Assessing Tissue Oxygenation

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2002;22:22-40Crit Care Nurse Barbara E. Berry and Agnes Eugine PinardAssessing Tissue Oxygenation

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22 CRITICAL CARE NURSE Vol 22, No. 3, JUNE 2002

Barbara E. Berry is director ofnursing at the Mailman Center forChild Development, Department ofPediatrics, School of Medicine,University of Miami, Miami, Fla.

Agnes Eugine Pinard is nursingproject manager at the MailmanCenter for Child Development,Department of Pediatrics, School ofMedicine, University of Miami.

To purchase reprints, contact The InnoVisionGroup, 101 Columbia, Aliso Viejo, CA 92656.Phone, (800) 809-2273 or (949) 362-2050 (ext532); fax, (949) 362-2049; e-mail,[email protected].

elements. The partial pressure ofoxygen (PO2) can therefore becalculated by multiplying thepercentage of oxygen by theatmospheric pressure4:

0.21 (oxygen) × 760 mm Hg =159.6 mm Hg.

The partial pressure of carbondioxide (PCO2) can be calculatedin the same manner:

0.0004 (carbon dioxide) × 760mm Hg = 0.3 mm Hg.

The concentrations of gases inalveolar air are not the same as theconcentrations in atmospheric air,however, because alveolar air isonly partially replaced by atmo-spheric air with each breath. Assoon as atmospheric air enters therespiratory passages, it is exposedto dead space air and fluids thatcover respiratory surfaces. Thus,oxygen reaches the alveoli atapproximately 103 mm Hg ( PAO2).Likewise, the carbon dioxide levelin the alveoli is approximately 40 mm Hg (PACO2).4

According to the principles ofdiffusion, gas exposed to a liquidwill dissolve in the liquid untilequilibrium of the gaseous phaseof the mixture is reached and willexert the same partial pressure inthe gaseous phase of the liquid asit did in the gaseous mixture.Diffusion of gases in the lungillustrates this point. Alveolar

Assessing TissueOxygenationBarbara E. Berry, RN, PhDAgnes Eugine Pinard, RN, BSN, MS/HSA

o provide thecomprehen-sive nursingcare that isn e c e s s a r yand is ex-pected byi n f o r m e d

consumers, nurses need anexpanded knowledge base. Thisneed is especially apparent inhospitals, where the acuity ofpatients is high. Accurateassessment, prompt recognition,a n d p r o p e r m a n a g e m e n t o fadverse changes are vital compo-nents in the nursing care ofp a t i e n t s w i t h c o m p r o m i s e dfunctioning. Although physicalexamination is important, then e e d f o r u n d e r s t a n d i n g t h eprinciples of gas diffusion andlaboratory assessment of tissueoxygenation, including interpre-tation of hemoglobin concen-tration, oxygen saturation, cardiacoutput, and acid-base balance(Table 1), must not be overlooked.

DIFFUSION OF GASES

At sea level , atmosphericpressure is 760 mm Hg. The airwe breathe is a mixture of gasescontaining 79% nitrogen, 21%oxygen, traces of carbon dioxide(approximately 0.04%), and other

This article hasbeen designatedfor CE credit. Aclosed-book, mul-tiple-choice exam-inat ion fo l lowsthis article, whichtests your knowl-edge of the fol-lowing objectives:

1. Describe the correlation ofhemoglobin concentration totissue oxygenation

2. Understand the role of labora-tory assessment in evaluationof tissue oxygenation

3. Recognize the relationship ofacid-base balance to tissueoxygenation

T



CRITICAL CARE NURSE Vol 22, No. 3, JUNE 2002 23

Table 1 Definitions of terms related to assessment of tissue oxygenation

Acid-base ratio – 1:20 ratio at an arterial blood pH of 7.4.The 1 represents acid or 1.2 mmol/L of carbonic acid (40mm Hg PaCO2); the 20 represents base or 24 mmol/Lbicarbonate1,2

Acidemia – pH lower than an acceptable level in arterialblood (ie, pH <7.35)1,3

Acidic substances – substances that donate hydrogen ionsin chemical reactions1,2,4

Acidosis – a pathophysiological state in which a markedbase deficit is present (pH <7.35)1,3

Alkalemia – pH greater than an acceptable level in arterialblood (ie, pH >7.45)1,3

Alkaline (or basic) substances – substances that accepthydrogen ions in chemical reactions1,2,4

Alkalosis – a pathophysiological state in which a significantbase excess is present (ie, pH >7.45)1,3

Anemia – a condition that can result in tissue hypoxia andmay be due to deficiency of hemoglobin in the blood,decreased number of red blood cells, inadequate flow ofblood, or reduction in oxygen-carrying capacity ofhemoglobin1,3

Base excess – a true nonrespiratory reflection of acid-basestatus reported in millimoles per liter of base greater thanor less than the normal range; arrived at by multiplying thedeviation from standard bicarbonate levels (24 mmol/L ×1.2)1,2,5 (ie, 34 mmol/L–24 mmol/L=10 × 1.2=+12, or12 mmol/L–24 mmol/L=-10 × 1.2=-12)

Bicarbonate (or HCO3) – an alkaline/basic substance inthe blood1,3

Buffer system – a system in the body that preventsexcessive changes in the pH of the body fluids1

Cardiac output – amount of blood pumped by the leftventricle into the aorta each minute (normal cardiac outputin adults is 5 L/min4)

Carbon dioxide combining power (carbon dioxidecontent) – a laboratory value reported with serumelectrolyte levels; a measure of the level of bicarbonate ionsin the plasma, because bicarbonate is broken down by theaddition of a strong acid, and the carbon dioxide emitted isa measure of the bicarbonate originally present (normalrange is 22-26 mmol/L)1,2,4

Hyperoxygenation – a condition in which the partialpressure of arterial oxygen is greater than 100 mm Hg3

Hypoxemia – deficient oxygenation due to inadequatearterial blood tension or partial pressure of arterial oxygen1,3,4

(ie, PaO2 ranges from relatively normal, 70-100 mm Hg; torelatively safe, 45-70 mm Hg; to dangerous, <45 mm Hg.)

Hypoxia – the condition of cellular oxygen deficiency3

Oxyhemoglobin dissociation curve – an S-shaped curvethat demonstrates the relationship between PaO2 andoxygen saturation of hemoglobin (ie, the progressiveincreased oxygen saturation or the percentage ofhemoglobin that is bound with oxygen as PaO2 increasesand the desaturation that develops when PaO2 decreases).Any PaO2 less than 40 mm Hg is incompatible with life formore than a few minutes4,6

P – pressure3

PO2 – partial pressure of oxygen3

PCO2 – partial pressure of carbon dioxide3

PAO2 – partial pressure of alveolar oxygen3

PACO2 – partial pressure of alveolar carbon dioxide3

PaO2 – partial pressure of arterial oxygen3

PaCO2 – partial pressure of arterial carbon dioxide3

P_vO2 – partial pressure of venous oxygen3

P_vCO2 – partial pressure of venous carbon dioxide3

pH – a logarithmic scale denoting hydrogen ionconcentration (ie, pH ranges from 1=acidic to 14=alkaline/basic)3

Polycythemia – an increase in red blood cells mostcommonly associated with an increase in hemoglobinconcentration in the blood1,3

Respiratory insufficiency – impairment of the normalability to oxygenate arterial blood or to eliminate carbondioxide, resulting in an inability to maintain normal arterialblood gas levels under conditions of increasing demand1

Shunting – passing of blood from the right side of the heartto the left side of the heart without gas exchange in thelungs3

Tension – partial pressure of a gas3




oxygen and capillary blood areseparated by a very thin alveolarmembrane. Oxygen di f fusesacross this membrane until thepartial pressure of the oxygen incapillary blood is the same as thatin the alveoli (103 mm Hg). Asmall amount of blood from theright side of the heart that fails topass through alveolar capillariesbecause of shunting mixes withthe oxygenated blood going to theleft side of the heart and slightlyreduces the partial pressure ofoxygen in the arterial blood (PaO2)to approximately 95 mm Hg.4

Because each gas is indepen-dent of the others in its ability todissolve in a liquid, the principlesof diffusion hold true for diffusionof carbon dioxide from the bloodto the alveoli. That is, net diffusionoccurs from areas of higherpressure to areas of lowerpressure until equilibrium isreached. Blood from the right sideof the heart contains carbondioxide at a higher pressure(P

_vCO2, ~46 mm Hg) than that of

alveoli (~40 mm Hg), so somecarbon dioxide diffuses out ofcapillary blood into the alveoli,from which it is expired into theatmosphere, and the blood that isreturned to the left side of theheart and into systemic circula-tion has a partial pressure (PaCO2)of approximately 40 mm Hg.4

OXYGENATIONPulmonary ventilation is de-

fined as the inspiration andexpiration of air (gases).4 Venti-latory failure is defined as havinga PaO2 of 50 mm Hg or less or aPaCO2 of 50 mm Hg or greater.1

Although ventilation is the onlymethod of eliminating carbondioxide, factors other than venti-lation influence oxygenation. Oxy-gen deficiency or tissue hypoxia

has many causes4 (Table 2).

OXYGEN TRANSPORTIN THE BLOOD

Hemoglobin transports almostall oxygen from the lungs to thetissues. Oxygen is transported inthe blood in 2 forms: a negligibleamount is dissolved in the plasma(~3% of total transported oxygen),and a considerably greater amount(97%) is bound to hemoglobin inred blood cells. The PaO2 deter-mines how much oxygen is trans-ported in each form.4

Oxygen Transport in the Plasma

Under normal conditions, 0.003mL of oxygen can be dissolved in100 mL of blood plasma for each 1 mm Hg of PaO2.3,4 For example,100 mL of blood plasma contains0.3 mL of dissolved oxygen at aPaO2 of 100 mm Hg:

If PaO2 × 0.003 = milliliters ofdissolved oxygen in 100 mL ofplasma,

then 100 × 0.003 = 0.3 mL ofdissolved oxygen in 100 mL ofplasma.

Oxygen Transportin Red Blood Cells

The amount of oxygen that can

be delivered to the tissues alsodepends on the hemoglobincontent of the blood. The normalrange of hemoglobin in adults is 12to 16 g per 100 mL (120-160 g/L) ofblood, and each gram of hemo-globin can bind with approx-imately 1.34 mL of oxygen at fullsaturation.3 For example, approx-imately 20 mL of oxygen is trans-ported in every 100 mL of bloodwhen the hemoglobin content is15 g, PaO2 is 100 mm Hg, and thehemoglobin is 100% saturatedwith oxygen:

If hemoglobin content (ingrams per milliliter of blood)× 1.34 × oxygen saturation =milliliters of oxygen bound tohemoglobin per 100 mL ofblood,

then 15 × 1.34 × 1.00 = 20.1mL of oxygen per 100 mL ofblood.

However, oxygen transportcan be reduced when eitherhemoglobin level or oxygen satu-ration is abnormal. For example,only 13.4 mL of oxygen is trans-ported at a hemoglobin content of10 g at the same PaO2 and oxygensaturation (PaO2 is 100 mm Hg,and the hemoglobin is 100%

Table 2 Some causes of oxygen deficiency or tissue hypoxia

Breathing a hypoxic mixture of gases such as that at high altitude, whereatmospheric pressure and oxygen tension are reduced, or near a fire, whereatmospheric oxygen is consumed by combustion

Inability of the lung to oxygenate the blood

Interference with oxygen delivery to the tissues, as occurs in heart/pumpfailure

Inability of tissues to use oxygen, as occurs in cyanide poisoning

A decrease in oxygen content of blood, as occurs in anemia. (PaO2 is normal,but the amount of hemoglobin is insufficient to carry an adequate amount ofoxygen.)




saturated with oxygen):If hemoglobin content (gramsper milliliter of blood) × 1.34 ×oxygen saturation = millilitersof oxygen attached to hemo-globin per 100 mL of blood,

then 10 × 1.34 × 1.00 = 13.4mL of oxygen per 100 mL ofblood.

Total Oxygen Content in the Blood

Total oxygen content in theblood can be dramatically reducedwhen hemoglobin content, PaO2,or oxygen saturation is abnormal.For example, consider the situationwhen oxygen saturation is 70%,PaO2 is 40 mm Hg, and hemoglobinis 12 g/100 mL of blood:

If 40 × 0.003 = 0.12 mL ofoxygen in plasma, and

12 × 1.34 × 0.70 = 11.26 mLof oxygen in red blood cells,

then total oxygen content =11.38 mL of oxygen in 100 mLof blood.

CARDIAC OUTPUTWhen tissue oxygenation is

assessed, another important con-sideration is cardiac output,which ultimately determines theamount of oxygen delivered. At ahemoglobin level of 15 g/mL, aPaO2 of 100 mm Hg, and an oxygensaturation of 100%, 20 mL ofoxygen is transported in 100 mL ofblood, which is equivalent to 200mL of oxygen per liter of blood.Normal (adult) cardiac output is 5L/min,4 so approximately 1 L ofoxygen can be delivered to thebody tissues per minute (5 L/min ×200 mL of oxygen per liter of blood= 1000 mL or 1 L of oxygendelivered per minute). If the heartcannot pump enough blood (eg,ventricular failure, arrhythmias,reduced heart rate), the cardiac

output and the amount of oxygendelivered to tissues are reduced.For example, if cardiac output isreduced by half, to 2.5 L/min, only500 mL of oxygen will be deliveredto the tissues per minute.

ASSESSMENT OF TISSUEOXYGENATIONOxyhemoglobin Dissociation Curve

Exposing hemoglobin to oxy-gen tensions of 0 to 150 mm Hgresults in an S-shaped curveknown as the oxyhemoglobindissociation curve (Figure 1). Theequation that reproduces theoxyhemoglobin dissociation curveis calculated by most blood gasanalyzers in clinical use.6 Normally,at a PaO2 of 27 mm Hg, hemo-globin is 50% saturated; at a PaO2of 40 mm Hg, 75% saturated; at aPaO2 of 60 mm Hg, 90% saturated;at a PaO2 of 80 mm Hg, 95% sat-urated; and at a PaO2 of 97 mm Hg,97% saturated1,3,7 (Figure 1).

Tissue oxygenation and pul-monary oxygen uptake dependcritically on the relationshipdemonstrated by the oxyhemo-

globin dissociation curve. Althoughhemoglobin has a certain affinityfor oxygen that allows blood tooxygenate tissue appropriately,various factors can alter thisaffinity and change the position ofthe oxyhemoglobin dissociationcurve1,3,6 (Figure 2).

For instance, a shift of the curveto the right results in a decreasedaffinity of hemoglobin for oxygen.Although this decreased affinityincreases the release of oxygen andis beneficial for tissue oxygenationwhen PaO2 is in a safe or normalrange, a deficiency in oxygenationof arterial blood limits the amountof oxygen available to the tissuesdespite easier release of oxygen tothe tissues when the PaO2 is lessthan 38 mm Hg.3,6 On the otherhand, a shift to the left increasesthe capacity of hemoglobin to carryoxygen, but decreases unloading ofoxygen to the tissues.1

A shift of the curve to the rightor left depends on the acidity of theblood, carbon dioxide tension,body temperature, and concen-tration of 2,3-diphosphoglycerate(an organic phosphate in red bloodcells that increases in level when

Figure 1 Oxyhemoglobin dissociation curve. With a normal hemoglobin level(~15 g/100 mL), a normal blood pH (~7.4), and a normal body temperature(~98.6°F/37°C), a PaO2 of 70 to 100 mm Hg is normal, a PaO2 of 45 to 70 mm Hgis relatively safe, and a PaO2 less than 45 mm Hg is dangerous.

Dangerous Relativelysafe

Normal

PaO2,mm Hg

Oxy

gen

satu

rati

on, %

20 40 60 80 100 150

100

90

75

50

25

0




anemia or chronic hypoxemiaoccurs). An increase in any of thesefactors will cause a shift of thecurve to the right, and a decrease inany of these factors will result in ashift of the curve to the left.4

A shift to the right due to in-creased body temperature reflectsincreased cell metabolism, and agreater need for oxygen and istherefore adaptive. A shift to theright may also be compensatory inconditions of anemia and chronichypoxemia.1 However, decreasedlevels of the enzymes that produce2,3-diphosphoglycerate, a circum-stance that may occur in blood thathas been stored for transfusion,will shift the curve to the left andthreaten the release of oxygen tothe tissues.3 On the other hand, ashift of the curve to the left is adap-tive in fetal blood, because thehemoglobin in fetal blood has agreater affinity for oxygen than doesadult hemoglobin and thereforerequires a lower tissue PO2 to releasecomparable amounts of oxygenmolecules from hemoglobin.6

Oxygen SaturationOximetry is a method of mea-

suring oxygen saturation. Pulseoximetry is based on measurementof the proportion of light trans-mitted by oxygenated forms ofhemoglobin; a sensor is placed overa finger, toe, earlobe, or the bridgeof the nose, and a numerical outputis produced.3 The measured satur-ation is accurate only if the probeadequately detects and measurespulsatile blood flow. Factors thatmay influence accuracy includenail polish, low perfusion states(which may be the result of hypo-volemia or hypothermia), andadministration of peripheral vaso-constriction agents, which make itdifficult to identify a pulse signal.8

Pulse oximetry is generally accurateonly for oxygen saturations greaterthan 80%; therefore, arterial bloodgas analysis is recommended foroxygen saturations less than 80%.8

Moreover, most clinicians consideran oxygen saturation of less than90% significant and will not relyexclusively on pulse oximetry formeasurement in such situations.3

Acid-Base BalanceBody fluids must maintain a

normal acid-base balance in orderfor normal cellular function tosustain health and life. Acid-basebalance can be described bymeasuring the pH (or acidity) of asubstance on a scale that rangesfrom 1 to 14 (Figure 3).1,4 Normally,blood has a pH of 7.35 to 7.45. A pHvalue outside this range indicates aserious acid-base imbalance. Thebody has numerous compensatorymechanisms to correct anabnormal pH; however, if thesemechanisms fail (Figure 4), cellularfunctions a r e i m p a i r e d , a n ddeath wil l eventually result.1,2

Respiratory acid-base imbal-ances (acidosis or alkalosis) aretriggered by respiratory disordersthat result from inspiratoryand/or expiratory dysfunction.Metabolic acid-base imbalances(acidosis or alkalosis) are trig-

Figure 2 Oxyhemoglobin dissociation curve with shifts. Shift to the left:higher oxygen saturation at any given PaO2, increased affinity of hemoglobinfor oxygen, decreased release of oxygen to the tissues. Shift to the right: loweroxygen saturation at any given PaO2, decreased affinity of hemoglobin foroxygen, increased release of oxygen to the tissues.

Shift to the left

PaO2,mm Hg

Shift to the right

Oxy

gen

satu

rati

on, %

Figure 3 Acid-base balance. The hydrogen ion concentration of a solution isexpressed as pH and indicates the acidity of the solution. The pH scale rangesfrom 1 to 14. As the concentration of hydrogen ions increases, the solutionbecomes more acidic, and the pH decreases. As the concentration ofhydrogen ions decreases, the solution becomes more alkaline, and the pHincreases. A neutral solution has a pH of 7.

AcidNeutrality

Base

20 40 60 80 100 150

100

90

75

50

25

0

7

141




gered by metabolic disorders suchas disorders of the gastroin-testinal or renal system.2,9

AcidosisAcidosis is the result of greater

than normal amounts of acid orless than normal amounts of base(alkaline) in the blood (pH <7.35).Respiratory acidosis occurs withretention of excess carbonic acid(due to decreased expiration ofcarbon dioxide) and can be

diagnosed on the basis of theincreased PaCO2 in arterial bloodgas sampling (Table 3). Metabolicacidosis occurs when body fluidscontain an excessive amount ofmetabolic acids or a deficit ofbases and can be diagnosed on the basis of the decreasedbicarbonate level or base excess inarterial blood samples (Table 3).

AlkalosisAlkalosis is the result of less

than normal amounts of acid orgreater than normal amounts ofbase (alkaline) in the blood (pH>7.45). Respiratory alkalosisoccurs when excess carbonic acidis excreted (via increased rate anddepth of expiration of carbondioxide) and can be diagnosed onthe basis of the decreased PaCO2in arterial blood gas sampling(Table 3). Metabolic alkalosisoccurs when body fluids containan excessive amount of bases or adeficit of acids and can bediagnosed on the basis of theincreased bicarbonate level orbase excess in arterial blood gassampling (Table 3).

Compensatory MechanismsThe ratio of bicarbonate to

carbon dioxide is 20:1, and thisratio is normally maintainedthrough compensatory mechan-isms or chemical buffers presentin the extracellular fluid, bodycells, blood cells, and plasma.Buffer systems maintain acid-base balance in 2 ways: bycorrecting or altering the compo-nent responsible for the imbal-ance and by compensatingthrough alterations in the com-ponent that is not primarilyresponsible for the imbalance.These buffer systems can actwithin a fraction of a second toprevent excessive changes inpH.2,9

Bicarbonate–Carbonic AcidBuffer System

The body’s major buffer sys-tem is the bicarbonatecarbonicacid compensatory mechanism.Normal blood pH is the result of abicarbonate to carbon dioxideratio of 20 to 1. The 20 in this ratiorepresents base or 24 mmol/L ofbicarbonate. The 1 in this ratiorepresents acid or 1.2 mmol/L of

Figure 4 Plasma pH. Normal plasma is slightly alkaline, with a pH ofapproximately 7.35 to 7.45. When the pH deviates outside this range in eitherdirection, signs and symptoms of acid-base imbalance will occur. Withoutcompensatory mechanisms or intervention, cellular dysfunction and deathmay occur.

Normal

Acidosis Alkalosis

Death Death

Table 3 Interpretation of arterial blood gas sampling*

pH <7.35Acidemia

PaCO2, <35mm Hg Alkalemia

Bicarbonate, <22mmol/L Acidemia

Base excess <-2Acidemia

PaCO2, <70mm Hg Hypoxemia

Parameter

7.35-7.45 >7.45Alkalemia

35-45 >45Acidemia

22-26 >26Alkalemia

-2 - +2 >+2Alkalemia

70-100 >100Hyperoxygenation

Low

*Statistical relationships are often used in medical laboratories to establish “normalranges.” Most laboratories consider 2 SDs from the mean as the normal range because thatrange includes 95% of the represented population. Therefore, normal ranges may varyslightly for different age groups and in different laboratories.

Normal High

Range

7.4

7.457.35

6.80 7.80



carbonic acid. The 1 in this ratiomay also represent a PaCO2 of 40mm Hg, because carbon dioxideis a potential acid. That is, whencarbon dioxide is dissolved inwater, it becomes carbonic acid.Thus, when the level of carbondioxide increases, the level ofcarbonic acid also increases, andwhen the level of carbon dioxidedecreases, the level of carbonicacid also decreases. If the level ofeither bicarbonate or carbondioxide is increased or decreasedso that the 20:1 ratio is notmaintained, acid-base imbal-ances occur.2

A ratio of less than 20:1 (20/1)indicates acidosis. A ratio of morethan 20:1 indicates alkalosis. Thediagnosis of acidosis or alkalosiscan be verified by using the 20:1formula. For example, for apatient with a pH of 7.22, abicarbonate level of 21 mmol/L,

and a PaCO2 of 55 mm Hg:

(Base) Given that the 20 in the20:1 ratio represents 24 mmol/Lbicarbonate, 21 mmol/L bicar-bonate would be equivalent toa 17.5 mmol/L. First set up thesimple proportion

20 = ?24 21

and then cross-multiply tosolve, (20 × 21)/24 = 420/24 =17.5.

(Acid) If the 1 in the 20:1ratio represents a PCO2 of 40mm Hg, then a PCO2 of 55 mmHg would be equivalent to1.37 mm Hg. Again, set up thesimple proportion

1 = ?40 55

and cross-multiply to solve, (1 × 55)/40 = 55/40 = 1.37.

(Diagnosis) The ratio isless than 20:1 (17.5/1.37 =12.8/1); therefore, the diagno-

sis is acidosis.

Respiratory Compensatory Mechanism

The respiratory center in themedulla is sensitive to concen-trations of carbon dioxide andhydrogen ion in body fluids.Compensation by the respiratorycenter can occur rapidly (inminutes or seconds). When acide-mia (decreased blood pH) occurs,the respiratory center in themedulla is stimulated. This stimu-lation results in increases in therate and depth of respirations,thereby reducing the carbondioxide (carbonic acid) level andincreasing the pH of the blood.When alkalemia (increased bloodpH) occurs, the respiratory centerin the brain is inhibited. Thisinhibition results in decreases inthe rate and depth of respirations,retention of carbon dioxide (car-bonic acid), and decrease in the



blood pH. The lungs compensatefor both respiratory and metabolicimbalances. However, the lungscannot compensate for acid-basedisturbances when pulmonarydysfunction is severe. In theseinstances, the kidneys must pro-vide compensation.2

Renal CompensatoryMechanism

Cells in the distal part of therenal tubules are sensitive tochanges in the pH of the filtrate.When the pH is less than normal,hydrogen ions are excreted andbicarbonate is formed and re-tained. When the pH is greaterthan normal, hydrogen ions areconserved and base-forming ionsare excreted. Renal compensationfor imbalances is slow (hours todays). The kidneys cannot com-pensate for acid-base imbalancesrelated to renal failure.2

Because total electrolyte levelsmust always be in electrochemicalbalance, electrolyte concentrationsmay change when acid-baseimbalances occur. The primaryelectrolytes that are exchangeableand may be stimulated by acid-

base imbalances to move in andout of intracellular and extra-cellular compartments are sodium,chloride, potassium, and bicar-bonate (Table 4). Metabolic pHdisturbances have a greater effecton electrolyte mechanisms than do

Table 4 Normal laboratory values

Ionized calcium, mmol/L 1.15-1.27

Serum sodium, mmol/L 135-145

Serum potassium, mmol/L 3.5-5

Serum chloride, mmol/L 95-105

Carbon dioxide combining power, mmol/L 22-26

Hemoglobin, g/100 mL blood 12-16

Urinary pH 4.5-8 (normal, ~6)

*Statistical relationships are often used in medical laboratories to establish “normal ranges.”Most laboratories consider 2 SDs from the mean as the normal range because that rangeincludes 95% of the represented population. Therefore, normal ranges may vary slightly fordifferent age groups and in different laboratories.

Variable Range



respiratory pH disturbances.2,10

CLINICAL STATES OF ACID-BASEIMBALANCE

Clinical states of acid-base

imbalance may be described as

acidosis or alkalosis. Acidosis is

the result of greater than normal

concentrations of acid or less

than normal concentrations of

base in blood. Respiratory acido-

sis is caused by any condition

that interferes with excretion of

carbon dioxide by the lungs, and

metabolic acidosis is caused by

abnormal losses of bicarbonate or

by accumulation of excess meta-

bolic acids2,5,10 (Tables 5 and 6).


Table 5 Respiratory acidosis

Respiratory acidosis is brought on by any condition that interferes with excretion of carbon dioxide by the lungs, such asHypoventilation or breath holdingDamage to the respiratory center in the medullaDepression of the respiratory center (eg, occurs with use of morphine, barbiturates, alcohol)Pulmonary damage or obstruction of air passageways (eg, pneumonia, emphysema, pneumothorax)Poor gas exchange during surgery

Clinical signs and symptomsDecreased rate and depth of respirationsDecreased central nervous system activity (lethargy, lack of judgment, disorientation)Headache or blurred vision, especially in the morningWeakness, cardiac arrhythmia, seizures if hyperkalemia is present

Arterial blood gas analysispH <7.35 (normal, 7.35-7.45)PaCO2 >45 mm Hg (normal, 35-45 mm Hg)Bicarbonate level normal (normal, 22-26 mmol/L)Base excess normal (normal, -2 to +2)

Other laboratory studies may revealPotassium level >5 mmol/L (normal, 3.5-5 mmol/L)Urinary pH <6 (normal, ~6)

Some compensatory mechanisms that may be occurringRespiratory—Hyperventilation will decrease carbonic acid level by blowing off excess carbon dioxide. However, the

ability to control respirations may have been lost because of the condition that is interfering with gas exchange, and, in this situation, hyperventilation can be accomplished only by mechanical ventilation.

Renal—Sodium is reabsorbed in exchange for hydrogen, which will contribute to the formation of ammonia and be excreted as urine; in addition, the reabsorbed sodium combines with bicarbonate to form sodium bicarbonate.

Electrolytes—Chloride moves from blood to cells in exchange for bicarbonate; bicarbonate moves to blood and begins to neutralize excess carbonic acid; potassium moves from cells to blood in exchange for hydrogen ions.

Most appropriate managementDetermining the cause of hypoventilationMaintaining adequate ventilation and hydrationAdministering oxygen therapy for severe hypoxemiaAdministering oxygen at low flow rates for patients with chronic lung disease in order to maintain the hypoxic drive

(because the medulla of these patients responds to lack of oxygen rather than to low carbon dioxide levels)Improving respiratory function through use of bronchodilators and chest physiotherapy, antibiotics for respiratory

infections, mechanical ventilation for a decompensating respiratory systemAvoiding narcotics, hypnotics, and tranquilizers because they depress the respiratory center further

Most appropriate nursing careBeing aware of common causes, signs and symptoms, expected laboratory findings if acidosis is suspectedPredicting which patients are at risk for respiratory acidosis, such as surgical patients who have chronic lung disease,

are obese, or smokeProviding interventions that will help increase lung expansion (eg, encouraging deep breathing, ambulation,

use of incentive inspirometer) for patients at risk for respiratory acidosisContinuing preceding measures for patients with confirmed respiratory acidosis in addition to measures to improve

respiratory function (eg, encouraging fluid intake to help thin secretions and performing chest physiotherapy, postural drainage, and suctioning unless otherwise contraindicated by patient’s condition)

Beginning seizure precautions when potassium level is elevated



Table 6 Metabolic acidosis

Metabolic acidosis results from abnormal losses of bicarbonate as occurs withSevere diarrheaProlonged vomiting of deep gastrointestinal contents

or by accumulation of metabolic acid, as occurs withKetosis resulting when proteins and fats are burned for energy rather than carbohydrates, as occurs in

Diabetes mellitusIncreased metabolism (eg, fever, anesthesia, infection)Starvation

Excessive ingestion of substances that increase concentrations of metabolic acids, such asSalicylic acidAmmonium chlorideFerrous sulfateEthylene glycol (antifreeze)Methyl alcohol (wood alcohol)

Inadequate renal function (inability to excrete hydrogen or conserve bicarbonate)Anoxia (anaerobic metabolism resulting in lactic acidosis)

Clinical signs and symptomsChanges in sensorium (lethargy progressing to coma)Hyperventilation (indicating respiratory compensation)Weakness, cardiac arrhythmias if hyperkalemia present

Arterial blood gas analysispH <7.35 (normal, 7.35-7.45)PaCO2 normal (normal, 35-45 mm Hg)Bicarbonate level <22 mmol/L (normal, 22-26 mmol/L)Base excess <-2 (normal, -2 to +2)

Other laboratory studies may revealCarbon dioxide combining power <22 mmol/L (normal, 22-26 mmol/L)

(ie, plasma bicarbonate)Potassium level > 5 mmol/L (normal, 3.5-5 mmol/L)Urinary pH <6 (normal, ~6)

Some compensatory mechanisms that may be occurringRespiratory—Hyperventilation begins involuntarily in an effort to decrease carbonic acid level and restore acid-base ratio.Renal—Sodium is reabsorbed in exchange for hydrogen, which is excreted in urine; in addition, sodium combines with bicarbonate to form sodium bicarbonate, which will help to restore acid-base ratio.Electrolytes—Potassium moves out of cells to blood in exchange for hydrogen, an attempt to neutralize excess acid.

Most appropriate managementDetermining the underlying mechanismPlanning appropriate interventions to correct mechanism (eg, administering insulin when ketoacidosis occurs)Assessing serum potassium level and treating as necessaryAdministering intravenous alkali, such as sodium bicarbonate (most frequently used, but care must be taken to avoid

overalkalinization, which could result in arrhythmias and tetany—no further bicarbonate should be given once the pH reaches 7.2)

Administration of salts of organic acids that are metabolized to bicarbonate, such as lactate, acetate, and citrateAdministration of tromethamine

Most appropriate nursing careBeing aware of common causes, signs and symptoms, expected laboratory findings if acidosis is suspectedPredicting which patients who are at risk for metabolic acidosis, such as those who have diabetes mellitus, have

advancing renal disease, are hypoxic, are malnourished, or are on low carbohydrate dietsTeaching ways to avoid this imbalance (eg, correct administration of medication, diet, testing urine and/or blood of

diabetic patients) as part of discharge instructions, even though most of the treatment specifically for metabolicacidosis is medical

Alkalosis is the result of lessthan normal concentrations ofacid or greater than normal

concentrations of base in theblood. Respiratory alkalosis iscaused by any condition that

causes an increase in rate anddepth of breathing, resulting inexcessive elimination of carbon




dioxide. Metabolic alkalosis iscaused by any condition thatcauses loss of metabolic acids fromthe body or retention of bicar-bonate2,5,10 (Tables 7 and 8).

ANALYSIS OF ARTERIAL BLOOD GASES

Analysis of arterial blood gas

s a m p l i n g ( F i g u r e 5 ) c a n b e

performed by following the 4 steps

described in Table 9. Examples of


Table 7 Respiratory alkalosis

Respiratory alkalosis is brought on by any condition that causes an increase in the rate and depth of breathing that results inexcessive elimination of carbon dioxide, as occurs with

PainSevere exerciseHysteria and anxiety reactionsHypoxia, anoxiaIntentional overbreathingDamage to the respiratory center in medulla, as occurs in

Central nervous system disease (eg, meningitis, encephalitis)Intracranial surgery

Overstimulation of the respiratory center, as occurs inFeverDrug overdose

Gram-negative bacteremia

Clinical signs and symptomsDeep, rapid respirationsLight-headedness and alterations in consciousness, inability to concentrate, tetany, convulsions (a low PaCO2 causes

cerebral vasoconstriction and thus cerebral ischemia)Cardiac arrhythmias if hypokalemia is presentNumbness and tingling of extremities if hypocalcemia is present

Arterial blood gas analysispH >7.45 (normal, 7.35-7.45)PaCO2 <35 mm Hg (normal, 35-45 mm Hg)Bicarbonate level normal (normal, 22-26 mmol/L)Base excess normal (normal, -2 to +2)

Other laboratory studies may revealPotassium level <3.5 mmol/L (normal, 3.5-5 mmol/L)Ionized calcium level <1.15 mmol/L (normal, 1.15-1.27 mmol/L)Urinary pH >7 or >8 (normal, ~6)

Some compensatory mechanisms that may be occurringRespiratory—Decreasing rate and depth of respirations will increase retention of carbonic acid. However, the

ability to control respirations may have been lost. In addition, attempts to slow rate and depth of respirations areoften inappropriate in the presence of a physiological response to hypoxemia.

Renal—Hydrogen is reabsorbed, and large amounts of potassium and sodium are excreted with excess bicarbonate.Electrolytes—Potassium moves from blood to cells in exchange for hydrogen ion; buffer systems attempt to

neutralize excess alkaline; in the presence of alkalosis, increased amounts of calcium are bound to protein,producing hypocalcemia.

Most appropriate managementDetermining and eliminating the underlying cause of hyperventilation (ie, for hysteria, reassurance, sedation, and

carbon dioxide inhalation)Providing oxygen and mechanical ventilation as neededAssessing serum levels of potassium and calcium and treating as necessary

Most appropriate nursing careBeing aware of common causes, signs and symptoms, expected laboratory findings if alkalosis is suspectedAssessing those patients with suspected respiratory alkalosis such as those with hysteria, hypoxemia, pain, drug

overdoseEliminating the underlying cause (ie, providing oxygen to hypoxemic patients, reassurance and emotional support to

hysterical patients, and encouraging hyperventilating patients to hold their breath for short periods or breathe intoa paper bag)

Beginning safety and seizure precautions if signs or symptoms of hypocalcemia are present



arterial blood gas sampling withcorresponding acid-base imbal-ances are given in Table 10. Apractice test for interpreting resultsof arterial blood gas sampling is

given in Table 11.Assessing trends of arterial

blood gas findings often providesmore information relating toprogress of the condition than does

a single isolated arterial blood gasanalysis. If compensation occurs,intervention is often unnecessary.Remember, treatment is con-sidered for an imbalance only

Table 8 Metabolic alkalosis

Metabolic alkalosis is brought on by any condition that causes loss of metabolic acids from the body or retention ofbicarbonate, such as

Loss of hydrochloric acid from the stomach, as occurs inVomitingGastrointestinal suctioning

Loss of chloride causing reabsorption of bicarbonate, as occurs withUse of diureticsExcessive vomiting

Retention of sodium causing reabsorption of bicarbonate, as occurs withIncreased secretion of aldosterone (stress, trauma)

Excessive ingestion of alkali, such asBicarbonate of soda (baking soda)Milk of magnesia

Intravenous administration of sodium bicarbonate for cardiopulmonary resuscitation

Clinical signs and symptomsSlow, shallow respirations (compensation by lungs)Dizziness, tingling of extremities, tetany, convulsions, hypertonicity of musclesIrritability, disorientationCardiac arrhythmias if hypokalemia is present

Arterial blood gas analysispH >7.45 (normal, 7.35-7.45)PaCO2 normal (normal, 35-45 mm Hg)Bicarbonate level >26 (normal, 22-26 mmol/L)Base excess >+2 (normal, -2 to +2)

Other laboratory reports may revealCarbon dioxide combining power > 26 mmol/L (normal, 22-26 mmol/L)

(ie, plasma bicarbonate)Potassium level <3.5 mmol/L (normal, 3.5-5 mmol/L)Ionized calcium level <1.15 mmol/L (normal, 1.15-1.27 mmol/L)Chloride level <95 mmol/L (normal, 95-105 mmol/L)Urinary pH >7 or >8 (normal, ~6)

Some compensatory mechanisms that may be occurringRespiratory—Hypoventilation begins involuntarily in an effort to retain carbonic acid.Renal—Hydrogen is reabsorbed, and large amounts of potassium and sodium are excreted with excess bicarbonate.Electrolytes—Potassium moves from blood to cells in exchange for hydrogen; buffer systems attempt to neutralize

excess alkaline; in the presence of alkalosis, increased amounts of calcium are bound to protein, producing hypocalcemia.

Most appropriate managementDetermining and treating the primary condition (ie, replacing fluids lost by vomiting or nasogastric suctioning)Assessing and correcting serum levels of potassium, calcium, chloride, and sodium as necessary

Most appropriate nursing careBeing aware of common causes, signs and symptoms, expected laboratory findings if alkalosis is suspectedPredicting which patients are at risk for metabolic alkalosis, such as patients who are self-medicating with

antacids, patients undergoing gastrointestinal suctioning or therapyTaking safety and seizure precautions for patients who have signs and symptoms of hypocalcemiaProviding discharge teaching (ie, overuse of antacids, misuse of baking soda in place of antacids, replacement of

fluids lost through vomiting) that may prevent alkalosis from occurring in the home





Table 9 Steps in analysis of arterial blood gases

1. Examine the pH, PaCO2, and bicarbonate level. Arethey all within normal limits?

2. Is the pH abnormal with abnormal level of therespiratory or acid (PaCO2) parameter and/or themetabolic or base (bicarbonate) parameter (see Table 3)?

a. Which parameter agrees with the pH? That is, if the pH indicates acidemia, does the

PaCO2 and/or bicarbonate level also indicateacidemia?

Or, if the pH indicates alkalemia, does the PaCO2and/or the bicarbonate level also indicatealkalemia?

b. Does the PaCO2 agree with the pH?c. Does the bicarbonate level agree with the pH?d. Do both PaCO2 and bicarbonate level agree with

the pH?

3. Is the pH abnormal with 1 parameter abnormal and in agreement with the pH, but the other parameter abnormal and not in agreement with the pH?

a. Is the PaCO2 abnormal and in agreement with the pH, and the bicarbonate level abnormal, but notin agreement with the pH?

b. Is the bicarbonate level abnormal and in agreement with the pH, and PaCO2 abnormal,but not in agreement with the pH?

4. Is the pH normal, but the PaCO2 and bicarbonate levelare abnormal?

a. Is the pH normal, but slightly alkaline (≥7.41)?

Does the PaCO2 (respiratory parameter) indicatealkalemia, but the bicarbonate level (respiratoryparameter) indicates acidemia?

Or, does the bicarbonate level (metabolicparameter) indicate alkalemia, but the PaCO2(respiratory parameter) indicates acidemia?

b. Is the pH normal, but slightly acidic (≤7.39)?

Does the PaCO2 (respiratory parameter) indicateacidemia, but the bicarbonate level (respiratoryparameter) indicates alkalemia?

Or does the bicarbonate level (metabolicparameter) indicate acidemia, but the PaCO2(respiratory parameter) indicates alkalemia?

Normal arterial blood gas levels

Acidosis and/or alkalosis

Acidosis

AlkalosisRespiratory acidosis or alkalosisMetabolic acidosis or alkalosis

Combination of respiratory and metabolic acidosis or respiratory and metabolic alkalosis

Partly compensated acid-base imbalance

Partly compensated respiratory acidosis oralkalosis (predominantly the result of metaboliccompensation)

Partly compensated metabolic acidosis or alkalosis(predominantly the result of respiratorycompensation)

Compensated alkalemic imbalance

Compensated respiratory alkalosis

Compensated metabolic alkalosis

Compensated acidotic imbalance

Compensated respiratory acidosis

Compensated metabolic acidosis

If Yes

If Yes

If Yes

If Yes If Yes If Yes

If Yes

If Yes

If Yes

If Yes

If Yes

If Yes

If Yes

If Yes

If Yes

If Yes




Respiratory alkalosis

pH 7.52PaCO2 30HCO3 24 (or BE +2)

Metabolic alkalosis

pH 7.57PaCO2 40HCO3 36 (or BE +14)

Respiratory and metabolic alkalosis

pH 7.68PaCO2 24HCO3 36 (or BE +14)

Partly compensated respiratory alkalosis

pH 7.46PaCO2 30HCO3 20 (or BE -4)

Partly compensated metabolic alkalosis

pH 7.46PaCO2 46HCO3 31 (or BE +7)

Compensated respiratory alkalosis

pH 7.42PaCO2 34HCO3 21 (or BE -4)

Compensated metabolic alkalosis

pH 7.43PaCO2 34HCO3 30 (or BE +7)

when the pH is abnormal. Be alertfor abnormal PaO2, indicating hyp-oxia, and provide adequate sup-plemental oxygen.2,10 A case study isprovided in Table 12 (page 40).

SUMMARYAlthough physical examination

remains an important part of thenursing assessment, assessment oftissue oxygenation provides ad-ditional vital information. Nurseswho are caring for patients withcompromised functioning musthave a basic understanding of thephysiological relationships be-tween oxygen saturation, cardiacoutput, and acid-base balance andmust be able to plan nursing carebased on this knowledge. ✙

AcknowledgmentsThe authors thank Debbie Newland, RN, BSN,

associate nurse manager of the pediatricintensive care unit, and Barry Gelman, MD,

associate professor of clinical pediatrics at theUniversity of Miami School of Medicine andattending physician in the pediatric intensivecare unit, Jackson Memorial Hospital, Miami,Fla, for their consultation and assistance withthis article.

References1. Price SA, Wilson LM. Pathophysiology:

Clinical Concepts of Disease Processes.5th ed. St Louis, Mo: CV Mosby; 1997.

2. Metheny N. Fluid and ElectrolyteBalance: Nursing Considerations. 3rd ed.Philadelphia, Pa: Lippincott-Williams &Wilkins; 1996.

3. Shapiro BA, Peruzzi WT. Clinical

pH low pH normal pH high

(7.35-7.45)

Acidemia Alkalemia

Bicarbonate level PaCO2 Bicarbonate level PaCO2

low high high low

Metabolic Respiratory Metabolic Respiratoryacidosis acidosis alkalosis alkalosis

Figure 5 Arterial blood gas analysis.

Mixed imbalance ifPaCO2 and bicarbonate level are both lowPaCO2 and bicarbonate level are both high

Table 10 Examples of arterial blood gas samples with corresponding acid-base imbalances

Respiratory acidosis

pH 7.23PaCO2 60HCO3 24 (or BE +2)

Metabolic acidosis

pH 7.11PaCO2 39HCO3 12 (or BE -14)

Respiratory and metabolic acidosis

pH 7.11PaCO2 58HCO3 18 (or BE -7)

Partly compensated respiratory acidosis

pH 7.34PaCO2 51HCO3 28 (or BE +7)

Partly compensated metabolic acidosis

pH 7.34PaCO2 34HCO3 20 (or BE -4)


pH 7.39PaCO2 49HCO3 29 (or BE +6)


pH 7.36PaCO2 32HCO3 19 (or BE -6)

BE indicates base excess; HCO3, bicarbonate level in millimoles per liter. Values for PaCO2are in millimeters of mercury.




Application of Blood Gases. 5th ed. StLouis, Mo: CV Mosby; 1994.

4. Guyton A, Hall J. Textbook of MedicalPhysiology. 9th ed. Philadelphia, Pa: WBSaunders Co; 1996.

5. Fischbach FT. Manual of Laboratory andDiagnostic Tests. 6th ed. Philadelphia,Pa: Lippincott; 1999.

6. Lamb AB. Nunn’s Applied RespiratoryPhysiology. 5th ed. Oxford, England:Butterworth-Heinemann; 2000.

7. Smeltzer SC, Bare BG, eds. Brunner andSuddarth’s Textbook of Medical-SurgicalNursing. Philadelphia, Pa: Lippincott;2000.

8. Pilbeam SP. Mechanical Ventilation:Physiology and Clinical Applications. 3rded. St Louis, Mo: CV Mosby; 1998.

9. Halperin M, Goldstein M. Fluid,Electrolyte, and Acid-Base Physiology.3rd ed. Philadelphia, Pa: WB SaundersCo; 1999.

10. Murray J, Nadel J. Textbook ofRespiratory Medicine. Vol 1. 2nd ed.Philadelphia, Pa: WB Saunders Co; 1994.

Note: Table 12 follows on page 40.

7. pH 7.51PaCO2 41HCO3 32

8. pH 7.47PaCO2 47HCO3 30

9. pH 7.44PaCO2 46HCO3 29

10. pH 7.68PaCO2 30HCO3 33

11. pH 7.51PaCO2 32HCO3 25

12. pH 7.34PaCO2 49HCO3 27

7. Metabolic alkalosisHCO3 is 32 mmol/L

(24 mmol:20 = 32 mmol:?)(20 × 32)/24 = 640/24 = 26.67

PaCO2 is 41 mm Hg(40 mm Hg:1 = 41 mm Hg:?)(1 × 41)/40 = 41/40 = 1.02

26.67 26.151.02 1

indicating alkalosis

8. Partly compensated metabolic alkalosis

9. Compensated metabolic alkalosis10. Metabolic and respiratory alkalosis11. Respiratory alkalosis12. Partly compensated respiratory

acidosis

Table 11 Practice test for arterial blood gas analysis

1. pH 7.29PaCO2 53HCO3 25

2. pH 7.33PaCO2 47HCO3 26BE +2

3. pH 7.38PaCO2 47HCO3 28BE +4

4. pH 7.62PaCO2 30HCO3 30

5. pH 7.44PaCO2 39HCO3 24

6. pH 7.38PaCO2 42HCO3 25

1. Respiratory acidosisHCO3 is 25 mmol/L

(24 mmol:20 = 25 mmol:?)(20 × 25)/24 = 500/24 = 20.8

PaCO2 is 53 mm Hg(40 mm Hg:1 = 53 mm Hg:?)(1 × 53)/40 = 53/40 = 1.32

20.8 15.81.32 1

indicating acidosis

2. Respiratory acidosis3. Compensated respiratory acidosis4. Metabolic and respiratory alkalosis5. Normal6. Normal

You may verify your answers by using the acid/base ratio:20 represents base (alkaline) or 24 mmol/L bicarbonate1 represents acid or 1.2 mmol/L of carbonic acid

(40 mm Hg PaCO2)

Therefore, a ratio <20/1 = acidosisa ratio >20/1 = alkalosis

= =

Answers




March 24 at 2:16 AM

PaO2, mm HgOxygen saturation, %pHPaCO2, mm HgBase excessBicarbonate, mmol/L

March 24 at 2:54 AM


March 24 at 6:30 AM

PaO2, mm HgOxygen saturation, %pHPaCO2, mm HgBase excessBicarbonate, mmol/LWhite blood cell count,x109/L

March 24 at 4:15 PM


March 25 at 5 AM

PaO2, mm HgOxygen saturation, %pHPaCO2, mm HgBase excessHCO3, mmol/L

March 26 at 11:10 AM


6891

7.2731-1214

10395

7.3534-8

18

30999

7.3840-2

23

20.2

11398

7.4336

024

9798

7.4535-1

22

10998

7.4337

024

Partly compensated metabolic acidosis (possibly attributed to blowing offcarbon dioxide via respirations with manual resuscitation bag)

Mechanical ventilation with 100% oxygen at a rate of 16 breaths perminute, controlled ventilations; intravenous infusion of 5% dextrose in0.45% sodium chloride started at 100 mL/h with antibiotics; givenalbuterol nebulizer treatment to be repeated every 4 hours

Compensated metabolic acidosisVentilations reduced to 10 breaths per minute in the assist/control mode

Normal acid-base balanceProbable respiratory infectionHyperoxygenationOxygen reduced gradually to 40% and assisted ventilations reduced to

8 breaths per minute

Normal acid-base balanceChest radiograph showed evidence of pneumonia; antibiotics continuedIntravenous infusion rate reduced to 50 mL/h; diuretic (furosemide) and

potassium replacement started

Normal acid-base balance

Normal acid-base balanceWeaning from ventilator begun

Findings Conclusion/intervention

Table 12 Case study: serial assessments, laboratory findings, results of arterial blood gas analysis, and interventions

A.G., an 86-year-old man, was admitted to the hospital at approximately 2 AM via the emergency department. Onarrival, he was having difficulty breathing and was responsive only to painful stimuli. Vital signs at admission werebody temperature, 97°F (~36.5°C); heart rate, 140/min; respirations, 37/min; and blood pressure, 177/110 mm Hg.Oxygen saturation measured by pulse oximetry was 76% on room air. Shortly after arrival, A.G. went into respiratoryarrest, with subsequent bradycardia (heart rate, 35/min). Resuscitation was initiated with intubation, and oxygen wasadministered via a manual resuscitation bag. Further interventions were guided by serial physical assessments, resultsof laboratory tests, and arterial blood gas analyses.




CE Test Form

Assessing Tissue Oxygenation

Objectives:

1. Describe the correlation of hemoglobin concentration to tissue oxygenation2. Understand the role of laboratory assessment in evaluation of tissue oxygenation3. Recognize the relationship of acid-base balance to tissue oxygenation

Mark your answers clearly in the appropriate box. There is only 1 correct answer. You may photocopy this form.

To receive CE credit for this test (ID C023), mark your answers on the form below, complete the enroll-ment information, and submit it with the $12 processing fee (payable in US funds) to the AmericanAssociation of Critical-Care Nurses (AACN). Answer forms must be postmarked by June 1, 2004. Within 3to 4 weeks of AACN receiving your test form, you will receive an AACN CE certificate.

This continuing education program is provided by AACN, which is accredited as a provider of continuing education in nursing by theAmerican Nurses Credentialing Center’s Commission on Accreditation. AACN has been approved as a provider of continuingeducation by the State Boards of Nursing of Alabama (#ABNP0062), California (01036), Florida (#FBN2464), Iowa (#332), Louisiana(#ABN12), and Nevada. AACN programming meets the standards for most other states requiring mandatory continuing educationcredit for relicensure.

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Mail this entire page to AACN, 101 Columbia, Aliso Viejo, CA 92656, (800) 899-2226

Test ID: C023Test writer: Kim Brown, RN, MSN, CS-FNP

Form expires: June 1, 2004Contact hours: 2.0

Passing score: 9 correct (75%)Category: A

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1. ❑a 2. ❑a 3. ❑a 4. ❑a 5. ❑a 6. ❑a 7. ❑a 8. ❑a 9. ❑a 10.❑a 11. ❑a 12. ❑a❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b ❑b❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c ❑c❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d ❑d




7. Which one of the following correlations is correct inaccordance with the oxyhemoglobin dissociationcurve?a. At a PaO2 of 27 mm Hg, hemoglobin is 30%

saturated.b. At a PaO2 of 80 mm Hg, hemoglobin is 85%

saturated.c. At a PaO2 of 40 mm Hg, hemoglobin is 75%

saturated.d. At a PaO2 of 60 mm Hg, hemoglobin is 80%

saturated.

8. Which one of the following does not affect the shiftof the oxyhemoglobin dissociation curve to the rightor left?a. Acidity of the bloodb. Carbon dioxide tension in the bloodc. Concentration of 2,3-diphosphoglycerate in red

blood cellsd. Serum sodium levels

9. Which one of the following factors influences theaccuracy of oximetry, the measurement of oxygensaturation in the blood?a. Low perfusion statesb. Hypothermiac. Oxygen saturations less than 80%d. All of the above

10. Which one of the following statements is trueregarding the bicarbonate-carbonic acid buffersystem?a. Normal blood pH is the result of a bicarbonate

to carbon dioxide ratio of 20 to 1.b. Carbonic acid when dissolved in water becomes

carbon dioxide.c. A ratio of less than 20:1 of bicarbonate to carbon

dioxide indicates alkalosis.d. A ratio of more than 20:1 of bicarbonate to

carbon dioxide indicates acidosis.

11. Which one of the following is not a likely cause ofrespiratory acidosis?a. Hypoventilationb. Damage to the respiratory center in the medullac. Severe diarrhead. Pulmonary damage or obstruction

12. Which one of the following is not a likely cause ofmetabolic alkalosis?a. Loss of hydrochloric acid secondary to vomitingb. Hyperventilationc. Excessive use of diureticsd. Intravenous administration of sodium

bicarbonate

1. Which one of the following statements is trueregarding diffusion of gases in the lungs?a. PaO2 is approximately 95 mm Hg.b. Partial pressure of oxygen at the point where

it reaches the alveoli is approximately 130 mm Hg.

c. The partial pressure of oxygen and carbon dioxide and their ability to diffuse into the capillary blood are dependent on one another.

d. Partial pressure of carbon dioxide at the alveoli is approximately 30 mm Hg.

2. Which one of the following does not contribute to thedecrease in the partial pressure of oxygen betweeninspired air and arterial blood?a. Dead spaceb. Water vapor in the airwayc. Shunting of blood from the right side of the heartd. Partial pressure of carbon dioxide in arterial

blood

3. Which one of the following best describes a patient inrespiratory failure?a. 66-year-old man with congestive heart failure

and a PaO2 of 40 mm Hg b. 50-year-old woman with emphysema and a

PaO2 of 72 mm Hgc. 33-year-old asthmatic man with a PaO2 of

55 mm Hgd. Both a and b

4. Which one of the following best describes pulmonaryventilation?a. Ability to maintain a PaO2 greater than 50 mm Hgb. Inspiration and expiration of air (gases)c. Ability to maintain a PaO2 greater than 30 mm Hgd. Dead space less than 30 mm Hg

5. Which one of the following statements is trueregarding hemoglobin and its relationship to oxygentransport in the blood?a. Ninety-seven percent of oxygen transported in

the blood is bound to hemoglobin.b. Each gram of hemoglobin can bind with

approximately 1.34 mL of oxygen at full saturation.

c. Oxygen transport can be reduced by either a hemoglobin level or oxygen saturation that is abnormal.

d. All of the above

6. Which factor ultimately determines the amount ofoxygen delivered at the tissue level?a. Serum potassiumb. Cardiac outputc. Core body temperatured. Peripheral vascular resistance

CE Test QuestionsAssessing Tissue Oxygenation



In the August 2002 issue,the article entitled “Met-hemoglobinemia: A CaseStudy” (2002;22:22-42), con-tained an error in Table 1.The methemoglobin level,reported as proportion oftotal hemoglobin, in Table 1showed an incorrect refer-ence range. The normal lev-els for methemoglobin are<0.01-0.02.

CRITICAL CARE NURSE Vol 22, No. 5, OCTOBER 2002 19

CORRECTIONSIn the article entitled “Assessing Tissue Oxy-

genation” (June 2002;22:22-42), the reference toFigure 4 (p.27) was incorrectly placed in the middleof the sentence. The sentence that refers readers toFigure 4 should read: “ The body has numerouscompensatory mechanisms to correct an abnormalpH; however, if these mechanisms fail, cellular func-tions are impaired, and death will eventually result(Figure 4).” Moreover, this figure contained an error.The corrected figure is published below.

In Table 3 (p.28) of this article, the last parametershould be PaO2, not PaCO2.

In “Prone Positioning of Trauma Patients WithAcute Respiratory Distress Syndrome and OpenAbdominal Incisions” (June 2002;22:52-56), the com-pany listed as the manufacturer of the CircOlectricbed was incorrect. This product is manufactured anddistributed by Stryker Medical, Kalamazoo, Mich.

On page 53 of this article, nitrous oxide was incor-rectly used instead of nitric oxide. The last sentencein the middle column and the third paragraph shouldread: “Other areas of research focus on the use of var-ious techniques of ventilator support and the use ofsurfactant and inhaled nitric oxide in the treatmentof ARDS.”

Figure 4 Plasma pH. Normal plasma is slightly alkaline, with a pH of approxi-mately 7.35 to 7.45. When the pH deviates outside this range in either direc-tion, signs and symptoms of acid-base imbalance will occur. Withoutcompensatory mechanisms or intervention, cellular dysfunction and deathmay occur.

Normal

Acidosis Alkalosis

Death Death

7.4

7.457.35

6.80 7.80



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Assessing Tissue Oxygenation