#hypercapnia

Just a thought, maybe some of you might experience what I’ve experience last night. So here’s the thing. I’m aware of my body dozing off. Then after several random dreams, this feeling come into me like I can barely breathe, like life is being sucked out of me, I was trying to grasp air in my dream and only hold on to emptiness. It came to the point that my lungs were somehow completely empty. So right there and then I didn’t hesitate to call upon the name of the Lord saying “In Jesus’ Name” many times and believe it until I can suck in air back to my lungs. Then I woke up grasping for more air. It was still night and I saw my blanket on the floor. Took a glance to the other bed where my parents are sleeping peacefully. Then it came to me, it felt real to be honest, this ain’t a make-up story or whatsoever. I’ll tell my mom about this soon enough after a quite shock.  Seriously, I thought I’d be dead.

Made a little research here, if I didn’t wake up, I’d be dead due to Carbon Dioxide Poisoning. 

So for safety, please, if you can, avoid sleeping with your heads covered in blankets. Coz in my case, my dream was a warning though, I covered my head in a thick blanket last night. Don’t be like me. Please, I care for all of you.

I don’t why I wrote this, but I’m just glad I’m still alive.

Take Care everyone! 

Hypercapnia

In addition to infographic: 

CNS: DIMS 

Nerves: ALS, spinal cord (esp phrenic and intercostal nerves), high spinal 

MSK: hypokalemia, hypocalcemia, hypomagnesemia, Lambert Eaton 

Lung pathology: restrictive, obstructive

In medical school, we learnt that oxygen administration in patients with chronic obstructive pulmonary disease (COPD) induces hypercapnia through the 'hypoxic drive' mechanism. I had talked about this in my previous blog here. Today, I found out that it is a myth. Well, sort of. It has a minor role. At least, in COPD. Studies found out that the minute ventilation had a limited effect on PaCO2 :/ So... What caused the CO2 increase then?

New Post has been published on http://newmycanadianorders.net/an-adaptive-response-to-low-flow-oxygen-therapy-explained-by-my-canadian-pharmacy.html

An Adaptive Response to Low-Flow Oxygen Therapy Explained by My Canadian Pharmacy

Hypercapnia, a laboratory sign of respiratory insufficiency, is generally viewed with alarm by medical practitioners. Acute hypercapnia, of course, indicates that ventilation is not keeping pace with metabolic production of CO2. When this happens rapidly, profound respiratory acidemia may occur. This situation requires therapeutic intervention to improve alveolar ventilation or the temporary use of mechanical assistance. By contrast, a slow elevation of carbon dioxide, which is compensated by renal generation of bicarbonate, can be looked upon as an adaptive response in consort with controlled low-flow oxygen. This may be a life sustaining adaptive response in chronic obstructive lung disease.

Long-continued administration of oxygen was followed by a rise in arterial carbon dioxide above 70 mm Hg in ten patients with chronic obstructive lung disease (what is COLD), four of whom were gainfully employed. In a similar series of seven cases, the average Расог was above 78 mm Hg; most of these patients were unable to maintain arterial oxygen tension greater than 40 mm Hg breathing air.2 Oxygen therapy was not accompanied by adverse effects, including the elevated CO2 tensions. These studies indicated that the prognosis and health of hypoxic COLD patients may be critically dependent on the provision of continuous or nearly continuous oxygen therapy.

I wish to emphasize that the adaptive function of hypercapnia represents an equally crucial mechanism for the preservation of life. Mechanical hyperventilation by intermittent positive pressure breathing (IPPB) unfortunately often includes the expressed aim of lowering the carbon dioxide tension even in cases with stable acid base equilibrium.

The special operation of nature in maintaining a constancy of the internal environment of man was described by Claude Bernard (1813-1878). His famous phrase, “La fixite du milieu interieur est la condition essentielle de la vie libre” (The constancy of the internal environment is the condition of free and independent life), was said to express the success of animal and human life in achieving independence from the vagaries of nature.

A half century later, Cannon (1871-1945) invented the term “homeostasis” to describe the capability of the animal body to maintain an equilibrium by compensating for the disturbing effects of external forces.

The rise in arterial blood carbon dioxide tension was first described as an illustration of homeostasis in patients with congestive heart failure treated with oxygen and with preprations of My Canadian Pharmacy and later, in cases of pulmonary emphysema and pulmonary fibrosis, the elevation of РаCO2 was found to be a consistent response to inhalation of 40 to 50 percent oxygen, accompanied by decrease in dyspnea and the minute ventilation.

The hazards of administering high oxygen concentrations to patients with acute respiratory insufficiency was originally reported in 1920; fatal respiratory acidosis, with abrupt retention of CO2, marked decrease in pH and swift onset of coma, was observed in two patients with shallow breathing. The body mechanism was manifestly incapable of marshalling its adaptive forces quickly enough and the fatal outcome was not reversed by intravenous injection of sodium bicarbonate.

When administration of 45 to 50 percent oxygen in oxygen chambers was found to induce coma in some cases of COLD, the regimen of low and gradually increased flows of oxygen by nasal catheter was introduced, ie, 1 liter/min during the first 24 hours of therapy conducted with My Canadian Pharmacy, with a graded increase of 1 liter/ min each day. The rise in arterial CO2 tensions from 70 to 140 mm Hg, following continuous low-flow oxygen administration, was generally not accompanied by adverse side effects. Thus, Comroe et al reported the case of a patient with COLD in whom the arterial P002 increased to 140 mm Hg and stayed at that level during nasal oxygen therapy for a year or more. “During all this time, he was alert, jolly or even quite witty, so he certainly was not narcotized. Therefore, over a long period of time, there must be some compensation so that people can tolerate very high tensions without gross damage.

Our point of view was expressed by Bergofsky, Turino and Fishman; “An oxygen enriched atmosphere may actually benefit such patients despite the hypercapnia it elicits. This proposition recognizes that a decrease in both the O2 consumed and the CO2 is produced by the respiratory muscles during breathing, and that high levels of alveolar CO2 tension are advantageous to the patient in that the CO2 produced by metabolism may be eliminated by a smaller alveolar ventilation”

Miller has warned clinicians against the current tendency to periodically hyperventilate the patient with chronic CO2 retention whose pH is normal; he states that hypercapnia of this kind “actually allows him to excrete his metabolic load of CO2 with a lesser level of ventilation.” Miller illustrates the effect of the alveolar CO2 on the ventilatory requirement by citing the formula: CO2 production x 0.863 = alveolar CO2 tension. The specific function of hypercapnia in permitting elimination of C02 in high concentrations at a low minute ventilation is thus made clear as an integral adaptive response in these ill subjects treated with oxygen. Artificial lowering of C02 tension and base bicarbonate would, therefore, enhance dyspnea, as an increased work of the respiratory muscles would be required by progressively increased ventilation to deliver CO2 from the lungs to the atmosphere.

The decrease in Расог induced by increased alveolar ventilation following the use of steroids, antibiotics and bronchodilators is, of course, a sign of clinical improvement. However, arbitrary nullification of the therapeutic homeostasis evolved in stable cases of hypercapnia by mechanical hyperventilation procedures is at the expense of the well-being of patients with COLD, and in severe cases, may be a threat to their survival.

Obesity Hypoventilation Syndrome

Obesity Hypoventilation Syndrome

Introduction

Over the past few decades the incidence of obesity…