Hypercapnic respiratory failure can be hard to detect; It may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. One must suspect it, and then test for it. And in the 21st century, we can now do exactly that.
But mostly we don’t.
Why not? Especially when our current treatments do not work or may make recovery harder? Altered mental status and severe depression can be a physical sign of hypercapnia. It is an easy hypothesis to test in the 21st century. Yet we aren’t. I do not know why. Lives, ….young adult lives are at stake. Dreams, ….young adult dreams are at stake.
We won’t even measure respiratory rate or minute volume and this is easy to do. [R.R. times Tidal Volume= Minute Volume].
Why not look at respiratory rate or minute volume and even arterial blood gas tests if indicated after these simple straightforward measurements are taken ? Do we not want to look for bodily causes of bipolar illness? Even though we are doing such a half assed job of diagnosing and treating it now? What about all the dreams and lives that are being destroyed as we speak? It is not like we have found convincing treatments? And we are willing to inflict horrible and life shortening side effects as well….Why? This is my question for the medical and scientific community.. I have been asking this question to different health professional leaders for over 20 years.. Why not test this hypothesis? All organ failure can be gradual, hidden, relentless and all organ failure can rob us of our reason and cause massive unpleasant indescribable internal sensations. All organ failure is insidious and unmasked by sudden death. Most organ failure will affect the brain and the mind. All organ failure will force the body to compensate for faulty PCO2 and this process is invisible, and ongoing, and will trigger the Stress Response to Trauma [eg. bleeding] and Surgery [involving bleeding] described by scientist surgeons such as Desborough .
Eur Respir J Suppl. 2003 Nov;47:3s-14s.
Author information 1Dept of Critical Care, University of Athens Medical School, Evangelismos Hospital, Athens, Greece. email@example.com
Respiratory failure occurs due mainly either to lung failure resulting in hypoxaemia or pump failure resulting in alveolar hypoventilation and hypercapnia. Hypercapnic respiratory failure may be the result of mechanical defects, central nervous system depression, imbalance of energy demands and supplies and/or adaptation of central controllers. Hypercapnic respiratory failure may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. In all these conditions, pathophysiologically, the common denominator is reduced alveolar ventilation for a given carbon dioxide production. Acute hypercapnic respiratory failure is usually caused by defects in the central nervous system, impairment of neuromuscular transmission, mechanical defect of the ribcage and fatigue of the respiratory muscles. The pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear. The most attractive hypothesis for this disorder is the theory of “natural wisdom”. Patients facing a load have two options, either to push hard in order to maintain normal arterial carbon dioxide and oxygen tensions at the cost of eventually becoming fatigued and exhausted or to breathe at a lower minute ventilation, avoiding dyspnoea, fatigue and exhaustion but at the expense of reduced alveolar ventilation. Based on most recent work, the favoured hypothesis is that a threshold inspiratory load may exist, which, when exceeded, results in injury to the muscles and, consequently, an adaptive response is elicited to prevent and/or reduce this damage. This consists of cytokine production, which, in turn, modulates the respiratory controllers, either directly through the blood or probably the small afferents or via the hypothalamic-pituitary-adrenal axis. Modulation of the pattern of breathing, however, ultimately results in alveolar hypoventilation and carbon dioxide retention.