Acid Base Disorders in Critical Care Medicine Edward Omron MD, MPH

Acid Base Disorders in the Intensive

Care Unit for Housestaff

Edward M. Omron MD, MPH, FCCP

Pulmonary and Critical Care Medicine

Morgan Hill, CA 95037

www.docomron.com

edofiron@gmail.com

OBJECTIVES

• A critical assessment of conventional acid-

base analysis

• A review of strong ion difference and

physicochemical analysis in acute illness

and major surgery

– Clinical applications in

• Electrolyte management

• Fluid resuscitation

• Complex acid-base disorders

• Metabolic acid-base status

– What is it?

– Why is it important?

– Why assess for it?

– Can we do better?

A 34-year-old white man presents with nausea, vomiting and has been

unable to consume any food or liquids. He admits to drinking about two pints

of vodka daily. Temperature is 99.6 F, pulse rate is 101 per minute supine and

126 per minute standing, respirations are 24 per minute, and blood pressure

is 110/85 mm Hg supine and 80/50 mm Hg when standing.

Sodium 134 mEq/L

Potassium 3.8 mEq/L

Chloride 83 mEq/L

Bicarbonate 24 mEq/L

PO2 89 mm Hg

PCO2 32 mm Hg

pH 7.48

Which of the following is the most likely explanation for these laboratory

findings?

(A) Respiratory alkalosis

(B) Respiratory alkalosis and metabolic acidosis

(C) Metabolic acidosis

(D) Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis

(E) Metabolic alkalosis, respiratory alkalosis, and respiratory acidosis

• Concept of pH

– pH H+

7.0 100 nmol/L

7.4 40

7.7 20

– pH = - log (H+): log linear

– Exponential in reality

“The duty of the physician is to discover that

the quantity of sodium bicarbonate in the

blood is diminished, to restore that quantity

to normal, and to hold it there. But while

restoring it, he must never increase the

quantity above normal.”

Henderson LJ; Science 1917;46:73-83

Figure 1. Henderson-Hasselbalch Equations

H+ + HCO3- H2CO3 CO2 + H2O

[H+] = 24 x PCO2/[HCO3-]

pH = 6.1 + Log [HCO3-] / [0.03 x PCO2]

pK = 6.1

Slope Intercept H-H Equation

• y = mx + b

• Log [PCO2] = -1 (pH) + Log [HCO3-]/K

• In-vitro log PCO2- pH equilibration curve

– Linear relationship between log PCO2 and

– Slope = -1

Log PCOLog PCO22--pH Curve in PlasmapH Curve in Plasma

Constable,P. J. Appl. Physiol. 1997; 83(1): 298

6.8 7.0 7.2 7.4 7.6 7.8 8.0 8.2

In-Vitro

6.8 7.0 7.2 7.4 7.6 7.8 8.0 8.2

2.0Blue : in vitro

Green: in vivo

Crit Care Med 1998;26:1173-1179

Gibbs Donnan Effect

6.8 7.0 7.2 7.4 7.6 7.8 8.0 8.2

Blue : in vitro

Green: in vivo

Red: Total Protein

Constable P. J Appl Physiol 1997; 83(1): 298

Gibbs Donnan Effect

HH Equation

• Explains the effect of PCO2 on pH

– PCO2 directly measured

– Linear relationship between pH and PCO2

• HH does not explain the effects of:

– Na+ (Hypernatremia, Hyponatremia)

– Cl- (Hypochloremia, Hyperchloremia)

– Unmeasured and measured anions and cations

• lactate, ketones, salicylates, lithium, serum globulins …

– hypoalbuminemia and hyperphosphatemia

– Resuscitation Fluids

Law of Electrical NeutralityLaw of Electrical Neutrality

Cations Cations == AnionsAnions

Plasma Strong IonsPlasma Strong Ions

• Strong cations and anions

– Na+, K+, Ca++, Mg++, Cl-, Lactate-

– Fully dissociated, exert no buffering effect

– Combined positive electrical effect

• Strong Ion Difference (SID)

– Collective unit of charge (mEq/L)

– Strong cations - anions

• Na++K++Ca+++Mg++-Cl- - lactate = +39 mEq/L

– Approximated by difference between Na+ and Cl-

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -106

SID = +39

Charge Balance at Standard Physiologic State

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -106

HCO3 = -24.6

A- = -14.4

Buffer Base = -39 SID = +39

pH = 7.40

PaCO2 = 40 mm Hg

BEp = 0 mEq/L

SBE = 0 mEq/L

ANG = 12 mEq/L

SIG = 5 mEq/L

Charge Balance at Standard Physiologic State

Strong Ions and Charge Balance

Na+ + K+ + Mg++ + Ca++ + H+ = Cl- + HCO3- + OH- + lactate- + A- + XA- + Pi-

Na+ + K+ + Mg++ + Ca++ - Cl- - lactate- - XA- = HCO3- + A- + Pi-

(Na+ + K+ + Mg++ + Ca++ - Cl- - lactate- - XA-) = (HCO3- + A- + Pi-)

+39 = ?-39

Strong Ion Difference = Buffer Base

Plasma Buffer Base

• Weak acids: pKa 5.8-8.9

• Volatile buffer anion bicarbonate

– HCO3- + H+ = H2CO3 = CO2 + H2O

– Open buffer system in plasma

• Nonvolatile Buffer Anions

– Albumin (imidazole amino protein groups)

– Inorganic Phosphorus (PI): H2PO42-

– Total Citrate

J Appl Physiol 1986; 61: 2260-2265

Plasma Buffer Base (BB)Plasma Buffer Base (BB)

• Total buffer capacity of plasma

– [HCO3-] - 24.6 mEq/L

– [Alb] + [PI] +[Citrate] - 14.4 mEq/L

NORMAL = - 39 mEq/L

http;/www.Figge-Fencl.org/

Standard physiological state in plasma for 70 kg test

subject (TBW = 60% total body weight)

SID, strong ion difference; Atot, plasma nonvolatile weak acid buffer content; SBE, standard

base excess; HCO3, bicarbonate; TBW, total body water; ECV, extracellular compartment

volume; PV, plasma volume

pH Regulating

Variables

Derived

Parameters

SID (mEq/L) 39 Weight (Kg) 70.0 pH 7.400

PCO2 (mm Hg) 40.0 TBW (L) 42.0 [HCO3]HH (mEq/L) 24.6

Atot ECV (L) 14.0 SBE (mEq/L) 0.2

Albumin (g/dL) 4.40 PV (L) 3.5

Phosphate (mmol/L) 1.16

Citrate total (mmol/L) 0.135

Calculation of the SID or Buffer Base

• Buffer Base [HCO3-] + 2.8 x [Alb-] g/dL + 0.6 x [Pi] mg/dL

– BB = -24.6 mEq/L- 2.8 x 4.4 g/dL – 0.6 x (3.6 mg/dL)= -39

• Figge-Fencl algorithm

– http://www.figge-fencl.org/

Δ SID Δ buffer base

• A change in SID forces a change in buffer

• Displacement from normal (+39 mEq/L)

quantitates metabolic acid-base disorders

• PCO2 independent index

Singer RB, Hastings AB. Medicine 1948; 27: 223-242

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -116

HCO3 = -15.8

A- = -13.2

pH = 7.209

PCO2 = 40 mm Hg

BEp = -10 mE/L

SBE = -11 mEq/L

ANG = 11 mEq/L

SIG = 5 mEq/L

Hyperchloremic Metabolic Acidosis

Buffer Base (BB) in Hyperchloremia

HCO3- = - 24.6 mEq/L

Albumin +PI = -14.4 mEq/L

HCO3- = -15.8

Albumin + PI = -13.2

BB = -39 mEq/L and

BB = -29 mEq/L and Cl- = 116

H+ +HCO3- H2CO3 CO2 +H2O

BEp = -10 mEq/L

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -106

HCO3- = -15.8

Alb- + PI = -13.2

Lactic Acidosis (Lactate- = 10 mmol/L)

pH = 7.208

PCO2 = 40 mm Hg

BEp = -10 mmol/L

Lac- = -10

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -106

HCO3- = -15.8

Alb- + PI = -13.2

Ketoacidosis (Ketones- = 10 mmol/L)

pH = 7.208

PCO2 = 40 mm Hg

BEp = -10 mmol/L

Ket- = -10

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -116

HCO3- = -15.8

Alb- + PI = -13.2

Hyperchloremic Phase of DKA

pH = 7.208

PCO2 = 40 mm Hg

BEp = -10 mmol/L

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -96

HCO3 = -33.8

A- = -15.2

Buffer Base = - 49 SID = +49

pH = 7.54

PCO2 = 40 mm Hg

BEp = 10 mEq/L

SBE = 11 mEq/L

ANG = 13

Hypochloremic Metabolic Alkalosis

15 20 25 30 35 40 45 50 55

SID (mEq/L)

pH = 7.4

PaCO2 = 40 mm Hg

SID = 39 mEq/L

AT = Standard State

pH as a function of SID

Etiology of Metabolic Acid-Base

Disturbances

• Changes in Strong Ion Difference

– Increased = Metabolic Alkalosis

• Excess of plasma cations

– Reduced = Metabolic Acidosis

• Excess of plasma anions

*Summarizes Acid-Base Status Circa 1962

Plasma Base Excess

-20 -15 -10 -5 0 5 10 15 20 25

Plasma Base Excess (mEq/L)H

24 29 34 39 44 49 54

SID (mEq/L)

– Excess Anions < -2 mMol/L (Metabolic Acidosis)

– Excess Cations > +2 mMol/L (Metabolic Alkalosis)

– Change from 39 reflects of degree of anion /

cation disparity only regarding strong ions

– Magnitude of metabolic component of acid-base

status in plasma compartment

• Not Standard Base Excess (SBE)

– PCO2 independent index

BE Scale for Metabolic Acid-Base Disorders

*Siggard-Anderson O. Scand J Clin Lab Invest 1962; 14: 598-604

• {+} value

• excess plasma cations = metabolic alkalosis

• {-} value

• excess plasma anions = metabolic acidosis

• Magnitude of metabolic component of acid-base

status in extracellular fluid compartment

• Adjusts for Gibbs Donnan effect unlike BEp

• Metabolic Acidosis

• PCO2 = SBE then normal compensation

• Respiratory acidosis/alkalosis (pure)

• SBE = 0

• PCO2 independent index

Standard Base Excess

Which profile has the most severe

metabolic acid-base derangement?

• A. pH = 7.19, PCO2 = 40, HCO3 = 15

• B. pH = 7.55, PCO2 = 18, HCO3 = 15

• C. pH = 7.10, PCO2 = 74, HCO3 = 22

Which profile has the most severe

metabolic acid-base derangement?

• A. pH = 7.19, PCO2 = 40, HCO3 = 15

– SBE = -11.6 mmol/L

• B. pH = 7.55, PCO2 = 18, HCO3 = 15

• C. pH = 7.10, PCO2 = 74, HCO3 = 22

Dehydration

• Dehydration and Water intoxication – Water loss/gain from intracellular and interstitial

compartments

– Associated with hypertonicity/hypotonicity and changes in plasma [Na+] (excludes uremia, DKA, NKHC, mannitol…)

– Symptoms: thirst, confusion, coma

– Quantitatively described as free water deficiency /excess

• Volume of water that must be removed/added to hypotonic/hypertonic plasma to make isotonic plasma

– Treatment: D5W with electrolytes, diuretics, and hypertonic saline

Language Guiding Therapy: The Case of Dehydration versus Volume Depletion

Ann Intern Med 1997;127:848-853

• Volume depletion/expansion (hypo and hypervolemia)

– Extracellular fluid compartment volume depletion/excess that affects the vascular tree

– Surrogate term for where cardiac function lies on the Starling Curve

– Diagnosis: • Macrocirculation Impairment: BP, HR, Orthostatics

• Microcirculation Impairment: Lactic Acidosis, Low venous Svo2

– Treatment: Crystalloids, Colloids, PRBC, or diuretics

Volume Depletion

Dehydration versus Volume Depletion

• Changes in extracellular and intracellular compartment volumes can be and often are dissociated

• Indiscriminate use of the terms dehydration and volume depletion risks confusion and therapeutic errors

Treatment of Dehydration Versus Hypovolemia

Language Guiding Therapy: The Case of Dehydration versus Volume Depletion

Ann Intern Med 1997;127:848-853

Free Water Excess/Deficit effects on [Cl-]

• Free H2O abnormality detected as an abnormal [Na+]

– Plasma [Cl-] has to be corrected for the dilution or concentration of plasma [Na+]

– [Cl-] predicted = [Cl-] normal x [Na+] observed / [Na+] normal

– If plasma [Na+] =155 mmol/L

• Then [Cl-] = 106 x 155/142 = 115 mmol/L

– If plasma [Na+] =131 mmol/L

• Then [Cl-] = 106 x 131/142 = 97 mmol/L

Free H2O excess/deficit effects on Plasma [Na+]

-3 L 155 115 +3 (42)

-2 L 150 111 +2 (41)

-1 L 146 108 +1 (40)

0 142 105 0 (39)

+1 L 138 102 -1 (38)

+2 L 134 99 -2 (37)

+3 L 131 97 -3 (36)

Free H2O [Na+] [Cl-] SID/SID

Standard State

Nguyen M. and Kurtz I: J Applied Physiology 2006; 100: 1293–1300

Concentr

ational

ilutional A

Sodium 134 mEq/L

Potassium 3.8 mEq/L

Chloride 83 mEq/L

Bicarbonate 24 mEq/L

PO2 89 mm Hg

PCO2 32 mm Hg

pH 7.48

Which of the following is the most likely explanation for these laboratory

findings?

(A) Respiratory alkalosis

(B) Respiratory alkalosis and metabolic acidosis

(C) Metabolic acidosis

(D) Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis

(E) Metabolic alkalosis, respiratory alkalosis, and respiratory acidosis

Cl-(corrected) =106 x 134/142

=100 mEq/L

Cl-(observed) = 83 mEq/L

17 mEq/L excess cations

BEp = +17 strong cations

ANGcorr = 33 or -17 anions

A 34-year-old white man presents with nausea, vomiting and has been unable to

consume any food or liquids. He admits to drinking about two pints of vodka daily.

Temperature is 99.6 F, pulse rate is 101 per minute supine and 126 per minute

standing, respirations are 24 per minute, and blood pressure is 110/85 mm Hg

supine and 80/50 mm Hg when standing.

• Changes in Strong Ion Difference – Increased = Metabolic Alkalosis

– Reduced = Metabolic Acidosis • Excess of plasma anions

• Water deficit/excess: • Hypernatremia = Alkalosis (Cation Excess)

• Hyponatremia = Acidosis (Cation Deficient)

• Cation/Anion Imbalance • Hypochloremia = alkalosis (Anion Deficient)

• Hyperchloremia = acidosis (Anion Excess)

• Organic Acids (lactate, Ketones…) = acidosis – Anion Excess

Etiology of Metabolic Acid-Base Disturbances

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -106

HCO3- = -24.6

Alb- + PI = -14.4

Standard Physiologic State [Pi] = 3.6 mg/dL

pH = 7.40

PCO2 = 40 mm Hg

BEp = 0 mEq/L

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -106

HCO3- = -21.2

Alb- + PI = -17.8

Hyperphosphatemic Metabolic Acidosis

[Pi] = 10 mg/dL

pH = 7.337

PCO2 = 40 mm Hg

BEp = -3.7 mEq/L

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -106

HCO3- = - 36.3

A- = - 2.7

Standard State Acid Base Status

[Alb-] = 0 mg/dL

pH = 7.571

PCO2 = 40 mm Hg

BEp = 13 mEq/L

SBE = 13 mEq/L

ANG = 1

pH As A Function of Serum Albumin

Concentration

1 1.5 2 2.5 3 3.5 4 4.5 5

Albumin (g/dL)

SID = 39 mEq/L

PCO2 = 40 mm Hg

Phosphate = 3.6 mg/dL

Fencl V, Rossing TH. Ann Rev Med 1989; 40:17-29

Hyperchloremic Acidosis

[Alb-] = 4.4 gm/dL

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -115

HCO3- = - 15.8

Alb- + PI = - 13.2

pH = 7.208

PCO2 = 40 mm Hg

BEp = -10 mEq/L

Cations Anions

Na+ = 142

K+ Ca++ Mg++

Cl- = -116

HCO3 = - 21.2

A- = - 7.8

pH = 7.338

PCO2 = 40 mm Hg

SBE = - 4 mEq/L

ANG = 6 mEq/L

Adj. ANG = 12 mEq/L

SIG = 5 mEq/L

Hyperchloremic strong ion acidosis with concurrent

hypoalbuminemic alkalosis ([albumin] = 2g/dL)

Hypoalbuminemic Alkalosis

HCO3- = -15.8 mEq/L

Charge =

-13.2 mEq/L

HCO3- = -21.2 mEq/L

Albumin

2.0 g/dL

BB = -29 BB = -29

H+ +HCO3- H2CO3 CO2 +H2O

Albumin

4.4 g/dL Charge =

-7.8 mEq/L

Hypoalbuminemia- an adaptive response

• Hypoalbuminemia independent risk factor

• Beneficial by restoring pH towards normal

• SBE = -10 mmol/L (Lactate = 10 mmol/L)

[Albumin-] = 4.4 g/dL, pH = 7.20

2.2 g/dL, pH = 7.33

1.1 g/dL, pH = 7.38

J Appl Physiol 1986; 61: 2260-2265

pH as a Function of [Alb] and SID

15 20 25 30 35 40 45 50 55

SID (mEq/L)

1.1 2.2 4.4Albumin (g/dL) =

AlbuminAlbumin

• Major nonvolatile plasma weak acid buffer

– (4 - 4.4 g/dL in plasma)

• 1 gm = 2.8 mEq of acid

• Accounts for 12.5 mEq/L of plasma fixed acid

– Hypoalbuminemia = alkalosis

– Hyperalbuminemia = acidosis

– Loss of weak acid = gain in basic equivalents

J Appl Physiol 1986; 61: 2260-2265

• Hypoalbuminemia pervasive in acute illness

and surgery

• Hypoalbuminemic alkalosis exists to some

extent in all critically ill patients

• Hypoalbuminemia corrects pH towards

standard state in acute illness

Am J Respir Crit Care Med 2000; 162: 2246-2251

• Changes in Strong Ion Difference – Increased = Metabolic Alkalosis

– Reduced = Metabolic Acidosis • Excess of plasma anions

• Water deficit/excess: • Hypernatremia = Alkalosis (Cation Excess)

• Hyponatremia = Acidosis (Cation Deficient)

• Cation/Anion Imbalance • Hypochloremia = alkalosis (Anion Deficient)

• Hyperchloremia = acidosis (Anion Excess)

• Organic Acids (lactate, Ketones…) = acidosis – Anion Excess

• Abnormal concentrations of plasma weak acids – Independent determinants of pH

– Hypoalbuminemia = metabolic alkalosis

– Hyperalbuminemia = metabolic acidosis

– Hyperphosphatemia = metabolic acidosis

Etiology of Metabolic Acid-Base

Disturbances

Am J Respir Crit Care Med Vol 162. pp 2246–2251, 2000

Anion Gap (1977)

• Law of electrical neutrality

– Discrepancy between cations and anions virtual

– Na+ + K+ = Cl- + HCO3- + XA-

– (Na+ + K+ - Cl- - HCO3) 16

– Facilitates differential diagnosis (easy to compute)

– Normal ANG entirely accounted for by [albumin] + PI

– ANG = 2.8*Albumin + 0.5 *PI

– Very Unreliable in critical illness

• Hypoalbuminemia

• pH changes

• Gibbs Donnan Effect

Oh MS & Carroll HJ. The Anion Gap. NEJM 1977; 297: 814-817.

Cations Anions

Na+ = 142

K+ = 4

Cl- = -105

HCO3 = -24.6

A- = -14.4

pH = 7.40

PCO2 = 40 mm Hg

SBE = 0 mEq/L

ANG = 12 mEq/L

SIG = 5 mEq/L

XA- = Unmeasured Anions:

Cyanide

Glycols

Isoniazid

Ketoacids

Krebs Cycle

Lactate

Methanol

Paraldehyde

Toluene

Salicylate

Uremia

Anion Gap

68 yo male UGI Bleed

Na =132, K = 4, Cl = 98, HCO3 = 22

Lactate = 4.5, Alb = 2.8

ANG = Na + K – Cl – HCO3 = 16 (“normal”)

ANG(c) = 16 + 2.8(4.4 - 2.8) = 20.5 (abnormal)

WHY? Adding back lost charge from hypoalbuminemia

Anion gap and hypoalbuminemia. Crit Care Med. 1998 Nov;26(11):1807–1810

Anion Gap as function of Albumin

Concentration

1 1.5 2 2.5 3 3.5 4 4.5 5

Albumin (g/dL)

Fencl V, Rossing TH. Ann Rev Med 1989; 40:17-29

Anion Gap = ( Na+ + K+ – Cl- – HCO3-)

Anion Gap as a function of pH

6.8 7 7.2 7.4 7.6

Anion Gap = ( Na+ + K+ – Cl- – HCO3-)

Anion GapAnion Gap

• Insensitive index of organic acidosis in acute

illness and post surgery (hypoalbuminemia, pH

effects)

• Adjusted Anion Gap for hypoalbuminemia

= ANG + 2.8( 4.4 - Observed alb.)

Increased anion gap = acidosis

Decreased anion gap = alkalosis

Strong Ion Gap

• Unmeasured Anions of Critical Illness

– All organic anions (ketones, lactate …)

• Codeterminants of Strong Ion Difference

– SIG = SID(apparent) – Buffer Base

– SIDa = Na+ + K+ +Ca+++ Mg++ - Cl- - Lactate-

• Not affected by pH or [Albumin]

• Equivalent to the Anion Gap (corrected)

Cations Anions

Na+ = 142 Cl- = -106

HCO3- = -24.6

Alb- + PI = -14.4

Strong Ion Gap: SIDa – BB = SIG

pH = 7.40

PCO2 = 40 mm Hg

BEp = 0 mmol/L

XA- K+ Ca2+ Mg2+

Lactate-

SIDa Buffer Base

Strong Ion Gap

SIDa = Na+ + K+ + Ca2+ + Mg2+ - Cl- - lactate- - XA-

Cations Anions

Na+ = 142

K+ = 4

Cl- = -105

pH = 7.40

PCO2 = 40 mm Hg

SBE = 0 mEq/L

ANG = 12 mEq/L

SIG = 5 mEq/L

Strong Ion Gap

SIDe or Buffer Base

Strong Ion Gap

Calculation of the SID and apparent SID

• Buffer Base [HCO3-] + 2.8 x [Alb-] g/dL + 0.6 x [Pi] mg/dL

– BB = -24.6 mEq/L- 2.8 x 4.4 g/dL – 0.6 x (3.6 mg/dL)= -39

• SIDa Na+ + K+ + (Mg2+ + Ca 2+) - Cl- - lactate-

– SIDa Na+ + K+ + 3 – Cl- - lactate- = 42 mEq/L

• SIG = SIDa – Buffer Base

• SIG = 42 – 39 3 mEq/L

Independent Determinants of pH

• Strong Ion Difference (SID)

• Strong Ion Gap

• Plasma Weak Acids

• CO2 production

• This is physico-chemical analysis!

Physico-Chemical Analysis

• Three independent determinants of acid-base

status

– Strong Ion Difference

– PCO2

– Variable weak acid total ([albumin-] + PI)

• Mechanistic and quantitative

• Guides diagnosis and therapy

Stewart P. Can J. Physiol. Pharmacology 1983; 61: 1444-1461

Normal Saline Lactated Ringer's 1/2 NS with 75 mEq/L NaHCO3 NaHCO3

Na 154 130 150 150

Cl 154 109 75

Acetate

Gluconate

Lactate 28

SID 0 28 75 150

*Caution must be exercised in patients with acute or chronic renal failure

and K containing solutions (LR)

*NaHCO3 solution: 3 Amps NaHCO3 in 1 Liter sterile water or D5W

Isotonic Crystalloid Solutions

-1.8 SBE/L +0.4 SBE/L +4 SBE/L +9 SBE/L

Crystalloid SID and serum [HCO3-]

• If crystalloid SID plasma [HCO3-] (24.6 mmol/L)

– No change in SBE or acid-base status

– Lactated Ringer’s, Hartman’s Solution, Hextend

• If crystalloid SID < plasma [HCO3-]

– Metabolic acidosis

– Normal Saline

• If crystalloid SID > plasma [HCO3-]

– Metabolic alkalosis

– Plasmalyte, ½ NS + 75 mEq/L NaHCO3, and isotonic

bicarbonate solutions

Omron E: J Int Care Med 2010. 25; 271-280

Metabolic Acid-Base Effects of Crystalloid Infusion

0 1 2 3 4 5 6 7 8 9 10

Crystalloid Infusion Volume (Liters)

Normal Saline (SID = 0)

Crystalloid SID = 24.5 mEq/L

Ringer's Lactate (SID = 28)

Plasmalyte 148 (SID = 50)

1/2 NS + 75 mEq/L NaHCO3 (SID = 75)

0.15 M NaHCO3 (SID = 150)

Physicochemical Resuscitation

• Principles – Patients in shock with a metabolic acidosis are

optimally managed with isotonic crystalloid

solutions that are alkaline when infused

– Patients with normal acid base status are best

managed with isotonic balanced solutions

– Patients with metabolic alkalosis are optimally

managed with isotonic solutions that are acidic

when infused

– The principles of Early Goal Directed Therapy are

to be done concurrently with physicochemical

resuscitation

Crystalloid Resuscitation Guidelines at albumin = 2.2 g/dL

-20 -15 -10 -5 0 5 10 15 20 25

SBE (mEq/L)

0** 3 4 4 0** 0** 1** 2 1

0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid

1 = Normal Saline (SID = 0), 1.8 mmol/L acid

2 = Lactated Ringers ( SID = 28), 0.4 mmol/L base

3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base

4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH

** Acetazolamide 250 mg IVP q12, no more than 500 mg qday Pulmonary / Critical Care

Dialysis

Isotonic (Normal) Saline

• 0.9% Sodium Chloride in sterile water

• Na+ = 154 mmol/L, Cl- = 154 mmol/L

• SID = 0

• Excellent choice in

– Hypovolemic, Hypochloremia with metabolic alkalosis

– SBE ≥ 0

• 1.8 mmol/L fixed acid generated (excess Cl-)

• -1.8 SBE/Liter infused

Lactated Ringer’s Solution

• Polyionic isotonic crystalloid that mimics plasma

electrolyte concentration

• Na+ = 130, K+=4, Cl- = 109, Lact- = 28, Ca++ = 3

• SID = 28

• Excellent choice in mild metabolic acidosis with

preserved renal function (SBE = -5 to +5)

• 0.4 mmol/L fixed base

• 0.4 SBE/Liter infused

1/2 NS with 75 mEq/L HCO3

• 1/2 NS + 1.5 Amps Na HCO3 per liter

• Isotonic resuscitation and maintenance

• Na+ =150 mmol/L, Cl- = 75 mmol/L HCO3 = 75

mmol/L

• SID = +75

• Hyperchloremic metabolic acidosis and reduced

renal function Plasma SBE -10 to -5

• 4 mmol fixed base/Liter infused

• +4 SBE/ Liter

Isotonic NaHCO3- Administration

• 3 Amps Na HCO3 in 1 liter sterile H2O

• Isotonic Resuscitation and maintenance

• Na+ = 150, HCO3 = 150

• SID = 150

• Excellent choice in malignant acidemias

• Bridge to acute dialysis: SBE ≤ -10

• +9 mmol fixed base/ Liter infused

• +9 SBE/Liter

Metabolic Acid-Base Effects of Crystalloid Infusion

during moderate metabolic acidosis

0 1 2 3 4 5

Crystalloid Infusion Volume (Liters)

Normal Saline

Crystalloid SID = 20 mEq/L

Ringer's Lactate

Plasmalyte

1/2 NS + 75 mEq/L NaHCO3

0.15 M NaHCO3

• Assumptions

– Normal renal function

– Acute and chronic kidney injury result

in marked impairment in chloride

excretion

– VD may change in acute illness and

surgery

– Ignores the effects of tissue buffering

Bicarbonate Solutions

• Historically: hyperosmolar solution – 1 amp = 50 mEq/50 cc or 1 mEq/cc (1 M)

– Correction of extracellular acidosis at the expense of massive intracellular derangement

– No defined physico-chemical endpoint

– Hypertonic volume expansion • Recently shown to increase mortality in shock

– Only use isotonic solutions: Sterile water or D5W + 3 amps Na HCO3! (0.15 M)

– Activates Phosphofructokinase !

– Aggravates minute ventilation !

Alkalosis activates PFK

**Aggravates lactic acidosis in shock states

28 yo male with ARDS undergoing

diuresis

• pH = 7.61, PaCO2 = 40 mm Hg,

• [HCO3-]HH = 39.4 mmol/L,

• SBE = 16.8 mmol/L

• Na+ = 144 mmol/L, Cl- = 91 mmol/L

• Cl- corrected = 106 x 144/142 = 107

– Cl- loss 16 mmol/L ( 107-91) = 16 mmol/L excess cations

• Severe hypochloremic metabolic alkalosis

– Mechanism?

– Treatment?

-20 -15 -10 -5 0 5 10 15 20 25

SBE (mEq/L)

0** 3 4 4 0** 0** 1** 2 1

2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base

** Acetazolamide 250 mg IVP q12, no more than 500 mg qd Pulmonary / Critical Care

Dialysis

67 yo female with ischemic bowel

• BP 80/40, HR 120, HCT= 25

• pH = 7.26, PaCO2 = 24, HCO3 = 11,

• SBE = -14.6

• Na+ = 143, Cl- = 118

• Cl- corrected = 106 x 143/142 106

• Excess Cl- (118 - 106) = 12 mmol/L

• Mechanism: Hyperchloremia

• How do you fix?

What are the resuscitation fluids of choice?

-20 -15 -10 -5 0 5 10 15 20 25

SBE (mEq/L)

0** 3 4 4 0** 0** 1** 2 1

Dialysis

78 yo with severe pneumonia and

sepsis

• pH=7.37, PCO2=26.9, HCO3=15.2,

• SBE = -9,

• Na = 134 and Cl = 113 and albumin = 3 g/dL

• Cl- corrected = 106 x 134/142 = 100 mmol/L – Excess chloride = 13 mmol/L

• Mechanism of metabolic acidosis

– Hyperchloremia

– Free water excess reducing Na

• Hypoalbuminemic Alkalosis • How do you fix?

• Resuscitation Fluid?

-20 -15 -10 -5 0 5 10 15 20 25

SBE (mEq/L)

0** 3 4 4 0** 0** 1** 2 1

Dialysis

Additional References

http://www.slideshare.net/edofiron

www.acidbase.org

http://www.figge-fencl.org/

Intensive Care Medicine 2011. 37; 461-468.

J. Intensive Care Medicine 2010. 25; 271-280.

Intensive Care Medicine 2009. 35; 1377-1382.

Critical Care Medicine 2005. 21; 329-346.

Best Practice Res Clin Anes 2004. 18; 113-127.

Kidney Inter. 2003. 64; 777-787.

Am. J. Respir. Crit. Care Med. 2000. 162; 2246-2251.

J. Applied Physiology 1999. 86; 326-334.

Annual Review Medicine 1989. 40; 17-29.

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