Page 82 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
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Distribution Abnormalities
       The concentration of O 2 and CO 2 in an alveolar  of the lung can be prevented by local scarring
       space and the related capillary are dependent  such as pleural thickening. Diaphragmatic
       on the ratio of ventilation (V ˙ A) to perfusion  paralysis has the same effect by preventing
       (Q ˙ ). In the ideal case this relationship (V ˙ A/Q ˙ )  expansion of basal lung segments. Functional
       and thus the O 2 and CO 2 concentration is iden-  arteriovenous shunts can also occur in pulmo-
       tical in all alveoli. Pulmonary vessels contract  nary fibrosis.
       in hypoxia and thus normally guarantee exten-  Perfusion of inadequately ventilated alveoli
       sive adaptation of perfusion to ventilation of  leads to an admixture of nonarterialized blood
    Acid–Base Balance  lation and perfusion in the basal lung seg-  hypoxemia (→ A; PA= partial pressure in alveo-
       individual alveoli. In an upright position venti-
                                       with pulmonary venous blood. This results in
       ments are greater than in the apical ones. Per-
                                       lar gas mixture), which cannot be compensat-
       fusion is more strongly affected and V ˙ A/Q ˙ is
                                       ed by hyperventilation of “intact” alveoli (this
       thus normally slightly higher apically than ba-
                                       is because O 2 uptake by the blood that passes
                                       along ventilated alveoli can be increased only
       sally.
         The term “abnormal distribution” describes
                                       minimally by hyperventilation; → p. 68). On
    Respiration,  the condition when the ratio of ventilation to  the other hand, hypercapnia hardly ever oc-
                                       curs because the reduced CO 2 release from un-
       perfusion in individual alveoli deviates to a
                                       derventilated alveoli (→ A, right) can be well
       functionally significant extent from that in the
                                       compensated by increased release into hyper-
       whole lung. In principle there are two possibil-
       ! Impaired perfusion of individual alveoli in
                                       the hypoxemia frequently leads to excess hy-
    4  ities:                          ventilated alveoli (→ A, left). On the contrary,
       relation to perfusion occurs in vascular occlu-  perventilation, and the development of hypo-
       sion, for example, in pulmonary embolism  capnia. If considerable venous admixture oc-
       (→ p. 80). In addition, capillaries can be sepa-  curs, the arterial hypoxemia cannot be stopped
       rated from their related alveoli by proliferating  even by breathing pure O 2 .
       connective tissue, as is the case in pulmonary  If the supplying airway is completely oc-
       fibrosis (→ p. 70,74). Lastly, capillary supply to  cluded, the alveoli collapse (atelectasis). Nor-
       the alveoli may also fade away if the alveolar  mally more O 2 is taken up in tissue than CO 2
       septa are destroyed, as is the case in pulmo-  is released, so that there is a greater decrease
       nary emphysema (→ p. 78).       in O 2 partial pressure than increase in CO 2 par-
         The impaired perfusion of ventilated alveoli  tial pressure (→ B1). The blood therefore takes
       increases the functional dead space, because the  more O 2 from the alveoli than it adds CO 2 , re-
       air in these alveoli no longer takes part in the  sulting in a decrease of the alveolar volume.
       gaseous exchange. This condition can be com-  As a consequence N 2 in the alveoli is concen-
       pensated by deeper breathing (increased VT).  trated and, following its gradient, also diffuses
       If a large proportion of alveoli are not perfused,  into the blood. Eventually, the entire alveolar
       the diffusion area also decreases (→ p. 70), and  volume is reabsorbed. The process is delayed
       this can no longer be compensated by deeper  by a fall in alveolar O 2 concentration and sub-
       breathing.                      sequent vascular contraction (see above). Ven-
       ! In impaired ventilation of perfused alveoli  tilation with O 2 can favor the development of
       (→ A) the blood is no longer adequately satu-  atelectases (→ B2), because O 2 uptake is in-
       rated with O 2 and rid of CO 2 . In an extreme  creased by the high alveolar O 2 partial pres-
       case a functional arteriovenous shunt devel-  sure and there is no constriction of the supply-
       ops. In obstructive lung disease, such as asth-  ing vessels.
       ma and chronic bronchitis (→ p. 76), some of
       the bronchi are narrowed and preclude normal
       ventilation of their alveoli. Ventilation of indi-
       vidual bronchi (or bronchioles) can also be
   72  prevented by occlusion through tumor. The
       opening up and therefore ventilation of parts
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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