Download P Gokal Whats in the pipeline

03 February 2012
No. 04
Whats in the pipeline?
P Gokal
Commentator: K Govender
Moderator: SS Ramsamy
Department of Anaesthetics
CONTENTS
INTRODUCTION ................................................................................................... 3
BASIC SCIENCE 32............................................................................................... 4
Fundamental bases and haemodynamic principles ...................................... 4
Hydrostatic and Hydrodynamic pressures ..................................................... 5
Resistance ........................................................................................................ 6
Hagen–Poiseuille Equation.............................................................................. 6
Stroke Volume .................................................................................................. 6
Ventricular Preload........................................................................................... 6
Wall Motion Abnormalities............................................................................... 8
DYNAMIC INDICES .............................................................................................. 9
Physiologic Explanation of Arterial Pressure Variation ................................ 9
Fig 3 17 ............................................................................................................. 11
Systolic Blood Pressure Variability (Δ SBP) ................................................ 11
Pulse Pressure Variability (ΔPP) ................................................................... 13
Limitations of the Dynamic Parameters........................................................ 17
DIASTOLIC, PULSE, AND SYSTOLIC BLOOD PRESSURES .......................... 19
Diastolic Blood Pressure ............................................................................... 19
Pulse Pressure ............................................................................................... 19
Systolic Blood Pressure ................................................................................ 19
CONCLUSION .................................................................................................... 22
REFERENCES.................................................................................................... 23
Page 2 of 24
INTRODUCTION
Fluid management and optimization involve an important part of daily decision
making in Anesthetics and Critical Care. The trouble is that it is difficult to
determine if hypotension is due to hypovolaemia or some other cause.
Hemodynamic management is related to the optimization of oxygen delivery to the
tissues and has been shown to be able to advance postoperative outcome and to
decrease the cost of surgery.1-3There are two distinctive complications when it
comes to fluid management – hypovolaemia on one side and hypervolaemia, or
fluid overload on the other. Both perioperative complications can result in a
decrease in oxygen delivery to the tissues and can also cause an increase in
postoperative morbidity.4
Hypovolaemia can be defined as a state of reduced blood volume. This definition
is less useful in clinical medicine as there is no one diagnostic test to quantify
blood volume. Generally speaking it is a state in which a patient has
hypoperfusion, which will improve with fluid therapy. In current literature,
hypovolaemia is most often defined as, the shocked patient in whom stroke
volume (SV) or cardiac output (CO) increases after a fluid bolus. This is also
termed Preload, Volume or Fluid Responsiveness.
Evidence shows that organ perfusion requires adequate perfusion pressure in
order to drive blood into the capillaries of all organs and adequate cardiac output
to ensure oxygen delivery. Data also exists showing the impact of cardiac output
optimization on postoperative outcome.5The issue is that determining organ
perfusion can be tricky. Cardiac output monitoring rarely is used in daily
anaesthetic practice simply because of availability and skills. Clinicians have to
therefore rely on clinical judgment and blood loss estimates to determine
intravascular volume.6
Clinical judgment may be guided by the more available and less invasive
monitoring. Blood Pressure is commonly used as a surrogate of Cardiac Output. It
is however a crude correlation. Blood Pressure is actually a function of Cardiac
Output and Stroke Volume. Intravascular volume is an important factor in
determining stroke volume. There are various indices that are commonly available
everyday which provides an idea of Intravascular Volume. Arterial Pulse Contour
analysis provides three types of data on the patient’s hemodynamic status. The
first type of data comes from Analysis of BP variations induced by applying
positive inspiratory pressure which provides specific information predicting
hemodynamic effects of volume loading. The second type of data is that of the
Static Indices. Those are the Mean Arterial Pressure (MBP), Systolic Blood
Pressure (SBP), Diastolic Blood Pressure (DBP), and Pulse Pressure (PP). The
third type of data is a mathematical analysis of the pulse wave shape.
Page 3 of 24
The capability of the circulation to increase cardiac output in response to volume
expansion is a well described concept.7-9
There is clear evidence that dynamic parameters of fluid responsiveness, based
on cardiopulmonary interactions in patients under general anaesthesia and
mechanical ventilation, are superior to Central Venous Pressure.10 Dynamic
indicators can be derived from the arterial pressure waveform. Systolic Pressure
Variations (SPV), including Δup and Δdown, and Pulse Pressure Variation (PPV)
are two of the concepts that will be reviewed.
Their aim is to diagnose the cause of the hypotensive type of hemodynamic
instability and attribute it to hypovolaemia. This is not an old concept and has
been described more than 40 years ago,11 and termed Dynamic Indices. These
indices have undergone significant improvement of late. During the past 3 years
new algorithms have been developed to constantly calculate these indices. Such
algorithms have been built into various modern devices such as the
Vigileo/FloTrac system.12
The various types of data available to the Anaesthetist in theatre provide good
information of a patient’s volume status. The Static parameters, Dynamic
parameters and analysis of the arterial pulse waveform can be used in clinical
practice as a means to guide fluid management.
BASIC SCIENCE 32
Fundamental bases and haemodynamic principles
Blood Pressure (BP)
Blood Pressure is the force per unit area exerted on the wall of a blood vessel by
its contained blood. It usually refers to blood pressure in aorta there is a pressure
gradient keeps blood flowing. This gradient varies through the vascular system.
Arterial Blood Pressure (ABP)
Arterial Blood Pressure varies with age, gender, weight, stress level, mood,
posture, physical activity. ABP depends on the compliance of elastic arteries and
stroke volume. Systolic pressure is the maximum pressure in arteries during
ventricular systole and diastolic pressure is the minimum pressure in arteries
during ventricular diastole.
Venous Blood Pressure
Venous Pressure is a low, steady pressure. Venous return is supported by; valves
that prevent backflow, the muscle pump, the respiratory pump, the changes in
thoracic and abdominal pressures during breathing.
Page 4 of 24
Mean Arterial Pressure
BP signal fluctuates around a mean value according to a complex mechanism.
Physiology responds to MAP. BP reaches Systolic Blood Pressure (SBP), and
then drops to Diastolic Blood Pressure (DBP). The difference between both values
is the Arterial Pulse Pressure (APP)
APP = SBP – DBP
The BP trace undergoes changes along its course from the proximal aorta (aortic
pressure) to the peripheral arteries (peripheral blood pressure) that may be
modelled by wave reflection and pulse wave amplification phenomena. The
arterial system may be considered as a functional unit interposed between the left
ventricle (LV) and the capillary exchange and is divided into two subunits
o the large arteries (characterized by their capacitive function)
o distal arterioles (characterized by high resistance)
This enables transformation of the pulsatile flow into a continuous flow. Major
haemodynamic principles are derived from the dynamics of a Newtonian fluid
(water) circulating continuously in rigid tubes. Neither conditions are met in
physiology where the assumptions are that the flow is described by linear
equations and that the pressure/flow relationship obeys Ohm’s law.
Continuous Flow
Cardiac output (CO) is continuous rather than pulsatile flow. MBP would be the
pressure required to obtain an identical CO in the absence of pulsatility.
Hydrostatic and Hydrodynamic pressures
Pascal’s first principle of fluid pressure establishes that below the fluid surface
there is a hydrostatic pressure. Hydrostatic pressure is the physical pressure
blood exerts on vascular wall. Mean Systemic Filling pressure can be observed
under no-flow conditions. Hydrodynamic pressure is the pressure created by
moving fluid which exerts additional pressure. This moving pressure is generated
by cardiac activity.
Controlling Factors
BF = P / R
When blood flows through a lumen the rate of flow is directly proportional to blood
pressure gradient (P) and inversely proportional to peripheral resistance (R).
Resistance is important in controlling local flow.
Page 5 of 24
Resistance
This is the amount of friction blood encounters as it passes through vessels.
Peripheral resistance is known as Systemic Resistance as peripheral vessels
accounts for most resistance in system
Sources of resistance:
1. Blood viscosity
 directly proportional to resistance
 affected by number of blood cells (e.g., polycythaemia)
2. Blood volume – directly proportional
 dehydration  decreases volume  decreases resistance
 overhydration  increases volume  increases resistance
3. Blood vessel length – directly proportional
4. Blood vessel diameter – main source affecting resistance
 Inversely proportional to resistance
o increased diameter  decreased resistance
o varies as inverse of radius to 4th power (1/r4)
 Controlled mainly at small arterioles
Hagen–Poiseuille Equation
Stroke Volume
There are five determinants of stroke volume, with the first three being most
important:
1. Preload: the stretch of the myocardium just before contraction
2. Afterload: tension against which muscle must contract.
3. Contractility: intrinsic property of the muscle that is related to the force of
contraction
4. Wall motion
5. Valvular Function
Ventricular Preload
Ventricular preload is defined as the degree of tension of the cardiac muscle when
it begins to contract. In practice, it is almost impossible to determine the degree of
tension of the cardiac muscle when it begins to contract. Clinicians may use
pressure or volume parameters for the assessment of preload. The pressure
parameters used are left and right ventricular filling pressures, and the volume
parameter used is mainly left ventricular end-diastolic volume obtained through
left ventricular end-diastolic area. Indices of preload have been used extensively
over the past decades to guide volume expansion.
Page 6 of 24
The underlying principle behind the use of these indices, to predict the effects of
volume expansion on stroke volume and cardiac output, is related to the FrankStarling relationship.
This relationship describes the intrinsic ability of the heart to adapt to increasing
volumes of inflowing blood. In essence, the greater the heart muscle is stretched
during filling, the greater is the force of contraction and the greater the quantity of
blood pumped into the aorta. Stated another way, within physiologic limits, the
heart pumps all the blood that returns to it by the way of the veins.13
Fig. 1 17
The Frank-Starling Curve has two portions. The first portion of this relationship is
called the steep portion, and the second portion is called the plateau. In a low
preload state the heart functions on the steep portion. Here an increase in preload
will induce a significant increase in stroke volume. This can be achieved by
volume expansion. On the steep portion the heart is said to be preload dependent
and the patient is a responder to volume expansion.
If the heart is functioning on the plateau (elevated preload), then an increase in
preload will not bring about any major increase in stroke volume. Here the heart
can be said to be preload independent, and the patient is a non-responder to
volume expansion.
It becomes apparent that knowing the preload will then help to predict fluid
responsiveness. However, the Frank-Starling relationship does not depend only
on preload and stroke volume, but it also depends on ventricular function because
the Frank-Starling curve is flattened when ventricular function is impaired (Fig 1).
Page 7 of 24
Consequently, for a given preload value or central venous pressure, it is not
possible to predict the effects of an increase in preload on stroke volume.10
Preload or its surrogates are therefore not accurate predictors of fluid
responsiveness.
Afterload
Afterload is the myocardial tension (force) required to overcome opposition to
ventricular ejection during systole and is related to the aortic pressure and
chamber radius as well as wall thickness. It is essentially the pressure the
ventricle must overcome to reduce its cavity. Myocardial Tension can be
explained using Laplace’s Law. Surface tension is directly proportional to the
transmural pressure and chamber radius. It is also inversely proportional to the
wall thickness. Ventricular wall tension is therefore directly proportional to the
transmural pressure and the ventricular chamber radius, and indirectly
proportional to the ventricular wall thickness. The other force the ventricle must
overcome to empty its volume is that of arterial impedance to ejection determined
by arteriolar tone. Arteriolar tone is the chief determinant of Systemic Vascular
Resistance. Cardiac output is inversely related to afterload, and the RV is more
sensitive to afterload than the LV because of its thinner wall. Patients with
myocardial dysfunction become increasingly more sensitive to increase in
afterload.
Contractility
Contractility is an intrinsic ability of the myocardium to pump in the absence of
changes in the preload, afterload or heart rate. It is related to the rate of
myocardial muscle shortening, which in turn is dependent on the intracellular
calcium. Factors which increase contractility are related to the amount of
intracellular calcium availability or degree of sensitization, ATP availability for
continued cycling, and enhanced states of relaxation (lusitripsy).
Wall Motion Abnormalities
When the ventricular cavity does not collapse symmetrically or fully, emptying
becomes impaired. Although contractility may be normal or even enhanced in
some areas, abnormalities in other areas of the ventricle can impair emptying and
reduce stroke volume.
Cardiac output is a function of stroke volume and heart rate. It is evident from this
physiology review that there are many factors affecting stroke volume. Essentially
clinicians would like to know a patient’s cardiac output. This is however a difficult
parameter to directly measure. Blood Pressure is used as a surrogate of cardiac
output. It is however also a function of Systemic Vascular Resistance. BP is
therefore a crude surrogate of CO. There are many variables effecting BP so the
difficulty is knowing how to treat the BP reading and when a patient is fluid
responsive. This gives place to Dynamic and Static Parameters which has proven
to be useful in diagnosing hypovolaemia.
Page 8 of 24
DYNAMIC INDICES
Physiologic Explanation of Arterial Pressure Variation
With volume expansion an increase in right ventricular end-diastolic volume, left
ventricular end-diastolic volume, stroke volume, and cardiac output is expected.
This is due to the positive relationship between them.
Increased preload
Fig. 2 30
Fig 2 32
With an increase in Preload, there is an increase in EDV due to an increase in
filling during diastole (Fig. 2). The EDV point therefore moves to the right and the
volume ejected (Stroke Volume) is also increased.
Page 9 of 24
The expected response to volume expansion is not so simple in practice. The
response is actually depends on several complicated parameters.
For example, the increase in end-diastolic volume induced by volume expansion
is related to the partitioning of the fluids into the different cardiovascular
compartments organized in series.
In theory volume expansion can result in an increase in cardiac output. In practice
there are many other variables which determine this. Ventricular function is one of
these variables.
In clinical practice, anaesthetists never know how fluids are partitioned or how
contractile the ventricles are. Therefore volume expansion does not always
achieve its main objective: an increase in cardiac output. More significantly, an
inappropriate volume can induce tissue oedema and oxygen delivery alteration,
counteracting the original goal of increased oxygen delivery. Therefore, it is of
major importance for anaesthetists to be able to predict the effects of volume
expansion before actually performing volume expansion.
Preload Dependence
Preload dependence is defined as the ability of the heart to increase stroke
volume in response to an increase in preload. The main question anaesthetists
have to answer before they perform volume expansion is if the fluid will increase
the patient’s cardiac output increase after volume expansion or really if the patient
is preload dependent or not. Preload on its own is not predictive of preload
dependence. In practice, cardiopulmonary interactions can be used to assess the
effects of fluid challenges on stroke volume.7
In patients under general anaesthesia, the changes in intrathoracic pressure
during positive-pressure ventilation induce cyclic changes in Inferior Vena Cava
blood flow, pulmonary artery flow, and aortic blood flow. During inspiration there is
an increase in intrathoracic pressure. This results in a decrease in vena cava
blood flow. There is a consequent decrease in venous return and therefore a
decrease in End Diastolic Volume. According to the Frank-Starling relationship
pulmonary artery flow decreases.7
Approximately 3 beats later this decrease in pulmonary artery flow is transmitted
to the left ventricle, inducing a decrease in aortic stroke volume. During an
expiratory pause, the inverse happens and the stroke volume increases.
Consequently, mechanically ventilated patients under general anaesthesia
present with cyclic changes in left ventricular stroke volume. Some variability in
stroke volume is therefore expected in normovolaemic states but during
hypovolaemic states there is excessive variability. This variability is a more
specific surrogate marker of hypovolaemia than hypotension alone.
Page 10 of 24
When the heart is working on the steep portion of the Frank-Starling relationship,
these respiratory variations are important because slight changes in right
ventricular preload induced by mechanical ventilation will induce significant
changes in stroke volume; whereas when the heart is working on the plateau of
this relationship, respiratory variations are small because changes in right
ventricular preload induced by mechanical ventilation have little impact on stroke
volume (Fig. 3). Because arterial pressure parameters are related to stroke
volume and arterial compliance, variations in arterial pressure parameters reflect
respiratory variations in left ventricular stroke volume if arterial compliance is
considered stable during a single respiratory cycle. This is translated into
excessive blood pressure variability during the inspiratory phase.
Fig 3 17
Systolic Blood Pressure Variability (Δ SBP)
ΔSBP is the difference between maximum and minimal SBP during a respiratory
cycle. ΔSBP can be broken down into two other indices: delta up (Δup) and delta
down (Δdown). The measurement of these two indices is performed with
reference to the SBP measured during an end-expiratory pause (SBPref). Δdown
is the difference between SBPref and the lowest value obtained during the
respiratory cycle. Δdown illustrates the decrease in LV preload and SV during
expiration as an out-of-phase response to the RV decrease in SV occurring during
insufflation. (Fig. 4
Page 11 of 24
Fig 4 18
Using Systolic Pressure Variation
Loosely the variability in Stroke Volume is referred to as “swing”. This is owing to
the morphology of the arterial line trace. Substantial amounts of literature have
confirmed the utility of the analysis of systolic pressure variation in the
assessment of fluid status.14,15 Excessive “swing” of the trace can be identified as
being either predominantly up or down. Where the “swing” is predominantly down,
hypovolaemia may be identified and a positive result of fluid administration
expected.
ΔSBP and Δdown as predictors of preload-dependence was also validated in a
study by Tavernier et al. involving septic shock patients.16 In that study the clinical
relevance of these predictors is apparent. There was at least a 15% response to
fluid administration when the ΔSBP > 10 mmHg and Δdown > 5 mmHg. Patients
with values above these cut points proved to be fluid responders as they were on
the steep part of the Frank Starling Curve.
These values we good surrogate predictors of a SV with excellent positive and
negative predictive values (>90%). Administration of fluid can therefore be
predicted from the net effect of the small variations in preload Δdown has been
shown repeatedly to be a sensitive predictor of preload.16 The same study also
showed that Δdown also predicted the response of cardiac output to volume load
better than either pulmonary capillary wedge pressure or left ventricular enddiastolic area as determined by echocardiography.16
Page 12 of 24
This has since proved to be a ground breaking finding, as these parameters have
traditionally been regarded as clinical gold standards for the assessment of
intravascular fluid status.
Figure 5 shows the Receiver Operating Characteristic (ROC) curves comparing
the ability of the Pulmonary Artery Occlusion Pressure (PAOP), the left ventricular
end-diastolic area index (EDAI), and the Δdown component of the positive
pressure ventilation induced arterial systolic pressure variation to discriminate
between positive (> 15% increase in stroke volume index) and negative (<15 %
increase in SVI) response to a subsequent volume loading step. The area under
the ROC for Δdown is greater than Pulmonary Artery Occlusion Pressure (PAOP),
the left ventricular end-diastolic area index (EDAI).
Fig. 5 16
Pulse Pressure Variability (ΔPP)
Pulse Pressure is a function of Stroke Volume and Arterial Compliance.
Considering the absence of significant changes in arterial compliance over the
respiratory cycle, it has been assumed that the respiratory variability of PP should
accurately predict fluid responsiveness.17 Figure 6 illustrates the calculation of Δ
PP.17
Page 13 of 24
A study by Michard et al.17 was conducted on mechanically ventilated septic shock
patients. In the 40 patient study a high ΔPP (ΔPP >13%) enabled differentiation
between responders and non-responders to volume expansion. What was found
was that the higher ΔPP before volume expansion, the more marked the increase
in cardiac index induced by volume expansion. What they looked for was an
increase in cardiac index of >15%. There was a 94% sensitivity and a 96%
specificity. Numerous other studies also confirmed the reliability of this parameter
9, 19
. The current evidence is that Δdown and ΔPP correlates with the degree of
response to volume administration. (Fig. 7)
Fig 6 15
Fig 6 17
Other work from Michard in 1999 demonstrated the effect of positive endexpiratory pressure (PEEP) on ΔPP analysis. It was shown that the higher ΔPP at
the zero PEEP (ZEEP), the higher the decrease in cardiac output induced by
application of PEEP in patients with acute respiratory distress syndrome
(ARDS).20
Page 14 of 24
Fig 7
17
Fluid challenge
This diagnostic test involves administering a fluid bolus of 250 – 500 ml and
observe changes in blood pressure. The technique is often used during the initial
phase of resuscitation, but once severe hypovolaemia has been corrected, better
markers of stroke volume or cardiac output are needed. This method has the
obvious drawback that the clinician has to give fluid to assess whether the patient
needs it or not. Fluid boluses may be of little use in most patients and in some
cases may result in hypervolaemia or even worsen cardiogenic shock. To avoid
this risk better diagnostic investigations are required to predict fluid
responsiveness.
Passive Leg Raising
The lower limbs hold blood which may be shifted to the central blood volume. A
Passive Leg Raise is a reversible autotransfusion maneuver by passive leg raising
combined with the assessment of changes in stroke volume has the potential to
diagnose hypovolaemia without the risk of volume overloading the patients. This
test has been less studied than those above, but may turn out to be applicable to
more patients, at least in emergency departments and general ICUs.
Page 15 of 24
Boulain et al. were the first to describe the relationship between radial artery pulse
pressure changes and passive leg raising.22
The passive leg raise was validated as a dynamic test of intravascular volume by
looking at the change in aortic blood flow using Esophageal Doppler 21, 22 Figure 8
illustrates the passive leg raising from the semi-recumbent position (likelihood
ratios can be calculated as 16 and 0.03).
Fig 8
20
Generally an increase in aortic blood flow of between 8 and 15% has been
reported to be diagnostic for hypovolaemia. The optimal technique for performing
passive leg raising is debatable. Controversies exist as to whether the passive leg
raising manoeuvre should be performed from the supine or semi-recumbent
position and whether a marker of preload should be used to ensure that a
sufficient shift of blood volume has occurred.
Page 16 of 24
Limitations of the Dynamic Parameters
Although Dynamic indices may seem to be the ‘silver bullet’ in diagnosing
intravascular fluid status there are many provisos as to their use. Studies have
been validated in Mechanically Ventilated patients under general anaesthesia.23 In
patients who are spontaneously breathing, the specificity of ΔPP is low.17 In the
instance where patients are spontaneously breathing another study suggests the
elevation of PP by more than 5 mmHg at the end of a 15-s end-expiratory pause
could be useful to predict a beneficial effect of fluid infusion.24
The reliability of dynamic parameters also depends on the tidal volume. Most
studies in which these indices have been validated use tidal volumes greater than
8 mL/kg and a PEEP of between 0 and 5 cmH2O.25,27 This is a major weakness in
the current literature. Studies in which dynamic variables validated fail to control
for intrathoracic pressure.
It can therefore be said that any patient can appear fluid responsive at excessive
levels of intrathoracic pressure. In patients with lung pathology, lung compliance the intrathoracic pressure from a given tidal volume - is variable and changing.
This occurs in theatre where position or other factors such as laparoscopy can
significantly influence effective lung compliance. Studies are limited by the fact
that they typically use volume ventilation, and intrathoracic pressure is not
reported.
The use of low tidal volumes during ARDS diminishes their sensitivity. As a result
of decreased pulmonary compliance, marked cyclic variations in alveolar pressure
are likely to occur during ARDS, generating marked cyclic variations in
transpulmonary pressure and Intrathoracic pressure, even in the case of low tidal
volume. 27 To this end Huang et al. suggests that ΔPP remains a valid parameter
of fluid responsiveness in ARDS patients ventilated with low tidal volumes and
high positive expiratory pressures.28
Static Indices
For 30 years, we used central venous pressure (CVP) and pulmonary artery
occlusion pressure (PAOP) to diagnose hypovolaemia. These markers of preload
have been an integral part of patient monitoring, which is perhaps why we were
late to assess them as diagnostic tests in clinical trials. When trialled, filling
pressures were shown to have no predictive power for hypovolaemia in the
majority of patients. A Review from Marik et al. included evidence from Shippy et
al.10
Page 17 of 24
The study determined that there was a poor correlation between CVP and blood
volume. 1500 simultaneous measurements of intravascular volume and CVP
demonstrated no association between these two variables (r = 0.27). (Fig. 9) This
was done in a heterogenous cohort of 188 ICU patients. The correlation between
CVP and change in intravascular volume was only 0.1 (r2 = 0.01). This study
essentially demonstrated that patients with a low CVP may actually have fluid
overload and similarly patients with a high CVP may yet be volume depleted.
Fig 9 8
Fig 9 10
Advances in technology allowed clinicians to measure heart volumes and areas,
including those of the right and left ventricles at end-diastole. These static indices
of preload were also shown to have low predictive power for hypovolaemia. It is
likely that extreme values of filling pressures or heart volumes/areas have
predictive power for hypovolaemia, but the cut-off points for what is a low or what
is a high value have not yet been established. Within the last ten years, clinical
researchers have challenged the static markers of preload in studies of dynamic
tests for the diagnosis of hypovolaemia.10
Page 18 of 24
DIASTOLIC, PULSE, AND SYSTOLIC BLOOD PRESSURES
Diastolic Blood Pressure
DBP remains nearly constant from the aorta to the peripheral arteries. The main
determinant of DBP is vascular tone. Low vascular tone (due to sepsis or
vasodilators) is responsible for a drop in DBP. The DBP also depends on the
duration of the diastole and BP decay time constant.
Therefore a short diastole (tachycardia) is associated with high DBP whereas a
prolonged diastole (bradycardia) is associated with low DBP. We may assume
that BP decreases monoexponentially during diastole. It has a time constant (Tau)
which is equal to the product of SVR multiplied by compliance. Tau shortening is
associated with a decrease in DBP which is related to either decreased
resistances (vasomotor tone decrease), or decreased arterial compliance. In
summary, low DBP is observed in cases of vasodilatation, bradycardia, or
decreased arterial compliance.
Pulse Pressure
PP is determined by SV and compliance of large arteries.
PP = SV/C
A decrease in SV is therefore associated with decreased PP, whereas a decrease
in compliance is associated with increased PP. The decrease in vascular
compliance with age causes a decrease in DBP along with an increase in PP and
SBP. Thus, detecting a lowered PP in the elderly is indicative of a decrease in
stroke volume. In a non pathological patient Pulse Pressure is a fair reflection of
stroke volume.24
Systolic Blood Pressure
SBP is determined by SV, arterial compliance, and SVR. SBP is physiologically an
essential determinant of LV afterload. In some cases, the combined analysis of
various BP indices (MBP, PP, SBP, and DBP) and patient characteristics (age
and cardiovascular disease) may allow for a precise assessment of
haemodynamic status.
Page 19 of 24
Pulse Pressure as a Measure of Stroke Volume
Fig 10 30
Pulse pressure is essentially the pressure rise from a baseline diastolic pressure.
The pressure rise during ventricular ejection is predominantly a function of:
1. The amount of blood ejected with each beat (stroke volume)
2. Central aortic stiffness or ‘compliance’
3. Peripheral run-off of the ejected blood or peripheral vascular resistance.
Intraoperatively the compliance can be said to be relatively constant. Under these
conditions stroke volume is the main determinant of pulse pressure.29 The
diagram shows the arterial pressure traces recorded from a patient during volume
resuscitation. Here a rapid infusion of a colloid (Voluven®) is administered. There
is a resultant increase in stroke volume. The increase in associated plasma
volume expansion is reflected as a corresponding increase in pulse pressure. The
progressive changes in pulse pressure during such a fluid challenge can even be
plotted against time as shown in Figure 10a.
This can be compared to the Frank-Starling curve which can be informative in
assessing volume responsiveness. Due to this direct relationship between stroke
volume and pulse pressure30, hypovolaemia may be characterized by a reduction
in pulse pressure. Hypovolaemia is usually associated with a reduced systolic
pressure as there is a reduction in stroke volume. There may also be a rise in
diastolic pressure. Vasoconstriction is a physiologic response to hypovolaemia
and may reflect in an elevation in diastolic pressure.
Page 20 of 24
Analysis of Pulse Pressure Waveform
Ventricular contraction creates a pulse wave. This is the pressure pulse that is felt
when determining a patient’s heart rate by palpation. The pressure is transduced
from an intra-arterial catheter into an electronic waveform. The normal arterial
pressure waveform is shown in Figure 11.
Fig 11 29
The systolic upstroke or Anacrotic limb (Gradient a) mainly reflects the pressure
pulse produced by left ventricular contraction. The pressure pulse is followed
slightly later by the flow wave caused by the actual displacement of blood volume.
The Anacrotic shoulder is the rounded part at the top of the waveform. Of many
things this represents a volume displacement. The dicrotic limb is evident by the
dicrotic notch. This notch occurs on the cardiac cycle as the aortic valve closes
secondary to subsequent retrograde flow. The location of the dicrotic notch varies
according to the timing of aortic closure of the cardiac cycle. Aortic closure may be
delayed in patients with hypovolaemia. As a result the dicrotic notch occurs farther
down on the dicrotic limb in hypovolaemic patients.31 Gradient (b) is the area
under the trace which reflects the stroke volume. 31 Gradient (c) or the run off
wave reflects the afterload. 31 The position of the dicrotic notch can therefore be
used as another marker of hypovolaemia. The evidence for this relationship is
weak as there are many other variables which impact on the location of the
dicrotic notch. It can however be used as another factor pointing towards
hypovolaemia. 31
Page 21 of 24
CONCLUSION
Over a period of almost twenty years numerous authors have progressively and
systematically researched and reviewed the utility of filling pressures and their
surrogates as tools for fluid assessment and optimization of cardiac output.
Recent publications on the validity of central venous and pulmonary capillary
wedge pressures only bear out concerns expressed almost seventy years ago
and first hinted at over a century ago.
The overwhelming consensus is that Central Venous Pressure and Pulmonary
Capillary Wedge Pressure measurement and interpretation are of little value in the
management of fluid status. Newer dynamic means, such as systolic pressure
variation, stroke volume variation and pulse pressure variation, all seem to hold
much in store for clinical practice. Already these new derivatives appear set to
displace our old stalwarts from the clinical arena.
Monitoring systolic pressure variation enables real time prediction and monitoring
of the left ventricular response to preload enhancement. It also aids in guiding
fluid therapy. Even the haemodynamic response to Passive Leg Raising would
appear to be a promising index of fluid responsiveness. Likewise, Static Indices,
although less specific, can tell us so much about the patients’ fluid state. From
simple insight into the physiology of Blood Pressure one can deduce more than
just taking it as yet another number. With the hype around fluids and the
endothelium, judging a patients intravascular fluid status will come under close
scrutiny. What is important to remember is that what exactly is in the pipeline (or
how much), can be guided by clinical judgment and simple indices that are
commonly available in patients with basic monitoring.
Page 22 of 24
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