Diaphragm paralysis?

Question

My mom is 60 and has COPD (Asthma & early Emphasema). Occasionally during her daily activities, which are not necesarilly stressful, she stops breathing -- that is to say mechanically (or neurologically) her diaphram momentarily ceases its natural rhythmic movement and she has to consciously force herself to breathe.

She say she feels as though her diaphram is temporarily paralised and with great determination she has to calmly force herself to breathe again.

Does anyone know what this is called or what can be done to help? Thanks so much.

My sense is that it has to do with the acid-base balance (O2/Co2), the pneumotaxic (breathing control) centre of her nervous system, or her Vagus nerve.

It's rather like having apnea during the daytime. It comes on suddenly and unpredictably;
it is also not a panic attack.

Phillipa - What an excellent answer! I'll have to reread that a couple of time to ingest it, but that is at least part of what I am looking for.

So this part of COPD, is there a diagnosis or more definative way to discribe it to her doctor? (Heck - I figure if it had a label, he'd pay better attention to it!)

She is under the care of a ?? GP, but feels like it's pulling teeth to get him to pay any worthy attention to her complaints...+she doesn't care to deal w/MD's anyhow!

Yes - and certainly not smoking would be a ideal, too!

Thanks!

Answer 1

This is a complicated process best considered by looking at normal physiology first.
Firstly you have to appreciate the relationship between CO2 and pH of body fluid.
CO2 + H2O = H2CO3 = HCO3- + H+
ie Carbon dioxide binds chemically with water to form carbonic acid (catalysed by the enzyme carbonic anhydrase). This dissociates into bicarbonate ions plus protons (hydrogen ions).
Normally breathing is regulated by chemoreceptors located on the ventral surface of the medulla oblongata of the brain stem. These are sensitive to cerebrospinal fluid (CSF) pH.
However, the blood brain barrier prevents dissociation of charged particles (such as H+) from the blood stream into the CSF. Hence, it is carbion dioxide dissolved in the blood which actually dissociated across the blood brain barrier into the CSF.
Normally blood is well buffered to the pH for a given CO2 is well maintained.
CSF is comparatively poorly buffered and hence once in the CSF CO2 rapidly lowers the pH by promoting H+ dissociation from the carbonic acid formed.
Thus an increase in blood CO2 lowers CSF pH and therby stimulates central medullary chemoreceptors (the person feels breathless) and hence increases neural discharge from the medullary respiratory centres via the phrenic nerve to stimulate diaphragmmatic contraction (ie you breath more). CO2 is thus expired, CSF pH drops and equilibrium returns.
However, the chemical CO2 itself has narcotic effects, not seen at normal physiological levels hence the need for the normal breathing reflex to keep levels low.
However, patients with COPD generally ventilate poorly, some more so than others.
A sub-group tend toi accumulate CO2. When this process is prolonged, the body will begin to retain HCO3- (bicarbonate, normally excreted by the kidneys) in order to maintain physiological blood pH. Thus the plasma CO2 levels are tolerated at a higher level.
This leads to correspondingly lower CSF pH which is also ultimately buffered (to a lesser degree) by the HCO3- retention.
However, the relatively increased stimulus to ventilation created by lower CSF pH (which is buffered by the HCO3-) is countered then by chronically high CO2 causing direct central narcotic effect.
The central respiratory stimulus is therefore dampened.
However, peripheral chemoreceptors (in the carotid bodies and aortic arch) respond to hypoxia and blood acidity (less important in the healthy individual) as respiratory stimuli. Low arterial pO2 and low pH cause afferent reflexes via the glossopharyngeal and vagus nerves (from carotid bodies and aortic arch respectively) to the medullary respiratory centres again increasing minute ventilation (ie volume of air ventilated over the period of one minute).
If for some reason the CO2 load increases, so does the central narcosis, so the sensation of breathlessness (ie the need to breath) is lost. This can literally mean the patient forgets to breath.
CO2 production will vary depending on diet and activity as does lung ventilation. Hence, the increased work of normal activity in the pathological emphysematous lung will disproportionately elevate CO2, the subsequent narcotic effect will supress ventilation until the pO2 or pH fall significantly and stimulate a breath OR the patient consciously initiates one and therefore increases ventilation to expire the accumulated CO2.
This is not an easy problem to treat and unfortunately COPD is a chronic incurable lung disease. There are centres (few and far between unfortunately) which specialise in pulmonary rehabilitation, involving a programme of chest physiotherapy to build up the respiratory muscles, which have often deconditioned in these patients, and long term LOW levels of home supplemental oxygen are often used (LTOT). This along with usual nebulised bronchodilators, steroids and theophyllines are often the best that can be done to palliate the disease.
Whatever stage of lung disease the patient is at, they must ALWAYS try to quit smoking as this is hugely important in preventing further disease progression.
COPD is largely a smoking related disease and, although not unheard of, it is extremely rare in non-smokers.

I hope this is useful for you.

Answer 2

I hope your mother is under the care of a good pulmonologist--a doctor for respiratory diseases. She needs to report these symptoms to the physician and get some tests done to determine the cause of her problem. The control of breathing is naturally an unconscious act. It sounds like for some reason she feels the need for more oxygen than she is getting... a check up is in order. Don't delay. With good care a COPD patient can live a full and rewarding life.

Answer 3

While coming out of a coma, I had a weak diaphragm after being on a ventilator so long. I had labored breathing sometimes, like I wanted to be back on oxygen - life is easier that way.
To strengthen my diaphram, I had a little device like a tube that I would blow in. There was a bead or something I had to try to move to the top of the tube. I strengthened my diaphragm. Ask for something like that. Her doctor will know, and should have already suggested it. Have her speak and sing as much as she is able, it will also strengthen the diaphragm.

Answer 4

the girl above is right -- your mother has both emphysema and asthma -- so that's like double the trouble.

however, with paralysis of the diaphragm, the only neuromuscular cause for it is the impairing of the C3,4,5 (cranial nerves) -- think christopher reeve -- this is the area that was damaged, so his muscles (for breathing) are paralyzed. with christopher reeve, i think they placed a device close to his diaphragm (like a pacemaker) that zaps the diagphragm muscles to contract again. (that's what i heard)

however, i've never heard of a condition that paralyzes the diaphragm that is connected to respiratory acidosis. i think you should have her tested to see where the problem is originating from.

Answer 5

It feels like a problem with the diaphram, butn it can be lung cancer, like T.B., and lung cancer. The diaphram could also be wearing out. There are other conclusions, but thjese r most likely, I tink.