CARDIOVASCULAR FUNCTION & FLUIDS
Churchill and Bungo have reflected that “Despite over 30 years of
experience with human spaceflight, we have yet to achieve a clear understanding
of how the cardiovascular system is affected by this unique combination of
environmental, emotional, and physiological challenges.” Moreover, classical
physiological and biophysical models of what “should” happen in microgravity
have not always generated predications that are supported by data from actual
spaceflight. Of course, this can be said of most other body systems as well; and,
in fact, in supports the value of spaceflight as a “tool” to explore and better
understand the workings of the human body. Still, we have learned much so far;
and many basic principles of cardiovascular and fluid changes seen in
spaceflight are understood today.
Basic Cardiovascular System and Terminology
The cardiovascular system refers to the heart and the vessels that pass to
and from the heart to the tissues of the body. These vessels include the large
arteries that receive blood from the heart, branching into smaller arterioles that
branch further into capillaries. From the capillaries, blood flows into small
collecting venules, then into larger and larger veins for return to the heart.

One estimate is that there is an
equivalent of over 62,000 miles of blood
vessels in the average adult body!
In discussing the cardiovascular system, it will also be important to discuss
the fluids within it and outside of it. In this case, we are concerned with the
entire “circulatory” system and the relation of blood flow to tissue fluids and the
lymphatic system.
The major functions of the cardiovascular system include: 1) delivery of
O2 and nutrients to all areas of the body, and 2) removal of CO2 and cell
metabolic wastes to specific organs, such as the lungs or kidneys, for removal.
Other functions of the cardiovascular system as it circulates blood include the
transport of hormones, transport of immune system components such as white
blood cells or antibodies, and heat regulation.
The overall organization of the cardiovascular system consists of a driving
pump, the heart, and two key circulatory systems that it powers: the pulmonary
circulation (the lungs) and the systemic circulation (the rest of the body).
The heart consists of four chambers: left and right atria at the top of the
heart, as well as left and right ventricles at the bottom. The two sides of the
heart act as a “double pump.” The atria receive blood from the veins that are
returning blood to the heart, and pump it to the ventricles. The ventricles then
pump blood into the arteries for distribution to the tissues of the body. Blood in
the right side of the heart has been deoxygenated during its passage through the
systemic circulation and is pumped into the lungs to pick up oxygen. After
returning to the left side of the heart, this oxygenated blood is pumped
throughout the rest of the body.
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Drawing of heart. SVC & IVC = Superior
and Inferior Vena Cava (large veins
returning to right side of heart); RA = Right
Atrium; LA = Left Atrium; RV = Right
Ventricle; LV = Left Ventricle; PA =
Pulmonary Artery. Right and left sides are
designated from the “anatomical” position
(i.e., from the viewpoint of the person’s
heart, not the viewer).
The pathway of blood from the right ventricle to the lungs and back to the left
atrium is the pulmonary circulation. This is a low-pressure system with low
resistance to blood flow. Blood is carried to the lungs from the right ventricle
via the pulmonary artery. As the blood flows through the capillaries in the lungs,
waste gases (i.e., CO2) are released and oxygen is absorbed by simple diffusion.
Blood then passes to the left atrium via the pulmonary veins. From there, the
oxygenated blood passes to the left ventricle to be pumped out of the heart again.
The pathway from the left ventricle to the capillaries of the general body
and back to the right atrium is the systemic circulation. This is a high-pressure
system that must push blood through the equivalent of tens of thousands of miles
of blood vessels, many with high resistance to blood flow, and about 40 billion
capillaries. Typically, the muscular wall of the left ventricle is 35 times thicker
(810 mm) than the wall of the right ventricle (23 mm) since the left ventricle
must perform significantly more work to accomplish this task.
Between the atria and ventricles are atrioventricular valves (the right
tricuspid valve and the left bicuspid, or mitral, valve) which prevent backflow
from the ventricles into the atria when the ventricles contract forcefully.
Similarly, there are semilunar valves (the pulmonary valve and the aortic valve)
in the blood vessels leaving the heart to prevent backflow from the pulmonary
and systemic circulations between heartbeats. The forceful closing of the valves
as they prevent backflow generates reverberations that can be picked up as
sounds via a stethoscope. The “lub” sound, heard first in a complete cardiac
cycle is caused by closing of the AV valves during contraction of the ventricles.
The second “dub” sound is caused by closing of the semilunar valves when
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pressure in the ventricles
(after contraction) falls
below the pressure in the
now-full elastic arteries.
Pulmonary veins returning to heart.
Aorta spreading into arteries in systemic circulation.

Diagram, from Human Physiology in Space, showing both pulmonary and systemic circulations.
AV Valves: Open (top) and closed (bottom)
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
The heart during one full contraction.
During the first phase, shown to the left, the
atria contract and push the blood they have
collected from veins through the open
atrioventricular valves. Next, shown to the
right, the ventricles contract and eject blood
into the pulmonary and system circulations.
Closing of the atrioventricular valves at this
time creates a “lub” sound via stethoscope.
When the ventricles finish ejecting blood
and begin to relax, a slight amount of initial
back-pressure from the arteries will snap
the semilunar valves closed to create a
“dup” sound. After a pause for re-filling of
the atria, the cycle begins again.
The contraction of the heart, first atria and then ventricles, is termed
systole. Between beats, the heart pauses briefly for the atria to refill with blood
for the next contraction. This period is termed diastole. Blood pressure in the
arteries fluctuates during these phases of the full cardiac cycle. The peak
pressure is achieved when the ventricles eject blood into them forcefully, and is
termed systolic pressure. Between beats, the pressure ebbs to a baseline level
maintained by the “filling pressure” of the blood and the natural tension in the
walls of the arteries—this is the diastolic pressure.
Blood pressures in the systemic circulation are sometimes reported as
“systolic over diastolic” such that a normal pressure might be “120 over 80”
mmHg pressure. In this example, this simply means that the maximal, systolic
pressure achieved is 120 mmHg; the minimal, diastolic pressure maintained is 80
mmHg. These values are obtained at the approximate level of the heart by a
blood pressure cuff or other measuring device. The reason they are measured at
the level of the heart is that gravity affects readings, due to the weight of blood
and its effect on hydrostatic pressure, above or below the heart. This will be
discussed more later. The difference between the systolic and diastolic pressures
is termed the pulse pressure. In the example used here, pulse pressure would be
40 mmHg.
To simplify discussion of arterial pressures, the calculated mean arterial
pressure (MAP) is often used. In effect, the MAP represents the average
pressure tending to push blood through the capillaries and other vessels of the
systemic circulation—it gives insight into average blood flow to the tissues. The
heart spends relatively more time in diastole than systole; therefore, the MAP is
not simply the average of systolic and diastolic pressures. Instead, the MAP in
the systemic circulation is taken as:
MAP = Diastolic Pressure + 1/3 Pulse Pressure
In the example begun above, then, the MAP would be:
MAP = 80 mmHg + 1/3 (40 mmHg) = 93 mmHg
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Blood pressure cuff (sphygmomanometer)
applied to upper arm at level of the heart.
One other pressure of special interest in cardiovascular physiology is the
central venous pressure (CVP). The CVP is the pressure in the vena cava,
which are the large veins returning blood to the right atrium from the systemic
circulation. It is this pressure that, compared to MAP, represents the pressure
differential across which blood flows. It also represents the blood “available” to
be picked up by the right atrium before each contraction cycle. If the heart is
weak and can’t move blood along quickly enough, blood “backs up” in the vena
cava and other large veins leading to the heart. CVP increases, and this fact can
be measured medically. If healthy, the heart can move this backlog of blood by
beating faster and/or harder.
The Skeletal Muscle Pump. Normally, CVP is quite low, and is usually
considered negligible—it doesn’t take much pressure to “push” blood into the
right atrium. The venous pressure is low because by the time the blood leaves
the capillaries the pressure pulses caused by the beating of the heart have been
damped out and pressure has been reduced markedly by vascular resistance. In
fact, the pressure in the systemic veins is, in itself, often insufficient to get blood
back to the heart in an efficient manner.
One adjunct to normal flow in the cardiovascular system is the so-called
skeletal muscle pump. The veins are a low-pressure system with very distensible
walls and, in many cases, blood would tend to pool in them unless something
aided flow. However, because most veins have valves in them, any movement
towards the heart is not followed by “backflow” and a periodic pushing of blood
forward can really assist venous return. This is the case every time skeletal
muscles in the legs contract; in doing so they bulge and squeeze veins inside the
leg. This “pumps” blood from valve to valve and eventually to the heart—it
helps maintain CVP and a pool of blood at the right atrium ready for the next
heartbeat.
People who must stand for long times often learn to flex their feet and
legs periodically, using the skeletal muscle pump to prevent pooling of blood in
the legs and overdistension of the veins there (perhaps leading to varicose veins).
It also helps maintain good return of blood to the heart and subsequent supply to
the vital organs. Besides the legs, some people know that periodically tightening
their abdominal skeletal muscles can more indirectly increase venous return and
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CVP by applying pressure to
the larger veins passing
through
the
abdominal
cavity.
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Body Fluids and the “Other” Circulatory System (Lymphatics)
Heart
(directional pumping force)
Veins
Arteries
(low-pressure transport
& flexible reservoirs)
(high-pressure transport)
Lymphatics
(pick up fluids between tissues)
Venules
Arterioles
(collection from capillaries)
(variable, high resistance with
nerve, hormone, & metabolic controls)
e.g., 15%
e.g., 85%
Precapillary sphincters
(fine-tune local flow)
Capillaries
(exchange with tissues)
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Blood Plasma
The total circulatory system actually manages a circulation of all
extracellular fluids, including a constant interchange between them. As will be
discussed later, as blood passes through the capillaries there is an exchange of
fluids between the plasma and the interstitial fluids. Although fluid moves both
ways and create a “mixing” effect, some estimates suggest that across the entire
systemic circulation the net effect is that about 15% of the blood plasma exits the
blood vessels to increase the interstitial fluid volume. If the system is to remain
in balance, this fluid volume must be returned to the cardiovascular system. This
is done by porous, blind-end lymphatic vessels that collect fluids from all the
interstitial spaces then merge into larger and larger vessels that eventually dump
the fluid into the larger veins returning to the heart. This lymphatic is a lowpressure system, with valves in the vessels to ensure one-way flow back towards
the heart. The following figure summarizes the basic circulatory system
discussed thus far.
Interstitial Fluids
The remaining 28 liters of water (2/3 of Total Body Water, and about 40%
of total body weight) is inside cells of the body—it is termed the intracellular
fluid (ICF) volume. Thus, in a simplified view, TBW = ECF + ICF, with ECF
further divided into interstitial fluids and blood plasma. =
Total Body Water
Intracellular Fluids
The cardiovascular system is well known as the major fluid transportation
system of the human body. Its regulated transport to and from the capillaries is
central to life from the cellular to whole-person level. Yet the cardiovascular
system contains only about 7% of the body’s water (about 3 liters in the plasma
of a total 42 liters Total Body Water, TBW, for a 70-kg “average” male).
Another 11 liters of water are located in the interstitial spaces (between cells)
and in the lymphatic vessels that drain those spaces. Together, these two fluid
compartments in the body are called the extracellular fluid (ECF) volume.
This is a simplified view of fluid
compartments. ere are other fluids. In fact,
other fluids expand on the view of those
“between” cells as classic intersititial fluid.
These fluids include digestive juices, fluid in
the eye, etc. These “transcellular” fluids are
generally
considered
negligible
in
discussions here.
Blood Volume and Body Fluid Dynamics
Blood Volume. Except in the case of bleeding or long-term whole-blood
shifts, changes in blood volume usually occur because of changes in the water
content of the blood plasma (liquid portion). Increasing total blood volume
ultimately increases the “filling pressure” of the vascular system and the amount
of blood to be ejected by the heart with each stroke.
Starling’s Law of the Capillary. Blood is not passively “trapped” within
the circulatory system; there is a dynamic interaction with the body tissues. On a
cellular level, mobile white blood cells can exit the bloodstream to forage for
invaders among the spaces between cells in the body tissues. On a strictly fluid
level, there is a constant exchange of fluid between blood plasma in the
capillaries and the interstitial fluid between cells of the various tissues. This
exchange is governed by physical forces and laws that can explain why areas of
the body can undergo dehydration (net fluid absorption) or swell with excess
fluid (net fluid filtration, or edema).
Pt
t
Pc
c
In the above figure, representing a length of capillary, there are competing
forces for filtration and absorption of fluid. The next transcapillary (“across the
capillary”) fluid shift is determined primarily by matching Starling forces of
fluid pressure (P) caused by blood pressure in the capillary and by interstitial
hydrostatic pressure in the tissues, or colloid osmotic pressure () caused by the
tendency of proteins or other substances in solution to draw water towards
themselves by osmosis.
The net filtration pressure tending to move fluid out of the capillary (c)
and into the tissues (t) can be given as:
Net Filtration Pressure = (Pc – Pt) – (C – t)
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Other factors can further modify the net transcapillary fluid shift in the
area of the body and limit the extent to which there is a net fluid shift. For
example, different capillaries have different permeabilities of their walls; more
permeable walls allow more flow of fluid and proteins. Fluid permeability is
sometimes hydraulic conductivity (L). The permeability of the capillary wall to
proteins is sometimes related to a reflection coefficient for plasma proteins (p).
Finally, increased total surface area (A) of a capillary network affects its
capacity to exchange net fluid with a tissue. Overall, our earlier equation can be
modified as:
Net Filtration Pressure = LA(Pc – Pt) – p(C – t)
Earth-related examples can clarify the implications of this equation and the
Starling forces in the formation of edema.
1) If blood pressure increases, so does capillary pressure (Pc). Thus, if
nothing else changes, there is an increased tendency for net filtration out of the
capillary and edema of the tissues.
2) In cases of severe malnutrition, often the body cannot maintain its
concentration of normal plasma proteins. In this case, the capillary has lower
colloid osmotic pressure (C), meaning the tendency of those proteins to retain
water. In this case edema or swelling of tissues also occur.
3) In normal inflammation, the permeability of capillary walls increases.
This allows an easier pathway for white blood cells to enter the tissues and
attack invaders. At the same time, this allows some capillary proteins to leak
into the tissues (increasing t ) and leading to edema or swelling as fluid is
drawn outward.
Conversely, in nature several adaptations can limit edema formation.
1) Precapillary sphincters can shut down flow to certain capillary beds,
limiting the total surface area there for filtration of fluids outward.
2) Tight skin (e.g., seen in the legs of giraffes) quickly increases the
hydraulic pressure in the tissues as any fluid leaks outward, acting as a “pressure
bandage” and preventing any more than a little flow.
3) Thicker capillary membranes (called the “basement membrane”) can
prevent much fluid flow even if there is a pressure or osmotic difference across
the capillary wall.
4) Finally, very large lymphatic vessels can act to quickly return any
leaked fluids to the main cardiovascular system. This doesn’t affect the basic
filtration mechanics (other than returning stray proteins that may have
accumulated in the tissues); but it does “keep pace” with the filtration and
prevent edema.
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Blood Pressure, Flow, and Resistance
Parallel to Ohm’s Law, which describes the relationship of voltage drop,
current flow, and resistance (V = IR) in an electrical circuit; fluid mechanics can
be described in simple terms by pressure drop, fluid flow, and resistance to that
flow. In general, for any segment of the cardiovascular system or for the system
as a whole
Pressure drop = Blood Flow x Resistance to Flow
The pressure drop across the systemic circulation, P, is equal to the
difference in pressures between the mean pressure in the aorta (the large, highpressure artery exiting the left ventricle) and the pressure at the end of the
venous system, as blood is re-entering the right atrium (sometimes called the
central venous pressure).
Unless there is some special medical or
physiological condition, central venous pressure is generally near zero; thus, the
mean pressure in the major arteries can be taken as the pressure differential.
Mean arterial pressure (MAP) is the main variable that the body
monitors and regulates, through a variety of means. It is this pressure that acts as
the central force for driving blood around the systemic circulation and through
the capillaries of the organs of the body. The total flow through the systemic
circulation is equal to the cardiac output (CO). The total vascular resistance to
flow is the sum resistance offered by the entire systemic circulation, and is
referred to as total peripheral resistance (TPR). Thus,
MAP = CO x TPR
Resistance in any particular vessel is dependent on the length of the vessel
(l), the viscosity of the blood as it flows (), and the radius to the fourth power
of the vessel as shown here:
Resistance = 8l/r4
Obviously, controlling blood vessel radius is an very powerful way for the
body to vary regional resistance, divert flow from one area to another, and vary
blood pressure overall.
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Increased
Blood Volume
Heart Rate
Stroke Volume
Peripheral Resistance
Blood Viscosity
Why Blood Pressure Increases
Increased total “filling pressure” in the semiflexible cardiovascular system; increased venous
return to the heart, leading to higher stroke
volume
Increased cardiac output which, without a
countering change in peripheral resistance,
increases pressure
Same as increased heart rate
Normally varied by changing vessel diameter,
particularly in the arterioles, increased
constrictive resistance increase pressure in the
vessels leading up to it
Increased resistance, as thicker blood does not
flow as easily and it
Cardiovascular & Body Fluid Control Mechanisms
Cardiac Output (CO). The total output of the heart over time is called
the cardiac output. It consists of two factors: stroke volume (SV), the amount
ejected from the heart with each beat; and heart rate (HR), the number of beats
per minute.
CO = SV x HR
Both heart rate and stroke volume can be varied, thus varying cardiac
output and the supply of blood to the entire circulation. Normal SV = 70 ml and
HR = 72 beats per minute, meaning the CO is about 5 L per minute. Since the
normal blood volume is about 5 L, this means the heart circulates the entire
blood supply about once per minute. During even moderate exercise, CO can
double or triple to increase gas transportation while the percentage of blood
shunted to the muscles can increase from 20% of CO to 60% or more.
“Starlings Law of the Heart” refers to an intrinsic regulatory mechanism to
balance venous return and cardiac output. Basically, if increased blood is
returned to the heart and pumped into the ventricles from the atria, the increased
stretch of the ventricles causes them to contract more forcefully. Thus, input
(venous return) and output (cardiac output) of the heart naturally balance.
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Peripheral Resistance . Resistance varies from vascular area to area,
with the main differences in resistance being the diameter of the blood vessels.
Smaller vessels offer much more resistance to fluid flow than larger ones.
The main site for controlling resistance is at the level of the arterioles, the
small blood vessels just preceding the capillaries in any area. By constricting or
dilating these vessels, the resistance to flow can be increased regionally or as a
whole. Factors that cause the arterioles to dilate (shunting more blood to an area
by lowering resistance to flow) include a build up of CO2, H+, or adenosine-signs that more oxygen might be needed. The sympathetic nervous system
(“fight or flight” response) can have variable effects, depending on the organ
system.
Baroreceptor Reflexes.
Baroreceptors (“pressure receptors”) are
specialized nerve endings located in both the arterial and venous systems. These
receptors monitor the “stretch” of the blood vessel walls caused by filling
pressure. They alter their signal rate to the brain when the vessels become more
or less stretched to stimulate corrective reflexes.
The arterial system has two main sites at which it monitors pressure. The
first is at the carotid sinus, located in the neck as the carotid artery ascends to the
brain. The second is in the aortic arch, immediately as blood leaves the heart in
the aorta. Stimulation of the baroreceptors increases when the arteries are
stretched by increased pressure. The result is a set of nervous reflexes that: 1)
decrease heart; 2) decrease heart contractility, and thus stroke volume; and 3)
vasodilate arterioles, to decrease vascular peripheral resistance. Alternately, a
decrease in blood pressure to the upper body leads to the reverse of these
reactions to maintain essential pressure to the vital organs.
Baroreceptors in the venous system are rather diffusely located and less
understood classically. In general, these receptors are scattered in the major
veins entering the heart (the vena cava), the atria, and the pulmonary vessels.
Classified as baroreceptors, these nerves also are sometimes referred to also as
volume receptors. This is because the large veins are very compliant, changing
greatly in volume with small pressure changes. Thus the venous baroreceptors,
by detecting slight stretch or pressure changes are actually monitoring rather
significant changes in venous blood volume in the upper body. Although less
well characterized than their arterial counterparts, it may be that these are the
first baroreceptors activated by fluid shifts seen in spaceflight.
For further thought. Note that the key baroreceptor sites in humans are located
in the upper body. What is the possible evolutionary or functional basis for this?
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The baroreceptor system responds rapidly to pressure changes for shortterm regulation needed to maintain normal blood pressure. In general, the
baroreceptors work with the sympathetic nervous system so that when blood
pressure is increased they stimulate a decrease in peripheral resistance and heart
rate and stroke volume (thus, cardiac output). In addition, secondary effects act
on the kidney to allow increased urine production. The reverse effects take place
if blood pressure is decreased. Overall, although the baroreceptors respond
rapidly to pressure changes, the response is not immediate.
Normally when a person stands upright, gravity causes blood to pool in the
relatively compliant leg veins. This is because the vascular system is essentially
a set of vertical “columns” of blood and pressure in these columns increases
hydrostatially with depth, just as pressure increases with depth in the ocean. As
noted before, in the lower body this can lead to swelling in the feet (as increased
pressure in the capillaries there upset the Starling forces and lead to increased
fluid leakage) and possible varicose veins in the leg (as the structure of the veins
eventually sags under constant pressure).
For the rest of the cardiovascular system, this pooling leads to decreases in
venous return, central venous pressure, filling of the heart between beats (called
end-diastolic volume, EDV), cardiac output, and arterial pressure. The
corrective response via the baroreceptors and sympathetic nervous system
includes increases in heart rate, cardiac contractility (to increases stroke
volume), peripheral resistance, and resultant arterial blood pressure. Anyone
who has stood very quickly though from a reclining or kneeling position, though,
knows that there can be a few seconds of dizziness during this process. This
dizziness is the period when the brain is receiving too little blood flow while the
body’s reflexes work to correct blood pressure in the upper body.
In a similar situation, fighter pilots beginning a high-g turn there is a “lag”
period before cardiovascular responses begin to accommodate to the g-induced
movement of blood downward from their heads to their feet. During, and even
before, this critical time pilots must be especially vigilant to maintain their blood
pressure by special straining maneuvers that increase blood pressure (further
aided by a rapid-reacting anti-g suit that inflates on their legs and abdomen to
push blood back towards the upper body).
Such lag times in body reflexes are not so important in microgravity,
because the headward fluid shift to which the baroreceptors are responding is a
more chronic condition, beginning as the astronauts recline in their seats for
launch and continuing on-orbit.
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Due to hydrostatic pressure, in the upright
posture, blood pressure and blood pooling
increase in the legs and feet. There is a
gradient established in hydrostatic pressure
from head-to-foot.
Blood Volume Regulation. Long-term regulation of blood pressure and
related blood volume primarily involves coordination with the kidney. The main
blood factor controlled is blood plasma volume, the liquid portion of the blood.
Ultimately, the cellular components of the blood can also be controlled (i.e., by
producing or destroying cells); however, this is a secondary and longer-term
phenomenon.
Overall, the kidneys maintenance of blood pressure and volume is a
phenomenon familiar to all of us. If we were to drink a large volume of fluids,
our body would respond by
Antidiuretic Hormone (ADH). ADH is a polypeptide hormone released
through the posterior pituitary gland of the brain when cells sense an increase in
plasma osmolarity (relative salt concentration). This hormone acts directly on
the kidneys to cause them to retain more water. This water then dilutes the
blood plasma and increases plasma volume. Alternately, a reduction in ADH
levels will cause the elimination of more water from the body. A more germane
mechanism here is that ADH release can also be triggered by decreased blood
volumes sensed in the right atrium of the heart, sensed by stretch receptors. This
reflex mechanism linking blood volume to water retention is classically termed
the Henry-Gauer reflex. The thinking of Gauer, in particular, has been a key
underpinning of efforts since the 1960s to anticipate and understand what might
happen to humans in microgravity. We are only now beginning to explore in
depth whether the Henry-Gauer reflex is of real significance there.
Renin-Angiotensin-Aldosterone System.
Certain kidney cells (the
juxtaglomerular apparatus) are sensitive to arterial pressure in a baroreceptor
fashion, sympathetic nervous system activity, or circulating epinephrine from the
sympathetic nervous system. In response to low blood pressure or increased
sympathetic nervous activity, these cells can release an enzyme, called renin,
into the bloodstream. Once there, renin interacts with a circulating peptide
(called angiotensinogen) that is made continuously in the liver and converts this
peptide into a 10-amino acid substance called angiotensin I (AI). Angiotensin I,
in turn, circulates in the bloodstream until it reaches the lungs. Yet another
enzyme in the lungs (angiotension converting enzyme, or ACE) converts
angiotensin I to an 8-amino acid angiotensin II (AII). Angiotensin II acts
immediately in the body as a vasoconstrictor, increasing peripheral resistance,
and to increase thirst. When it reaches the adrenal glands, it also stimulates the
release of a steroid hormone called aldosterone. Aldosterone enters the
bloodstream and arrives at the kidney, where it completes a negative-feedback
cycle by causing the kidneys to retain salt (actually, Na+) and water to increase
blood volume and pressure. This rather complex, multi-stage process serves to
retain or eliminate a “balanced” fluid of water and electrolytes; as such, it is a
powerful regulator of blood volume.
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Feedback mechanism, involving many
organs, by which kidney senses decreased
pressure and initiates chain reaction that
causes Na+ and, with it, water retention;
also increased fluid intake and increased
peripheral resistance.
Atrial Natriuretic Factor/Protein/Hormone (ANF or ANP or ANH).
The several names of this biological substance reflect the fact that several teams
of investigators eventually tracked it down and explored its role in Na+ and
water retention in the body. Depending on the team, they called it a nebulous
“factor” that seemed to affect Na+ excretion, a protein (which it is
biochemically), or a full-fledged hormone. By whatever name, this substance is
released by the atria of the heart when the atria are stretched beyond the normal
amount. ANF then acts on the kidneys to cause an increase in salt (i.e., Na +)
excretion in an effect opposite to that of aldosterone. Water tends to be carried
along with this salt, resulting in a decrease in plasma and blood volume; this, in
turn, relieves the stretching of the atria in another classic negative-feedback
response. This hormonal mechanism would normally work in parallel with the
Henry-Gauer reflex, with ADH then joining in to further help eliminate water
when the atria are overly stretched.
The Hypothesis: What “Should” Happen in Microgravity
Expectations for what might happen to the cardiovascular system and body
fluids during spaceflight what we know about them on Earth and in spaceflight
simulations. Without gravity to pull blood and body fluids downward from the
human head, we expect to see a relative redistribution of fluids headward. This
is similar to what happens when people move from a standing or sitting position
into one in which they are lying down.
For Further Thought. Would less “vertically challenged” organisms than
humans (i.e., quadrupeds and others that tend to move and orient horizontally)
have as much problem coping with microgravity-induced fluid shifts?
On Earth, a headward fluid shift in humans leads to an increase in central
venous pressure and blood available to fill the heart. This change leads to a
transient increase in stroke volume, via the Starling Law of the Heart (i.e., the
heart’s self-regulation of contractility to move blood onward). The increase in
stroke volume leads to increased cardiac output and, in turn, to increased blood
pressure. The increased blood pressure triggers reflexes to decrease heart rate
and total peripheral resistance, acting to re-normalize blood pressure through
these short-term mechanisms. If there is a persistent headward fluid shift and
thoracic filling, even if blood pressure has been readjusted, other reflexes are
triggered by stretching of vessels and atria of the heart to decrease total bloodplasma volume via the kidneys and help normalize function for the longer term.
Does all this really happen in microgravity? It is difficult to say,
especially if we want to consider microgravity alone as a factor. Currently,
microgravity effects are obscured by the pre-launch and launch changes
(astronaut seated position, understandable excitement and stress, vibration,
noise, etc.), activities upon reaching orbit, possible use of medications for Space
Motion Sickness and the effects of that sickness itself, and so forth. Beyond
this, we have data on a very small population of astronauts—the individual
variation from person to person still obscures a general “picture” of major
physiological mechanisms.
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 Head-down bed-rest studies, where volunteers have stayed in a slight head-down lying position from 1 day to about 1
year, have shown that there is an early increase in stroke volume of ~ 20%. Over time, cardiac output is maintained at
roughly normal levels, though, as heart rated decreases somewhat.
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Changes Seen in Spaceflight
We do know that one of the principal factors related to cardiovascular
changes seen in space actually is a change in the volume and distribution of body
fluids. The generally described major response is indeed a shift of fluids
headward, which then triggers follow-on events.
The shift of fluids actually begins before launch, when astronauts recline
in their seats for several hours with feet somewhat elevated. Gravity causes
fluids and blood to shift from the legs and settle headward. In fact, this position
often leads to a reflexive increase in kidney output and urine volume in the
bladder. Shuttle astronauts wear undergarments to absorb this urine if the urge
to urinate becomes excessive. Other astronauts have apparently tried to
compensate for this natural response by dehydrating themselves somewhat
before flight. This may work in the short term; however, it puts them into orbit
in a fluid-depleted state.
Once launch is over, the headward fluid shift continues in microgravity
relative to normal Earth conditions. This headward fluid shift actually creates a
more even distribution of fluids and a more even distribution of blood pressures
than is seen on Earth; it is just that our bodies are adapted to a more upright
posture that leads to subsequent effects.
Puffy Face & Chicken Legs. Effects of headward fluid shift occur
immediately, tend to last throughout flight, and are diverse. Most obvious is a
visible distension of veins in the head and neck region, as well as puffiness
around the eyes. As fluid remains in the head area a “puffy face” syndrome
occurs with general facial edema. Accompanying this may be sinus congestion
and a stuffy or runny nose due to further edema and fluid leakage in the nasal
areas. The senses of smell and taste may be altered, as happens on Earth when
one has a cold. Spacelab D-2, in 1993, even reported increased pressures inside
the eye for a few days. Occasional headaches have been reported, and
intracranial pressure is still being studied to see how and if it changes in
microgravity as a possible correlate to this and other effects (such as nausea).
For Further Thought. Some puffy-face effects (e.g., the nasal stuffiness) may
be temporarily alleviated during heavy exercise. Why might this be so?
In contrast to the upper body, the legs experience a net loss of fluids as
general capillary pressures decrease there. This leads to a so-called “chicken
leg” syndrome as leg volume decreases with time in microgravity. US studies
dating from Skylab onward and Russian studies have shown that leg
circumference may decrease 10-30%, mostly in the fleshier thighs, as up to 2
liters of fluid shift headward. Fluid shifts clearly account for the first phase of
this decrease.
For Further Thought. Astronauts with larger, more muscular thighs and legs,
tend to have a larger relative decrease in leg volume. Why might this be so?
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Consider the vascular needs
of muscle; also consider that
fat tissues contain about
10% water by weight, while
other
tissues
generally
contain 70-75% water.
Generalized schematic of launch position. Knees and legs are up, and head is even tilted slightly downward. Fluid shifts
headward into the upper body.
Normally “lean” astronaut, Guion Bluford, with puffy face on orbit.
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This initial fluid shift occurs rapidly and is virtually complete within the
first 610 hours of flight, though leg volume may slightly decrease for a few
days as body fluid compartments adjust and if further fluids are eliminated from
the body. Eventual muscle loss due to atrophy is believed to account for a later
phase of decreased leg volume.
Central Venous Pressure (CVP). As occurs on Earth, it was early
assumed that a headward shift of blood volume would increase the pressure in
the large veins returning blood to the heart (central venous pressure) and, when
this extra blood as ejected through increased cardiac output, also increase blood
pressure. This, in turn would trigger the reflexes that would correct blood
pressure in the short term and generate increased urine output to correct for the
perceived “overfilling” of the circulatory system in the long term. The first
study of CVP was in the 1969 Biosatellite III program. The subject, a male pigtailed macaque monkey named Bonnie, spent 9 days in space of a planned 30day flight (terminated early because of the monkey’s deteriorating health).
Among the many tests done while in space, Bonnie was surgically fitted with
long indwelling catheters that placed pressure sensors in the veins at the entrance
of the heart (to record CVP) and in arteries (for mean arterial blood pressure).
As expected, increases in CVP and initial arterial pressure were seen.
One method to determine leg volume is to
carefully measure its circumference at
various points, then sum the computed
volume of the segments, which can be
modeled as truncated cones.
Early expectations have not been carried though in human studies, though.
The first human studies of CVP date from the mid 1980s and did not involve
deep catheters—instead they used catheters extending only to the elbow or
indirect, ultrasound-related ways to collect data. The results indicated that, if
anything, CVP was decreased within 20 minutes of flight and could decrease
somewhat after that! Tests in Skylab and thereafter have shown little fluctuation
and certainly no consistently significant increase in CVP on-orbit.
The first direct measurements of CVP in humans finally occurred in SLS1, though subjects included only one payload specialist with a catheter extending
into the inferior vena cava near the heart. Data indicated an increase in CVP
pre-launch (in the knees-up seated position), and CVP increased even further
during launch. In microgravity, though, CVP immediately (within one minute)
decreased below pre-launch levels and stayed lower than normal. These results
have been generally confirmed in such later flights as SLS-2.
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Monitor and catheter, threaded through
veins from foream to heart.
no
It is possible that the increased CVP pre-launch and during launch
generate the reflex cardiovascular responses anticipated, so that the short-term
reflexes have already acted by the time orbit is reached.
On-orbit, the decreased CVP may indicate that venous compliance of
thoracic blood vessels increases rapidly to hold the increased fluids at a lower
pressure. This increased space for fluid build-up around the heart could be
enhanced, for example, removal of the weight of the lungs on veins that surround
the heart. Even if CVP does not remain elevated in microgravity, then, the fact
that there is increased fluid available to the heart may lead to altered cardiac
filling and stroke volume. Echocardiography (ultrasound imaging of the heart)
provides some answers here—it can lead to estimates of stroke volume and,
when combined with heart rate, cardiac output.
Cardiac & Pressure Variables. Data generally support some increase in
total cardiac filling and stroke volume early in flight (e.g., Days 1-3).
Experiments in SLS-2 and SLS-2, as well as other, missions have indicated
an increase in left-ventricular end-diastolic volume (LVEDV) early in flight.
This volume is the “filling” of the ventricle just before contraction. This
increase translates, then as an increased stroke volume that tends to produce an
increased cardiac output, when calculated based on a normal or slightly
increased heart rate. A slightly decreased heart rate in some cases actually can
compensate and keep cardiac output relatively constant. As shown in the figure
above, values for ventricular filling decrease again later in flight after a few days
of adaptation. Blood pressure values remain extremely individual, and there are
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firm
or

CVP recordings from various phases of flight in one astronaut. The catheter is removed after one or more
days in flight.
Astronaut Rhea Seddon performing echocardiography on Jeff Hoffman during STS-51D.

Data shown here indicate a 20% increase in left-ventricular filling volume, which then begins to decrease as fluids are
accommodated in the body or eliminated. By Flight Day 5-6 left-ventricular filling is actually below normal—the heart
shrinks in size and has an easier “load” than on Earth.
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generalized conclusions on how the transient increase in cardiac output
ultimately interacts with changing peripheral resistance to affect blood pressure.
The role that altered pressure might have in triggering short-term pressure
regulation via the baroreceptors is also not well understood.
Fluid Regulation & Volume. Total fluid regulation in microgravity, and
the expected triggering of fluid loss through the kidneys because of perceived
“overfilling” in the upper body, is also hard to study. Confounding factors
include voluntary pre-launch dehydration by some astronauts to avoid getting a
full bladder (especially if there are launch delays). Also, the legs-up pre-launch
position, headward fluid shift on the launch pad, and well-document reflexes (on
Earth) caused by this shift lead to increased urine output and depletion of body
water even before reaching orbit.
Thirst is generally decreased early in flight, and astronaut fluid intake is
down. In part, this may be due to headward fluid shifts and suppression of
normal thirst reflexes. In part, it may be due to the effects of Space Motion
Sickness in many crew for the first 13 days of spaceflight. Use of anti-motion
sickness drugs, mission activities, and many other factors can also impact
hydration and urine volume in space.
Increased ADH levels and decreased urine production, indicating an effort
by the body to fight relative dehydration, are not uncommon on some missions
and in some astronauts. These results are not consistent with a classic HenryGauer reflex, though the reflex could be happening very early in flight and other
factors could be obscuring it. Similarly, one would expect that increased atrial
filling would lead to increased atrial natriuretic protein release, but this did not
prove to be the case on SLS-1 and SLS-2—so it may be, as discussed earlier, that
the vessels around the heart quickly accommodate the excess fluid and prevent
overfilling to a degree that would trigger this hormonal response. On the other
hand, SLS-1 and SLS-2 results have also indicated that renin and aldosterone
may be decreased early in flight, which would tend to aid electrolyte and fluid
loss.
In the end, data support the fact that plasma volume and overall
extracellular fluid volume decrease within hours of spaceflight. As an example,
for 9 Skylab astronauts plasma volume declined within hours and fell to about
12% below normal. Total body water, measured by monitored dilution of
tritiated water as a tracer in the body, also dropped by about 2%. Shuttle
experiments also have shown decreases in total body water of about 3% within
about 3 days of flight. Secondary evidence for a decrease in plasma volume is
that there is a general increase in the concentration of red cells in the blood
(hemoconcentration). The mechanisms for fluid volume decreases remain
unknown. Decreased fluid intake could play a part, as might some combination
of nervous and hormonal reflexes triggered by the headward fluid shift. Other
hypotheses are also being generated as actual research during space missions
continues.
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Cardiovascular Deconditioning.
First considering cardiac
deconditioning, it was noted before that heart size decreases. In part, this is due
to decreased plasma volume and ventricular filling. However, physical work
requirements also are generally less in space; related to this, an actual decrease
in thickness of left ventricular muscle has been seen postflight, especially on
longer flights.
Tests on Skylab 4 showed that vascular compliance in the lower
extremities (i.e., the change in vessel volume caused by a given change in
pressure) increased for up to 10 days of spaceflight. There may be some reversal
of these changes, but it is quite possible that the lower-body blood vessels will
more readily allow blood to “pool” in them after spaceflight may contribute to
orthostatic intolerance. Compliance does seem to return to normal soon after
landing, though.
Baroreceptor Sensitivity. Bed-rest studies, which produce a headward
fluid shift, have indicated that baroreceptor reflexes may be impaired with time.
In effect, when continuously exposed to increased pressure, the baroreceptors
apparently become less sensitive and responsive—they “adapt” somewhat to the
new situation and blood-pressure “setpoint.” Similar findings have been
indicated in spaceflight. These changes in sensitivity and responsiveness may
take days to occur and, similarly, may take several days to readjust upon return
to Earth. Ongoing studies are being conducted to verify these results.
Arrhythmias. Altered, even dysfunctional, heart rhythms have been
observed on several space missions. Some of these abnormalities have been
attributed to electrolyte balance or stress. No consistent or persistent pattern has
been detected, though arrhythmias do seem more prevalent during extravehicular
activities, exercise, and lower-body negative pressure tests or other stress on the
cardiovascular system. The effects of such arrhythmias have not been profound.
Lower-Body Negative Pressure (LBNP) Tests. If the lower body is
place in an enclosed environment and the air pressure in side is reduced, the net
effect is forces that “pull” blood and fluids into the lower body. You can mimic
this effect my sucking lightly on your own arm—an area of slight redness and
edema is formed. When applied to the entire lower body, this mimics the effect
of standing in a gravitational field. The lowering of air pressure can be adjusted
to provide a variable stress to the cardiovascular system. As in standing, the
cardiovascular system responds by increasing blood pressure to maintain flow to
the upper body and head.
LBNP tests performed on-orbit provoke a larger increase in leg volumes,
as fluid is shifted rapidly footward, than in control tests on Earth. There is also a
much larger increase in heart rate (to maintain upper-body blood pressure) than
on Earth. These results may indicate a loss of muscle tone in leg blood vessels
and less resistance to expansion by fluids, as well as weakened ability to respond
to short-term blood pressure changes in general
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Astronaut floating in LBNP gear.
Time-Course of Changes. On orbit, Skylab experiments showed that the
cardiovascular system reaches a new “baseline” or level of adaptation in 46
weeks. Russian studies support about 1 month as a period of re-stabilization of
the cardiovascular system at new levels of function. During this month
cardiovascular responses are more variable, as each person’s system adjust to the
new conditions.
countermeasures have been
developed, though (as noted)
they still are not totally
effective.
For further thought. As a review, relate the biophysical and physiological
principles you have read about to explain each of the following Earth-related
circumstances: 1) swelling of the feet and ankles after prolonged standing; 2)
growing faint when suddenly standing up from a squatting or reclining position,
3) getting swollen veins in the head and neck after a headstand. Now, how does
each compare to changes in the body during spaceflight and microgravity?
Changes on Re-entry
Fluid Shifts. Almost all leg volume is recovered soon after reentry, due to
rapid footward fluid shifts. Although real-world results are variable, there is
some tendency for leg fluid content to actually be greater than pre-flight, as fluid
pools more easily in veins which have become more compliant during
spaceflight. The other factor affecting leg size, deconditioning of skeletal
muscle, takes longer to recover and is one reason legs may remain somewhat
smaller for a time.
Orthostatic Intolerance or Orthostatic Hypotension. The main
cardiovascular concern upon re-entry and return to Earth relates to the decrease
in circulating blood volume and cardiovascular deconditioning that has occurred
after several days in space. Once the body is again exposed to a gravitational
field, the remaining blood is once again redistributed in the footward direction.
This leads to a relative decrease in blood pressure in the upper body and head.
In fact, this decrease in blood pressure can easily exceed the ability of the
baroreceptor response to maintain pressure to the brain. This leads to low blood
pressure (hypotension) in the upper body during standing posture (orthostasis).
The results are dizziness, weakness, faintness, and syncope (fainting and loss of
consciousness). Along with this, as the body attempts to maintain blood
pressure, may be heart palpitations and reflexive “cold sweats.”
Some such effects are seen most in flights longer than 5 hours or so, and
some symptoms occur in about half of returning astronauts even though
countermeasures have been taken. Early flights showed that orthostatic
intolerance got worse as flight duration increased, leading to some concerns that
this effect could be severely limiting on re-entry operations. Specifically, there
were concerns about piloting in Shuttle-like spacecraft that generate g forces in
the head-to-foot (+Gz) direction upon re-entry and about the ability of crew to
quickly exit a spacecraft in an emergency after landing. Longer Russian and US
flights did show that the tendency for orthostatic intolerance does plateau after
awhile in space. On-orbit exercise may help ease symptoms, and other
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Cosmonauts being removed in wheelchairs
after a long spaceflight.
The decrease in blood volume is exacerbated upon re-entry by any decrease in
the reflexive ability of the cardiovascular system to return blood pressure to
normal. Thus, loss of baroreceptor sensitivity to pressure drops is a contributing
factor to orthostatic intolerance. Similarly, deconditioning of the heart muscle
and smooth muscle of the blood vessels makes it harder to increase peripheral
resistance and cardiac output. Finally, deconditioning of leg muscle makes it
harder for the “skeletal muscle pump” during movement to help force blood from
the legs back up to the heart.
Upon re-entry crew experience orthostatic intolerance upon standing.
They can be tested for the degree of their intolerance either by laying them on a
“tilt table” that holds them at a certain head-up angle (e.g., 70o head up in
Gemini tests, which led to presyncopal symptoms), by conducting a stand test
(e.g,, Gemini and Apollo astronauts leaned on a wall with their heels 15 cm from
the wall’s base), or a comparison of heart rates and blood pressure between
supine rest and upright standing (as used in Shuttle).In one example of
orthostatic intolerance and stand tests, 14 astronauts were tested after flights of
up to 2 weeks in Shuttle life science missions SLS-1, SLS-2, and D-2. Of these
astronauts, 64% could not complete a 10-minute stand test that all had completed
pre-flight. This simple test consisted of about 30 minutes of supine rest and
baseline data collection followed by 10 minutes of standing (with subjects told
remain quiet and not to contract their leg muscles actively).
70
100
30
100
100
100
200
100
160

Numbers
reflect
idealized
Mean
Arterial
Pressures
For further thought. A current medical test for the state of dehydration in
patients with vomiting, diarrhea, or other gastrointestinal complaints includes
comparison of heart rate and blood pressure in a 3-step series: reclining, sitting,
and standing. In what way are returning astronauts “dehydrated” so that tests for
their physiological function can be so similar? In what way are they different?
Cardiac and Vascular Function. Tests indicated that there is a tendency
for decreased venous return, cardiac filling (end-diastolic volume), and stroke
volume upon return to a 1-g environment.
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One possible diagram to compare preflight (left), in-flight (center), and post-flight
(right) fluid distributions. Pre-flight has been
discussed before. In-flight changes include
a relative headward fluid shift that is actually
an evening of pressures—head pressure
does not exceed foot pressure in space.
During this period, plasma volume has
decreased; however, this is adaptive to
microgravity. Post-flight in the upright
posture, blood again pools in the legs and
there is a lowered blood volume to
distribute—this leads to orthostatic
intolerance.
A very evident response is a markedly elevated heart rate. This is
probably a reflexive action to increase cardiac output and, thus, blood pressure.
In Shuttles 4 & 5, for example, heart rate generally increased by about 35% from
pre-flight conditions while astronauts were upright. This increased heart rate
seems especially important to cardiovascular function, since tests have shown
that other mechanisms to increase short-term blood pressure (i.e., increasing
peripheral resistance or increasing stroke volume through increased heart
contractility) via
the sympathetic nervous system seem blunted after spaceflight. Decreased
baroreceptor sensitivity, acquired in spaceflight, can also slow the total response.
Post-flight exercise stress tests indicate that heart rate can still meet
normal stress levels, but stroke volume is decreased versus pre-flight, again
leading to more reliance on heart rate increases. Upright and maximal exercise
capability is decreased for a short time, but it is recovered.
Venous compliance is also increased post-flight, meaning that the vessels
have lost some smooth muscle “tone” and are more compliant—they allow blood
to pool in the legs more easily. Overall, even with all these changes, the body is
generally able to maintain cardiac output and blood pressure. However, blood
pressure may not be maintained at pre-flight equivalent levels or adjusted as
quickly, leaving astronauts susceptible to orthostatic intolerance.
Body Weight and Total Body Water. Body weight increases within a
few hours of landing, related to increased thirst and fluid intake that begin to
increase total body water. Concurrent with these changes are observed increases
in the hormones ADH and aldosterone (which help to retain water and salt) and a
decrease in urine output.
These data are further indications that the body has plasma volume and
total body water while on orbit by as much as 10-15%. Upon return to Earth,
there is a relative “underfilling” of the circulatory system and a concurrent
decrease in extracellular fluids able to shift into it—the body is in a functionally
“fluid depleted” that is no longer adaptive to its environment. Reflexes are
triggered to regain extracellular fluid levels and total body water.
Recovery Times
US flights of 12 weeks have shown that astronauts generally exhibit a
normal stand test and other cardiovascular parameters within about 3 days of
landing, indicating a basic return to normal cardiovascular function in terms of
maintaining blood pressure. Longer Russian flights of 812 months show that
cardiovascular recovery may take about 4 weeks. However long recovery takes,
though, cardiovascular function is one that does return to normal upon return to
Earth.
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
In the previously mentioned standtest results where 64% of the astronauts
showed orthostatic intolerance, all
showed increased heart rates and
decreased stroke volumes.
Though
cardiac
output
was
relatively
unchanged, the key difference in those
that were able to maintain arterial blood
pressure was that those 46% able to
complete the test had a higher increase
in total peripheral resistance due to
vasoconstriction.
On-Orbit Countermeasures
For many of the physiological changes that occur in spaceflight there
remains debate over which are “normal adaptive” and which we should try to
prevent. Much of what occurs in the cardiovascular system and body fluid
volume in spaceflight is adaptive to that environment. Some of the results, such
as facial congestion, are bothersome and arrhythmias can be of concern;
however, they have not proven to be major operational impediments. A primary
concern, though, has been to limit the impact of spaceflight on a successful and
enjoyable return to Earth. For this reason, several countermeasures have been
developed for use by astronauts.
Lower-Body Negative Pressure. Lower-body negative pressure (LBNP)
can be used to aid cardiovascular conditioning, as well as to judge its extent via
LBNP stress tests. Periodic exposure to LBNP helps shift blood back from
upper body and into the legs. This creates a more Earth-like “upright” condition
that forces the heart to deal with decreased venous return. This, then, forces
increased cardiac response and adjustment of peripheral vascular resistance in
order to meet this stress. Levels of LBNP that have been used on orbit have
ranged from –30 to –50 mmHg versus atmospheric pressure. Care is used in this
approach since, if LBNP levels are too high, similar effects to long-term standing
and orthostatic intolerance can occur.
Exercise. Just as on Earth, appropriate exercise can aid cardiovascular
conditioning. Cardiovascular function tests during exercise can help monitor
cardiovascular status and the level of deconditioning in individual astronauts.
The two major forms of exercise on Shuttle flights are the bicycle
ergometer and the treadmill. Special restraint systems (e.g., bungee cords) are
required on both to hold the astronauts in place during exercise sessions.
Another practical issue regarding exercise in space is that it must be timed so
that vibration caused by the exercise itself, and transmitted through the structure
of the Shuttle, doesn’t impact other planned operations or experiments.
The duration of needed exercise to balance mission needs and achievable
cardiovascular conditioning, remains debated. Russians aboard space station
Mir would often use the treadmill about 2 hours per day. Other exercise regimes
might include a mix of 30-40 min biking and 45-80 minutes on the treadmill
(again constituting up to 2 hours/day). In discussing exercise, realize that the
discussion here is aimed at cardiovascular conditioning. Other types of exercise
(i.e., resistance training) can also be important as countermeasures for skeletal
and bone loss seen in microgravity.
Combined LBNP & Exercise. Proposals have been made, and tested in
the laboratory, for combining the benefits of LBNP and cardiovascular exercise
in space. A LBNP chamber built around a treadmill would offer several
benefits. First fluid would be pulled into the legs to an even greater extent than
that increased bloodflow needed for increased muscle activity. This could add
an
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increased “load on the heart for further conditioning. Also, the negative pressure
could actually help “pull” the astronaut down against the treadmill to gain a footstrike impact (or “ground reaction force”) more like that experienced on Earth—
this might help in preventing bone losses that stem from decreased loads on bone
in microgravity.
Unfortunately the levels of negative pressure to cause that 1-g equivalent
ground reaction force (e.g., –100 mmHg) would probably also be excessive
regarding the level of LBNP best withstood by the body. For this reason an
elastic garment or inflatable anti-LBNP suit, like a fighter pilot’s anti-g suit,
might be added. With these equipment items both in use, an astronaut could
adjust LBNP effects separate from exercise load.
Anti-g suits. Despite any other on-orbit conditioning efforts, orthostatic
intolerance still occurs. In the critical period of re-entry and landing, Shuttle
astronauts routinely may wear anti-g suits. These garments inflate to prevent
pooling of fluids in the lower body and can also, via an abdominal bladder, help
maintain venous return to the heart.
Hydration & Fluid Loading. Studies in the late 1970s showed that
drinking about one liter of a balanced salt solution would lead to an increased
blood plasma volume loads, by about 400 mL for at least 4 hours. Why is this so
and why do we care?
The extracellular fluid is basically 0.9% NaCl solution in water—medical
supplements that match this concentration are called “normal” saline. If a person
is given normal saline intravenously or ingests it (as is the case here), the volume
is distributed primarily across the extracellular fluid volume compartment. Since
the plasma volume is the lesser portion of the extracellular fluid, it retains a
smaller percentage of the normal saline. The rest moves into the interstitial
spaces of the tissues. Eventually, some of the fluid may enter cells (though Na +
is generally excluded) and some may be excreted.
Studies in the mid-1980s verified that this technique of temporarily
increasing plasma volume could be used by Shuttle astronauts in the short term
to ease the orthostatic intolerance on landing. For example, for 26 astronauts,
those who had practiced “fluid loading” had lower heart rates, maintained blood
pressure better, and reported no faintness (compared to 33% astronauts having
faintness in a control group).
Since 1984 the general NASA protocol for fluid loading has been for crew
to ingest about 32 ounces (1 quart, or about 1 liter) of water or juice and 8 salt
tablets about 1 hour before leaving orbit. This produces 1 liter of isotonic saline
in the digestive track, which then leads to absorption and subsequent increase in
plasma volume. A variant of this technique that was tested combined fluid
loading concurrent with several hours of LBNP at about –30 mmHg. The LBNP
“loads” more fluids into the interstitial spaces when applied; after it is removed
(close to re-entry) the fluids redistribute themselves across the extracellular
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space, again increasing
plasma volume and helping
to maintain blood pressure
upon landing.
Later tests showed that fluid loading is most beneficial for shorter flights
of up to 10 days, with relative benefits (versus. no loading) decreasing with
longer time in orbit. It may be that other factors such as cardiovascular
deconditioning itself become more important on longer flights with regard to
causing orthostatic intolerance.
Drugs. Drugs are not now used to boost blood pressure, cause water
retention and increased plasma volume, or so forth before landing. However,
some such drugs have been proposed if their side effects could be minimized.
Further Research
Further research is planned to better understand, and perhaps better
control, the cardiovascular and fluid changes in spaceflight. Some of the areas
for further work include studying baroreceptor and sympathetic nervous system
reflexes, hormonal effects, vascular compliance changes, capillary permeability,
and Starling forces. Almost every aspect discussed in this reading is subject to
further, deeper study.
References
Churchill, SE, & MW Bungo. Response of the Cardiovascular System to
Spaceflight, Chapter 4 in Fundamental of Space Life Sciences, Vol I,
SE Churchill, ed., Krieger Publ. Co., Malabar FL, 1997.
Charles, JB, MW Bungo, & GW Fortner. Cardiopulmonary Function, Chapter
14
in Space Physiology and Medicine, 3rd ed. AE Nicogossian, CL Huntoon,
& SL Pool, eds. Lea & Febiger, Philadelphia, 1994.
Hargens, AR. Recent bed rest results and countermeasure development at
NASA.
Acta Physiol Scand, 150, Suppl 616: 103-114, 1994.
HB107, Biology and Space Exploration. Course reader, compiled and edited by
Malcolm Cohen, Stanford University, Spring 1995.
Lujan, BF, and RJ White. Human Physiology in Space: Curiculum Supplement
for Secondary Schools. Produced by NASA, the National Institutes of
Health, Universities Space Research Associates, and the University of
Southwestern Medical Center, 1993.
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Other Resources
<http://www.nsbri.org/humanphysiologyspace/indexb.html> Human Physiology
in Space online, presenting a classroom supplement for secondary schools
to parallel the work by Lujan and White. Includes some figures used here.
<http://www.nsbri.org/research/cardiod.html> Cardiovascular research area of
the National Space Biomedical Research Institute (NSBRI).
<http://www.vesalius.com/archv1.asp> Vesalius Image Archive, and excellent
source of clinical images and anatomical drawings. Includes some figures
used here.
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