The PACO2 of an awake, preoxygenated adult with normal lungs rises 7 mm Hg/minute for the first 10 seconds, 2 mm Hg/min for the next 10 seconds, then 6 mm Hg/minute afterwards [Stock MC et. al. J Clin Anesth 1: 96, 1988], so essentially 6 mm Hg/min or 1 mm Hg every 10 seconds. According to UVa lectures, CO2 increases 3-4 mm Hg / min in a cardiac arrest patient.
In awake, normal adults, the apneic threshold for PaCO2 is ~ 32 mm Hg, although awake adults will still voluntarily breathe at this level. At 80 mm Hg, the ventilatory response to CO2 becomes parabolic (i.e., increase in V tails off), and at 100-120 mm Hg CO2 narcosis occurs. 1.0 MAC of CO2 is 200 mm Hg.
There are only three true causes of a left-shift or steepening CO2 response curve [and subsequent hyperventilation]: 1) hypoxemia 2) metabolic acidemia 3) central causes [ex. drugs, intracranial HTN, fear, and norepinephrine]. A right-shift or flattening can be caused by opiates and inhaled anesthetics [partially but unpredictably reversed by surgical stimulation], metabolic alkalemia, sleep, and drugs.
The most common cause of acutely increased pulmonary dead space is sudden drop in cardiac output (and not pulmonary embolus). Emboli are the 2nd most common cause. Note that the majority of cardiac output reduction in pulmonary emboli are due to vasoconstriction/inflammatory response and not the obstruction itself.
Yamanaka and Sue [Yamanaka et. al. Chest 92: 832, 1987] studied 17 mechanically-ventilated patients with some form of lung injury and found that the average difference in PETCO2 and PaCO2 was 18 mm Hg (STDEV 10). P[a-ET]CO2 was related to dead space in a linear relationship. Thus, according to Barash, PETCO2 is useful as an indicator of deadspace, but not adequacy of ventilation (since PaCO2 is still unknown).