Overview:

Hyperventilation probably isn’t what you think it is. Hyperventilation is when ventilation exceeds metabolic demands and PaCO₂ drops below 5 kPa. The result will be an alkalosis that affects the function of every protein in the body, producing a confusing spectrum of symptoms with a single cause. Shallow, rapid breathing is probably just that, not necessarily hyperventilation.

The importance of CO₂

The body’s main mechanism for altering breathing patterns uses CO₂ as the trigger, not O₂. It sounds counterintuitive, like many topics in physiology, but because CO₂ levels determine blood pH and changes in pH fundamentally alter biochemical processes, it’s the thing the body is most interested in regulating. Oxygen comes second.

Whether someone is adequately ventilated can be determined from the partial pressure of CO₂ in arterial blood (PaCO₂), not from how they appear to be breathing. A patient might appear to be hyperventilating, but in fact be taking lots of shallow breaths and actually hypoventilating. Similarly, when we exercise, breathing increases to get rid of excess CO₂; this increase is appropriate (hyperpnoea), since the body is producing increased CO₂ that needs to be “blown off”. Ventilation comes down to metabolism: how much CO₂ is the body producing, and what alveolar ventilation is required to blow it off to keep PaCO₂ at 5 kPa.

Metabolism

If you fuelled the body exclusively with glucose, the amount of O₂ consumed and CO₂ produced would be the same. This is due to the stoichiometry of burning glucose in O₂:

For every molecule of glucose (C₆H₁₂O₆), six molecules of O₂ are required, and six molecules of CO₂ are produced. We don’t live on pure glucose though. Imagine if we lived on pure fat instead. The chemistry is rather different (this is palmitin, a common plant and animal fat):

In this case, the ratio of CO₂ to O₂ is 102÷140 or 0.73. We call this ratio the respiratory exchange ratio. For glucose it is 1.0, for fats it is closer to 0.7. On a mixed diet, it’s fair to assume that this ratio is around 0.8; we normally produce around 250 mL/min CO₂, burning 300 mL/min O₂ in the process. Adequate ventilation is a matter of getting those gas flow rates working, and it’s the CO₂ that the body is keeping an eye on the most, because (PaCO₂) regulates pH and every process in the body is altered by pH disturbances.

Alveolar ventilation (V̇A)

Breathing in and out doesn’t completely replenish the stale air in the lungs. In fact most of the volume of the lungs stays in the lungs, and each breath dilutes fresh air in the functional residual capacity (FRC) of the lung. Furthermore, the air in the conducting airways doesn’t contribute to gas exchange at all and constitutes dead space. At rest, with a typical tidal volume VT; the depth of each breath) of around 500 ml, 150 ml is lost in dead space (VD), and the remaining 350 mL is mixed into the much larger 2350 mL existing FRC. So, it’s not a matter of breathing in, exchanging gases and breathing out. The process of gas exchange goes on continuously, and breathing is just the mechanism for removing a little stale air and adding a little fresh stuff. If we treat the lung as one big alveolus connected to a single airway it works out as shown in Figure 1.

The actual volume of air that reaches the alveoli is tidal volume (VT) minus the dead space (VD):

That’s just thinking about volumes (L) though. We need to think in terms of flow: L per minute (L/min). This is simple enough. Say you take 12 breaths per minute (your respiratory frequency, or f), each of 500 ml VT. From this we can calculate your minute ventilation (V̇E, in mL/min) by multiplying the two:

Of course, not all that ventilation reaches the alveoli because some of it is lost in dead space, so if we wanted to calculate the true alveolar ventilation we’d have to factor VD into the equation:

The natural reaction to seeing someone breathe at, say, 40 breaths per minute, with a VT of 150 mL might be to think that they are hyperventilating. To be sure, we’d need to see their PaCO₂ to see if they were hypocapnic. Repeating the above calculations with those values should give you a clue about the degree of alveolar ventilation in such a person. Their V̇E would be 6000 mL/min, but their V̇A would have to be zero, so they must be hypoventilating.

Gas exchange:

By the time fresh air is diluted down in the somewhat staler alveolar environment (and water vapour is added), PAO₂ is 14 kPa, and is mixed with 6 kPa CO₂ (equal to PvO₂). In fact, you can calculate what the PAO₂ should be based on PaCO₂ using the alveolar gas equations. If the airways become obstructed, the alveoli become less ventilated and the air in them is staler as a result: PAO₂ will drop and PACO₂ will rise closer to venous blood levels. Indeed, if the airway leading to a series of alveoli becomes completely obstructed, the partial pressures of O₂ and CO₂ in those alveoli will equilibrate with venous blood. The process of gas exchange is summarised in Figure 2 below:

Hyperventilation and hypoventilation

Figure 3 below illustrates the relationship between alveolar ventilation (V̇A) and the partial pressure of CO₂ (PO₂) in the alveoli (PACO₂). Remember, under normal circumstances the (PACO₂) will be equal to the arterial partial pressure of CO₂ (PaCO₂)

Hyperventilation is excessive V̇A such that too much CO₂ is blown out of the body, not breathing too quickly as the word is commonly (mis)used. Hypoventilation is the opposite; you retain too much CO₂. So: