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Keywords
acid–base balance, colloids, crystalloids, strong ions, unmeasured ions
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324 Intravenous fluids
Recall that all crystalloid fluids are prepared in a water the cells—NaCl is not freely diffusible and creates an
base. Thus, administration of 1000 ml of any crystalloid osmotic gradient between the internal environment of
provides 1000 ml of water regardless of the additional the cell and solution. By contrast, cells placed in a
electrolyte content. Although seemingly simple, this solution of urea will swell, as urea is freely diffusible
cornerstone concept is often misunderstood when addres- and has no osmotic effect. This is why a solution contain-
sing disorders of sodium balance, in particular dilutional ing dextrose may be isotonic (and hence not cause injury
hyponatremia. Crystalloids for human infusion that are to vessles when infused) but hypoosmotic when infused
used for resuscitation purposes are constructed with into a patient. Commonly available resuscitation fluids
sufficient electrolyte additives to approximate human and their compositions are provided in Table 1.
plasma osmolality and tonicity. These requirements help
support retention of the administered fluid and salt Maintenance fluids are hypotonic by design, providing
within the vascular space, as opposed to the extravascular electrolytes that meet the minimum daily requirements
extracellular space. The reader should note that in health, for salt administration (see Fluids and Their Clinical
approximately 75% of an administered normotonic crys- Effects). Some fluids are constructed to be hypertonic
talloid infusion extravasates into the extracellular extra- and have specific uses such as hypertonic saline (HTS)
vascular space; fluids of lesser tonicity demonstrate whose use is designed to provide concentrated salt with-
greater extravasation and less resuscitative efficacy. out an accompanying large volume of water for the acute
Assuming a typical 5000 ml circulating blood volume, a therapy of severe and symptomatic hponatremia. How-
10% PVE bolus (500 ml of retained fluid) requires the ever, HTS may also be used as an initial resuscitation
administration of 2000 ml of a normotonic fluid, and is fluid for those with traumatic brain injury when elevated
consistent with advanced trauma life support directed plasma osmolality is desired as part of a management
resuscitation [5]. strategy for cerebral edema. As crystalloid fluids are
protein-free and comprised of only small particles, their
Osmolality and tonicity ability to remain in the vascular space is limited.
Proper fluid management is aided by understanding the
properties of osmolality and tonicity. Osmolality refers to
the concentraiton of osmotically active particles per Water and electrolytes
1000 ml of fluid and is generally expressed as millios- Although crystalloids are water based, they contain a
moles (mOsm)/l of H2O; normal blood osmolality is 285– variety of electrolytes. Each of the electrolyte additives
295 mOsm/l H2O. Tonicity is a relative term reflecting a to the fluid base carries a charge in an aqueous milieu.
comparison of the osmolality of a particular fluid to that of Using physicochemical principles articulated by Peter
plasma. Thus, a normotonic solution has an osmolality Stewart in 1983 [6], and reviewed elsewhere [7–9], ions
similar to that of plasma – a general property of resuscita- in an aqueous milieu are termed strong ions if at physio-
tion fluids such as lactated Ringer’s solution and 0.9% logic pH, they separate from their partners and contribute
normal saline solution (NSS). However, tonicity also a charge to the aqueous milieu. Such strong ions are
refers to the effects in a given environment with respect commonly used to construct resuscitation and mainten-
to the permeability of membranes in that environment. ance fluids and include Naþ, Kþ, Cl, Ca2þ, Mg2þ and
Thus, a solution that is isotonic to plasma may not be PO42þ. As such, these electrolytes establish a net charge
isoosmolar if the particles in question are freely diffusible that will influence plasma pH as they are infused intra-
and create no osmotic effect. venously (see Physicochemistry of Aqueous Solutions).
On the basis of the particular composition of electrolytes
For example, if red blood cells are placed in a solution in the fluid preparation, each fluid should impact plasma
containing 400 mOsm/l of urea they will behave comple- pH in a predictable fashion that may be utilized in a
tely differently if they are placed in a solution of therapeutic fashion. Moreover, a particular therapeutic
400 mOsm/l of NaCl. Placed in the hypertonic saline goal may help guide the clinician to select a parti-
solution the cells will shrink as water diffuses out of cular fluid for resuscitation or maintenance use, most
0.9% NSS, normal saline solution; Lact, lactate; Acet, acetate; Glucon, gluconate; mOsm, milliosmoles/l; var, variable as this solution is locally prepared
without pH balancing; pH may be further influenced over time with CO2 equilibration; Plasma, normal human plasma.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Fluids, pH, ions and electrolytes Kaplan and Kellum 325
commonly to impact plasma electrolyte composition and hydroxylation retards the rate of hydrolysis by plasma
pH (see how fluids influence pH below). nonspecific a-amylases. Starches are characterized by
their average molecular weight and average molecular
size, as they exist as a polydispersed preparation of
Chemical properties of colloids different molecular weight and sizes. Thus, starches
Colloids are defined as preparations of homogeneous may be further classified by their average molecular
noncrystalline substances that are dispersed throughout weight into high molecular weight (>450 kDa), medium
another substance that is usually water based (for medical molecular weight (200kDa), and low molecular weight
use) [10]. The colloid may be large macromolecules or (70–130 kDa). Furthermore, they are characterized by
smaller particles, but do not precipitate and are not the C2/C6 substitution ratio also known as the degree of
separable from their suspending solution by filtration substitution or molar substitution ratio; ratios are expressed
or centrifugation. Colloids are generally polydispersed, as a number spanning 0–1. The greater the degree of
representing a span of molecular sizes that characterize a substitution or molar substitution ratio, the longer the
single preparation. Molecular weight may be described in plasma persistence and plasma half-life (t / ). 1 2
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
326 Intravenous fluids
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Fluids, pH, ions and electrolytes Kaplan and Kellum 327
resuscitation fluid in the emergency department (ED), correcting hyponatremia using IVF.
operating room or ICU, it is the rare patient who has not
received salt far in excess of their minimum require- D Na for 1 liter of IVF ¼ ½ðinfusate Na þ infusate KÞ
ments. This excess is complicated by a commonly high- serum Na=½Total body water
ADH level that supports water retention, and may be
especially marked on those with heart failure. Thus, a þ 1
falling Naþ generally indicates free water excess, rather Where total body water ¼ weight (kg) correction factor
than a true total body sodium deficit. Frequently, those
with dilutional hyponatremia have a normal or nearly (1) Correction factors
normal plasma Cl and a high urinary Naþ as well. The (a) Children: 0.6
therapy for this disorder is fluid restriction to decrease (b) Nonelderly men: 0.6
free water, not the delivery of a higher Naþ content fluid. (c) Nonelderly women: 0.5
Judicious diuretic use may also help correct dilutional (d) Elderly men: 0.5
hyponatremia, and particular efficacy may be realized (e) Elderly women: 0.45
with the use of the new class of diuretics – the aqua-
porins – based on their pure aquaretic effect; though For example, a liter of NSS (Naþ 154 mEq) would result
experience is limited with these agents in patients with in a modest 0.8 mEq increase in the serum Naþ concen-
critical illness and the authors recommend limiting use to tration when given to a 70 kg man with a serum Naþ of
refractory cases and only with careful monitoring even 120 mEq/l:
then [18].
D Na ¼ ½ð154 þ 0Þ 120=½42 þ 1 ¼ 0:8
A special note is made regarding the correction of hypo-
natremia with regard to timing. The Naþ concentration However, if 40 mEq/l of Kþ was added to the infusate, the
may be corrected at the same rate as that with which it change would be 1.7 mEq:
was acquired. When the condition has developed over
D Na ¼ ½ð154 þ 40Þ 120=½42 þ 1 ¼ 1:7
several days (chronic hyponatremia), one should avoid
raising the Naþ more rapidly than 0.5–1 mEq per hour to
avoid central pontine myelinolysis (CPM) [19]. This is This is because Kþ and Naþ are ‘exchangeable’ cations
especially important in those with a Naþ less than and Kþ administration will increase the plasma Naþ
120 mEq/l for more than 48 h. CPM may result in per- concentration by exchanging with intracellular Naþ.
manent injury with devastating neurological effects. Indeed, NSS with 40 mEq KCl is modestly hypertonic.
Extrapontine demyelination may also occur. These time Failure to appreciate this effect can result in an overly
rules also apply to true total body salt depletion. In rapid correction of serum Naþ and can be dangerous.
general, the rapidity of correction is also driven by the Note that the earlier formula is used to determine the
presence or absence of neurologic symptoms. Three effect of administration of a liter of fluid, in order to
percent saline is commonly used to raise the Naþ con- determine the effect of administration of multiple liters
centration above 120 mEq/l in symptomatic patients but of fluid it is necessary to use the following formula:
should always be used with careful monitoring of the
serum Naþ concentration. New Na ¼ ½ðserum Na total body waterÞ
þ infused Na=ðtotal body water
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
328 Intravenous fluids
(4) Asymptomatic chronic hypernatremia should be cor- additional 1540 mEq Naþ and 1540 mEq Cl into a new
rected at a rate not exceeding 0.5 mEq/l per hour, and total body water of 52 kg (42 kg þ 10 kg H2O from the NSS
not more than 10mEq/l over 24 h. infusion). Thus, one may derive the new Naþ concen-
tration by totaling the existing Naþ 5880 plus the infused
Intravenous free water, commonly provided as D5W, is Na 1540 and dividing by the new water volume of 52 kg to
most commonly used but may be supplemented by yield 142.7 mEq/l. However, the same calculation for Cl
gastrointestinal luminal free water using either pure yields 4200 þ 1540/52 ¼ 110.4 mEq/l. The net impact of
water, or diluted tube feeds. The same formula used this infusion, in addition to an increase in plasma volume is
for correcting hyponatremia may be used to calculate free the induction of a hyperchloremic metabolic acidosis with
water deficit: an important, but tolerable decrease in pH in this healthy
individual. However, large volumes such as those used in
D Na ¼ ½ðinfusate Na þ infusate KÞ this example are not provided to the healthy, but are
serum Na=½Total body water þ 1 instead infused in those with critical illness or injury. In
this patient population, the pCO2 and pH prior to infusion
For example, administration of 1 l of D5W to a 70 kg man are typically abnormal, and the patients often suffer from
with a serum Naþ of 160 would result in a decrease of lactic acidosis, or other metabolic acidoses from preexisting
3.7 mEq/l assuming no loss of water. organ failure or ketoacidosis. These acidoses may be
aggravated by a rising pCO2 from impending respiratory
Hypokalemia failure as well. In these circumstances, the induction of a
Hypokalemia is much more common in hospitalized HCMA may be disastrous and potentially lethal.
patients than hyperkalemia. In those with normal renal
function, hypokalemia is often related to diminished
intake, the infusion of Kþ free fluids, and/or the use of Physical chemistry of aqueous solutions
kaliuretic diuretics (i.e. loop diuretics such as furose- Biological solutions are both water based and primarily
mide). It is important to recall that serum Kþ deficit does alkaline (as opposed to being acidic) in nature. Using
not demonstrate linearity with the amount needed to Stewart’s physicochemical approach to acid–base bal-
restore a normal concentration. As Kþ is principally an ance, there are only three independent variables that
intracellular cation, extracellular deficits draw on intra- determine pH in human plasma: pCO2; the strong ion
cellular stores to maintain homeostasis. Thus, a total body difference (SID); and the sum of the total weak acid
deficit exists when serum Kþ is less than 3.0 mEq/l, and concentration (ATOT) [6,7]. The last two components
patients generally require 200 mEq Kþ (and often more) represent nonvolatile acids, whereas CO2 serves as a
to replace intracellular and extracellular Kþ to normal, volatile component. Note that HCO3 does not serve as
especially in the setting of ongoing renal or gastrointes- an independent determinant of pH.
tinal losses. As acute and potentially life-threatening
dysrhythmias are common with Kþ less than 3.0 mEq/l, Strong ions
and the concentration of the replacement solutions is Plasma contains a variety of ions that are classified as
typically higher than may be administered on the general positive (cations) or negative (anions) depending on their
ward, continuous ECG monitoring is warranted. Addi- charge. Some ions, as noted earlier, exist completely
tionally, restoration of normokalemia relies on the esta- dissociated from their ionic partners at physiologic pH
blishment of normomagnesemia as both Kþ and Mg2þ and are termed strong ions to separate them from weak
cotransport in the kidney. ions, species that may exist in dissociated or associated
forms; only the dissociated species manifest a charge.
Hyperchloremia and hyperchloremic metabolic acidosis Strong ions include Naþ, Kþ, Caþþ, Mgþþ, Cl, and
As NSS is the most commonly prescribed fluid in the lactate (LA), whereas albumin and PO42 are weak ions.
United States, and 1L provides the minimum daily By way of example, a solution of only water and NaCl, has
requirements for maintenance electrolyte balance, let us equal amount of strong cations (Naþ) and strong anions
consider the impact of infusing a large volume of NSS into (Cl), establishing a SID of zero. Normal plasma does not
a healthy individual with no acid–base disturbance, a have a SID of zero as in the earlier example. Instead
normal pco2 and normal pH before examining the results plasma has more strong cations (mainly Naþ) than strong
from the same infusion into a patient with critical illness. anions (mainly Cl). The difference between the sum of
Using a prototypical 70 kg male, one may calculate total all strong cations minus the sum of all strong anions is
body water as 42 l (70 0.6). Assuming standard electro- known as the strong ion difference (SID).
lytes including a Naþ of 140 mEq/l and a Cl of 100 mEq/l,
we may calculate the total body Na (140 42 ¼ 5880 mEq) Plasma SID normally ranges between 40–42 mEq/l in
and total body Cl (100 42 ¼ 4200 mEq). Infusing 10 l of health but is typically much lower in those with critical
0.9% NSS (154 mEq/l of each Naþ and Cl) contributes an illness. As SID is positive, it must be balanced by an equal
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Fluids, pH, ions and electrolytes Kaplan and Kellum 329
negative charge to conform to the principle of electrical to note that the loss of weak acid (ATOT) is an alkaliniz-
neutrality. These balancing charges stem from both CO2 ing process [23]. However, the critically ill are only
and the weak acids (A). In the absence of renal failure or infrequently alkalemic despite often profound hypo-
ketoacidosis, the total weak acid concentration derives albuminemia. This seemingly counterintuitive obser-
principally from albumin’s exposed histidine residues vation is understood by recalling that the SID and
and PO42. As weak acids, ATOT exists in both associated ATOT are best evaluated in relation to one another
and dissociated forms represented by the following rather than as absolute values. Hypoalbuminemic
equation: ATOT ¼ AH þ A. In order to preserve electo- patients often also manifest a reduced SID, perhaps
neutrality, it then follows that plasma SID may be as compensation for their reduced ATOT from hypo-
derived from the remaining negative charges: SID – albuminemia [24,25].
(CO2þA) ¼ 0. This estimated value of SID is termed
the effective SID (SIDe) and is also known as ‘buffer
base’ [20]. These relationships also enable one to use the How do fluids influence plasma pH?
base excess to understand an additional aspect of the Metabolic acidoses and alkaloses are categorized accord-
SID. As the base excess is the change in ‘buffer base’ ing to the ions that are responsible. Thus, there is lactic
required to reestablish a pH of 7.4 when pCO2 ¼ 40 torr acidosis and chloride responsive alkalosis, etc. It is
base excess identifies the change require in SID to important to recognize that metabolic acidosis is pro-
normalize pH [21]. duced by a decrease in the SID [26]. A decrease in
SID may be brought about by the generation of organic
A more clinically appealing and clinically malleable anions (e.g. lactate, ketones) the loss of cations (e.g.
method of estimating SID is (Naþ þ Kþ þ Caþþ þ diarrhea), the mishandling of ions (e.g. renal tubular
Mgþþ) – (Cl þ lactate). This value is termed the acidosis) or the addition of exogenous anions (e.g. iatro-
‘apparent’ SID (SIDa) reflecting the fact that some genic acidosis, poisonings). By contrast metabolic alka-
‘unmeasured’ ions might also be present. Although both loses occur as a result of an inappropriately large SID,
SIDe and SIDa are convenient and fairly readily measur- although the SID need not be greater than the ‘normal’
able, neither value is a completely accurate representa- 40–42 mEq/l. This may be brought about by the loss of
tion of the actual SID. The discrepancy stems from the anions in excess of cations (e.g. vomiting, diuretics), or
presence of clinical entities that generate unmeasured rarely by administration of strong cations in excess of
ions such as the sulfates and ketones mentioned earlier. strong anions (e.g. transfusion of large volumes of banked
blood).
Regulation of the strong ion difference
It is important to recall that regulation of the SID utilizes In the acute setting, acidosis is usually more of a problem
three interrelated organ systems: the kidney, the liver and than alkalosis and in the critically ill, the most common
the gastrointestinal tract. The kidney is the dominant sources of metabolic acidosis are disorders of chloride
organ and discharges its role principally via Cl excretion. homeostasis, lactate, and other anions. Hyperchloremic
With each Cl that is not reclaimed after filtration, the metabolic acidosis occurs either as a result of chloride
SID will increase, and so will pH (hypochloremic alka- administration or secondary to abnormalities in chloride
losis). As normal dietary intake is rich in strong ions, handling or related to movements of chloride from one
gastrointestinal uptake is sufficient to maintain a normal compartment to another. The effect of chloride admin-
balance. As regulation of intravascular volume, especially istration on the development of metabolic acidosis has
during critical illness and after injury establishes a strong been known for many years [27,28]. Recently, new
imperative for Naþ uptake and reclamation, and Kþ attention has been paid to this area in light of better
handling is driven by plasma concentration as well as understanding of the mechanisms responsible for this
glucose and insulin levels, renal Cl handling is especi- effect [29–32]. It has now been shown in animal models
ally important in pH maintenance [22]. of sepsis [29] and in patients undergoing surgery [23,
30–32] that 0.9% saline causes metabolic acidosis not by
Albumin and the weak acids ‘diluting’ HCO3 but rather by its chloride content
The second nonvolatile determinant of blood pH is the [33,34]. From a physical chemical prospective this is
total weak acid concentration (ATOT). The weak acids, completely expected. HCO3 is a dependent variable
are mostly proteins (predominantly albumin) and phos- and cannot be the cause of the acidosis. Instead, Cl
phates, and they contribute the remaining charges to administration decreases the SID (an independent vari-
satisfy electroneutrality such that SID – (CO2 þ able) and produces a decrease in pH. The reason this
A) ¼ 0. As A varies with changes SID and pCO2, A occurs with 0.9% saline administration is that although
cannot be an independent variable. Instead, the inde- 0.9% saline contains equal amounts of both Naþ and Cl,
pendent variable is the sum of the associated and dis- the plasma does not. When large amounts of salt are
sociated weak acids represented by ATOT. It is important added, the Cl concentration increases much more than
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
330 Intravenous fluids
the sodium concentration as per the example provided attention to the potential for harm as well as benefit.
earlier. Intravenous fluids can correct or induce electrolyte and
acid–base abnormalities. In experienced hands, intra-
There are other important causes of hyperchloremia venous fluids can be life saving—if used improperly, like
(renal tubular acidosis, diarrhea, etc.) and in addition, most drugs, they can lead to adverse effects and contribute
this form of metabolic acidosis is common in critical to morbidity and even mortality in critically ill patients.
illness, especially sepsis. Although 0.9% saline resuscita-
tion undoubtedly plays a role, there appear to be unex-
plained sources of Cl, at least in animal models of sepsis References and recommended reading
Papers of particular interest, published within the annual period of review, have
[29]. One possible explanation is that this Cl is coming been highlighted as:
of special interest
from intracellular and interstitial compartments as a of outstanding interest
result of the partial loss of Donnan equilibrium due to Additional references related to this topic can also be found in the Current
albumin exiting the intravascular space [29]. However, World Literature section in this issue (pp. 394–395).
this hypothesis is yet unproven. 1 Kellum JA, Song M, Venkataraman R. Effects of hyperchloremic acidosis on
arterial pressure and circulating inflammatory molecules in experimental
sepsis. Chest 2004; 125:243–248.
2 Kellum JA, Song M, Li J. Lactic and hydrochloric acids induce different
Consequences of hyperchloremia: immune patterns of inflammatory response in LPS-stimulated RAW 264.7 cells. Am
activation and inflammation J Physiol Regul Integr Comp Physiol 2004; 286:R686–R692.
A growing body of literature documents that crystalloid 3 Kaplan LJ, Maerz LL, Schuster K, et al. Uncovering system errors using a rapid
response team: cross-coverage caught in the crossfire. J Trauma 2009;
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activation triggers [35,36]. Importantly, evidence sug- This manuscript details the relevant impact of ACGME work hours restrictions as it
applies to postoperative care. One major deleterious impact was inadequate fluid
gests, at least in a cell-culture model, that the impact management.
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when comparing lactic acidosis to HCMA [2]. Intact 5 Shock. Advanced Trauma Life Support, 8th ed. In: J Fildes and J Wayne
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As the first such publication from this multispecialty group, this manuscript is
Conclusion comprehensive and provides an up-to-date review of the available evidence
addressing renal-hepatic dynamics. A well done and detailed review of fluid
It is important to remember that intravenous fluids are management as it applies to hepatorenal syndrome, tense ascites, and hepatic
drugs. They should be prescribed with care and with failure is provided.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Fluids, pH, ions and electrolytes Kaplan and Kellum 331
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