Wednesday, May 25th 2011
June 2, 2011 4 Comments
Fright of my life
It had been a good day up until that horrific moment. I’d been able to spend some of the morning out in the back garden on my level access patio soaking up the rays of the sun whilst listening to birdsong. Later in the afternoon I’d had a visit from one of the lovely carers who used to look after me and we had been able to enjoy a good chat and a catch up. But by late evening when I was being prepared for bed I started to experience difficulties in getting my breath. Each breath was getting shorter and shorter and the situation was developing rapidly. Debbie, to her credit reacted immediately and called the emergency services and placed an oscillating fan in front of me. By this time I was struggling to get any breath at all. My heart was pounding, my skin felt very hot and my whole body was screaming for oxygen. The voices around me seemed to be fading out and all I could cry out in a pitiful voice was ‘I’m dying, I’m dying’. Honestly that’s exactly how it felt. Instinctively in that moment I thought I was going to die as I was thinking ‘so this is how it all ends for me then, on Wednesday evening’. It was a truly frightening experience.
The first responders arrived on the scene very quickly and administered oxygen. Apparently my oxygen saturation had dropped right through the floor. The paramedics arrived shortly afterwards and I was rushed to hospital hooked up to oxygen. I then spent the next few hours having a battery of tests including chest x-rays, blood/gas tests, heart readings. Nothing obvious was picked up (or at least communicated to me) apart from the fact that my CO2 levels were a bit high. Initially there was the possibility that they might have wanted to send me home again but by midnight that was not practical as I had no care package in place for these hours so it was agreed that I would stay in the hospital overnight for observation.
Before signing off I would like to express my deepest gratitude to Debbie for reacting to the situation quickly and professionally. Had she not done so I might not be here now as I have a DNR (do not resuscitate) stipulation for situations like this written into my ADRT (Advanced Decision to Refuse Treatment) should I slip into unconsciousness. I would also like to say a big thank you to the first responders and the paramedics who took such good care of me.
Mark
Living with Motor Neurone Disease - One Day at a Time! 
Hi Mark,
You certainly had me and Laura scared that night. I’m just so relieved that you’re geting better. It just goes to show the beneifit of having regular carers and a stable care package., All of us that look after you know you so well and can recognise any changes in your condition and react quickly to ensure you have the help you need immediately.
We all look forward to having you back home again.
lots of love
Debbie xx
Mark i can only imagine how scared you must have felt. I have just found out my husband has MND hope that we can both cope the way in which you are doing. Hope that I will be able to react the same way has Debbie did.
Your posts have shown a great desire.
I can definitely say, brother, that you gave us all quite a scare that day. Chery and I raced up to the hospital to see you. I’m glad the hospital saw sense in the end to keep you in. Still not sure what would have happened gone midnight if they’d tried to send you home. Crazy!
Mark, so sorry about this. I am copying an extensive piece on use of oxygen in MND, I think it is worth noting some of the issues.
You might find the following information helpful:
Patients with neuromuscular diseases who are developing progressive respiratory failure due to respiratory muscle weakness will die unless mechanical ventilation is used. The rate of progression is often hard to predict. Some patients seem suddenly to experience life-threatening hypercapnic respiratory failure. They may not have been aware of gradually increasing symptoms and signs, particularly since they are often not physically active and are often not being regularly monitored with simple pulmonary function tests.
Administering oxygen does not provide assistance to the weakening respiratory muscles, but gives both the patient and the doctor the false impression that appropriate treatment is being provided. While in fact hypoventilation is mistaken for an oxygen transfer problem. Indeed, administering oxygen can mask the problem. Also there is a danger of causing respiratory depression by giving oxygen (see reference to the article by Dr. Peter Gay – Mayo Clinic – below). Oxygen is NOT the treatment for hypoventilation. It will improve the SaO2, but not the hypoventilation and may increase the danger of dying of sudden respiratory failure.
In hypercapnic respiratory failure due to hypoventilation, the SaO2 falls due to the rise of the CO2. The alveoli in the lungs (tiny gas exchange units) should clear most of the CO2 out with each breath. Instead, with hypoventilation, CO2 accumulates and thus there is decreased room in the alveoli for oxygen. When mechanical ventilation using room air is provided, it lowers the CO2 in the alveoli, corrects the SaO2, and rests the respiratory muscles. The ventilator should be adjusted to achieve a normal SaO2, on room air. If oxygen is being administered, one cannot use noninvasive oximetry to tell whether enough assisted ventilation is being provided; repeated arterial blood gas specimens (ABGs) would be needed.
When there is respiratory failure in neuromuscular patients (ALS, post-polio, SMA, muscular dystrophy, etc.) who have no additional pulmonary disease that impairs oxygen transfer, the ventilator set-up is adjusted to:
be comfortable for the patient;
achieve SaO2 of 95% or higher on room air (this can be measured with a finger-sensor oximeter);
assist the patient to effectively cough and clear secretions;
provide improved oral communication (if vocal communication is possible).
It has been common for people using noninvasive nasal ventilation (NPPV) with a bi-level positive pressure unit to use inadequate settings; frequently, they are not monitored with clinical evaluation and oximetry. The EPAP is often set too high – usually it should not be higher than 3-4 cm H2O; the IPAP is set too low – usually it needs to be 12-16 cm H2O and adjusted to achieve an oxygen saturation of 95% or higher.
Some situations may require administering oxygen temporarily, such as pneumonia due to infection or aspiration. If this occurs in patients with respiratory muscle weakness and hypoventilation, then it is important to provide both assisted ventilation and supple-mental oxygen, and use ABGs to monitor them.
(The late Dr. Oppenheimer, former head of pulmonary medicine at UCLA, sent me that article a few years back. He went on to tell me that when PALS are given oxygen it tricks the brain into thinking the body doesn’t need to put forth the effort to breathe.)