Normal Circulation |
The cardiovascular system has ten unique characteristics that
make it an unusually complicated hydraulic system. Understanding
how the cardiovascular system functions requires insight into a
larger set of variables than that which governs the function of
most pump, pipe, and fluid systems found in the world of
man-made machines. The ten unique characteristics peculiar to
the cardiovascular system are:
- The system is a closed circle rather than being
open-ended and linear.
- The system is elastic rather than rigid.
- The system is filled with liquid at a positive mean
pressure ("mean cardiovascular pressure"), which exists
independent of the pumping action of the heart.
- The right and left ventricles, which pump into the
same system that they pump out of, are in series with
two interposed vascular beds (systemic and pulmonary).
- The heart fills passively, rather than by actively
sucking.
- As a consequence of the heart's passive filling, the
circulation rate is normally regulated by
peripheral-vascular factors, rather than by cardiac
variables.
- The flow from the heart is intermittent, while the
flow to it is continuous.
- Normally, there is an excess expenditure of energy
by the heart needed for the circulation rate imposed by
peripheral vascular regulators ("pump energy excess").
- Normally, ventricular capacity is in excess of the
diastolic filling volume ("pump capacity excess").
- The slowing effect of any vascular resistance on
flow rate depends on its location, with reference to
upstream compliance, as well as its magnitude.
In order to understand circulatory
phenomena in the elastic circular hydraulic system (Fig.
1), where every point is both upstream and downstream from
every other point, and where the non-sucking ventricles pump out
of the same system they pump into, we need to examine the ten
unique factors individually, before we can amalgamate them into
a meaningful whole.
VENTRICLES (THE
PUMPS)
To clarify and facilitate understanding
of the features peculiar to the heart, it is helpful to compare
three major types of pumps. The heart�s unique characteristics
as a pump are of paramount importance in understanding how the
cardiovascular system works.
PUMP TYPE #1: This type of pump both sucks and
forcibly ejects fluid. This pump uses energy both to
actively fill at its inlet and to empty its contents at its
outlet. Two examples of this type of pump are: (1) a piston
pump, which expends energy to suck in the stroke volume
which is then forcibly ejected; and (2) a roller pump, which
sucks at its inlet by the recoil of the resilient tubing
that has been compressed by the roller as it moves forward,
ejecting the fluid in front of it. With type #1 pumps, the
output in a hydraulic system is determined exclusively by
two pump variables: the stroke rate and the stroke volume.
The reason for discussing this is that the heart is a
different type of pump, and those two variables are
frequently and erroneously projected onto cardiovascular
function, in a way in which they do not apply.
PUMP TYPE #2: This pump sucks and blows but,
instead of producing a specific flow rate, creates a
specific pressure gradient between its inlet and outlet.
Centrifugal pumps fall into this category. With this type,
two pump factors (rate and power), as well as two non-pump
factors (pressure and resistance in the system), effect
output. As the heart is not such a pump, there is danger in
borrowing explanations of cardiovascular function from
hydraulic systems containing centrifugal pumps.
PUMP TYPE #3: This type of pump is passive
filling, and does not suck at its inlet. It expends no
energy to fill, it only expends energy to empty. An example
of this type of pump is the urinary bladder. It is a
flaccid, hollow organ that does not create any negative
pressure or suck on the ureters or kidneys to fill. The
bladder merely exerts energy to empty. To calculate the flow
of urine for any given period, you can obtain the answer by
multiplying the stroke rate times the stroke volume.
However, it is important to underline here that those two
things, stroke rate and volume, are not determinants of
bladder output. You cannot increase the output merely by
changing the rate of bladder contraction (stroke rate). The
urinary bladder cannot expend energy to increase its filling
and thus its stroke volume. This type of pump, even though
it does the work and thus produces the flow, is totally
dependent upon external factors (e.g., renal function) to
determine the output. At a given rate of urinary production,
stroke rate and stroke volume are reciprocals of one
another. If the bladder is emptied twice as often, the
stroke volume will be one half as much.
THE RIGHT AND LEFT VENTRICLES ARE TWO TYPE #3 PUMPS:
The heart, like the urinary bladder, is
a hollow muscular organ that does not suck to fill, but produces
circulation by ejecting whatever fluid enters it at diastole.
During normal function, the heart not only doesn't develop a
pressure negative to the intrathoracic pressure, but it offers
an impediment to filling because of its limited volume-pressure
compliance.
The evidence that the heart fills
passively, and does not suck to fill, is found in the data from
innumerable heart catheterizations, which all show a positive
diastolic pressure in the ventricles (Fig.
2, a to c). In fact, as ventricles fill, they not only do
not suck, but they offer an increasing impediment to filling, as
noted by the progressive increase in pressure toward the end of
diastole (Fig. 2,
c). Negative ventricular pressure, in relation to intrathoracic
pressure, has not been found in physiologic states. The heart,
like all other muscles in the body, expends energy and does work
by contracting. It cannot expend energy to do mechanical work by
forcibly elongating its fibers to suck like the type #1 pump,
which uses energy to suck in a stroke volume. Do not confuse the
negative pressure created in the chest by inspiration as
negative heart pressure (Fig.
2, b). The chest can suck, the heart cannot.
One can calculate cardiac output in the
same way as in the urinary bladder example: by multiplying
stroke rate times stroke volume. Also, just as in that example,
while stroke rate multiplied by stroke volume measures the
amount of output, those variables are not determinants of that
output. The heart, by filling passively, pumps out blood at a
rate determined by the rate of blood coming to it. Given that
the heart is a pump that produces the flow but has a flow rate
determined by extra-cardiac factors, let us examine those
factors that determine circulation rate.
DETERMINATION OF
CARDIAC OUTPUT IN A CIRCULAR ELASTIC SYSTEM WITH PASSIVE FILLING
PUMPS
With pumps that cannot suck to fill,
there must be a positive pressure at the inlets for any blood to
run into the ventricles, in order for there to be any pump
output. If there is no pressure in the cardiovascular system, no
blood can run into the ventricles and there can be no flow.
Normally, there is a mean cardiovascular pressure above zero,
which the heart distributes. The heart, rather than being
responsible for the pressure in the vascular system, is a
circulating device. It lowers the pressure at the ventricular
inlets and raises it at the ventricular outlets. With a positive
pressure in the cardiovascular system, when blood is ejected
into the arterial side of the circle, a pressure gradient is
created between the arteries and veins. This gradient causes
blood to flow around the circle back to the ventricular inlets.
Therefore, the output rate varies directly with the magnitude of
that mean cardiovascular pressure. The higher the pressure,
the higher the gradient, the greater the flow rate. The
circular system being elastic, and having resistance and other
impediments to flow, the energy from ventricular contraction
does not transfer instantaneously around the circle after each
heart beat, as would occur in a rigid system. The energy of
venous flow is several heart beats behind that of ventricular
ejection. The greater the elasticity and impediments to flow,
the slower the flow rate.
Therefore, during normal function,
cardiac output varies directly with the mean cardiovascular
pressure and inversely with the impedance to blood flow to the
heart.
I. MEAN CARDIOVASCULAR PRESSURE
Definition: The mean cardiovascular pressure is the
pressure in the cardiovascular system with the circulation
stopped, after the pressure has equalized between the arteries,
capillaries, veins, and cardiac chambers. Do not confuse this
pressure with central venous pressure, venous filling pressure,
or mean-arterial pressure. Mean cardiovascular pressure is the
pressure related to the blood volume and the compliance of the
entire elastic cardiovascular compartment.
Measurement: Mean cardiovascular pressure is expressed
in centimeters of water above ambient pressure, with zero being
at mid-heart level. The mean cardiovascular pressure can be
approximated during cardiac arrest. After arrest, a pressure
equalization occurs between the various cardiovascular
compartments in about thirty seconds. The arterial pressure
falls and the venous pressure rises as some of the arterial
blood moves into the veins during pressure equalization.
Therefore, the mean cardiovascular pressure is always above
venous pressure and below arterial pressure. Normally, mean
cardiovascular pressure is between 15 and 18 cm. of water above
mid-heart level. We have some approximation of its magnitude
from fortuitous records of the arterial and venous pressures
equalizing, obtained during short periods of cardiac arrest of
patients in coronary care settings, in emergency rooms, or in
operating rooms during heart surgery. Even in these situations,
the resulting pressure can be regarded as only an approximation,
as the shift in fluid, from hypoxia caused by lack of
circulation, may have altered the vascular compliance. (See
Appendix
for clinical measurement technique)
Significance: Without mean cardiovascular pressure
there would be no circulation. The heart doesn't generate the
pressure in the vascular system, it merely distributes the mean
cardiovascular pressure. The cardiac ventricles take the mean
cardiovascular pressure and distribute it by raising the
pressure on the arterial sides while lowering it on the venous
sides. The two ventricles, being passively filling pumps, cannot
suck, so they lower the inlet pressures toward — but never below
— zero, in relation to the ambient pressure in the chest.
The higher the mean cardiovascular
pressure, if the ventricles are not failing, the higher the
ventricles can elevate the arterial pressure while reducing the
venous pressure toward zero, and thus the greater the cardiac
output. Conversely, the lower the mean cardiovascular pressure,
the less the heart can raise the arterial pressure by lowering
the venous pressure, and thus the lower the cardiac output.
Origin of the mean cardiovascular pressure: The mean
cardiovascular pressure results from the volume of blood and the
compliance of the cardiovascular system. The volume in the
cardiovascular system results from an equilibrium between the
rate of water, electrolytes, and other blood constituents
entering the body by way of the gastrointestinal tract, and
leaving the body primarily by the kidneys (Fig.
3). The mean cardiovascular pressure is the result of a
continuing dynamic process.
MEAN CARDIOVASCULAR PRESSURE =
energy forcing fluid into the body / resistance to fluid
loss from the body |
Homeostatic maintenance of normal mean cardiovascular
pressure:
(1) Slow feedback mechanism:
A slow homeostatic feedback
mechanism tends to keep the mean cardiovascular pressure at
a constant level: Elevation of the mean cardiovascular
pressure above normal —› causes increase in cardiac output
—› causes increased renal blood flow —› results in increased
renal output —› thereby lowering blood volume and mean
cardiovascular pressure back to normal. Conversely, low mean
cardiovascular pressure —› low cardiac output —› low renal
blood flow —› decreased renal output until the mean
cardiovascular pressure is restored to normal by continuing
fluid intake. With elevated mean cardiovascular pressure,
the rate of return to normal is dependent on renal function,
whereas, with low mean cardiovascular pressure the rate of
return can vary greatly, depending on the rate of
restoration of blood volume.
Clinical evidence of the homeostatic mechanism:
- Response to weightlessness by going into orbit: In
the absence of gravity, normal blood volume shifts
centrally from the lower part of the body, thereby,
increasing the mean cardiovascular pressure at heart
level —› resulting in increased cardiac output —›
causing greater renal blood flow —› leading to greater
urinary output —› causing a decrease in blood volume
and, thus, a decrease in mean cardiovascular pressure
back to normal. The converse is found when astronauts
return to gravity. It takes a few hours to restore
normal mean cardiovascular pressure by intake of fluid
and electrolytes after returning to earth, during which
transition time they conserve the fluid they take in by
putting out very little urine.
- During any hypovolemic shock state, such as massive
hemorrhage or severe dehydration, the urinary output
goes abruptly down and remains low until restoration of
normal mean cardiovascular pressure.
(2) Rapid mean cardiovascular pressure buffer
mechanisms:
(a) Elasticity: The elasticity of the vascular system
prevents sudden blood volume loss or gain from causing a
linear, temporary change in mean cardiovascular
pressure. Elasticity has, of course, an instantaneous
buffer effect. Evidence of this is found in one's
ability to give a pint of blood at the blood bank
without going into severe low cardiac output. This
buffer effect bolsters circulation while the blood
volume — and, thus, mean cardiovascular pressure — is
restored by subsequent oral intake of fluid.
(b) Vascular/extravascular equilibrium: There is a
pressure equilibrium between the various extravascular
compartments of the body and the cardiovascular space (Fig.
3). Changes in mean cardiovascular pressure result
in shifts of fluid back and forth which tend to buffer
sudden changes. This buffer system is fairly rapid but
not instantaneous, as evidenced by the observation that
a person going into severe shock from sudden loss of
blood would not have had the same severe shock state if
the loss had occurred more gradually over a period of an
hour or so.
(3) Humeral and neuro-muscular-vascular reflexes:
These responses from stimuli, which
alter vascular compliance, act as buffer systems. They
prevent sudden changes in mean cardiovascular pressure from
sudden position changes, such as going from lying to
standing. They also buffer the effect of sudden loss of
blood volume from hemorrhage.
II. IMPEDANCE TO THE FLOW OF BLOOD FROM THE OUTLETS
AROUND TO THE INLETS OF THE VENTRICLES
Four factors tend to impede the flow of
blood in the cardiovascular circle. Therefore, they are inverse
determinants of cardiac output: (1) resistance, (2) elasticity,
(3) limited compliance of the ventricles to filling, and (4)
inertia of intermittent blood flow to the ventricles. The
interrelationship of these four factors makes flow determination
much more complicated than plain resistance, which is the single
impediment in rigid, open ended, linear hydraulic systems.
(1) Resistance and (2) Elasticity
Unlike rigid linear hydraulic
systems, where a given resistance may have the same effect
on flow, irrespective of its location, the elasticity of the
vascular system makes location of the resistance a
significant parameter. Because of the elasticity of the
circle, the location of any particular resistance determines
to what extent that resistance has on impeding blood flow. A
given resistance may have little or no effect in determining
cardiac output if it is near the outlet of the ventricles,
yet the same magnitude of resistance may have tremendous
slowing effect on circulation if located near the inlets of
the heart. Resistance points that have little compliant
vascular bed "upstream" (arteriolar resistance), increase
pump work but may not affect cardiac output significantly.
The heart, except during failure, exerts enough energy to
force the blood past any resistance near its outlet, with no
hold up in flow. On the other hand, resistance located with
a large compliant bed upstream has a tremendous effect on
flow rate by slowing blood return to the ventricles. Venous
sided resistance, with the compliance of the whole vascular
bed upstream, is a major inhibitor of circulation rate.
Thus, venous sided resistance is a major determinant of
cardiac output, but arterial resistance is not.
Interpolation of the additive effect of all resistance
points in the circle on cardiac output must include the
amount of compliant bed upstream from each resistance point.
All resistance factors — including
blood viscosity, cross-section area of any vascular bed,
margination of blood constituents, etc. — play roles in flow
rate determination only when linked with their location to
compliance upstream. Adding venous sided resistance of a
magnitude that results in only a few mm. water pressure
gradient may cause a marked reduction of flow. Whereas,
increasing arteriolar resistance to the point of severe
arterial hypertension may not appreciably change cardiac
output.
In human cardiovascular physiology,
the significance of resistance can only be understood when
coupled with upstream compliance. It is not just the
magnitude of resistance but the location of that resistance
that determines its effect on circulation rate.
(3) Impediment to Ventricular Filling
The end-diastolic pressure:
Ventricles not only do not suck to fill, they offer an
impediment to filling. The left ventricle has thicker and
stiffer walls than the right, so it tends to retard filling
more than the right ventricle. Catheterization data shows
end-diastolic pressure of five to ten centimeters of water
above intrathoracic pressure. Don't confuse the negative
pressure of inspiration, transmitted to the heart, as the
heart sucking. The intracardiac pressure is always above
that intrathoracic pressure (Fig.
2 at C).
(4) Inertia of Intermittent Blood Flow Offset by "The
Atrial Effect"
Atrial function facilitates
circulation by preventing the retarding effect that would
otherwise occur from the intermittent inflow to the
intermittent outflow ventricles. By being partially empty
and distensible, atria prevent the interruption of venous
flow to the heart that would occur during ventricular
systole if the veins ended at the inlet valves of the heart.
Atria have four essential
characteristics that cause them to promote continuous venous
flow. (1) There are no atrial inlet valves to interrupt
blood flow during atrial systole. (2) The atrial systole
contractions are incomplete and thus do not contract to the
extent that would block flow from the veins through the
atria into the ventricles. During atrial systole, blood not
only empties from the atria to the ventricles, but blood
continues to flow uninterrupted from the veins right through
the atria into the ventricles. (3) The atrial contractions
must be gentle enough so that the force of contraction does
not exert significant back pressure that would impede venous
flow. (4) The "let go" of the atria must be timed so that
they relax before the start of ventricular contraction, to
be able to accept venous flow without interruption.
By preventing the inertia of
interrupted venous flow that would otherwise occur at each
ventricular systole, atria allow approximately 75% more
cardiac output than would otherwise occur. The fact that
atrial contraction is 15% of the amount of the succeeding
ventricular ejection has led to the false conclusion that
atria have their benefit by pumping up the ventricles (the
so-called "atrial kick"). The real benefit is in preventing
inertia and allowing uninterrupted venous flow.
The 20% to 25% increase in cardiac
output from synchronized atrial function over that of atrial
fibrillation doesn't belie the 75% contribution of the
atrial effect, as atrial fibrillation eliminates only part
of that effect. Atrial compliance, elasticity, and gravity
help in emptying the atria at ventricular diastole during
atrial fibrillation. Also, cardiac output during atrial
dysfunction is buffered: the initial fall in circulation
rate during atrial fibrillation reduces renal flow, thereby
causing retention of water and the subsequent rise in mean
cardiovascular pressure, which then partially offsets the
slowing effect on circulation.
Thus, four factors impede the flow of
blood around the cardiovascular circle: (1) resistance with (2)
upstream compliance, (3) ventricular non-compliance, and (4)
inertia if there is intermittent venous flow. The combined
effect of these factors that impede the flow of blood to the
inlet of the ventricles and, therefore, determine cardiac output
in a negative way, will be referred to as: inlet impedance.
In summary,
during normal physiology:
CARDIAC OUTPUT=FUNCTION OF MEAN CARDIOVASCULAR
PRESSURE / INLET IMPEDANCE
|
AUTOMATIC
BALANCING OF THE PULMONARY AND SYSTEMIC BLOOD VOLUMES
The passive filling characteristic of
the ventricles is the feature that accounts for the automatic
maintenance of blood volume equilibrium between the pulmonary
and systemic vascular beds. With passively filled pumps, the
relative blood volume in the two circuits is determined by their
relative size and elasticity. On the other hand, if the
ventricles were type #1 pumps, which actively fill, any
discrepancy in the output of the two pumps, or flow through
normal physiological shunts between the two vascular systems,
would very quickly shift all of the blood volume into one
circuit at the expense of the other, resulting in disaster.
The right and left ventricles, by
filling passively, pump out whatever amount comes to them,
determined by extracardiac factors. The blood volume
equilibrium, therefore, is determined by the relative size and
compliance of the two circuits and, to a minor extent, by the
relative impediment of flow to the two pumps. It has been noted
that the output of the two sides of the heart is never equal
because there are physiological shunts, which connect one
vascular bed to the other. The largest of these shunts, in
normal physiology, are the bronchial arteries, which go from the
systemic circuit to the lungs. The bronchial blood flow is a
left-to-right shunt that accounts for the left ventricular
output normally being at least 10% larger than the right.
Because of the shunt, more blood returns to the left ventricle
than the right, the left ventricle passively fills more than the
right, thereby causing it to produce a greater output and thus
the equilibrium is maintained. With other types of pumps this
would not occur.
A dramatic illustration of this volume
equilibrium, automatically being maintained during a massive
discrepancy in output of the two pumps, is seen in atrial septal
defects. In this case, the right ventricular output may be four
or five times that of the left. Yet, the volume equilibrium is
maintained. A large atrial septal defect virtually results in a
single atrium above the two ventricles. The shunt occurs during
ventricular diastole, because the right, thin walled ventricle
is more distensible than the non-compliant thicker walled left
ventricle. The blood in the common atrium goes the way of least
resistance. The greater filling into the more compliant right
ventricle results in greater right ventricular output. The
greater right output goes to the lungs and then directly back to
the right ventricle, returning again through the septal defect.
Because of the passive filling, this results in no progressive
increase in the blood volume in the lungs, and no disturbance in
the maintenance of the blood volume equilibrium. After closure
of the septal defect, resulting in much smaller right heart
output, the volume equilibrium remains. This equilibrium, which
persists after such sudden, massive changes in right heart
output, occurs automatically because of the passive filling
characteristic of the ventricles. It is the physical
characteristics of the two vascular beds (e.g., relative size,
compliance, and impediment to flow), that determines the volume
balance with passive filling ventricles.
The passive
filling of the ventricles accounts for the maintenance
of blood volume equilibrium between the systemic and
pulmonary vascular systems.
|
HEART RATE AND
STROKE VOLUME
Normally, the passively filling
ventricles are not maximally filled at diastole. Also, they are
exerting excess energy over that needed to eject blood at the
flow rate of blood entering the ventricles. With such volume and
energy reserve, if blood enters the heart faster, the flow rate
can go up without any change in strength of contraction or heart
rate, unless the heart is being filled maximally (heart
failure). Conversely, if blood enters the ventricles at a slower
flow rate, the output will go down irrespective of any lowering
of the rate or decrease in strength of cardiac contraction.
Thus, at a given flow rate, with the
normal excess pump power, in both strength and rate, the heart
rate and stroke volume become reciprocals of one another, as
long as the heart doesn�t go into failure. At a given flow rate,
decreasing the heart rate increases the stroke volume; while
increasing the heart rate decreases the stroke volume. The
observation — that cardiac output usually parallels the cardiac
rate and strength of contraction — has resulted in the
fallacious conclusion, based on post hoc ergo propter hoc
reasoning ("following this, therefore because of this"), that
they are cause and effect.
Even though these two variables do not
normally control cardiac output, their variability has
physiological benefit in energy conservation. During low
circulation rates, when the heart is not filling to its maximal
volume during diastole, the heart down shifts its rate and
strength of contraction, thus conserving energy. Also, during
high output states, it increases its rate and strength of
contraction, thus preventing failure from any limitation of
output that might be imposed by ventricular chamber size. If the
heart functioned at its maximum strength of contraction and a
rate of 150 beats a minute, the cardiac output would go up and
down just as it does normally. But what a waste of energy would
result! So the variability of rate and strength of contraction
have only ecological value: that of conserving world food
supply.
Two mechanisms cause the heart to
roughly parallel its energy expenditure with cardiac output,
preventing failure during high output states and saving energy
during low output: (1) The neural and humeral stimuli that
increase mean cardiovascular pressure are also those that
increase heart rate and strength of contraction. (2) Increased
stretching of the ventricles at diastole causes some increased
strength of contraction at systole (Starling's law of the
heart). While this observation of Starling is true and
contributes to the paralleling of cardiac output to strength of
contraction, it is probably not a major determinant of energy
expenditure, as strong cardiac contractions continue even when
the heart is completely empty, as seen during cardiac bypass
surgery.
The reciprocal relationship of heart
rate and stroke volume can be demonstrated in patients with
complete heart block by varying the rate of firing of their
pacemakers. Variations in rate, within physiological levels,
above that required to prevent complete diastolic ventricular
filling, are associated with no change in cardiac output.
Therefore, a compromise rate of 78 is a commonly used setting
that allows a wide range of activity acceptable to most
patients.
Conclusion: During normal physiologic states, there
is always pump energy excess over that used in
circulation. |
EXERCISE AND
CARDIAC OUTPUT INCREASE
Two factors cause the increase in
cardiac output during exercise: Exercise causes the
cardiovascular impedance to be decreased and the mean
cardiovascular pressure to be increased. The intermittent
skeletal muscle contractions around venous beds, which contain
one-way valves, act as a peripheral pump which overcomes
significant impedance to flow. Neuro-humeral reflexes speed the
heart rate, which slightly lowers the inlet impedance to the
heart, by lowering the end-diastolic pressure over what it would
otherwise be. The increased heart rate guarantees excess energy
expenditure, thus preventing cardiac power failure at the higher
circulation rate. The neuro-humeral response to exercise also
throws the vascular system into spasm, thereby increasing the
mean cardiovascular pressure from the "G-suit" effect of tensing
the body in general. These are temporary changes, lasting only
during the exercise period, which do not effect the long term
homeostatic control of circulation.
DISTRIBUTION OF
BLOOD FLOW: PULSATILE BLOOD FLOW AND ARTERIOLAR RESISTANCE
Pulsatile arterial blood flow tends to
result in diffuse, fairly equal distribution of blood to all
tissues of the body. This phenomenon would not occur with a non-pulsatile
steady flow. Arteriolar resistance variability from time to time
and from place to place, superimposed on the otherwise diffuse
distribution, controls preferential blood flow to specific
areas, with physiologic benefit. The diverting of a greater
portion of cardiac output to the digestive tract after meals and
the increased flow to muscles during exercise are examples of
changes in distribution of blood flow controlled by variable
arteriolar resistance. Peripheral arteriolar resistance, rather
than having a cardiac output control function, has its
physiological significance by its determination of distribution
of blood flow. |
|
Abnormal Circulation |
Now that we have amalgamated the ten unique characteristics into
an integrated concept of normal cardiovascular function, we
proceed to examine the implications of those ten unique
characteristics during pathological states.
HEART FAILURE
(PUMP ENERGY FAILURE)
CONTRASTED WITH PUMP ENERGY EXCESS
Heart failure is the only situation where the non-sucking
heart determines its output. In this state, the heart is pumping
at its maximum output and therefore, in effect, by limiting the
output, it determines the output.
Normally, the heart rate and pump energy are in excess of
that needed to eject enough blood at systole, so that the
ventricles are empty enough at diastole to allow unobstructed
passive filling. Normally ventricles are not maximally filled so
there is reserve compliance which allows cardiac output to be
determined by the extra-cardiac factors, rather than being
limited by the heart. If the heart fails, it pumps less than the
normally controlling extra-cardiac factors would dictate. During
pump energy failure the heart's output is being limited
by whatever amount it is able to pump. The heart in such a
situation of failure, by limiting output, becomes the sole
regulator of cardiac output.
Definition: Heart failure exists whenever heart
function is inadequate to produce the output which would be
allowed by the mean cardiovascular pressure and inlet impedance.
Heart failure is present when cardiac function is limiting and,
therefore, determining cardiac output. Normally, extra-cardiac
factors being constant, if the heart contracts more strongly,
efficiently, or rapidly, no increase in output occurs. Normally,
the heart is exerting excess energy over that used to produce
cardiac output and thus a reserve is present, so that increases
in circulation rate are not impeded by the heart. Normally, at a
given circulation rate, an increase in heart rate or increase in
strength of cardiac contraction does not increase the output.
However, during failure where the heart is pumping out the
maximal circulation rate that it can produce at the moment,
increases in the rate and strength of contraction do increase
cardiac output, up until venous pressure is reduced to normal,
at which time the heart is no longer in failure.
When heart failure occurs, blood volume equilibrium shifts to
the system behind the failing ventricle with an increase in the
venous pressure at the inlet of the failing ventricle. The other
ventricle, in the presence of the slowed circulation rate, is
able to maintain a low inlet pressure, with the resulting shift
in blood volume equilibrium toward the circuit behind the
failing ventricle. With left ventricular failure, for instance,
the circulation slows to the rate limited by the left ventricle
and a new equilibrium occurs with a shift of blood volume from
the systemic circuit to the pulmonary vascular bed. Pulmonary
edema occurs if this shift in equilibrium is severe.
The high end-diastolic ventricular pressure and high end
systolic volume, from a low ejection fraction in heart failure,
would also be factors limiting flow, if the heart weren't
already determining a lower output.
A secondary change occurs when the left ventricle fails. The
lowered cardiac output decreases renal blood flow, thereby
causing retention of fluid and elevation of the mean-vascular
pressure. Fluid equilibrium, which exists between the
cardiovascular system and extra-vascular spaces, then results in
edema, liver engorgement, and the other fluid abnormalities of
congestive heart failure. Heart failure can intensify in a
descending spiral if the blood volume progressively expands. The
over-stretching of the heart puts it at a poor mechanical
advantage, thus further increasing its failure (the descending
limb of Starling's curve).
An extreme example of right heart failure is seen after a
"Glen" right atrial-pulmonary artery anastomosis procedure for
palliation of tricuspid atresia. Here, the person has virtually
complete failure of a non-functioning right heart, with a
surgical bypass of the right ventricle so that, in effect, the
circulation is by the left ventricle alone. Circulation is
slowed by the increase in impediment that normally would be
overcome by the right ventricle. As a consequence of the slowed
circulation, the kidneys receive slow flow, causing retention of
fluid, resulting in a permanent elevation in the homeostatic
level of mean cardiovascular pressure, resulting in some
compensatory increase in cardiac output at the new equilibrium.
Causes of Heart Failure:
Cardiac causes (low myocardial power):
- Myocardiopathies � viral, arteriosclerotic, toxic,
rheumatic
- Incompetent leaky valves, e.g., mitral or aortic
- Abnormally slow heart rate, e.g., complete heart block
Peripheral vascular causes:
- Abnormally high mean cardiovascular pressure causing
potentially higher circulation rate than a normal heart is
able to deliver, e.g., renal shutdown resulting in high
output failure
- Abnormally low impedance to the heart, e.g.,
arteriovenous fistula
Signs and Characteristics of Heart Failure:
- High venous pressure is the major pathognomonic finding
in cardiac failure. If the heart were not in failure, the
pressure would be normally low.
- A new equilibrium occurs between the two vascular
systems with a shift in volume to the field behind the
failing ventricle. I.e., left ventricular failure shifts the
equilibrium with a greater volume in the pulmonary circuit,
resulting in x-ray evidence of pulmonary vascular
engorgement and high pulmonary venous pressure. With right
heart failure, the neck vein pressure is seen to be
elevated. However, the systemic system initially is large
enough to accommodate the shift in blood volume from the
lungs without significant venous engorgement until secondary
changes (as seen below) occur.
- With either left or right heart failure, increased fluid
accumulation in the body progresses in a descending spiral
caused by slowed cardiac output —› less than optimum renal
blood flow —› low renal output —› retained fluid in the
vascular system —› increased mean cardiovascular pressure —›
edema —› liver engorgement and ascites.
NORMAL |
HEART FAILURE |
Heart energy excess |
Heart energy deficit |
Low ventricular inlet
pressure |
High inlet pressure |
Incompletely filled
ventricles |
Completely filled
ventricles |
Increase in rate —› no
increase in cardiac output |
Increase in rate —›
increase in cardiac output |
Increase contraction
—› no increase in cardiac output |
Increase contraction
—› increase in cardiac output |
Cardiac output = f
mcvp/inlet impedance |
Heart determines
cardiac output |
Body water equilibrium |
Progressive water
retention |
Normal cardiac output |
Low cardiac output |
Pathologic Conditions Resulting in Heart Failure:
- Complete heart block with slow pulse
- Extremely rapid pulse
- Intermittent, pulsatile venous flow
- Low ejection fraction
- Myocardiopathy with weak myocardial contraction
- Myocardial infarction to the point of low ejection
volume
- Valvular heart disease with stenosis or insufficiency
- Myocardial failure
- Pericardial tamponade
- Constrictive pericarditis
Goals in the Treatment of Heart Failure:
- Make the heart contract stronger and faster.
- Lower the resistance to ejection of blood from the
ventricles.
- Lower the mean cardiovascular pressure by salt and water
restriction and diuretics
- Restore the atrial effect if it is compromised by atrial
fibrillation or nodal rhythym.
If failure is due to myocardial contractility, lessening the
failure state by lowering mean cardiovascular pressure to the
point of producing normal venous pressure, without increasing
myocardial energy, may create hypovolemic shock rather than
restoring normal circulation.
SHOCK
Shock is a low cardiac output state that results from low
mean cardiovascular pressure. The low mean cardiovascular
pressure can result from altering of one or the other of the two
determinants of that pressure: (1) Increasing vascular
compliance, and (2) Loss of blood volume.
- Low output with resulting hypotension from sudden loss
of vascular tone is frequently seen after inducing spinal
anesthetics. A dramatic example was seen following total
central nervous system anesthesia, induced when marcaine was
inadvertently injected into the spinal canal during an
attempt to do an intercostal nerve block. In this case,
sudden total relaxation of the entire vascular system
resulted in severe hypotension. Loss of vascular tone can be
reversed by the use of vasopressors and the addition of
fluid.
- Shock from loss of blood volume can be temporarily
compensated for by decreasing vascular compliance by
vasopressor drugs, but ultimately needs to be corrected by
blood volume restoration.
A combination of the two mechanisms of shock is seen in
anaphylaxis, where there is both relaxation of the vascular
system plus a shift in blood volume to the extra-vascular space,
caused by increased capillary porosity.
Whatever the cause, the resulting low mean cardiovascular
pressure in shock can be restored to normal by rapid infusion of
fluid and electrolytes, aided by the use of vasopressor drugs.
During both of the shock mechanisms, the heart is already
spending excess energy, so increasing the heart rate or strength
of contraction will not increase the cardiac output. The obvious
increase in output that follows the use of epinephrine, or other
vasopressors, in such states is not caused by the inotropic
effect on the heart, but by their effect of increasing the mean
cardiovascular pressure by decreasing vascular compliance. Thus
another temporary therapeutic measure, which increases mean
cardiovascular pressure by making the system less compliant, is
the surrounding of the vascular system by a "G-suit" such as
those used by emergency medical personnel. It matters little how
fast or how strongly the heart contracts: If there is no
pressure in the cardiovascular system, there can be no
circulation.
ARTERIAL
HYPERTENSION
(LOW AND HIGH OUTPUT TYPES)
Arterial hypertension results from two radically different
mechanisms. One is caused by increased arteriolar resistance in
a system with normal mean cardiovascular pressure. The other
results, in the presence of normal arteriolar resistance, from
elevated mean cardiovascular pressure.
- In arterial hypertension from increased arteriolar
resistance, there is no slowing of the circulation rate from
the resistance. The heart, which normally expends excess
energy, just forces whatever blood that comes to it right
past the resistance point. The only change in circulation is
the elevated arterial pressure. Such arterial abnormal
resistance may have its origin from transient neuro-humeral
stimuli. However, with longstanding arterial hypertension,
changes eventually occur, resulting in more permanent
structural resistance increase. If, eventually, the vascular
changes effect blood flow to the kidneys, the second type of
hypertension may develop.
- High mean cardiovascular pressure hypertension: The most
graphic example of this state is seen during renal shutdown,
from whatever cause. Here, if fluid and electrolyte intake
continues, and there is reduced fluid leaving the body, the
vascular volume progressively rises, with a corresponding
increase in mean cardiovascular pressure. If the heart is
strong enough that it continues to exert excess energy over
that necessary to maintain a low ventricular inlet pressure,
cardiac output increases. With the increased flow, even in
the presence of unaltered arteriolar state, the resulting
arterial pressure is elevated. If the heart is normal, but
the pressure becomes so high that venous pressure rises,
high output heart failure occurs. Severe high output failure
has been seen where the systemic arterial pressure was
350/200, the systemic venous pressure was elevated with the
neck veins at 30 cm., the pulmonary artery pressure was
doubled, and the pulmonary capillary pressure was so high as
to cause pulmonary edema with frothing of blood from the
mouth and nose. This is in marked contrast to the
distribution hypertension caused by arteriolar resistance
increase.
The spectrum of hypertension states varies greatly between
these two extremes and combinations of the two. Determination of
the mean cardiovascular pressure helps delineate the
significance of each in diagnosis. (See
Appendix.)
Therapy for the two types of hypertension should be aimed at
the etiology. For high mean cardiovascular hypertension,
improving renal blood flow by removing renal arterial
obstruction, diuretics, low salt diet, and water restriction to
lower mean cardiovascular pressure or even renal transplant may
be indicated. For hypertension caused by high arteriolar
resistance, arteriolar vaso-relaxing drugs and changing the
patient's response to stress may be effective.
ARTERIOVENOUS
FISTULA
An arteriovenous fistula, with blood flow going directly from
an artery to a vein without going through arterioles,
capillaries, and venules, bypasses most of the resistance that
has upstream compliance. Therefore, depending on size, a fistula
can cause tremendous increase in cardiac output. If a shunt is
great enough, high output failure can result. If a shunt is in
an extremity, where it can be occluded by manual pressure,
alternating decrease and increase of cardiac output can be
observed, as the shunt is intermittently occluded and opened.
This maneuver is a good demonstration of the peripheral vascular
control of circulation rate.
Arteriovenous fistula shunts occur in a number of disease
states. For example, blood flow is shunted from arteries to
veins in thyrotoxic goiters. Rather than there being one large
arteriovenous channel, there are many small shunting vessels.
The blood may be flowing so rapidly through the many small
shunts that a loud, continuous murmur may be heard over the
thyroid gland. This arteriovenous shunting of blood flow
accounts, in part, for the high cardiac output associated with
toxic goiter.
CHANGES IN SIZE OF
THE
VASCULAR SYSTEM
Because of the peripheral control of cardiac output, changing
the size of the vascular bed, permanently (such as by a leg
amputation) or by short term decrease (such as by cross-clamping
the aorta and vena cava during surgery), causes an instantaneous
decrease in cardiac output, mechanically, without any
involvement or need of neurologic or humeral reflexes.
COMPLETE HEART
BLOCK AND
FIXED RATE PACEMAKERS
Patients with heart block, with a very slow pulse rate, have
maximal ventricular filling before the completion of diastole,
thereby restricting venous flow. This restriction in venous flow
causes high venous pressure and low cardiac output. As the rate
is incrementally increased by the use of a pacemaker, pressure
gradually falls, until the ventricles are no longer maximally
filled at diastole. Further increase in pacemaker rate above
that level causes no more increase in output and no further drop
in the venous pressure, as ventricular capacity is no longer
restrictive to flow. A rate of 60 produces this plateau in most
adults at rest and in a recumbent position. If the patient is
active, the pacemaker rate may need to go to 80 or even 100
before further increases in pacemaker rate cause no
corresponding increase in cardiac output. When the rate is fixed
at 80 and the patient is resting, the output goes down normally
with a waste of energy expended by the heart, the excess not
being used for circulation. The rate of 80 allows a great
variation in activity without exceeding a need for pulse
increase to prevent failure. If the pacemaker is set at 120,
such a rate would probably accommodate cardiac output for any
violent activity. However, at rest, even though the output goes
down to normal, the 120 pulse tachycardia is uncomfortable, the
excess myocardial energy waste is great, and myocardial oxygen
availability may be taxed. Therefore, fixed pacemaker rates are
usually set at about 76 to 80 as a compromise between excess
myocardial energy spent for circulation at rest and needed
cardiac energy for strenuous activity.
From pacemaker experience we conclude that: (1) The heart,
when not in failure, is always expending excess energy over that
necessary to produce cardiac output. (2) The ability to lower
pulse rate below maximum during periods of low cardiac output
has implications for energy conservation rather than cardiac
output.
LEFT VENTRICULAR
BOOSTER PUMPING
Myocardial energy failure is a frequent finding during acute
myocardial infarction and for short periods of time after coming
off of bypass after open heart surgery. In both of these
situations, left ventricular booster pumping has proved useful
during a recovery period.
A competent, passive filling, pulsatile outflow, continuous
inflow assist pump, placed between the left atrium and aorta
will automatically lower the left atrial pressure and restore
circulation rate to normal. A passive filling booster pump,
which expends excess energy, put in parallel with the failing
left ventricle, will make the combined output of the two normal.
The combined output of two non-sucking pumps in parallel will
act as one pump which produces excess to that needed for normal
cardiac output. Their combined output will be controlled by the
extra-cardiac factors that normally control circulation rate.
Whatever amount the ventricle is unable to pump will run
automatically into the booster ventricle and be ejected into the
aorta. When the heart has recovered, the left atrial and
arterial blood pressure will remain the same whether the pump is
on or off. One method of weaning the patient off of the booster
pumping is to raise the pump a few centimeters above the left
atrium. Blood will then run preferentially into the heart's
ventricle and be pumped out by it, if the heart is no longer in
power failure. If the ventricle is still in failure, the venous
pressure will rise only those few centimeters. Then whatever the
heart does not pump the booster pump will.
From cardiac booster pumping, we conclude that the
non-failing heart is expending excess energy to that needed at
any moment to produce its output. Expenditure of energy by a
parallel passive filling booster pump cannot increase the
circulation rate above that dictated by extra-cardiac
determinants.
SUMMARY: The
cardiovascular system is a closed elastic circle,
containing two passive filling pumps in series with two
vascular beds, systemic and pulmonary. Normally, the
circulation rate made by the two pumps is controlled by
mean cardiovascular pressure and inlet impedance. It is
only during heart failure, when heart function is
limiting the cardiac output, that the heart is
regulating circulation rate. |
|
|
Open-Heart Surgery with
Passive Filling Pumps |
The advent of
open-heart surgery has provided a wealth of data and
observations regarding cardiovascular physiology. Furthermore,
our expanding ability to correct cardiovascular defects has been
a stimulus to better understand how the system works.
Delineation of the essential mechanical features of the heart
has allowed construction of heart replacement pumps that: (1)
automatically provide normal circulation during heart bypass,
with the flow rate remaining under control of normal
physiological mechanisms; (2) allow research, in animals, by
isolating the peripheral vascular versus cardiac effect on
circulation rate from responses to various drug, humeral, and
neural stimuli; and (3) provide a mechanical model having the
ten unique characteristics of the cardiovascular system, for
teaching and the study of circulatory phonomena.
THE MECHANICAL
HEART
REPLACEMENT PUMPS
The pumps have the four characteristics in common with the
heart that allow them automatically, without pump regulation, to
reproduce circulation under control of normal physiologic
mechanisms: (1) The pumps fill passively and don't suck at their
inlets. (2) The output of the pumps is pulsatile. (3) The pumps
have atria that allow uninterrupted inflow to the intermittent
outflow pumps. (4) The capacity of the pump ventricles is
greater than any anticipated diastolic filling.
Many designs of pumps with the above characteristics could be
made. One of the six variations that the author has used is
shown in Figure
4. The pump consists of a flat atrial-ventricular silicone
rubber tube with a reinforcing flat cotton cover (Fig.
5). The flat configuration, which prevents rebound to a
round cross-section after being compressed, is responsible for
the passive filling characteristic. The tube is mechanically
compressed, sequentially, by four plates activated by cams and
lifters (Fig. 6).
Two narrow plates act as inlet and outlet valves to the
ventricular portion of the tube. Two wide plates act as atrial
and ventricular impellers (Fig.
4). The atrial impeller compression and sequence are
critical in preventing interruption of venous inflow when the
ventricles are being emptied. Therefore, atrial compression is
incomplete, leaving the atria with a 3/16" channel at maximum
compression. The slope of the atrial cams is gentle, to prevent
any sharp rise in pump atrial pressure that might interrupt
venous flow. The cam's timing is such that the "compression let
go" occurs just before the inlet valve closes.
CLINICAL SURGERY
USING THE
HEART-SIMULATING PUMP
Cardiac surgery using both right and left heart bypass pumps
has one significant advantage over conventional cardiopulmonary
bypass: No oxygenator is used, as the lungs are left in the
perfusion circuit and are provided with normal circulation. With
normal pulmonary blood flow during the operation, post-operative
pulmonary insufficiency is less of a problem than when the lungs
are bypassed using an oxygenator.
By connecting the unique pumps in parallel to the heart's
ventricles and with the pumps at heart level, cardiac function
can be temporarily interrupted during surgical procedures
without any interruption in normal circulation. When both the
heart and bypass pumps are functioning simultaneously, the
combined output remains the same as when the heart alone is
pumping. Because both fill passively, the combined output
remains regulated by the mean cardiovascular pressure and inlet
impedance. Any amount that goes to the pumps doesn't go to the
heart, and vice versa. If the heart function is then
interrupted, by induced fibrillation or diversion of all the
venous flow from one or both ventricles, the flow automatically
goes to the pumps and circulation is uninterrupted and continues
at the same rate. Subsequently, when the heart is defibrillated,
or when the flow to the heart is no longer interrupted, the
heart output takes over part of the circulation, with the total
circulation rate still remaining the same. Weaning off of bypass
is done simply by sequentially elevating the pumps a few
centimeters at a time, thereby diverting more and more of the
venous flow to the heart. Myocardial competence to take over the
entire circulation becomes evident if the circulation rate and
blood pressure remain unchanged after the incremental elevations
are made. By appropriate elevation of the pumps above heart
level, booster pumping can be done to maintain any desired
atrial pressure in the heart during a recovery period.
The advent of open-heart surgery has provided a wealth of
data and observations regarding cardiovascular physiology.
Furthermore, our expanding ability to correct cardiovascular
defects has been a stimulus to better understand how the system
works. Delineation of the essential mechanical features of the
heart has allowed construction of heart replacement pumps that:
(1) automatically provide normal circulation during heart
bypass, with the flow rate remaining under control of normal
physiological mechanisms; (2) allow research, in animals, by
isolating the peripheral vascular versus cardiac effect on
circulation rate from responses to various drug, humeral, and
neural stimuli; and (3) provide a mechanical model having the
ten unique characteristics of the cardiovascular system, for
teaching and the study of circulatory phonomena.
THE MECHANICAL
HEART
REPLACEMENT PUMPS
The pumps have the four characteristics in common with the
heart that allow them automatically, without pump regulation, to
reproduce circulation under control of normal physiologic
mechanisms: (1) The pumps fill passively and don't suck at their
inlets. (2) The output of the pumps is pulsatile. (3) The pumps
have atria that allow uninterrupted inflow to the intermittent
outflow pumps. (4) The capacity of the pump ventricles is
greater than any anticipated diastolic filling.
Many designs of pumps with the above characteristics could be
made. One of the six variations that the author has used is
shown in Figure
4. The pump consists of a flat atrial-ventricular silicone
rubber tube with a reinforcing flat cotton cover (Fig.
5). The flat configuration, which prevents rebound to a
round cross-section after being compressed, is responsible for
the passive filling characteristic. The tube is mechanically
compressed, sequentially, by four plates activated by cams and
lifters (Fig. 6).
Two narrow plates act as inlet and outlet valves to the
ventricular portion of the tube. Two wide plates act as atrial
and ventricular impellers (Fig.
4). The atrial impeller compression and sequence are
critical in preventing interruption of venous inflow when the
ventricles are being emptied. Therefore, atrial compression is
incomplete, leaving the atria with a 3/16" channel at maximum
compression. The slope of the atrial cams is gentle, to prevent
any sharp rise in pump atrial pressure that might interrupt
venous flow. The cam's timing is such that the "compression let
go" occurs just before the inlet valve closes.
SPECIFIC
APPLICATIONS OF THE
MECHANICAL PUMPS
Coronary Bypass Surgery:
Cardiac bypass during coronary surgery is used to provide a
non-moving target with decompressed ventricles and the security
that adequate circulation is being maintained during
manipulation of the heart. Coronary artery surgery is not an
open heart procedure, as the coronary arteries are on the
surface of the heart. Therefore, closed bypass is applicable.
Four cannulae are used. One pump is connected from the left
atrium to the aorta, and the other from the right atrium to the
pulmonary artery (Fig.
7).
It is important to start the left-sided bypass before the
right. If the right one is started and the heart happens to
fibrillate before the left bypass is started, blood will be
pumped into the pulmonary circuit while no blood is leaving it.
The result would be acute pulmonary engorgement ("liver lungs")
with a fatal outcome. Likewise, the left-sided bypass should be
discontinued last.
The heart is electrically fibrillated while the
coronary-graft anastomoses are made. Then the heart can be
defibrillated before the aorta-graft anastomoses are made. If,
during the coronary-graft anastomoses, greater decompression of
the ventricles is desired, the atrial cannulae can be advanced
into the ventricles to drain them as well as the atria.
Figure 8
shows arterial blood pressures staying relatively constant
before and during a coronary bypass procedure, using right and
left heart bypass.
During cardiac bypass with the two pumps, with the lungs
functioning and without the use of an oxygenator, the
anesthesiologist maintains ventilation and support of
circulation just as he would in other non-cardiac procedures.
Circulation rate reacts to blood loss, fluid infusion, and
vasoactive drugs, just as when the heart is functioning.
Pulmonary Stenosis:
While it might appear that pulmonary stenosis could be
repaired by using a right-sided bypass alone, one laboratory
experience has demonstrated this to be too hazardous for
clinical application. During the course of a right heart bypass,
with the left ventricle functioning, the heart unexpectedly
fibrillated. With the left ventricle suddenly not pumping, and
before the right heart bypass pump could be turned off and the
heart defibrillated, the lungs became irreparably overloaded
with blood. The resulting "liver lungs" were not reversible,
causing the death of the animal. Therefore, for safety, total
heart bypass is always used, even when a right heart bypass
alone could allow adequate access for correction of the lesion.
Use of a Passive Filling Pump with a Bubble Oxygenator:
During open-heart surgery, two pump bypass is precluded
because of the difficulty in bypassing the left atrium, with its
many pulmonary veins. Therefore, cardiopulmonary bypass with an
oxygenator is necessary whenever the cardiac chambers need to be
opened.
The passive filling, pulsatile output, continuous inflow pump
has advantages over other types of pumps when used in a
pump-oxygenator circuit. It can automatically produce normal
circulation rate with a normal pulse wave, without any control
adjustments, and without the hazard of oxygenator blood level
fluctuations or air emboli.
If the inlet of the pump is placed at the priming level in
the oxygenator (Fig.
9), because the pump is non-sucking, the blood will never
fall below that level. Any blood that runs into the oxygenator
that would tend to raise the level is automatically pumped back
into the patient. The oxygenator is positioned at such a level
that normal venous pressure is maintained by gravity drainage
during bypass.
With this pump-oxygenator setup, circulation rate is
determined by the patient's mean cardiovascular pressure and
inlet impedance, just as it does in the intact body. During the
bypass, circulation rate is modified by using vasoactive drugs,
blood and fluid replacement to change the mean cardiovascular
pressure, not by pump alteration.
This technique — beginning partial bypass in parallel with
the heart — results in normal circulation rate, as both the
heart and the extra-corporeal system fill passively. When
complete bypass is produced, by occluding the vena cava around
the caval catheters, the circulation rate remains the same.
Terminating bypass is very simple. The occluding tapes around
the vena caval tubes are released and the venous drainage tubing
is occluded in increments. As more and more blood is diverted to
the heart, the venous pressure will indicate whether or not
further decrease in extra-corporeal pumping will be tolerated.
In this way, the pump-oxygenator can be used as an automatic
booster device during the myocardial reovery period, following
the cardiac repair procedure.
Figure 10
shows the blood pressure before, during, and after bypass,
including the parallel bypass at the end of the procedure, in a
patient with wide-open aortic insufficiency. The wide, abnormal
pulse wave of aortic insufficiency is followed with a normal
pulse wave while on bypass and after valve replacement.
Figure 11
shows typical pulse waves during bypass and
Figure 12
shows superimposed waves during circulation produced by parallel
pumping of the heart and extra-corporeal pump.
Figure 13
illustrates a safety feature of the passive filling pump used
with an oxygenator. Bypass was just underway, during a mitral
valve replacement, when the inferior vena cava cannula slipped
back into the right atrium. The inferior vena cava being
temporarily occluded by the circumferential tape, caused the
venous drainage to the pump to drop to one liter per minute. The
oxygenator did not run out of blood and no air was pumped into
the patient during this low output episode. After the tube was
re-advanced properly into the inferior vena cava, the blood flow
to and from the pump automatically returned to normal.
The Non-Sucking Pump Used with a Membrane Oxygenator:
The non-sucking heart replacement pump is ideal for use with
a membrane oxygenator. It automatically allows a constant blood
volume in the system with this closed-volume oxygenator. There
is no need for a reservoir for volume monitoring of changing
blood levels, which would occur and require alteration of pump
rate with other types of pumps. In effect, the passive filling,
continuous inflow pump used with a membrane oxygenator provides
a closed automatic bypass system.*
*NOTE:
In all clinical applications of passive filling pumps,
it is important to use large caliber venous drainage
tubing so as not to add to the vascular system's normal
inlet impedance to the pumps. |
Pulsatile Blood Flow During Bypass Surgery:
Cardiac bypass during heart surgery has given an opportunity
to observe the benefit of pulsatile blood flow, by comparing it
with techniques using non-pulsatile flow. Pulsatile flow ensures
diffuse normal distribution of blood flow to all the organs and
tissue of the body, while non-pulsatile flow results in reduced
flow to certain vascular beds and excessive flow to others. With
non-pulsatile flow, the brain and kidneys receive reduced blood
supply. Also, incomplete metabolism from islands of under-perfused
tissue results in acidosis, not found when pulsatile flow is
provided. When hypothermia is used, the need of pulsatile flow
to insure diffuse distribution of circulation is increased.
While the adverse effects of non-pulsatile flow can be offset by
the use of vaso-relaxers, blood dilution, and other methods, the
value of pulsatile flow in normal function is illustrated by
comparing findings from the two types of pumping systems.
Ventricular Compliance — an Inlet Impedance Factor:
Open-heart surgery on a patient with severe hypertrophy of
the left ventricle, from longstanding aortic stenosis,
illustrated how ventricular compliance can be a factor in the
inlet impedance determination of cardiac output. This patient's
left ventricle measured three-fourths of an inch in thickness.
After replacement of the aortic valve, the bypass was
discontinued. The heart contracted very strongly, with a normal
pulmonary venous pressure of 12 cm. water. However, there was
practically no cardiac output and the blood pressure remained at
only 55/25. The blood volume was, therefore, increased by
increments while watching the pulmonary venous pressure go to
16, 18, 20, 25, and 30 cm., with no effect on output or blood
pressure. The heart continued to beat very forcibly. Suddenly,
at a pulmonary venous pressure of 35 cm., almost at the point of
causing pulmonary edema, the heart distended during diastole,
cardiac output went beyond normal with a resulting blood
pressure of 160/90. The non-compliance of this thick ventricle
was a significant impediment to passive filling and cardiac
output. |
|
Hydraulic Model of the Cardiovascular System |
A model, incorporating many of the unique characteristics of the
cardiovascular system, allows the opportunity to observe the
significance of each of those features. The characteristics
reproduced in the model are: (1) the hydraulic system is a
circle; (2) it is an elastic system, (3) it is filled with fluid
producing a mean pressure; (4) there are two pumps in series
between two vascular beds; (5) the pumps fill passively; (6)
pump output is intermittent; (7) the pumps have atria that allow
continuous, unimpeded flow to the pumps; (8) the pumps are
capable of pumping out a greater volume than the system will
produce; and (9) there are resistance points near the pumps'
inlets as well as near their outlets.
Studying the model has an advantage over studying in vivo
preparations in that the effect of altering one variable at a
time can be directly observed. Furthermore, the model eliminates
the possibility that some simultaneous, hidden, undetected
change might have occurred that would invalidate cause and
effect conclusions (Fig.
37). The model has proven to be a very effective study and
teaching tool.
The Model:
Figure 38
shows the layout of the model pictured in
Figure 39.
The Pumps:
The model pumps share the three unique characteristics of the
heart: They are non-sucking, and therefore fill passively at
their inlets, they have a pulsatile outflow, and they have atria
which allow uninterrupted inflow to the intermittent, pulsatile
outflow ventricles.
Figure 40
shows one of the two assembled pumps.
Figure 41
shows the unassembled parts of a pump.
The atrial and ventricular pump chambers consist of a rigid
side (Fig. 41
at A) and an opposing pliable silicone rubber side (Fig.
41 at B). The ventricular half of the rigid side has both an
inlet and an outlet port containing inlet and outlet valves,
respectively. The atrial half of the rigid side has a single
port with no valve. There is a "Y" connection between the atrial
port, inlet port to the ventricle and the venous line. This "Y"
inlet allows venous fluid to run both into the atrium, when the
inlet ventricular valve is closed during systole, and into the
ventricular chamber during both ventricular diastole and atrial
systole. This arrangement reproduces the "atrial effect" by
allowing continuous uninterrupted flow from the veins to the
intermittent outflow ventricles, thus preventing the need of
overcoming inertia by starting stopped flow after each pump
beat.
The impeller part of the pump also consists of a rigid side (Fig.
41 at E) and an opposing pliable rubber side (Fig.
41 at D). Each half of the rigid part has a port through
which air can be forced into or sucked out of the impeller
chambers. When the impeller chambers are inflated, their rubber
side exerts pressure on the silicone rubber side of the
ventricle or atrial chambers, thus emptying the ventricle or
atrium.
A spacer (Fig.
41 at C), placed between the opposing impeller and pumping
chambers, has many side holes which allow air to pass freely to
and fro between the ambient air and the space between the
impeller and pump ventricles. This free communication prevents
any negative pressure, caused by suction used to deflate the
impeller spaces, from being transmitted to the pump ventricles.
Thus, the ventricles fill passively from venous pressure.
The power supply to the pumps is from compressed air and
vacuum sources, delivered alternately to the impeller spaces
timed in the desired sequence. An electronic regulator triggers
solenoid valves to control pulse rate and the ratio of systole
to diastole. The pulse rate is variable from 1 to 160 strokes
per minute at an impeller pressure of one to thirty p.s.i.
Reducer valves regulate peak pressure and onset to peak time.
Impeller deflating suction is strong enough that passive
ventricular filling is not impeded.
Simulated Vascular Network:
The major vessels are silicone tubing, while the capillary
beds are made of more compliant Penrose drain material. Variable
resistance points are at various sites in both arterial and
venous lines. Pressure transducers connect to a direct writing
recorder and pressure tubes connect to an electromagnetic flow
meter. A transfusion reservoir provides opportunity to change
the fluid volume within the system. Different weights placed on
a plate resting on the "capillary beds" allow changes in the
system compliance to be made. The system was filled with water.
Hundreds of pieces of #0 silk suture material, 2 millimeters in
length (found to be isobaric with water), were suspended in the
water to allow visualization of the circulation.
MODEL FINDINGS
CORRELATE WITH OBSERVATIONS IN HUMAN PHYSIOLOGY:
EXPERIMENT #1
The relationship of mean cardiovascular pressure to volume in
the system
With the pumps turned off, the compliance remaining
unchanged, and starting with the system full of water, at a
volume of 2000 cc. at a pressure of zero, pressure was recorded
as fluid was added by way of the transfusion reservoir.
Figure 43
shows the non-linear relationship between the mean system
pressure and the volume.
EXPERIMENT #2
The relationship of circulation rate to mean system pressure
Starting with a mean system pressure of zero, and with
arbitrary settings of the resistance points, the pumps were
started. Appropriate amounts of fluid were added to increase the
mean system pressure by increments of 2 cm. water pressure (Fig.
44)
Findings:
- Figure
44 shows a direct correlation between pump output and
mean system pressure over the range of 0 to 20 cm. of water
pressure. The greater the mean system pressure, the greater
the pumps' output.
- At no time, over the range of pressure studied, did the
ventricles fill to capacity at diastole. There was always a
"pump capacity excess."
- At no time was there any interruption of venous flow by
the intermittent closing of the inlet valves of the
ventricles at systole, as the atria had been emptied during
ventricular diastole.
EXPERIMENT #3
Pump rate correlation with pump output
The pump rate in the model was varied from 0 to 170 beats per
minute with other variables remaining constant (Fig.
45). The mean system pressure was kept at 12 cm. water
pressure, with the impeller pressure at 14 p.s.i. and the
resistance kept constant.
Findings:
- At pump rates between 0 and 20/min.:
- The pump output correlated in a linear way with the
pump rate (Fig.
45, from A to halfway to B).
- The ventricles filled to capacity at each
ventricular diastole.
- The atria filled to capacity during each ventricular
systole.
- At pump rates between 20 and 40/min.:
- The pump rate correlated in a non-linear way with
the pump output (Fig.
45, from halfway in between A and B, to B).
- The ventricles filled slightly less than capacity at
ventricular diastole.
- The atria were filled to capacity at the end of
ventricular systole.
- Venous flow was slowed but not completely
interrupted before the end of ventricular systole.
- Increasing the pump rate from 50 to 110:
- Caused no increase in pump output (Fig.
45, B to C).
- Was associated with progressive decrease in
ventricular end-diastolic volume.
- Caused progressive decrease in atrial diastolic
volume.
- Was unaccompanied by any interruption in venous
flow.
- The pump rate and stroke volume were reciprocals of
one another.
- Increasing the pump rate from 110 to 170 beats/min. (Fig.
45, C to D) was accompanied by a progressive increase in
residual air pressure in the ventricular impeller after
ventricular systole which:
- Progressively decreased pump output.
- Impeded ventricular filling at ventricular diastole.
- Caused venous flow interruption at ventricular
systole.
EXPERIMENT #4
Ventricular impeller-force correlation with pump output
The ventricular impeller pressure was varied from 0 to 20
p.s.i., in increments of 2 p.s.i., while keeping other variables
constant (Fig.
46). The pump rate was 80, the mean system pressure was 12
cm. water pressure and all resistances remained unchanged.
Findings:
- At impeller pressures between 0 and 10 p.s.i. there was:
- Linear correlation between impeller pressure and
pump output (Fig.
46, from A to B).
- The ventricles were never completely emptied at
ventricular systole.
- The ventricles were completely filled at ventricular
diastole.
- Venous flow to the pumps was interrupted at each
ventricular systole.
- At impeller pressures between 10 and 18 p.s.i. there
was:
- No increase in the output as the pressure increased
(Fig.
46, from B to C).
- Maximal ventricular emptying at systole.
- Sub-maximal filling of the ventricles at diastole
- No venous flow interruption at any time.
- As the impeller pressure was progressively increased
above 18 p.s.i. (Fig.
46, from C to D) there was progressively incomplete
evacuation of compressed air in the ventricle during
diastole which:
- Progressively decreased pump output.
- Impeded ventricular filling at diastole.
- Caused venous flow interruption at ventricular
systole.
EXPERIMENT #5
Relationship of resistance to pump output
Resistance at a variety of sites was changed in the model's
vascular network while maintaining other factors constant, with
the mean system pressure at 12 cm. water pressure, pump rate at
80 beats per minute, and an impeller pressure of 16 p.s.i. There
was a marked difference in response to a given resistance
depending on where the resistance was placed in the model.
Responses fell into two categories which became more obvious the
closer the resistance was to either the inlet or outlet of a
pump. Therefore, resistance was studied in two situations: near
a pump inlet, where there was a large compliant bed upstream;
and near a pump outlet, with no compliant bed upstream.
Relationship of Resistance Near a Pump Outlet to Pump
Output: (Fig.
47)
A variable resistance clamp was placed 20 cm. from the left
heart homologue pump outlet (Fig.
38, #9), across which a pressure gradient could be monitored
by transducers (Fig.
38, #8).
Findings:
- As the resistance is progressively increased (Fig.
38, #9), the superimposed arterial pressure
tracings, which demonstrated no gradient initially (Fig.
47 at A), separated as resistance was added (Fig.
47, from A to C).
- With increase in outflow resistance up to 100 mm.
Hg. gradient, there was no drop in pump output (Fig.
47 at C).
- Further increase in gradient from 100 to 250 mm. Hg
did cause a corresponding drop in flow (Fig.
47, from C to D).
- In the range where there was no drop in flow (Fig.
47, A to C), the left ventricle did not fill
maximally, but did empty maximally, and there was no
interruption of venous flow at any time during the
pumping cycle.
- However, when the gradient became great enough that
the flow slowed (Fig.
47, C to D), the left ventricle progressively
emptied less completely, and the residual volume
resulted in complete left ventricular filling at
diastole and interruption of venous inflow at each
systole.
- Whenever the left ventricle was being filled
completely at diastole, increasing the mean system
pressure caused no concomitant increase in pump output.
- As slowing of flow occurred (Fig.
47, C to D), there was gradual increase in a greater
than previous volume in the pulmonary circuit at the
expense of the systemic circuit. The greater the
slowing, the more the volume equilibrium shifted to the
simulated pulmonary circuit.
The Effect of Resistance Near a Pump Inlet on Pump
Output: (Fig.
48)
An adjustable resistance clamp was placed 20 cm. from the
left pump's inlet (Fig.
38, #7), across which a pressure gradient could be monitored
using the transducers (Fig.
38, #6). The clamp was progressively closed. The resulting
inflow resistance magnitude is represented by the pressure
gradient between the transducers.
Figure 48
shows the two superimposed pressure lines (Fig.
48, A to B) in the absence of resistance. When resistance is
progressively increased, starting at B, a pressure gradient
becomes evident (Fig.
48, B to C).
Findings:
- There was a direct inverse correlation between pump
output and inflow resistance to the pump (Fig.
48, B to C) over the whole range studied. This is in
marked contrast to outflow resistance of the previous
experiment (Fig.
47, B to C), where decrease in flow did not occur
until there was pump failure.
- As inlet resistance increased there was
progressively less filling of the ventricles at
diastole. Maximal emptying did occur at each ventricular
systole, and venous flow remained uninterrupted at all
times.
- Progressive increase in left pump inflow resistance
shifted the fluid equilibrium between the pulmonary and
systemic circuits toward the pulmonary bed.
- The circuit with the greatest inflow resistance was
the major determinant of the output of both.
EXPERIMENT #6
The Atrial Effect
In the model, to eliminate the atrial effect, the air
pressure in the atria can be left continuously obliterating the
atrial chambers, while not impinging on the connection of the
venous tubes to the ventricles. By intermittently producing
circulation with and without the atrial effect, its contribution
to pump output was determined. At pump rates between 60 and 90
there was four times the pump output (2400 cc./min.) with the
atria functioning as with no atrial effect (600 cc./min.). The
output without atria progressively decreased as the rate was
increased. At 130 beats per minute, flow stopped completely. It
is demonstrated that atria markedly increase flow when used with
pulsatile, passively filling pumps. They prevent inertia, which
would otherwise occur if the inlet valves were allowed to stop
venous flow at each beat.
EXPERIMENT #7
Pulsatile Flow
A branching hydraulic system was made with twenty, 3/16 inch
diameter, transparent tubes, six to twelve inches in length,
linked together with "Y" connectors in the configuration of a
simulated vascular bed.
Findings:
- With pulsatile flow there was flow in all parts of the
system. It fairly danced with the pulsation. There were
areas where flow was in one direction during most of the
cycle and reversed in the other direction for the rest of
it. With pulsatile flow, the distribution remained stable
for a long period of time.
- With continuous non-pulsatile flow, the distribution
started out in a diffuse manner. Very shortly, some channels
had higher flow than others. Yet there was some flow in all
of them. However, within a short time the 2 mm. silk
particles began clustering at "Y" junctions, eventually
totally blocking some and partially blocking others. Before
long, almost all of the flow was in just a few channels and
very little was in the others. When pulsatile flow then
replaced the steady flow, the aggregates of silk were broken
up, the whole bed began dancing with the pulse, and flow was
again established in a diffuse manner, with flow fairly
equal in all channels.
Conclusion:
There is obviously a difference in the mechanism of
aggregation of silk particles in this system and the
mechanism that caused poor distribution with non-pulsatile
flow in the animal in the previous chapter. However, this
experiment does show that the simplest way to guarantee
diffuse, equal distribution of fluid in a hydraulic system
is to make flow pulsatile.
THE MODEL AS A
TEACHING TOOL
An example of the teaching and learning benefit of the
model is illustrated by an incident. One day I had scheduled a
replacement of an aortic and mitral valve in a woman who had
severe mitral and aortic stenosis. The student on my service
came to me and said, "This woman is so critically ill that she
may have difficulty surviving such a big operation. Maybe it
would be the better part of valor to correct only one valve.
Then, when she is better, go back and replace the other one." I
asked him which valve he thought I should replace first. He
responded that he would go to the model and put an inlet and
outlet obstruction on the circuit. Then remove one and then the
other and see what improvement would result from a single
obstruction removal. When he only removed the inlet obstruction,
the increased flow to the pump put it into power failure. When
he removed only the outlet obstruction it decreased the workload
of the pump, but the output didn't increase.
We would have sealed the woman's fate if we had corrected
only one of the valves. She would have remained in low output
failure if we had corrected the aortic valve alone; and she
would have gone into acute left ventricular failure if we had
relieved the mitral stenosis alone. Therefore, we replaced both
valves and the patient made an excellent recovery.
The close
correlation of model findings to physiological
observations in man makes the model useful in
understanding how the cardiovascular system works, and
helps to anticipate cause and effect in human
physiology. |
|
|
The significance of ten unique characteristics of the
cardiovascular system has been demonstrated by clinical
observations, cardio-bypass data, animal mechanical heart
replacement experiments, and a simulated cardiovascular model.
All of the evidence validates that:
- The cardiovascular system is a circle containing a
mean cardiovascular pressure dependent upon volume and
compliance.
- The heart is a passively filling pump.
- Atria increase cardiac output by causing continuous
venous flow to the intermittently contracting
ventricles, not by pumping up the ventricles.
- Circulation rate is normally determined by the
extra-cardiac factors: mean cardiovascular pressure and
inlet impedance.
- It is only during heart failure that the heart is
the regulator of cardiac output.
|
|
Clinical Determination of Mean-Cardiovascular Pressure |
A useful approximation of the mean-cardiovascular pressure can
be made without the need of stopping the heart and letting the
pressure equalize in the entire cardiovascular system. The
assumption is made that the same pressure would be found by
isolating a representative sample of the arteries, capillaries,
and veins at ventricular diastole, and letting the pressure
equilibrate in that sample. By instantaneously interrupting
arterial inflow to the arm and venous outflow from it, the
pressure will fall in the arteries and rise in the veins until
they are equal. This equalized pressure, which will occur within
30 seconds, approximates that found when circulation is stopped
in the entire body.
Equipment:
A narrow pneumatic blood pressure cuff (approximately one
inch in width) is used so that during inflation it will not
displace any blood volume distally into the arm.
A one liter air pressure reservoir, pressurized to 300 mm.
Hg, is connected to the pressure cuff with a valve interposed to
allow instantaneous inflation of the cuff. The reservoir is
pressurized by a regular blood pressure inflating bulb and
valve, interposed with a "Y" connecter between the reservoir and
the valve.
Two pressure transducers and recorders are needed, to allow
pressure recording without any loss of fluid from the vascular
bed, which would occur with a simple manometer system.
Technique:
- The patient should be lying perfectly horizontal.
- Both an artery and a vein are cannulated at the
antecubital area of the arm and connected to the pressure
transducers.
- The blood pressure cuff is applied above the biceps
bulge of the arm. It must be applied loose enough that it
does not cause any venous obstruction, as evidenced by the
observation that it produces no elevation of venous pressure
above that seen before its application.
- The cuff must be applied tight enough that its
inflation, to 300 mm. Hg pressure, completely interrupts the
arterial flow to the arm. Complete interruption can be
assumed if arterial and venous pressure approach
equalization after 30 seconds, and do not continue to rise
thereafter.
- The arm should be abducted sufficiently from the side of
the body, so as to obtain the lowest venous pressure
reading, thereby being certain that any abduction is not
mechanically interfering with venous flow in the axilla.
- The arm should be horizontal, with the anterior surface
of the antecubital skin at mid- chest position.
- The thickness of the chest should be accurately
measured. The pressures are small, so careful
standardization is necessary in order to get meaningful
data.
- The patient is instructed to leave the arm perfectly
relaxed, and not to contract any muscle.
- The valve or switch in the pressure line is turned,
thereby inflating the cuff, which simultaneously interrupts
venous and arterial flow to and from the arm.
Pressure readings are made 30 seconds after the occlusion. As
the equalization process progresses, the pressure gradient
becomes so small between the arteries and veins that the
pressures may never completely equalize. However, the average of
the arterial and venous pressures recorded at 30 seconds can be
interpreted as the mean-cardiovascular pressure.
Establishing such a standardization makes these approximate
readings clinically useful. In any low arterial blood pressure
situation, the mean-cardiovascular pressure indicates whether
the problem is from low blood volume or myocardial failure.
Mean-cardiovascular pressure is a diagnostic tool that can
separate high output hypertension from the more common
arteriolar resistance hypertension, thus indicating the proper
therapy regimen. |
|
Blood circulates through a network of vessels
throughout the body to provide individual cells with oxygen and
nutrients and helps dispose of metabolic wastes. The heart pumps the
blood around the blood vessels. Blood is made up of about 45% solids
(cells) and 55% fluids (plasma). The plasma is largely water, containing
proteins, nutrients, hormones, antibodies, and dissolved waste products.
Functions of blood and circulation:
- Circulates OXYGEN and removes Carbon Dioxide.
- Provides cells with NUTRIENTS.
- Removes the waste products of metabolism to the excretory organs
for disposal.
- Protects the body against disease and infection.
- Clotting stops bleeding after injury .
- Transports HORMONES to target cells and organs.
- Helps regulate body temperature.
General types of blood cells: (each has many different sub-types)
ERYTHROCYTES (red cells) are small red disk shaped cells. They
contain HAEMOGLOBIN, which combines with oxygen in the lungs and is then
transported to the body's cells. The haemoglobin then returns carbon
dioxide waste to the lungs. Erythrocytes are formed in the bone marrow
in the knobby ends of bones.
LEUKOCYTES (white cells) help the body fight bacteria and
infection. When a tissue is damaged or has an infection the number of
leukocytes increases. Leukocytes are formed in the small ends of bones.
Leukocytes can be classed as granular or non granular. There are three
types of granular leukocytes (eosinophils, neutrophils, and basophils),
and three types of non-granular (monocytes, T-cell lymphocytes, and
B-cell lymphocytes). See also the lymphatic system.
THROMBOCYTES (platelets) aid the formation of blood CLOTS by
releasing various protein substances. When the body is injured
thrombocytes disintegrate and cause a chemical reaction with the
proteins found in plasma, which eventually create a thread like
substance called FIBRIN. The fibrin then "catches" other blood cells
which form the clot, preventing further loss of blood and forms the
basis of healing.
ARTERIES carry oxygenated blood away from the heart. They are
thick hollow tubes which are highly ELASTIC which allows them to DILATE
(widen) and constrict (narrow) as blood is forced down them by the
heart. Arteries branch and re-branch, becoming smaller until they become
small ARTERIOLES which are even more elastic. Arterioles feed oxygenated
blood to the capillaries. The AORTA is the largest artery in the body,
taking blood from the heart, branching into other arteries that send
oxygenated blood to the rest of the body.
CAPILLARIES distribute the nutrients and oxygen to the body's
tissues and remove deoxygenated blood and waste. They are extremely
thin, the walls are only one cell thick and connect the arterioles with
the venules (very small veins).
VENULES (very small veins) merge into VEINS which carry
blood back to the heart. The vein walls are similar to arteries but
thinner and less elastic. Veins carry deoxygenated blood towards the
lungs where oxygen is received via the pulmonary capillaries. The
PULMONARY Veins then carries this oxygenated blood back to the heart.
The heart is a hollow muscular organ which beats over 100,000 times a
day to pump blood around the body's 60,000 miles of blood vessels. The
right side of the heart receives blood and sends it to the lungs to be
oxygenated, while the left side receives oxygenated blood from the lungs
and sends it out to the tissues of the body. The Heart has three layers;
the ENDOCARDIUM (inner layer), the EPICARDIUM (middle layer), and
MYOCARDIUM (outer layer). The heart is protected by the PERICARDIUM
which is the protective membrane surrounding it.
The heart has FOUR CHAMBERS, in the lower heart the right and left
Ventricles, and in the upper heart the right and left Atria. In a normal
heart beat the atria contract while the ventricles relax, then the
ventricles contract while the atria relax. There are VALVES through
which blood passes between ventricle and atrium, these close in such a
way that blood does not backwash during the pauses between ventricular
contractions. The right and left ventricles are divided by a thick wall
(the VENTRICULAR SEPTUM), babies born with "hole in the heart" have a
small gap here, which is a problem since oxygenated and deoxygenated can
blood mix. The walls of the left ventricle are thicker as it has to pump
blood to all the tissues, compared to the right ventricle which only
pumps blood as far as the lungs.
This is a large flat oval organ located below the diaphragm, it's main
function is to STORE BLOOD. The size of the spleen can vary, for example
it may enlarge when the body is fighting infection also it's size tends
to decrease with age. It is a non-vital organ and it is possible to
survive after removal of the spleen.
Perinicious anaemia is a Vitamin B12 deficiency resulting in a
reduction in number of erythrocytes.
Aplastic anemia is a failure of the bone marrow to produce the
enough red blood cells.
Septicaemia - bacterial toxins in blood.
component
|
meaning
|
example
|
CARDIO-
|
heart
|
echocardiogram = sound wave image of the heart.
|
CYTE-
|
cell
|
thrombocyte = clot forming cell.
|
HAEM-
|
blood
|
haematoma - a tumour or swelling filled with blood.
|
THROMB-
|
clot, lump
|
thrombocytopenia = deficiency of thrombocytes in the blood
|
ETHRO-
|
red
|
ehtrocyte = red blood cell
|
LEUKO-
|
white
|
leukocyte = white blood cell
|
SEP, SEPTIV-
|
toxicity due to micro-organisms
|
septicaemia
|
VAS- |
vessel / duct
|
cerebrovascular = blood vessels of the cerebrum of the
brain.
|
HYPER-
|
excessive
|
hyperglycaemia = excessive levels of glucose in blood.
|
HYPO-
|
deficient / below
|
hypoglycaemia = abnormally low glucose blood levels.
|
-PENIA |
deficiency
|
neutropenia = low levels of neutrophilic leukocytes.
|
-EMIA
|
condition of blood
|
anaemia = abnormally low levels of red blood cells.
|
- Overview of Haematological Malignancies
- The most common haematological malignancy is leukaemia - cancer
of the white blood cells. There are many types of leukaemia;
Acute types progress rapidly, while Chronic types develop
more slowly. Leukaemia is often accompanied by anaemia because the
red oxygen carrying cells in the blood are crowded out by the
cancerous white cells. There are a number of malignancies and
disorders affecting other types of blood cells.
-
Internet Resources for Leukaemia
- Acute Lymphoblastic Leukaemia (ALL)
- Acute lymphoblastic leukaemia (also known as acute lymphocytic
leukaemia or ALL) is a disease where too many immature lymphocytes
(a type of white blood cell) are found in the blood and bone marrow.
Symptoms can include persistent fever, weakness or tiredness,
achiness in the bones or joints, or swollen lymph nodes. Adult ALL
and its treatment is usually different to childhood ALL. Almost a
third of adult patients have a specific chromosome translocation;
"Philadelphia Positive" ALL.
-
Internet Resources for Acute
Lymphocytic Leukaemia
- Acute Myeloid Leukaemia (AML)
- Acute myeloid leukemia (AML) is a disease in which too many
immature granulocytes (a type of white blood cell) are found in the
blood and bone marrow. There are a number of subtypes of AML
including acute myeloblastic leukemia, acute promyelocytic leukemia,
acute monocytic leukemia, acute myelomonocytic leukemia,
erythroleukemia, and acute megakaryoblastic leukemia.
-
Internet Resources for Acute
Myeloid Leukaemia
- Other Types of Leukaemia
Chronic Lymphocytic Leukaemia
Chronic Myelogenous Leukaemia
Hairy Cell Leukaemia
-
Internet Resources for Leukaemia
- Childhood Leukaemia
- Childhood leukaemias tend to have different characteristics and
treatments compared to adult leukaemias. There is a "childhood peak"
of Acute Lymphoblastic Leukaemia, there is a lower proportion of
Acute Myeloid Leukaemias compared to adult patients. Clinical
prognostic factors include age, White Blood Cell count (WBC) at
presentation, and Central Nervous System (CNS) involvement. Infants
less than 1 year and adolescents over 10 years of age, WBC greater
than 50,000, or CNS involvement are associated with a less
favourable prognosis.
-
Internet Resources for Childhood
Leukaemia
- Other Haematological Malignancies
-
- - Myelodysplastic Syndromes
- Myelodysplastic syndromes, sometimes called "pre-leukaemia"
are a group of diseases in which the bone marrow does not
produce enough normal blood cells. Common symptoms are anaemia,
bleeding, easy bruisability, and fatigue. These Myelodysplastic
syndromes can occur in all age groups but are more common in
people aged over 60. Myelodysplastic syndromes may develop
spontaneously or be secondary to treatment with chemotherapy /
radiotherapy. There is an association with Myelodysplastic
syndromes and acute myeloid leukaemia.
- - Myeloproliferative Disorders
- Myeloproliferative disorders are diseases in which too many
blood cells are made by the bone marrow, there are 4 main types
of myeloproliferative disorders: chronic myelogenous leukaemia,
polycythemia vera, agnogenic myeloid metaplasia, and essential
thrombocythemia. Chronic myelogenous leukaemia is where an
excess of granulocytes (immature white blood cells) are found in
the blood and bone marrow. Polycythemia vera is where red blood
cells become too numerous often resulting in a swelling of the
spleen. Agnogenic myeloid metaplasia is a condition in which
certain blood cells do not mature properly, this may result in a
swelling of the spleen and anaemia. Essential thrombocythemia is
a disease in which the body produces excessive numbers of
platelets (cells in the blood that make it clot) which impedes
the normal circulation of blood.
- - Aplastic Anaemia
- Anaplastic Anemia is not a cancer. AA is a rare disease in
which the bone marrow is unable to produce adequate blood cells;
leading to pancytopenia (deficiency of all types of blood
cells). AA may occur at any age, but there is a peak in
adolescence / early adulthood, and again in old age. Slightly
more males than females are diagnosed with AA, also the disease
is more common in the Far East. Patients successfully treated
for aplastic anemia have a higher risk of developing other
diseases later in life, including cancer.
- - Fanconi Anaemia
- Fanconi Anaemia is not a cancer, it is a rare disorder found
in children that involves the blood and bone marrow. The
symptoms include severe aplastic anemia, hypoplasia of the bone
marrow, and patchy discoloration of the skin. Recent research
has shown an association between Fanconi anaemia and leukaemia.
- - Waldenstrom's Macroglobulinemia
- This is a rare malignant condition, involving an excess of
beta-lymphocytes (a type of cell in the immune system) which
secrete immunoglobulins (a type of antibody). WM usually occurs
in people over sixty, but has been detected in younger adults.
-
Internet Resources for
Haematological Malignancies
- French-American-British (FAB) Classification
Scheme
- Leukaemia can be classified using the French-American-British
(FAB) criteria. for cell morphology:
L1 - ALL: small lymphoid cells, regular nuclei
L2 - ALL: large lymphoid cells, irregualr nuclei
L3 - ALL: large homogeneous cells with prominent nucleolus
M1 - Myeloblastic leukemia without maturation
M2 - Myeloblastic leukemia with maturation
M3 - Promyelocytic leukemia
M4 - Myelomonocytic leukemia
M5 - Monocytic leukemia
M6 - Erythroleukemia
M7 - Megakaryoblastic leukemia
M0 - AML with minimal differentiation
- CNS Prophylaxis
- Leukaemia can sometimes spread to the spinal cord and brain
(Central Nervous System). Intrathecal chemotherapy (injection into
the fluid around the spine) may be given to combat or prevent CNS
relapse.
- Blood Counts
- Blood counts are done to test the number of each of the
different kinds of cells in the blood. This may be an aid to
diagnosis or done to monitor toxicity after each course of
chemotherapy. The next course of chemotherapy may be delayed until
white cells, neutrophils, and platelets have recovered to a safe
level.
- Cardiotoxicity
- Cardiotoxicity (damage to the heart) is associated with certain
anti cancer drugs, especially Adriamycin. As such the total dose of
these drugs may be limited to reduce the risk of cardiotoxicity.
- Echocardiagram
- An Echocardiogramis where an image of the heart is formed when
high frequency sound waves are reflected from the muscles of the
heart. An echocardiogram may be done before treatment starts to
establish a baseline from which to compare future tests.
- Metastases through the cardivascular system
- The network of blood vessels reach all parts of the body and may
provide one of the routes for cancer cells to spread to secondary
sites.
Related Abbreviations and Acronyms:
-
-
AA |
Anaplastic Anaemia
|
ALL |
Acute lymphoblastic leukaemia
|
AML |
Acute Myeloid leukaemia
|
ANC |
Absolute neutrophil count
|
ANLL |
Acute non-lymphatic leukaemia
|
ASH |
American Society for Hematology
|
B-ALL |
B-cell Acute Lymphoblastic Leukaemia
|
BP |
Blood pressure
|
CALGB |
Cancer and Leukemia Group B (USA)
|
cALL |
Common ALL
|
CGL |
Chronic Granulocytic Leukaemia
|
CHF |
Congestive heart failure
|
CLL |
Chronic lymphocytic Leukaemia
|
CML |
Chronic myeloid leukaemia
|
CMML |
chronic myelomonocytic leukemia
|
CPR |
Cardio pulmonary resuscitation
|
CVA |
Cardiovascular Accident (stroke)
|
CVC |
Central venous catheters
|
ECG |
Electrocardiogram - heart scan
|
FAB |
French American and British classification scheme for
leukaemia
|
FBC |
Full Blood Count
|
G-CSF |
Granulocyte colony stimulating factor promotes
production of white blood cells
|
GM-CSF |
Granulocyte and macrophage colony stimulating factor
|
Hb |
Haemoglobin
|
HCL |
Hairy Cell Leukaemia
|
HD |
Hodgkin's Disease (lymphoma)
|
HTLV |
Human T-cell leukemia-lymphoma virus
|
IV |
Intravenous - into a vein
|
LRF |
Leukaemia Research Fund (UK)
|
LVEF |
Left Ventricular Fjection Fraction - a heart function
test
|
LVSF |
Left Ventricular Shortening Fraction - a heart function
test
|
MM |
Multiple Myeloma
|
RBC |
Red blood cell / red blood count
|
WBC |
White blood cell count
|
WCC |
White cell count |
5-FU |
5-Fluorouracil (anti cancer drug)
|
6-MP |
6-Mercaptopurine (anti cancer drug)
|
6-TG |
6-Thioguanine (anti cancer drug)
|
AA |
Anaplastic Anaemia
|
ABC |
Advanced Breast Cancer
|
ABMT |
Autologous bone marrow transplant
|
ADR |
Adverse Drug Reaction
|
AE |
Adverse event
|
AFP |
Alphafetoprotein - eg. expressed by germ cell tumours
and other cancers
|
AIDS |
Acquired immune deficiency syndrome
|
ALAT |
Alanine aminotransferase / alinine transaminase
|
ALCL |
Anaplastic Large-cell Lymphoma
|
ALL |
Acute lymphoblastic leukaemia
|
ALT |
Alanine Aminotransferase
|
AMKL |
acute megakaryocytic leukemia
|
AML |
Acute Myeloid leukaemia
|
ANC |
Absolute neutrophil count
|
ANED |
Alive no evidence of disease
|
ANLL |
Acute non-lymphatic leukaemia
|
ARMS |
Alveolar rhabdomyosarcoma
|
ASR |
Age Standardised Rate (Incidence)
|
AUC |
Area under the curve
|
B-ALL |
B-cell Acute Lymphoblastic Leukaemia
|
BAER |
Brainstem Auditory Evoked Responce
|
BCC |
Basal Cell Carcinoma
|
BID / BD |
Twice a day (bis in die)
|
BM |
Bone Marrow
|
BM |
Blood Monitoring (eg for glucose)
|
BMJ |
British Medical Journal
|
BMR |
Basal Metabolic Rate
|
BMT |
Bone Marrow Transplant
|
BNF |
British National Formulary
|
BP |
Blood pressure
|
BRM |
Biological Response Modifier
|
BSA |
Body Surface Area
|
BSE |
Breast Self Examination
|
Bx |
Biopsy
|
C/O |
Complaining of
|
C/W |
Continue With
|
C1 - C7 |
Cervical vertebrae (spine eg. C7 = seventh cervical
vertebra)
|
Ca |
Cancer; carcinoma
|
Ca |
Calcium
|
cALL |
Common ALL
|
CAT |
Computerised axial tomography (scan)
|
cc |
Cubic centimeter
|
CCF |
Congestive Cardiac Failure
|
CCR |
Continuous complete remission
|
CEA |
Carcinoembryonic Antigen (tumour marker)
|
CGH |
Comparative Genomic Hybridisation - cytogenetics method
|
CGL |
Chronic Granulocytic Leukaemia
|
cGy |
Centi Gray (unit of radiation)
|
CHF |
Congestive heart failure
|
CLL |
Chronic lymphocytic Leukaemia
|
cm |
centimeter - 0.01 meters
|
CML |
Chronic myeloid leukaemia
|
CMML |
chronic myelomonocytic leukemia
|
CMV |
Cytomegalo virus
|
CNS |
Central nervous system - the brain and spine
|
CPM |
Cyclophosphamide (anti cancer drug)
|
CPR |
Cardio pulmonary resuscitation
|
CR |
Complete remission / complete response
|
CRA |
Clinical Research Associate
|
CRC |
Colorectal carcinoma
|
CRF |
Case Report Forms
|
CRF |
Chronic renal failure
|
CRO |
Contract Research Organisation
|
CSF |
Cerebro spinal fluid
|
CSF |
Colony-stimulating Factor
|
CT |
Computerised axial tumography (scan)
|
CT |
Chemotherapy
|
CTC |
Common Toxicity Criteria
|
CTCL |
Cutaneous T-Cell Lymphoma
|
CTO |
Clinical Trials Office
|
CTX |
Clinical Trials Exemption
|
CVA |
Cardiovascular Accident (stroke)
|
CVC |
Central venous catheters
|
CVP |
Central Venous Pressure
|
CXR |
Chest X-Ray
|
D/C |
Discharge
|
D/H |
Drug History
|
D/W |
Discussed With
|
DCIS |
Ductal Carcinoma In Situ - type of breast cancer
|
DDAVP |
Desmopressin test for urine osmolality
|
DDx |
Differential diagnosis
|
DFI |
Disease Free Interval
|
DFS |
Disease Free Survival - time without disease prior to
relapse or last follow-up
|
DI |
Diabetes Incipidus
|
dl |
deciletre - 0.01 litres
|
DLBCL |
Diffuse Large B-cell Lymphoma
|
DLCL |
Diffuse large-cell lymphoma
|
DLS |
Date last seen
|
DLT |
Dose limiting toxicity - determined by phase 1 studies
|
DMC |
Data Monitoring Commitee
|
DNA |
Deoxyribonucleic acid
|
DNA |
Did Not Attend (clinic)
|
DNR |
Do Not Resusitate
|
DOA |
Dead on Arival
|
Dx |
Diagnosis
|
EBM |
Evidence-Based Medicine
|
EBV |
Epstein-Barr Virus
|
ECG |
Electrocardiogram - heart scan
|
EDTA |
ethylendiaminetetraacetic acid - used in measuring
kidney function
|
EEG |
Electroencephalogram - brain scan
|
EFS |
Event Free Survival - time from diagnosis to defined
events (eg relapse or deat
|
EJC |
European Journal of Cancer
|
EMC |
Extraskeletal Myxoid Chondrosarcoma
|
EMUO |
Early Morning Urine Osmolality (evaluating urine
concentration)
|
ENT |
Ear nose throat
|
ESR |
Erythrocyte Sedimentation rate
|
ETS |
Environmental Tobacco Smoke
|
F/H |
Family history
|
FAB |
French American and British classification scheme for
leukaemia
|
FBC |
Full Blood Count
|
FEV |
Forced expectorant volume (a lung test)
|
FFA |
For Further Appointment
|
FIGO |
Federation Internat. Gyn. Obst. (FIGO Gynaecological
staging system)
|
FISH |
Flourescence in situ Hybridisation
|
FMTC |
Familial Medullary Thyroid Carcinoma
|
FNA |
Fine Needle Aspiration - a type of biposy using a thin
needle (or FNAB)
|
FU |
Follow up
|
FVC |
Forced Vital Capacity
|
g |
gram - unit of weight
|
G-CSF |
Granulocyte colony stimulating factor promotes
production of white blood cells
|
GA |
General Anaesthetic
|
GCP |
Good Clinical Practice (guidelines)
|
GCT |
Germ Cell Tumour
|
GCT |
Giant Cell Tumour Context: bone tumours
|
GFR |
Gromerular filtration rate
|
GI |
Gastrointestinal
|
GIST |
Gastrointestinal Stromal Tumours
|
GM-CSF |
Granulocyte and macrophage colony stimulating factor
|
GPR |
Good Partial Remission
|
GU |
Genito-urinary
|
GvHD |
Graft versus Host Disease
|
Gy |
Grays (units of radiation)
|
H&E |
Hematoxylin and Eosin (stain)
|
H/O |
History of
|
Hb |
Haemoglobin
|
HCC |
Hepatocellular Carcinoma
|
HCG |
Human Chorionic Gonadotrophin (hormone)
|
HCL |
Hairy Cell Leukaemia
|
HCO3 |
Bicarbonate
|
HD |
Hodgkin's Disease (lymphoma)
|
HD |
High dose
|
HDC |
High Dose Chemotherapy
|
HIV |
Human Immunodeficiency Virus
|
HL-A |
Human Leukocyte Associated antigens (HL-A matching for
BMT)
|
HNPCC |
Hereditary NonPolyposis Colorectal Cancer
|
HPV |
Human Papilloma Virus - implicated in some gynacological
cancers
|
HR |
High risk
|
HRT |
Hormone replacement therapy
|
HTLV |
Human T-cell leukemia-lymphoma virus
|
I-131 |
Radioactive Iodine
|
ICD |
International Classification of Diseases (coding system)
|
ICDO |
International Classification of Diseases for Oncology
(coding system)
|
ICF |
Intercellular fluid
|
ICU |
Intensive Care Unit
|
IL2 |
Interleukin2
|
IM |
Intramuscular - into a muscle
|
IMRT |
Intensity-Modulated Radiotherapy
|
INSS |
International Neuroblastoma Staging System
|
ITU |
Intensive Therapy Unit
|
IU |
International units
|
IV |
Intravenous - into a vein
|
IVP |
Intravenous Pyelogram - type of Xray after injection
with iodine dye
|
JCO |
Journal of Clinical Oncology
|
K+ |
Potassium
|
kg |
Kilogram - a thousand grams
|
l |
liter - unit of volume
|
L1 - L5 |
Lumbar vertebrae 1 - 5 (spine eg. L1 = 1st lumbar
vertebra)
|
LCH |
Langerhans cell histiocytocis
|
LCIS |
Lobular Carcinoma In Situ - type of breast cancer
|
LDH |
Lactic dehydrogenase -high levels correlate with tumour
volume in some cancers
|
LMM |
Lentigo Maligna Melanoma
|
LMP |
Low Malignant Potential (context: ovarian tumours)
|
LN |
Lymph Node
|
LP |
Lumbar puncture
|
LVEF |
Left Ventricular Fjection Fraction - a heart function
test
|
LVSF |
Left Ventricular Shortening Fraction - a heart function
test
|
Lx |
Lumpectomy
|
m |
meter (unit of length)
|
M/H |
Medical history
|
MAB - mAb |
Monoclonal antibody
|
MDR |
Multi drug resistant
|
MDS |
Myelo dysplastic syndrome
|
MEN |
Multiple Endocrine Neoplasia - (familial) a.k.a. FMEN
|
mEq/l |
milliequivalent per liter
|
mets |
Metastases (where the tumour has spread to secondary
sites)
|
Mg |
Magnesium
|
mg |
milligram - 0.001 gram
|
MI |
Miocardial Infarction
|
mIBG |
Radioactive Iodine Metaidobenzoguanidine (mIBG scans or
mIBG therapy).
|
ml |
millilitre 0.001 liter
|
MM |
Malignant Melanoma
|
mM |
millimole
|
mm |
millimeter - 0.001 meters
|
MM |
Multiple Myeloma
|
mOsm |
milliosmole
|
MPNST |
Malignant Peripheral Nerve Sheath Tumour
|
MPO |
Medical and Pediatric Oncology (journal)
|
MRI |
Magnetic resonance imaging (scan)
|
MRT |
Malignant Rhabdoid Tumour
|
MSSU |
Mid stream specimen urine
|
MTD |
Maximum tolerated dose - phase 1 studies
|
MTX |
Methotrexate (anti cancer drug)
|
MUD |
Matched Urelated Donor - for bone marrow transplant
|
Mx |
Mastectomy
|
N/V |
Nausea and vomiting
|
Na+ |
Sodium
|
NAD |
No Abnormality Detected
|
NBCCS |
Nevoid basal cell carcinoma syndrome
|
NBM |
Nil by mouth
|
NED |
No evidence of disease
|
ng |
nanogram - 0.000000001 gram
|
NHL |
Non Hodgkin's Lymphoma
|
NK |
Natural Killer cells (large lymphocytes, part of the
immune system)
|
NK |
Not known
|
NM |
Nodular Melanoma
|
NMR |
Nuclear magnetic resonance (scan)
|
NMSC |
Non Melanoma Skin Cancer
|
NOS |
Not otherwise specified (see ICDO)
|
NPC |
Nasopharyngeal Carcinoma
|
NRSTS |
Non-Rhabdomyosarcoma Soft Tissue Sarcoma
|
NSCLC |
Non-small cell lung cancer
|
NSE |
Neuron-Specific Enolase - a neural marker
|
NSR |
Non significant result
|
NSR |
Normal Sinus Rhythem
|
O/E |
On Examination
|
ONB |
Olfactory Neuroblastoma
|
OS |
Overall Survival
|
OS |
Osteogenic sarcoma (context bone tumours)
|
PBSC |
Peripheral Blood Stem Cell (see PBSCT)
|
PBSCH |
Peripheral Blood Stem Cell Harvest
|
PBSCR |
Peripheral Blood Stem Cell Rescue (transplant)
|
PBSCT |
Peripheral Blood Stem Cell Transplant
|
PD |
Progressive disease
|
PDQ |
Physician's Data Query (CancerNet)
|
PET |
Positron Emmission Tomography- a scan after a small
radioactive injection.
|
PET |
Pancreatic Endocrine Tumor
|
PFS |
Progression Free Survival
|
pg |
picogram - 0.000000000001 gram
|
pH |
hydrogen-ion concentration - acid / alkaline
|
PH |
Past History
|
PLB |
Primary Lymphoma of Bone
|
PNET |
Primitive neuroectodermal tumour Context: CNS
tumours
|
PNET |
Peripheral neuroectodermal tumour Context: Bone
tumours - see Ewing's tu
|
PNS |
Peripheral nervous system - nervous system outside the
brain and spine.
|
PR |
Partial Responce / Partial Remission
|
PR |
per rectum
|
prn |
as required
|
prn |
whenever necessary (pro re nata)
|
PSA |
prostate-specific antigen - PSA test used in screening
for prostate cancer
|
PUD |
Peri-Urethral Diathermy (associated with superficial
bladder cancer)
|
QALY |
Quality-Adjusted Life Year
|
qid |
Four times a day (quater in die)
|
QoL |
Quality of Life
|
RBC |
Red blood cell / red blood count
|
RCT |
Randomised Controlled Trial
|
RFS |
Relapse free survival - Time from diagnosis to relapse
or death.
|
RIGS |
Radioimmunoguided surgery
|
RMS |
Rhabdomyosarcoma
|
RNA |
ribonucleic acid
|
RT |
Radiotherapy
|
RTPCR |
Reverse transcriptase polymerase chain reaction
|
Rx |
Treatment
|
SA |
Surface area (see BSA)
|
SAE |
Serious Adverse Event
|
SC |
Subcutaneous
|
SCC |
Squamous Cell Carcinoma
|
SCLC |
Small cell lung cancer
|
SD |
Stable Disease
|
SDV |
Source Data Verification
|
SGOT |
Serum glutamic oxalacetic transaminase - a liver
function test
|
SGPT |
Serum glutamic pyruvic transaminase - a liver function
test
|
SH |
Social history
|
SHO |
Senior House Officer
|
SIADH |
Syndrome of Inappropriate Antidiuretic Hormone
|
SNP |
Single Nucleotide Polymorphism
|
SOB |
Short of breath
|
SSM |
Superficial Spreading Melanoma
|
T1 - T12 |
Thoracic vertebrae 1-12 (spine eg. T10 = tenth thoracic
vertibra)
|
TAMs |
tumour-associated macrophages
|
TBI |
Total body irradiation
|
TCC |
Transitional Cell Carcinoma (usually bladder cancer)
|
TCP |
Thrombocytopenia
|
tds / tid |
Three times a day (ter in die)
|
TNF |
Tumour Necrosis Factor
|
TNM |
Staging system - primary tumour
|
TPN |
total parenteral nutrition
|
TRK |
Transketolase
|
U&Es |
Urea and Electrolites
|
UA |
Urine analysis
|
ug |
microgram - 0.000001 gram
|
ULN |
Upper Limits of Normal
|
URTI |
Upper respiratory tract infection
|
US |
Ultasound (scan)
|
UTI |
Urinary Tract Infection
|
UVR |
Ultra Violet Radiation
|
VEF |
Ventricular ejection fraction (tests lung function)
|
VM-26 |
Teniposide (anti cancer drug)
|
VMA |
Vanillylmandelic Acid
|
VP-16 |
Etoposide (anti cancer drug)
|
WBC |
White blood cell count
|
WCC |
White cell count
|
XRT |
Radiotherapy (external)
|
YST |
Yolk sac tumour - (aka. germ cell tumour) |
Shortcuts: ABCDEFGHIJKLMNOPQRSTUVWXYZ
|
Blood circulates through a network of vessels
throughout the body to provide individual cells with oxygen and
nutrients and helps dispose of metabolic wastes. The heart pumps the
blood around the blood vessels. Blood is made up of about 45% solids
(cells) and 55% fluids (plasma). The plasma is largely water, containing
proteins, nutrients, hormones, antibodies, and dissolved waste products.
Functions of blood and circulation:
- Circulates OXYGEN and removes Carbon Dioxide.
- Provides cells with NUTRIENTS.
- Removes the waste products of metabolism to the excretory organs
for disposal.
- Protects the body against disease and infection.
- Clotting stops bleeding after injury .
- Transports HORMONES to target cells and organs.
- Helps regulate body temperature.
General types of blood cells: (each has many different sub-types)
ERYTHROCYTES (red cells) are small red disk shaped cells. They
contain HAEMOGLOBIN, which combines with oxygen in the lungs and is then
transported to the body's cells. The haemoglobin then returns carbon
dioxide waste to the lungs. Erythrocytes are formed in the bone marrow
in the knobby ends of bones.
LEUKOCYTES (white cells) help the body fight bacteria and
infection. When a tissue is damaged or has an infection the number of
leukocytes increases. Leukocytes are formed in the small ends of bones.
Leukocytes can be classed as granular or non granular. There are three
types of granular leukocytes (eosinophils, neutrophils, and basophils),
and three types of non-granular (monocytes, T-cell lymphocytes, and
B-cell lymphocytes). See also the lymphatic system.
THROMBOCYTES (platelets) aid the formation of blood CLOTS by
releasing various protein substances. When the body is injured
thrombocytes disintegrate and cause a chemical reaction with the
proteins found in plasma, which eventually create a thread like
substance called FIBRIN. The fibrin then "catches" other blood cells
which form the clot, preventing further loss of blood and forms the
basis of healing.
ARTERIES carry oxygenated blood away from the heart. They are
thick hollow tubes which are highly ELASTIC which allows them to DILATE
(widen) and constrict (narrow) as blood is forced down them by the
heart. Arteries branch and re-branch, becoming smaller until they become
small ARTERIOLES which are even more elastic. Arterioles feed oxygenated
blood to the capillaries. The AORTA is the largest artery in the body,
taking blood from the heart, branching into other arteries that send
oxygenated blood to the rest of the body.
CAPILLARIES distribute the nutrients and oxygen to the body's
tissues and remove deoxygenated blood and waste. They are extremely
thin, the walls are only one cell thick and connect the arterioles with
the venules (very small veins).
VENULES (very small veins) merge into VEINS which carry
blood back to the heart. The vein walls are similar to arteries but
thinner and less elastic. Veins carry deoxygenated blood towards the
lungs where oxygen is received via the pulmonary capillaries. The
PULMONARY Veins then carries this oxygenated blood back to the heart.
The heart is a hollow muscular organ which beats over 100,000 times a
day to pump blood around the body's 60,000 miles of blood vessels. The
right side of the heart receives blood and sends it to the lungs to be
oxygenated, while the left side receives oxygenated blood from the lungs
and sends it out to the tissues of the body. The Heart has three layers;
the ENDOCARDIUM (inner layer), the EPICARDIUM (middle layer), and
MYOCARDIUM (outer layer). The heart is protected by the PERICARDIUM
which is the protective membrane surrounding it.
The heart has FOUR CHAMBERS, in the lower heart the right and left
Ventricles, and in the upper heart the right and left Atria. In a normal
heart beat the atria contract while the ventricles relax, then the
ventricles contract while the atria relax. There are VALVES through
which blood passes between ventricle and atrium, these close in such a
way that blood does not backwash during the pauses between ventricular
contractions. The right and left ventricles are divided by a thick wall
(the VENTRICULAR SEPTUM), babies born with "hole in the heart" have a
small gap here, which is a problem since oxygenated and deoxygenated can
blood mix. The walls of the left ventricle are thicker as it has to pump
blood to all the tissues, compared to the right ventricle which only
pumps blood as far as the lungs.
This is a large flat oval organ located below the diaphragm, it's main
function is to STORE BLOOD. The size of the spleen can vary, for example
it may enlarge when the body is fighting infection also it's size tends
to decrease with age. It is a non-vital organ and it is possible to
survive after removal of the spleen.
Perinicious anaemia is a Vitamin B12 deficiency resulting in a
reduction in number of erythrocytes.
Aplastic anemia is a failure of the bone marrow to produce the
enough red blood cells.
Septicaemia - bacterial toxins in blood.
component
|
meaning
|
example
|
CARDIO-
|
heart
|
echocardiogram = sound wave image of the heart.
|
CYTE-
|
cell
|
thrombocyte = clot forming cell.
|
HAEM-
|
blood
|
haematoma - a tumour or swelling filled with blood.
|
THROMB-
|
clot, lump
|
thrombocytopenia = deficiency of thrombocytes in the blood
|
ETHRO-
|
red
|
ehtrocyte = red blood cell
|
LEUKO-
|
white
|
leukocyte = white blood cell
|
SEP, SEPTIV-
|
toxicity due to micro-organisms
|
septicaemia
|
VAS- |
vessel / duct
|
cerebrovascular = blood vessels of the cerebrum of the
brain.
|
HYPER-
|
excessive
|
hyperglycaemia = excessive levels of glucose in blood.
|
HYPO-
|
deficient / below
|
hypoglycaemia = abnormally low glucose blood levels.
|
-PENIA |
deficiency
|
neutropenia = low levels of neutrophilic leukocytes.
|
-EMIA
|
condition of blood
|
anaemia = abnormally low levels of red blood cells.
|
- Overview of Haematological Malignancies
- The most common haematological malignancy is leukaemia - cancer
of the white blood cells. There are many types of leukaemia;
Acute types progress rapidly, while Chronic types develop
more slowly. Leukaemia is often accompanied by anaemia because the
red oxygen carrying cells in the blood are crowded out by the
cancerous white cells. There are a number of malignancies and
disorders affecting other types of blood cells.
-
Internet Resources for Leukaemia
- Acute Lymphoblastic Leukaemia (ALL)
- Acute lymphoblastic leukaemia (also known as acute lymphocytic
leukaemia or ALL) is a disease where too many immature lymphocytes
(a type of white blood cell) are found in the blood and bone marrow.
Symptoms can include persistent fever, weakness or tiredness,
achiness in the bones or joints, or swollen lymph nodes. Adult ALL
and its treatment is usually different to childhood ALL. Almost a
third of adult patients have a specific chromosome translocation;
"Philadelphia Positive" ALL.
-
Internet Resources for Acute
Lymphocytic Leukaemia
- Acute Myeloid Leukaemia (AML)
- Acute myeloid leukemia (AML) is a disease in which too many
immature granulocytes (a type of white blood cell) are found in the
blood and bone marrow. There are a number of subtypes of AML
including acute myeloblastic leukemia, acute promyelocytic leukemia,
acute monocytic leukemia, acute myelomonocytic leukemia,
erythroleukemia, and acute megakaryoblastic leukemia.
-
Internet Resources for Acute
Myeloid Leukaemia
- Other Types of Leukaemia
Chronic Lymphocytic Leukaemia
Chronic Myelogenous Leukaemia
Hairy Cell Leukaemia
-
Internet Resources for Leukaemia
- Childhood Leukaemia
- Childhood leukaemias tend to have different characteristics and
treatments compared to adult leukaemias. There is a "childhood peak"
of Acute Lymphoblastic Leukaemia, there is a lower proportion of
Acute Myeloid Leukaemias compared to adult patients. Clinical
prognostic factors include age, White Blood Cell count (WBC) at
presentation, and Central Nervous System (CNS) involvement. Infants
less than 1 year and adolescents over 10 years of age, WBC greater
than 50,000, or CNS involvement are associated with a less
favourable prognosis.
-
Internet Resources for Childhood
Leukaemia
- Other Haematological Malignancies
-
- - Myelodysplastic Syndromes
- Myelodysplastic syndromes, sometimes called "pre-leukaemia"
are a group of diseases in which the bone marrow does not
produce enough normal blood cells. Common symptoms are anaemia,
bleeding, easy bruisability, and fatigue. These Myelodysplastic
syndromes can occur in all age groups but are more common in
people aged over 60. Myelodysplastic syndromes may develop
spontaneously or be secondary to treatment with chemotherapy /
radiotherapy. There is an association with Myelodysplastic
syndromes and acute myeloid leukaemia.
- - Myeloproliferative Disorders
- Myeloproliferative disorders are diseases in which too many
blood cells are made by the bone marrow, there are 4 main types
of myeloproliferative disorders: chronic myelogenous leukaemia,
polycythemia vera, agnogenic myeloid metaplasia, and essential
thrombocythemia. Chronic myelogenous leukaemia is where an
excess of granulocytes (immature white blood cells) are found in
the blood and bone marrow. Polycythemia vera is where red blood
cells become too numerous often resulting in a swelling of the
spleen. Agnogenic myeloid metaplasia is a condition in which
certain blood cells do not mature properly, this may result in a
swelling of the spleen and anaemia. Essential thrombocythemia is
a disease in which the body produces excessive numbers of
platelets (cells in the blood that make it clot) which impedes
the normal circulation of blood.
- - Aplastic Anaemia
- Anaplastic Anemia is not a cancer. AA is a rare disease in
which the bone marrow is unable to produce adequate blood cells;
leading to pancytopenia (deficiency of all types of blood
cells). AA may occur at any age, but there is a peak in
adolescence / early adulthood, and again in old age. Slightly
more males than females are diagnosed with AA, also the disease
is more common in the Far East. Patients successfully treated
for aplastic anemia have a higher risk of developing other
diseases later in life, including cancer.
- - Fanconi Anaemia
- Fanconi Anaemia is not a cancer, it is a rare disorder found
in children that involves the blood and bone marrow. The
symptoms include severe aplastic anemia, hypoplasia of the bone
marrow, and patchy discoloration of the skin. Recent research
has shown an association between Fanconi anaemia and leukaemia.
- - Waldenstrom's Macroglobulinemia
- This is a rare malignant condition, involving an excess of
beta-lymphocytes (a type of cell in the immune system) which
secrete immunoglobulins (a type of antibody). WM usually occurs
in people over sixty, but has been detected in younger adults.
-
Internet Resources for
Haematological Malignancies
- French-American-British (FAB) Classification
Scheme
- Leukaemia can be classified using the French-American-British
(FAB) criteria. for cell morphology:
L1 - ALL: small lymphoid cells, regular nuclei
L2 - ALL: large lymphoid cells, irregualr nuclei
L3 - ALL: large homogeneous cells with prominent nucleolus
M1 - Myeloblastic leukemia without maturation
M2 - Myeloblastic leukemia with maturation
M3 - Promyelocytic leukemia
M4 - Myelomonocytic leukemia
M5 - Monocytic leukemia
M6 - Erythroleukemia
M7 - Megakaryoblastic leukemia
M0 - AML with minimal differentiation
- CNS Prophylaxis
- Leukaemia can sometimes spread to the spinal cord and brain
(Central Nervous System). Intrathecal chemotherapy (injection into
the fluid around the spine) may be given to combat or prevent CNS
relapse.
- Blood Counts
- Blood counts are done to test the number of each of the
different kinds of cells in the blood. This may be an aid to
diagnosis or done to monitor toxicity after each course of
chemotherapy. The next course of chemotherapy may be delayed until
white cells, neutrophils, and platelets have recovered to a safe
level.
- Cardiotoxicity
- Cardiotoxicity (damage to the heart) is associated with certain
anti cancer drugs, especially Adriamycin. As such the total dose of
these drugs may be limited to reduce the risk of cardiotoxicity.
- Echocardiagram
- An Echocardiogramis where an image of the heart is formed when
high frequency sound waves are reflected from the muscles of the
heart. An echocardiogram may be done before treatment starts to
establish a baseline from which to compare future tests.
- Metastases through the cardivascular system
- The network of blood vessels reach all parts of the body and may
provide one of the routes for cancer cells to spread to secondary
sites.
Related Abbreviations and Acronyms:
-
-
AA |
Anaplastic Anaemia
|
ALL |
Acute lymphoblastic leukaemia
|
AML |
Acute Myeloid leukaemia
|
ANC |
Absolute neutrophil count
|
ANLL |
Acute non-lymphatic leukaemia
|
ASH |
American Society for Hematology
|
B-ALL |
B-cell Acute Lymphoblastic Leukaemia
|
BP |
Blood pressure
|
CALGB |
Cancer and Leukemia Group B (USA)
|
cALL |
Common ALL
|
CGL |
Chronic Granulocytic Leukaemia
|
CHF |
Congestive heart failure
|
CLL |
Chronic lymphocytic Leukaemia
|
CML |
Chronic myeloid leukaemia
|
CMML |
chronic myelomonocytic leukemia
|
CPR |
Cardio pulmonary resuscitation
|
CVA |
Cardiovascular Accident (stroke)
|
CVC |
Central venous catheters
|
ECG |
Electrocardiogram - heart scan
|
FAB |
French American and British classification scheme for
leukaemia
|
FBC |
Full Blood Count
|
G-CSF |
Granulocyte colony stimulating factor promotes
production of white blood cells
|
GM-CSF |
Granulocyte and macrophage colony stimulating factor
|
Hb |
Haemoglobin
|
HCL |
Hairy Cell Leukaemia
|
HD |
Hodgkin's Disease (lymphoma)
|
HTLV |
Human T-cell leukemia-lymphoma virus
|
IV |
Intravenous - into a vein
|
LRF |
Leukaemia Research Fund (UK)
|
LVEF |
Left Ventricular Fjection Fraction - a heart function
test
|
LVSF |
Left Ventricular Shortening Fraction - a heart function
test
|
MM |
Multiple Myeloma
|
RBC |
Red blood cell / red blood count
|
WBC |
White blood cell count
|
WCC |
White cell count |
More Cancer Related Abbreviations
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