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86 Cards in this Set

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Describe the XYZ coordinate system used in describing aircraft acceleration
x-axis is oriented front to back or perpendicular to a coronal plane, the y-axis is oriented is oriented laterally or perpendicular to a sagittal plane, and the z-axis is oriented vertically or perpendicularly to a horizontal plane. Place your right hand I front of you with the thumb pointed up, index finger pointed directly forward, and middle finger pointed toward toward the left so that each finger is perpendicular to the other two. Now each of the three pointing fingers indicates a “positive” direction (axis) of the centripetal acceleration forces: (a) the thumb points to headward acceleration (+gz); the index finger points forward acceleration (+gx); and the middle finger points leftward acceleration (+gY).One must still remember the sign change associated with eyeballs-in (-x reaction) for +x acceleration. Similarly, +z is eyeballs-down and +y is eyeballs-right.Longitudinal (vertical) is denoted z; lateral (right/left) is y; and horizontal (supine/prone) is x.
Right hand rule
Define linear centripetal acceleration.
When the linear velocity of an object changes over time, the difference in velocity, divided by the time require for the moving object to make the change, gives it a mean linear acceleration. Formula is a=(v2 – v1)/Δt where v1 is the initial velocity and v2 is the final velocity, and Δt is the elapsed time. It is a vector quantity with magnitude and direction. Measured in m/second2. To convert to units of g, simply divide by 9.81.
Measurement units
Convert to g
Define angular acceleration.
Anuglar acceleration, ω, is the rate of change of angular displacement. Formula is ω=(θ2 – θ1)/Δt, where θ1 is the initial angular displacement and θ2 is the final angular displacement. The fact that an object may be undergoing curvilinear motion during a turn in no way effects the calculation of its angular velocity. Because radial or centripetal linear acceleration results when rotation is associated with a radius from the axis of rotation, centripetal acceleration can be calculated with this formula: ac= ω2r. The rate of change of angular velocity is angular acceleration, α. Formula is α=(ω2/ω1)Δt, where ω1 is initial angular velocity and ω2 is the final angular velocity. Measured in degrees/sec or rad/sec. One cannot express angular acceleration in g units.
Does an object undergoing curvilinear motion during a turn have an effect?
How calculate centripetal?
Measurment units
Convert to g
Define centripetal acceleration.
Centripetal acceleration is a type of linear acceleration that results in curvilinear, usually circular motion. This acceleration acts along the line represented by the radius of the curve and is directed toward the center of the curvature. Its effect is a continuous redirection of the linear velocity, in this case called tangential velocity of the object subjected to the acceleration. The value can be calculated if one knows the tangential velocity, vt and the radius, r of the curved path followed. Formula is ac=vt2/r. Measured in m/second2. To convert to g, divide by 9.81.
Measurment units
Convert to g
Define “G force” as it applies to the aviation environment.
Unit of linear and centripetal (radial) acceleration is the "G" which expresses the magnitude of a force (or acceleration) acting on a body. jolt is the rate of change in acceleration (G/sec). It is of particular consequence when discussing short term accelerations such as ejection or crash forces. The effects of acceleration on the body are also classified by duration. Dehart has 2 categories: (1) transitory which is <1 sec and (2) sustained which is >1 sec. Ernsting has 3 categories: (1) short duration which is <1 sec, e.g. crash forces; (2) intermediate duration 0.5-2 sec, e.g. ejection, cat shots, traps; and (3) long duration which is >2 sec, e.g. aircraft maneuvers. Long duration lateral acceleration (+GY) is rare in aviation and won't be discussed
DeHart classification categories
Ernsting classification categories
Which classification category is rare in aviaiton?
State the systems that are effected by +Gz on the body.
Cardiovascular, pulmonary, central nervous system, renal system, mobility, hormonal response, +Gz tolerance
What are the effects of +Gz on the cardiovascular system
Cardiovascular response, heart rate changes, and coronary blood flow.
What Is the effect on Heart rate with +Gz
Howard reports that HR increases directly (but not linearly) w/max +GZ level of exposure. Rate will vary between and w/in subjects on individual runs. Burton suggested HR response during high +GZ has 3 separate components: (1) physical work (straining), (2) acceleration, and (3) psychological stress.
What is the effect on coronary blood flow from +Gz
Controlled by aortic diastolic BP and remains adequate during +GZ exposure and increase w/ increasing +GZ. However, subclinical coronary artery disease could manifest itself during a high +GZ exposure.
What is the cardiovascular response to +Gz?
The cardiovascular reflexes respond to blood pooling below the heart level due to the hydrostatic column effect. Pooling of blood occurs mainly in lower limbs w/some occurring in abdominal area. BP decreases above the heart and increases below the heart which has an immediate effect on the size of blood vessels which is based on transmural pressure (difference between intra- and extravascular tissue pressure), distensibility of vessel and amt of blood available to fill it. In comparison, BP at rt and lt atria remain unchanged up to +4.5 GZ. Transmural pressure increases in arteries and arterioles below the heart will decreases peripheral resistance and increases local blood flow. Transmural pressure decreases in veins above the heart can produce complete collapse and cease blood flow. The transmural pressure  in the skin capillaries can increase enough that vessels rupture, especially in the lower extremities. This leads to petechial hemorrhages (petechiae or "G-measles") after prolonged or repeated exposure > +4GZ. The decrease in both central BP and apparent blood vol causes stimulation of the high pressure stretch receptors in the carotid sinus and aortic arch causing decrease parasympathetic (vagal) inhibition and increase sympathetic stimulation resulting in increase HR, increase vasoconstriction, increase venoconstriction and increase heart contractile force. Venous return to the rt side of the heart starts to increase 10-15 sec after onset of exposure and CO increase w/in a few beats.
Blood pooling
Blood vessel size
Heart BP
Transmural pressure
Cause of G-measles
Vagal effect
What are the effects of +Gz on the pulmonary system
Pulmonary ventilation and lung volume, regional plumonary blood flow, Pulmonary Gas Exchange and Arterial Gas Saturation, G-Induced Atelectasis
What are the effects on Pulmonary ventilation and lung volume from +Gz
As +GZ increase resp. rate and VTHowever, VT starts to increase between +5-7 GZ because of G pushing diaphragm and abdominal contents down and G-suit pushing diaphragm up into thoracic area. W/out G-suit counterpressure FRC would decrease by 500 ml at +3 GZ . At +5-7 GZ the physiologic dead space incresae and in spite of incresae resp. rate the arterial PCO2 changes very little w/ increasing GZ . Normally, ventilation is greater at the base areas of the lungs than the apex because of the incresae plural pressure from apex to base. The pleural pressure gradient results in increase alveolar distention in apex alveoli while the base alveoli are near min vol. Upon inhalation, the base alveolar expansion is > apex alveolar expansion. With high +GZ, the pleural pressure gradient increase by 0.2 cm H2O/cm lung/+GZ which increase differences in expansion between apex and base of lung. At +5GZ the pleural pressure at base is 30 cm H2O > the apex. The increase pleural pressure in the base will cause collapse of base alveoli (airway closure). The anti-G suit abdominal bladder decrease FRC and increase amt of non-ventilated basal due to increase pleural pressure.
Pleural pressure
What are the effects on the regional pulmonary blood flow from +Gz
The +GZ has great effect on blood flow distribution in lung because of ventilatory (alveolar gas) pressures which remain constant and unaffected by +GZ and the low pulmonary BP. Mean pulmonary arterial (15 mm Hg) and venous (0 mm Hg) BP at junction of middle and lower thirds of lung are unaffected by +GZ.. The arterial BP above and below junction is affected by hydrostatic forces.Blood flow increase descending down the lung and the increase blood flow/cm down the lung increase w/ increasing +GZ.
What are the effects on the pulmonary and arterial gas exchanges from +Gz
The +GZ increase accentuates the ventilation-perfusion inequalities that normally exist. The area of the lung which is ventilated but non-perfused increases w/increasing +GZ. PO2 in non-ventilated alveoli (closed terminal airways) is absorbed by the blood and reaches equilibrium w/mixed venous blood w/in few sec. Blood flowing in this area constitutes a rt-to-lt shunt and proportion of blood in shunt increases w/increasing +GZ. This shunt markedly increases O2 saturation and arterial PO2. Arterial blood desaturation is evident at +3GZ and oxyHb saturation decrease to 85% at +5GZ. Breathing 100% O2 prior to onset helps delay desaturation. Inflation of G-suit abdominal bladder increase desaturation due to raising of diaphragm and increase alveoli closure
what can you do to help delay desaturation
Inflation of G-suit abdominal bladder
What are the effects on G-induced atelectasis from +Gz
Exposure to +GZ causes closure of alveoli in base of lung which prevents their ventilation even though their perfusion continues. The number of closed alveoli increases w/increasing +GZ and w/inflation of abdominal bladder of anti-g suit. Blood absorbs trapped gas at rate limited by rate which least soluble gas (N2) is removed. If little of no N2 present - such as when breathing 100% O2 - gas is absorbed rapidly, the alveoli are rendered free of gas and the alveoli collapses and will remain so until an inspiration provides gas pressures high enough to exceed the alveolar wall surface forces. Atelectasis seen as low as +3GZ w/g-suit and breathing 100% O2. Symptoms usually apparent after exposure include dry cough w/or w/out substernal discomfort. Deep inspirations are used to reinflate the alveoli and can cause reflexive bouts of coughing. PPB and AGSM can increases FRC and decreases the magnitude of alveoli collapse. However, the use of counter-pressure w/PPB will decrease or negate this improvement. Smoking is thought to increase chance for atelectasis
What causes it
The min N2 needed in breathing gas to prevent atelectasis is?
What are the effects of +Gz on the central nervous system
LOC and a progressive decrease of peripheral vision (greyout) and central vision (blackout) are caused by decrease blood flow to cerebral and retinal tissue. Intraocular pressure is 20 mm Hg and the retinal artery BP must be > 20 mm Hg to maintain blood flow to eye. If retinal artery BP is < 20 mm Hg then blackout occurs 4-6 sec later w/delay due to O2 stored in retinal extravascular fluid. After blood returns to eye there is also several sec lag in recovery to restore the retinal O2 store.
What is the cause of peripheral light loss due to G forces
The early peripheral loss is due to the anatomical arrangement of these vessels which increase sensitivity to +GZ.
What are some other visual indications caused by G forces?
Other visual indications of decrease retinal blood flow are pupillary dilation, decrease ocular motility, progressive and concentric narrowing of visual field and decrease visual acuity.
What defines a person's blackout threshold in regard to G forces
A person's blackout threshold is defined as that G exposure (w/onset rate of 1G/sec) where blackout occurs and vision then returns in 2 sec due to the compensatory reflex. Redistribution - through autoregulatory vasodilatation and siphon effect - of blood flow found near upper +GZ tolerance level so that cerebellum and brain stem blood flow is preserved even w/ decreasing cerebral blood flow. At +5GZ this provides a pos pressure increase between the arterial and venous sides of cerebral circulation of 50-60 mm Hg w/a corresponding jugular bulb pressure of -50 mm Hg. This redistribution overcomes what would be expected if predicting BP based on hydrostatic column effect. However, as +GZ increase jugular veins collapse which breaks the siphon and empties cerebral vessels leaving 3-4 sec worth of intratissue O2 and consciousness remaining. At moderate +GZ (5-6GZ) blackout precedes LOC, but increase or rapid onset +GZ LOC may occur w/out any visual symptoms in about 4-6 sec. Consciousness after LOC occurs in about 15 sec w/a similar period of confusion. Amnesia of event is common.
Can prolonged exposeure to lower levels of +Gz cause LOC? If so, how?
Prolonged exposure to lower levels of +GZ can also cause LOC by vasovagal syncope when there is also pallor, sweating and bradycardia.
What % TACAIR aircrews reported LOC due to G-forces?
12% of USAF/USN/USMC TACAIR crews report LOC.
What % is estimated to be the true number of TACAIR aircrew who have LOC'd?
Since 50% of centrifuge LOC's don't remember incident, it is extrapolated that 24% of TACAIR crews have LOC'ed
What are the effects of +Gz on the renal system?
Data based on non-human studies show that renal blood flow decrease w/+GZ exposure and wearing an anti g-suit.
Why is the renal system important in regards to +Gz?
Renal system is important as small decrease in Na+and H2O decrease +GZ tolerance
Renal system is important as small decrease in Na+and H2O decrease +GZ tolerance
The increase wt of soft tissues and limbs makes unassisted emergency egress and raising from a sitting position impossible at +3GZ. If properly supported, fine motor movements are unhindered at +8GZ. Helmeted head movements are severely hindered at +4-6GZ. This is exacerbated w/HMD's as it shifts the CG forward relative to the atlanto-occipital junction and upper thoracic vertebrae. Back, neck and limb injuries are commonly associated w/ high, rapid onset +GZ. The neck in a flexed and rotated position is particularly vulnerable to include ruptured intervertebral discs
What are the effects of +Gz on hormonal response?
Acceleration stress psychologically induces an epinepherine release. The stress itself increase serum cortisol and catecholamine levels. The cortisol increase is too slow for acute exposure but may be significant for prolonged or repeated exposures. The catecholamine release and ADH may also increase tolerance by increase peripheral resistance, HR and heart contractility
What are the effects of +Gz on G tolerance?
Difficult to define tolerance because of 3 factors: (1) magnitude of the acceleration stress which varies from LOC w/out preceding blackout at high levels down to vasovagal syncope or fatigue at low levels; (2) G-onset rate as increase onset rates usually elicit G-stress response at decrease G levels; and (3) large individual variations. However, DeHart states that using 100% peripheral light loss and 50% central light loss are reliable reference points for determining tolerance
What factors effect G tolerance?
Heat, hypoglycemia, alcohol, hyperventilation, hypoxia, and gastric distention
What effect does heat have on G tolerance?
. For every 1oC increase in core temp the blackout tolerance decrease 30-40% due to cutaneous vasodilatation which shifts blood flow to periphery. The decrease peripheral vascular resistance and increase central blood vol decrease arterial BP
What effect does hypoglycemia have on G tolerance?
A 50% decrease in blood glucose from base line decrease blackout threshold by 0.6 +GZ. However, if blood glucose decrease is enough to elicit hypoglycemic reaction the blackout threshold increase by 0.5 +GZ due to the arterial hypertension produced by epinepherine secreted in response to reaction
What effect does alcohol have on G tolerance?
A moderate dose decrease tolerance by +0.1-0.4GZ and will increase severity of symptoms produced by a given +GZ
What effect does hyperventilation have on G tolerance?
Markedly decrease tolerance as the increase in cerebral vascular resistance produced by hypocapnia accentuates the decrease in blood flow through brain. A decrease of arterial PCO2 by 20-25 mm Hg decrease tolerance by 0.6 G. Moderate hyperventilation can cause LOC at + 3 GZ
What effect does hypoxia have on G tolerance?
Decrease inspired PO2 to 70 mm Hg decrease blackout threshold by 0.6 G and decrease inspired PO2 to 55 mm Hg decrease threshold by 0.8-1.2G
What effect does gastric distention have on G tolerance?
Stomach distention increase tolerance due to distended stomach decrease descent of diaphragm and heart during exposure. Ingestion of 1.5 L H2O increase blackout threshold by 0.6-1.3 G
That is the most important system in the body that determines the tolerance and response to +Gz in the body.
The cardiovascular system is by far the most important system that determines the tolerance and response to +GZ
State the general effects of -Gz on the body.
Feeling of heaviness and interference w/limb movement similar to +GZ. The specific effects of -GZ occur primarily in the head and neck. At -1GZ there is a sense of fullness in head and head pressure which becomes very disagreeable at -2GZ and causes post-exposure headaches. At -2.5GZ there is congestion of air passage mucosal lining that can cause breathing difficulties, eyelids swell, and petechiae appear on the face and neck. Between -2.5 and -3.0GZ the eyes feel like they're popping out of head and vision is blurred by subconjunctival hemorrhages. Exposure to >-4GZ can cause mental confusion and unconsciousness
What effect on the cardiovascular system does-Gz have?
The initial hydrostatic effect is increase in regional arterial BP above the heart and decrease below the heart. Eye level arterial BP increase by 20-25 mm Hg/-GZ. It takes several sec to level off venous BP as blood has to flow thru the capillaries to fill them to capacity. Eye level venous BP = 100 mm Hg at -3GZ. The increase arterial BP stimulates the carotid sinus baroreceptors which causes bradycardia, cardiac arrhythmias and generalized arteriolar vasodilatation. Arrythmias usually occur at -1GZ and asystole can occur w/a 5-7 sec -2.5GZ exposure. The decrease CO and vasodilatation decrease arterial BP. The increase in cerebral venous BP is countered by increase in CSF which decrease risk of vessel rupture. The decrease CO and increase venous BP combine to decrease arteriovenous BP changes across the cerebral vascular bed causing decrease cerebral blood flow which leads to mental confusion and LOC. LOC can also be caused immediately by cardiac asystole or ectopic rhythm
What effect on the pulmonary system does -Gz have?
-GZ causes headward displacement of diaphragm which decrease VC, FRC, and pulmonary ventilation. Changes in pulmonary regional blood flow are opposite to those produced by +GZ. With -GZ the apical region is better ventilated and perfused than the basilar region, but most of the lungs remains perfused. Airway closure and atelectasis can occur in the apical region and a rt-to-lt shunt occurs because of decrease FRC
How does -Gz affect G tolerance?
-GZ isn't well tolerated, max are 5 sec at -5GZ; 10-15 sec at -3GZ; and 60 sec at -2GZ. There is some adaptation as some aerobatic pilots can tolerate -6GZ
Describe the “push/pull” effect and the resultant reduction in G tolerance.
This is a negative synergy between –Gz and +Gz. This can occur when –Gz maneuvering, accomplished by “pushing” the stick, is immediately followed by +Gz “pulling”. Cardiovascular adaptation decreases, and the incidence of G-LOC increases, in proportion to the level and duration of preceding –Gz acceleration.
What mechanisms have been proposed to explain push-pull effect?
1. Increased cephalad blood flow during

2. Prior –Gz induces upper body vasoconstriction and lower body vasodilation

3. To prevent cerebral overperfusion during –Gz, vasoconstriction occurs
Why would increased cephalad blood flow affect push-pull effect?
Increased cephalad blood flow during –Gz stimulates carotid sinus baroreceptors, leading to bradycardia and peripheral vasodilation, thus lowering systemic blood pressure. When the aviator then induces +Gz by pulling, there is a delay in the onset of the compensatory sympathetically mediated increase in heart rate, cardiac output, and peripheral vascular resistance because of the hypotensice effect of the previous –Gz
Why would prior -Gz inducing upper body vasoconstriction and lower body basodialation affect push pull effect
Prior –Gz induces upper body vasoconstriction and lower body vasodilation. Greater net vasodilation. Greater net vasodilation than vasoconstriction during –Gz leads to lowered systemic blood pressure, predisposing to G-LOC under +Gz stress.
Why would vasoconstriction to prevent cerbral overperfusion during -Gz affect push-pull effect?
To prevent cerebral overperfusion during –Gz, vasoconstriction occurs. This is increased cerebral vessel resistance seems to persist for about 20 seconds after cessation of –Gz and onset of +Gz, thus predisposing to cerebral hypoperfusion and G-LOC.
Describe the principal central nervous system factors that limit short-duration, high +Gz exposure tolerance.
Positive Gz is a downward force that attempts to force blood into the lower extremities. Physiological reflexes that attempt to counteract the positive Gz forces are an increased heart rate, vasoconstriction of the blood vessels in the lower body and vasodilatation of blood vessels in the brain.
What are the physiological reflexes to G forces designed to do?
All of these reflexes are designed to increase blood return to the heart and blood delivery to the brain.
What happens when the physiological reflexes can't compensate enough against G-forces?
When these physiological reflexes cannot compensate enough to maintain blood flow to the brain, brain hypoxia ensues. Brain hypoxia can result in a loss of consciousness episode (G-LOC). G-measles (cutaneous petechiae) occur in the unsupported areas of the body during +Gz exposure.
Where are the most common areas for G-measles to occur?
Most common areas are the feet and ankles, followed in decreasing frequency in the legs and arms.
What is the probable cause of G-measles
The probable cause of these G-measles is either rupturing of capillaries or diapedesis in response to high intravascular pressure.
Given a G-time Tolerance curve, describe the regions of the curve and how they relate to human performance while experiencing Gs
This curve shows tolerance to +Gz acceleration and effect of onset rate. A brief rapid onset run (10G/s) can be tolerated to 12 G without visual loss, but if prolonged for more than 4-5 seconds loss of conscious may occur without visual warning. Even a moderately fast onset rate exceeds the cardiovascular reflexes, though loss of consciousness will be preceded by visual symptoms of greyout, tunnel vision, and blackout. A slow onset rate allows cardiovascular reflexes to develop during the G stress and development of visual signs at a higher G level. Also allows time for the cardiac reflex to kick in increasing resting G tolerance as a result of vasoconstriction mediated by the sympathetic nervous system via the baroreceptors that increase arterial tension at head level. Gs lower than resting G tolerance will not result in light loss or GLOC.
Rapid onset
Slow onset
List the symptoms of grayout as they apply to the +Gz environment.
100% peripheral light loss (PLL), and 50% central light loss (CLL), consciousness and hearing remains undisturbed.
List the symptoms of blackout as they apply to the +Gz environment.
100% PLL, 100% CLL, consciousness and hearing remains undisturbed
List the symptoms of G-induced loss consciousness (GLOC), as they apply to the +Gz environment.
Consciousness and hearing functions are interrupted
Once actual loss of consciousness results due to G forces, what is the total average incapacitation time
24 seconds
Describe the differences between absolute and relative incapacitation as they relate to GLOC
Absolute incapacitation signifies complete loss of brain blood flow. It is during this phase that the flyer is unconscious. Usually the G’s are unloaded and slowly blood flow to the brain resumes. Relative incapacitation represents the period of time when the brain is being “rebooted”. This is a period of confusion and disorientation. Some basic senses like vision, hearing, and speech come back on line as well as some reflex capabilities, but cognitive thought and higher processing is unlikely to occur. A pilot is unable to maintain aircraft control during either of these periods.
What are the two distinct phases that incapacitation from G-LOC can be divided into?
Absolute and relative incapacitation.
What is the time range for absolute incapacitation in GLOC?
This period has ranged from 2 - 38 seconds, the average time is 12 seconds.
What is the time range for relative incapacitation in GLOC?
The relative incapacitation time averages also 15 seconds but ranges from 2 - 97 seconds.
What is the total incapcitation time for GLOC?
Averaging 28 seconds with a range of 9 to 110 seconds.
Differentiate between Almost Loss of Consciousness (ALOC) and GLOC.
ALOC is a transient incapacitation, without loss of consciousness which occurs during and after short duration, rapid onset +G2 pulses. ALOC is considered to be part of the G-LOC syndrome. Therefore, it has many of the same symptoms of G-LOC including a similar psychological impact, dreamlets, confusion, and sensory and motor symptoms. The duration of incapacitation is much shorter than with G-LOC, reflecting a more transient degree of ischemia.The GLOC syndrome is the transition from normal consciousness to a neurological state of unconsciousness that results when blood flow to the nervous system is reduced below the critical level necessary to support conscious function.
What is ALOC characterized by?
ALOC is characterized by unresponsiveness to voice communication and loss of numerical skills, with various degrees of memory compromise and may include transient paralysis and convulsive motor activities.
List physical and physiological factors that may reduce an individual’s tolerance and/or endurance to G forces.
Age, Reduced height, High diastolic and systolic arterial tension, Increase in ambient (cockpit) temperature, Cold stress, Dehydration, Inhaled gas mixtures that are hypoxic or hyperoxic, Nutrition, Experience, Recent Illness, Conditioning, Fatigue, Alcohol & Self Meds
How does hydration affect G tolerance?
Hydration is critical to G-tolerance. At 3% dehydration (2 qts low, 170lb man), 50% of G-tolerance is lost. As blood volume drops due to fluid loss, the cardiovascular system is unable to maintain or generate adequate blood pressure needed to counter the effects of G-forces.
How does repeated exposure to the G environment affect G tolerance?
It is important to emphasize the increase in G-tolerance attained through repeated exposure to the high G environment, specifically it is important to note the benefit of recency of experience. Not only does the body become more tolerant of G-forces, the pilot becomes better trained at countering the effects through greater anticipation and practice. When significant lay-off periods happen, it is prudent to re-enter the high G environment with anticipation of a lower than normal G-tolerance.
How does illness affect G-tolerance?
Any recent illness, especially if the aircrew member is still recovering, can reduce G-tolerance. The body is expending a lot of energy fighting off disease and leaves little energy available to “fight off the Gs”. The great aspect of the human body is its adaptability and improvement in performance while exposed to stress.
How does exercise affect G-tolerance?
Aircrew can specifically train to perform better under G. Several studies have indicated that aircrew who exercise have a higher G-tolerance than those who don’t, specifically those who engaged in weight training and moderate aerobic exercise.
List the methods available to increase a crewmember’s tolerance to +Gz forces.
Anti G Straining Manuever, anti G-suits, positive pressure breathing, centrifuge training, physical training, posture, breathing CO2, drugs, inducement of positive cardiac reflex and G-warm up.
State the benefits of wearing an anti-G suit
The anti-g suit increases tolerance by: (1) increasing peripheral resistance and decreasing blood pooling by providing counter pressure in the lower limbs and abdomen; (2) raises the diaphragm which decreases the heart-to-eye distance; (3) prevents loss of plasma into tissue; and (4) plays minor role in venous return. The inflation must be rapid (2-3 sec) to ensure effectiveness. The anti-G suit is also effective in reducing the physiologic stress response of the G exposure by reducing the amount of fluid shift below the heart and increasing blood flow to all organs of the body.
4 benefits
How much G protection does a G suit give?
1-1.5 G protection
The G-suit is a combinat ion of what and how does it work?
Is a combination of the garment and the aircraft mounted anti-g valve. The anti-g valve controls the pressure in the garment in proportion to the applied acceleration, usually 1.25lb/in2/G,
When does the G-suit begin to inflate?
Doesn't begin to inflate until > 1.75-2 G's to avoid unnecessary and distracting inflations during routine maneuvering.
What are some improvements that have been made to the G-suit?
Improvements to anti-g suit include more responsive valves, pre-inflated suits, and use of multiple bladders that inflate sequentially to aid venous return.
Why is the G-suit effective in reducing the physiologic stress response of G exposure?
Because it reduces the amount of fluid shift below the heart and increases blood flow to all organs of the body.
Describe the elements of the anti-G straining maneuver (AGSM) and how they interrelate.
The AGSM is a forced exhalation effort against a closed (L-1 maneuver) or partially closed (M-1 maneuver) glottis while tensing leg, arm, and abdominal muscles which increases intrathoracic pressure that is directly transferred to the arterial pressure at heart level. The breathing rate is 3- to 4- second intervals. This brief-rapid effort allows adequate venous return because of a low intrathoracic pressure. Although the head level arterial tension (Pa) falls to nearly zero in conjunction with a lowered thoracic pressure, the period is so brief (less than 1 second) that the brain and retinal tissue maintain unaltered function (vision and consciousness). It is a two phase act - phase one is isometric tensing of the leg muscles, the abdomen and upper body. The leg tensing is of critical importance and the G-suit will assist this muscular work in preventing the pooling of blood in the lower extremities. This muscle tensing must be maintained while at G. Phase two is the cycle of breath holding. Take a big breath prior to the pull, bear down against a closed glottis, hold breath until at max G, and then exchange the air in quick, small amounts in three second cycles. Any longer breath holding can result in “starving the pump” and imminent G-LOC.
The AGSM can prodive how much G protection?
The AGSM can provide 3.5 - 4 +Gz of protection provided it is performed correctly.
What is the purpose of the breath holding cycle during the anti-G straining maneuver?
The purpose of the breath-holding cycle is to generate and maintain pressure in the thoracic cavity which will assist in getting blood flow to the brain. The air exchange (quick release of pressure) is needed to allow for adequate venous return (helped by the G-suit).
The respiratory aspect of the anti-G straining maneuver is an adaptation of what?
The respiratory aspect of the AGSM is an adaptation of the Valsalva maneuver that produces a high intrathoracic pressure (125mm Hg). However, unlike the Valsalva maneuver test that challenges the circulatory system to cope with a reduced VR, the AGSM interrupts the effort at 3- to 4- second intervals with a rapid expiration and inspiration effort (less than 1 second).
Describe common errors in performing the AGSM.
•  Too little time tensing and straining and too much time breathing can result in little venous return to the heart, thus starving the pump.

•  Holding the breath longer than needed also starves the pump from venous return.

•  Exhaling and/or grunting without muscle tensing and straining will cause early fatigue and possible hyperventilation.

•  Delaying the start of AGSM until onset.

•  Over or under-tensing and straining.
Describe exercises (physical training) that can be performed in order to improve an individual’s G-tolerance.
A combination of whole-body strength (wt training) and aerobic conditioning will increase performance of AGSM, especially for repeated or prolonged exposure.
What are the two types of physical training that can impact anti-G straining maneuver ability?
Aerobic and anaerobic
Describe aerobic training in terms of G tolerance affect
Aerobic training helps you avoid the fatigue associated with flying against high G forces. As you increase your aerobic capacity, your body increases its ability to move oxygen and utilize that oxygen to a maximum efficiency. It has been documented that excessive aerobic training can lead to decreased G tolerance. This is due to the resting blood pressure decreasing as an individual becomes more aerobically conditioned.
Describe anaerobic training in terms of G tolerance effect
Otherwise known as weight training. As you weight train, your skeletal muscles increase in muscular tone which allows you to more efficiently perform the AGSM. Weight training also improves the muscles’ endurance so they don’t fatigue as quickly after repeated isometric contraction in response to repeated G exposure.
Research has shown that a 10- to 12- week weight lifting program can increase G-duration tolerance approximately by what % with an individual correlation between what?
50% with a direct individual correlation between muscular strength and D-duration tolerance.
According to Dehart does aerobic conditioning have an effect on G-tolerance?
Aerobic conditioning has no effect on G tolerance.
Excessive aerobic conditioning in some individuals can have what effects on G related issues?
1) cause serious cardiac dysrhythmias associated with reduced G tolerance

2) increase susceptibility to motion sickness on the centrifuge

3) increase the length of time of incapacitation of GLOC.