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atmosphere and a high probability that the device has been bled out of the body,
should trigger a prompt gas venting and failsafe device shutdown procedure. This
is particularly important in the case of oral bleeding, since respirocytes could
explode if crushed between two hard planar surfaces with no avenue of escape as
might occur during dental grinding [1z]—tooth enamel is the hardest natural
substance in the human body, and a patient with an oral lesion could spread
respirocyte-impregnated blood over the teeth. Of course, single-device explosions
of a micron-size pressure tank caused by dental grinding would probably be
undetectable by the patient.
Self-test algorithms monitoring tank filling rates, unaccounted pressure drops
(indicating a leak), clutch responses, etc. may detect significant device malfunc-
tion, causing the respirocyte to place itself in standby mode ready to respond to an
acoustic command to execute the filtration protocol for nanapheresis. Basic self-
diagnostic routines should be able to detect simple failure modes such as jammed
rotor banks, plugged flues, gas leaks, and so forth, and to use backup systems to
place the device into a fail-safe dormant mode pending removal by filtration.
Dormant mode can also be triggered by thermal shutoff protocols which activate
upon self-detection of any of at least four failure scenarios: (1) A normally
functioning respirocyte is deposited in a relatively dry (e.g., osteal or cartilagi-
nous) location, losing contact with the aqueous heat sink; (2) one or more glucose
engines become jammed at full open throttle; (3) inbound sorting rotors overload
pressure vessel; or (4) device fragmentation or combustion.
Using onboard (21 nm) 3 pressure transducers, respirocytes can detect, record,
or respond to changes in heart rate or blood pressure, since arterial pressure is
normally 0.1-0.2 atm (
100 zJ/(21 nm) 3 sensor) and systolic/diastolic differential
is 0.05-0.07 atm (40-60 zJ/(21 nm) 3
B
sensor), both well above the mean thermal
noise limit of k B T
4 zJ at human body temperature. Outmessaging [1aa]
protocols could allow the population of respirocytes to communicate systemwide
status (e.g., ''low oxygen,'' ''low glucose,'' ''under immune attack,'' ''cyanide
detected'' [39]) directly with the patient by inducing recognizable physiological
cues (fever, shivering, gasping) or by transmitting the information to implanted
GUIs accessible to the patient [1bq], or with the physician by generating subtle
respiratory patterns requiring diagnostic equipment to detect, either automatically
or in response to an acoustically transmitted global inquiry initiated by patient or
physician. Attempted phagocytosis of bloodborne respirocytes by the RES [2b],
particularly Kupffer cells in the liver [2c], bloodborne white cells, macrophages, or
other natural phagocytic cells could, upon detection by the respirocyte, activate
appropriate phagocyte avoidance and escape protocols (Section 15.4.2) using
techniques detailed elsewhere [2d].
Other useful control protocols may enable in vivo respirocytes to be com-
manded to cease or resume operating locally/globally, to enable/disable one or
another class of sorting rotors, to alter sensor sensitivities, to blow tanks or to run
all engines continuously, and so forth. Note that the long-term bloodstream
presence of a therapeutic dose of working respirocytes would preclude tissue
hypoxia, possibly reducing EPO secretion as low as 1% of normal levels [40], thus
B
 
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