Acute respiratory failure is characterised by mismatch of ventilation with perfusion (VA/Q). The multiple inert gas elimination technique (MIGET) is a complex method which allows the description of a virtually continuous distribution of VA/Q ratios. We investigated VA/Q relationships in patients admitted to the intensive care unit due to acute respiratory failure and thus requiring for mechanical ventilation.
Method: Eight patients (mean APACHE 11 = 22 +/- 4) who suffered from acute pneumonia (n = 4), traumatic lung contusion (2), toxic lung failure (1) or massive bilateral atelectasis (1) were investigated by MIGET within 3 days after the begin of mechanical ventilation. A mixture of six inert gases, dissolved in isotonic saline, was infused continuously. Arterial and mixed venous blood samples and expired gas samples were obtained and analysed by gas chromatography. Blood-gas partition coefficients were determined, and the ratios of retention and excretion were calculated. The data were transformed in a 50-compartment model of blood flow and ventilation against VA/Q ratio. We assessed the amount of intrapulmonary shunt (VA/Q = 0), low VA/Q regions (VA/Q = 0.005-0.1), normal VA/Q regions (VA/Q = 0.11-10), high VA/Q regions (VA/Q = 11-100) and dead space ventilation (VA/Q > 100). Furthermore, we calculated the logarithmic standard deviation of pulmonary perfusion distribution (logSDQ).
Results: In all patients we found moderate to severe intrapulmonary shunt and VA/Q mismatching. The data are expressed as median values and ranges. Inert-gas-measured shunt was 21% (3-45.5%), whereas low VA/Q regions were little affected. Normal VA/Q regions ranged from 41.5% to 96.0% (median 76.8%). The amount of alveolar dead space ventilation was 28% (19.7-41.8%). Median logSDQ (normal range 0.3-0.6) was calculated to be 0.855 (0.540-1.490). In patients presenting with moderate lung injury (Murray score < 3), a moderate increase in shunt and a moderate VA/Q mismatch were observed. In contrast, patients with severe lung failure and critically decreased oxygenation (Murray score > 3) were characterised by massive shunting and VA/Q mismatching. Additionally, low VA/Q and high VA/Q compartments and an increase in dead space ventilation was found in these patients.
Conclusions: The impairment of oxygenation in patients with acute respiratory failure is due to several pathophysiological mechanisms: increase in intrapulmonary shunt, VA/Q-mismatching and dead space ventilation, according to the severity of lung failure. We conclude from our results that the prevention and/or reduction of non-ventilated lung areas (atelectasis) is an outstanding therapeutic strategy in the treatment of patients with acute respiratory failure. From this point of view, several techniques of systemic changes in body position should be integrated as supportive therapeutic strategies.