Download Pulse Pressure Variation Predicts Fluid Responsiveness Following

Pulse Pressure Variation Predicts Fluid
Responsiveness Following Coronary
Artery Bypass Surgery*
Andreas Kramer, MD; David Zygun, MD; Harvey Hawes, MSC;
Paul Easton, MD, FCCP; and Andre Ferland, MD
Study objective: To determine whether the degree of pulse pressure variation (PPV) and systolic
pressure variation (SPV) predict an increase in cardiac output (CO) in response to volume
challenge in postoperative patients who have undergone coronary artery bypass grafting (CABG),
and to determine whether PPV is superior to SPV in this setting.
Design and setting: This was a prospective clinical study conducted in the cardiovascular ICU of
a university hospital.
Patients: Twenty-one patients were studied immediately after arrival in the ICU following CABG.
Intervention: A fluid bolus was administered to all patients.
Measurements: Hemodynamic measurements, including central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), CO (thermodilution), percentage of SPV (%SPV), and
percentage of PPV (%PPV), were performed shortly after patient arrival in the ICU. Patients were
given a rapid 500-mL fluid challenge, after which hemodynamic measurements were repeated.
Patients whose CO increased by > 12% were considered to be fluid responders. The ability of
different parameters to distinguish between responders and nonresponders was compared.
Results: In response to the volume challenge, 6 patients were responders and 15 were
nonresponders. Baseline CVP and PAOP were no different between these two groups. In
contrast, the %SPV and the %PPV were significantly higher in responders than in nonresponders.
Receiver operating characteristic curve analysis suggested that the %PPV was the best predictor
of fluid responsiveness. The ideal %PPV threshold for distinguishing responders from nonresponders was found to be 11. A PPV value of > 11% predicted an increase in CO with 100%
sensitivity and 93% specificity.
Conclusion: PPV and SPV can be used to predict whether or not volume expansion will increase
CO in postoperative CABG patients. PPV was superior to SPV at predicting fluid responsiveness.
Both of these measures were far superior to CVP and PAOP.
(CHEST 2004; 126:1563–1568)
Key words: cardiac output; preload; pulse pressure variation; systolic pressure variation
Abbreviations: CABG ⫽ coronary artery bypass grafting; CO ⫽ cardiac output; CVP ⫽ central venous pressure;
HR ⫽ heart rate; LV ⫽ left ventricle, ventricular; LVEDA ⫽ left ventricular end-diastolic area; MAP ⫽ mean arterial
pressure; PAOP ⫽ pulmonary artery occlusion pressure; PPV ⫽ pulse pressure variation; %PPV ⫽ percentage of pulse
pressure; RV ⫽ right ventricle; SPV ⫽ systolic pressure variation; %SPV ⫽ percentage of systolic pressure;
SVV ⫽ stroke volume variation
measurement of intravascular volume status
T heto guide
fluid management is an important aspect of caring for critically ill patients. Central
venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) are still commonly used by
clinicians in determining whether or not to adminis*From the Brandon Regional Health Center (Dr. Kramer),
Brandon, MB, Canada; the Department of Critical Care Medicine (Drs. Zygun, Easton, and Ferland), Foothills Medical Center, Calgary, AB, Canada; and the Faculty of Medicine (Mr.
Hawes), University of Calgary, Calgary, AB, Canada.
Manuscript received December 2, 2003; revision accepted June
15, 2004.
www.chestjournal.org
ter fluid. This practice persists despite numerous
studies showing that cardiac filling pressures are
often misleading when used to predict the effects of
volume expansion on cardiac output (CO).1–5 Even
the assessment of left ventricular end-diastolic area
(LVEDA) with echocardiography is not necessarily a
good predictor of fluid responsiveness.5,6
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail:
[email protected]).
Correspondence to: Andreas H. Kramer, MD, Intensive Care
Unit, Brandon Regional Health Center, 150 McTavish Ave East,
Brandon, MB, R7A 2B3 Canada; e-mail: [email protected]
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Systolic pressure variation (SPV) and pulse pressure variation (PPV) during mechanical ventilation
have been shown to predict the hemodynamic effects of volume expansion in patients with septic
shock.5,7 Positive pressure in the thorax has the effect
of decreasing preload and increasing afterload in the
right ventricle (RV). This leads to a decrease in RV
stroke volume during inspiration, which in turn
induces a subsequent decrease in LV preload and
stroke volume, usually reaching its nadir during
expiration.8 In addition, LV stroke volume may
increase slightly during inspiration as a consequence
of increased LV filling from enhanced pulmonary
venous return,9,10 increased LV compliance because
of decreased RV dimensions,11 decreased LV afterload,12 and external pressure on the LV.13 Thus,
respiratory variations in arterial pressure reflect, in
large part, the corresponding cyclic variations in LV
stroke volume. These variations are exaggerated
when the LV is functioning on the steep portion of
the Frank-Starling curve, whereby small changes in
preload induce large changes in stroke volume.14
SPV is also due in part to the direct effects of positive
pleural pressure on the aorta.15 This effect is potentially avoided with the use of PPV because pleural
pressure affects systolic and diastolic BP to the same
degree. Indeed, PPV has been shown in one study to
be a better index of fluid responsiveness than SPV.7
Patients undergoing coronary artery bypass grafting (CABG) often require postoperative hemodynamic support in the ICU. LV and RV function are
known to be depressed for several hours following
CABG, probably as a result of multiple factors,
including the lingering effects of cardioplegia, myocardial ischemia, reperfusion injury, hypothermiainduced vasoconstriction, and the perioperative use
of ␤-blockers. The use of PPV and SPV as predictors
of fluid responsiveness may not be as reliable in
patients with impaired LV function. Pizov et al16
showed in a dog model that LV depression caused a
reduction in SPV. Moreover, with the induction of
cardiac failure, a larger proportion of the SPV was
due to the “delta up” (ie, the increase in systolic
pressure during inspiration) rather than the “delta
down” (ie, the decrease in systolic pressure during
expiration). SPV may therefore also be indicative of
the stroke volume enhancement that occurs due to
the afterload-reducing effects of mechanical ventilation rather than reflecting only preload dependence.
For this reason, numerous previous studies5,17–19
excluded patients with reduced LV function. In a
study of patients undergoing CABG, BennettGuererro et al20 actually found SPV to be inferior to
PAOP as a predictor of fluid responsiveness. In
contrast, Reuter et al21,22 showed that the degree of
stroke volume variation (SVV), assessed using pulse
contour analysis, correlated well with changes in CO
in response to volume loading in postoperative
CABG patients, even when LV function was depressed. The objective of this study was (1) to
determine whether PPV and SPV could be used to
predict fluid responsiveness in patients recently separated from cardiopulmonary bypass following
CABG and (2) to determine whether PPV was
superior to SPV in this setting.
Materials and Methods
Patients
The study protocol was approved by the Conjoint Health
Research Ethics Board at the University of Calgary. Informed
written consent was obtained. Any patient undergoing elective or
emergency CABG met the inclusion criteria for the study.
Patients were excluded if they had arrhythmias, valvular heart
disease, a temperature of ⬍ 34.5°C, PAOP ⬎ 24 mm Hg, or the
need to change vasoactive medications during the study protocol
because of hemodynamic instability. A total of 21 nonconsecutive
patients were studied.
Hemodynamics
All patients were monitored using an arterial catheter (Cook
Critical Care; Bloomington, IN) and a pulmonary artery catheter
(Abbott Critical Care Systems; Morgan Hill, CA). Transducers
were positioned at the level of the fourth intercostal space in the
midaxillary line and were zeroed to atmospheric pressure. BP,
heart rate (HR), and CVP were measured continuously. PAOP
was assessed at end-expiration. The CO level was determined by
thermodilution using the mean of at least three measurements
performed at end-expiration.
Mechanical Ventilation
All patients were sedated with propofol and an opiate to ensure
that there was no evidence of spontaneous breathing effort.
Mechanical ventilation was performed with tidal volumes of 8 to
10 mL/kg, a positive end-expiratory pressure of 5 mm Hg, and a
fraction of inspired oxygen of 0.6. Chest wall excursion was
recorded using a band placed around the thorax in order to time
BP variation to different phases of the respiratory cycle.
BP Variation
The arterial pressure tracing was recorded continuously during
the first postoperative hour using an analog-to-digital converter
and data acquisition software (Datasponge; Bioscience Analysis
Software; Calgary, AB, Canada). The mean percentage of PPV
(%PPV) and percentage of SPV (%SPV) over 1 min were
determined before and after the administration of fluid. These
values were calculated as follows:
%SPV ⫽ (SBPmax ⫺ SBPmin)/
[(SBPmax ⫹ SBPmin)/2] ⫻ 100%
%PPV ⫽ (PPmax ⫺ PPmin)/[(PPmax ⫹ PPmin)/2] ⫻ 100%
where SBPmax is maximum SBP, SBPmin is minimum SBP,
PPmax is maximum pulse pressure, and PPmin is minimum pulse
pressure.
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Clinical Investigations
Table 1—Patient Characteristics*
Characteristics
Values
Gender
Male
Female
Age, yr
Weight, kg
Elective surgery
Recent ACS
␤-blocker
Calcium blocker
ACE Inhibitor
ARB
Dopamine,† ␮g/kg/min
Phenylephrine,† ␮g/kg/min
Epinephrine,† ␮g/kg/min
Pump time, min
Cross-clamp time, min
15
6
64.7 ⫾ 9.4
87.8 ⫾ 19.9
11 (52)
10 (48)
15 (71)
12 (57)
11 (52)
5 (24)
8/2.8 ⫾ 1.0
7/0.4 ⫾ 0.2
1/0.06
69.5 ⫾ 22.2
49.0 ⫾ 17.7
Values given as No. (%) or mean ⫾ SD, unless otherwise indicated.
*ACS ⫽ acute coronary syndrome; ARB ⫽ angiotensin receptor
blocker; ACE ⫽ angiotensin-converting enzyme.
†Values given as No. of patients/mean dose.
Fluid Challenge
For volume expansion, we used 500 mL “pump blood,” which
is collected during the separation of patients from cardiopulmonary bypass. The fluid bolus was administered rapidly over 10 to
15 min. Hemodynamic measurements were performed immediately before and after the volume challenge. Changes to vasoactive and sedative infusions or to ventilator settings were not
permitted during the study period. Based on the work of Stetz et
al,23 patients whose CO levels increased by ⱖ 12% in response to
volume expansion were considered to be “responders.” The
ability of different hemodynamic parameters to predict whether
patients would be responders or nonresponders was compared.
Statistical Analysis
All variables were explored in a univariate manner using
classical descriptive statistics. The change in hemodynamic variables associated with volume loading was assessed using the
paired Student t test. Between-group comparisons were accomplished with the Student t test when variables were normally
distributed and the Mann-Whitney U test if they were not. A p
value of ⬍ 0.05 was considered to be statistically significant.
Logistic regression models were created to assess the ability of
each preload index to predict fluid responsiveness. The discriminative ability of each model was assessed by calculating the area
under the receiver operating characteristic curve.
Results
Overall, 32 patients were recruited, but 11 had to
be excluded for the following reasons: insufficient
pump blood available (4 patients); spontaneous
breathing not suppressed with additional sedation (3
patients); bradycardia requiring pacing (3 patients);
and hemodynamic instability (necessitating the use
of a cardiac assist device) (1 patient). The characteristics of the remaining 21 patients are described in
Table 1. Eleven patients underwent surgery for
chronic ischemic heart disease, while 10 patients
required urgent revascularization for a recent acute
coronary syndrome with high-risk coronary artery
blockages.
Preoperative investigations revealed that cardiac
function was abnormal in numerous patients. Echocardiograms were performed in 17 patients, and
were interpreted as showing depressed LV function
in 7 patients (41%) and LV hypertrophy in 5 patients
(29%). Preoperative cardiac catheterization revealed
regional wall motion abnormalities in 16 of 21
patients (76%). Ejection fraction was determined by
ventriculogram in 19 of 21 patients and was estimated to be ⬍ 50% in 5 of 19 patients (24%). A total
of 9 of 21 patients (43%) had LV end-diastolic
pressure measured at ⬎ 18 mm Hg.
Hemodynamic measurements at baseline and following volume expansion are shown in Table 2. CO
level, mean arterial pressure (MAP), CVP, and
PAOP all increased significantly, while HR, %PPV,
and %SPV all decreased in response to fluid administration. There was little correlation between base-
Table 2—Hemodynamic Variables Before and After Volume Expansion in Fluid Responders and Fluid
Nonresponders*
Fluid Responders
Fluid Nonresponders
Variables
Baseline
Volume Expansion
Baseline
Volume Expansion
HR, beats/min
MAP, mm Hg
CO, L/min
CVP, mm Hg
PAOP, mm Hg
% PPV
% SPV
92.8 ⫾ 13.8†
65.5 ⫾ 3.7†
5.6 ⫾ 1.4
13.5 ⫾ 4.1
11.5 ⫾ 6.1
16.3 ⫾ 4.0‡
9.3 ⫾ 2.1‡
88.8 ⫾ 12.8
78.7 ⫾ 12.9
6.7 ⫾ 1.5
16.5 ⫾ 5.2
15.7 ⫾ 5.3
9.1 ⫾ 4.7
5.6 ⫾ 2.2
76.7 ⫾ 12.6
73.1 ⫾ 8.8
6.3 ⫾ 1.7
13.3 ⫾ 2.9
11.9 ⫾ 3.4
7.1 ⫾ 2.7
4.8 ⫾ 1.7
75.1 ⫾ 11.2
80.7 ⫾ 10.6
6.6 ⫾ 1.8
15.3 ⫾ 2.8
14.7 ⫾ 4.2
4.8 ⫾ 1.7
3.7 ⫾ 0.9
*Values given as mean ⫾ SD.
†p ⬍ 0.05 vs baseline value in nonresponder.
‡p ⬍ 0.001 vs baseline value in nonresponder.
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1565
line values of both CVP and PAOP and the percent
change in CO following fluid challenge (Fig 1)
(r ⫽ ⫺0.13, p ⫽ 0.58 and r ⫽ ⫺0.16, p ⫽ 0.50, respectively). In contrast, the baseline %SPV and the
%PPV correlated significantly with the change in CO
induced by fluid (r ⫽ 0.65, p ⫽ 0.001 and r ⫽ 0.66,
p ⫽ 0.001, respectively).
Of the 21 patients, 6 were found to be responders
(increase in CO, ⱖ 12%), while 15 were nonresponders. Baseline CVP and PAOP were no different
in responders compared with nonresponders. In
contrast, the baseline values of %SPV and %PPV
were significantly higher in responders than in nonresponders (Table 2). The area under the receiver
operating characteristic curve, showing the ability of
different hemodynamic parameters to discriminate
between responders and nonresponders, was greatest for the %PPV (0.99), followed by the %SPV
(0.93) [Table 3]. A PPV of ⱖ 11% predicted an
increase in CO of ⱖ 12%, with a sensitivity of
100% and a specificity of 93%. PAOP was only
slightly better than chance at predicting fluid responsiveness.
Discussion
Our results show that variations in arterial pressure during mechanical ventilation can be used to
accurately predict the effects of volume expansion in
cardiac surgical patients. In contrast, both CVP and
PAOP were poor predictors of fluid responsiveness.
These findings support those of a systematic review24
that concluded that “dynamic” measures of preload
responsiveness (ie, SPV, PPV, inspiratory decrease in
CVP, and respiratory changes in aortic blood velocity) are superior to “static” preload parameters (ie,
CVP, PAOP, and LVEDA) at guiding fluid management. This review acknowledged that there are still
relatively few studies validating dynamic parameters.
PPV was the best predictor of fluid responsiveness, with a threshold value of 11% being optimal.
Michard et al7 previously found a PPV of 13% to
have the highest sensitivity and specificity in predicting an increase in CO in response to volume expansion in a study of septic patients. The rationale for
using PPV rather than SPV is that it is more reflective of variations in stroke volume. SPV occurs not
only because of variations in stroke volume, but also
because of the direct effects of positive pleural
pressure on the aorta during inspiration. Therefore,
a degree of SPV is observed even if the stroke
volume remains constant. In contrast, pleural pressure is transmitted to the aorta during both systole
and diastole, such that there should be no impact on
PPV.
Our findings are of particular interest given the
patient population studied. A significant proportion
of the patients were recognized preoperatively as
having LV dysfunction. Even in those without preoperative cardiac dysfunction, it is well-recognized
that LV ejection fraction is usually reduced significantly following CABG. Breisblatt et al25 found that
the mean LV ejection fraction of CABG patients was
reduced from 58% preoperatively to 46% immediately postoperatively, reaching a nadir of 37% in the
first few hours following surgery. Despite the concern that variations in BP in patients with LV
dysfunction may reflect the beneficial afterloadreducing properties of mechanical ventilation rather
Table 3—Area Under the Receiver Operating
Characteristic Curve Showing Ability of Various
Hemodynamic Parameters to Predict Fluid
Responsiveness*
Baseline
% PPV
% SPV
HR
MAP
PAOP
CVP
Figure 1. Correlation between the percent change in CO and
the baseline values of PAOP and %PPV
AUROC
95% CI
0.99
0.94
0.81
0.81
0.63
0.49
0.96–1.00
0.83–1.00
0.61–1.00
0.62–1.00
0.32–0.94
0.18–0.81
*AUROC ⫽ area under the receiver operating characteristic;
CI ⫽ confidence interval.
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Clinical Investigations
than only preload dependence, both PPV and SPV
were good predictors of fluid responsiveness. It is
possible, however, that these measures may not be as
useful in patients with more severe cardiac depression than the ones included in this study.
Reuter et al21 used pulse contour analysis to
determine SVV in a patient population that was
similar to ours. In patients with normal preoperative
LV function, SVV was superior to PAOP and
LVEDA at predicting fluid responsiveness. However, while SVV was still useful in patients who were
known preoperatively to have a reduced ejection
fraction, it was no better than conventional preload
measures in predicting fluid responsiveness in these
patients.22 Our study sample was too small to allow a
comparison of the utility of PPV in patients with
normal preoperative LV function and those with
depressed LV function.
Bennett-Guerrero et al20 studied CABG patients
preoperatively and found SPV to be significantly
higher in fluid responders than in nonresponders,
but they were unable to determine an optimal
threshold value to distinguish the two groups. PPV
was not specifically assessed. SPV was reported as an
absolute value rather than as a percentage, even
though the latter is likely more meaningful.14,26 The
methodology used to determine variations in BP
from the arterial tracing differed somewhat from that
used in our study.
Although all information was obtained in a prospective manner, the analysis of the BP tracing was
performed after completion of the study protocol,
thereby introducing the possibility of bias. This is a
weakness that has been apparent in most previous
studies of arterial pressure variation. At the time of
this study, monitors with the capability of determining these values “on-line” in an automated fashion
were not yet available. Because SPV and PPV were
determined as the mean value over a whole minute,
and therefore several respiratory cycles, we believe
that our measurements were very accurate.
In our center, pump blood is routinely reinfused
into patients on admission to the ICU following
coronary bypass surgery. In order to interfere as little
as possible with standard patient care, we used this
pump blood, rather than colloid or crystalloid, as our
means of volume expansion. It should be kept in
mind that because properties such as the viscosity
and hematocrit of pump blood are not completely
consistent, the potency of our fluid challenge will
have varied slightly from patient to patient. Given
that the goal of our study was to evaluate the ability
of SPV and PPV to predict fluid responsiveness in
general, rather than predicting the magnitude of
response, we do not believe that minor differences in
www.chestjournal.org
the degree of volume expansion would have influenced our results significantly.
The purpose of assessing intravascular volume
status in critically ill patients is primarily to determine whether or not they will benefit from
the administration of fluid. The overuse of catecholamines without adequate volume resuscitation
may result in tissue ischemia. Conversely, the excessive use of fluids with no resultant increase in CO
may cause edema and contribute to further tissue
injury and organ dysfunction. Despite the inability of
conventional static preload parameters such as
PAOP and CVP to predict fluid responsiveness,
these measures are still commonly used in making
decisions about fluid management.27,28 It is possible
that the measurement of cardiac filling pressures
may help to predict whether or not volume expansion will contribute to edema formation, and therefore act as a safeguard against excessive fluid administration.
In summary, both PPV and SPV during controlled
mechanical ventilation are useful predictors of increased CO in response to volume expansion in
postoperative CABG patients. In this study, PPV was
slightly superior to SPV, and far superior to CVP and
PAOP at predicting fluid responsiveness.
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