Posts Tagged ‘pah’

Pulmonary circulation  is a  low pressure  , low impedance  but  a high capacitance  system  . The job  of  pulmonary circulation  is  not only  to  ferry  the  blood from  right ventricle to  left atrium  ,   it should also ensure smooth gas exchange as it traverses the circuit . (How vital  it’s job is  . . . but we tend to be  obsessed with heart !)

The paradox is ,  for  the  flow of blood to occur you need a pressure head . (Note :  the pressure head is 120mmhg in systemic circulation.) The pulmonary  pressure head  is  only about 5-10mmhg it has to push the entire blood .(Pulmonary   pressure head  = Mean pulmonary artery pressure -mean LA pressure )

In  healthy persons

  • Pulmonary artery pressure (PAP)  is not supposed to increase beyond few mmhg.
  • The diastolic pulmonary artery pressure can not  afford to increase  even  those  few mm.

If it does , it  can cause serious hemodynamic and oxygenation issues. Both these statements are  based on  strong scientific  beliefs But now we realise the margin of these elevation has been revised a little higher  in normal persons .

  • In health ,  athletes can reach a systolic PAP  up to 40mmhg .
  • Diastolic PAP still largely remain a mystery . You can’t measure it when the patient is running you know !

Here is a recent article from chest  (2011) which documents pulmonary artery systolic pressure in trained athletes .

Relationship between exertional dyspnea and PA pressure.

The mechanism of  exertional dyspnea in any  individual is largely attributable  to  exercise induced pulmonary vascular  stretch .(J receptors etc ) . Many still believe  human functional  capacity is limited primarily by  the  lung function and the cross sectional areas of  pulmonary microvascular  bed .( Is this the  reason  two  patients with 25% EF  has vastly different functional capacity ?)

* Note : Exercise induced  pulmonary artery pressure  elevation are well-recognized in pathological states.

  • Mitral valve disease
  • In established COPD
  • In patients  with LV dysfunction


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 Excercise physiology has been studied most extensively in the last century.The hemodynamic impact of excercise in various disorders of heart has been well established.
Dyspnea on exertion is the commonest symptom in clinical cardiology practice. It is well-known pulmonary stretch receptors located in pulmonary vasculature is one of the  major mechanism of dyspnea.

Excercise increases the cardiac output manyfold.Transporting  up to 10-12 litres of blood every minute across the lungs with a narrow pressure  head (about 10 mmhg ) is not an easy job . It needs lot of lung discipline .

It is surprising to note, there is little data on excercise induced pulmonary hypertension in the evaluation of patients with unexplained dyspnea.

We know, excercise increases the systemic blood pressure ,we  presume it should not raise the PAP (however severe the exertion is 1 )as pulmonary circulation  is a  high compliant low pressure system. 

Is our presumption correct ?

Exercise induced PAH can occur in both   health and disease 

In patients with preexisting disease

  • Stress induced LV dysfunction and resultant raise in LVEDP-PCWP-PAP .This is the most common mechanism in valvular and myocardial  disease.

Apparently healthy population

  • Excercise  induced PAH as a  marker for silent CAD .
  • Transient Hyperkinetic PAH* (Note :Here PCWP is usually normal )

This is similar  to hypertensive response to EST in systemic circulation.Existence  of this entity , is controversial, But this may reflect  reduced pulmonary vascular reserve  or reduced pulmonary nitric oxide secretion.

*The main difference here is the PAH is more often an  isolated systolic PAH. While LV dysfunction induced PAH is  a combined diastolic and systolic PAH .
How to assess excercise induced  PAH ?
It is not an easy job. Invasive catheter derived pressure measurements have been done ,but it is not practical .

The simplest way is to look for the TR /PR jet in echo in both pre and post excercise phase.

Final message

Excercise induced PAH is an inadequately studied entity in cardiology , in spite  it’s great significance .
This phenomenon is observed  in both diseased and normal heart.

The quantum of excercise induced PAH  is  widely variable depending upon the cardiac  status especially  LV function and the  functional integrity of pulmonary microvasculature .

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PAH  is  the major determinant of surgical outcome of left to right shunts. In this  modern era of cardiac care  allowing a child  with   left to right shunt   to progress to a  stage of   Eisenmenger syndrome  is  considered  as a  huge medical failure . But  , this is still rampant in many of the developing countries .

Cardiologists are divided over the issue of  operability of Eisenmenger syndrome .The confusion is largely due to the conflicting data of outcome in these patients. While  there is strong   data  when  PVR exceeds  SVR  ,  the death is imminent in the post operative period .

What has complicated the issue is   there are  many case reports  where severe PAH patients have been successfully operated. Most would think it is a statistical exception and one can  not alter the traditional criteria based on few case reports.

But ,it remains an irony as on 2009 ,  we do not have a proper methodology to assess reversibility of PAH in Eisenmenger syndrome . Further ,  there is a  significant number of  patients with high PVR  , who continue to experience  an  unabated left to right shunting .  We do not have an answer  for either the mechanism of such shunts and  how to manage these patients.

Click over the slide  to view full  PPT  presentation in PDF format .

This short paper was presented in the Annual scientific sessions of cardiological society of India 2009 regarding the usefulness of a new parameter to assess reversibility of PAH. This may not be called as  a study rather a report of  our experience  in  five  patients  with eisenmenger syndrome

Download the full PPT presentation in PDF  format.

pulmonary artery pulse pressure

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                                  Even as cardiology community is preoccupied with systemic hypertension & CAD  ,  pulmonary arterial hypertension(PAH) is a much neglected , still  an important clinical cardiac problem encountered . The irony is self evident , there are half a dozen methods to grade systemic hypertension not even a single stadardised grading available for pulmonary arterial hypertension. The WHO  working group defined pulmonary hypertension  few decades ago and was not clinically graded .The only grading available is based on  the pulmonary vascular biopsy changes (Heath Edwards) 

                                   Currently PAH management has gone through revolutionary changes. There is an urgent  need for grading  this entity .This will facilitate to  diagnose , manage and assess the efficacy of the currently available treatment.

                                Developing countries like ours have a great number of PAH due to rampant rheumatic heart disease.  A simple study was done in  100 patients with PAH .Bulk of the study population had RHD .Few had primary pulmonary  hypertension .Systolic , diastolic, and mean pressure was assessed by doppler echocardiographic analysis of tricuspid regurgitation (TR) and pulmonary regurgitaion(PR) jets. TR jet provided the systolic PA pressure , PR jet provided mean as well as diastolic PA pressure .TR jet was available in all patients. PR jet was available only in 60 patients .Hence the diastolic andmean PA pressure data has been extrapolated in some  and  was plotted in a scatter diagram. Five equal quintiles were divided. Patients in first  and 2nd quintiles were graded 1   and third  and 4th  quintile were  graded 2 ,  5 th  was graded 3 respectively. From this cut off points for  various grades of PAH were identified .The top 3% of patients  with highest PAP were graded as grade 4 and all of them had supra systemic PAH. 

The following grading is suggested for PAH* 

 *This is a preliminary  attempt to grade PAH. This could be applicable mainly in rheumatic heart disese and primary pulmonary hypertension .Further refining of methodology is  required.PAH grading may be little different in congenital left to right shunts.

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