Posts Tagged ‘lvedp’

Thorax is a rigid bony box with a fixed space.The intra thoracic organs are snugly arranged within the cavity.The two lungs on either side with the heart in the middle fill the major volume of the mediastinum .In physiological conditions the volume of mediastinum remain almost constant , except for the respiratory swings.

heart lungs pulmonary function test dyspnea cardiomegaly ct ratio

It is to be noted the two major organs inside the thorax has a distinct behavioral pattern. Lung a very pressure sensitive structure tend to collapse whenever confronted with external pressure .This is evident in all cases of large pleural effusion (Note :The heart collapses only in a fraction of patients with large pericardial effusion -ie tamponade) . Similarly in any mediastinal syndromes , first the lung function is affected , logics then dictate , the low pressure venous system to get compressed resulting in SVC /IVC syndrome.Finally the right heart chambers may get interfered with .This is due the dynamic intracardiac pressures that resists any compression from exterior.

So, it is obvious , lung function is affected with raised intrathoracic volume or pressure .The increase in intrathoracic volume can be due to any thing .

cardiomegaly massive dyspnea mechanism lvedp

The volume of heart in cardiac failure can increase very significantly .For a fraction raise of CT ratio there is many fold raise in it’s volume.A CT ratio of 75% can cause a huge ” housing & accommodation ” problem for the lungs on either side . As we have discussed , the lung is passive organ has absolutely no other option but to bow down like a touch me not plant . The lung , reduces it’s ventilatory function impairing the already poor exercise capacity .The terminal respiratory units collapse significantly. This collapse is not visible in x rays as there is no intrinsic obstruction within the airways as happens in lung pathology.

The course of events in progressive cardiomegaly is often silent and heart successfully encroaches the the human breathing space until the heart failure is corrected and normal heart size is restored. Complete reversal of heart size may not be possible always !

A new unrecognized mechanism for cardiac dyspnea ?

Yes,the mechanism of cardiac dyspnea always been centered around elevated LVEDP , lung congestion etc and the resultant stimulation of lung receptors.

Now we realise a reduction in the lung ventilatory capacity may also contribute significantly in every patient with cardiac failure and cardiomegaly.

When a person with single pnemonectomy lead a comfortable life what is the big issue of heart compressing few respiratory segments of a patient ?

It is true a single normally functioning lungs is sufficient for living but what we are dealing here is patients with compromised cardiac function.Recruitment or non recruitment of even few respiratory bronchooles may have a bearing on patients symptoms and exercise capacity.

Final message

Cardiomegaly is not an inert consequence of cardiac failure. It can have important functional impact on the pulmonary ventilatory and perfusion capacity .It should be emphasised this mechanical encroachment on the lung space is over and above the hemodynamic effects on pulmonary capillary circulation .

Youngsters should recognise this fact as this offers one more explanation for cardiac dyspnea. This is not often discussed in the clinical classes.



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                                    Competence of mitral valve is vital  for proper hemodynamics of  heart .A trivial mitral regurgitation ,is observed in nearly 10-20% of normal population detected by doppler echocardiograpgy .This is other wise clinically insignificant. In fact , it is expected  , the sonographers do not report this,  as it might increase the patient anxiety.

Can a mildly incompetent mitral valve be a hemodynamic advantage ?

Left ventricle , physiologically can have only one exit, namely LVOT and aortic valve.If there is normal  impedance , at this level (LV after load )  it  is refered to as  physiological .In disease states , as in cardiac failure there is raised after load or LV wall stress.this makes the LV struggle to pump blood into aorta.The more the dilatation the more the wall stress (Laplace law). more the wall stress more the after load.

 The  main principle of management of cardiac failure  for decades  has been promoting  LV inotropism .Now we have realised this is fundamentally a wrong concept, (Except in acute heart failure). Hence the main option available now is to reduce the after load , ACEI do that most effectively and proven to improve survival.

What is the effect of  trivial or mild MR on LV after load  ?

It is a hemodynamic fact for MR  to increase LV contractility  and Dp/Dt  due to a relative reduction of after load.

In patients with cardiac failure , even a mild improvement in LV contractility can give a  symptomatic improvement .



Can mitral valve act as controlled safety valve allowing only a trivial or mild MR ?

This may be difficult . But it happens naturally in many of our patents in cardiac failure .

Probably , these are same  patients who come under the 20% incidence of physiological  doppler  MR .Other group could  form the  functional MR*

We have found, patients with  DCM  with mild mitral regurgitation tolerate excercise better than patients who have very competent and rigid mitral valve.It is presumed a mitral valve which gives in a little bit , decompresses the LV with a symptomatic benefit.But if the MR , is occurs in an eccentric path or it results in significant volume burden the potential advantage becomes a liability.

Related issues

*Functional mitral regurgitation. Functional MR is said to occur , when patients with cardiac failure, and resultant dilatation of mitral annular ring, and lack of opposition of leaflets

While milder forms of MR are well tolerarted  , when it occurs  acutely ( even if it is mild) ,  it can be dangerous and result in sudden pulmonary edema  .This usually happens in acute MI or infective endocarditis etc.

 Final message

  • Minimal or mild  mitral regurgitation without any significant volume overloding  in some of the patients with dilated cardiomyopathy  could bring  a hemodynamic advantage .
  • So one may not unduly worry about , a mild MR (central jet) in patients with DCM.It could be after all a safety exit for overstrained LV

We will report the results of the ongoing study about the impact of presence /absence    of  mild MR on the 6 minute walk test in patients with dilated cardiomyopathy.

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Humans have roughly 5 to 6 liters of blood at any given time in their  body  . Out of  this*

50% (2500ml)  is located in the systemic venous compartment.
18% is within the pulmonary circulation participating in the vital oxygenation
12% (500-600ml) is within the cardiac chambers.
8%  is in the arterial tree of  the body.
5%  is  within the  capillaries.
2%  is in the aorta.
* Source : Best & Taylor Physiological basis of  medical practice 1966, 8th edition

What is the implication of this predominantly venous distribution of blood  at rest ?

  • A competent venous tone is essential  for the human beings to maintain the erect posture.
  • Bulk of the cause of syncope in humans is due to peripheral  mechanism like loss of vascular tone and resultant venous pooling.
  • The  concept of venous reservoir is so important in emergency situations like  hypotension  as  simple elevation of legs  is equivalent to  infusing 500 -800 ml of intravenous saline .
  • Similarly during acute left ventricular failure trunk elevation and legs dangling down can reduce the pulmonary congestion very significantly and reduce pulmonary capillary wedge pressure (LVEDP)

 Autonomic dysfunction and venous insufficiency

 Autonomic dysfunction and resultant  orthostatic hypotension is directly related  to venous reservoir dysfunction.Increasing effective circulatory volume by elastic stockings or administration of mineralocorticosteroids like fludrocortisone (.5mg/day ) can be useful in this condition

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