End-tidal tensions of oxygen (PETO2) and carbon dioxide (PETCO2) are values that can determine a precise estimate of arterial oxygen and carbon dioxide pressures (PaO2, PaCO2). The method of obtaining these values is done non-invasively by sampling the end of exhalation at the mouth so that the CO2 and O2 measured at the end of a tidal breath reflects alveolar CO2 (LeMura, 2004). PETCO2 is also helpful in determining the adequacy of gas exchange (hypercapnia).
The normal resting value of PETO2 is 90mmHg and increases during exercise to allocate the extra work load placed on muscles in the production of energy (Wasserman, 2004). PETO2 has been found to be closely related to PaO2 through changes in VO2 and RER, in young and old patients with normal lung function. When corrections are made for dry or wet gases, the difference seen between PETO2 and PaO2 is very minimal. PETO2 like PETCO2 is helpful as it is easy to measure it also automatically adapts to the actual RER and it allows for the use of an alternative respiratory index entirely based on measured values and not of an assumed RER (Bengtsson, 2001). Normal resting values of PETCO2 are 36-42mmHg and increases by 3-8 mmHg during submaximal exercise, but decreases during heavy, maximal exercise (Babb, 1998).
Effects of Disease
Though PETCO2 is a good indicator of gas exchange in healthy adults the accuracy decreases when compared to PaCO2 when measured in patients with lung disease or chronic obstructive pulmonary disease (Babb, 1998). PETCO2 and PETO2 can also show changes when measured in the obese, in severe heart failure and in patients with pulmonary vascular disease (Fig.1.0). In obese individuals PETCO2 is greater than that of normal individuals and PETO2 is severely decreased. This is due to a mechanical restriction caused by the heavy chest wall and abdomen preventing ventilation from keeping the precise pace with the increase of CO2 production.
Patients that have severe heart failure evidence a decrease in PETCO2. This is due to blood flow being slow in relation to ventilation in regional lung units. Irregular breathing patterns associated with severe heart failure also make PETCO2 quite variable. This is shown by two sets of values appearing when measuring PETCO2 at rest in patients with severe heart failure. A reduction in PETCO2 can be seen in pulmonary vascular occlusive disease. This is due to an increase of dead space provided by a lack of perfusion of ventilating lung. This increase in dead space dilutes the CO2 and thus a reduction in PETCO2 is seen when compared to healthy individuals (Wasserman, 2004).
In healthy patients the rise in PETCO2 is regarded to be closely linked with lactate and the lactate threshold. When undertaking an incremental exercise test and PETCO2 and O2 are graphed you can see two distinct phases (Fig. 2). The first phase is at a medium to heavy intensity range and this is called isocapnic buffering. In this phase excess CO2 is produced from the buffering of lactic acid as part of an ‘open system’.
The second phase is the respiratory compensation phase where an increase rate of ventilation becomes apparent to get rid of the excess CO2 from the buffering phase. These two phases can be distinctly seen in Fig.2. In this review both of these phases will be examined in respect to lactate, PETCO2 and O2. There will also be matters addressing the use of different types of muscle mass with these phases.
During the medium to heavy intensity phases of an incremental exercise test blood and muscle alike become saturated with CO2 in conjunction with the increase of lactate associated protons. This provides the basis for the estimation of the lactate threshold by non-invasive methods. This is the start of the isocapnic buffering phase which is widely believed to fall in conjunction with the lactate threshold. H+ ions from the lactate become exposed to a mix of buffers in the blood which include inorganic phosphate (Pi) and bicarbonate (HCO-3).
These mix of buffers constrain the acidaemia that results from the acidosis. All of the many buffers are involved in the role of buffering ions, but to varying degrees. Even though the initial 0.3-0.5mm of the lactate increase is constrained by buffers other than HCO-3 bicarbonate does make up for more than 90% of the buffering (Visser, 1964). The buffering of H+ ions from the use of bicarbonate can be said to be part of an open system as the reaction is completely reversible (Levitzky, 2003). H+ + HCO-3 H2CO3 H2O+CO2
From this equation you can come to the conclusion that CO2 production from bicarbonate is at the same rate at which HCO-3 buffers the lactic acid. Wasserman et al states that 22.3mL of CO2 will be produced over that generated from aerobic metabolism for each mmol of lactic acid buffered by HCO-3. The increase in cell lactate and decrease in cell HCO-3 concentrations stimulate transmembrane exchange of these ions, with HCO-3- decreasing in the blood almost mmol for mmol with the increase in lactate concentration (Beaver, 1986). Thus the greater rate of increase of lactate, the greater the rate of the pulmonary exchange rate. This is evidenced by a higher VCO2 being seen when at a given VO2 in conjunction with rising lactate levels during a rapid increasing incremental test (Scheuermann, 1998).
In comparison, a slow incremental test shows that CO2 production can be several times greater than that for a rapid incremental test (Ward, 1992. As lactate increases and bicarbonate decreases CO2 is produced from the contracting muscle units. This results in an increase in CO2 output from the muscle and finally from the lungs. This is the basis for characterizing the onset of metabolic acidosis, as estimated from pulmonary gas exchange, as a metabolic rate rather than a work rate (Ward, 1992). The CO2 produced by the buffering of lactic acid is quantitatively large. This is seen by an almost 2.5 fold increase in VCO2 and a 12.5 fold increase in the glycogen utilization rate (Whipp, 1991).
This large increase predominantly from the buffering of lactic acid makes VCO2 analysis as a function of VO2 a reliable and accurate way of identifying the lactate threshold (Beaver, 1986). This is done by using a simple method called the V-slope method. This method consists of plotting CO2 production over O2 utilization and identifying a breakpoint in the slope of the relationship between these two variables.
The level of exercise intensity corresponding to this breakpoint is considered the anaerobic threshold. The slope that is graphed in the method falls under two terms. The first term being S1 and this is the first part of the slope that is characterized by a relatively linear relationship over the moderate intensity range (Beaver, 1986). At this point isocapnic buffering occurs and PETCO2 increases slightly due to the extra metabolic CO2 being produced by the buffering of lactate (Takano, 2000) The second phase is evidenced by an increased slope (S2) that occurs during the isocapnic buffering phase and extends up to the respiratory compensation point. This area is characterized by a decrease in PETCO2 (Wasserman, 1973). It is the intersection of these two phases that has been shown to agree closely with the onset of lactate (Beaver, 1986).