University of PennsylvaniaScholarlyCommons

Miscellaneous Papers Miscellaneous Papers

1-1-2001

Critical Care Nursing of Infants and ChildrenMartha A. Q. CurleyUniversity of Pennsylvania, curley@nursing.upenn.edu

Patricia A. Moloney-HarmonThe Children's Hospital at Sinai

Copyright by the author. Reprinted from Critical Care Nursing of Infants and Children, Martha A.Q. Curley and Patricia A. Moloney-Harmon(Editors), (Philadelphia: W.B. Saunders Co., 2001), 1,128 pages.

NOTE: At the time of publication, the author, Martha Curley was affiliated with the Children's Hospital of Boston. Currently, she is a faculty memberin the School of Nursing at the University of Pennsylvania.

This paper is posted at ScholarlyCommons. http://repository.upenn.edu/miscellaneous_papers/4For more information, please contact repository@pobox.upenn.edu.

Please Note: The full version of this book and all of its chapters (below) can be found on ScholarlyCommons (from the University of Pennsylvania) at http://repository.upenn.edu/miscellaneous_papers/4/ Information page in ScholarlyCommons Full book front.pdf - Front Matter, Contributors, Forward, Preface, Acknowledgements, and Contents Chapter 1.pdf - The Essence of Pediatric Critical Care Nursing Chapter 2.pdf - Caring Practices: Providing Developmentally Supportive Care Chapter_3.pdf - Caring Practices: The Impact of the Critical Care Experience on the Family Chapter_4.pdf - Leadership in Pediatric Critical Care Chapter 5.pdf - Facilitation of Learning Chapter_6.pdf - Advocacy and Moral Agency: A Road Map for Navigating Ethical Issues in Pediatric Critical Care Chapter_7.pdf - Tissue Perfusion Chapter 8.pdf - Oxygenation and Ventilation Chapter_9.pdf - Acid Base Balance Chapter 10.pdf - Intracranial Dynamics Chapter 11.pdf - Fluid and Electrolyte Regulation Chapter 12.pdf - Nutrition Support Chapter 13.pdf - Clinical Pharmacology Chapter_14.pdf - Thermal Regulation Chapter_15.pdf - Host Defenses Chapter 16.pdf - Skin Integrity Chapter_17.pdf - Caring Practices: Providing Comfort Chapter 18.pdf - Cardiovascular Critical Care Problems Chapter 19.pdf - Pulmonary Critical Care Problems Chapter 20.pdf - Neurologic Critical Care Problems Chapter 21.pdf - Renal Critical Care Problems Chapter 22.pdf - Gastrointestinal Critical Care Problems Chapter_23.pdf - Endocrine Critical Care Problems Chapter_24.pdf - Hematologic Critical Care Problems Chapter_25.pdf - Oncologic Critical Care Problems Chapter_26.pdf - Organ Transplantation Chapter 27.pdf - Shock Chapter_28.pdf - Trauma Chapter_29.pdf - Thermal Injury Chapter 30.pdf - Toxic Ingestions Chapter_31.pdf - Resuscitation and Transport of Infants and Children back.pdf - Appendices and Index

Acid-Base BalanceAnn Powers

DEFINITION OF ACID-BASE BALANCENormal metabolism results in the production of acids. Anacid is a proton or hydrogen ion (H+) donor, and abase is a proton or hydrogen ion acceptor. A largenumber of potential hydrogen ions exist in the body, mostof which are buffered and therefore not in free form. Thenonnal concentration of free H+ in the extracellular fluid(ECF) is extremely small, approximately 40 nmEqlL,which is equivalent to one millionth of a mEqlL con­centration of sodium. The term pH expresses the negativelogarithm of free H+ concentration. The relationship isinversely proportional in that as free H+ concentrationincreases, pH decreases, and vice versa. A normal arterialpH of 7.40 correlates with a free H+ concentration of 40nmEqlL. For each O.QJ-unit (U) change in pH from 7.40,H+ concentration changes I nmEqlL in the oppositedirection, provided that the pH range is between 7.20and 7.50.

Normal metabolism produces hydrogen in the form ofvolatile and fixed acids. To maintain pH within its normalnarrow range of 7.35 to 7.45, acids must be buffered orexcreted. A buffer is defined as a substance that reduces thechange in a solution's free H+ concentration when an acid orbase is added to it. In other words, the presence of a bufferin a solution increases the amount of acid or base that mustbe added to change the pH.

The largest amount of acid load in the body is in the formof carbonic acid (H2C03), which is a volatile acid. Carbonicacid is formed, or dissociated, into either hydrogen andbicarbonate or carbon dioxide and water. This is illustratedby the following equation:

DEFINITION OF ACID-BASE BALANCE

REGULATION OF ACID-BASE BALANCE

Buffer SystemRespiratory SystemRenal System

ELECTROLYTES AND ACID-BASE BALANCE

MATURATIONAL FACTORS

ANALYZING ACID-BASE BALANCE

ACID-BASE DISTURBANCES

Respiratory AcidosisRespiratory AlkalosisMetabolic AcidosisMetabolic Alkalosis

MIXED ACID-BASE DISORDERS

Respiratory Acidosis With Metabolic AlkalosisRespiratory and Metabolic AcidosisRespiratory Alkalosis With Metabolic AcidosisRespiratory and Metabolic AlkalosisTriple Acid-Base Disorders

SUMMARY

A II patients who are admitted to the pediatric criticalcare unit are at risk for acid-base disturbances that

may complicate their underlying disorder and furthercompromise their overall status. Acid-base balance ismaintained through a variety of physiologic processes,which may be disrupted with serious illness or in­jury. Knowledge of acid-base balance is essential to thepractice of pediatric critical care nursing so that appro­priate assessment, monitoring, and intervention can beprovided in a timely manner to optimize the child'soutcome.

309

H+ +Hydrogen

Carbonic acid

HC03 ­

Bicarbonate

CO2

Carbondioxide

+

310 Part III Phenomena of Concern

The specific reaction (dissociation or formation ofcarbonic acid) is determined by the underlying acid-baseenvironment.

Hydrogen that is generated in the form of a fixed acidincludes lactic acid, ketoacid, phosphoric acid, and sulfuric

Box 9·1 ..

~ Physiologic Effects.of Alterations in pH ..

Increase pHIncrease

Insulin-induced glycolysisResponsiveness to catecholaminesLactate production

Decrease

Krebs cycle oxidations in muscles and renal cortexGluconeogenesis in the renal cortex2,3-Diphosphoglycerate concentration with a corresponding

left shift in the oxyhemoglobin dissociation curveVascular tone and resistance

Decrease pHIncrease

GlycolysisLipolysisKrebs cycle oxidations in muscles and renal cortexGluconeogenesis in the renal cortex2,3-Diphosphoglycerate concentration with a correspond-

ing right shift in the oxyhemoglobin dissociation curvePulmonary vascular resistance

Decrease

Quantities of liver glycogenLactate productionInsulin secretion and binding to receptorsPancreatic amylase secretionThreshold for ventricular fibrillationRespoosiveness to catecholaminesPeripheral vascular resistanceMesenteric blood flowPulmonary macrophage functionGranulocyte functionImmune response

Data from Czekaj L: Promoting acid base balance. In Kinney MR el al. eds:MeNs clinical referellcefor ailicaJ care nursing, St Louis. 1998. Mosby,pp 135-144.

acid. These are buffered by extracellular bicarbonate andeventually excreted by the kidneys. Dietary intake of acidsand alkal i are also metabolized and buffered to preventchanges in pH balance.

Biochemical processes are extremely sensitive to minutechanges (0.1 to 0.2 U) in body fluid pH. Cardiac, centralnervous system, and metabolic function may be significantlyaltered by changes in pH. Box 9-1 summarizes the physio­logic effects of alterations in pH. An interval of 1 pH unit(6.8 to 7.8) is the widest range compatible with human life.

REGULATION OF ACID-BASE BALANCEThree systems function interdependently to regulate andmaintain acid-base balance. They are the buffer, respiratory,and renal systems.

Buffer SystemThe buffer system can be activated within seconds and thusis considered the first line of defense against changes in pH(Table 9-1). The most important of these buffers is thebicarbonate-earbonic acid (HC03--H2C03) pair, which isresponsible for buffering ECF. This buffer pair consists of aweak acid (H2C03), which is activated when the pH isthreatened by a strong base, and a weak base (HC03-),

which is activated when the pH is threatened by a strongacid. Whenever a buffering reaction occurs, the concentra­tion of one member of the pair increases while the otherdecreases. The bicarbonate-earbonic acid system is assessedclinically by arterial blood gas pH, Pc02, and HC03-. Inclinical settings where arterial plasma HC03- measurementis unavailable, it can be estimated as being approximatelyI mEqlL less than the venous serum total CO2 content asmeasured with electrolytes. Therefore an elevated total CO2

would suggest buffering of a strong base. Arterial blood gasanalysis also reveals whether other systems (respiratory orrenal) are involved in maintaining or attempting to restoreacid-base balance.

A simple and clinically relevant way of relating pH toalterations in the acid-base ratio is:

pH =Base/Acid =HC03-1H2C03 =20/1

The second most abundant buffer pair is hemoglobin andoxyhemoglobin, an important buffer of carbonic acid. As

Weak Acid Weak Base % Total Buffer Action

TABLE 9-1 Buffer System Pairs

533535

732

Sodium bicarbonate (NaHC03 )

Potassium hemoglobinate (KHb)Potassium oxyhemoglobinate (KHb02 )

Proteinate (NaPr)Alkaline organic phosphate (Na2P04 )

Alkaline inorganic phosphate (NaHP04 )

Carbonic acid (H2C03)

Hemoglobin (Hb)Oxyhemoglobin (Hb02 )

Plasma protein (HPr)Acid organic phosphate (NaRHP04 )

Acid inorganic phosphate (NaH2P04 )

,;Prom Baer CL: Regulation and assessment of acid base balance. In Kinney MR et ai, eds: AAeNs clinical reference for critical care nursing. ed 3.FIi:,]!~ew York, 1993. McGraw-HilI.

Chapter 9 Acid-Base Balance 311

Fig. 9·1 pH effect on oxyhemoglobin dissociation curve. (Mod­ified from Shapiro B: Clinical application of blood gases. ed 5,St Louis. 1994. Mosby.)

blood passes from the arterial to the venous end of acapillary, cellular COz enters erythrocytes and combineswith water to fonn carbonic acid. At the same time,oxyhemoglobin gives up its oxygen to the cells, some ofwhich becomes reduced hemoglobin carrying a negativecharge. The hemoglobin ion then attracts the H+ fromcarbonic acid, resulting in a weaker acid than carbonic acid.When this system is active, the exchange demonstrates whyerythrocytes tend to give up oxygen more rapidly when Pcoz

is elevated (as in respiratory acidosis), resulting in a shift tothe right of the oxyhemoglobin dissociation curve. Eryth­rocytes hold on to oxygen when Pcoz is decreased (as inrespiratory alkalosis), resulting in a shift to the left in theoxyhemoglobin dissociation curve (Fig. 9-1). This is tennedthe Bohr effect. I

The protein buffer pair is the most abundant intracellularand ECF buffer. Proteins are composed of amino acids,which contain at least one carboxyl and one amine group.The carboxyl group tends to function like an acid, whereasthe amine group tends to act like a base. Thus proteins canact as both acid and base buffers.

The phosphate buffer pair, which works in the samemanner as the bicarbonate--{;arbonic acid pair, is an impor­tant regulator of both erythrocyte and renal tubular pH. Thisbuffer pair consists of acid-alkaline organic and inorganicsodium phosphate.

Respiratory SystemVentilation also plays a major role in maintaInIng pHbalance. The respiratory system can activate changes in pHwithin I to 3 minutes and can eliminate or conserve CO2(which directly affects acid-base status) more quickly andefficiently than all the buffer systems combined.

As discussed, when a strong acid is present in the body,the bicarbonate--{;arbonic acid buffer pair is activated tobuffer the acid. This results in a net increase of carbonicacid, which dissociates into COz and HzO. Carbon dioxideis then eliminated by the lungs (Fig. 9-2). An increase in H+concentration in the blood stimulates the breathing center inthe medulla to increase the respiratory rate, which facilitatesCOz elimination. If, on the other hand, pH is elevatedsecondary to an increase in HCO]-, the respiratory center isinhibited, and the respiratory rate decreases. This results in

100806040

Partial pressure O2

20

100

75Right shift

c Lph0

~ i PC02

'" iTempa;50en

N

0~0

25

Equilibrium Decreased H + ionconcentration

Fig.9·2 Regulation of hydrogen ion concentration by the respiratory system. (From Baer CL: Acid-basebalance. In Kinney MR et ai, eds: AACN's clinical reference for critical care nursing, ed 3, St Louis, 1993,Mosby. P 211.)

312 Part III Phenomena of Concern

Renal SystemCompared with the respiratory system, which operates bypassive CO2 diffusion, the kidneys control acid-base bal­ance through several highly developed acti ve transportprocesses. Renal compensation is a slower process, requir-

Fig. 9-3 Chemical reactions for (I) secondary active secretion ofhydrogen ions into the tubule, (2) sodium ion reabsorption inexchange for the hydrogen ions secreted, and (3) combination ofhydrogen ions with bicarbonate ions in the tubules to form carbondioxide and water. (From Guyton AC: Hllmall physiology alldmechallisms of disease, ed 6, San Diego. 1996. Harcourt. Brace.)

ing I to 2 days for complete activation, with disordersresulting in respiratory alkalosis, and 3 to 5 days to be fullyfunctional, with disorders resulting in respiratory acidosis.The length of time a primary acid-base disturbance has beenpresent is an important factor in determining the expecteddegree of renal compensation.

The kidneys react to changes in pH by regulating theexcretion or conservation of Wand HC03- (Fig. 9-3). Alow pH stimulates excretion of H+ into the urine. As H+enters the urine, it displaces another positive ion, usuallyNa+. At the same time, HC03- is reabsorbed in exchange forthe H+. The Na+ is then reabsorbed into the tubule cell,where it combines with HC03- to form NaHC03• which isthen available to buffer other H+ in the blood. The rale ofH+excretion, and therefore the rate of HC03- reabsorption, isproportionate to arterial Pc02. This reaction is reversed forincreases in pH.

The transport of H+ in the renal tubules is facilitated bythe buffer's phosphate (as previously discussed) and ammo­nia, which is classified as a base. Most ammonia isconverted to urea by the liver and is eliminated from thebody in urine. The remaining ammonia combines with H+to form the ammonium ion (NH4+) in the renal tubules(Fig. 9-4). NH/ also displaces Na+ and is eliminated in theurine. The Na+ is then reabsorbed into the tubule cells,where it combines with HC03- to form NaHC03, which isabsorbed into the blood to buffer excess H+.

The amount of H+ excreted in the urine can be measuredby determining the amount of alkali required to neutralizethe urine and is called titratable acidity. As a result of H+and NH4+ excretion, urine usually has an acidic pH of 6. Inthe clinical setting, checking urine pH can be a useful indi­cator of the degree of renal compensation when assessingacid-base status. For example, a low or acidic blood pH willbe accompanied a few days later by a low or acidic urine pHwhen renal compensatory mechanisms are active. Thereverse is true in alkalotic states.

TUBULEEXTRACELLULAR

FLUID

CO2 retention, which then becomes available to formcarbonic acid, which buffers the excess bicarbonate. Therespiratory system is thus able to compensate for changes inpH related to metabolic disorders (e.g., diabetic ketoacido­sis) by regulating Pc02 , which alters the bicarbonate­carbonic acid ratio. The respiratory system cannot, however,produce any loss or gain of hydrogen ions. Respiratorycompensation is activated within minutes and is usuallyfully functional within I to 2 days.

ELECTROLVTES AND ACID-BASE BALANCE

Fig. 9·4 Primary active transport of hydrogen ions through theluminal membrane of the tubular epithelial cell. Note that onebicarbonate ion is absorbed for each hydrogen ion secreted, and achloride ion is secreted passively along with the hydrogen ion.(From Guyton AC: Humall physiology alld mechallisms ofdisease,ed 6. San Diego. 1996. Harcourt. Brace.)

EXTRACELLULARFLUID

TUBULE In the clinical setting, recognizing how H+ interacts withother ions is extremely important so that metabolic andelectrolyte imbalances can be anticipated and managed in atimely and appropriate manner. Fig. 9-5 illustrates thelocation of the major concentrations of electrolytes that areaffected by acid-base balance. As discussed, an increase inplasma CO2 results in an increased renal excretion of H+ andreabsorption of HC03-, which then buffers excess H+ in thebody. This is a very important compensatory mechanismthat can stabilize pH.

Potassium (K+) also interacts in very important wayswith H+; the two share a reciprocal relationship. When H+concentration is elevated in the ECF, as occurs in metabolicacidosis, H+ moves into the cell, and K+ moves out. Thisexchange allows H+ access to the intracellular proteinbuffers, which can minimize changes in pH. However,during this process, the shift in K+ from the intracellularfluid (lCF) to the ECF results in hyperkalemia. A shift in avery small amount of the ICF K+ will produce a significant

increase in ECF K+ concentration and may lead to thepotentially lethal cardiac dysrhythmias associated withhyperkalemia (see Chapter 11). When H+ concentration isdecreased (as in metabolic alkalosis), H+ moves out of thecell, and K+ moves in, which can result in a hypokalemicstate. Cardiac dysrhythmias are also possible with hypoka­lemia but are usually not life threatening.

Sodium is affected by H+ balance, as previously dis­cussed. When H+ concentration is elevated, Na+ is displacedin the renal tubules so that excess H+ can be eliminated inthe urine. The displaced Na+ is reabsorbed, which tends toincrease HC03- reabsorption. Normally, this process alonedoes not affect pH. However, if tubular Na+ reabsorption issignificantly elevated (as in prolonged sodium deprivation),a metabolic alkalosis with hyponatremia may result.

The chloride ion (Cn can also contribute to acid-baseimbalance because it usually follows Na+ passively. Anincrease in Cl- results in a decreased reabsorption of HC03-

Chapter 9 Acid-Base Balance 313

with Na+ in the renal tubules, which can result in ametabolic acidosis associated with hyperchloremia. Thereverse of this (increase in HC03- resulting in a decreasedreabsorption of Cl- with Na+) can result in a hypochloremicmetabolic alkalosis.

Calcium (Ca+) is another ion that is affected by acid-basebalance. Maintaining Ca+ levels within their normallynarrow range is critical to normal neuromuscular andcardiac function. When pH is normal, 40% of the totalplasma Ca+ is bound to protein (mostly albumin) and 60%is present as ionized calcium in the plasma. Changes in pHalter the amount of Ca+ bound by proteins, which, in tum,alters ionized Ca+ levels. A change in pH of 0.1 U will effecta corresponding change in protein-bound calcium of0.12 mg/dl. When metabolic alkalosis is present in a childwith a low serum Ca+, the ionized Ca+ is likely to be verylow and can lead to neuromuscular and cardiac dysfunction.In a child with a metabolic acidosis and a low Ca+ level, the

Metabolic Balance

pH 7.35 - 7.45

ECF

Metabolic Acidosis

pH < 7.35 - 7.45

104 NLort

ECF

Ca++2.5 NL or.j,

ECF

Metabolic Alkalosis

pH> 7.35 - 7.45

ECF

Fig. 9-5 Location of major concentrations of electrolytes that affect acid-base balance (in mEqIL). ECF,Extracellular fluid; ICF, intracellular fluid. (Redrawn from Mathewson-Kuhn M: Pharmacotherapeutics: anursing process approach, ed 3, Philadelphia, 1994, FA Davis.)

314 Part III Phenomena of Concern

ionized Ca+ may be within normal limits. Chronic metabolicacidosis increases renal clearance of Ca+. NaHCO} admin­istration reestablishes normal calcium reabsorption.

MATURATIONAL FACTORSThe systems that regulate and maintain acid-base balancebecome fully operational at different developmental pe­riods. The buffer systems are functional in utero. Respi­ratory system control of acid-base balance is mature innewborns, provided that pulmonary function is adequate.Any respiratory, neuromuscular, or neurologic disorderthat alters CO2 elimination can result in an acid-basedisturbance.

Renal system control of acid-base balance is not fullyfunctional at birth. Newborns have a limited ability toexcrete hydrogen and ammonium ions. Because H+ excre­tion matures rapidly, the ability of the kidney to excrete amaximal acid load is achieved by 2 months of age in bothterm and preterm infants. Ammonium production may notfully mature until age 2. Newborns also have a low serumbicarbonate level, which is secondary to a lower renalthreshold for bicarbonate. The mechanism for this isunknown, but it may be related to an expanded ECF volumeand immaturity in the transport capacity for bicarbonatereabsorption. Because of these immature renal functions,infants have a diminished renal capacity for dealing withacid-base disturbances.

ANALYZING ACID-BASE BALANCEBefore discussing specific acid-base disturbances, a reviewof terminology and guidelines for analyzing acid-basebalance are presented. The terms base excess and basedeficit are often used in the clinical setting in relation toacid-base balance. Base excess describes the presence of anexcessive amount of base (HCO}-) or a deficit in the amountof fixed acid (not including H2CO}).

Base excess or deficit can be determined clinically byapplication of three rules. 2 These rules assist in determin­ing if a disorder is respiratory, metabolic, or mixed. Rule Istates that an acute change in Pc02 of 10 torr is associatedwith an increase or decrease in pH of 0.08 U. Normally, ifpH is 7.40, the Pc02 would be 40 torr in the absence ofmetabolic acidosis. Application of rule I would reveal thefollowing:

Pco2 50 (40 + 10) = pH 7.32 (7.40 - 0.08)Pco2 30 (40 - 10) = pH 7.48 (7.40 + 0.08)

Rule II states that for every 0.0 I-V change in pH not causedby a change in Pc02, there is a 2/3 mEqlL change in the base.For example, if the pH is 7.26 and the Pc02 is 50 torr, theincrease in PC02 would indicate respiratory acidosis. Thecalculated pH would be 7.32 (according to rule I). Becausethe measured pH is 7.26, there is a pH difference of 0.06 VBy applying rule II (6 x ¥3), the calculated base deficitwould be 4 mEqlL. Thus a metabolic and respiratoryacidosis are both present.

Rule III states the following:

Total body bicarbonate deficit =Base deficit (mEqlL) x Patient's weight (kg) x 0.3

HCO}- is located primarily in ECF, which is equal to 30%of body weight; thus total base deficit can be determined bymultiplying base deficit by body weight by 0.3. In a lO-kgchild with a PC02 of 50 and a pH of 7.24, the Pc02 is 10 torrabove normal, suggesting that the pH would be 7.32 if thechild had a respiratory acidosis. The unexplained pHdifference of 0.08 U must therefore be attributed to ametabolic acidosis with a base deficit of 6 mEqlL (accordingto rule II). Application of the preceding equation wouldreveal the following:

Total bicarbonate deficit = Base deficit x Weight (kg) x 0.3

18 = 6 x 10 x 0.3

To avoid overcorrection and a rebound metabolic alkalo­sis, total bicarbonate correction is not recommended. Onequarter to one half of the calculated dose is most oftenused. Note that the usual recommended dose of NaHC03

for correction of moderate metabolic acidosis, I mEq/kg,(which is approximately one fourth of the calculateddose), is very close to the more complicated calcula­tion using rule III. Therefore a standard dose of I mEg/kgis acceptable for quick determination of bicarbonatereplacement.

ACID-BASE DISTURBANCESThe buffer, respiratory, and renal compensatory mecha­nisms function interdependently at specific time inter­vals to restore acid-base balance. Signs and symptoms andthe clinical significance of acid-base disturbances aredirectly related to the rate at which the pH changes.Disorders that develop slowly, such as chronic renalor respiratory failure, allow time for maximum compen­sation to occur and thus are accompanied by minimalchanges in pH. Rapidly progressing or sudden insults,such as a cardiac arrest, allow little or no time forcompensation to occur, resulting in profound alterations inpH that may be fatal if immediate and effective inter­vention is not initiated. The arterial blood gas (ABG) isthe most useful diagnostic tool in detern1ining acid-baseimbalances in the clinical setting. Normal blood gas valuesare listed in Table 9-2. The steps used to analyze arterialblood gases to determine the acid-base imbalance areillustrated in Fig. 9-6.

Respiratory AcidosisRespiratory acidosis is an excess of ECF carbonic acid thatis caused by conditions resulting in hypoventilation and CO2retention. These conditions are summarized in Box 9-2.Buffer response to hypercapnia occurs immediately and iscomplete within 10 to 15 minutes. Renal compensatorymechanisms are activated within 2 to 5 hours but take 3 to5 days to function at maximum capacity.

Signs and symptoms depend on the severity of the

Chapter 9 Acid-Base Balance 315

Normal or(Won't help)

r~'~-Respiratory

{ elevated acidosis as wellHCO"B D Decreased - PC02 Normal

Decreased -Respiratory

compensation

Normal or(Won't help) Metabolic

-[decreased -

r~'~-PC02 compensation

Elevated - HCO"B.D. Normal

Decreased -Metabolic

acidosis as well

Normal or (Won't help)

r~"'-Respiratory

-[decreased compensationHCO"B.D. Elevated - PC02 Normal

Decreased -Respiratory

alkalosis as well

Normal or (Won't help)

f"~··'-Metabolic

{ elevated alkalosis as wellPC02

HCO"Decreased - . B.D. Normal

Decreased -Metabolic

compensation

What is the pH?

Below (Acidosis)7.35

Above .7.45 (AlkalosIs)

Fig. 9-6 Arterial blood gas analysis to determine acid-base imbalance. B.D., Base deficits. (FromDonIen J: Interpreting acid-base problems through arterial blood gases. Reprinted with permission ofCrit Care Nurs 3:38, 1983.)

Parameter Arterial Mixed Venous Capillary

pH 7.35-7.45 7.31-7.41 7.35-7.45P02 80-100 mmHg 35-40 mmHg Less than arterial *O2 saturation 95%-97% 70%-75% Less than arterialPc02 35-45 mmHg 40-50 mmHg 35-45 mmHgHC03 22-26 mEqlL 22-26 mEqlL 22-26 mEqlLTotal CO2 content 20-27 mEqlL 20-27 mEqlL 20-27 mEqlLBase excess +2 to -2 +2 to-2 +2 to -2

r T"'£9-2 .o,mal Blood Ga. ValUe.

iij.,~.,t.·~.api1lary POz is approximately 10 mmHg less than arterial POz except when decreased tissue perfusion is present, that is, cardiovascular collapse or!!ibypothennia. In these states, capillary samples will not accurately reflect arterial Po2 •iii;;

respiratory acidosis (Table 9-3). Changes in respiratoryfunction, such as decreased respiratory rate and shallowbreathing, occur secondary to the underlying problem thathas triggered the alveolar hypoventilation. Dyspnea iscaused by stimulation of the respiratory center in themedulla and peripheral chemoreceptors that are trig­gered by a decrease in blood pH. Cardiovascular effectssuch as tachycardia, increased cardiac output, and increasedblood pressure occur secondary to sympathetic stimulationand epinephrine release from the adrenal medulla. Thismechanism is stimulated by hypercapnia and a low pH.Although receptor response to catecholamines is bluntedin acidosis, this is initially offset by a surge in catechol-

amine release. Acute hypercapnia has opposing effects onperipheral vasculature. Vasodilation occurs by its directeffect on vascular smooth muscles. Vasoconstriction issimultaneously produced by catecholamine release. Thisusually results in either a mild vasoconstriction orvasodilation.

Important exceptions to this occur in the pulmonaryand cerebral vessels. Cerebral vascular resistance de­creases and cerebral blood flow increases proportion­ately with an increase in PC02' whereas the oppositeoccurs in the pulmonary vascular bed. Increased cerebralblood flow precipitates the headache associated withhypercapnia and respiratory acidosis. An acute increase

316 Part III Phenomena of Concern

Box 9·2~ Disorders Associated

With Respiratory Acidosis

Acute Obstructive Airway DisordersCroupEpiglottitisForeign bodyAsthmaBronchiolitis

Chronic Obstructive Airway DisordersBronchopulmonary dysplasiaCystic fibrosis

Pulmonary Restrictive DisordersPneumoniaAspirationAdult respiratory distress syndromePulmonary edemaInterstitial lung diseasePleural effusionPneumothoraxFlail chestKyphoscoliosisPierre Robin syndrome

Neuromuscular DisordersMuscular dystrophyMultiple sclerosisSpinal muscular atrophyGuillain-Barre syndromeBrainstem injury or tumorBotulismSpinal cord injury or tumorMyasthenia gravisDiaphragmatic paralysisPickwickian syndromePoliomyelitis

Central Nervous System DepressantsNarcoticsGeneral anesthesiaSedativesCerebral trauma or infectionBrain tumorCircu latory crisesCardiac arrestSevere pulmonary edemaMassive pulmonary embolism

Iatrogenic Causes

Inadequate mechanical ventilationHyperalimentation with high carbohydrate contentSorbent regenerative hemodialysis

in Pc02 may preCIpItate pulmonary vasospasm, result­ing in an abrupt increase in pulmonary vascular resis­tance and decreased pulmonary blood flow. Any in­crease in pulmonary vascular resistance may worsenthe underlying disorder responsible for the respiratoryacidosis.

The pathophysiologic effects on the central nervoussystem (CNS) are unclear. Cerebrospinal fluid (CSF) pHchanges in relation to blood pH. CO2 permeates theblood-brain barrier, so increases in arterial Pc02 are seenimmediately in the CSF. However, the CSF contains fewerbuffers than the blood, so CSF pH falls more dramatically,which may contribute to the CNS symptoms that occur withrespiratory acidosis. CNS symptoms can vary greatly indifferent individuals. For example, similar increases in Pc02cause some children to become somnolent and others tobecome apprehensive and agitated.

In respiratory acidosis, the arterial pH is less than 7.35,the Pc02 is greater than 45 torr, and the HC03- is normal orelevated (depending on the degree of renal compensation).It is important to note that hypoxemia may be a very latesign of respiratory acidosis; therefore cyanosis may not bepresent until the child progresses to respiratory failure.Serum potassium increases 0.1 mEqlL for each O.I-Udecrease in blood pH and therefore would be normal toslightly elevated with respiratory acidosis. Blood lactatelevels fall slightly, and phosphorus becomes mildly ele­vated. Urine pH may be decreased, again depending on thedegree of renal compensation.

Clinical management of respiratory acidosis is directedtoward reestablishing effective ventilation and treating theunderlying problem. The child may require intubation,mechanical ventilation, or a change in the ventilation planwhile the primary problem is being treated. Oxygen andNaHC03 may be given based on the ABG results. Althoughhypoxemia does not usually affect acid-base balance, a P02

of less than 35 torr may induce a lactic (metabolic) acidosis.NaHC03 is administered only to correct severe metabolicacidosis. Effective ventilation must be established before theadministration of NaHC03 ; otherwise, the acidosis willworsen.

The clinical significance of respiratory acidosis dependson the child's general health and the physiologic effects ofthe acidosis and hypoxemia. Nursing assessment parametersinclude vital signs, noting heart and respiratory rate, rhythm,character, and pattern; blood pressure, perfusion status,peripheral and distal pulses, level of consciousness, andurine output; muscle strength and movement; oxygenationstatus, noting color of nail beds and mucous membranes,and Sa02 ; gastrointestinal function; degree of comfort; andlaboratory data.

Nursing interventions include positioning the child tooptimize ventilation, administering oxygen, and suctioningto clear the airways and enhance CO2 elimination. Care isdirected to minimize 02 consumption by providing anenvironment with minimal stimulation and uninterruptedperiods of rest. Inherently important is providing the childand family with appropriate explanations, support, andreassurance.

Chapter 9 Acid-Base Balance 317

TABLE 9·3 Signs and Symptoms Associated With Acid·Base Imbalance

li!'Jtespiratory AcidosisF

i;i)ecreased respiratory rate~Shallow breathingit·~pyspnea

~1:Tachycardia

~i'Headachef~:

liliDecreased responsiveness~;IDisorientation

iRestlessness(Apprehension~Agitation

!f:Fatiguej;iWeaknessri!Diminished reflexes~£Seizures~:n'

~cNausea and vomiting

1-1""~L~:;

uV'·!!,'

Respiratory Alkalosis

HyperventilationBreathlessnessCardiac dysrhythmiasHypotensionExtremity and perioral

paresthesiasVertigoSyncopeAnxietyNervousnessConfusionDecreased level of

consciousnessDecreased psychomotor

performanceHyperreflexiaMuscle crampsTwitchingTetanySeizures

Metabolic Acidosis

Tachypnea --.. Kussmaulrespirations

Tachycardia --.. bradycardiaCardiac dysrhythmiasHypotensionPoor perfusion with a

grayish pallorDecreased peripheral pulsesIncreased capillary refill timeDecreased urine outputDecreased level of

consciousnessCongestive heart failureFatigueDrawsi nessConfusionApathyUnresponsivenessSeizuresNausea and vomitingAbdominal distension

and pain

Metabolic Alkalosis

HypoventilationCardiac dysrhythmiasDecreased perfusionHypotensionConfusionLethargyUnresponsivenessHyperreflexiaMuscle crampsTwitchingTetanySeizuresNausea, vomiting, and

diarrhea

Respiratory AlkalosisRespiratory alkalosis is an ECF deficit of carbonic acidcaused by conditions resulting in alveolar hyperventilationand CO2 deficit. Rare as a primary problem, disordersassociated with respiratory alkalosis in children are summa­rized in Box 9-3, Buffer response to hypocapnia beginsimmediately and is complete within 10 to 15 minutes. Renalcompensatory mechanisms are activated within 2 to 5 hoursin respiratory alkalosis and take I to 2 days to be fullyfunctional.

Hyperventilation results from stimulation of the respira­tory center in the medulla and stimulation of peripheralchemoreceptors and nociceptive receptors in the lungs.Hyperventilation may also occur when signals from thecerebral cortex override the chemoreceptors, as in voluntaryhyperventilation.

Heart rate increases secondary to sympathetic stimula­tion and the resultant catecholamine release from theadrenal medulla, This response can cause atrial and ventric­ular tachydysrhythmias. There is usually no major change incardiac output and blood pressure in awake children.Cardiovascular response to hypocapnia differs in anesthe­tized children. Although tachycardia may not develop,cardiac output and perfusion may decrease. This responseoccurs secondary to increased intrathoracic pressures asso­ciated with passive hyperventilation, resulting in decreasedvenous return. Pulmonary vasodilation occurs with hypo­capnia; however, peripheral vasoconstriction also occurs.This results in decreased blood flow to the skin andcontributes to paresthesias. Cerebral blood flow (CBF) is

also drastically reduced secondary to cerebral vasoconstric­tion. This vasoconstriction decreases intracranial and intra­ocular hydrostatic pressure. Cerebral oxygen consumptiondoes not decrease when blood flow is reduced, so cerebralhypoxemia and hypoxia may develop, leading to light­headedness, syncope, anxiety, altered levels of conscious­ness, and seizures.

Calcium binding, resulting in hypocalcemia, occurs withalkalemia. This condition also contributes to the develop­ment of seizures, as well as neuromuscular irritability,hyperreflexia, muscle cramps, twitching, and tetany.

In respiratory alkalosis, the arterial pH is greater than7.45, the Pc02 is less than 35 totT, and the HC03- is normalor decreased (less than 25 mEqlL). Potassium concentrationdecreases 0.1 mEqlL for each O.I-U increase in pH andtherefore should be normal or slightly decreased. Urine pHis normal to increased, depending on the degree of renalcompensation.

The clinical management of respiratory alkalosis isdirected toward restoring effective ventilation and treatingthe underlying cause. Sedation, breathing exercises, andrelaxation with controlled breathing can correct the imbal­ance (if the child is developmentally capable of participatingin such activities). Administration of 3% to 5% CO~ andneuromuscular paralysis with intubation and mechanicalventilation may also be necessary if respiratory alkalosis issevere and other measures are ineffective.

The clinical significance of respiratory alkalosis dependson the presence and extent of neuromuscular effects.Seizures from respiratory alkalosis can be life threatening.

318 Part III Phenomena of Concern

Metabolic Acidosis

Normal Anion Gap (Hyperchloremic)

DiarrheaIntake of chloride-containing compounds (HCI, NH4 Cl,

CaCI2' MgC12 , arginine HCI, cholestyramine)HyperalimentationPancreatic, small bowel. or biliary tubes or fistulasUreterosigmoidostomy, ileal conduitCarbonic anhydrase inhibitors (acetazolamide)Extracellular fluid volume expansionMineralocorticoid deficiency (adrenal disorders)Renal tubular acidosisEarly uremic acidosis

Box 9-4

~ Disorders Associated. With Metabolic Acidosis

Increased Anion Gap (Normochloremic)

Cardiovascular collapseDiabetic ketoacidosisLactic acidosis (tissue hypoxia)StarvationDrugs/toxins (methanol, ethanol, salicylate, fructose, sorbitol,

cyanide, carbon monoxide, paraldehyde)Organic acid metabolism (pyruvate)Hepatic failureRenal failureCongenital enzymatic defectsGlucose 6-phosphate deficiencyFructose l,6-diphosphatase deficiencyPyruvate carboxylase deficiencyMethylmalonic aciduria

Box 9-4. Note that the most common cause of metabolicacidosis in the pediatric population is insufficient tissueperfusion. Situations that produce an increase in fixed acidsresult in a normochloremic acidosis with an increased aniongap. Situations that cause a bicarbonate loss result in ahyperchlorernic acidosis with a normal anion gap. Thenormal range for the anion gap is 8 to 16 mEqlL and iscalculated using the following formula:

Anion gap =Na+ - (0- + HC03-)

Buffer and respiratory compensatory mechanisms are acti­vated within minutes with metabolic acidosis. Respiratorycompensation results in an increased respiratory rate toeliminate excess CO2; however, it is not usually effective incorrecting the imbalance.

Signs and symptoms depend on the severity of themetabolic acidosis (see Box 9-4). Tachycardia results fromsympathetic stimulation and the subsequent release of epi­nephrine from the adrenal medulla, which is stimulated byacidosis. As pH falls below 7.10, heart rate progressivelyslows. This reaction is most likely related to the inhibitoryeffect that acidosis has on the action of catecholamines oraccumulation of acetylcholine caused by the inhibition ofacetylcholinesterase. Ventricular dysrhythmias are usuallyrelated to the electrolyte imbalances seen with acidosis, par­ticularly hyperkalemia. Acidosis also decreases the fibrilla-

.Box.9-3D~ord~rsAsspclatedwithJtespiratory Alkalosis

I

Intoxications

AlcoholSalicylateParaldehydeXanthine

Miscellaneous

High altitudeVoluntary hyperventilationAnxietyHysteriaHepatic failureCongestive heart failure with hypoxemiaMechanical ventilation

Increased Intracranial Pressure

MeningitisEncephalitisHead traumaVascular accidentsBrain lesions

Metabolic acidosis is an ECF deficit of bicarbonate causedby conditions that result in a loss of bicarbonate or anincrease in fixed acids. These conditions are summarized in

Pulmonary Disorders

PneumoniaPulmonary edemaPulmonary emboli

Nursing assessment parameters include vital signs, notingheart and respiratory rate, rhythm, character, and pattern,blood pressure, perfusion status, peripheral and centralpulses, level of consciousness, and urine output; musclemovement and strength; sensation in the extremities andaround the perioral area; and seizure activity.

Nursing interventions with respiratory alkalosis includemaintaining seizure precautions. If age and clinical condi­tion indicate, interventions may include assisting withrelaxation and slow breathing techniques or having the childbreathe through a paper bag. Care is directed towardproviding a safe environment with age- and condition­appropriate activities, minimal stimulation, and uninter­rupted periods of rest.

Increased Metabolic Rate

FeverHyperthyroidismExerciseAnemiaGram-negative sepsisInterstitial lung disease

tion threshold, so the child is at greater risk for ventricularfibrillation. As pH falls from 7.40 to 7.20, the negativeinotropic effect of acidosis and the positive inotropic effectof catecholamine release offset each other so that effectivemyocardial contraction is maintained. However, as pH fallsbelow 7.20, the negative inotropic effect dominates, whichresults in poor perfusion and hypotension. Calcium entryinto the cell is also inhibited at this point, which furtherdecreases effective myocardial contraction. Although epi­nephrine facilitates calcium entry into the cells in early aci­dosis, this becomes inhibited as H+ concentration increases.Infants and children who are receiving p-adrenergic antago­nists or calcium channel blocking agents, as well as thosewho are chronically stressed and have limited endogenouscatecholamine stores, are more susceptible to the negativeinotropic effects of acidosis. A pH of less than 7.20 alsoeffects arterial and venous tone. The arterial system dilateswhile the venous system constricts, which forces blood toflow centrally. This increases the workload of the heart andcan result in congestive heart failure.

Tachypnea results from stimulation of the respiratorycenter in the medulla. Kussmaul respirations develop withacute severe metabolic acidosis as the child increases tidalvolume and respiratory rate to improve oxygenation andeliminate CO2, Oxygen delivery to the tissues is enhancedby metabolic acidosis as the oxyhemoglobin dissociationcurve shifts to the right (see Fig. 9-1). However, if acidosisprogresses, glycolysis slows, and red blood cell 2,3­diphosphoglycerate (DPG) is depleted, which eliminates thebeneficial Bohr effect as previously described. Hypoxemiaand tissue hypoxia then progress. Neurologic changes arerelated to decreased perfusion to the brain, hypoxemia,hypoxia, and metabolic and electrolyte imbalances.

The gastrointestinal symptoms associated with metabolicacidosis are likely related to either ketogenesis or electro­lyte and biochemical changes that accompany acidosis.Normal tone and contraction of the gastrointestinal tract arealtered, resulting in abdominal pain, distension, nausea, andvomiting.

In metabolic acidosis, the arterial pH is less than 7.35, thePc02 is decreased (a normal or elevated PC02 would indicatefailing respiratory compensation and the development ofrespiratory acidosis), and HC03- is less than 25 mEqlL.Serum potassium is elevated 0.1 rnEqlL for each 0.01 Udecrease in pH; chloride is normal or elevated (dependingon the cause); and urine pH is normal or decreased, againdepending on the cause of the acidosis.

Clinical management of metabolic acidosis is directedtoward identifying and treating the underlying problem andwould include restoring fluid and electrolyte imbalance,preventing or treating a catabolic state, and providingadequate ventilation. Bicarbonate losses should be replacedin severe acidosis. NaHC03 is now used conservatively,most often indicated for a pH below 7.20, when there isdepressed myocardial function, and when compensatoryrespiratory efforts cannot be maintained and respiratoryfailure is imminent. NaHC03 should be administered toachieve a slight undercorrection and thus prevent a reboundmetabolic alkalosis from occurring. A recommended dose ofI mEq/kg will provide approximately one fourth to one half

Chapter 9 Acid-Base Balance 319

of calculated bicarbonate losses (see previous discussionunder Analyzing Acid-Base Balance). Adverse effects asso­ciated with NaHC03 administration include a transientincrease in Pc02, which may further compromise cellularfunction, myocardial contractility, and cerebral acidosis.Hyperosmolarity, hypernatremia, and iatrogenic metabolicalkalosis may also occur. The alkalosis may decreaseionized calcium and potassium levels, shift the oxyhemo­globin dissociation curve to the left (inhibiting 02 release tothe tissues), and predispose the patient to life-threateningdysrhythrnias. The potential risks and benefits must becarefully considered in individual clinical situations whendeciding if NaHC03 is indicated. It is critical to rememberthat to maintain the buffering capacity of NaHC03 , effectiveventilation or mild hyperventilation must be present.

The clinical significance of metabolic acidosis dependson the severity of the disorder. The body does not toler­ate changes in H+ concentration well. Without appropri­ate intervention, metabolic acidosis will progress to life­threatening alterations in cardiac, neurologic, and metabolicfunction. Nursing assessment parameters include vital signs,noting heart and respiratory rate, rhythm, character, andpattern, blood pressure, perfusion status, peripheral andcentral pulses, level of consciousness, and urine output;seizure activity; gastrointestinal function; intake and output;muscle strength; signs of hyperkalemia; the child's level ofcomfort; and appropriate laboratory data.

Nursing interventions include administering medicationsand fluids, positioning the child to optimize ventilation,maintaining seizure precautions, and providing comfortmeasures for gastrointestinal upset. Care is directed towardproviding a safe environment with age- and condition­appropriate activities, minimal stimulation, and uninter­rupted periods of rest.

Metabolic AlkalosisMetabolic alkalosis is an ECF excess of HC03- caused byconditions resulting in excess base because of loss of H+,reabsorption of HC03-, or loss of other ions (i.e., chloride,sodium). These conditions are summarized in Box 9-5.Buffer and respiratory compensatory mechanisms are acti­vated immediately with metabolic alkalosis. Respiratorycompensation results in a decreased respiratory rate toconserve CO2; however, this response is ineffective anddoes not correct the imbalance.

Hypoventilation results from stimulation of the respira­tory center in the medulla, which attempts to conserve Pc02by decreasing alveolar ventilation. This condition may resultin hypoxemia, which can further compromise the child'sstatus. Cardiac dysrhythmias with a subsequent decrease incardiac output and blood pressure usually occur secondaryto hypoxemia or hypokalemia.

Changes in level of consciousness occur secondary todecreased CBF, which results from the cerebral vasocon­striction that is associated with alkalosis. Seizures candevelop secondary to hypoxemia, hypocalcemia, or hypo­magnesemia. Calcium binding increases with alkalemia,resulting in hypocalcemia. Magnesium levels decrease inrelation to calcium. Hypocalcemia also contributes to the

320 Part III Phenomena of Concern

..

Bj)~ 9-5

Disorders AssociatedWith Metabolic Alkalosis

VomitingGastrointestinal suctioningCI--wasting diarrheaCI--deficient formulaDiureticsHypokalemiaHypocalcemiaHypochloremiaExogenous alkali intake: HC03-, citrate, lactate, acetateExcessive steroid useRenal failureExtracellular fluid volume depletionCystic fibrosisExcess mineralocorticoidHyperaldosteronism, Cushing's syndrome. adrenogenital

syndromeLaxative, licorice abuseExcessive tobacco chewingBartter's syndrome

development of neuromuscular irritability, muscle cramps,and tetany. Gastrointestinal effects are usually associatedwith the underlying problem, which results in nausea,vomiting, and diarrhea.

In metabolic alkalosis, the arterial pH is greater than7.45, HC03- is greater than 30 mEqlL, base excess isgreater than +2, and Pco2 is normal or elevated. Serumelectrolytes usually reveal a hypokalemia, with a 0.1 mEqlLdecrease in potassium for each 0.0 I U increase in blood pH.Hypocalcemia and hypochloremia may also be present.Urine chloride is usually decreased, and urine pH is normalor increased; the degree depends on the cause.

The clinical managemell1 of metabolic alkalosis isdirected toward identifying and treating the underlyingcause of the imbalance. This approach usually involvesexpanding ECF volume with saline, administering chloride(arginine or ammonium chloride if the NaCl is insufficientto replace the lost ion), correcting hypokalemia withpotassium chloride, and facilitating excretion of HC03­

with carbonic anhydrase-inhibiting diuretics (e.g., acetazol­amide) or dialysis if renal impairment is present.

The clinical significance of metabolic alkalosis dependson the severity of the disorder and the accompanyingneuromuscular and respiratory effects. Nursing assessmentparameters include vital signs, noting heart and respiratoryrate, rhythm, character, and pattern, blood pressure, perfuc

sion status, peripheral and central pulses, level of conscious­ness, and urine output; neuromuscular function; musclemovement and strength; Chvostek's and Trousseau's signsfor hypocalcemia; strict intake and output; stooling patternand characteristics; and laboratory data.

Nursing interventions with metabolic alkalosis includeadministering medications and fluids, maintaining seizureprecautions, and providing comfort measures for gastroin-

testinal upset. Care is directed toward providing a safeenvironment with age- and condition-appropriate activities,minimal stimulation, and uninterrupted periods of rest.

MIXED ACID-BASE DISORDERSMixed acid-base disturbances often occur in infants andchildren with a variety of multisystem problems. Mixeddisturbances can result in excessive or diminished compen­sation. The clinical significance of the imbalances dependson the net change in pH.

In general, mixed disorders that drive the pH in oppositedirections (respiratory acidosis with metabolic alkalosis) arebetter tolerated because each compensates for the other tokeep the pH near or within normal limits. Mixed disordersthat drive the pH in the same direction (respiratory andmetabolic acidosis) have profound effects on pH becausecompensation is impossible. Because the body is unable totolerate significant changes in pH, mixed disorders cansignificantly alter cardiac, neurologic, and metabolic func­tion and be life threatening without appropriate intervention.Treating each component of the mixed disorder simulta­neously is important to avoid exacerbating one whilecorrecting the other. Accurate interpretation of ABGs andmonitoring of the child's clinical response to therapy arecritical nursing interventions because the patient's responseto therapy may be asynchronous.

Respiratory AcidosisWith Metabolic AlkalosisRespiratory acidosis and metabolic alkalosis can occur inchildren with obstructive pulmonary disease (e.g., broncho­pulmonary dysplasia, or cystic fibrosis) who are receivingdiuretics as part of their management plan. Such childrenusually live in a state of compensated respiratory acidosissecondary to CO2 retention related to their pulmonarydisease. Chronic diuretic therapy with potassium-wastingdrugs (such as furosemide) can lead to hypokalemia andmetabolic alkalosis. A similar scenario also occurs inchildren with congestive heart failure and chronic respira­tory acidosis who are receiving long-term diuretic therapy.The pH with this mixed imbalance is usually near or withinnormal limits because of compensation. If, however, the pHrises with the metabolic alkalosis, respiratory drive may bedepressed in the medulla, resulting in a decrease in P02 andan increase in Pc02• which can progress to respiratoryfailure.

Clinical management of this mixed imbalance is directedtoward correcting the metabolic alkalosis, which is accom­plished by administering sodium and potassium chloride tofacilitate renal excretion of HC03-. This must be donecautiously to avoid inducing or exacerbating congestiveheart failure. Although pH may fall to acidemic levels, thiswill stimulate respiration and subsequently increase P02 anddecrease Pc02 levels. Oxygen must be administered care­fully because increasing the P02 above the patient's normalthreshold may depress the respiratory drive in the medulla.Knowing the baseline ABG status for the patient with

chronic lung disease is extremely helpful in establishingappropriate treatment goals.

Nursing assessment and interventions would be the sameas those listed under each disorder. Consideration must begiven to these children's underlying disease process and tothe degree that they are compromised when planning,implementing, and evaluating clinical management.

Respiratory and Metabolic AcidosisRespiratory and metabolic acidosis may develop in infantsand children with chronic obstructi ve pulmonary diseasewho are in shock, who have any type of metabolic acidosisand develop respiratory failure, and in those who suffercardiopulmonary arrest. Compensation is not possible withthis mixed disorder, and the pH falls dramatically, evenwhen changes in Pc02 and HC03- are moderate. The clinicalsignificance is related to the fall in pH and can result incardiac, neurologic, and metabolic dysfunction.

Clinical management ofthis imbalance is directed towardcareful correction of both the respiratory and metaboliccomponent to normalize pH. Knowing the baseline status ofthe patient with chronic lung disease is helpful, as previ­ously discussed. Special consideration must be given to thecare of these children because the goal will be to return themto their baseline compromised status, which will includenormalizing pH but not necessarily other ABO parameters.Mechanical ventilation may be necessary to eliminateexcess CO2 and return these children to their baseline status.NaHC03 is usually administered after adequate ventilationis established. Nursing assessment and intervention are asdiscussed under each disorder.

Respiratory AlkalosisWith Metabolic AcidosisThe mixed imbalance of respiratory alkalosis with meta­bolic acidosis may be seen in children with hepatic failure.The respiratory alkalosis is due to hyperventilation (second­ary to restrictive lung capacity with liver enlargement), andthe metabolic acidosis is due to hepatic failure with lacticacidosis, renal failure, or renal tubular acidosis. Thisimbalance can also' occur in children with chronic renalfailure and acute sepsis. The respiratory alkalosis developssecondary to the hyperventilation that accompanies sepsis,and the metabolic acidosis is associated with the renalfailure. Salicylate intoxication also results in a respiratoryalkalosis, which is related to stimulation of the breathingcenter in the medulla, and metabolic acidosis, which occurssecondary to disruption of the Krebs cycle with accumula­tion of lactic and other organic acids.

Clinical management of the child with this mixedimbalance is directed toward correction of the underlyingproblem. The pH is usually close to or within normal limitsbecause of effective or excessive compensation and may notrequire specific treatment. Nursing assessment and interven­tions are as discussed under each disorder.

Chapter 9 Acid-Base Balance 321

Respiratory and Metabolic AlkalosisThe combination of respiratory and metabolic alkalosis isseen in children with chronic hepatic failure who arereceiving diuretics or who develop vomiting. The respira­tory alkalosis is due to hyperventilation from restrictive lungdisease related to hepatic enlargement, and the metabolicalkalosis is due to potassium or fixed acid loss related todiuretic therapy or vomiting (respectively). This condition isalso seen in children with chronic respiratory acidosis (fromchronic lung disease) with appropriately elevated HC03­

levels who are supported on mechanical ventilation and areoverventilated, resulting in a drastic fall in PC02 leading torespiratory alkalosis. Neither disorder is able to compensatefor the other, and pH rises dramatically.

Clinical management of this imbalance is directed towardtreating the underlying problem and normalizing the pH.The respiratory component is managed by treating the causeof hyperventilation or adjusting the ventilator. The meta­bolic component is corrected with sodium and potassiumchloride. Fluids must be administered cautiously to avoidinducing congestive heart failure or pulmonary edema.Nursing assessments and interventions are as listed undereach disorder.

Triple Acid-Base DisordersTriple acid-base disorders may occur in children withdisorders affecting more than one body system, such asthose with chronic liver failure. Hyperventilation andrespiratory alkalosis result from restrictive lung capacityrelated to the enlarged abdomen. Metabolic alkalosis occursif the child is receiving diuretics, develops vomiting, orrequires nasogastric suctioning. Finally, metabolic acidosismay develop secondary to renal tubular acidosis, diarrhea,uremic acidosis, and lactic acidosis. Clinical management ofsuch a complicated disorder involves careful assessment andcorrection of each component simultaneously to normalizepH. Nursing assessment and intervention would includethose listed under each disorder.

SUMMARYAcid-base disturbances are associated with many disordersand diseases seen in the pediatric critical care unit. Thenurse must be able to accurately assess the child's acid-basestatus, to recognize imbalances, and to anticipate thepotentially life-threatening complications that may resultfrom them. Appropriate interventions can then be imple­mented to prevent or minimize these complications and thusimprove the patient's outcome.

REFERENCES1. Antonini E, Brunori M: Hemoglobin, Ann Rev Biochem 39:977-1042,

1970.2. Chameides L, Hazinski MF: Fluid and medication therapy. In Pediatric

advanced life support. ed 3, Dallas, 1997, American Heart Association.