Page 92 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Pathophysiology of Breathing Regulation
Numerous factors influence the respiratory quent decrease in HCO 3 – concentration in
neurons in the medulla oblongata (→ A): plasma and (after a delay) in CSF.
Ventilation is increased by acidosis, hyper- Barbiturates (soporific drugs) and chronic
capnia, hypoxia, and a decrease of Ca 2+ and respiratory failure decrease the sensitivity of
Mg 2+ in cerebrospinal fluid (CSF). Pain, inten- the respiratory neurons to pH or CO 2 in CSF.
sive cold or heat stimuli to the skin, an increase Lack of O 2 thus becomes the most important
or moderate fall in body temperature, a drop in stimulus to breathing. In both cases the supply
blood pressure, and muscular activity (joint in- of O 2 -enriched air leads to hypoventilation and
Acid–Base Balance ulating factors are epinephrine and norepi- is increased by, for example, uremia (→
nervation) all increase ventilation. Other stim-
respiratory acidosis (→ p. 88ff.). This response
p.110ff.) or sleep. Because O 2 uptake varies
nephrine in the blood, histamine, acetylcho-
within a wide range independently of alveolar
line and prostaglandins in the central nervous
ventilation (→ p. 68), breathing is stimulated
system (CNS), progesterone, testosterone, and
corticotropin.
only when there is a marked diminution in al-
Conversely, ventilation is reduced by alkalo-
veolar O 2 partial pressure and a fall in O 2 sat-
Respiration, sis, hypocapnia, peripheral hyperoxia, and Ca 2+ uration in the blood. The resulting increase in
2+
increase in the CSF. Hypoxia in the
and Mg
ventilation will again cease as soon as O 2 sat-
uration in the blood is normal; breathing is
CNS, deep hypothermia, rise in blood pressure,
therefore irregular.
ganglion blockers as well as high concentra-
The reduced sensitivity of the respiratory
and glycine in the CNS also diminish ventila-
4 tions of atropine, catecholamines, endorphins neurons to CO 2 can also result in sleep apnea,
tion. an arrest of breathing during sleep lasting a
Normally the pH around the respiratory few seconds. It is more likely in the presence
neurons or the pH in the CSF has a decisive in- of a metabolic alkalosis.
fluence on ventilation. A shift in pH in the Damage or massive stimulation of the re-
brain following rapid changes in P CO 2 is accen- spiratory neurons can cause pathological
tuated by the low buffering power of CSF (low breathing (→ C):
protein concentration). Because CO 2 , but not ! Kussmaul breathing (→ C1) is an adequate
– +
HCO 3 or H , quickly passes through the response of the respiratory neurons to
blood–CSF and blood–brain barriers, changes metabolic acidosis. The depth of the individual
in CO 2 concentration in the blood result in breaths is greatly increased but breathing is
very rapid adaptation of ventilation, while regular.
adaptation after changes in blood pH or blood ! Cheyne–Stokes breathing (→ C2) is irregu-
–
HCO 3 occurs only after a delay of several days. lar. The depth of breathing periodically be-
If sudden metabolic acidosis occurs (→ B, top; comes gradually deeper and then gradually
see also p. 88ff.), respiratory compensation more shallow. It is caused by a delayed re-
will thus occur only slowly. Conversely, treat- sponse of respiratory neurons to changes in
ment of a partly compensated respiratory blood gases resulting in an overshooting reac-
–
acidosis, for example, by infusion of HCO 3 , of- tion. It occurs when there is hypoperfusion of
ten leaves behind respiratory alkalosis (→ B, the brain, or when breathing is regulated by a
bottom). Also, with a sudden fall of O 2 partial lack of oxygen (see above).
pressure in inspiratory air (at high altitude) ! Blot breathing (→ C3) consists of a series of
ventilation is not immediately and adequately normal breaths interrupted by long pauses. It
raised. The onset of hyperventilation leads to is an expression of damage to respiratory neu-
hypocapnia, and the resulting intracerebral al- rons. Gasping (→ C4) also signifies a marked
kalosis will then transiently inhibit any further disorder in the regulation of breathing.
rise in ventilation. Complete adaptation of
breathing to a reduced O 2 supply requires an
–
82 increase in renal HCO 3 excretion with subse-
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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