Disclaimer: I do not own "Transformers," nor any characters or related indicia thereof. No money is being made and no copyright infringement is intended.

This is the first chapter of a guide written by Alirion of Frey's Hope for the use of other medics in the treatment of Cybertronians and other cybernetic lifeforms. Guided toward the neophyte in cybermedicine. This will probably not interest you.

Cybernetic Physiology and Internal Medicine

1) Overview

The cybernetic races possess a distinct and individualistic physiology which both parallels and diverges from organic humanoid physiology. Analogous systems exist in the two basic models, but the importance of each system is specific to the species, rather than as a general rule of thumb. As the Cybertronian race of cybernetic lifeforms is the most commonly encountered, it is this basic model we will be using in our discussion.

2.) Circulatory/Fuel Systems

2i. The Cybertronian physiology features two discrete but related circulatory systems, the fuel system and the circulating coolant system. These serve different but related purposes. The fuel system comprises the energon intake, holding and conversion tanks, and the distributary conduits that provide fuel to the body's systems. The main energy distribution pathway in the body is via wiring: fuel is consumed—either orally or intraconduitally--, converted into electrical energy, and held in central batteries which power the individual between fuel intakes. However, the various musculoskeletal systems—separated for multiple redundancy to ensure that damage to one sector of the body does not result in widespread deactivation of systems—have their own liquid fuel supply and conversion modules. This auxiliary energon supply is recirculated via a small pump located below the main energon conversion tanks. Thus, if damage or blockage to the main cable bus feeding power to a limb prevents mainline power transfer, the auxiliary energon feed systems will allow that limb to continue functioning without interruption.

Once the fuel has been processed through the conversion tanks, changing the electrical potential in the liquid energon into electrical energy, the liquid matrix remains. This liquid now passes through a filtration barrier into the circulating coolant fluid reservoir, combining with the CLA (q.v) in the coolant fluid, and is pumped out into the circulovascular cooling network.

The circulating coolant system is the most vital of the basic somatic functions of the Cybertronian physiology. While in deep interstellar space, the heat produced by normal functioning is able to disperse through the external armour plating; however, in temperature ranges above 273 degrees Kelvin/0 degrees Celsius, heat transfer is required to maintain optimal functioning efficiency. Thus, a liquid coolant network draws heat away from the circuitry and disperses it via heat-transfer modules located close to the external surface. The coolant fluid itself is contained within a vascular network of conduits which are capable of expanding and contracting to adjust flow and pressure within the system. This vascular tension is autonomically controlled, and the stimuli which cause these autonomic corrections can be artificially induced to produce particular effects.

The conversion process which transforms the energy matrix present in energon into usable electrical power produces a great deal of heat as a byproduct; therefore the vascular network surrounding the conversion tanks is extremely dense. The coolant is circulated by a pump module which is located sternoventrally from the conversion tanks—separated by the filtration system which clears any obvious debris from the energy matrix fluid after conversion—and is powered by a separate, redundant battery array designed to maintain coolant flow in the event of major power loss. Circulatory fluid reservoirs flank the coolant pump module and are protected by internal armour shell plating.

Circulatory systems—both fuel and coolant—are regulated by the autonomic array of the central neuroprocessor (neurocable bus 8 and 9).

2ii. Approach to the Patient with Possible Circulovascular Malfunction

The first and most important aspect of circulovascular care is to verify that the circulation of fluids is unimpeded. Without proper circulation of coolant, vital systems will begin to overheat and shut down, and potential permanent damage may result. In some cases of circulatory failure, cooling is completely referred to the oxygen intakes; thus, the patient may present with oxygen intake distress as well as temperature spikes and localized or general system failure. It is important to determine whether oxygen intake distress is secondary to circulation failure or caused by a separate malfunction; all cases of oxygen intake distress should be checked for circulatory function and monitored to ensure that the circulatory systems remain patent. If the circulation is compromised due to physical damage or blockage of the conduits, the patient must be stabilized and cooling maintained by external means while repairs on the vessels are carried out. Most cases of circulovascular derangement are due to mechanical trauma and the consequent loss of circ fluid, but pathogenic involvement remains a possibility and must be investigated if symptoms and scan results warrant it.

Supportive therapy during the intense diagnostic phase consists of external auxiliary coolant and recirc connections, external power supply, and sedation via neurocircuitry block if shock—categorized by a sudden fall in vascular tension, fluctuation in central core temperature, and feedback loops in the autonomic control system—appears imminent.


2iii. Pump Function and Circulatory Control

As remarked above, the coolant is circulated via a shielded pump located in the main chest compartment ventral to the conversion tanks. This pump is run via neurocable bus 8, which traverses down the spinal column and is accessible via the cervical access panel before it splits into cable bunches to feed the systems of the upper torso. The connections with the local circuitry occur just below the split, and are difficult to access without cableties and retractors. The anatomy of the neurocable bundles should be familiar to the student of cybermedicine, but for reference a diagram is provided at the end of this chapter.

The pump itself is a simple and elegant piece of machinery which works on a two-chambered suction principle: returning coolant enters the first chamber as the second chamber is emptied, then the central valve closes as the second chamber fills; when it is full, the central valve opens to permit the coolant to flow into the second chamber under pressure, until the presseals are at their set limit, whereupon the interchamber valve shuts, the second chamber is emptied, and the circuit begins again. The pump is set at baseline to run at a certain rate, which may be overridden by increased cooling demands from the somatic systems due to exertion, temperature change, or pathogenic involvement. There are cascade failsafes guarding the operational circuitry for the pump, but in case of complete systemic failure it can be restarted by connecting a GS7 power coupling to the connector on the outside of the pump housing (anterior oblique connector 5). It is wise, in any case presenting with acute circ-pump failure, to check the circ fluid itself for the presence of foreign nanorobotic matter which may be causing malfunctions.

2iv. Hypertension

As noted above, the recirculating coolant fluid is contained within a vascular network, the tension of which is normally under autonomic control (neurocable bus 8). However, this control may be deranged due to energy overload (as in cases of electric shock) or stress. In rare cases, idiopathic vascular tension fluctuations have been noted; these are often ascribed to secondary circuit fluctuations consequent to minor system shock. Pathogens (q.v.) are capable of damaging the neurocircuitry which controls vascular tension; specifically, DHX-1 and CR-alpha have been recorded as producing tension fluctuations which cause secondary system malfunctions. Hemicrania (q.v.) also involves changes in cerebrovascular tension which are not fully understood, but which are believed to be associated with overstress in certain cerebral network bundles.

2v. Atherosclerosis-Thrombosis and Vascular Structure

The thrombotic subclassification of the CLA (q.v.) is limited in its actions, in normal functioning, to the repair of breached vessels. Local sensors in the vascular wall relay damage signals to the cerebral circuitry, which activates the thrombic CLA and directs them to the damaged area to repair the vascular wall. However, these signals may be spuriously activated by pathogenic or physical damage to the neural net. In certain degenerative neurocircuitry disorders, atherosclerosis of the vascular network may develop due to overactivation of the thrombic CLA despite the lack of vascular breach. Illegal substances such as "syk" also derange the normal functioning of neurocircuitry controlling vascular tension, and may cause permanent damage.

The vascular network itself is constructed of three layers of delicate myocircuitry. The inner and outer layers run transverse around the central layer, which runs longitudinally up the length of the vessel itself. Each of these layers is capable of contraction and expansion both locally and generally, under the control of the neurocable bunches for that particular sector. This flexibility allows for the preservation of the vascular integrity despite vessel breach in any given sector; the damaged area is contracted to shutdown by the local myocircuitry, while flow is resumed in subsidiary vessels to maintain cooling in the surrounding systems. All vascular breaches must be repaired as soon as possible to avoid the danger of localized overheating and circuitry damage subsequent to vessel damage.

Atherosclerosis may, as referenced above, be caused by damage to the autonomic immune system circuitry. The second major cause of atherosclerosis is inappropriate fuel additives; certain performance-enhancing additives contain large quantities of incontrovertible substances that are unfortunately able to pass through the filtration core between the conversion module and the circ-fluid reservoirs. These substances adhere to the vascular walls and integrate thrombic CLA bodies to form plaques of hard material which grow to sclerose the vascular lumen. Ultrasonic thrombotripsy may be useful in breaking up these plaques and releasing them for the detritophagic CLA to dispose of; otherwise, physical debridement of the vascular lumen is indicated, which may involve major surgery if the vessel involved is a deep one. At-risk patients must be counseled about the dangers of performance enhancers, both immediate and long-term.