Ventilation/Perfusion Mismatch

[ResTech]

Could someone give a easy to understand explanation of ventilation/perfusion mismatch and how it relates to COPD? I am studying pulmonology and am beginning to have a good understanding of cor pulmonale and pulmonary hypertension. I have gotten some good sources from Google but thought I would post here to get even more.

My specific questions are:
How does ventilation/perfusion mismatch relate to COPD?

Why do the pulmonary arteries constrict in response to hypoxia which is reverse of systemic tissue that is hypoxic?

Any elaboration is greatly appreciated! Thanks!

 

[VentMedic]

Respiratory Physiology and V/Q relationships
http://medschool.slu.edu/pharmphys/respiratory_physiology_2.pdf

Pathophysiology of Hypercapneic and Hypoxic Respiratory Failure and V/Q Relationships
http://www.indiachest.org/teaching_material/Respiratory failure.pdf

Matching of Ventilation and Perfusion in the Lung
http://www.asahq.org/rcls/RCLS_SRC/185_Pearl.pdf

ATS site for everthing you want to know about COPD:
http://www.thoracic.org/sections/copd/for-health-professionals/index.html

All about Oxygen (includes shunting and V/Q)
http://www.ccmtutorials.com/rs/oxygen/index.htm

Here's a good one:
Why is the patient still hypoxic despite being ventilated?
http://www.rcsed.ac.uk/Journal/vol45_4/4540007.htm

Cor Pulmonale (everything you need to know)
http://www.medscape.com/viewpublication/144_toc?vol=24&iss=3
Log in is simple and it offers a great search engine for additional medical articles.

 

[VentMedic]

I posted all the links because there is so much "basic" information that you need to understanding this. There is not one factor that can easily sum everything up nor is all COPD alike. I could make a statement but that could be taken out of context with an assumption like "All COPD patients will cease to breathe if given high concentrations of oxygen".

The explanations on the links I provided are fairly self explanatory provided you have had some college level A&P.

 

[Veneficus]

I posted all the links because there is so much "basic" information that you need to understanding this. There is not one factor that can easily sum everything up nor is all COPD alike. I could make a statement but that could be taken out of context with an assumption like "All COPD patients will cease to breathe if given high concentrations of oxygen".

The explanations on the links I provided are fairly self explanatory provided you have had some college level A&P.

cmon vent you know I don't understand all that book learnin nonsense. I'm gonna go find out how it works on the street

 

[BruceD]

Why do the pulmonary arteries constrict in response to hypoxia which is reverse of systemic tissue that is hypoxic?

Any elaboration is greatly appreciated! Thanks!

Currently, there are some theories on why this happens, but the full pathways have not been discovered.

I just find it easiest to remember, if a portion of lung won't oxygenate, better that blood be diverted elsewhere so it can pick up some good 'ole O2

stay safe
-B

 

[JPINFV]

Why do the pulmonary arteries constrict in response to hypoxia which is reverse of systemic tissue that is hypoxic?

I don't have my physio book with me to give a how (I believe it went over a mechanism, but I can't remember right now). As for a "why," think of it in terms of function.

Answer the following questions:

What is the purpose of the lungs?

Can that purpose be achieved if a portion of the lungs isn't being ventilated?

If that purpose can't be achieved, why send blood that way?

 

[VentMedic]

I just find it easiest to remember, if a portion of lung won't oxygenate, better that blood be diverted elsewhere so it can pick up some good 'ole O2

stay safe
-B

True but when alveolar hypoxia is global, as in diseases such as emphysema and cystic fibrosis (as I stated earlier -many disease processes), Hypoxic Pulmonary Vasocontriction leads to Hypoxic Pulmonary Hypertension and right heart failure. Hypoxic Pulmonary Vasocontriction is driven by the response to hypoxia of two different cell types, namely the pulmonary arterial smooth muscle and endothelial cells. When chronic conditions exist, pulmonary remodeling takes place. The right ventricular hypertrophy that occurs in cor pulmonale is a direct result of chronic Hypoxic Pulmonary Vasoconstriction and subsequent Pulmonary Artery Hypertension, leading to increased right ventricular work and stress.

 

[VentMedic]

Why do the pulmonary arteries constrict in response to hypoxia which is reverse of systemic tissue that is hypoxic?

Hypoxia-induced vasodilation may be direct (inadequate O2 to sustain smooth muscle contraction) or indirect via the production of vasodilator metabolites. (Lactic Acid, Hydrogen Ions, Carbon Dioxide)

Hypoxic Pulmonary Vasocontriction involves the formation of reactive oxygen species, endothelin-1 or productions of arachidonic acid metabolism.

Some treatments for Pulmonary Hypertension:
Nitric Oxide treatment may modulate circulating endothelin-1.

Smooth muscle cells in blood vessels produce prostaglandins. When they need help, inhaled prostaglandins are administered.
http://www.rcjournal.com/contents/06.04/06.04.0640.pdf

 

[rhan101277]

True but when alveolar hypoxia is global, as in diseases such as emphysema and cystic fibrosis (as I stated earlier -many disease processes), Hypoxic Pulmonary Vasocontriction leads to Hypoxic Pulmonary Hypertension and right heart failure. Hypoxic Pulmonary Vasocontriction is driven by the response to hypoxia of two different cell types, namely the pulmonary arterial smooth muscle and endothelial cells. When chronic conditions exist, pulmonary remodeling takes place. The right ventricular hypertrophy that occurs in cor pulmonale is a direct result of chronic Hypoxic Pulmonary Vasoconstriction and subsequent Pulmonary Artery Hypertension, leading to increased right ventricular work and stress.

Many paramedics couldn't rattle this off.

 

[Sasha]

Many paramedics couldn't rattle this off.

Remember, Vent is not only a paramedic, but an RRT, with more years of experience than some people have been alive. She's not your "average paramedic".

Not excusing lax educational standards, by the way.

 

[VentMedic]

Many paramedics couldn't rattle this off.

This comes from years of listening to rounds and explaining the concepts over and over to young doctors or new RNs. The advanced education and a couple of college degrees help also.

If you break that paragraph into one sentence at a time, it is more understandable.

True but when alveolar hypoxia is global, as in diseases such as emphysema and cystic fibrosis (as I stated earlier -many disease processes), Hypoxic Pulmonary Vasocontriction leads to Hypoxic Pulmonary Hypertension and right heart failure.

Hypoxic Pulmonary Vasocontriction is driven by the response to hypoxia of two different cell types, namely the pulmonary arterial smooth muscle and endothelial cells.

When chronic conditions exist, pulmonary remodeling takes place.

The right ventricular hypertrophy that occurs in cor pulmonale is a direct result of chronic Hypoxic Pulmonary Vasoconstriction and subsequent Pulmonary Artery Hypertension, leading to increased right ventricular work and stress.

 

[rhan101277]

Remember, Vent is not only a paramedic, but an RRT, with more years of experience than some people have been alive. She's not your "average paramedic".

Not excusing lax educational standards, by the way.

I didn't know ventmedic was a female. All this time I thought she was a he. :blush:

 

[Sasha]

I didn't know ventmedic was a female. All this time I thought she was a he. :blush:

Psht. She's too smart to be a he.

 

[BruceD]

True but when alveolar hypoxia is global, as in diseases such as emphysema and cystic fibrosis (as I stated earlier -many disease processes), Hypoxic Pulmonary Vasocontriction leads to Hypoxic Pulmonary Hypertension and right heart failure. Hypoxic Pulmonary Vasocontriction is driven by the response to hypoxia of two different cell types, namely the pulmonary arterial smooth muscle and endothelial cells. When chronic conditions exist, pulmonary remodeling takes place. The right ventricular hypertrophy that occurs in cor pulmonale is a direct result of chronic Hypoxic Pulmonary Vasoconstriction and subsequent Pulmonary Artery Hypertension, leading to increased right ventricular work and stress.

Sorry, wasn't paying enough attention, I was just thinking about localized v/q totally missed that his question was about generalized hypoxic-vasoconstriction.

 

[8jimi8]

Could someone give a easy to understand explanation of ventilation/perfusion mismatch and how it relates to COPD? I am studying pulmonology and am beginning to have a good understanding of cor pulmonale and pulmonary hypertension. I have gotten some good sources from Google but thought I would post here to get even more.

My specific questions are:
How does ventilation/perfusion mismatch relate to COPD?

COPD is characterized by chronic inflammation in the airways, parynchema and pulmonary vasculature. This is not the only mechanism involved in the pathogenisis of COPD, but it is the primary process. The label COPD includes two types of obstructive airway diseases. Chronic Bronchitis (in which other causes of chronic coughing have been ruled out) and Emphysema (structural remodeling and enlargement of air-spaces distal to the terminal bronchioles w/o obvious fibrosis). Most people suffering from COPD have a mixture of the two diseases. Air is able to move in, but not out.

Chronic bronchitis starts with an insult to the lungs in the form of an inhaled irritant. Inlammatory cells (macrophages, lymphocytes and later neutrophils) respond and release inflammatory mediators (leukotrienes, interleukins, and tumor necrosis factor) which damage the tissues of the lungs.

Now go to your knowledge of the inflammatory response: Excess mucous production, constriction of airways. These repeated cycles and repeated insults result in collagen deposits / scar tissue formation / fibrosis.

Tissue destruction of the parynchema is theorized to be a consequence of inflammation (but there are also genetic causes such as a deficiency in alpha 1-antitrypsin) and includes a loss of attachments (which hold airways open and leads to the collapse of peripheral airways) and destruction of alveolar capillary beds. Inflammatory cells also infiltrate the smooth muscle of pulmonary vasculature causing them to thicken as the disease progresses.

With the concurrent loss of the integrity alevolar walls and their surrounding cappillaries, the surface area available to diffuse O2 is decreased... Ventilation is still availble; however perfusion is diminished :. ventilation / perfusion mismatch (also known as v/q mismatch)

Hope that helps! Sorry I don't have an answer to your pulmonary artery vasoconstriction: My best guess is that since COPD'ers are hypoxemic the body is trying to increase perfusion to the lungs.



***referenced Medical Surgical Nursing: Assessment and Management of Clinical Problems 7th edition (Lewis, Heitkemper, Dirksen, O'brien, and Bucher)