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  • Type I respiratory failure, characterized by severe, oxygen-refractory hypoxemia, is caused by shunting due to airspace filling.
  • When blood transport of oxygen is inadequate, treatment includes optimizing cardiac output, hemoglobin concentration, and arterial saturation, and lowering oxygen consumption.
  • Optimizing does not mean maximizing, and the end point of each therapeutic approach needs to be selected for the individual patient.
  • Type II respiratory failure is characterized by alveolar hypoventilation and increased PCO2, caused by loss of CNS drive, impaired neuromuscular competence, excessive dead space, or increased mechanical load.
  • Type III respiratory failure typically occurs in the perioperative period when factors that reduce functional residual capacity combine with causes of increased closing volume to produce progressive atelectasis.
  • Type IV respiratory failure ensues when the circulation fails and resolves when shock is corrected, as long as one of the other types of respiratory failure has not supervened.
  • Liberation from mechanical ventilation is enhanced by identifying and correcting the many factors contributing to increased respiratory load and decreased neuromuscular competence.


Respiratory failure (RF) is diagnosed when the patient loses the ability to ventilate adequately or to provide sufficient oxygen to the blood and systemic organs. Urgent resuscitation of the patient requires airway control, ventilator management, and stabilization of the circulation, while effective ongoing care for the patient with RF necessitates a differential diagnosis and therapeutic plan derived from an informed clinical and laboratory examination supplemented by the results of special ICU interventions. Recent advances in ICU management and monitoring technology facilitate early detection of the pathophysiology of vital functions, with the potential for prevention and early titration of therapy for the patient's continual improvement. The purpose of this chapter is to provide an informed, practical approach to integrating established concepts of pathophysiology with conventional clinical skills. This chapter does not provide a course in pulmonary physiology nor a comprehensive review of how to treat respiratory failure. Rather, it attempts to provide a conceptual framework of principles useful in approaching the patient with RF, first by discussing an approach to tissue hypoxia, and then by describing the mechanisms causing four types of RF, showing how correcting each derangement allows the patient to resume spontaneous breathing effected by respiratory muscles that are not fatigued.


Patients with RF are susceptible to anaerobic metabolism, either because they deliver inadequate O2 to their systemic organs or because their tissues develop an abnormal inability to extract oxygen from the blood.1 During air breathing, arterialized blood leaves the normal alveoli with a partial pressure of oxygen (PaO2) of about 100 mm Hg. When the hemoglobin concentration is 15 g%, arterial O2 content (CaO2) is about 20 mL per 100 mL blood on the fully saturated hemoglobin and about 0.3 mL in physical solution. Accordingly, a cardiac output (Q̇t) of 5.0L/min transports approximately 1000 mL/min of O2 to the tissues (transport of oxygen; Q̇O2). There, ...

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