On general physical examination, Bukowskii had increased respiratory rate (22 breaths per minute), deep and laboured breathing and saturations of 89 percent on oxygen of 6L per minute. Respiratory system examination revealed intercostal muscle recession on inspection and diminished air entry to both bases and crepitations in the right base on auscultation. Arterial blood gas analysis revealed PaO2 less than 60mmHg (58mmHg) and PaCO2 more than 50 mmHg (54mmHg) with pH of 7.3. These are the four pieces of evidence pointing towards acute respiratory failure.
Respiratory failure may be acute or chronic. In case of Bukowski, the respiratory failure is acute and this is indicated by the drastic change in the acid-base status (pH= 7.3). The cause of respiratory failure in him is the right lower lobe collapse-consolidation secondary to pneumonia. Lower respiratory tract infection is known as pneumonia. The pathology lies in the parenchyma of the lungs which consist of alveolar sacs. There are several causes to pneumonia, the most common of which is bacterial (Stephen, 2009). Bacterial pneumonia can be community acquired or hospital acquired. In case of Bukowski, the pneumonia is hospital acquired.
The most common respiratory failure is acute hypoxemic respiratory failure or type-1 which is seen in pneumonia. In acute respiratory failure, the pH is less than 7.3 (Nettina, 2009) as in Bukowski.
Decreased oxygen saturation: Acute respiratory failure occurs when the body is unable to maintain gas exchage at a rate on par with the demands of the body like in paneumonia. The damage to lung parenchyma in pneumonia results in release of inflammatory mediators and fluids because of which intrapulmonary shunting, ventilation-perfusion mismatching, hypoventilation and diffusion defects occur (Stephen, 2009). All these eventually lead to hypoxemia which is evident in the blood gas analysis of Bukowski (Ranjit, 2001). In ventilation-perfusion mismatch, areas which have lower ventilation as against perfusion contribute to hypoxemia. Intrapulmonary shunt causes deoxygenated blood to bypass ventilation in the alveoli resulting in venous admixture of blood (Roussos and Koutsoukou, 2003). Both these mechanisms cause a widening in the alveolar-arterial oxygen difference. The normal difference is less than 15mmHg and when the difference exceeds this value, respiratory failure ensues (Kaynar and Sharma, 2009). The hypoxemia causes increased work of breathing resulting in respiratory fatigue. Respiratory fatigue and reduced alveolar ventilation in turn cause hypercarbia (Roussos and Koutsoukou, 2003).Thus, Bukowski developed hospital-aquired pneumonia because of which adequate gas exchange commensurate with the needs of the body was not met, resulting in acute hypoxemic respiratory failure. Elevated respiratory rate and work of breathing: Increased respiratory rate and accessory muscle usage are indicators of increased work of breathing (Stephen, 2009), secondary to decreased oxygen in the blood. Respiratory acidosis: The hypoxemia causes increased work of breathing resulting in respiratory fatigue. Respiratory fatigue and reduced alveolar ventilation inturn causes hypercarbia (Roussos and Koutsoukou, 2003). Auscultation: Pneumonia occurs secondary to immune and inflammatory response secondary to bacteria. Due to this, fluid and pus accumulate in the airspaces. This is heard as crepitations on auscultation.