Prospective targeting and control of end-tidal CO2 and O2 concentrations

Abstract

Current methods of forcing end-tidal PCO2 (PETCO2) and PO2 (PETO2) rely on breath-by-breath adjustment of inspired gas concentrations using feedback loop algorithms. Such servo-control mechanisms are complex because they have to anticipate and compensate for the respiratory response to a given inspiratory gas concentration on a breath-by-breath basis. In this paper, we introduce a low gas flow method to prospectively target and control PETCO2 and PETO2 independent of each other and of minute ventilation in spontaneously breathing humans. We used the method to change PETCO2 from control (40 mmHg for PETCO2 and 100 mmHg for PETO2) to two target PETCO2 values (45 and 50 mmHg) at iso-oxia (100 mmHg), PETO2 to two target values (200 and 300 mmHg) at normocapnia (40 mmHg), and PETCO2 with PETO2 simultaneously to the same targets (45 with 200 mmHg and 50 with 300 mmHg). After each targeted value, PETCO2 and PETO2 were returned to control values. Each state was maintained for 30 s. The average difference between target and measured values for PETCO2 was +/-1 mmHg, and for PETO2 was +/-4 mmHg. PETCO2 varied by +/-1 mmHg and PETO2 by +/-5.6 mmHg (s.d.) over the 30 s stages. This degree of control was obtained despite considerable variability in minute ventilation between subjects (+/-7.6 l min(-1)). We conclude that targeted end-tidal gas concentrations can be attained in spontaneously breathing subjects using this prospective, feed-forward, low gas flow system.

Figures

Figure 1

Schematic of the modified sequential gas delivery circuit The manifold attached to the non-vented mask is separated into inspiratory and expiratory limbs using one-way low resistance valves. The two limbs are connected via a bypass limb with a one-way cross-over valve that has an opening pressure greater than that of the other two valves. During exhalation, all of the exhaled gas is directed through the expiratory limb into the atmosphere, with the last portion of the exhaled breath trapped in the expiratory reservoir. At the same time, Gas 1 (G1) collects in the inspiratory reservoir. At the beginning of inhalation, G1 is drawn from the Gas 1 inlet and the inspiratory reservoir. If minute ventilation exceeds the flow of G1 during inhalation, G1 in the reservoir is depleted and the reservoir collapses. The negative pressure in the inspiratory limb causes the cross-over valve to open and the balance of the breath is then made up of Gas 2 from the expiratory reservoir.

Figure 2

Changes in end-tidal partial pressure of CO2 (, ○) in response to progressive decrease in the flow of Gas 1 () Also shown in the figure is the stylized raw capnograph tracing (continuous line). At the top of the figure, the observed results are explained with a lung model consisting of anatomical dead space (VDAN) in series with alveolar volume (VA). If exceeds minute ventilation (), then the lung is only filled with Gas 1 (G1). When, on average, the inspiratory reservoir of the SGD circuit collapses at the end of each inspiration, equals (stage A). If is less than , Gas 2 (G2) starts to enter the lungs via a bypass conduit of the SGD circuit. This is confirmed by a characteristic rebreathing ‘shoulder’ at the end of the inspiratory portion of the raw CO2 tracing. G2 remains trapped in VDAN (stage B), however, and therefore has no effect on . only starts to increase when G2 starts to enter alveoli (stage D). The when values start to increase corresponds to the alveolar ventilation (). At this point, all of VDAN is occupied by G2 (stage C).

Figure 3

The effect of changes in tidal volume (VT) on alveolar ventilation when breathing on a sequential gas delivery (SGD) circuit When the flow of Gas 1 exceeds alveolar ventilation (panel A), the increase in VT causes G1 trapped in the anatomical dead space (VDAN) to enter alveoli (VA), providing extra alveolar ventilation. If the flow of G1 is equal to or less than alveolar ventilation (panel B), all of VDAN is filled with the previously exhaled gas (G2) that is ‘neutral’ with respect to alveolar ventilation (see Rule 2 in text). An increase in VT causes G2 to enter VA, but because the volume of G1 available for gas exchange is not altered, alveolar ventilation does not change.

Figure 4

Experimental protocol A total of three experiments were performed. During experiment I was varied to + 5 (I-T1) and + 10 mmHg (I-T2) from baselines (I-B1 and I-B2) before being returned to baseline II-B1. During experiment II was varied to +100 (II-T1) and +200 mmHg (II-T2) from baselines (II-B1 and II-B2) before being returned to baseline III-B1. During experiment III, both and were varied simultaneously to the same targets as those attained during experiments II and III.

Figure 5

End-tidal partial pressure of CO2 () and O2 () and minute ventilation () data from all subjects Note that subjects were asked to empty the inspiratory reservoir at the end of most breaths. Since was set to 15 l min−1 in order to speed up transitions between steady-states, the baseline was at least 15 l min−1 or greater in all subjects. As a result, the normal increases in ventilation that would be seen during a significant hypercapnic challenge and natural breathing are not observed in this experiment.

Figure 6

Pooled end-tidal and data from all subjects Continuous lines represent ideal target responses at each stage of the protocol. Circles represent experimental data (mean ± s.d.). *Statistically significant differences (P < 0.05).