Page 392 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

262 PART 3: Cardiovascular Disorders

• Kumar A, Roberts D, Wood KE, et al. Duration of hypotension regarding the details of shock resuscitation, including the role and type of
before initiation of effective antimicrobial therapy is the critical fluid therapy, metrics for assessing the response, and clinical end points.
determinant of survival in human septic shock. Crit Care Med. Initial resuscitation transforms a hypovolemic, hypodynamic circula-
2006;34(6):1589-1596. tion into one where oxygen transport is normal or high, at least at the
2,3
whole body level, in most septic adults and even following trauma
• Myburgh JA, Finfer S, Bellomo R, et al. Hydroxyethyl starch and cardiac arrest. In contrast to the average patient entering the early
4
or saline for fluid resuscitation in intensive care. N Engl J Med. goal-directed trial (EGDT), once fluids, antimicrobials, vasoactive
2
2012;367(20):1901-1911. drugs, and perhaps blood have been given, resuscitated patients typi-
• Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy cally display elevated central venous pressure (CVP), cardiac output, and
in the treatment of severe sepsis and septic shock. N Engl J Med. mixed and central venous oxyhemoglobin saturations (Sv and Scv ,
O 2
O 2
2001;345(19):1368-1377. respectively). There is no longer global hypoperfusion as judged by any
• Russell JA, Walley KR, Singer J, et al. Vasopressin versus norepi- measure of oxygen transport, even when hypotension, lactic acidosis,
nephrine infusion in patients with septic shock. N Engl J Med. and organ dysfunction persist. Nevertheless, the circulation remains
2008;358(9):877-887. grossly impaired and mean arterial pressure is rarely restored to normal.
Indeed, persistent hypotension and progressive organ failures often
• Shakur H, Roberts I, Bautista R, et al. Effects of tranexamic acid on prompt further fluid administration. When given additional fluid, some
death, vascular occlusive events, and blood transfusion in trauma patients will respond: Blood pressure, cardiac output, oxygen delivery,
patients with significant haemorrhage (CRASH-2): a randomised, Scv , or urine output increases. Other patients will not: Hemodynamics
placebo-controlled trial. Lancet. 2010;376(9734):23-32. fail to improve and the fluid bolus is ineffective, at best. Moreover, ineff-
O 2
5
• Sprung CL, Annane D, Keh D, et al. Hydrocortisone therapy for ective fluid challenges often lead to additional boluses, culmi nating in
patients with septic shock. N Engl J Med. 2008;358(2):111-124. a grossly edematous patient (still hypotensive and oliguric). Critically
• Walley KR. Use of Central Venous Oxygen Saturation to Guide ill patients also receive nutrition, sedatives, analgesics, antimicrobials,
Therapy. Am J Respir Crit Care Med. 2011;184(5):514-20. vasoactive drugs, insulin infusions, and agents to reduce the risk of gas-
tric hemorrhage, all of which contribute to a surprising degree of fluid
overload. For example, in the liberal fluid arm of the fluid and cath-
6
REFERENCES eter treatment trial (FACTT ) subjects received more than 4 L per day.
The consequence was a 7-day net positive fluid balance of 7 L. Fluid
Complete references available online at www.mhprofessional.com/hall balance in the earlier ARDS Network trials (where fluid therapy was at
the discretion of the intensivist, not guided by a protocol) was found to
be essentially superimposable on the liberal arm of the FACTT. Thus
6
routine critical care appears to be associated with large fluid loads and a
very substantial net positive fluid balance.
Just as too little fluid resuscitation risks harm, too much fluid may
CHAPTER Judging the Adequacy also be deadly. Identifying patients who are likely to respond to fluids
34 of Fluid Resuscitation (so that sufficient fluid can be given timely) and those who are not
(focusing attention on effective treatment and sparing them useless
Gregory A. Schmidt fluids) is a daily challenge in the intensive care unit (ICU). Yet predicting
fluid responsiveness is not a trivial task. This chapter reviews the asso-
ciation between fluid resuscitation and outcomes in critical illness; the
KEY POINTS limitations of static predictors of fluid response (such as CVP); the phys-
iological underpinning of dynamic predictors (such as stroke volume
• Of critically ill patients with conventional indications for a fluid variation [SVV]) and their role in guiding fluid therapy; and a clinical
bolus, only about half will respond with a meaningful increase in approach to the patient. Few patients in the first hours of sepsis, trauma,
perfusion. or other forms of shock have been studied with regard to endpoints of
• Fluid therapy that does not boost perfusion may cause harm by fluid therapy. For example, in the trial of early goal-directed resuscita-
impairing lung function or producing edema in other organs. tion, the target was the central venous oxyhemoglobin saturation—CVP
2
• Static hemodynamic parameters, such as central venous pressure, goals were identical between groups. Although the EGDT subjects
were given more fluid in the first 6 hours (4981 ± 2984 vs 3499 ± 2438;
have little value in guiding fluid therapy. p < 0.001), they also received more dobutamine and packed cell trans-
• Fluid responsiveness can be predicted using cardiopulmonary inter- fusion, making it difficult to attribute any particular benefit to the
actions to probe circulatory function or through passive leg raising. fluid, per se. Further, there is no evidence that goal-directed resuscita-
• Dynamic fluid-responsiveness predictors are accurate, but require tion after the first 6 hours confers any benefit. Moreover, concerns
7-9
careful attention to preconditions for validity. have been raised about the generalizability of the EGDT study in light of
the atypical patient population and other problems. Thus we empha-
10
size here the patient who is hypoperfused following initial resuscitation
Critical illness often cripples the circulation. For example, septic shock and for whom additional fluid therapy is considered.
combines ventricular dysfunction; arteriolar dilation; vascular obstruc-
tion; and volume depletion due to transudation of fluid from the vascular EXCESS FLUID CAUSES HARM
space into tissues, venodilation, reduced oral intake, and heightened
insensible loss. Trauma produces similar effects through hemorrhage, Fluid infused into the vascular space ultimately equilibrates with other
spinal injury, cardiac tamponade, tension pneumothorax, acidemia, and fluid compartments. Unnecessary fluid (ie, fluid that does not enhance
cardiac dysfunction. These join to compromise perfusion globally, threat- perfusion) will cause or exacerbate edema in lungs, heart, gut, skin, brain,
ening the function of vital organs. Urgent resuscitation improves out- and other tissues. At times, this creates clinically obvious organ failure,
come in shock, showing that time is of the essence, a concept captured in such as respiratory failure, abdominal compartment syndrome, 11,12 or
the phrase “the golden hour.” Treating hypovolemia has been a central cerebral edema and herniation. Multiple studies have correlated positive
1,2
tenet of shock management. Nevertheless, many controversies remain fluid balance with reduced survival in acute respiratory distress syndrome

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