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.
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 .
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.
Reference
Dr.S.Venkatesan MD 
I agree with your comments. In 1976 an international meeting on the “Cardiac lung” was held in Florence Italy with the participation of the most important cardiac and pulmonary physiologist of the world to discuss these items