Management of the Patient on a Ventilator

  • J. B. Hall
  • L. D. H. Wood
Conference paper
Part of the Anaesthesiologie und Intensivmedizin / Anaesthesiology and Intensive Care Medicine book series (A+I, volume 178)


Consider a one compartment lung model ventilated via one airway and perfused by the total pulmonary blood flow. Inspired gas having no CO2 enters the airspace perfused by mixed venous blood. In the steady state, the CO2 production (VCO2 = 250 ml/min), which was added to the arterial blood in the peripheral tissues, now moves by diffusion to equilibrate with the alveolar ventilation (VA = 41/min). Accordingly, the alveolar gas fraction is about 6%, so the alveolar PCO2(PACO2) is about 40 torr. Because PACO2 is determined by the ratio VCO2/VA, arterial CO2 retention signals alveolar hypoventilation when the CNS drive to breathe decreases (drug intoxication, head trauma), when the respiratory muscles become excessively weak (ascending polyreticulitis, myasthenia gravis, botulism), or when the load on the respiratory muscles exceeds their normal strength (status asthmaticus, acute on chronic respiratory failure). In the latter conditions, alveolar ventilation is further reduced because large amounts of the minute ventilation are wasted as dead space; increased dead space in each tidal volume (Vd/Vt) is signalled by the mixed expired CO2 becoming much less than the alveolar PCO2, because a large fraction of the tidal volume does not equilibrate with pulmonary blood flow in the alveoli (Vd/Vt) = (PACO2 - PECO2)/(PACO2). Hypercapnia is the sine qua non of hypoventilatory (Type II) respiratory failure, which is associated with arterial hypoxemia accounted for by alveolar hypoventilation (normal alveolar-arterial gradient) and correctable with supplemental oxygen [1, 2].


Chronic Obstructive Pulmonary Disease Respiratory Muscle Pulmonary Blood Flow Alveolar Ventilation Status Asthmaticus 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Owens GR, Rogers RM (1982) Managing respiratory failure in chronic airflow obstruction. J Respir Dis 3: 24–37Google Scholar
  2. 2.
    Aubier M, Murciano D, Milic-Emili J, et al (1980) Effects of administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Resp Dis 122: 747–754PubMedGoogle Scholar
  3. 3.
    Hall JB, Wood LDH (1984) Acute hypoxemic respiratory failure. Med Grand Rounds 3 (2): 183–195Google Scholar
  4. 4.
    Malo J, Ali J, Wood LDH (1984) How does positive end-expiratory pressure reduce intrapulmonary shunt in canine pulmonary edema? J Appl Physiol: Respirat Environ Exerc Physiol 57 (4): 1002–1010Google Scholar
  5. 5.
    Don HF, Craig DB, Wahba WM, Couture JG (1971) The measurement of gas trapped in the lungs at functional residual capacity and the effects of posture. Anesthesiology 35: 582–590PubMedCrossRefGoogle Scholar
  6. 6.
    Murciano D, Aubier M, Lecocguic Y, Pariente R (1984) Effects of theophylline on diaphragmatic strength and fatigue in patients with chronic obstructive pulmonary disease. NEJM 311 (6): 349–379PubMedCrossRefGoogle Scholar
  7. 7.
    Dantzker DR, Brook CH, DeHart P, et al (1979) Gas exchange in adult respiratory distress syndrome and the effects of positive end-expiratory pressure. Am Rev Resp Dis 120: 1039PubMedGoogle Scholar
  8. 8.
    Roussos C, Macklem PT (1982) The respiratory muscles. NEJM 307: 786–797PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1985

Authors and Affiliations

  • J. B. Hall
  • L. D. H. Wood

There are no affiliations available

Personalised recommendations