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Figure 1.

Model schematic representing O2 uptake, transport and consumption.

O2 stores are represented by the alveolar, arterial, and venous compartments. Two dynamically-independent levels of O2 uptake are denoted: pulmonary O2 uptake () and metabolic consumption (). R-L shunt is also included. Ta is the arterial transit time. Symbols are described in Table 1.

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Table 1.

Mathematical symbols.

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Table 2.

Typical parameters for the preterm infant at term equivalent age.

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Table 2 Expand

Figure 2.

Pulmonary gas exchange during apnea.

(A) Rate of pulmonary O2/CO2 exchange. and fall from resting levels during apnea. (B) Net alveolar-capillary gas uptake () and respiratory exchange ratio ()during apnea. (C) Changes in alveolar, arterial and mixed venous during apnea. Contrast the time-course in and as they fall/rise towards . (*) represents the fall in if was assumed equal to . S1 = stage 1; S2 = stage 2.

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Figure 3.

The time course of during apnea.

Panel (A) shows the increase in the slope of the oxy-hemoglobin dissocation curve at the level of alveolar (), and the fall in pulmonary oxygen uptake () that occurs during apnea. Panel (B) shows that changes in the product explain the time course of the instantaneous slope of arterial O2 desaturation () during apnea. Note that the peak occurs when is substantially less than its resting value. Note also that the rate of fall of mixed-venous saturation () and become equal and constant after 20 s.

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Table 3.

Impact ratios describing the effect of cardiorespiratory factors on .

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Figure 4.

Impact of pre-apneic alveolar (ventilation, supplemental O2) on .

(A) Effect of three levels of alveolar (), (i) 100 mmHg, (ii) 80 mmHg and (iii) 60 mmHg, on arterial () and mixed venous () O2 desaturation during apnea. Note that arterial O2 desaturation is substantially right-shifted with increased . (B) Sensitivity of to changes in pre-apneic (). Note that reduced has a major impact on but little impact on ; the influence on is small in the normal range but becomes stronger at low . n = ‘normal’ 'values; S1, stage 1 slope; S2, stage 2 slope.

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Figure 5.

Impact of lung volume (VL) and blood volume (Qb) on .

(A) Effect of three levels of VL, (i) 30, (ii) 20 and (iii) 10 ml kg−1, on arterial () and mixed venous () O2 desaturation during apnea. (B) Sensitivity of to changes in VL. Note that reduced VL has a strong impact on and but no impact on . (C) Effect of three levels of Qb, (iv) 120, (v) 80 and (iv) 40 ml kg−1, on and during apnea. (D) Sensitivity of to changes in Qb. Note that reduced Qb has little impact on or but has a large impact on . n = ‘normal’ values; S1, stage 1 slope; S2, stage 2 slope.

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Figure 6.

Impact of metabolic O2 consumption () on .

Panel (A) shows the effect of doubling on arterial () and mixed venous () O2 during apnea; (i) 10 ml min−1kg−1, (ii) 20 ml min−1kg−1 with cardiac compensation (CC), and (iii) 20 ml min−1kg−1 with no CC (nCC). Note that with CC, increased , from (i) to (ii), elevated uniformly at all levels of during both stages 1 and 2; note that the level of at the inflection point (shown by short black lines) is unchanged. With nCC (iii), increased caused a reduced resting and lower inflection, and greater during stage 1, compared to (ii). (B) Sensitivity of to changes in . Note that with increased : a uniform increase in occurred with CC, and a more-than-proportional increase was seen with nCC; is elevated in both cases, but more so with nCC; a uniform increase in is shown regardless of CC. n = ‘normal’ values; S1, stage 1 slope; S2, stage 2 slope.

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Figure 7.

Impact of hemoglobin content (Hb) and O2 affinity (P50) on .

(A) Effect of three levels of Hb, (i) 12 g dl−1, (ii) 8 g dl−1 and (iii) 4 g dl−1, on arterial () and mixed venous () O2 desaturation during apnea. Note the fall in at the inflection point (shown by short black lines). Note also that the reduced Hb has little impact on desaturation above . (B) Sensitivity of to changes in Hb. (C) Effect of three levels of P50, (iv) 18 mmHg, (v) 24 mmHg, and (vi) 36 mmHg, on . (D) Sensitivity of to changes in P50. n = ‘normal’ values; S1, stage 1 slope; S2, stage 2 slope.

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Figure 8.

Impact of cardiac output () on .

(A) Effect of three levels of resting , (i) 375 ml min−1kg−1, (ii) 250 ml min−1kg−1, and (iii) 125 ml min−1kg−1, on arterial () and mixed venous () O2 during apnea. Note that reduced elevates , associated with a reduction in resting and reduction in at the stage 1–2 transition or inflection point (shown by short black lines). (B) Sensitivity of to changes in . Note the strong influence of on , but negligible effect on and . (C) Simulations in (A) repeated for a step change in at apnea onset by (iv) +125 ml min−1kg−1 (e.g. tachycardia), (v) 0 ml min−1kg−1, and (vi) −125 ml min−1kg−1 (e.g. bradycardia), following resting . Note that the transient effect of is opposite to the resting effect of on arterial desaturation during apnea. (D) Sensitivity of to acute changes in during apnea. Note the strong influence of a step-change in on , but negligible effect on and . n = ‘normal’ values.

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Figure 9.

Impact of R-L shunt (Fs) on .

(A) Effect of three levels of Fs, (i) 0%, (ii) 15%, and (iii) 30%, on arterial () and mixed venous () O2 during apnea. Note that resting R-L shunt fraction has a negligible impact on during apnea. (B) Sensitivity of to changes in Fs. n = ‘normal’ values; S1, stage 1 slope; S2, stage 2 slope.

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Figure 10.

Conceptual framework depicting the temporal sequence of influence of the key cardiorespiratory factors on .

Note the regions of influence of lung volume (), cardiac output () and blood volume (), each with respect to metabolic O2 consumption (). Hemoglobin content (Hb) influences the latter phase of stage 1 as well as stage 2. The impact of reduced is limited to stage 1, and blood volume to stage 2. Reduced causes a leftward shift in the desaturation trajectory. Note that the point of inflection at the transition between stages reveals the resting .

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Figure 11.

Relationship between the slope of the oxy-hemoglobin dissociation curve and alveolar .

Note that reduced alveolar () causes a substantial increase in the slope of the oxy-hemoglobin dissociation curve (; see inset) and in at apnea onset (; based on Equation 12).

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