Pathophysiology of Chronic Respiratory Failure

Pathophysiology of Chronic Respiratory Failure A. Hypoxemic Respiratory Failure 

For a given level of CO2 production (VCO2), hypercapnic respiratory failure results only from an inadequate VA. A simple equation describes these relationships quantitatively under steady state conditions  

Since VA = minute ventilation (VE) - dead-space ventilation (VD), this equation can be expressed as 

From these equations, it follows that VA decreases and so Pacx 2 increases when VE decreases. Likewise, when VE and VD remain unchanged but VT decreases and respiratory frequency (RF) increases (rapid shallow breathing), Pacx)2 increases. Patients adopt a rapid shallow breathing pattern to minimize respiratory work per breath, but this form of compensatory behavior can be deleterious to gas exchange and is a major factor producing chronic hypercapnic respiratory failure in patients with COPD and neuromuscular disorders (6-10). 

The function of the ventilatory pump is critically dependent on three factors the respiratory workload, the respiratory muscle strength, and the ventilatory drive (Fig. 1). Chronic hypercapnic respiratory failure can result from one or more of these abnormalities inadequate ventilatory drive, excessive respiratory load, and inadequate inspiratory muscle 

---

In patients with kyphoscoliosis the severity is quantified by measuring the angle between the upper and lower portions of the spinal curve (Cobb angle). When this angle exceeds 100° (severe scoliosis), the vital capacity falls below 50% of the predicted value (48). A major factor in the pathophysiology of chronic respiratory failure in patients with kyphoscoliosis is the decrease in the compliance of the chest wall and limgs (49,50). In severe scoliosis the compliance of the chest wall may be about 25% of the predicted value. 

---