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118 F. M. Pieracci
However, artificial attainment of this level of oxygen delivery (1) is extremely
difficult and (2) requires excessive volume expansion. Results of clinical
trials randomizing critically ill patients to supra-normal oxygen delivery have
not demonstrated improved outcomes, and have observed an increased
risk of pulmonary edema, intestinal ischemia, and ambominal compartment
syndrome.
• Corticosteroids for septic shock: See Chapter 11-(ii).
Resuscitation markers
• No one marker is superior to the other; use multiple markers when possible;
be aware of the limitations of each marker; follow trends, not isolated values.
• SvO
• Lactate: Advantages include specificity for tissue hypoperfusion (as
• Base deficit: Advantages include rapidity and unaffected by hepatic and renal
: Advantages include potentially earlier recognition of shock (prior to
2
initiation of anaerobic metabolism). Disadvantages include (1) invasive and
(2) false negatives seen with septic shock and cell death.
compared to the base deficit). Disadvantages include the need to differentiate
type A lactic acidosis (over-production) from Type B lactic acidosis (impaired
clearance). This distinction can be made by calculating the lactate to pyruvate
ratio, which is high in Type A lactic acidosis and normal in Type B lactic
acidosis.
clearance. Disadvantages include lack of specificity. One common problem is
that of non-anion gap, hyperchloremic metabolic acidosis. Specifically,
volume expansion with chloride rich fluid results in hyperchloremia and,
to maintain electroneutrality, excretion of bicarbonate. A non-anion gap
metabolic acidosis ensues, which can be misinterpreted as worsening shock.
The incorrect reaction is to give more chloride-rich fluid, exacerbating the
problem. Avoid this trap by obtaining a serum chloride concentration and
calculating an anion gap on every patient with a metabolic acidosis [see also
Chapter 7-(v)].
Resuscitation Strategies 119
Practical Algorithm(s) /Diagrams
Fig. 1. Algorithm for the management of shock. ACS indicates abdominal compartment
syndrome; CVP, central venous pressure; PAOP, pulmonary artery occlusion pressure;
PEEP, positive end expiratory pressure; PLR, passive leg raise; PPV, pulse pressure variation; SPV, systolic pressure variation (Reproduced with permission from Pieracci and
Biffl).
Review of Current Literature with References
• Kern et al. conducted a meta-analysis of 21 randomized trials comparing
goal-directed therapy to conventional management of patients in shock. The
majority of studies involved optimization of PAOP, cardiac output, and DO2
to either normal or supranormal levels. A benefit to such therapy was
observed only among those studies that maximized DO2 either before or early
after the onset of organ dysfunction (Crit Care Med 2002; 30: 1686).
• The largest individual trial of crystalloid vs. colloid is the Saline versus
Albumin Fluid Evaluation (SAFE) study, which randomized nearly 7,000
critically ill patients to resuscitation with either 4% albumin or saline.
Mortality, organ failure, and length of stay were equivalent between groups.
120 F. M. Pieracci
A priori subgroup analyses revealed a trend toward an increased mortality
for the albumin as compared to the saline group among trauma patients
(13.6% vs 10.0%, respectively, P ¼ .06) and a decreased mortality among
patients with severe sepsis (30.7% vs 35.3%, respectively, P ¼ .09). However,
reduced statistical power in these subgroup analyses precluded meaningful
interpretation (New Engl J Med 2004; 305: 2247).
Chapter 5-(iv)
Measurements of Preload Responsiveness
Fredric M. Pieracci, MD, MPH*
* Acute Care Surgeon, Denver Health Medical Center
Take Home Points
• The relationship between left ventricular end diastolic volume (LVEDV),
commonly termed preload, and stroke volume (SV) is described by the
Starling Curve (Fig. 1).
• Preload responsiveness refers to the ability of an increase in LVEDV to result
in a clinically meaningful increase in SV. A clinically meaningful increase in
generally considered to be ≥10%.
• Achievement of a clinically meaningful increase in SV is the fundamental
intention of volume expansion of critically ill patients in shock. Volume
administration that does not result in a clinically meaningful increase in SV
provides no benefit in terms of increasing cardiac output (and ultimately oxygen
delivery), and exposes the patient to the deleterious effects of overzealous fluid
administration.
Contact information: Denver Health Medical Center, 777 Bannock Street, MC 0206, A388,
Denver, CO 80206. Email: Fredric.pieracci@dhha.org
121
122 F. M. Pieracci
• Many ICU variables are routinely misused as measurements of preload
responsiveness, when in fact they provide no such information. These include
heart rate, blood pressure, and urine output.
• Measurements of preload responsiveness may be divided into static and
dynamic.
• Static measurements of preload responsiveness provide a point-in-time
estimation of LVEDV. These measurements are then used to predict if
volume expansion will result in a clinically meaningful increase in
SV. Although most static variables measure pressure as a surrogate for
volume, it is possible to measure LVEDV directly using echocardiography
(Chapter 13). Commonly used static measurements of preload responsiveness include the central venous pressure (CVP) and pulmonary capillary
wedge pressure (PCWP).
• Whereas static measurements predict preload responsiveness, dynamic
measurements actually measure it. This measurement is done by exploiting
natural changes in LVEDV that occur during respiration (either spontaneous
or while ventilated), and their corresponding effects on SV or its surrogates.
Commonly used examples of dynamic measurements of preload responsiveness include stroke volume variation (SVV), systolic blood pressure variation
(SPV), and pulse pressure variation (PPV). For any of these variables, respiratory variation of ≥12% predicts preload responsiveness with a high
degree of accuracy.
• Multiple comparative studies have documented the superiority of dynamic
measurements over static measurements of preload responsiveness. A basic
understanding of Starling Curve physiology explains this discrepancy. In
addition to improved accuracy, dynamic measurements are also generally
less invasive, and able to predict preload responsiveness prior to fluid
administration.
• Clinical situations in which the accuracy of dynamic measurements of preload
responsiveness may be compromised include cardiac dysrhythmias and ventilator dysynchrony. In these cases, a modified “preload challenge,” achieved by
either passive leg raise (PLR) or exogenous fluid administration, may be
employed to determine an accurate measurement of preload responsiveness.
• Despite strong evidence documenting superiority, dynamic measurements of
preload responsiveness are still employed infrequently in ICUs, mostly
because of unfamiliarity. However, the prevalence of these techniques has
increased, and they are now included in several professional organizations’
recommendations, including the most recent Surviving Sepsis Campaign
Guidelines.
Measurements of Preload Responsiveness 123
Background
• The extremes of intravascular volume are equally deleterious. Hypovolemia
results in impaired tissue perfusion due to decreased cardiac output. However,
hypervolemia also results in decreased tissue perfusion due to increased
hydrostatic pressures within tissues (resulting in increased afterload), and
organ dysfunction from tissue edema.
• Volume expansion of critically ill patients is exceedingly common. The
average critically ill patient is 2–4 L positive each day.
• A positive fluid balance correlates linearly with mortality among ICU patients.
• Common, organ-specific sequellea of overzealous volume expansion include
worsening intra-cranial hypertension in patients with traumatic brain injury
[Chapter 4-(ii)], worsening gas exchange in mechanically ventilated patients
with acute lung injury [Chapter 6-(v)], and intra-abdominal hypertension
[Chapter 8-(vii)].
• On the most fundamental level, the purpose of volume expansion is to
improve oxygen delivery to tissues by increasing cardiac output, which is
in turn increased by increasing stroke volume, that is then increased by
increasing preload (assuming preload responsiveness) [Chapter 5-(i)].
• It may be extrapolated from the previous point that volume expansion will be
useful only if (1) there is evidence of impaired tissue perfusion and (2) an
increase in preload will result in a clinically meaningful increase in SV.
• Unfortunately, many studies have reported that only about 50% of patients
who are considered to be preload responsive, and therefore receive a fluid
bolus, actually realize a clinically meaningful increase in SV. Therefore, the
other half of patients was exposed to the risks of volume expansion without
any benefit.
• As a result of the deleterious effects of overzealous volume expansion, it is
imperative to utilize tests that estimate preload responsiveness with a high
degree of accuracy, thereby minimizing the likelihood of unnecessary fluid
administration.
Main Body
• According to the Starling Curve (Fig. 1), increases in preload have variable
effects on SV depending on the baseline preload; whereas a low baseline
preload corresponds to a large increase in SV following volume expansion,
a high baseline preload results in no increase in SV following volume
expansion.
124 F. M. Pieracci
• Every patient’s Starling Curve is different. Furthermore, multiple Starling
Curves exist within any individual patient; both the slope and position of the
curve are affected by changes in cardiac dynamics, vasopressor requirements,
and afterload, among other variables.
• Most static measurements of preload responsiveness attempt to estimate base-
line preload by using pressure as a surrogate for volume. This strategy is
problematic for several reasons:
Intravascular pressure is affected by multiple other variables besides
preload, including intra-thoracic pressure, intra-abdominal pressure, and
intra-cranial pressure.
The intravascular pressure within more proximal structures is used to
estimate left ventricular end diastolic pressure; superior vena caval/right
atrial pressure in the case of CVP and pulmonary capillary pressure in the
case of PCWP. This accuracy of this estimation is decreased in the setting
of any mechanical abnormality between the two structures (e.g., valvular
disease).
Even when pressure is a reliable surrogate for volume, a static measurement
provides no information about (1) the patient’s current Starling Curve and
(2) the baseline preload location on that curve. This is the fundamental
limitation of static measurements. For example, a CVP of two may
correspond to any baseline preload location on any of the curves shown in
Fig. 1. Furthermore, as shown in Fig. 1, the same baseline preload
(A) results in a markedly different response in SV following volume
expansion depending on the underlying Starling Curve (a to b vs. a'
to b'). This limitation holds true even at the extremes of preload estimation
(e.g., CVP of 1 or CVP of 20), as well as when using trends as opposed to
absolute values.
Static measurements typically are invasive, requiring a central venous catheter
in the case of CVP, and a pulmonary artery catheter in the case of PCWP.
• These theoretical limitations of static measurements have been borne out by
outcomes data (see Review of Current Literature section): multiple publica-
tions have documented the inability of both the CVP and PCWP to predict
preload responsiveness in a variety of clinic scenarios, even when accounting
specifically for both extreme values and trends.
• In contrast to static measurements, dynamic measurements of preload
responsiveness estimate on which portion of the Starling Curve a patient is
Measurements of Preload Responsiveness 125
currently operating. They are therefore able to predict preload responsiveness with a high degree of accuracy.
• All variations of dynamic measurements exploit inherent respiratory-
mediated changes in both preload and corresponding SV. These natural variations are summarized in Fig. 2.
• Patients who are operating on the steep (preload responsive) portion of the
Starling Curve demonstrate exaggerated respiratory variation in SV, and thus
both cardiac output and blood pressure.
• A respiratory variation in stroke volume (SVV), systolic blood pressure
(SPV), and pulse pressure (PPV) of ≥12% has been found to be highly accurate for predicting a clinically meaningful increase in SV following volume
expansion.
• The value of 12% corresponds to the maximum value minus the minimum
value, and divided by their average. In the case of SPV:
SPV = (SPV
For example, inputting SPV
– SPV
max
of 130 and SPV
max
min
) / (SPV
+ SPV
max
of 127 would result in SPV
min
min
/ 2)
of 2.3%. This value would not suggest preload responsiveness. By contrast,
inputting SPV
of 130 and SPV
max
of 115 would result in SPV of 12.2%.
min
This value would not suggest preload responsiveness.
• Both the SPV and PPV can be measured accurately in mechanically venti-
lated patients with a functional arterial catheter in place (Chapter 15).
• Measurement of SVV requires a specialized catheter that uses arterial pulse
contour analysis to provide both SVV and continuous cardiac output. This is
advantageous as (1) measurement of cardiac output helps differentiate the
various etiologies of shock [Chapter 5-(ii)] and (2) the effect of volume
expansion on cardiac output may be assessed real time. These devices are
commercially available from multiple vendors.
• In addition to improved accuracy for predicting preload responsiveness,
dynamic measurements have the following advantages over static
measurements:
They are less invasive, requiring only a functional arterial line as opposed
to a central venous catheter.
They predict preload responsiveness prior to giving a fl uid bolus, such
that unnecessary volume expansion is avoided.
The measurement is continuous, such that a response to volume expansion
may be accessed real-time.
126 F. M. Pieracci
• Multiple publications have demonstrated high accuracy for predicting preload
responsiveness for SPV, PPV, and SVV, with a receiver operator characteristic
area under the curve in the 0.85 range.
• The accuracy of dynamic measurements of preload responsiveness is limited
in the presence of either cardiac arrhythmias or ventilator dysynchrony. In
these cases, either the systolic blood pressure (SBP) or SV (most commercially available devices also provide continuous measurement of SV) may be
exploited to determine preload responsiveness. First, the baseline SV is noted.
Volume expansion using 10 cc/kg is then given. The SV measurement is again
noted. A change in SV of ≥10% is considered preload responsive, and the
volume expansion is repeated until either (1) the patient is no longer in shock
or (2) the change in SV is <10%.
• A PLR may be used in place of the exogenous fluid bolus in order
to avoid a potentially unnecessary volume expansion. This maneuver,
shown in Fig. 3, involves tilting the patient in order to return venous
blood pooled in the lower extremities into the cardiac circulation. Studies
have shown that a PLR results in approximately 250–500 mL of venous
blood return in a 70 kg patient. Thus, in order to determine preload
responsiveness in a patient with either cardiac arrhythmia or ventilator
dysynchrony, the SV or SBP is noted, a PLR is performed, and the SV or
SBP is repeated. A change of ≥10% suggests preload responsiveness.
Note that in this example, no fluid bolus is necessary to determine
preload responsiveness.
• These relatively non-invasive measurements should be performed in all criti-
cally ill patients when volume expansion is being considered (e.g., hypotension,
oliguria, tachycardia). Current data suggest that only one half of these patients
will demonstrate evidence of preload responsiveness. In this case, utilization
of dynamic measurements not only avoids unnecessary volume expansion,
but also expedites the search for other sources of the original derangement
(e.g., blunt cardiac injury as a cause of tachycardia, or acute tubular necrosis
as a cause of oliguria).
Measurements of Preload Responsiveness 127
Practical Algorithm(s)/Diagrams
Fig. 1. The starling curve.
The Starling Curve depicts the relationship between cardiac preload (x axis) and stroke
volume (SV, y axis). The curve begins at its steepest, wherein small changes in preload
corresponding to large changes in SV. It then begins to flatten exponentially, such that
further increases in preload achieve smaller corresponding increases in SV. Finally, the
curve becomes flat; over this range, further increases in preload result in no increase in SV.
In this graph, a family of Starling Curves is shown, reflecting the heterogeneity of curves
both between and among critically ill patients. As can be seen in the graph, an identical
volume expansion (from A to B) results in a drastically different effect on SV depending
on the curve (from a to b on the bottom curve, as opposed to from a' to b' on the top curve).
In this case, the static measurement A would be unable to predict the effect of volume
expansion without knowing under which Starling Curve the patient is operating.