Novel Tools For Hemodynamic Monitoring in Critically Ill Patients With Shock - UpToDate

Novel tools for hemodynamic monitoring in critically ill patients with shock - UpToDate 07.02.
2020, 11:25
Authors: Mark E Mikkelsen, MD, MSCE, David F Gaieski, MD, Nicholas J Johnson, MD
Section Editor: Scott Manaker, MD, PhD
Deputy Editor: Geraldine Finlay, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2020. | This topic last updated: Nov 26, 2019.
INTRODUCTION
Central venous and pulmonary artery catheters (PAC) are invasive tools that have traditionally
been used for hemodynamic monitoring in patients who present with shock. However, these
tools have drawbacks and inaccuracies. Thus, several, less invasive, novel technologies are
available or being investigated for use to assess parameters such as cardiac output,
intravascular volume status, responsiveness to intravenous fluid administration, and tissue
perfusion. They can potentially be used in the emergency department, intensive care unit, and
operating room when caring for patients with shock or hypovolemia.
This topic will discuss novel techniques for hemodynamic monitoring. The evaluation and
treatment of shock, central venous pressure and PAC monitoring are discussed separately.
(See "Evaluation and management of suspected sepsis and septic shock in adults" and
"Evaluation of and initial approach to the adult patient with undifferentiated hypotension and
shock" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and
waveforms in adults".)
GENERAL PRINCIPLES
Deficiencies of standard techniques — For many years, the gold standard for
hemodynamic monitoring was the pulmonary artery catheter (PAC). However, several studies
have demonstrated that the PAC fails to improve outcome in critically ill patients and may be
associated with harm. In the late 1990s central venous pressure (CVP) monitoring via central
venous catheterization (CVC) emerged as a less invasive alternative that was incorporated
into guideline management of sepsis; however, this practice has also been questioned [1-3].
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Novel tools for hemodynamic monitoring in critically ill patients with shock - UpToDate 07.02.2020, 11:25
(See "Pulmonary artery catheterization: Indications, contraindications, and complications in

adults" and "Evaluation and management of suspected sepsis and septic shock in adults".)
CVP and PAC monitoring suffer from the following inadequacies:
● Inconsistent prediction of fluid responsiveness – Both CVP and pulmonary alveolar

occlusion pressure have been shown to have poor predictive value for predicting fluid
responsiveness (arbitrarily defined as an increase of at least 15 percent in cardiac output
[CO] in response to a 500 mL bolus fluid challenge, as measured by PAC) [3-6].
Furthermore, CVP is affected by a number of other physiologic derangements, including
valvular regurgitation, right ventricular dysfunction, pulmonary hypertension, and variation
in intrathoracic pressure with respiration.
● Complications associated with invasiveness – CVCs and PACs require central

venous access and have been associated with a number of complications, including
arrhythmias, injury to vascular or cardiac structures, catheter-associated bloodstream
infection, pneumothorax, and venous thromboembolism. (See "Pulmonary artery
catheterization: Indications, contraindications, and complications in adults", section on
'Complications' and "Complications of central venous catheters and their prevention".)
● Data interpretation is difficult – Data from CVCs and PACs may be challenging to
interpret both due to the lack of standardization of technique and the hemodynamic
complexity of patients receiving them. Several studies have documented poor
interobserver reliability and challenges interpreting intravascular pressures from PACs,
even among trained intensivists [7,8]. (See "Pulmonary artery catheterization:
Interpretation of hemodynamic values and waveforms in adults".)
Indications — A plethora of techniques aimed at overcoming the deficiencies associated with

standard hemodynamic monitoring tools have been developed, many of which use complex
imaging technology and computer algorithms to estimate the following:
● Fluid responsiveness and volume status (see 'Volume status and fluid
responsiveness' below)
● Cardiac output (see 'Cardiac output' below)
● Tissue perfusion (see 'Measurement of tissue oxygen saturation' below and

'Measurement of microcirculatory blood flow' below and 'Tissue perfusion' below)
While no large randomized trials of resuscitation guided by noninvasive hemodynamic

monitors have been conducted, a systematic review of 13 trials enrolling over 1600 subjects
found that such practice was associated with reduced mortality, ICU length of stay, and
duration of mechanical ventilation [9]. These findings will likely only increase the interest in
use of these tools in critically ill patients.
Limitations — The devices discussed in this topic have several limitations, some of which
explain why their use is not widespread. First, many of these tools use proprietary algorithms
or imaging technology, making it difficult to confirm their validity. Second, some devices
produce data that still require complex interpretation which can be challenging even for expert
clinicians. Third, no large randomized trials of resuscitation guided by noninvasive
hemodynamic monitors have been conducted.
Physiologic principles
Upstream versus downstream monitors — A greater understanding of tissue and

cellular hypoxia as a cardinal feature of shock has led to the concept of "upstream" and
"downstream" indicators of organ perfusion [10].
● Upstream – "Upstream" ("macro") markers assess flow and pressure in the heart, vena
cava, pulmonary artery, and aorta and are the traditional variables that have been used to
assess the hemodynamic status of critically ill patients. The majority of existing
hemodynamic monitors are upstream monitors. (See 'Volume status and fluid
responsiveness' below.)
● Downstream – Shock with end-organ dysfunction occurs at the capillary and tissue
levels [11]. Tools have been developed that follow alterations in tissue oxygenation and
microvascular blood flow. These techniques are known as the "downstream" (or "micro")
markers of resuscitation. (See 'Measurement of tissue oxygen saturation' below and
'Measurement of microcirculatory blood flow' below.)
Heart-lung interaction during mechanical ventilation — The underlying physiologic

principle common to a number of the monitoring tools discussed in this topic is the heart-lung
interaction [12]. During the inspiratory phase of positive pressure ventilation, intrathoracic
pressure increases, passively increasing right atrial pressure, causing venous return to
decrease and the vena cava to distend. If both the right ventricle (RV) and left ventricle (LV)
are fluid responsive, this leads to decreased RV output and, after two or three heartbeats,
decreased LV output [12,13]. In preload-dependent patients, cyclic changes in LV stroke

volume (SV) and its coupled arterial pulse pressure are seen, and the magnitude of the
changes is proportional to volume responsiveness. The inverse is true during spontaneous
negative pressure breathing, though this has not been well-studied. (See 'Pulse contour
analysis (fluid responsiveness)' below.)
VOLUME STATUS AND FLUID RESPONSIVENESS
The devices listed in this section rely on the principles that underlie the heart-lung interaction
during mechanical ventilation and/or visually assess flow in the heart and major vessels (ie
"upstream" monitors). (See 'Physiologic principles' above.)
Pulse contour analysis (fluid responsiveness)
Pulse pressure variation (PPV) — Pulse pressure (ie, the difference between systolic
and diastolic arterial blood pressure) varies with respiration induced by positive pressure
ventilation. Variation in pulse pressure is thought to be an indicator of a patient's position on
the Frank-Starling Curve, a curve that denotes a patient's response to pre-load (ie, fluid
responsiveness) (figure 1) [14]. Patients operating on the flat part of the curve are insensitive
to changes in preload induced by mechanical ventilation and thus have a low variation in the
pulse pressure, indicating a lack of fluid responsiveness. In contrast, patients operating on the
steep portion of the curve, are sensitive to cyclic changes in preload induced by mechanical
ventilation and hence, exhibit greater variation in the pulse pressure (ie, fluid responsive).
Numerous studies have demonstrated that a PPV of at least 13 to 15 percent is strongly

associated with volume responsiveness [4,13,15]. As an example, one systematic review of
29 studies reported a higher area under the receiver operating characteristic curve (AUROC)
for PPV compared with CVP (0.94 versus 0.55) as an indicator of fluid responsiveness
(sensitivity and specificity were 0.88 each) [15].
PPV is typically calculated as the ratio of the maximum pulse pressure (systolic blood
pressure minus diastolic blood pressure; PPmax) minus the minimum pulse pressure (PPmin)
to the mean pulse pressure (PPmean), usually averaged over three or more breaths.
Although it can be measured from pressures derived from manual cuff-inflation,
measurements are generally more accurate when an arterial catheter is used such that the
latter is preferred (figure 2):
PPV = 100 x (PPmax – PPmin)/PPmean
A number of commercially available devices and monitors capable of measuring PPV exist,
and several use complex proprietary algorithms to additionally calculate stroke volume (SV)
and cardiac output (CO).
While encouraging, this technique is limited to patients who are mechanically ventilated,
receiving ≥8 mL/kg of tidal volume, in sinus rhythm, and not spontaneously triggering the
ventilator, factors that limit its general applicability in the intensive care unit [12]. In addition,
sensitivity for volume responsiveness is decreased in patients ventilated with tidal volumes of
≤6 mL/kg, as the cyclic changes induced by mechanical ventilation are less pronounced [16].
Although patients with intra-abdominal hypertension often have markedly abnormal
respiratory system compliance, PPV is thought to be accurate in this setting [17,18].
Stroke volume variation (SVV) — SV is linearly related to pulse pressure. SVV functions
on the same physiologic principle as PPV (see 'Pulse pressure variation (PPV)' above).
Studies have consistently found that SVV >10 percent is associated with fluid responsiveness
[12,18-21]. As an example, in a study of 40 mechanically ventilated liver transplant patients,
an SVV threshold of >10 percent discriminated fluid responsive patients with a sensitivity and
specificity of 94 percent each [19].
Analogous to PPV, SVV is typically defined as the ratio of the maximum (SVmax) SV minus
the minimum SV (SVmin) to the mean SV (SVmean), averaged over several respiratory
cycles.
SVV = 100 x (SVmax - SVmin)/SVmean
The SV can be calculated from the arterial pressure waveform if the arterial compliance and
systemic vascular resistance are known, values typically derived from an arterial catheter.
SVV is typically measured by several commercially available devices. SVV can also be
determined by measuring aortic blood flow velocity using esophageal Doppler, bioimpedance,
and bioreactance technology, which are discussed below. (See 'Thoracic electrical
bioimpedance or bioreactance' below.)
SVV has the same limitations as PPV (see 'Pulse pressure variation (PPV)' above). Although
there is evidence that suggests that SVV may also be applied to spontaneously breathing
patients, this has not been validated [22]. Patient position may also affect SVV accuracy. In
one study, the 30 degree head-up and prone positions were associated with increased SVV
because of the associated decreased SV associated with these positions [23]. Another study
reported poor correlation with pulmonary artery catheter assessment of volume status [24].
A meta-analysis of 11 randomized trials (total 1015 patients) reported that measuring fluid
responsiveness using the SVV resulted in a shorter length of hospital stay and (weighted
mean difference -1.96 days, 95% CI -2.34 - -1.59) [25]. In addition, there was a reduction in
mortality that was not significant (odds ratio 0.55, 95% CI 0.3-1.03).
Oximetric waveform variation — Using the same principles as PPV and SVV, variation in
the plethysmographic waveform of the pulse oximeter has been proposed as a predictor of
fluid responsiveness. The pleth variability index (PVI) is an automated algorithm that has been
shown to modestly predict fluid responsiveness in the operating room [26-28]. However, PVI
was not associated with fluid responsiveness in two intensive care unit-based studies and has
not been systematically studied in the emergency department setting [28,29].
Passive leg raising or fluid bolus challenge — Many devices used for measuring CO, PPV,
or SVV may be combined with a provocative maneuver to assess whether or not a patient is
fluid responsive. (See 'Cardiac output' below and 'Pulse pressure variation (PPV)' above and
'Stroke volume variation (SVV)' above.)
Provocative maneuvers include:
● Intravenous fluid bolus – These parameters may be measured before and after a small
"test" bolus of intravenous fluid (250 to 500 mL administered over 5 to 10 minutes) to
assess whether a patient is fluid responsive.
● Passive leg raising (PLR) – PLR is thought to provide a bolus of the patient's own
intravascular blood from the capacitance veins of the lower extremities into the thorax
(figure 3) [30]. PLR is accomplished by the following steps:
• Position the patient in the semi-recumbent position with the head and torso elevated
at 45 degrees.
• Obtain a baseline measurement (eg, baseline of CO).
• Lower the patient's upper body and head to the horizontal position and raise and
hold the legs at 45 degrees for one minute.
• Obtain subsequent measurement.
Although poorly defined, a 10 percent increase in CO has been shown in several studies to
predict fluid responsiveness [30-35] whereas a reduction in SVV and PPV is expected in
those who are fluid responsive when provocative maneuvers are used. One meta-analysis of
23 studies reported a sensitivity of 86 percent and a specificity of 92 percent for PLR for
predicting fluid responsiveness; the predictive value of PLR was best when a flow variable
such as CO was used in conjunction with PLR [36]. Another review of 50 studies also
reported that augmentation of CO (or other related parameters) on PLR had a likelihood ratio
of 11 and specificity of 92 percent, better than other measurements of fluid responsiveness
including physical examination, central venous pressure, and respiratory variation in vena
cava diameter [37]. (See 'Vena cava assessment' below.)
Point-of-care ultrasonography — Although point-of-care bedside ultrasonography (POCUS)

is not traditionally considered a monitoring device, evaluation of the lung and heart are
important components of the evaluation of hemodynamically compromised patients [38-43].
Although the data on its use are limited, a randomized trial demonstrated that use of POCUS
for patients with undifferentiated hypotension in the emergency department did not reduce
mortality [44]. Data that supports the use of POCUS in critically ill patients who present with
shock or trauma are discussed separately. (See "Evaluation of and initial approach to the
adult patient with undifferentiated hypotension and shock", section on 'Point-of-care
ultrasonography' and "Emergency ultrasound in adults with abdominal and thoracic trauma"
and "Indications for bedside ultrasonography in the critically-ill adult patient".)
POCUS techniques that assess volume status are discussed here while point-of-care
echocardiography to assess CO is discussed below. (See 'Point-of-care echocardiography'
below.)
Vena cava assessment — Vena cava diameter and dynamic measures of vena cava
collapse have been proposed as tools for estimating intravascular volume status.
Because there is no valve between the vena cava and right atrium, fullness of the vena cava
is thought to correlate with increased right atrial pressure [45,46]. During spontaneous
breathing, a decrease in intrathoracic pressure with inspiration draws blood from the vena
cava into the heart, leading to collapse of the vessel. Conversely, during positive pressure
ventilation, increased intrathoracic pressure pushes blood from the heart into the vena cava,
leading to distention of the vessel. The magnitude of these changes has been proposed to
correlate with intravascular volume status and fluid responsiveness.
Typically, the inferior vena cava (IVC) is identified in its longitudinal axis in the subcostal view
as it enters the right atrium. Diameter should be measured approximately 2 centimeters from
the junction of the IVC and right atrium.
Static measurement of IVC diameter and variation with spontaneous respiration has been
shown to correlate with central venous pressure (CVP) [45,47,48]. A change in IVC diameter
with respiration of 12 to 18 percent has been associated with fluid responsiveness (defined as
an increase in CO of >15 percent after a fluid bolus) in mechanically ventilated patients
[49,50].
A general disadvantage of this technique, and POCUS in general, is that it requires training,
and images obtained are operator-dependent. Several patient factors such as pulmonary
hypertension, valvular regurgitation, and right ventricular dysfunction may also confound
findings. In addition, obtaining accurate serial measurements may be time consuming and
difficult.
Lung ultrasonography — Advocates of the concept of "fluid tolerance" believe that

patients should receive fluid resuscitation until they develop signs of volume overload, such
as pulmonary edema [30,51]. Radiographic and clinical signs of pulmonary edema and clinical
evidence of anasarca are late signs of volume overload and poor endpoints for fluid
resuscitation [30]. Sonographic assessment of B-lines, indicative of interstitial or alveolar
pulmonary edema, and measurement of extravascular lung water (EVLW) are techniques that
may aid in the assessment of early volume overload, but is poorly studied [52-54]. (See
"Bedside pleural ultrasonography: Equipment, technique, and the identification of pleural
effusion and pneumothorax".)
Femoral vein diameter — Preliminary studies measuring femoral vein diameter in

mechanically ventilated patients suggested acceptable correlation with central venous
pressure measurements but additional studies are warranted to validate these findings [55].
CARDIAC OUTPUT
Several invasive and noninvasive technologies have been developed to measure cardiac
output (CO).
Arterial pulse waveform analysis — Several commercially available devices calculate CO

based upon the arterial pulse waveform derived from an arterial catheter. A study of 17
postoperative patients that compared some of these devices to the thermodilution method
using a pulmonary artery catheter (PAC) found that, although the devices produced similar
mean CO values, their dynamic responses and trends correlated poorly with each other [56].
Lithium dilution-based devices — Lithium-based dilution devices use the lithium dilution
method for calibration and subsequent measurement of cardiac output. Lithium is injected via
a central or peripheral vein, and a lithium analyzer is connected to an arterial line, which
measures the wash-out curve over time, generating a curve similar to the thermodilution curve
of a pulmonary artery catheter (PAC; that is also used to calculate the CO). Based upon this
initial calibration, the root mean square method applied to the arterial pressure signal is used
for subsequent measurements, so no additional lithium injections are required. Correlation
between lithium dilution and thermodilution has been reported to be acceptable [10,57].
Recalibration must be performed after significant hemodynamic changes or other
interventions that alter vascular impedance. (See "Pulmonary artery catheterization:
Interpretation of hemodynamic values and waveforms in adults", section on 'Indicator
thermodilution method'.)
Thermodilution-based devices — This device uses pulse contour analysis of the aortic
transpulmonary thermodilution curve for initial calibration. Typically, a small volume of cold
saline is injected into the central vein. Various hemodynamic parameters can be obtained
through analysis of variations in blood temperature taken by the temperature sensor of an
arterial catheter. One device produces CO data by determining the area under the systolic
arterial waveform with some evidence suggesting that its performance is comparable to
thermodilution derived from a PAC [58,59]. As an example, a retrospective study of 46
patients with subarachnoid hemorrhage complicated by Takotsubo cardiomyopathy reported
good correlation between pulse contour cardiac output analysis (PiCCO)-based
measurements of CO and echocardiography [60]. However, in another study of 25
postoperative patients, thermodilution-based measurements did not correlate well with PAC
measurements of CO but reliably tracked changes in CO over time [59].
Arterial waveform-based devices — These devices transduce multiple pressure points
along the arterial pressure curve and calculate cardiac index using these data combined with
vascular resistance data (calculated from age, gender, height, weight, and body surface area)
[61]. Although some studies suggest improved performance among more contemporary
devices [19,30,56,62-67], several studies have shown that the devices inconsistently predict
CO, fluid responsiveness, and SV in hemodynamically compromised patients receiving fluid
boluses or vasoactive agents [61,65,68-70]. These devices may be more promising in the
operating room (OR) setting among high-risk patients undergoing noncardiac surgery [71].
Thoracic electrical bioimpedance or bioreactance
● Thoracic electrical bioimpedance (TEB) – Using low-voltage electrodes placed on the

chest wall, electrical impedance (ie, opposition of flow to an electrical current) across the
thoracic cage is measured. The higher the fluid content within the chest cavity, the lower
the impedance, since fluid conducts electricity. As the heart cycles through systole and
diastole, the volume of blood in the thorax changes, and this can be measured electrically
and extrapolated to determine CO [10].
While early studies demonstrated poor correlation between TEB and invasive measures
of CO [10,72], studies since then report improved accuracy, in patients who have recently
undergone cardiac surgery [73-78]. It has traditionally been thought that TEB is
inaccurate during states of volume overload, but one study demonstrated that it performs
well in patients with decompensated heart failure [79].
● Thoracic bioreactance – Thoracic bioreactance is a modification of bioimpedance

technology, designed to reduce the "signal-to-noise" ratio [61]. Bioreactance technology
determines the "phase shift" in alternating current voltage across the thorax. It is
proposed that the phase shift almost exclusively depends on pulsatile flow and is
therefore less influenced by other intravascular and extravascular fluid in the thorax.
Because the overwhelming majority of pulsatile flow in the thorax comes from the aorta,
the bioreactance signal correlates with aortic flow.
One commercially available device uses four electrode patches each consisting of two
electrodes and calculates CO separately for the right and left side of the body, with the
final CO being the average of these two values [61]. This device reports a number of
hemodynamic parameters, including CO and SV.
Several studies have demonstrated that CO determined by bioreactance technology
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correlates with measurements using pulmonary artery catheter thermodilution or pulse

contour analysis [31,61,80-82]. However, other studies have reported a poor correlation
between bioreactance and thermodilution techniques [83,84]. One observational study
demonstrated that this technology, when incorporated into usual clinical care, was
associated with lower fluid balance, fewer days requiring mechanical ventilation, shorter
ICU length of stay, less hemodialysis, and a shorter time on vasopressors [85].
Electrocautery and external pacemakers interfere with the bioreactance signal, limiting its
use in certain locations (eg, OR) and certain patients [61]. Severe aortic insufficiency or
other thoracic aorta pathology may impact accuracy.
Aortic Doppler — Aortic Doppler measures blood flow velocity in the aorta by means of a
Doppler probe, which may be inserted blindly into the esophagus (esophageal Doppler) or
placed on the anterior chest wall (ie, transcutaneous Doppler). With esophageal Doppler
(usually performed under sedation in a ventilated patient), the CO is calculated based on the
diameter of the aorta, the distribution of the CO to the descending aorta, and the measured
flow velocity of blood in the aorta. Transcutaneous devices use Doppler to calculate CO, using
a proprietary algorithm that determines velocity-time integral (VTI) measurements in the left
and right ventricle outflow tracts. Esophageal Doppler uses similar proprietary algorithms.
Esophageal Doppler has been used with success to guide fluid management in the OR
[61,86-88]. Studies of the transcutaneous device have produced varying results [89-92].
The major limitation of this technology is that the Doppler waveform is highly dependent on
correct positioning, as it must be well aligned with the direction of blood flow. Poor positioning
tends to underestimate true CO.
Point-of-care echocardiography — In addition to a global assessment of ventricle and

valvular function in patients with hemodynamic compromise, CO can be assessed using
bedside echocardiography. (See "Evaluation of and initial approach to the adult patient with
undifferentiated hypotension and shock", section on 'Point-of-care ultrasonography' and
"Indications for bedside ultrasonography in the critically-ill adult patient", section on 'Basic
critical care echocardiography'.)
Cardiac output may be calculated by determining the velocity-time integral (VTI) of the
spectral Doppler envelope (or tracing), most commonly at the level of the left outflow tract
(LVOT). Most ultrasound machines equipped with pulsed wave Doppler may be used. First,
the cross sectional area (CSA) of the LVOT is measured, typically in the parasternal short-axis
view. Next, a pulsed wave Doppler signal of the LVOT is obtained, usually in the apical five-
chamber view to determine the LVOT VTI, from which the CO can be calculated when the
heart rate (HR) is known:
CO = VTI x CSA x HR
Many devices contain software that automate these calculations. Analogous measurements
may be taken of the carotid artery.
Trained physicians are capable of determining CO using these methods with fair reliability [93-
95]. CO determination using carotid blood flow has been shown to be feasible in a number of
disease states, including cardiac arrest [31,96-100]. Serial measurements before and after
fluid bolus have been associated with volume responsiveness [32,33].
Point-of-care echocardiography is highly operator-dependent. Serial measurements may be

challenging, as slight changes in patient or transducer position may lead to large variations in
measurements.
TISSUE PERFUSION
In compensated shock, macrocirculatory measures such as arterial pressure and cardiac

output (CO) may be normal in the face of markedly abnormal oxygen delivery and utilization
[12]. Devices have been developed to measure indices of shock at the tissue level. (See
'Upstream versus downstream monitors' above.)
Measurement of tissue oxygen saturation — Tissue oxygen saturation (StO2)

measurement using near-infrared spectroscopy (NIRS) has been proposed as a downstream
hemodynamic monitoring tool to survey the microcirculation and assess the balance of
oxygen delivery and consumption at the tissue level.
StO2 is measured transcutaneously using NIRS via a number of commercially available

devices that measure tissue absorbance values in a defined range of wavelengths.
StO2 with VOT has been shown to predict outcome and organ dysfunction in patients with
sepsis and congestive heart failure in two small studies, and preliminary studies have
demonstrated its usefulness in trauma patients [101-103].
However, the value of StO2 value is limited because StO2 remains within normal range until
shock is quite advanced. The addition of a dynamic ischemic challenge such as the vascular
occlusion test (VOT; application of a tourniquet or sphygmomanometer above systolic arterial
pressure for brief, defined intervals) may improve the predictive ability of StO2 to identify
tissue hypoperfusion [104].
Measurement of microcirculatory blood flow — There is considerable interest in shock-

induced microcirculatory dysfunction, most notably in the case of sepsis.
The sublingual mucosa is the preferred means to evaluate the microcirculation in critically ill
patients because it shares embryological origin with the splanchnic circulation and can be
easily accessed at the bedside.
Imaging of the sublingual microvasculature is typically obtained using advanced microscopy

techniques, such as sidestream dark field imaging, or by near-infrared spectroscopy (NIRS).
Early studies demonstrated alterations in microvascular flow in patients with sepsis and
cardiogenic shock [11,105]. Multiple subsequent studies have demonstrated that alterations in
sublingual microcirculatory blood flow are associated with poor outcome among patients with
septic shock [106-112].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Sepsis in children and
adults".)
SUMMARY AND RECOMMENDATIONS
● Central venous and pulmonary artery catheterization (PAC), the traditional tools used for
hemodynamic monitoring of patients who present with shock, are invasive and frequently
inaccurate. (See 'Introduction' above and 'Deficiencies of standard techniques' above.)
● Several, less invasive, novel technologies are available or being investigated for use to
assess hemodynamic parameters such as cardiac output (CO), intravascular volume
status, responsiveness to intravenous fluid administration, and tissue perfusion. Although
novel, many of these tools use proprietary algorithms or imaging technology rather than
direct measurements, data interpretation can be challenging, and no randomized studies
have demonstrated improvement in clinical outcome with their use. (See 'General
principles' above.)
● Several devices have been proposed for assessing volume status and fluid
responsiveness. These include measurements of pulse pressure variation (PPV) and
stroke volume variation (SVV) as well as ultrasonography of the vena cava and lung.
Measurements of PPV and SVV typically require an arterial catheter; they are also limited
to patients who are in normal sinus rhythm, mechanically ventilated, and not
spontaneously breathing. Ultrasonography is noninvasive but more time consuming and
expertise-dependent. Their performance compared with PAC monitoring is variable. (See
'Volume status and fluid responsiveness' above.)
● Several invasive and noninvasive technologies have been developed to measure CO

including devices that analyze the arterial waveform, devices that measure thoracic
bioimpedance and bioreactance, aortic Doppler, and point-of-care echocardiography.
Arterial pulse waveform analysis requires an arterial catheter while the others are
noninvasive but require complex algorithms or operator skill. Their performance
compared with standard echocardiography or PAC-determined CO is variable. (See
'Cardiac output' above.)
● There are few commercially available "downstream" monitoring tools capable of

noninvasively assessing oxygen delivery and utilization at the tissue level (eg, near-
infrared spectroscopy). Data are lacking regarding their value in the evaluation and
management shock at the tissue level. (See 'Tissue perfusion' above.)
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Topic 107337 Version 14.0

Novel Tools For Hemodynamic Monitoring in Critically Ill Patients With Shock - UpToDate

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Novel tools for hemodynamic monitoring in critically ill patients with shock - UpToDate 07.02.

(See "Pulmonary artery catheterization: Indications, contraindications, and complications in

CVP and PAC monitoring suffer from the following inadequacies:

● Inconsistent prediction of fluid responsiveness – Both CVP and pulmonary alveolar

● Complications associated with invasiveness – CVCs and PACs require central

Indications — A plethora of techniques aimed at overcoming the deficiencies associated with

● Cardiac output (see 'Cardiac output' below)

● Tissue perfusion (see 'Measurement of tissue oxygen saturation' below and

While no large randomized trials of resuscitation guided by noninvasive hemodynamic

Upstream versus downstream monitors — A greater understanding of tissue and

Heart-lung interaction during mechanical ventilation — The underlying physiologic

decreased LV output [12,13]. In preload-dependent patients, cyclic changes in LV stroke

VOLUME STATUS AND FLUID RESPONSIVENESS

Pulse contour analysis (fluid responsiveness)

Numerous studies have demonstrated that a PPV of at least 13 to 15 percent is strongly

PPV = 100 x (PPmax – PPmin)/PPmean

SVV = 100 x (SVmax - SVmin)/SVmean

Provocative maneuvers include:

• Obtain a baseline measurement (eg, baseline of CO).

hold the legs at 45 degrees for one minute.

• Obtain subsequent measurement.

Point-of-care ultrasonography — Although point-of-care bedside ultrasonography (POCUS)

Lung ultrasonography — Advocates of the concept of "fluid tolerance" believe that

Femoral vein diameter — Preliminary studies measuring femoral vein diameter in

Arterial pulse waveform analysis — Several commercially available devices calculate CO

Arterial waveform-based devices — These devices transduce multiple pressure points

Thoracic electrical bioimpedance or bioreactance

● Thoracic electrical bioimpedance (TEB) – Using low-voltage electrodes placed on the

● Thoracic bioreactance – Thoracic bioreactance is a modification of bioimpedance

Several studies have demonstrated that CO determined by bioreactance technology

correlates with measurements using pulmonary artery catheter thermodilution or pulse

Point-of-care echocardiography — In addition to a global assessment of ventricle and

Point-of-care echocardiography is highly operator-dependent. Serial measurements may be

In compensated shock, macrocirculatory measures such as arterial pressure and cardiac

Measurement of tissue oxygen saturation — Tissue oxygen saturation (StO2)

StO2 is measured transcutaneously using NIRS via a number of commercially available

Measurement of microcirculatory blood flow — There is considerable interest in shock-

Imaging of the sublingual microvasculature is typically obtained using advanced microscopy

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● Several invasive and noninvasive technologies have been developed to measure CO

● There are few commercially available "downstream" monitoring tools capable of

Use of UpToDate is subject to the Subscription and License Agreement.

2. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of

severe sepsis and septic shock. N Engl J Med 2001; 345:1368.

5. Coudray A, Romand JA, Treggiari M, Bendjelid K. Fluid responsiveness in

8. Gnaegi A, Feihl F, Perret C. Intensive care physicians' insufficient knowledge of right-

9. Bednarczyk JM, Fridfinnson JA, Kumar A, et al. Incorporating Dynamic Assessment of

management of patients with shock. Crit Care 2007; 11:131.

17. Renner J, Gruenewald M, Quaden R, et al. Influence of increased intra-abdominal

19. Biais M, Nouette-Gaulain K, Cottenceau V, et al. Uncalibrated pulse contour-derived

20. Biais M, Nouette-Gaulain K, Roullet S, et al. A comparison of stroke volume variation

25. Dave C, Shen J, Chaudhuri D, et al. Dynamic Assessment of Fluid Responsiveness in

compliance. Crit Care Med 2012; 40:152.

43. Jasudavisius A, Arellano R, Martin J, et al. A systematic review of transthoracic and

endorsed by the European Association of Echocardiography, a registered branch of the

60. Mutoh T, Kazumata K, Terasaka S, et al. Impact of transpulmonary thermodilution-based

64. Compton FD, Zukunft B, Hoffmann C, et al. Performance of a minimally invasive

67. Scolletta S, Franchi F, Romagnoli S, et al. Comparison Between Doppler-

77. Kööbi T, Kaukinen S, Kauppinen P. Comparison of methods for cardiac output

80. Squara P, Denjean D, Estagnasie P, et al. Noninvasive cardiac output monitoring

89. Beltramo F, Menteer J, Razavi A, et al. Validation of an Ultrasound Cardiac Output

103. Masip J, Mesquida J, Luengo C, et al. Near-infrared spectroscopy StO2 monitoring to