Posts Tagged ‘ispah’

What is the incidence of Isolated systolic pulmonary arterial hypertension (ISPAH) and its Implication? We attempted to answer this question and found some interesting answers. It was published in the Indian heart journal  December 2007 Abstract issue. More than a decade gone. I think this issue is still largely misunderstood. Fellows may pursue this. One more parameter that can be explored is pulmonary artery pulse pressure and effect on progressive pulmonary vascular disease and PVR. Mean while  PAH definition and classification has changed many times, ISPAH definitely requires a place in the new scheme of things.

The abstract

S.Venkatesan ,G.Gnanavelu,V.Jaganathan , Madras Medical College. Chennai

Pulmonary circulation is a classical example of a low-pressure low impedance circulation. It is generally presumed high output states generally do not increase the systolic blood pressure in the pulmonary circulation. In systemic circulation, there can be divergence of systolic and diastolic blood pressure depending upon the cardiac output and peripheral vascular resistance. This has resulted in separate clinical entity -Isolated systolic hypertension.(ISH). It has been our observation many of the patients with PAH during echocardiographic and cath study were found to have an elevation of systolic pulmonary artery pressure(PAP) with normal diastolic PAP . In this context, this study was undertaken to specifically identify whether there is an entity of Isolated systolic PAH
( ISPAH ) and it’s the incidence in various clinical situations.
We analyzed the echocardiographic data of patients who were referred to our echo lab retrospectively. A total of 4000 echocardiograms over a period of 6 months were reviewed. Majority of these patients were referred for routine screening echo from our OPD. Data from patients who were assessed to have PAH were thoroughly scrutinised. They constituted shunt lesions, RHD,PPH, COPD, pregnancy, and patients with unexplained dyspnea for evaluation Those Patients who had both TR and PR jet were only considered for analysis .The Systolic PAP was estimated with TR jet and diastolic PAP with End diastolic PR Jet. ISPAH was diagnosed when the calculated systolic PAP was more than 30mmhg. And the diastolic PAP was less than 16mmhg  Antenatal women formed 2 % of the study population. A total 72 patients fulfilled the criteria of ISPAH Among the shunt lesions it was most common in large VSD( 4/10), followed by ASD(14/35) and PDA( 1/3) . In patients with RHD it was observed in 12%(15/110) , COPD 10%(15/150), in pregnancy and general population it was 5%(23/450). None of the patient with PPH had ISPAH.The mean Systolic PAP was 38mmhg(R 32- 74) The mean diastolic PAP was 14mmhg(R 8-15).The highest systolic PAP was 74mmhg recorded in patient with large VSD.
It is often presumed hyperkinetic states elevate systolic PAP and reactive elevates diastolic PAP .But it is clear from our study the rule is not that simple. Surprisingly many of the RHD patients had only the systolic PAP raised.It is important to recognize systolic PAP was very high in some of the shunt lesions. Taking this alone as an index of severe PAH is fraught with the risk of declining corrective surgeries in these patients.
Perhaps the most important observation from the study is the incidence of PAH in apparently healthy individuals, which is very significant as it could be the marker of continuously increasing chronic lung disorders due to the worsening environment of the 21st century.


A PowerPoint presentation of the paper is available with the author and may be requested.

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The primary determinant of pulmonary artery systolic pressure is . . . ?

  1. Pulmonary arterial tone
  2. Pulmonary venous pressure
  3. RV contractility
  4. Pulmonary blood flow

Answer : All of the above

But what is the relative contribution of each ?

I am  100 %  sure  ,  no  one can answer this question  correctly !

It is  true  , in some  pathological situations  one can  be  fairly certain about  cause of   elevated pulmonary arterial pressure .

When we confront a patient  with left heart disease  it is the transmission of  mean venous pressure .

Whatever be  our understanding ( Pre/Post capillary pulmonary hyper tension and the related stuff !  ), the one parameter that makes mystery contribution  to PA pressure is RV contractility !

In physiology  RV   generates  about 30mmhg systolic pressure that becomes the  pulmonary systolic  pressure .The  diastolic pressure  will be around 15 and mean around 20 . During exercise  contractility of both RV and LV increase .There has been documented PASP up to 50 mmhg in normal healthy adults during   exertion .

Here one can assume RV contractility is causing  a entity called transient Isolated  systolic  pulmonary arterial  hypertension.(ISPAH)

Consider a entirely different situation

A patient with COPD  with raised  PASP .  The right ventricle pressure has to equilibrate with PASP  during systole .For this to happen   it has to generate the 60mmhg .  If the RV fails  to augment it’s contractility for some reason ,  will the  ineffective RV contraction will  lower the  PASP  ? This is the perplexing question !

While the popular understanding is ,  RV dysfunction will under- estimate the severity of   pulmonary hypertension   . . . still  . . .  we are not sure whether RV dysfunction will  reduce the PASP   per-se  ( and  subsequently PA  diastolic pressure as well )

We often see a  good example  . A patient who develops tricuspid valve disease and RV  dysfunction get symptomatic relief  from  lung congestion .

Final message

The relationship between RV function and pulmonary artery pressure is a real enigma. Though hyper functioning  RV is expected to elevate PASP  and hypo functioning  RV would pull  it down  , the relationship  is not that simple. If only we decode this  mysteries   we can try  specific  RV negative inotropic  agents  as a  modality to treat pulmonary hypertension .

After thought

Total artificial hearts  are going to come in a big way in the coming decades .It  will specifically address this issue  ,  as RV and LV contractility  need to  be individually tuned to avoid pulmonary congestion.

Coming soon

While  RV function is critical for human survival  ,  Fontan  principle  simply says entire RV is dispensable . How ?

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