[Basis of respiratory insufficiency]

Setting out from the components of respiratory function, i.e., ventilation, distribution, diffusion, circulation, respiratory mechanics, and regulation of breathing, the pathogenic mechanisms leading to respiratory failure are discussed. In every case, the vital capacity is decreased by 4 factors, namely loss of ventilated lung parenchyma, diminished compliance of lungs, thorax or both, airway obstruction, and insufficient respiratory airflow. With few exceptions, these alterations can be attributed to the two general groups of obstructive and restrictive disturbances of ventilation. Essential for the understanding of airway obstruction from the viewpoint of mechanical ventilation is the dependence of the airway caliber on lung volume, thoracic pressure, and bronchial gas flow. The functional differentiation of restrictive disorders between forms with lung retraction(fibrosis, scarring) and with lung fettering (pleural thickening) is important for adequate correction of complications during the intensive care phase. Respiratory failure is the consequence of these alterations which usually impede pulmonary gas exchange. Hypoxemia results in most situations through disturbance of ventilation/perfusion ratio, especially increase of anatomical or functional pulmonary right-to-left shunting. Disturbance of diffusion or alveolar hypoventilation are far less frequently leading mechanisms for hypoxemia. The differential diagnosis of these hypoxemic mechanisms is generally by arterial blood gas analysis under resting conditions breathing air and 100% oxygen, and during exercise. Respiratory failure often leads to hypertension in the lesser circulation. Pulmonary arterial hypertension must be subdivided into the active, the passive and the hyperdynamic forms, of which only the active component is important for the evaluation of pulmonary insufficiency since only this kind of elevated pressure in the pulmonary circulation is connected with increased vascular resistance due to thoracopulmonary disease. By restoration of normoxic conditions, the functional variant of active pulmonary hypertension can be efficiently improved by correction of respiratory disease or directly by treatment with oxygen and by mechanical ventilation. Finally, disturbances of gas transport in the blood may have an essential bearing on respiratory failure, but are often overlooked in diagnostic and therapeutic considerations. Shifting of the oxygen-dissociation curve to the left may, by increased oxygen affinity of hemoglobin, create a lack of oxygen in the peripheral tissue, while right wardshifting impedes oxygenation of hemoglobin in the lung. Thus, the correction of acidosis and elevated body temperature may become an important factor in the treatment of respiratory failure.