United States Naval Flight Surgeon's Manual: Third Edition 1991: Chapter 2: Acceleration and Vibration
Naval Aerospace Medical Institute
Peer Review Status: Internally Peer Reviewed
Sustained acceleration most significantly affects the circulatory system and secondarily affects mental and sensory function. Of less significance, musculoskeletal effects impede movements necessary to control the aircraft or execute emergency procedures. At very high acceleration levels, musculoskeletal injury as been reported.
Three types of sustained acceleration are commonly seen in aviation:linear, which is a change in speed without a change in direction; radial or centripetal, which results from a change in direction without necessarily a change in speed; and angular, which is rotation around a body axis. Each of these types of acceleration has disorienting aspects, however, these are discussed in the chapter on vestibular function.
The physiological effects of G differ markedly, depending on the direction of the G related to the body. Because of this, each G direction will be discussed separately.
"Eyeballs Down" (+Gz) Acceleration
"Eyeballs down" or +Gz acceleration is the most common sustained acceleration experienced by naval aviators, and it is the most likely to have serious consequences. This type of acceleration is usually a result of radial acceleration due to a c hange in direction.
For an aircraft in a level turn, the G can be calculated by the following formula:a = v2/r
The following example is a calculation of G in an aircraft flying at 500 knots and turning with a radius of 2000 ft. (Note that there are 6080 ft/knot and 3600 s/h.)
As we shall see, this is well beyond the limits of most naval aviators' capability.
For a naval aviator of average stature seated upright, the height of the column of blood from the aortic valve to the eye is about 30 centimeters (cm). At 1 +Gz, this column of blood would result in an app roximate pressure drop from heart to eye of 22 millimeters of mercury (mm Hg). Thus, with a mean blood pressure of 100 mm Hg at the aortic valve level, the systolic blood pressure at eye level at 1 +Gz would be 100 minus 22, or 78 mm Hg. For each additional +Gz, the eye level blood pressure is lowered by 22 mm Hg, until at 4.5 G, the mean eye level blood pressure is 0. Therefore, if only the hydrostatic column is considered, the theoretical limit of +Gz tolerance for eye and brain blood flow, and thus eye and brain function, is approximately 4.5 G, unless either the blood p ressure at the aortic valve level is increased, or the effective height of the aortic valve to eye blood column is decreased.
Other complexities are added, however, in vivo. As the +Gz level increases, compensatory mechanisms begin to act. Baroreceptors in the aortic arch and carotid arteries sense the decrease in pressure and act to increase the blood flow to the he ad by three mechanisms:peripheral vasoconstriction, increased heart rate, and increased contractile force of the cardi ac muscle. These responses occur about 6-10 seconds after stimulation (see Figure 2-1 and Guyton, 1981), and in very fast onset rates of G, may be too slow to avoid serious neurological consequences. (See section on +Gz neurological effects. ) Chemoreceptors play a role as pressure drops and as the arterial oxygen partial pressure (Pa02) decreases from the respiratory effects of G. The central nervous system (CNS) ischemic response probably plays a role in recovery when head blood pressure drops to 0 for greater than 5 seconds, resulting in loss of consciousness.
Dysrhythmias are frequently seen when subjects are electrocardiographically monitored while undergoing G stress. The most common dysrhythmias associated with +Gz exposure are marked sinus arrhythmia, premature ventricular contractions, and prem ature atrial contractions (Leverett & Whinnery, 1985, p.216). It is questionable whether acceleration is more dysrhythmogenic than other physical stresses, such as hard exercise, or whether mechanisms unique to G, such as distortion of heart muscle, have an effect. In healthy aviators, the effects of these dysrhythmias are usually slight, except in rare instances when they may reduce brai n blood flow enough to cause neurological symptoms (Whinnery, Laughlin, & Uhl, 1980).
There has been concern for many years that subclinical cardiovascular system damage might occur from high G exposure, causing long-term adverse health eff ects. In fact, endocardial hemorrhages have been reported in pigs exposed to high G, but there is no evidence that cardiac damage occurs in humans who are exposed acutely or chronically to G within tolerance limits (Leverett & Whinnery, 1985, p.227).
Most of the CNS and sensory effects of +Gz are a direct result of the cardiovascular effects. For CNS and eye tissue to function, only brief blood flow interruption can be tolerated. If blood flow to t hese tissues is interrupted, the tissue reserves of oxygen last approximately 5 seconds. As this minuscule reserve is used up, the tissue ceases its normal function. If blood flow is restored after a brief period of malfunction, the tissue resumes functi oning with no residual damage. There is, however, a profound and critical difference between the response of the eye and the response of the brain to blood flow loss from +Gz. First, blood flow to the eye ceases before blood flow to the brain does, because of the internal pressure of the eye (approximately 16 mm Hg average). Because of this early blood loss difference, vision will fail at about 0.7 G below the +Gz level at which cerebral function fails. This is fortuitous for aviat ors since it can provide a visual warning of impending loss of consciousness. Aviators frequently use grayout or tunneling of vision as a way to titrate the G load to avoid more serious consequences, but this technique becomes less reliable as the G onset rate increases. To understand this phenomenon, it is necessary to examine the interactions between the 5-second lag from stoppage of blood flow to eye or brain until the development of eye or brain symptoms, and the onset rate of G. Figure 2-2 illustrat es this warning time change at a slow and a fast onset rate of G.
Figure 2-3 further illustrates the physiology of G-induced visual symptoms and loss of consciousness. Note especially the 5-second oxygen reserve during which no eye or brain symptoms occur. This reserve explains why an aviator can bend an airplane with momentary excessive G, have no ill effects, and as a result, develop an inflated perception of his G tolerance. The dip in the curve in Figure 2-3 illustrates the problem caused by the lag in physiological compensatory mechanisms, especially with high onset rates of G. Figure 2-4 illustrates the G-titration strategy using vision symptoms that pilots can use effectively with slow onset rates of G. It also illu strates why this strategy will not always work with aircraft such as the F/A-18 that are capable of high onset rates of G. There simply is not enough time for the visual symptoms to provide warning before G-induced loss of consciousness (GLOC).
Another profound difference between eye and brain response to +Gz is the failure and recovery mode. The eye fails and recovers smoothly when blood flow stops. This can be easily demonstrated by digital pr essure on the eye to stop the blood flow (Whinnery, 1979). After about 5 seconds of pressure, vision is progressively lost from peripheral vision to central vision. When blood flow is allowed to resume, vision is smoothly and rapidly recovered. Cerebral failure and recovery is much less graceful and predictable (Houghton, McBride, & Hannah, 1985). After about 5 seconds of blood flow stoppage to the brain, GLOC occurs suddenly and lasts from 10 to 30 seconds (average about 13 seconds). When consciou sness is regained, it is usually accompanied by brief seizure-like activity and a period of confusion,which lasts about 12 seconds. During this 12 seconds, the aviator is unable to function effectively. An additional period of up to 2 minutes is required before cognitive and psychomotor performance ability recovers to normal.
Although amnesia for the event of GLOC is common (Whinnery & Shaffstall, 1979), 13 percent of naval aviators questioned in an anonymous survey admitted having GLOC in an aircraft, at least once in their career (Johanson, Flick, & Terry, 1986). Total loss of the ability to control a high performance, unstable aircraft for half a minute is obviously a condition to be avoided.
There are two primary effects of +Gz on respiratory function. The most serious effect results from a perfusion/ventilation mismatch. As the +Gz increases, the pressure gradient in the lung increas es, resulting in reduced per fusion of the upper part of the lung and increased perfusion in the lower part of the lung. This results in an increased physiological dead space in the upper portion and a physiological shunt in the lower portion of the lung, both of which result in a re duced Pa02. In healthy subjects exposed to +7 Gz for 45 seconds, the Pa02 decreased from 91.6 mm Hg to 50.1 mm Hg despite an almost two-fold increase in tidal volume (Leverett & Whinnery, 1985, p 221). This reduced Pa 02 is added to the insult of reduced blood flow to the head and would be expected to contribute to decrements in performance capability.
A second problem is G-induced oxygen atelectasis, or aero-atelectasis. The U.S. Navy uses 100 percent oxygen in most tactical jet aircraft breathing systems to simplify the breathing system, to provide an underwater breathing capacity, and to maximize nig ht vision. Aero-atelectasis, especially in the compressed alveoli of the dependent portion of t he lung, occurs more readily when 100 percent 02 is used than when an inert gas dilutes the breathing gas, due to the more rapid absorption of 02 from poorly aerated alveoli. The aero-atelectasis sometimes causes mild transient chest pain and coughing after high +Gz maneuvering, but the symptoms are generally not thought to be severe enough to offset the advantages of the 100 percent 02 systems. This is a controversial subject. The USAF and the RAF have elected to use systems that dilute the oxygen in the breathing system with cabin air up to a preset cabin altitude, while the Navy continues to consider that underwater breathing capability more than offsets the mild symptoms of aero-atelectasis.
At 6 +Gz, a 160 pound aviator is pressed into his seat with an equivalent of 960 lbs. As +Gz levels increase, purposeful limb movements become progressively more difficult. Neck and back pain may occ ur a nd may be the limiting factor for G tolerance in some aviators. Musculoskeletal physical fitness is very important in limiting this performance decrement and discomfort, and enabling the aviator to accomplish the neck and body movement required to search for enemy aircraft. Weight training is currently being evaluated for its cardiovascular and its musculoskeletal effects on G tolerance and shows promise in both areas.
Tolerance to +Gz varies considerably f rom person to person, and in a given aviator, varies from day to day. A simplified theoretical case was discussed earlier with the assumption of an aortic valve to eye column height of 30 cm, and a mean blood pressure at the aortic valve level of 100 mm H g. The point of loss of brain blood flow would theoretically occur at 4.5 G. In actual practice, determination of G tolerance requires defining the measurement method, which is affected by a complex array of compensatory mechanisms and individual differe nces. Any measurable, repeatable end point could be chosen; for example, mild peripheral vision loss, total vision loss, or loss of consciousness. An accepted measure of tolerance limits is loss of peripheral vision to a central cone of 60o as measured by the subject tracking his peripheral vision on a light bar (Air Standardization Coordinating Committee, 1986). This degree of vision loss occurs roughly 0.7 to 2.0 G lower than GLOC occurs.
Figure 2-5 illustrates G tolerance measur ed by peripheral light loss (PLL) in an experiment using a moderately rapid (2-second rise time) onset rate with non-aviator subjects (Cohen, 1983). These G tolerance levels are for a specific group of experimental subjects and, therefore, will vary with the population being tested. Figure 2-5 also shows the increase that can be gained by use of the anti-G suit (AGS), the M-1 straining maneuver, and the pelvis and legs elevating seat (PALE), which is equivalent to a 75o seat back angle.
A number of factors affect individual G tolerance. Some of them are:
Protective Measures for +Gz.
1. Anti-G suit (AGS).
The Navy AGS contains inflatable bladders, which cause constriction around the calves, thighs, and abdomen. The suit prevents pooling of blood in the lower extremities and abdomen, thus improving venous return to the heart, and el evates the diaphragm, thus slightly reducing the aortic valve to eye column height, reducing the distortion of the heart by G, and assisting in increasing the intrathoracic pressure. The suit is inflated by an aircraft-mounted G valve, which senses G and inflates the G suit in proportion to the G force. Careful fitting of the G suit is critical to its function. A well-fitted G suit will increase G tolerance by about 1 G.
2. Straining Maneuvers.
Straining maneuvers increase G t olerance by reducing blood pooling in the extremities and abdomen, and by increasing intrathoracic pressure rhythmically to assist the heart in maintaining head level blood pressure. The "M-1" maneuver consists of tightening the muscles of the extremities , abdomen, and chest; pulling the head down between the shoulders; and grunting against a partially closed glottis. This grunt is maintained for about 3 to 5 seconds, relaxed very briefly to allow inhalation and thoracic venous blood return, and then repe ated. A properly performed M-1 increases G tolerance by about 2 G and is roughly additive to the G suit protection, together providing about 3 G additional protection. An improperly performed M-1 may actually reduce G tolerance, probably by reducing card iac return.
Training is critical for the performance of an optimum M-1. The maneuver should be carefully explained and should be practiced with supervision under +Gz conditions. (It is uncomfortable and perhaps dangerous to practi ce at 1 G because it markedly increases head level blood pressure. ) Practice in an aircraft usually precludes adequate training feedback. A centrifuge provides the best environment for training of the maneuver.
The "L-1" maneuver is identical to the M-1 maneuver except that the glottis is completely closed instead of partially closed. It is as effective as the M-1 and probably preferable because is causes less throat irritation.
3. Reclined Seat.
Reclining the sea t improves G tolerance by reducing the effective aortic valve/eye column height. Figure 2-6 illustrates the effect of various seat back angles (Burns, 1975). The improvement in G tolerance is roughly linear with reduction in effective column height (i.e. at 75o seat back angle, column height is reduced to one half and G tolerance is almost doubled). At high G in the reclined position, G tolerance becomes progressively limited by pain from contact with the seat, from chest compression, and from difficulty inhaling due to the increased weight of the anterior chest wall. These symptoms limit this technique to about 14-15 G maximum. Although reclined seats can dramatically improve G tolerance, they are seldom used because of difficulty providing full use of displays and controls while providing adequate outside vision.
4. Experimental Protective Techniques.
Several methods for increasing +Gz tolerance are under investigation. These methods include:
a. Positive pressure breathing with a chest counterpressure garment. This technique provides a mechanical assist for increasing intrathoracic pressure, and it may be more effective and less tiring than performing a standard straining maneuver.
b. Pulsating G suits, synchronized to the electrocardiogram. This technique would provide a pulse superimposed on the systolic pulse, producing a higher systolic pressure at head level.
c. Positive pressure breathing with reclined seat. This technique may alleviate inhalation difficulty caused by the increased weight of the anterior chest wall, and thus overcome one disadvantage of the reclined position.
d. Optimization of physical fitness training procedures. This may allow a more forceful straining maneuver with less fatigue.
e. Drugs to increase head level blood pressure on a short-term basis.
"Eyeballs Up" (-Gz) Acceleration
Cardi ovascular Effects.
In -Gz, arterial and venous pressure cranial to the heart are increased. It should be remembered that -1 Gz differs by 2 G from the normally experienced G. The increased pressure in the aortic arch and carotid arteries results in a pronounced bradycardia. Increased venous pressure may result in facial edema, petechiae, sinus pain, and headache. A commonly reported "red out" or visual red veil is probably due to the lower lid being forced over the pupi l or perhaps to blood staining of the lacrimal fluid from ruptured conjunctival vessels. A rapid transition from -Gz to +Gz would obviously exacerbate the problem of the delayed physiological compensatory mechanisms and may increase the risk of GLOC.
Sensory disturbances and severe headache have been reported, as well as confusion and loss of consciousness. These responses are subject to considerable individual variation.
The main musculoskeletal effects are impairment of the aviator's ability to operate controls. For example, in an inverted spin, an inadequately restrained aviator may not be able to manipulate the controls well enoug h to recover from the spin or to reach the ejection firing control.
Discomfort is the primary limiting factor in voluntary exposure to -Gz. Research on the limits has been sketchy due to volunteer subject d iscomfort and researchers' fears of untoward side effects. An estimate of reasonable limits is -4.5 Gz for 15 seconds and -3 Gz for 30 seconds (Christy, 1971).
Serious respiratory effects have not been reported at the otherwise tolerable levels of -Gz.
The only protective measure currently available is to maintain restraints tight enough to allow operation of both normal and emergency controls.
"Eyeballs In" (+Gx) Acceleration
"Eyeballs in" acceleration is experienced during forward acceleration, such as catapult shots, with minimal effects other than decreased musculoskeletal control and increased risk of disorientation. The cardiovascular and respiratory effects are simply ex tensions of those discussed under +Gz in the special case of a 90o seat back angle.
"Eyeballs Out" (-Gx) Acceleration
This is a condition seldom experienced by a naval aviator except for impact or for brief periods during a carrier landing or a ditching. It may occur in abnormal conditions such as a flat spin. For example, a flat spin in an F-14 may exert as much as -6 Gz. The primary problem in this instance is musculoskeletal (e.g. difficulty in operating the aircraft controls). A special problem occurs when the pilot's shoulder harness is not locked, and the onset of -Gx is not rapid enough to automatically lock the harness. In this c
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