arterial blood gases: as easy as a b g

AORN JOURNAL MAY 1989, VOL. 49, NO 5

Arterial Blood Gases AS EASY AS A B G

Karen York, RN; Gail Moddeman, RN

rterial blood gas (ABG) testing has become increasingly common in nursing A practice, from the operating room to

home care. As people live longer and chronic disease management improves, more patients with chronic lung disorders are considered candidates for surgery. Operating room nurses will find that they are seeing ABG tests in a wider variety of surgical procedures. In a recent survey, we found one 770-bed hospital that recorded an average of 60 ABG tests per week in the operating rooms. Approximately three fourths of those were associated with major cardiovascular surgery.

Arterial blood gas results generally contain five values: pH, partial pressure of carbon dioxide (PaCO,), bicarbonate (HCO;), partial pressure of oxygen (PaO,), and oxygen saturation (0,sat). Some laboratories report base excess and/or total CO, instead of, or in addition to, HCO;. All three of these are indicators of alkaline substances, or bases, in the blood.

Analysis of ABGs usually is done in two sections: oxygenation and acid-base status. The PaO, and O p t indicate how effectively the patient's lungs are ventilating and d i h i n g 0, from the atmosphere to the bloodstream. The pH,

PaCO,, and HCO; permit evaluation of acid- base imbalance and possible compensatory mechanisms. Because low 0, states can produce life-threatening changes more quickly than acid- base imbalances, the oxygenation status should be assessed h t .

Oxygenation

xygen in the blood is measured as the partial pressure it exerts in comparison 0 to the total amount of atmospheric

pressure. The partial pressure of 0, in arterial blood is abbreviated PaO,. The value that is measured is the 0, dissolved in the plasma, although this accounts for only 3% of the total 0, contained in the blood.' The majority of 0, in the blood is combined with hemoglobin and cannot readily be analyzed.

When the 0, is combined with hemoglobin, it creates oxyhemoglobin. Each hemoglobin molecule accepts four 0, molecules to become fully saturated. Oxygen saturation refers to the percentage of hemoglobin molecules that are fully saturated with 0,. The normal range for oxygen saturation is from 90% to 100%.

Karen York, RN, MSN, k a pulmonav clinical coordinator, div~ion of surgical services, Miami nurse special& Advance Home Health Services, Valley Hospital Dayton, Ohio. She earned her Cincinnati She earned her bachelor of science diploma in nursing from St Elizabeth Hospital and master of science degrees in nursing from School of Nursing, Covington, Ky, and her the University of Cincinnati bachelor of science and master of science degrees

in nursing from Wright State Univers@, Dayton, Gail Mod&mn, RN, MS I;Ci the education Ohio.

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% Hemoglobin saturation

Fig 1 Oxyhemoglobin Dissociation Curve

100

80

60

40

20

0 0 20 40 60 80 100 120

PaO, mmHg

In many laboratories, the O p t is calculated based on a standard hemoglobin level rather than what is actually measured. If the patient’s actual hemoglobin level is dserent from the laboratory standard, the 0,sat reported will be quite inaccurate. The actual 0,sat depends on the PaO, and the amount of hemoglobin. As the PaO, levels fall, so does the percent of hemoglobin molecules that are fully saturated with 0,.

The 0,sat can be monitored using a pulse oximeter, a noninvasive device that gives second- by-second readings. Clinically, noninvasive O p t monitoring can be a useful adjunct to ABGs because it permits instantaneous observation of 0,sat changes without the delays and need for removal of blood required by ABGs.

A hemoglobin molecule prefers to be either fully saturated or fully desaturated. When fully saturated, the hemoglobin tends to resist unloading its 0, at the tissue where the 0, is needed for cellular activity. For this reason, when 0, is in short supply, the percent of hemoglobin saturation drops much more rapidly than the PaO, levels. This lower percentage of fully saturated hemoglobin molecules means that the little 0, that is

available is more easily given up at the cell where it is needed. This relationship between the PaO, and 0,sat is described by the oxyhemoglobin dissociation curve (Fig 1).

This curve is particularly important in surgery because of the factors that modify the relationship in this curve: body temperature, pH, and use of banked blood or blood that has been stored for more than 72 hours. Acid pH, fever, and increased 2,3diphosphoglycerate (DPG), an enzyme that decreases rapidly in old blood, cause the curve to shift to the right. This means that the percent of fully saturated hemoglobin is below normal for a given PaO, level? This decreased saturation means that the 0, is given up more readily at the cellular level, and this is sometimes desirable in situations where 0, is in short supply.

The curve shifts to the left, and therefore 0, is less readily available to the tissues, when the patient is alkalotic, cold, or receiving blood stored longer than three days.

Decreased temperature lowers the metabolic demands for 0, so that the decreased availability is somewhat counterbalanced in this common situation. Note that the 0,sat does not fall in direct

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Modem anesthesia equipment generally reduces the problem of alterations in inhaled gas combinations

that reduce the concentration of inhaled oxygen.

proportion to PaO, levels; instead, the body provides a protective mechanism whereby 0,sat falls only slightly until the PaO, drops below 60 mmHg.3 For this reason, as well as inaccuracy due to a discrepancy between actual and standard hemoglobin levels, the O F t is a less sensitive measure of oxygenation status than the PaO,. Therefore, PaO, is given the most attention when assessing ABGs.

The normal range for PaO, is 80 to 100 mmHg. Levels below 60 mmHg indicate hypoxemia and generally require 0, treatment. In the elderly, however, changes in the lungs produce decreased PaO, levels without indicating serious lung disease. Altitude is the other major factor that affects PaO, levels; people at high altitudes will have lower PaO, levels than they would at sea level due to the decreased atmospheric pressure.

Low PaO, levels are caused by: decreased ventilation, decreased lung perfusion, decreased permeability of alveolarcapillary

decreased concentration of 0, in inhaled air! Patients in surgical areas may have disturbances

in one or more of these processes from preexisting diseases as well as from events in the perioperative experience itself. Analgesics and anesthetics can decrease or eliminate spontaneous ventilation. Blood loss and positive pressure ventilation can decrease lung perfusion. Pulmonary edema and respiratory irritants can decrease diffusion of gases across the alveolarcapillary membrane. Alteration in inhaled gas combinations can reduce the concentration of inhaled 0,; however, modern anesthesia equipment generally reduces this problem? These changes often are accentuated by body responses to anesthesia and surgery that may increase 0, requirements.

Pain and analgesia in the postoperative period further limit respiration, and pooling of respiratory secretions in immobile patients contributes to

membranes, and

decreased oxygenation. While the 0, in room air is fairly stable at 21’76, perioperative patients frequently receive gas mixtures other than room air. People breathing in small airtight spaces, such as children playing with plastic bags, also are affected in this manner.

The major symptoms of hypoxemia are caused by changes in the functioning of the central nervous system. Mild hypoxemia can produce apprehension and difficulty with concentration. As hypoxemia worsens, apprehension becomes anxiety and panic, and decision-making ability deteriorates. Confusion and lethargy ensue with coma later. Acute hypoxemia may produce changes in heart rate, respiratory rate, and blood pressure? People who are chronically hypoxemic adapt to low PaO, and symptoms may be evident only at PaO, levels that would be lethal to the healthy person?

Ms C., an atypical patient, illustrates the process of chronic hypoxemia. She is a 56-year-old nursing home employee who came to the emergency department for the first time complaining of “seeing blue.” She also was experiencing shortness of breath that limited her ability to walk to the bus stop to get to work. Her PaO, was 26 mmHg. With further questioning, Ms C. admitted to “trouble thinking straight” and her family said that sometimes she got very “blue looking” and could not make decisions.

Ms C. reluctantly agreed to be admitted to the hospital and required two weeks of therapy. Discharge plans included home 0, and counseling about symptom recognition and appropriateness of working with patients during symptomatic

The goal of oxygen therapy is to maintain the individual’s PaO, at an acceptable level. Some conditions, such as carbon monoxide poisoning, frequently require high pressure or hyperbaric 0, therapy? For people with acute or short-term hypoxemia, treatment is aimed at bringing PaO,

perid.

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Signs and symptoms of hypoventilation include headache, lethargy, and confusion

that can progress to a coma.

levels to between 80 and 100 mmHg. Patients with chronic hypoxemia, however, frequently will be maintained at PaO, levels between 60 and 80 mmHg. In patients who have chronic hypoxemia and hypercapnea (elevated PaCO, levels), the normal stimulus to breathe provided by the PaCO, levels is blunted, and the hypoxic drive to breathe may be the only stimulus to maintain breathing. If the hypoxemia is alleviated in these people, breathing may cease unless ventilation is maintained by mechanical means. Early indicators of decreased hypoxic drive are increased PaCO, levels and lethargy.

In the intraoperative period, concerns about blunting hypoxic drive often may be secondary to providing optimal oxygenation during anesthesia. Anesthesia often causes a postoperative decrease in ventilation/perfusion relationships and elastic recoil of the lungs and an increase in airway resistance? Taking these factors into consideration, anesthesia personnel should increase the percentage of 0, in the inhaled air.

Acid-Base Balance

nce the oxygenation status has been ascertained and treatment for life- 0 threatening hypoxemia begun, the acid-

base balance is assessed. The first step in acid- base analysis is to assess the pH level. The pH value is a negative logarithm of hydrogen ion concentration, which indicates acid activity. Because pH measures hydrogen ion concentration in a negative manner, a low pH value represents a high acid level.

The normal blood pH, in which acids and bases are in balance with each other, is 7.40, with an acceptable range from 7.35 to 7.45. When the pH is outside this range, the body attempts to return to the normal range by juggling acids or bases as necessary.

A pH below 7.40 is acidic. A pH above 7.40

is alkalotic-it has an increase in bases or a decrease in acidic substances. The ABG report uses two substances to represent the amount of acids and bases present in the blood.

The acid indicator. Carbon dioxide is a volatile substance-the waste or residue produced by the metabolism of 0, in the cells. The PaCO, is regulated primarily by the lungs through respiration. The normal value for the PaCO, is 40 mmHg with a normal range of 35 to 45 mmHg. When carbon dioxide combines with water in the bloodstream, carbonic acid (H2C03) is formed.lo Therefore, an increase in PaCO, results in a more acidic, or lower, pH.

The lungs regulate the amount of CO, in the blood on a minute-by-minute basis by increasing or decreasing the rate and depth of respiration. The more gas exchanged by the lungs by faster or deeper breathing, the more CO, will be eliminated from the body and the lower the PaCO, will be. When less air is ventilated by the lungs, less CO, will be eliminated and the PaCO, eventually will rise. Chemoreceptors in the medulla respond to pH changes by sending signals to the lungs to alter the rate of breathing and thus bring the pH back into normal range. When the lungs are able to function normally, they will regulate ventilation to maintain the PaCO, levels within normal limits and thus maintain a normal PH.

Problems with CO, regulation occur when the lungs are unable to respond to changes in PaCO, and pH. Major causes include chronic and acute lung diseases and disturbances of neural control of breathing, such as anesthesia, analgesia, or central nervous system problems. When the lungs are unable to increase ventilation to respond to high PaCO, levels, the patient is said to be hypoventilating. Signs and symptoms of elevated PaCO, (hypoventilation) are headache, lethargy, and confusion that can progress to a coma. Because CO, also is carried by the hemoglobin molecule,

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elevated PaCO, levels may decrease the amount of hemoglobin available for 0, transport.

Hyperventilation, on the other hand, is characterized as a PaCO, level below 35 mmHg. This condition is produced by breathing faster or deeper than necessary and eliminating too much COT It produces carpopedal spasms, progressing to tetany, and constriction of cerebral blood vessels, which can produce dizziness and light- headedness. '

Treatment for abnormal PaCO, levels involves modifying either ventilation or CO, production. Ventilation may be changed by altering the rate and depth of breathing. Sometimes a patient who is awake can be coached to pace his or her rate and depth of breathing. In a patient who is unable to respond, however, manual or mechanical ventilation is required. In addition to those primary interventions, e x m CO, production also may be manipulated by promoting muscle rest and relieving hypermetabolic states such as fever.

The base indicator. The HCO; represents the balance between bases and fixed, or metabok acids.'* The HCO,' is regulated mainly by renal excretion and reabsorption. The primary blood base is HCO; which is the alkaline substance measured in most laboratories as part of ABGs. The normal value is 24 mEq/L, with a normal range from 22 to 26 mEq/L. Because HCO; is a base, increases in HCO,' produce an alkaline, or higher, pH level. When HCO; is lowered beyond normal limits, the pH also is lowered, or more acidic.

The bicarbonate is regulated primarily by the kidneys, and it is called the metabolic indicator. Bicarbonate values also are affected by amounts of tixed acids in the blood. The major sources of such acids are dietary acids produced in the absorption and metabolism of proteins, lactic acid produced during anaerobic metabolism, and keto acids produced during insulin deficiency or whenever glucose is not available for metab~lism.'~ Acids dissociate and liberate hydrogen ions (H') which combine with HCO; in their function as blood buffers. As the acid production increases, H+ increases and combines with HCO; forming H,CO, (carbonic acid) and decreasing the available HCO;.

Compensatory Mechunhm

ecause the body functions best when the pH is within normal limits, it has three B mechanisms to help maintain this neutral

state. These three mechanisms are blood buffer systems, the respiratory system for CO, regulation, and the renal system for HCO; regulation.

Blood buffer systems are pairs composed of a weak acid and its complementary base. One of the major buffer systems is the CO, and HCO; pair. These two, with the addition of water, can convert from an acid to a base almost instan- taneously to maintain the pH in its normal range. This reaction is demonstrated by the chemical symbols:

co, + H,O <--> H,CO, <--> H+ + HCO;

Other major buffer systems are protein buffers and a phosphate pair.

The respiratory system compensates for pH abnormalities caused by other acids or bases within the blood. Respiratory compensation is the second system to go into action to normalize pH, taking seconds to minutes to begin its work. The lungs compensate for abnormal pH levels by either increasing or decreasing CO, excretion. When the pH is too acidic, the lungs will increase ventilation to eliminate CO, and thus reduce the total acid load in the bloodstream. When the pH is too alkalotic, the lungs will retain CO, by decreasing ventilation.

The third, and slowest, compensatory mechanism is the kidney. The kidney works to increase or decrease HCO; levels and H+ ion concentration. In acidic pH situations, H+ is excreted in exchange for sodium. When the pH is alkaline, HCO; is excreted and H+ is retained.

Clinical Interpretation

W 'hen interpreting a patient's acid-base status, there are four steps that must be followed. These steps are the

following. A: Assess the pH-is it acidic or alkalotic?

Remember, pH values between 7.35 and 7.45 are

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MAY 1989, VOL. 49, NO 5 AORN JOURNAL

Case Study 1 Acute Respiratory Acidosis

Mr J. is a 57-year-old man with moderately severe emphysema and benign prostatic hypertrophy. His lung disease is stable and preoperative ABGs showed a mild compensated respiratory acidosis. Surgery was uneventful. Arterial blood gas values in the recovery area on 0, at 2 L/min were

pH = 7.30 PaCO, = 63mmHg HCO; = 28mEq/L

PaO, = 65mmHg

Analysis A: pH is acidic-acidosis B: PaCO, is elevated (acidic); HCO; is slightly increased (alkalotic) C acid PaCO, matches the acid pH-respiratory D: compensation is just beginning as evidenced by increased HCO;,

PaO, is below normal limits but not low enough to be called but pH is still outside normal limits

h ypoxemia.

Interpretation Acute respiratory acidosis

Plan of care Position for optimal respiratory excursion; coach and stimulate deep

breathing; use analgesics judiciously; give respiratory treatments as ordered and medications to maximize bronchodilation. Additional 0, is probably contraindicated; raising the PaO, too much may cause depres- sion of the hypoxic drive to breathe.

normal. A pH below 7.35 is considered acidosis; values above 7.45 are considered alkalosis.

B: Break any abnormalities in the PaCO, and HCO; into their acid or base directions. Levels of PaCO, that are higher than normal add acid to the system and may cause acidosis; lower than normal PaCO, levels produce alkalosis. Bicarbo- nate is a base. Elevated levels of HCO; add alkaline substance to the blood, causing alkalosis; a decreased HCO; produces acidosis.

C: Compare the PaCO, and HCO; to the pH abnormality. The acidity or alkalinity of the PaCO, and HCO; are compared to the pH. Whichever of these two matches the pH is generally considered to be the source of the

abnormal pH. For example, if the pH imbalance is caused by the PaCO, then the acidic or alkalotic status is referred to as respiratory; if the imbalance is caused by the HCO,-, the imbalance is metabolic.

D: Determine whether compensation has occurred. In analyzing the ABG values, it is helpful to compare the test results to the ideal values. This can help identify the tendency or direction of the acid-base abnormality even when the value is within normal limits.

Compensation takes place when the noncaus- ative factor is able to balance the primary causative factor enough to bring the pH back to normal limits. Generally, compensation brings the pH to

d) 1317


Case Study 2 Compensated Respiratory Alkalosis

Ms S., a 22-year-old with a full-term pregnancy, has been in and out of labor for 36 hours and is scheduled for a cesarean section. Preoperative ABG tests reveal

pH = 7.44 PaCO, = 29 mmHg HCO; = 20 mEq/L

PaO, = 75 mmHg

Analysis A pH is slightly alkalotic, within normal limits-either normal or

B: PaCO, is decreased (alkalotic); HCO; is decreased (acidic) C: alkaline PaCO, matches pH-respiratory D: compensation has ocurred as evidenced by the acidic HCO; and

PaO, is below normal but not low enough to be considered h ypoxemia

compensated alkalosis

pH within normal limits

Interpretation Compensated respiratory alkalosis

Plan of care This is a common finding in third trimester pregnancy, especially

during labor. This abnormality will most likely reverse spontaneously after the birth, because the alkalosis is primarily caused by hyperventilat- ing in response to the hypbxemia. The hypoxemia, in turn, is caused by the restriction to breathing produced by the decreased movement of the diaphragm caused by the uterine contents.

Further, rapid breathing during contractions can accelerate the loss of CO,. Slower, deeper breathing should be encouraged between contractions.

normal limits, but not all the way back to the perfect value of 7.40.

Respiratory acidosis is caused by the inability to eliminate enough CO, from the body, or hypoventilation. (See “Case Study 1: Acute Respiratory Acidosis.”) Common causes include lung disease, respiratory depressant drugs, neuromuscular disorders, abdominal distension, sleep, and splinting from pain, particularly with torso incisions. Respiratory acidosis can occur quite easily in the intraoperative and postoperative periods because of anesthetics, analgesics,

decreased consciousness, increased respiratory secretions, and pain.

Anesthesia and nursing personnel must be careful to prevent hypoventilation by ensuring adequate ventilation either with manual or mechanical means or by stimulating or coaching the conscious patient.

Respiratory alkalosis is produced by breathing faster and/or deeper than the level of PaCO, demands, and thus eliminating CO, faster than it is produced by the tissues. (See “Case Study 2: Compensated Respiratory Alkalosis.”) Hypoxe-

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Case Study 3 Partially Compensated Metabolic Acidosis

Ms J. is a 27-year-old diabetic. She is brought to the OR for open reduction for multiple right arm and leg fractures following an automobile accident. ABG values in the recovery area are


PaO, = 85 mmHg

Analysis A pH is acidic-acidosis B: PaC0,is decreased (alkaline); HCO; is decreased (acidic) C: acid HCO; matches pH-metabolic D: compensation has begun as shown by alkaline PaCO,; however,

pH remains outside normal limits, therefore, only partial compensation has taken place

PaO, is within normal limits

Interpretation Partially compensated metabolic acidosis

Plan of care Stat blood sugar; treat underlying problem (eg, administer insulin

intravenously), assess for dehydration, ensure adequate intravenous fluids, monitor blood-sugar levels frequently.

mia may produce hyperventilation or low PaCO, because the patient breathes faster and CO, crosses the alveolar-capillary membrane about 20 times faster than 0, does.14 Some lung disorders, such as asthma and pulmonary embolus, can produce respiratory alkalosis in response to hypoxemia. Other causes include pain, fever, anxiety, central nervous system disorders, and overventilation by mechanical ventilators. Treatment usually is directed at correcting the underlying problem. Hyperventilation is sometimes used therapeutically to help reduce intracerebral pressure by constrict- ing cerebral blood vessels.15

Metabolic acidosis is caused by either a loss of bases or an increase in nonvolatile acids. Causes include renal failure, diabetic ketoacidosis, and lactic acidosis. (See “Case Study 3: Partially Compensated Metabolic Acidosis.”) Metabolic

acidosis is a frequent finding in the immediate postoperative period. Treatment is based on correction of the underlying problem. Either NaHCO, or THAM’” may be used to correct the acidosis but must be used judiciously because the HCO; cannot cross the blood-brain barrier.

Metabolic alkalosis occurs with an increase in bases in the body or a decrease in the fixed, nonvolatile acids. (See “Case Study 4 Partially Compensated Metabolic Alkalosis.”) Metabolic alkalosis can be difficult to treat because the compensatory mechanism is to decrease ventilation to conserve CO,; this may cause or worsen hypoxemia. Also, in the alert patient, the drive to breathe will frequently override the compensatory need.16 Major causes of metabolic alkalosis include:

loss of gastric acids through suction

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MAY 1989. VOL. 49, NO 5 AORN JOURNAL

Case Study 4 Partially Compensated Metabolic A lkalosis

Mrs F. is a 64-year-old woman with a small bowel obstruction. She was admitted through the emergency department with repeated vomiting. Preoperative ABG values were


PaO, = 63 mmHg

Analysis A: pH is alkaline-alkalosis B: PaCO, is slightly elevated (acidic); HC0,- is elevated (alkalotic) C: alkalotic HCO; matches pH-metabolic D: the PaCO, is acidic in an attempt to compensate for the alkalosis;

however, the pH remains outside normal limits, therefore only partial compensation has taken place

PaO, is below normal but not low enough to be considered h ypoxemia

Interpretation Partially compensated metabolic alkalosis

Plan of care Careful intake and output and fluid replacement; careful observation

of both respiration and gastric fluid losses. The compensatory mechanism of respiratory retention of CO, is not to be encouraged because shallow respirations may predispose to complications of ineffective airway clear- ance and atelectasis. Supplemental 0, is probably indicated because there is no history of lung disease.

or vomiting, hypokalemia (low serum potassium), hypochloremia (low serum chlorides), and administration of sodium bicarbonate.

All of these causes are relatively common in patients in the perioperative areas.

Drawing ABGs

n arterial blood sample is necessary for ABGs because it more accurately reflects A the levels of PaCO, and PaO, of the blood

leaving the lungs than does venous blood. The sites most commonly used are the radial, brachial, or femoral arteries. Because the radial artery is

the safest and most accessible site, it is most commonly used by nurses to draw ABGs.

In the operating room, however, the patient’s position on the OR bed determines the selection of a puncture site. Patients who require repeated ABG samples may have an indwelling arterial catheter inserted. The arterial catheter also can be used to monitor arterial blood pressure.

Radial artery puncture. Arterial circulation to the hand is supplied by the radial and ulnar arteries, both of which connect to the palmar arches in the hand. Because possible complications of arterial puncture are spasms of the vessel and clotting, the adequacy of collateral circulation must be tested. The Allen’s test must be carried out

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MAY 1989, VOL. 49, NO 5 AORN J O U R N A L

Breath holding or tachypnea can affect the arterial

blood gas results.

before the radial artery is used for ABGs. The procedure is as follows.

1. Close the hand tightly to force as much blood out of the hand as possible.

2. Apply pressure over both the ulnar and radial arteries until the hand blanches and then relax the hand.

3. Release the pressure on the ulnar artery only. The color should return to the hand within 15 seconds if ulnar circulation is adequate.

Puncture technique. Use a commercially prepared blood gas kit or obtain the following supplies: 21- to 23-gauge needle, 3 to 5 mL glass syringe, sterile airtight stopper, skin preparation supplies, and a container of ice. Glass syringes are preferred because the pulsations can fill the syringe without pulling on the plunger. Heparinize the syringe (if it is not preheparinized) by flushing with heparin (1,000 units/mL) and then emptying the excess heparin, taking care to avoid leaving air bubbles in the syringe. The sterile stopper may be a rubber plug into which the needle can be inserted or a plastic syringe cap that fits securely on the hub of the syringe. It is critical that the syringe be airtight to avoid contamination of the syringe with room air. Also, any air bubbles must be carefully expelled. The specimen must be placed on ice immediately to stop metabolism in the blood

used to decrease discomfort. The wheal of anesthetic may, however, obscure the pulsations and may increase the number of skin punctures required.

5. Insert the needle at a 45-degree angle or less, with the needle barrel up, and advance it until it enters the artery. Piercing the back wall of the artery can increase the risk of blood loss or clotting. If a glass syringe is used, a flash of blood can be seen in the syringe when the artery is entered.

6. Obtain 2 to 3 mL of blood, making sure there is no air in the syringe, cap the syringe, and place the sample on ice immediately.

7. Apply firm pressure to the site for 5 minutes. If the patient has been anticoagulated, pressure should be maintained until no bleeding is present.

In infants, blood gases are measured on capillary blood drawn into capillary tubes to minimize blood loss. An area with a thick capillary network, such as an earlobe, heel, great toe, or finger, is used. Heat is applied to increase blood flow in the area as much as possible.

Arterial blood gases need not be a mystery to the perioperative nurse. The four steps: assess, break into acid and base, compare with pH, and determine whether compensation has occurred, can help clarify

0 the nurse’s understandmg of this test.

cells themselves, which i n alter the ABG results. Gloves should be worn to prevent contact with possibly contaminated blood. Povidone-iodine is

Notes

and the Art (New york City: John Wiley 1982) 61.

1. G A Traver, ed, Respiratory Nursing: The Science Sons,

the cleansing agent of choice in many institutions

procedure is as follows. 1. If the patient is alert, explain the procedure.

Ask the patient to breathe normally during the procedure, because breath holding or tachypnea are common responses to pain or anticipation of pain and can affect the ABG results.

2: B A Shapiro, R A Harrison, J R Walton, Clinical and is included in many prepared kits. m e Application of Blood Gases, second ed (Chicago: Year

Book Medical Publishers, 1977) 85. 3. Ibid 82. 4. Traver, Respiratory Nursing: The Science and

5. W D Wylie, H C Churchill-Davidson, A Practice of Anesthesia, second ed (Chicago: Year Book Medical Publishers, 1984) 135.

6. Traver, Respiratory Nursing: The Science and the Art, 64.

7. Shapiro, Harrison, Walton, Clinical Application of Blood Gases, 178-179.

theArt, 63.

2. Palpate the radial artery carefully. 3. Cleanse the skin at the puncture site carefully. 4. In an alert patient, local anesthesia may be

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MAY 1989, VOL. 49, NO 5 AORN JOURNAL

8. M Glowacki, N Chew, “Hyperbaric oxygen therapy: A guide for the perioperative nurse,” AORN Journal 47 (June 1988) 1374.

9. Wylie, Churchill-Davidson, A Practice of Anesthesia, 103.

10. Shapiro, Harrison, Walton, Clinical Application of Blood Gases, 96.

11. Traver, Respiratory Nursing: The Science and the Art, 58.


13. hid, 96. 14. Traver, Respiratory Nursing: The Science and

the Art, 66. 15. K York, “The lung and fluid-electrolyte and acid-

base imbalances,” Nursing Clinics of North America 22 (December 1987) 810.


Suggested reading Butts, D E. “Fluid and electrolyte disorders associated

with diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic coma.” Nursing Clinics of North America 22 (December 1987) 830-832.

Panic Attacks May Indicate Anxiety Disorders A panic attack is defined by the American Psy- chiatric Association as a sudden onset of intense fear or terror, often associated with a fear of dying, going crazy, or doing something uncon- trollable. Symptoms include dizziness, difficulty breathing, chest pain, trembling, sweating, hot and cold flashes, choking sensations, and tingling in the hands or feet.

In a study of 410 adults, researchers at the University of Houston Department of Psychol- ogy have found that nearly 15% (61) suffered such attacks. Most (58) experienced infrequent panic attacks, but 6% (3) of that group had three or more attacks in a three-week period, with four to 12 symptoms during each attack, according to a report in volume 2 of the 1988 edition of Jour- nal of Anxiety Disorders.

The most common (90%) coping response was to discuss the matter with a spouse or friend. Other responses included ignoring the attack (40%), avoiding the situation that caused panic (34%), and seeking medical help (30%). Fourteen people (23%) took tranquilizers or other medications.

Researchers say this type of behavior may indicate an early stage of clinical anxiety disorders. It also implies that general avoidance behavior, common in agoraphobia, may result from spontaneous panic attacks.

Noninvasive Finger Cuff Measures Blood Pressure A new method of measuring blood pressure has been developed that is both continuous and noninvasive, according to a press release from the American Society of Anesthesiologists. The device is a small cuff that fits around a patient’s finger. Infrared beams from the cuff shine through the tissue in the finger and measure the pressure of the blood flow from one heart beat to the next.

Using 15 high-risk surgical patients, physicians at the Pennsylvania State University, University Park, compared the finger cuff to a commonly used invasive technique. The intraarterial pressure (IAP) technique uses a thin tube inserted into an artery to measure blood pressure. The traditional technique of using a cuff around the arm was not used in the study because it does not provide continuous monitoring.

A computer was used to compare the mea- surements of both methods. The readings from the finger cuff method agreed with the IAP mea- surements about 84% of the time. Because of these transient differences, researchers recom- mend using the finger cuff in situations when more information than the traditional cuff around the arm is necessary, but not in situations when accurate, continuous blood pressure monitoring is essential.

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arterial blood gases: as easy as a b g

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