Effects of changing in inspired gases graphs provided V T, RR, VE

3.3.3 Hypoxia alone

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ventilatory acclimatization to hypoxia produces a timedependent increase in ventilation, a decrease in arterial Pco

2(PaCO2), and an increase in the hypoxic ventilatory response

(HVR). This process has been well characterized in humans which

exhibits the most humanlike ventilatory acclimatization to hypoxia.

3.3.4 Hyperoxia

The idea of pre-oxygenation is to replace air in the

Functional Residual Capacity (that is the residual volume of air in

the lungs after the end of a normal breath) with 100% oxygen.

The volume of the FRC in a 70kg adult is about 2.5 liters. The
total oxygen demand of the same person at rest is about

250ml/min. With no pre-oxygenation the total amount of oxygen

in the FRC will be 500ml (2.5L * 21%) - exhausted in approx. 2

min. With pre-oxygenation you can increase the time until your
lung stores of oxygen are depleted by about 5 times to 10
minutes.

In that 10 minutes, arterial CO2 levels will climb by about

0.5 kPa/min, from about 5 kPa to 10, the blood pH will probably
drop to about 7.2. This is not ideal, but it really isn't life

threatening. Lack of oxygen will kill you way before the build up
of CO2 does.

The caveat to that is that the urge to breath is predominately

driven by CO2 build up, and inhaling one breath of O2 wouldn't

do anything much to your CO2 levels so it would be difficult to

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resist your urge to breath, although probably not impossible with

enough will power.

Our blood has evolved to capture the oxygen we breathe in

and bind it safely to the transport molecule called haemoglobin. If

you breathe air with a much higher than normal O2 concentration,

the oxygen in the lungs overwhelms the blood's ability to carry it
away. The result is that free oxygen binds to the surface proteins
of the lungs, interferes with the operation of the central nervous
system and also attacks the retina. Contrary to popular myth,

hyperventilating air at ordinary pressures never causes oxygen

toxicity (the dizziness is due to CO2 levels dropping too low
3.3.5 Hypercapnia alone
Optimal V/Q matching occurs when the ratio of the volume

of gas to the volume of blood into the lungs approximates 1.

Pulmonary venoarterial shunts and alveolar hypoventilation result

in V/Q mismatch, which is probably the most important

mechanism of gas exchange impairment in infants with respiratory

failure due to various causes, including respiratory distress

syndrome (RDS). Hypoventilation is frequently seen in infants with

apnea of prematurity.

The effect of assisted ventilation on hypercapnia strongly

depends on the mechanism of gas exchange impairment.
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Hypercapnia secondary to severe V/Q mismatch may be treatable

with CMV or could require high-frequency ventilation (HFV).
Hypercapnia secondary to hypoventilation is usually easily

managed with CMV. CO2 normally diffuses readily from the blood
into the alveoli. Elimination of CO2 from the alveoli is directly

proportional to alveolar minute ventilation, which is determined by

the product of tidal volume (minus dead-space ventilation) and
frequency.

Relationships among ventilator-controlled variables (shaded circles)

and pulmonary mechanics (unshaded circles) that determine minute
ventilation during pressure-limited time-cycled ventilation. The

relationships between the circles joined by solid lines are described

by simple mathematical equations. The dashed lines represent
relationships that cannot be calculated precisely without

considering other variable such as pulmonary mechanics. Thus,

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simple mathematical equations determine the time constant of the

lungs, the pressure gradient, and the inspiratory time. In turn, these
determine the delivered tidal volume, which, when multiplied by

the respiratory frequency, provides the minute ventilation. Alveolar

ventilation can be calculated from the product of tidal volume and
frequency when dead space is subtracted from the former

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Effects of incomplete inspiration (A) or incomplete expiration (B)

on gas exchange. An incomplete inspiration leads to decreases in
tidal volume and mean airway pressure. Hypercapnia and

hypoxemia may result. An incomplete expiration may lead to

decreases in compliance and tidal volume and an increase in mean
airway pressure. Hypercapnia with a decrease in PaO2 may result.
However, gas trapping and its resulting increase in mean airway

pressure may decrease venous return, decreasing cardiac output and

impairing oxygen delivery

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