Download This educational slide module includes notes and diagrams of slides

This educational slide module includes notes and diagrams of slides to be used in
presenting the concepts of volumetric monitoring using the Edwards Vigilance®
monitoring system. This system provides the clinician with the ability to monitor
continuous cardiac output (CCO), continuous mixed venous oxygen saturation
(SvO2) and continuous end diastolic volume (CEDV). This module will discuss the
concepts and methodology related to volumetric monitoring. Research studies
supporting the use of this technology will also be discussed.
Strategies to implement the use of these new volumetric parameters at the
bedside will be discussed in a case scenario format at the end of the module.
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
The major components of oxygen delivery (DO2) are depicted on this slide. DO2
reflects the amount of oxygen leaving the heart to be delivered to the tissues. It is
determined by multiplying cardiac output (CO) by arterial oxygen content (CaO2).
One of the most important goals in managing the critically ill patient is to maximize
the delivery of oxygen to prevent the occurrence of tissue hypoxia.
16
One of the major components of oxygen delivery is cardiac output. Cardiac output
is the volume of blood that is ejected from the heart per minute. It is equal to
stroke volume (volume of blood ejected per heart beat) times heart rate (number
of times the heart contracts per minute). Stroke volume is influenced by preload,
afterload and contractility.
17
Stroke volume is the amount of blood that is ejected from the heart per heart beat.
Preload, afterload and contractility influence stroke volume. All three of the
components of SV are interrelated and a change in one component may impact
the others.
Each of the three components of stroke volume will be discussed in the next few
slides beginning with contractility.
18
Contractility is the inherent property of the myocardial fibers to shorten and
therefore contract. This allows the heart to increase its extent and force of muscle
shortening. The degree of inherent contractility is referred to as the inotropic state
of the myocardium.
19
Several different parameters are used to reflect contractility. These include stroke
volume (SV), stroke volume index (SVI), left ventricular stroke work index
(LVSWI) and right ventricular stroke work index (RVSWI).
The normal values and formulas for each of the measures is found on this slide.
20
Afterload refers to the resistance or pressure that the ventricles must overcome to
eject their contents into the systemic and pulmonary circulations. Subsequently,
afterload is the pressure against which the contractile force of the ventricles is
exerted.
Afterload is determined by many factors including; the wall thickness of the
ventricle, volume and mass of blood in the pulmonary or systemic circulation, and
the impedance of the vasculature.
21
In the clinical setting, a common measure of right ventricular afterload is
pulmonary vascular resistance (PVR).
The normal value and formula is found on this slide.
22
In the clinical setting, a common measure of left ventricular afterload is systemic
vascular resistance (SVR).
The normal value and formula is found on this slide.
23
Preload is the amount of myocardial fiber stretch at the end of diastole, or the
amount of blood in the ventricles at the end of diastole.
24
The Frank Starling Law describes the relationship between myocardial fiber length
and the force of contraction. This law states that the greater the diastolic volume
or fiber stretch at the end of diastole, the stronger the subsequent force of
contraction during systole.
This phenomenon will occur until a physiological limit has been reached. Once
this limit is reached, the force of contraction will begin to decline, regardless of the
increase in fiber stretch.
Manipulating of preload influences stroke volume and subsequently cardiac
output.
25
Historically, it has been very difficult to actually measure fiber length or volume at
the bedside. Clinically, it has been acceptable to measure preload as a pressure.
Preload has been indirectly measured for both the right and left ventricle.
The central venous pressure (CVP) and right atrial pressure (RAP) are used to
evaluate right ventricular preload.
Left ventricular preload is evaluated by assessing pulmonary artery diastolic
pressure (PAD), pulmonary artery wedge pressure (PAWP) and left atrial
pressure (LAP).
26
Traditionally, preload has been measured as a pressure since it has been very
difficult to actually measure fiber length or volume at the bedside.
This was based on the assumption that pressures correlate with left ventricular
end-diastolic volume (LVEDV) and that ventricular compliance does not change.
27
Traditionally, preload has been measured as a pressure since it has been very
difficult to actually measure fiber length or volume at the bedside.
This was based on the assumption that pressures correlate with left ventricular
end-diastolic volume (LVEDV) and that ventricular compliance does not change.
28
29
A comprehensive understanding of the anatomy and physiology of the right
ventricle (RV) and its relationship to the left ventricle (LV) is important in order to
appreciate the unique role of the RV in biventricular function.
The location and shape of the RV has made it more difficult to study than the LV.
The RV lies anterior to the LV and posterior to the sternum.
The LV has a conical shape where as the RV has a crescent shape. The
interventricular septum (IVS) separates the two ventricles, acting as a common
wall.
30
The lateral free walls of the right and left ventricles are very different in structure
due to the pressure that they encounter from the pulmonary and systemic
circulations.
The right ventricle (RV) has a very thin free wall. The RV normally encounters low
pressure as it pumps blood into the pulmonary circulation. Unlike the left ventricle,
the RV is very sensitive to changes in afterload.
The left ventricle (LV) in contrast has a thick and muscular free wall. This ventricle
normally encounters high pressure as it pumps blood into the systemic circulation.
31
The right ventricle (RV) is a very compliant, distensible chamber. It is referred to
as a volume pump.
In contrast, the left ventricle is a thick walled, less distensible chamber. It is
referred to as a pressure pump.
32
The right coronary artery (RCA) supplies blood to the right atrium, free wall of the
RV, portions of the LV and one third of the interventricular septum (IVS).
The left anterior descending artery (LAD) branch of the left coronary artery (LCA)
supplies a small portion of the LV free wall and the anterior two-thirds of the
interventricular septum.
The left circumflex artery (Cx) supplies blood to the lateral and posterior wall of
the left ventricle.
It is clinically important to keep in mind that there is dual blood supply to both the
right and left ventricles. This becomes clinically relevant when occlusion of the
RCA or LAD occurs. Occlusion of either of these arteries may result in
biventricular dysfunction.
33
34
35
Over the years there has been an abundance of articles in the literature describing
the right ventricle (RV) and its significance, especially the role of the RV in the
critically ill patient.
Historically, the right ventricle (RV) was once viewed as a passive conduit with
little influence in overall ventricular performance. It is now known that the right
ventricle plays a significant role in global ventricular performance.
36
The right and left ventricles work together to maintain adequate cardiac output
and hence oxygen delivery to the tissues.
The goal of the right ventricle (RV) is to take the blood or volume it receives and to
deliver it to the left ventricle (LV).
If RV function is compromised, this will affect delivery of preload to the left side of
the heart.
37
Even though the ventricles are structurally different, they are interdependent for
several reasons. The four reasons are listed on this slide and will be discussed in
the subsequent slides.
38
The two ventricles are also joined in a series by the pulmonary circulation. This
allows blood to flow from the right side of the heart to the left side.
39
The right and left ventricles are separated by a mobile interventricular septum
(IVS).
Normally the septum is curved or bowed into the right ventricle (RV) secondary to
the higher pressure and tension generated in the left ventricle (LV).
Enlargement of either ventricle or changes in pressures within the ventricles may
cause this septum to shift toward the opposite chamber.
40
The ventricles are encased in a relatively rigid pericardial sac. This sac normally
acts as a restraining force during ventricular filling.
41
To fully apppreciate the role of the right ventricle, it is important to be familiar with
the most common causes of RV dysfunction.
RV function is most commonly threatened by an increase in impedance to ejection
(RV afterload -PVR).
The thin RV free wall limits this ventricle’s ability to respond to acute changes in
resistance (PVR). So in response to an acute increase in pressure or resistance,
the RV compensates very differently than the LV.
The next several slides will discuss causes of RV dysfunction and compensatory
mechanisms that come in to play when RV function is threatened.
42
RV dysfunction most commonly results from an increase in pulmonary vascular
resistance (PVR).
There are many causes of increased PVR. Some of the more common causes
are listed on this slide.
43
It is important to understand the compensatory mechanisms that come into play
when the ventricles encounter an increase in afterload. The thicker, muscular
walled left ventricle (LV) responds to increased afterload (SVR) by generating a
higher pressure or tension to overcome the increase in pressure.
The RV normally does not encounter a high pressure as it pumps blood into the
pulmonary circulation since pulmonary artery pressures are normally much lower
than the systemic blood pressure. The thinner free wall of the RV limits this
ventricle’s ability to respond to changes in afterload.
When the RV does encounter an increase in afterload (PVR) it cannot
compensate like the LV by just overcoming the pressure. The RV compensates
by dilating its free wall in order to maintain adequate stroke volume (SV).
Dilation of the RV free wall augments preload as described by the Frank-Starling
Law which states that an increase in volume (preload) will result in an increase in
the subsequent force of contraction, therefore leading to increased SV and CO up
to a physiological limit.
44
This diagram illustrates how the right ventricle (RV) compensates when it
encounters an increase in afterload (PVR).
The RV compensates for an increase in afterload by dilating out its free wall. As
the RV dilates, the interventricular septum (IVS) is displaced into the left ventricle
(LV). This RV dilation and septal displacement affects the relationship between
pressure and volume in the LV.
Although the LV has the same volume, there is less space in the chamber,
resulting in an increase in LV pressure. Because of this, pressure and volume
within the LV are no longer equal.
The goal of this RV dilation therefore is to maintain adequate delivery of stroke
volume (SV) to the left side of the heart. This is necessary in order to maintain
adequate LV function and cardiac output (CO).
45
Right ventricular dilatation results in displacement of the mobile interventricular
septum. It may also result in decreased blood flow to the right coronary artery
which creates an imbalance between oxygen supply and demand.
46
47
Until the early 1970’s, there was no way to clinically assess preload at the
bedside. The introduction of the Edwards Swan-Ganz® catheter allowed for the
bedside measurement of preload as a pressure.
Traditionally, pulmonary artery catheters (PAC) have been used for bedside
assessment of cardiac performance in the critically ill. This technology allows for
the measurement of cardiac output (CO) and has historically used pressure based
measurements to assess the determinants of stroke volume (SV), including
preload, afterload and contractility.
48
We have already described the Frank-Starling Law under the previous discussion
of preload.
Manipulation of preload is one of the most common ways to increase stroke
volume (SV) and hence cardiac output (CO).
49
Historically we have assumed that right atrial pressure (RAP)/central venous
pressure (CVP) reflect right ventricular (RV) preload and that pulmonary artery
diastolic (PAD)/pulmonary artery wedge pressure (PAWP)/left atrial pressure
(LAP) reflect left ventricular (LV) preload.
When we use pressures to reflect preload we make the above assumptions that
pressures correlate with volume, assuming that the atrioventricular valves are
competent.
50
When we make the assumption that pressure reflects volume we are assuming
that there is a linear relationship between pressure and volume. That a change in
pressure would reflect a change in volume and similarly, a change in volume
would reflect a change in pressure.
51
It is important to realize that the actual relationship between end-diastolic volume
and end-diastolic pressure is dependent upon the compliance of the muscle wall.
This relationship between pressure and volume is referred to as compliance and
is not linear but is said to be curvilinear.
A normal compliance curve is illustrated above. It is important to assess where a
critically ill patient falls on the compliance curve.
52
A normal compliance curve is seen on this slide. It is important to assess where a
critically ill patient falls on the compliance curve in order to understand the
relationship between volume and pressure.
When preload (volume) is low (on lower portion of the curve); relatively large
increases in volume create relatively small increases in pressure.
A clinical example might involve a very hypovolemic trauma patient that is
receiving large amounts of volume who has very little change in right atrial (RA) or
pulmonary artery wedge pressure (PAWP). This patient would be on the lower
portion of this compliance curve.
53
When preload (volume) is high (on upper portion of the curve), a small change in
volume will result in a large change in pressure.
A clinical example might involve a patient who has been receiving large amounts
of fluid with very little change in right atrial (RAP) or pulmonary artery wedge
pressure (PAWP), who receives just a little more fluid and a dramatic increase in
pressure is seen.
54
Compliance is not a static state but is a dynamic and ever changing state in the
critically ill patient.
There is not only one compliance curve, but many compliance curves as
illustrated by the picture above.
It is important to remember that patient condition and therapeutic interventions will
alter the relationship between pressure and volume (compliance).
The compliance curve will change in response to many factors including:
therapeutic interventions (such as administration of vasopressors or vasodilators),
disease states (such as cardiomyopathy or ischemia) and pressures surrounding
the heart.
55
The relationship between pressure and volume changes when the ventricles
become stiffer or less compliant. In a less compliant ventricle, a greater pressure
is generated with very little increase in volume. This results in a shift of the
compliance curve to the left, where a given volume (preload) is recorded as a
higher pressure. The end result is that pressure does not reflect volume.
Many clinical conditions and interventions result in decreased compliance.
Examples of some of these causes of decreased compliance are listed above.
56
Changes in pressures surrounding the heart from the clinical conditions listed
above may also cause compliance to be decreased, resulting in a shift of the
compliance curve to the left, where a given volume (preload) is recorded as a
higher pressure. The end result is that pressure does not reflect volume.
57
Increased compliance of the ventricles allows for large changes in volume with
little rise in pressure. When a ventricle is more compliant, it is able to hold more
volume while reflecting a smaller pressure. The compliance curve shifts to the
right as compliance is increased, so that for the same volume, less of a change in
pressure is seen. The end result is that pressure no longer reflects volume
(preload).
Many clinical conditions and interventions result in increased compliance.
Examples of some of these causes of increased compliance are listed above.
58
59
This section will review the new continuous volumetric parameters including
stroke volume (SV), end-diastolic volume (EDV), end-systolic volume (ESV) and
right ventricular ejection fraction (EF).
60
Stroke volume is not a new parameter. It can be calculated by taking cardiac
output (CO) divided by heart rate (HR) and then multiplied by 1000.
Normal ranges are listed above. These are just textbook reference values. Keep
in mind that normal ranges will vary for each critically ill patient and that normal
values must be individualized for each patient.
61
End-diastolic volume (EDV) is a parameter that is measured when using the
continuous volumetric technology. EDV is simply a measure of preload as a
volume rather than a pressure. It is the volume of blood stretching the fibers prior
to ventricular contraction or at the end of diastole.
Normal ranges are listed above. These are just text book reference values. Keep
in mind that normal ranges will vary for each critically ill patient and that normal
values must be individualized for each patient.
62
End-systolic volume (ESV) is another volumetric value that can be measured
continuously with the volumetric technology. It is the amount of blood left over
after contraction or the volume of blood in the ventricles at the end of systole.
Normal ranges are listed above. These are just textbook reference values. Keep
in mind that normal ranges will vary for each critically ill patient and that normal
values must be individualized for each patient.
63
The end-systolic volume (ESV) may be increased by many clinical situations,
including situations where there is an increase in afterload or a decrease in
contractility.
As the ventricle meets more resistance or has less contractile force, less is
pumped out and more blood remains in the ventricle.
64
Similar to stroke volume (SV), ejection fraction (EF) is not a new parameter.
Normally however, EF is obtained from various tests such as angiography and
echocardiography. In these situations, EF is a static number. However, in looking
at EF, which is simply the percent of blood ejected with each beat, or SV/EDV, EF
is realized as a dynamic number, one that may change anytime SV or EDV are
manipulated.
In looking at EF, it is simply the relationship between EDV and SV, the SV divided
by the EDV or the amount of volume ejected over the preload (amount of volume
available).
A normal range is listed above. This is just a textbook reference value. Keep in
mind that normal ranges will vary for each critically ill patient and that normal
values must be individualized for each patient.
65
66
The Vigilance® Monitor System consists of a modified pulmonary artery catheter
and the Vigilance® Monitor.
This system measures right heart volumes using continuous cardiac output (CCO)
technology to obtain indicator dilution curves.
The next few slides will describe the continuous volumetric technology.
67
The various continuous volumetric values are measured by a modified pulmonary
artery catheter that has a thermal filament that lies between 14 and 25 cm from
the tip of the catheter. The proximal lumen exits in the RA at 26 cm and a
standard thermistor lies 4 cm from the tip of the catheter for measuring pulmonary
artery (PA) temperature.
68
Volumetric measurements including end-diastolic volume (EDV) are measured by
periodically warming the blood in the right atrium and ventricle via the thermal
filament with a known quantity of thermal energy, and by sensing heart rate from a
“slaved” ECG signal.
This technology eliminates the need for fluid bolus injections because the signal is
now using small energy impulses. Because of this, all the technical errors
associated with bolus injection are eliminated.
The catheter thermistor detects the small change in blood temperature
downstream, and the Vigilance® Monitor computes an ejection fraction by using
thermodilution principles. Ejection fraction is computed based on the curve’s
exponential slope and the continuous average heart rate that is obtained from the
slaved-in patient’s ECG signal.
Subsequently, right ventricular volumes including continuous EDV are then
calculated using ejection fraction, heart rate and CO without the need for user
calibration or intervention.
69
The next few slides will briefly describe the technology that is used to continuously
measure end-diastolic volume (EDV), end-diastolic volume index (EDVI), endsystolic volume (ESV), end-systolic volume index (ESVI), ejection fraction (EF),
stroke volume (SV) and stroke volume index (SVI).
70
71
The input signal is small energy impulses that are emitted directly into the blood
stream via the thermal filament in a random on-off pattern.
This random on-off pattern (pseudo-random-binary sequence) is repeated
approximately every 60 seconds. This provides a unique input signal for the
Vigilance® computer to evaluate when determining cardiac output (CO) and
ejection fraction (EF).
72
73
74
Right ventricular volumes including continuous end-diastolic volume (CEDV) are
calculated using ejection fraction, heart rate and cardiac output.
75
The value displayed is updated from new cross-correlated information
approximately every 60 seconds.
The updated value reflects an average of the last 6-9 minutes of data is and
referred to as “time averaging”.
A change in CEDV and CCO will usually be reflected in 6-9 minutes as new
values are collected.
76
Using the previous described technology, the Vigilance® Monitor system displays
continuously monitored volumetric measurements.
This screen is referred to as the STAT screen. It displays both continuous cardiac
output (CCO) and continuous end-diastolic volume (EDV). Each value in the
small box represents a fast estimate of CCO and CEDV values. The most recent
value is time stamped. All other values are accompanied by the duration of time
that has passed since that value and the most recent value was first displayed.
The CCO is found in the top portion of the box and the CEDV in the lower portion.
In this example, the first box in the upper left hand corner of the screen shows the
most recent CCO and CEDV values. The small box to the right shows the value
obtained approximately 60 seconds earlier; the one to the right of that shows the
value obtained approximately 60 seconds prior and so on. Each value has a time
stamp above it indicating the time that has passed since that value and the most
recent value were obtained.
77
Some of the common indications for the use of volumetric monitoring are listed on
this slide.
78
79
Due to concern about the patient’s urine output, a decision was made to improve
renal perfusion and oxygen delivery DO2. What would be your recommendation?
Based on the PAWP of 24 mmHg, the clinician might assume the patient is
volume overloaded. However, does the wedge of 24mmHg indicate that the
patient is volume overloaded?
80
After looking at the volumetric data, the EDVI indicates that the patient is not
volume overloaded. Based on this information, the clinician decided to administer
volume in an effort to increase oxygen delivery and renal perfusion. Increasing
inotropic support might have been the initial therapeutic response based on the
initial hemodynamic information. However, because of the low EDVI, fluid rather
than inotropic support was attempted.
81
Fluid therapy greatly increased the cardiac output / index and oxygen delivery
resulting in an increased urine output. Note that the PAWP did not change after
the administration of the volume. In this instance PAWP, a measure of pressure
rather than volume, failed to reflect the true volume status of the patient. In
addition, notice that the heart rate slowed and the SVR lowered at same time the
cardiac output increased.
82
Note the improvement in RVEF following the administration of volume. The EDVI
increased from 68mL/m2 to 100mL/m2 resulting in increased right ventricular
contractility and overall myocardial performance.
83
What is your differential diagnosis based on the above hemodynamic data? Does
this patient have cardiac tamponade or right ventricular failure?
84
Does adding the volumetric information clarify the problem? The RVEDV is low
indicating the ventricle is not filling adequately. When the other hemodynamic
parameters are reassessed, note the PAWP, PAD and RAP are within 2-3 mmHg
of each other. This is termed “diastolic plateau” or equilibration of filling pressures
and is a classic sign of cardiac tamponade. However, it is often missed. By adding
the volumetric measurements to the picture, the clinician is able to validate the
presence of cardiac tamponade and intervene much more quickly. This patient
was returned to the operating room for evacuation of a large clot.
85
After returning to the ICU following evacuation of the clot in the mediastinum, the
filling pressures fell back to more “normal” values, the RVEDV increased and the
CO and CI increased as well. Jones, et al, demonstrated that EDV was a much
better indicator of cardiac tamponade when compared to pressure measurements.
The volumetric parameters changed much earlier than the pressure
measurements, providing an earlier warning sign.
JW Jones, et al.
Usefulness of right ventricular indices in early diagnosis of cardiac tamponade
Ann Thorac Surg 1992, vol 54: 44-49
86
What parameters are less than optimal? There was much concern about the
patient’s low urine output. The PAWP of 14 was noted and the decision was made
to administer fluids, hoping the urine output would improve.
87
Note that the CO / CI and urine output is not significantly increased. The PAWP
remained at 14 mmHg. The decision was made to administer more volume.
88
Following the additional volume administration, the urine output remained low and
there were no significant changes in the hemodynamic parameters. There was a
suggestion that an additional 250cc of Albumin be administered for the low urine
output. Prior to additional volume administration, the RV parameters were plotted.
89
Initially, the patient’s RVEF was 38%. Following each 250cc of Albumin, the EDV
increased, but the RVEF fell, indicating the ventricle was volume overloaded and
myocardial contractility was impaired. The decision was made to start an inotrope.
90
Plotting this patients Frank-Starling Curve illustrates clearly what has happened.
The improvement in stroke volume and decrease in end diastolic volume is
indicative of the movement to a higher ventricular function.
91
Following the initiation of inotropes, myocardial contractility was improved as
evidenced by the increased CO/CI and RVEF. If the decreased RVEF had been
assessed following the initial 250cc of Albumin, the clinicians might have
considered initiating the inotrope sooner, resulting in improved myocardial
performance, renal perfusion and urine output.
92
This slide reflects the intermittent measurements of RVEDVI and CI prior to and at
approximately two hour intervals following the administration of fluids during the
resuscitation of this patient. While one can identify the trend indicating an
increase in both CI and RVEDVI, the clinician cannot see what the response to
each of the interventions was.
93
This slide has the continuous parameters of cardiac index and RVEDVI
superimposed upon the intermittent measurements. The “positive” response to
each of the interventions is demonstrated, providing the clinician with more
information. Having the continuous information available provides the clinician
with more information. If the clinician knew the response to the initial 2 liters of
fluid, additional volume could have been given to maintain what had been
achieved with the initial volume administration.
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
116
117
118
119