Hi there, I know this question might sound very unprofessional but I am not familiar with the English term of dependent and independent lungs.
I will appreciate the help
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Hi there, I know this question might sound very unprofessional but I am not familiar with the English term of dependent and independent lungs.
I will appreciate the help
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For memory the dependent lung is the one where the blood is more likely to be, i.e. the one where gravity sends the most blood. So in sitting this is the bases, in lying this is the posteior aspects of the lobes, when standing on the head it would be the apical segments. The relevance of this relates to ventilation/perfusion. In the normal subject ventilation tends to go the the dependent lung, i think due to less resistance of the lung tissue with relatively less blood flow. This may not be the case in the person with pulmonary disease? It has been a while since I was involved directly in cardiopulmonary physio so please correct me if i am wrong.
The concept of dependent and non-dependent should be considered when performing postural drainage. Read below for my additional notes on breathing at low lung volumes and the ventilated patient. 8o
also important in vq matching eg deep breathing exs in sidelying, say dfecreased air entry rRLL, then put patient lying on right, empashize DBE and as a result of more perfusion due to dependncy, vq matching is enhanced
vq highest in standing/sitting
The dependent lung refers to the lung that is lowermost ie bases in the upright position, the left lung in left side lying etc. In the spontaneously breathing person ventilation perfusion is best matched in the dependent lung. It is the reverse in someone who is receiving positive pressure ventilation and in children: V/Q matching is best in the non- dependent lung. This contradicts one of the previous entries.
The dependent and non- dependent lung is not really important with postural drainage: the lung with secretions should be uppermost. This therefore means that in the spontaneously breathing person V/ Q matching will be best in the dependent (ie unaffected) lung.
OK, thanks Fiona. Here's some more info as things are never cut and dry and even reading more on this today I learnt a few new points (be they theory or not).
Dependent lung—the lung in the lowest part of the gravitational field, i.e., the base when in the upright position; the dorsal portion when supine.
Why put it uppermost? Gravity yes, but also to increase alveolar perfusion to the dependent segment so as to decrease any hypoxic stress to the patient? In a general sense I feel there is some thought process that considers the dependent lung in postural drainage other than just gravity. The non-dependent lung, in the case of a patient with widespread secretions/infection etc would be breathing at a lower tidal volume. In this case I thin the ventilation is preferentially distributed to the non-dependent lung? Also I read that "in the anaesthetised patient, however, irrespective of the mode of ventilation, the upper lung receives more gas flow." So one might actually have to consider the implications of the definition as it relates to the actual patient situation.Quote:
The dependent and non- dependent lung is not really important with postural drainage: the lung with secretions should be uppermost.
Regional Variation in Lung VentilationA few more notesQuote:
Ventilation within the lungs is greatest near the bases, in the upright position. This is probably mainly due to variation in intra-pleural pressure as we move from apex to base - pressure is more negative near the apex. Effectively, this probably causes more expansion of the apices at FRC. As the person inhales, it is easier to expand the bases, as these are less distended than the apices! Note that at lower lung volumes, the situation may be reversed, with poor ventilation of the bases.
Ventilation-perfusion mismatch
This is an important cause of hypoxaemia affecting patients on the intensive care unit. Relative ventilation and perfusion, in different areas of the lung are unequal, resulting in inefficient gas transfer.
The distribution of ventilation in normal subjects varies depending on the mode of ventilation and position. More ventilation occurs in the right lung due to its larger size, both in the upright and supine positions. In the upright position there is greater ventilation towards the apex of the lungs than to the bases. In the lateral position, the lower lung is preferentially ventilated irrespective of which side is lain upon. This is due to the dependent diaphragm lying higher in the thorax, with increased length of muscle fibres providing more efficient contraction during inspiration. In the anaesthetised patient, however, irrespective of the mode of ventilation, the upper lung receives more gas flow.
Pulmonary blood flow is greater at the bases than at the apices in the erect subject. The distribution of flow through the lung is uneven due to the relatively low pressures in the pulmonary circulation and gravity assumes a very important role. Similarly, in the lateral position, the dependent lung is perfused more than the upper lung.
Although both perfusion and ventilation increase from the apices to the bases the increase in ventilation is less than that of perfusion and, in order to understand the relationship between the two is described as the ventilation/perfusion ratio (V/Q). The resting values are approximately 4 l/min for ventilation and 5 l/min for pulmonary blood flow, giving a ratio of 0.8 throughout the whole lung (assuming ventilation and perfusion of all alveoli are equal). However, some alveoli will receive no ventilation and some will receive no perfusion.
Hypoxic pulmonary vasoconstriction
Hypoxic pulmonary vasoconstriction (HPV) is a potent regulator of the distribution of blood flow to match areas of ventilation. HPV normally acts to improve gas exchange by reducing the blood flow to lung regions with low V/Q ratios.
In conditions producing inflammatory mediators such as sepsis and trauma, HPV is impaired with blood flowing to poorly ventilated lung resulting in hypoxia. Drugs such as sodium nitroprusside and nitroglycerine can also impair HPV. Hypoxic pulmonary vasoconstriction can also be abolished in the presence of raised pulmonary artery pressures leading to V/Q mismatch and hypoxia.
Ventilation perfusion mismatch is responsible for the hypoxaemia seen in pulmonary oedema, chronic obstructive airways disease, pulmonary embolism and interstitial lung disease. The hypoxaemia worsens with increasing V/Q mismatch for two reasons. Firstly, with V/Q mismatch, a greater percentage of the cardiac output passes through lung units with lower V/Q ratios (perfusion > ventilation) so that less well saturated blood makes a greater contribution to total pulmonary blood flow. Secondly, in relation to shunts, the oxygen content of blood from lung units with low V/Q ratios exerts a greater effect on the saturation of blood flowing to the left side of the circulation because of the shape of the oxygen dissociation curve.
Thanks for that- it might be helpful to put the reference on the site that you have used in relaying this information. I think it is important to point out that the majority of what we know about ventilation and perfusion distribution is derived from animal studies and studies of normal lungs. Not a lot of research has been carried out looking at diseased lungs and situations where there are secretions resulting in hypoventilation.
The point I was making about postural drainage is that the MAIN AIM of this technique is the drainage of secretions. It is fortunate that in the spontaneously breathing patient you have the added advantage of preferentially ventilating the unaffected lung (when secretions are unilaterally distributed). This obviously needs to be taken into consideration when the patient is ventilated and the affected lung is placed uppermost for drainage of secretions as air will go into the affected lung preferentially and a degree of desaturation may be observed.
Quote
The non-dependent lung, in the case of a patient with widespread secretions/infection etc would be breathing at a lower tidal volume. In this case I thin the ventilation is preferentially distributed to the non-dependent lung?
Regardless of whether or not there are secretions in the non- dependent lung by nature of the definition the non- dependent lung (in a spontaneously breathing person) is less preferentially ventilated than the dependent lung. So I am not quite sure of the point you are trying to make here?
Quo:) te
Also I read that "in the anaesthetised patient, however, irrespective of the mode of ventilation, the upper lung receives more gas flow." So one might actually have to consider the implications of the definition as it relates to the actual patient situation.
I think this statement supports my previous statement that ventilation in the ventilated person goes preferentially to the non- dependent lung (ie the uppermost lung).
I agree that we tend to take simplistic view of what is happening with ventilation and perfusion distribution in abnormal states but believe that is because we do not have the evidence to tell us. If you have any useful references of the effect of hypoventilation on V/ Q distribution I would be interested in reading them.
OK I understand your point here. The dependent lung is the only one defined, the non-dependent is whatever is left over. I think I was trying to say in the case of breathing at low volumes, the dependent lung will not be the base, but the apex (in an errect posture). Hence was was the non-dependent lung has become the dependent lung doe to the reduced volume and I suppose reduced resistance to expansion.Quote:
Regardless of whether or not there are secretions in the non- dependent lung by nature of the definition the non- dependent lung (in a spontaneously breathing person) is less preferentially ventilated than the dependent lung. So I am not quite sure of the point you are trying to make here?
My comments were actually a collection of bits and pieces spliced together so no specific reference was given. I will look for a few good ones over the next day or so and also post them to this topic area. I feel we are opening a can of worms here in an often misunderstood and still largely theoretical model/s. But to be honest it feels quite refreshing to look at a topic I have had little to do with for the past 10 years. :D
Thanks- I look forward to chasing up whatever references you locate. I agree that it is a can of worms but having worked in respiratory care for a number of years we are often relating what we are doing to theories of physiology in normals- not ideal but not sure what we can do about it (in an ethical research format!).