Page 382 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

252 PART 3: Cardiovascular Disorders

Vital signs, laboratory data, cardiac monitoring,
pulse oximetry, urinary catheterization,
arterial and central venous catheterization

Intervention Dose Goal

CVP 8–12 mm Hg
Crystalloid resuscitation Minimum: 500 mL q30m
1
(warmed) Moderate: 1000 mL q10m
MAP 65 mm Hg
2 Norepinephrine 0.5–50 µg/min

Scv 70%
O 2
3 Red blood cell transfusion Hct 30%

4 Dobutamine 2–20 µg/kg/min

FIGURE 33-2. An approach to initial resuscitation of the circulation based on Early Goal-Directed Therapy. Cardiac monitoring, pulse oximetry, urinary catheterization, and arterial and
central venous catheterizations must be instituted. Volume resuscitation is the initial step. If this is insufficient to raise mean arterial pressure (MAP) to 65 mm Hg, then vasopressors are the
second or simultaneous step. Adequate tissue oxygenation (reflected by central venous O saturation [Scv ] >70%) is a goal of all resuscitation interventions. If this Scv goal is not met by
2
o 2
o 2
volume resuscitation and vasopressors, then red blood cell transfusion and inotrope infusion are the third and fourth interventions, respectively. When the goals of resuscitation are met, then
reduction of vasopressor infusion, with further volume infusion if necessary, becomes a priority. CVP, central venous pressure; Hct, hematocrit.
Early echocardiography is a useful adjunct to the above measure- above 90 g/L is no more beneficial than maintaining a hemoglobin
ments to distinguish poor ventricular pumping function from hypo- level above 70 g/L and only incurs additional transfusion risk. 12
volemia; a good study can exclude or confirm tamponade, right heart Is There a Role for Delayed Resuscitation of Hypovolemia? During brisk ongoing hemor-
failure, pulmonary hypertension possibly due to pulmonary embolism, rhage, massive crystalloid or colloid resuscitation increases blood pressure
or significant valve dysfunction, all of which influence therapy, and can and the rate of hemorrhage, so patient outcome may be worse. This
13
replace more invasive pulmonary artery catheterization. does not mean that resuscitation is detrimental; rather, control of active
Volume Aggressive volume resuscitation up to the point of a heart that bleeding is more important than volume replacement. Preventing blood
is too full is the first step in resuscitation of the circulation. The rate loss conserves warm, oxygen-carrying, protein-containing, biocompat-
and composition of volume expanders must be adjusted in accord with ible intravascular volume and is therefore far superior to replacing ongo-
the working diagnosis. The Early Goal-Directed Therapy algorithm for ing losses with fluids deficient in one or more of these areas. Delayed or
resuscitation of septic shock calls for 500 mL saline every 30 minutes, inadequate volume resuscitation, after blood loss is controlled, is likely a
but this is much too slow in hypovolemic patients in whom 1 L every significant error that will have a detrimental effect on patient outcome. 11
10 minutes, or faster, is initially required. During volume resuscita- Vasopressors Whereas adequate cardiac output is more important than
tion, infusions must be sufficient to test the clinical hypothesis that the blood pressure (because adequate tissue oxygen delivery is the underly-
patient is hypovolemic by effecting a short-term end point indicating ing issue), effective distribution of flow by the vascular system depends
benefit (increased blood pressure and pulse pressure and decreased on an adequate pressure head. At pressures below an autoregulatory limit,
heart rate) or complication (increased jugular venous pressure and normal flow distribution mechanisms are lost, so significant vital organ
pulmonary edema). Absence of either response indicates an inadequate system hypoperfusion may persist in the face of elevated cardiac output
challenge, so the volume administered in the next interval must be due to maldistribution of blood flow. In this case, where inadequate
greater than the previous one. In obvious hemorrhagic shock, immedi- pressure is the dominant problem, an assessment of organ system perfu-
ate hemostasis is essential ; blood must be obtained early, warmed and sion is made (urine output, mentation, and lactic acid concentration),
11
filtered; blood substitutes are administered in large amounts (crystalloid and then a vasopressor agent such as norepinephrine is initiated to raise
or colloid solutions) until blood pressure increases or the heart becomes MAP. The increased afterload will decrease cardiac output, so this
14
too full. At the other extreme, a working diagnosis of cardiogenic shock intervention as single therapy is appropriate only when cardiac output is
without obvious fluid overload requires a smaller volume challenge high. If cardiac output and oxygen delivery are inadequate, then combi-
(250 mL 0.9% NaCl in 20 minutes). In each case, and in all other types nation of vasopressor therapy with inotropic agents should be consi dered
of shock, the next volume challenge depends on the response to the first; (see below).
it should proceed soon after the first so that the physician does not miss Vasopressor therapy increases MAP and can increase cardiac output
the diagnostic clues evident only to the examining critical care team at the (venoconstriction increases venous return) and, therefore, often masks
bedside during this urgent resuscitation (Table 33-3). inadequate volume resuscitation and confounds the diagnosis of the
Role of Red Blood Cell Transfusion During Initial Resuscitation Transfusion of red blood etiology of shock. Thus, vasopressor use as part of Early Goal-Directed
cells is a component of the initial volume resuscitation of shock when severe Therapy must be reassessed during ongoing volume resuscitation. Even
or ongoing blood loss contributes to shock. In addition, when anemia con- when the numerical CVP and MAP goals have been attained, additional
tributes to inadequate oxygen delivery so that mixed venous oxygen satura- rapid volume challenge generally should be used to test for further clini-
tion, or its surrogate Scv <70% despite an adequate CVP (8-12 mm Hg) cal improvement (increased MAP, decreased heart rate, increased urine
O 2
and an adequate MAP (>65 mm Hg), then transfusion of red blood cells output, and increased Scv ) and to determine whether this will allow
O 2
to hematocrit greater than 30% is a reasonable component of Early Goal- titration of vasopressor use down or off.
Directed Therapy and improves outcome. After initial resuscitation and Assessment of organ system perfusion (adequacy of organ function)
3
stabilization, transfusion of red blood cells to maintain a hemoglobin is the most important component of vasopressor therapy; increase in

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