E Casadei

Ventilatory-metabolic monitoring and analysis of arterial pulse

The assessment of cardiac output (CO) continues to challenge physiologists who study human endurance, clinical pharmacologists interested in the effects of treatment on cardiac output, and intensivists concerned with the measurement of oxygen consumption/oxygen delivery (VO2/DO2) dependency and the prevention of organ dysfunction or failure in haemorrhagic, cardiogenic, or septic shock. In clinical exercise testing, employed for the evaluation cardiac function in patients with chronic heart failure (CHF), the measurement of CO is mainly used to record the stroke volume in patients who have an unexpectedly high heart rate during exercise. A low stroke volume implies impaired cardiac function. If cardiac function is normal and output is high, the tachycardia is presumed to be due to impaired control of the peripheral circulation [1].

Combined gas exchange and pulse wave monitoring for detecting anaerobic metabolism in critically ill patients

The anaerobic metabolism causes lactate to increase. This is accompanied by a reduction in bicarbonate concentration in the blood, causing CO2 production (VCO2) to accelerate, evidenced as an increased respiratory CO2 output. Over the physiological range of CO2 content the CO2 tension is linearly related to CO2 content, and the venoarterial CO2 tension difference (DPCO2) could be used as a surrogate for the difference between mixed venous and arterial CO2 contents. Under anaerobic metabolism the respiratory quotient increases. The venoarterial CO2 tension difference/arteriovenous O2 content difference ratio [DPCO2/C(a-v)O2] therefore increases. We tested the DPCO2/C(a-v)O2 ratio and mixed venous oxygen saturation (SvO2) values as potential predictors of anaerobic metabolism.