With  the  advent of echocardiography  diagnosing  RVH by ECG would  appear  redundant. Still , it gives vital information about the electro-physiologcal basis  of RVH. Knowing different mechanisms of RVH helps us decode  regional variations in RVH.

Type A , Type B  are easy to diagnose as they fulfill the conventional criteria of tall R in lead V1

Type A  RVH occur in severe  pulmonary hypertension and critical valvular pulmonary stenosis.

Type B  RVH occur in  volume overload states like ASD and moderate  forms of mitral stenosis.

( Severe  MS may cause Type A pattern  if RV pressure exceed systemic pressure)

Type C  RVH    has  no classical signs of RVH. Here  RVH  is diagnosed by proxy . Look for RAE  and a  vertical QRS axis . ( For all practical purposes RAE will indicate  RVH  except in isolated tricuspid stenosis.

Type C RVH occurs classically in COPD and in some cases  of acute pulmonary embolism .In other- words type C  RVH  reflects  predominantly  RV dilatation rather than  hypertrophy.

Why Type C  RVH is important ?

It is important  for two  reasons

  • It  is  basically a  masked   RVH .
  • It mimics Anterior MI

Missing the first  one and erring  in  later  both  can have major  implications  in clinical cardiology  especially during emergencies.

What is  the mechanism of poor  R wave in precardial leads in  Type C RVH of COPD ?

The fact that  poor  R wave  in precardial  leads occur in  most  cases of  COPD  (whether or not RVH is present or not)   convey an important message.

The  lack of  R wave  progression   is probably  less to  do  with   rotation of  RV  than  the insulation effect  lung  . Further, the  elongated lungs   drags   the heart down , and  make it more vertical and in spite of RVH tall  R  is not picked up by v1 v2 .

Unlike primary PAH and critical MS where the RVH  can dominate the LV  ,  the  quantum of  RVH is never huge in pure COPD . However , presence of RBBB  could  alter  the R wave amplitude .

ECG in acute pulmonary embolism

This resembles the type  C  RVH . The  R  waves in V 1  and  V 2 can not gain the voltage acutely.

The S 1 . Q 3 , T 3  pattern if present indicate the  acute RV strain and  the resultant  RV wall motion defect.

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Clinical scenario : Practical utility of  decoding    RVH   by ECG ?

A  middle aged female came  to our CCU  with acute  dyspnea with tachycardia .

Echo revealed a dilated  RA and RV . She had  mild TR and moderate to severe PAH (The TR jet measured 3.8m/sec)

The MPA showed a hazy shadow suspicious of thrombus . The patient  had no evidence for DVT .

The fellows  arrived at  a conclusion about a  severe  PAH  but , the etiology was debated.

One is chronic thrombo-embolic PAH . Other groups argued for acute massive pulmonary embolism and resultant PAH.

This raised an  important    therapeutic   issue  as one of them wanted to lyse the thrombus  ,  the  other argued for simple heparin .The  argument continued as the first fellow reminded ,  presence of RA, RV dilatation is a sign of acute RV strain  . The other countered the  same  as  it could be  a  chronic response  to pre existing PAH.

How do you know  in an emergency ,  whether the RA, RV dilatation is new onset  or a chronic one ?

In spite of  good   echocardiogram  we were confused .  Then it struck  to us ,  ECG would solve our problem . It indeed helped us. She had a tall  monophasic  R  in  V1  indicating   Type A RVH , which suggested chronic PAH   and  the thrombus in MPA  in all likely hood  was a sequel  to PAH  and  not vice versa . A type C RVH  would have voted  in favor of  acute pulmonary embolism.

Meanwhile a  CT pulmonary angiogram  report was available   . It showed a small  thrombus in MPA and LPA with no clearcut perfusion defects ruling out acute pulmoanry embolism . The thrombus was probably  de-nova in- situ thrombus due to PAH.

 

 

Final message

It may  appear  funny for the  present day cardiologists to waste so much time  to analyze  the  RVH  by surface ECG . But please remember ECG remain the only simple and cheap  investigation that transmit live data from the heart instantly  .Most importantly unlike other imaging  modalities  ECG data do not vary with person who records it !

Reference

A very good referen from   Basic and Bedside Electrocardiography   By Romulo F. Baltazar

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It sounds  to be a  simple question . But, cardiology literature is sparse  on the subject.

RV mimics a three dimensional triangular chamber .The inflow, body and outflow align themselves in complex planes .This makes measurement difficult.

What  are the measurements to be made  ?

  • RV inflow tract (RVIT)
  • RV body
  • RV outflow tract (RVOT)
  • RV Free wall thickness

How to measure RV size ?

  • Inflow diameter is assessed in inflow view ( Para sternal long axis,probe  tilted down towards lower  sternal edge (cool . . .That is were tricuspid valve is located !)
  • RV body can be assessed in long axis or 4 chamber view
  • RVOT in short axis view.

What is the normal range ?

RV Body

< 3 cm in parasternal long axis view

<8 cm Long axis ( RV apex to mid point of TV )

RV inflow(RVOT)

<  3- 4cm

RV outflow (RVOT)

1.8 to 3 cm

Note :

  • All measurements are taken in end diastole .
  • The largest diameter of RV is at its inflow(it is roughly equivalent to tricuspid annulus)
  • RVOT size can vary  , generally tapers as it reaches near the pulmonary valve .

How common is the  differential RV enlargement*?

The complex shape and architecture of RV  make  the  direction , sequence  and magnitude of  RV enlargement less predictable .

  • Diastolic loading of RV generally have more uniform enlargement of RV .(Inflow, body, outflow )
  • In dilated cardiomyopathy RV enlargement  common in short axis > long axis
  • Pressure over  loading may not result in uniform enlargement as the pressure points on RV surface is not homogeneous.
  • In congenital heart disease , RV shape and size  depend more on the morphology(location of VSD, infundibular  anatomy, muscle bundles, extent of trabeculations etc)
  • In arrhythmogenic  RV dysplasia (ARVD) outflow  tract enlargement is more dominant.

* The fact that ,  RV can enlarge  in focal and localised manner make it mandatory to measure RV dimension in multiple views and in all possible diameters.

At what  pressure RV begins to enlarge ?

RV is believed to enlarge at > 60mmhg .Hypertrophy is usually precedes dilatation  .

At what volume overload RV begins to enlarge ?

Our experience with ASD indicate when the pulmonary  blood flow  is twice that of systemic blood flow RV is distinctly enlarged. May be it begins to enlarge at>  1.5: 1 shunt

RV begins to enlarge horizontally or longitudinally ?

this aspect is not studied much.  Generally volume overload causes more uniform enlargement.

How does acute RV enlargement differ from chronic RV enlargement ?

Dilatation is more conspicuous in acute RVE ( Pulmonary embolism, RV infarct ) associated wall motion defects and thinning favors acute RVE.

Normal or increased thickness is expected in chronic RV enlargement

Here is a  five-star rated  article on RV dimension

Published in 1986 , still considered a  land mark paper  . . .

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