an argument for colloid resuscitation for shock

572 ACADEMIC EMERGENCY MEDICINE NOV/DEC 1994 VOL 1/NO 6

An Argument for Colloid Resuscitation for Shock Mohanzed Rady, MD, PhD

81 ABSTRACT

A focused review of the physiologic mechanisms of colloid and crystalloid fluid resuscitations for acute critical illness is presented. This review suggests that postresuscitation plasma volume, cardiac output, left ventricular mechanical performance, and global and microcirculatory O2 supplies are more favorable with colloid therapy. Conversely, crystalloid may adversely affect microcirculatory blood flow and resultant 0, supply and use by ischemic tissues in shock. Poor relief of global and regional hypoxia may persist in critically ill patients after resuscitation with crystalloid.

Acad. Emerg. Med. 1994; 11572-579.

Fluid resuscitation in acute critical illness has been extensively discussed for different insults (e. g., traumatic, hemorrhagic, cardiogenic, and septic shock).14 However, the choice of crystalloid vs colloid fluid for resuscitation in acute critical illness continues to be debated.5 This focused review article addresses the underlying pathophysiologic changes in acute critical illness and delineates the physiologic advantages to colloid therapy.

DEFINITION OF ACUTE CRITICAL ILLNESS AND SHOCK Acute critical illness has been defined as an acute illness that has a predicted mortality rate in excess of 30%.6 With many acute crirical illnesses, shock evolves when an imbalance between systemic 0, delivery and tissue 0, consumption results in a cumulative O2 debt that over- whelms normal cardiorespiratory compensatory mechanisms. '$8 A hemodynamically compensated shock state can be difficult to detect clinically during the early stages of critical illness because, by definition, patients have normal vital signs, which conceal occult tissue hypoxia and cumulative 0, debt .9-12 Only when systemic hypotension and cardiorespiratory collapse ( i .e., hemodynamically decompensated shock state) develop in a critically ill patient does the severity of illness becomes apparent, even to the novice.

THERAPEUTIC GOALS

Initial therapy for shock, whether for an early hemodynamically compensated or a late decompensated shock state, should restore an optimal circulating plasma volume and hematocrit to maintain an adequate cardiac output (CO) and 0, delivery to satisfy global 0, requirenients.'3-15 Oxygen delivery should be enhanced to repay cumulative 0, debt and to meet elevated 0, consumption and metabolic demands induced by endo- genous release of catecholamines and cytokines. lC1* Therefore, optimal plasma volume, CO, and 0, delivery may be higher than normal values found among healthy individual^.^^-^^

~ ~

Colloid Resuscitation, Rudy 573

NORMAL STRESS

HEllORRHAGE HYPDXIA

I FIGURE 1. Pathophysiologic changes in the distribution of body water among the three major fluid compartments [intracellular fluid (ICF), interstitial fluid (ISF), and plasma volume (PV)] in acute critical illness. Neuro- humoral response to stress and microvascular endothelial in,jury induces a water shift from PV to ISF, occult cellular hypoxia induces a water shift from ISF to ICE and hemorrhage or trans- epithelial exudate loss reduces absolute PV. A relative and/or an absolute reduction of PV is common in acute critical illness. Based on data obtained from Suzuki et aI.,l9 Forrester et al.,'O Shoemaker et al.,22 B r ~ a n - B r o w n , ~ ~ and Isbis- ter.24

Shock states secondary to a vari- ety of primary insults (e.g., hemorrhagic, traumatic, cardiogenic, and septic disorders) are characterized by an absolute and/or a relative deficien- cy of circulating plasma volume.l9-2l External or internal hemorrhage and exudative fluid loss can reduce absolute plasma volume. In contrast, the neurohumoral stress response and tissue hypoxia secondary to the acute critical illness can redistribute water from the intravascular to the interstitial and intracellular fluid compartments, even in the absence of frank plasma or blood ~ O S S . ~ J - ~ ~ An absolute and/or a relative depletion of plasma volume is a common finding in shock due to acute critical illness, irrespective of the primary insult. Hence, after appropriate ventilatory support, the infusion of a fluid to selectively increase the intravascular volume should be the first maneuver to support circulatory function in a critically ill patient (Fig. 1).

The relationships between plasma volume, CO. stroke volume, and stroke work are complicated by changes of left ventricular (LV) diastolic compliance and systolic contractility in shock.25 Left ventricular

diastolic compliance influences end- diastolic pressure for a given end-diastolic volume (Fig. 2). A reduced diastolic compliance leads to high end-diastolic pressures and is mani- fested as an elevated pulmonary capillary wedge pressure at a relatively low end-diastolic filling volume. However, in such patients, maximal stroke volume and CO are achieved at an optimal end-diastolic volume, requiring an adequate blood volume. Therefore, isolated measures of elevated filling pressures (central venous and pulmonary capillary wedge pressures) commonly used to reflect right ventricular (RV) and LV preloads become unreli- able indicators of circulatory or ventricular volume overload.26-28

TYPES OF FLUIDS

Fluids can be classified by their abili- ty to bind and transport molecular 0,; i.e., 0,-transporting and non-0,- transporting fluids. Oxygen-transporting fluids (e.g., polymerized stro- ma1 hemoglobin) bind, transport, and release molecular 0, and promise to promote 0, flux to ischemic tissues in

Unfortunately, as yet no study has supported this theoretical advantage for critically ill patients.

0) I c

v) v)

a L

a

a

Non-0,-transporting fluids are most commonly used in clinical prac- tice. Colloid is composed of a large macromolecular moiety (e.g., albumin, polypeptide gelatin, dextran, or hydroxyethylstarch) in iso-osmotic saline. Commercial solutions are made to different concentrations and colloidal oncotic pressures. Solutions of strength less than 2% are hypo- oncotic, 3-5% are iso-oncotic, and 6- 25% are hyperoncotic to human plasma colloid oncotic pressure.

Crystalloid solutions are composed predominantly of sodium (Na) salts. Commercial solutions are made of different concentrations and osmo- larities: hyposmotic (< 75 mmol/L), isosmotic (150 mmol/L), or hyperosmotic (> 1,500 mmol/L) to human plasma osmolarity. A single anion or a mixture of anions (e.g., C1, lactate, bicarbonate, and acetate) is added to buffer the final solution pH to the desired level . , * , 3 O

PHYSIOLOGIC PROPERTIES OF FLUIDS Several physiologic features distin- guish crystalloid from colloid when used for resuscitation of shock. Plas- ma volume kinetics, CO, and LV

B

250 al 1 0

Lef t ventricular end-diastolic volurnehl)

I FIGURE 2. The relationship between left ventricular (LV) end-diastolic volume and pressure in health (A, solid line) and in acute critical illness (B, dotted line). The upward and leftward shift of curve B (i.e., a reduced LV diastolic compliance) implies that LV end-diastolic volume will be lower for a critically il l patient (B) compared with that for a healthy subject (A) at identical end-diastolic filling pressures. Based on data obtained from Sibbald'5 and Baek et

574 ACADEMIC EMERGENCY MEDICINE NOV/DEC 1994 VOL I /NO 6

stroke work, 0, transport and use patterns, and pulmonary and systemic interstitial edema are affected by infusion of exogenous fluid and determine morbidity and mortality in critically ill patients.

Plasma volume responds differ- ently to infusion of colloid vs infusion of crystalloid in acute critical ill- ne~s.31-3~ There are greater increases in plasma volume after infusion of equal volumes of colloid than there are for crystalloid in hypovolemic states (Fig. 3). The colloid moiety has a higher water-binding capacity than do the Na cations found in crystalloid and can retain a large fraction of infused water within the vascular space. After completion of infusion, the increase in plasma volume persists for longer periods with colloid than it does with crystalloid.33 Many colloids have a long intravascular half- life than have the Na cation (main

’7 Volume (ml)

500

0 -r

constituent of crystalloid solutions), thereby prolonging retention of water within the vascular space.31.32

Addition of a colloid can be beneficial to maximize and prolong the increase in circulating plasma volume observed for a given water and Na load infused in a critically ill patient. Iso- osmotic crystalloid has to be infused at four times the volume of colloid to achieve a similar increase in plasma v o l ~ r n e . ~ ~ ~ ~ ~ Alternatively, hyperosmotic crystalloid can be infused in smaller volumes than iso-osmotic crystalloid to produce greater increases in plasma volume.35 Hyper- osmotic Na solutions draw water from the intracellular compartment and induce a rapid increase in plasma volume; the plasma volume decreases quickly as both Na and water escape into the interstitial fluid space.36 A colloid moiety added to the hypertonic saline prolongs intravascular re-

- T

Plasma volume after lnhrslon of imrnl:

1 dearan 70 ( 6 % )

2 hespan ( 6 % )

3 slbumln ( 5% )

4 haemsccel ( 3.5% )

5 salln ( 0.9% )

I FIGURE 3. Plasma volume responses to infusion of equal volumes of either crystalloid or colIoid in acute hypovolemia. Plasma volume increased 800 mL (dextran 701, 750 rnL (Hespan), S O 0 mL (albumin), 300 mL (Haemaccel), and 180 mL (saline). Reproduced with permission from: Larnke LO, Liljedahl SO. Plasma volume changes after infusion of various plasma expanders. Resuscitation. 1976; 5:93-102.

tention of water and the desired plasma volume expansion.36

Fluids increase CO, stroke volume, and stroke work in proportion to the increase in plasma volume and ventricular preload in hypovolemic p a t i e n t ~ . ~ * , ~ ~ . ~ ~ J ~ However, the CO response to similar increments in plasma volume is dependent on the type of fluid infused.31.34 The relationship between CO and plasma volume for two types of fluids are illustrated in Figure 4. Further examination of the LV stroke work response to plasma volume suggests that a limited increase in stroke work can explain different CO responses to plasma volume with different types of fluid (Fig. 5) . An interaction between the type of fluid given and LV mechanical performance may explain the diverse stroke work response to similar plasma volume increments induced by either crystalloid or colloid fluid.’s Hemo- dilution secondary to infusion of fluids reduces blood viscosity and lowers LV afterload. This effect may improve LV mechanical performance after resuscitation.3840

However, non-0,-transporting fluids may adversely affect myocardial performance in critically ill patients. Crystalloid can reduce LV compliance and ~ont rac t i l i ty .~ l Myocar- dial edema, reperfusion injury secondary to free-radical generation, and electrolyte shifts are some of the possible mechanisms by which crystalloid can depress LV mechanical per- fo r rnan~e .~* Infusion of colloid is less prone to induce myocardial edema and may also scavenge free radicals and protect against reperfusion injury.42 Isotonic crystalloid may not maintain adequate coronary blood flow, especially to the subendothelium, after resuscitation from hernor- rhagic s h o ~ k . ~ 3 In contrast, colloid can maintain a supranormal coronary blood flow and preferential perfusion of ischemic subendothelium, which may maximize LV mechanical perfor-

In fact, abnormalities of to- tal coronary and regional blood flows and 0, supply may prolong cardiac

Colloid Resuscitation, Rady 575

A

0 2

A Plasma volume (L) I FIGURE 4. The physiologic response of cardiac output to plasma volume increments produced by two types of fluids in hypovolernic states (A and B). Cardiac output is increased to a higher level after fluid A (a colloid, solid h e ) than it is after fluid B (an iso-osmotic crystalloid, doffed line) at similar increments of plasma volume. Based on data obtained from: Shippy et al.,’* Shoemaker and Monson,” and Hauser et a1.33

ischemia and exacerbate myocardial injury in shock. Maldistribution of blood flow and O2 supply also can depress myocardial metabolism and 0, uptake and thereby limit recovery of normal cardiac func- t ion .44.45

Infusion of non-0,-carrying fluid can increase 0, delivery by improving CO in critically ill patient^.^^,^^.^^ Al- though fluids also reduce arterial 0, content by hemodilution, the net result on 0, delivery represents the bal- ance between the two opposing effects (Fig. 6). Lactated Ringer’s solutions and isotonic saline solution have been shown to cause significant hemodilution with moderate increses in C O and a relative small increase in 0, delivery.31v33,34,47 In contrast, the colloids (e. g ., albumin, dextran, hydroxyethylstarch) produce significant increases in C 0 with moderate hemodilution and large increases in 0,

Fluid therapy is intended to enhance microcirculatory 0, delivery and use to meet the aerobic demands of ischemic organ sy~tems.~9-5’ Oxy- gen consumption, global or regional, is determined by a tissue’s 0, requirements and the availability of the sup- plied 0, (or delivery) (Fig. 7). Con- vection and diffusion of 0, at the microcirculatory level become critical factors for relief of tissue hypoxia and

delivery. 34.37 .J7.48

help clear ischemic metabolites produced by anaerobic metabolism.52 In- deed, the pattern of O2 consumption is dependent on the type of fluid used for re~uscitation.5~ Isotonic crystalloid minimally increases and in certain in- stances decreases 0, consumption in critically ill patients with evident global ischemia.47.53 On the other hand, the colloids (e.g., albumin, hydroxyethylstarch, gelatin, and dextran) support large increases in 0, consumption and rapid relief of global ischemia under similar condi- t i o n ~ . ~ ~ ~ * In fact, the electrolyte load of NaCl can interfere with the microcirculatory 0, cascade and hinder 0,

extraction or use by ischemic tis- s u e ~ . ~ ~ ~ ~ ~ , ~ ~ Some colloids may theo- retically enhance microcirculatory 0, supply and use in shock states. Colloid can disperse RBC aggregates, attenu- ate excessive activation of WBCs, scavenge free radicals, reduce microvascular endothelial edema, and es- tablish nutritive capillary blood flow.40,56-59 Neither Na nor C1 per se have any beneficial effect on the mi- crocirculation; in fact, their preferential sequestration in the interstitial space produces intercellular edema and occludes capillary blood flow, thereby reducing 0, supply and diffusion to tissues.50,51,54,55

Small volumes of hyperosmotic NaCl with or without an added colloid have been used to limit the loss of NaCl into the inter~titium.30.~6.56 Hy- perosmotic crystalloid fluid offers the advantage of a temporary high osmotic Na load that draws water from the intracellular and interstitial compartments to reduce microvascular endothelial swelling and reopen occluded capillaries to ischemic tissues.36359 Hyperosmotic NaCl increases 0, consumption immediately after resuscitation, coinciding with reestablished microcirculatory blood f l 0 ~ . ~ 6 How- ever, blood lactic acid concentrations (and 0, debt) may remain elevated in spite of a simultaneous increase in 0, consumption after resuscitation from

A

0) x

z c M

L 4

0 L ” c 0) 5

- a .-

L - 0 J

0 , 4 0 2

A Plasma volume [L) I FIGURE 5 . Left ventricular stroke work response to plasma volume expansion with two types of fluids in hypovolemic states. Fluid A (a colloid, solid l ine) produced a higher stroke work response than did fluid B (an iso-osmotic crystalloid, dotred line) at similar increments of plasma volume. Based on data obtained from Foglia et al.41


- c .- E

h 3 0 0 - E - L r

2 2 0 0 - Q) V

E

I- -

El00 - X 0

0 -

hemorrhagic-traumatic shock. In fact, a short burst of high Na load can increase intracellular Na flux and concentrations in ischemic tissues. This flux may increase the energy demands and activity of the plasma membrane Na-potassium pump. It is conceivable that hyperosmotic NaCl may divert 0, use to meet plasma membrane energy requirements and maintain intracellular osmotic integrity. This may delay the correction of cellular anaerobic metabolism and 0, debt. Sodium and C1 loads also may modify local produc- tion of vasodilator (e.g., nitric oxide) and vasoconstrictor (e.g., thrombox- anes, endothelin) mediators by injured microvascular endothelium following ischemia and reperfusion.58.6*,61

Pulmonary microvascular endothelial dysfunction secondary to hypoxia or hypoperfusion is the inciting insult for the development of adult respiratory distress syndrome (ARDS).62v63 Local activation of WBCs and platelets generates high concentrations of inflammatory mediators within alveolar-capillary units and perpetuates lung injury in acute critical i l l n e ~ s . ~ ~ J j 5 When the pathophysiology of ARDS is considered,

5 -

- .r 4 - E -. -1

c1 3 - n 3

J 0

"

2 - g

0

.HCT

400 1

fluids per se do not act as a primary inciting stimulus, as commonly per- ceived.66.67 On the contrary, dextran has been shown to reduce the incidence of posttraumatic ARDS by early augmentation of macrocirculatory and microcirculatory 0, transport and

However, isotonic crystalloid solutions, when given in large volumes to improve central hemo- dynamics, frequently worsen pulmonary gas exchange function (in terms of pulmonary shunt fraction) for patients with established or evolving ARDS.68.69 However, the severity and duration of ARDS are causally related to the primary insult and not the type of fluid used. Further, ARDS can be exacerbated by infusion of large volumes of either fluid type.62.67.68

Crystalloid fluid (especially NaCl and water) preferentially sequesters in the interstitial space of many organ systems (Fig. 8). Interstitial fluid sequestration reflects a breakdown or enhanced permeability of systemic capillaries induced by hypoxic insult and perpetuated by the inflammatory reaction to the acute critical illness.70 Mobilization of fluid from this space is dependent upon the recovery of nor-

Daz [ " r:

H - - 0

0-1 I

0 2

A Plasma volume (L l

FIGURE 6 . Physiologic response of cardiac output (CO), arterial hematocrit (HCT), and O2 delivery (D02) in response to plasma volume expansion by a non-02-carrying fluid in hypovolemic statcs. As fluid increases plasma volume, there is a simultaneous increase in CO and a reduction of HCT, with an initial increase and later a decrease of D02. A maximal increase of DO2 would be achieved by a maximal increase of CO and a minimal decrease in HCT for a critically ill patient. Based on data obtained from Rackow et a1.,34 Lazrove ef a1..37 Voerman and Groeneveld,@ and Tait and L a r ~ o n . ~ )

ma1 permeability of systemic capillaries. Since isotonic crystaloid solutions are required in large infusion volumes to achieve an adequate henio- dynamic response during initial resuscitation, their use may exacerbate interstitial fluid gain in critically ill p a t i e n t ~ . ~ ~ . ~ 4 . 7 1 The gain in extravascular water content results in edema of many organ systems and can hinder the convection and diffusion of 0, to these t i ~ s u e s . 2 ~ Some investiga- tors speculate that colloids also may leak into the interstitial space and exacerbate extravascular water gain in the presence of leaky capillaries in many organ However, this hypothesis is not supported experi- mentally. Indeed, a large fraction of administered colloid remains in the intravascular space and can be effi- ciently cleared from extravascular fluid space.31-34.36,37,46,47

CRITERIA FOR EFFECTIVENESS OF FLUIDS Based on the above physiologic properties of colloid and crystalloid solutions, it is possible to formulate a set of ideal criteria to guide the choice of fluid for resuscitation of a critically ill patient. Plasma volume should be expanded by the smallest volume of infusion that will result in an adequate expansion of the vascular space. 'The plasma volume response should persist for several hours. Cardiac output and LV stroke work should respond to the increase in ventricular end-diastolic filling volume and demonstrate enhanced myocardial diastolic compliance and contractility. Administered fluid should support supranormal coronary blood flow and preferential perfusion of the subendothelium to satisfy myocardial 0, requirements and improve the mechanical per-for- mance of the ventricles. Although plasma volume expansion with a non- 0,-carrying fluid is invariably linked to a reduced arterial 0,-carrying capacity, the increase in CO should off- set hemodilution and result in a net increase in 0, delivery.47 Fluid in-

Colloid Resusci ta t ion, Rady 577

N- 80 - E 2 E 1. 60 - E

E 40 -

.-

- C

CL c

I * 0 A Oxygen delivery 120

0 (ml/m~n.m’)

4

X

C -20 -

I FIGURE 7. Variation of O2 consumption in response to increases of O2 delivery after resuscitation with three types of fluids in hypovolemic states. Fluid A (dextran) induced a larger increase of oxygen consumption than did fluid B (albumin) for similar increases of O2 delivery. Fluid A may enhance peripheral O2 use by ischemic tissues, compared with fluid B. In contrast, O2 consumption is reduced in the face of an increase in O2 delivery after fluid C (isotonic crystalloid). Fluid C has reduced microcirculatory nutritive blood flow and peripheral O2 uptake by ischemic tissues. Based on data obtained from Shoemaker et a1.,47 Matsuda and Shoemaker,48 Messmer and Kreimeier.50 and Wang et al.51

fused should reverse any obstructed blood flow in the affected capillaries and enhance microcirculatory 0, convection and diffusion to maintain adequate 0, uptake and abate anaerobic metabolism by ischemic tissues.50 To meet these physiologic goals, colloids should always be used for resuscitation of a critically i l l patient.

ENDPOINTS OF THERAPY WITH FLUIDS There are several useful parameters to monitor during titration of fluid ad- ministration. Measurement of plasma volume before and after infusion is impractical and time-consuming and requires the use of radioactive-labeled albumin or R B C S . ~ ~ , ~ , Vascular pressures, especially RV and LV filling pressures, are popular measurements to evaluate blood volume in critically ill patients.73 The RV and LV filling pressures usually reflect changes in compliance and competency of the

respective ventricles to maintain for- ward blood flow. However, elevated ventricular filling pressures (right atrial and pulmonary wedge pressure) should not be assumed to indicate hyper volemi a .26-2*

Echocardiography (transthoracic or transesophgeal) provides a nonin- vasive method to directly evaluate ventricular volumes.27 Alternatively,

Normel

the stroke volume and stroke work can be measured by a thermodilution pulmonary artery catheter, and the infusion of fluid can be titrated to obtain a maximal increase in stroke volume and work, as described by Starling- Sarnoff (Fig. 9). This method assesses the response of both ventricles and functional limitations due to preexist- ing myocardial disease.74

After After After Hemorrhage

I S W

After After Crystallolds Colloldo mIv miv

I FIGURE 8. The immediate effects of crystalloids and colloids on the three major body water compartments [intracellular water (ICW), interstitial water (ISW), and plasma volume (PV)] after resuscitation from shock. hemorrhage, or trauma. Crystalloid expanded ISW (with depleted ICW and PV) to cause multiple organ system edema. In contrast, colloid selectively increased PV without deleterious effects on either ISW or ICW. Based on data obtained from Zadrobilek et al..67

Tranbaugh et a1.,68 Haupt et al.,69 and Lucas.’O

0 20 torr 200 mL Preload

(Wedge pressure or left ventricular end-diartollc volume1

I FIGURE 9. Left ventricular (LV) stroke work response to increments of preload from fluid infusion in hypovolemic states. The LV preload can be measured indirectly by pulmonary artery catheter (pulmonary capillary wedge pressure) or directly by echocardiography (LV end-diastolic volume). The volume of fluid infused can be titrated to obtain the maximal response in LV stroke work. Based on data obtained from Rady et aI.l4


Oxygen delivery can be assessed with successive measurements of CO and arterial 0, content (proportional to hematocrit) (Fig. 6 ) . Hemodilution may reduce arterial 0, content and net 0, delivery and therefore obscure the infusion volume required to maximize LV stroke volume and work. Oxygen consumption (measured by indirect calorimetry or calculated from CO and arteriovenous O2 content differ- ence) and elimination of elevated blood lactic acid concentrations can indicate the effectiveness of fluid ad- ministration for restoration of microcirculatory perfusion and 0, use by ischemic tissues.52

CONCLUSIONS Fluid therapy should aim to expand plasma volume, augment ventricular work performance, and maintain effi- cient O2 delivery and use by ischemic tissues i n shock. Given these physiologic goals, colloid solutions are de- sirable because they can achieve and maintain the desired endpoints of global and microcirculatory oxygena- tion with small volumes of infusion. The use of colloid for resuscitation should decrease the incidence of fluid overload and related morbidity associated with shock resuscitation.

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~~~ ~

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