Reduced vital capacity



Pathophysiology of Breathing Regulation

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Numerous factors influence the respiratory neurons in the medulla oblongata A):

Ventilation is increased by acidosis, hyper-capnia, hypoxia, and a decrease of Ca2+ and Mg2+ in cerebrospinal fluid (CSF). Pain, intensive cold or heat stimuli to the skin, an increase or moderate fall in body temperature, a drop in blood pressure, and muscular activity (joint innervation) all increase ventilation. Other stimulating factors are epinephrine and norepinephrine in the blood, histamine, acetylcho-line and prostaglandins in the central nervous system (CNS), progesterone, testosterone, and corticotropin.

Conversely, ventilation is reduced by alkalosis, hypocapnia, peripheral hyperoxia, and Ca2+ and Mg2+ increase in the CSF. Hypoxia in the CNS, deep hypothermia, rise in blood pressure, ganglion blockers as well as high concentrations of atropine, catecholamines, endorphins and glycine in the CNS also diminish ventilation.

Normally the pH around the respiratory neurons or the pH in the CSF has a decisive influence on ventilation. A shift in pH in the brain following rapid changes in Pco2 is accentuated by the low buffering power of CSF (low protein concentration). Because CO2, but not HCO3- or H+, quickly passes through the blood-CSF and blood-brain barriers, changes in CO2 concentration in the blood result in very rapid adaptation of ventilation, while adaptation after changes in blood pH or blood HCO3- occurs only after a delay of several days. If sudden metabolic acidosis occurs (^ B, top; see also p. 88 ff.), respiratory compensation will thus occur only slowly. Conversely, treatment of a partly compensated respiratory acidosis, for example, by infusion of HCO3-, often leaves behind respiratory alkalosis (^ B, bottom). Also, with a sudden fall of O2 partial pressure in inspiratory air (at high altitude) ventilation is not immediately and adequately raised. The onset of hyperventilation leads to hypocapnia, and the resulting intracerebral al-kalosis will then transiently inhibit any further rise in ventilation. Complete adaptation of breathing to a reduced O2 supply requires an increase in renal HCO3- excretion with subse quent decrease in HCO3- concentration in plasma and (after a delay) in CSF.

Barbiturates (soporific drugs) and chronic respiratory failure decrease the sensitivity of the respiratory neurons to pH or CO2 in CSF. Lack of O2 thus becomes the most important stimulus to breathing. In both cases the supply of O2-enriched air leads to hypoventilation and respiratory acidosis (^ p. 88 ff.). This response is increased by, for example, uremia (^ p. 110 ff.) or sleep. Because O2 uptake varies within a wide range independently of alveolar ventilation (^p. 68), breathing is stimulated only when there is a marked diminution in alveolar O2 partial pressure and a fall in O2 saturation in the blood. The resulting increase in ventilation will again cease as soon as O2 saturation in the blood is normal; breathing is therefore irregular.

The reduced sensitivity of the respiratory neurons to CO2 can also result in sleep apnea, an arrest of breathing during sleep lasting a few seconds. It is more likely in the presence ofa metabolic alkalosis.

Damage or massive stimulation of the respiratory neurons can cause pathological breathing (^ C):

♦ Kussmaul breathing (^C1) is an adequate response of the respiratory neurons to metabolic acidosis. The depth of the individual breaths is greatly increased but breathing is regular.

♦ Cheyne-Stokes breathing (^C2) is irregular. The depth of breathing periodically becomes gradually deeper and then gradually more shallow. It is caused by a delayed response of respiratory neurons to changes in blood gases resulting in an overshooting reaction. It occurs when there is hypoperfusion of the brain, or when breathing is regulated by a lack of oxygen (see above).

♦ Blot breathing (^ C3) consists of a series of normal breaths interrupted by long pauses. It is an expression of damage to respiratory neurons. Gasping (^ C4) also signifies a marked disorder in the regulation of breathing.

I— A. Modulators of Respiratory Neurons


Acidosis (pH I ) Hypercapnia (CO2 f ) Hypoxia (O2 | ) Calcium and magnesium in CSF I

Body temperature f Pain, anxiety Blood pressure Muscle work Hormones Transmitters

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