Failure of respiratory drive, effects on mind and body.

Breathing is a complex process that relies heavily on the coordinated action of the muscles of respiration and the control center in the brain.………..Central and peripheral chemoreceptors, as well as mechanoreceptors in the lungs, convey neural and sensory input to the brain to help modulate respiratory drive. The respiratory center responds in return by changing its firing pattern to alter breathing rhythm and volume. Physiology, Respiratory Drive Joshua E. Brinkman; Fadi Toro; Sandeep Sharma. StatPearls [Internet].

1] Paula seems to have lost the autonomic nervous system reflex that modulates respiratory drive at rest when awake. This is true in health and does not change with illness. Something is not right with her respiratory drive. This is only unmasked by outright routine measurement of respiratory rate and depth at rest when awake. When physically ill [with the common cold, seasonal flu or allergies] her breathing rate does not increase normally at all. Her respiratory drive with respect to motor activity or exercise is sluggish, compared to normal responses.

Each respiratory cycle begins with inspiration and ends with expiration. During inspiration, the diaphragm and the external intercostals contract, causing enlargement of the thoracic cavity. As a result, intra-pleural pressure decreases, and so does alveolar pressure, forcing the lungs to expand and air to move in. Expiration, on the other hand, occurs passively when the diaphragm relaxes, owing to the lungs’ elastic properties. The respiratory control system drives respiratory cycles and consists of three components: the central neural respiratory generator, the sensory input system, and the muscular effector system. The rate and strength at which the diaphragm contracts, hence the frequency and volume of respiration, depend heavily on the firing pattern of pacemaker cells in the brainstem. The sensory input system, on the other hand, sends signals to the brain to modulate respiratory patterns depending on metabolic demand. Physiology, Respiratory Drive Joshua E. Brinkman; Fadi Toro; Sandeep Sharma. StatPearls [Internet].

2] Paula does not seem to have “passive exhalation” ever when at rest and awake. Upon close examination, she seems to actively squeeze the air out of her lungs using abdominal and other muscles. Exhaling is always active for her. She is always using accessory muscles to breathe. Paula is not aware of this because this seems to be “normal” for her. She is aware of the extra effort it takes to breathe at rest, but she thinks that this is “normal” and that everyone breathes the way she does. She does not feel dyspnea [discomfort when breathing] in health, unless she is asked to breathe faster, which she cannot keep up for long, as breathing faster [normal for most] results in dyspnea.

Carbon dioxide is a lipid-soluble molecule that freely diffuses across the blood-brain barrier and forms hydron ions within the cerebrospinal fluid. Chemoreceptors, in turn, respond to pH changes as they become more acidic and send sensory input to the brain to stimulate hyperventilation. The result is a slow and deep breathing pattern that helps eliminate carbon dioxide from the body. Likewise, when arterial PCO2 drops, pH in the cerebrospinal fluid becomes alkalotic, and hypoventilation ensues. Therefore, arterial PCO2 is the chief determinant of the respiratory drive under normal conditions.Physiology, Respiratory Drive Joshua E. Brinkman; Fadi Toro; Sandeep Sharma. StatPearls [Internet].

3] Paula’s breathing pattern in health or illness is too unlike the norm to be able to tell anything about her PCO2 levels in health or in illness. Paula exchanges only 1.5 Litres of air with each breathe. I guess that this is hypoventilation – inadequate breathing- in health or in illness, yet Paula is alive, and she is well – most of the time. No one suspects that she has hypoventilation and is well. No one worries what happens should she become very ill, with her hypoventilation and problems with her respiratory drive and ANS reflexes. No one has checked her vital signs and respiratory rate and volume together to get her minute ventilation. No one has given her an arterial blood gas test to try to figure out what is going on. And many people like Paula have been discovered and described by researchers in the last century, some healthy like Paul, and others who are in poor condition and insane but not permanently brain damaged.

Respiratory centers located within the medulla and the pons are responsible for generating the baseline respiratory rhythm. However, an aggregated sensory input from the peripheral sensory system monitoring oxygen levels and the central sensory system monitoring pH modifies the rate and depth of respiration. These signals, along with several other sensory inputs coming from peripheral mechanoreceptors, modulate the respiratory rhythm to create a unified neural signal, sent to the primary muscles of respiration. The total input culminates in a respiratory rate of approximately 12 breaths per minute for an average adult while at rest. Physiology, Respiratory Drive Joshua E. Brinkman; Fadi Toro; Sandeep Sharma. StatPearls [Internet].

Paula found out at a basic first aid class that her breathing rate is only 3 breathes per minute. And her respiratory centre seems to have difficulty increasing her breathing rate when ill. Her tidal volume is normal at .5 L.

Patients with failure of ventilatory drive are not short of breath and typically demonstrate bradypnea or apnea.

Paula has bradypnea at rest when awake when healthy , awake, at rest and the also when physically ill at rest. She is not aware of her respiratory defect.

Patients with underlying abnormalities of ventilatory drive who develop respiratory infections, congestive heart failure, or other acute illnesses are more likely to develop acute ventilatory failure compared with individuals without such defects. Pathophysiology of Acute Ventilatory Failure. The Thoracic Key Website.

This applies to Paula. And seems to apply to Kraepelin’s patients, also found to have respiratory rate defects., 1921Topics Psychiatry — Early works to 1900Manic-depressive illnessParanoiaPublisher Edinburgh : LivingstoneCollection gersteintorontomedicalheritagelibraryuniversity_of_torontoDigitizing sponsor MSNContributor Gerstein – University of TorontoLanguage English

Yet no one has officially screened her for a respiratory defect and she found out by accident.

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