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THE ABCs of Arterial Blood Gasses
PATHO CORNER
THE ABCs of Arterial Blood Gasses Kim A. Noble, PhD, RN, CPAN
THE RAPID ANALYSIS, interpretation, and treatment of abnormal lab values is imperative for all perioperative patients, and this is especially true for the critically ill patient in the Phase I PACU. Because arterial blood gas (ABG) analysis is the most frequently performed laboratory testing in critically ill patients,1 the ability to accurately interpret and report abnormal results is required by the PACU nurse. This column begins with a case study of a fictitious patient with abnormal ABG results, followed by a description of normal acid base balance, forms of compensation, and common abnormalities associated with blood gas derangement.
100% oxygen, 2 mg midazolam, 100 mcg fentanyl, 200 mg propofol, and succinylcholine. Surgical anesthesia was maintained with nitrous oxide, sevoflurane, and vecuronium, and 10 mg of morphine sulfate was given in divided doses during the final hour of the procedure. He was not reversed and is planned for overnight ventilation. AA’s blood pressure was slightly labile during the procedure, and he was treated with intermittent fluid boluses. His estimated blood loss was 1,800 mL; he received 4,000 mL of normal saline solution (NSS), 1,500 mL of lactated Ringer’s, and 3 units of packed red blood cells (1,075 mL).
Arnold Aneurysm (AA) is a 62-year-old male who was emergently admitted to the hospital after reporting approximately 45 minutes of severe, midline ‘‘tearing’’ abdominal pain. He was taken for a computerized axial tomography (CAT/CT) scan and was found to have a 7-cm dissecting abdominal aneurysm. He was transferred immediately to the operating room.
Kim A. Noble, PhD, RN, CPAN, is an Assistant Professor at Temple University, Philadelphia, PA, USA. Address correspondence to Dr Kim A. Noble, Department of Nursing, Temple University, 3307 Broad St, Philadelphia, PA 19140; e-mail address: [email protected]. Ó 2009 by American Society of PeriAnesthesia Nurses 1089-9472/09/2406-0010$36.00/0 doi:10.1016/j.jopan.2009.08.005
Mr. AA has a past medical history of smoking approximately 112⁄ packs per day for 40 years, hypertension treated daily with losartan, high serum cholesterol controlled with simvastatin, angina, and prostatic hypertrophy. AA’s surgical history includes only a tonsillectomy at age 8. His preoperative lab work was minimal because of the emergent need for surgery, and it included a type and screen, hemoglobin 14.9 g/dL and hematocrit 46%, Na1 141 mEq/L; Cl2 98 mEq/L; K1 3.1 mEq/L. Your admission assessment includes the following: unresponsive, overweight adult male; sinus tachycardia, rate 112 beats/ minute with rare unifocal premature ventricular contractions; BP 102/61; femoral pulse present on the left femoral area. Right popliteal pulse is palpable and distal pulses present with use of Doppler only. Feet are cool to the touch with decreased refill. AA is intubated orally with an 8.0 endotracheal tube (ETT) taped at the 12-cm lip mark. Ventilator settings include 70% FIO2, assist/control at a rate of 14 breaths/minute, tidal volume 650 mL. Bilateral breath sounds are present with rhonchi scattered throughout. A large midline abdominal dressing is dry and intact. He has a nasogastric tube (NGT) that is connected to low suction and is draining scanty dark bilious fluid. Mr. AA has a urinary catheter in place that is draining clear light yellow urine. He has bilateral large-bore intravenous lines and has NSS infusing rapidly into each one. He is noted to have very cool skin and a tympanic temperature of 93.2 F. A forced-air warming device is applied. After 30 minutes in the PACU, the following lab results are obtained: Na1 146 mEq/L; Cl2 101 mEq/L; K1 4.0 mEq/ L; Ca11 7.2 mg/dL; Mg11 1.2 mg/dL; Hgb. 7.1; Hct 29%; platelets 130,000; PT 14.3 seconds; International
Journal of PeriAnesthesia Nursing, Vol 24, No 6 (December), 2009: pp 401-405
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You are post-call and arrive for work as scheduled at 1600 hours. You assume care, receive report on several patients, and are told of the difficult abdominal aortic aneurysm (AAA) repair that is underway. At 1830 you are notified of the impending arrival of Mr. AA to the Phase I PACU, and a ventilator is requested. You currently do not have a patient assignment, so you are assigned to set up a critical care bay for AA’s arrival. Mr. AA arrives at 1910 with a fanfare of personnel and equipment. He has undergone an open AAA repair with cross-clamping of the aorta above the renal arteries, lasting 95 minutes. The procedure took over 4 hours and was complicated by blood loss and a left femoral embolectomy. Mr. AA received a rapid-sequence induction with
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Normalized Ratio (INR) 1.0; PTT 50 seconds; pH 7.31; PCO2 41 mm Hg; PO2 212 mm Hg, HCO3– 18 mmol/L; saturation 100%. Lab results reported an additional 4 units of PRBCs are to be crossed and 2 units infused; 10 units of platelets are to be infused and the FIO2 on the ventilator reduced to 50% and repeat ABG labs 30 minutes after the change in ventilator settings.
The Physiology of Acid-Base Balance A delicate balance between acid and base is closely maintained in the human body and if the scale tips with changes in metabolism, mechanisms are built in to again balance the scale. The measurement of the concentration acid or H1 ions is termed pH and the amount of acid in the body is inversely proportional to the pH; as acid accumulates, the pH declines in an inverse fashion and losses of acid lead to an increased pH. The process of metabolism leads to the production of acidic byproducts both in the production of adenosine triphosphate (ATP) from glucose and fat, termed fixed acids, and again as ATP is degraded, to provide energy for body processes,2 termed volatile acids. Fixed acids, such as ketone bodies, released when fat is broken down or lactic acid produced by anaerobic metabolism are strong acids and are usually produced in relatively small amounts. Carbonic acid (H2CO3) is a volatile acid produced when CO2 is combined with water to form the weak carbonic acid (Fig 1). Volatile acids are produced in large quantities by cellular metabolism from the break-down of ATP. The balance between acid and buffers in the body is pH homeostasis, maintained in a narrow range of 7.35 to 7.45. Acidosis is seen if the pH declines below 7.35 and alkalosis if the pH rises above 7.45. Finally, the scale can be tipped by altering either substance in balance. For instance, acidosis or a decrease in pH can follow either an increase in the production of acid or a loss of buffer from the body.
Acid-Base Compensation Three mechanisms are found in the body to maintain the pH within its normal, narrow range. These compensatory mechanisms differ in their action and timing, but their final outcome of a normalized pH in consistent. The goal of a compensatory mechanism is not to correct the original problem but to do whatever is necessary to normalize the pH homeostasis. The three mechanisms will be described briefly in the sequence based on the timing of their response. When metabolic changes affect pH, the protein buffer system is immediately put to use. Proteins, present in all body cells and in the blood, are amphoteric and can function as either an acid or a base.3 These proteins have a variety of functions based on location and provide a tremendous source of ‘‘hidden’’ buffer, immediately accessible for alterations in pH. For instance, as H1 begins to accumulate in the body or HCO3– or bicarbonate is lost,
KIM A. NOBLE
Figure 1. Production of carbonic acid from CO2 and water. This figure is available in color online at www.jopan.org.
a hydrogen-potassium (H1/K1) exchange mechanism immediately shuttles the excess H1 into the cell in exchange for K1. The addition of acid is accommodated by the intracellular protein acting as a buffer. The movement of K1 from the intracellular to extracellular space leads to the rise in serum K1 associated with an acidotic pH. This first compensation is very efficient—limited because only so much acid can move into the cell before it will affect intracellular pH homeostasis. The second compensatory mechanism, mobilized with alterations in pH, is the respiratory system. Carbon dioxide (CO2) is enzymatically combined with water to form carbonic acid, a weak acid (Fig 1). Manipulating the amount of CO2 by changing ventilation is the second mechanism to compensate for changes in pH. For example, as the pH increases or becomes alkalotic, ventilation decreases, retaining CO2 and therefore forming carbonic acid, which in turn leads to normalization of the pH. In diabetic ketoacidosis, characteristic increases in ventilatory rate and depth, termed Kussmal respirations, are used to eliminate CO2 and normalize the pH. Compensation for pH abnormalities with the manipulation of CO2 levels begins within minutes of pH abnormalities, but is limited to approximately 12 to 24 hours because of the impact on respiration. Although respiratory compensation has only approximately 50% to 75% efficiency as a buffer system,3 large swings in pH are prevented until the third, much more efficient compensation is activated. The third compensatory mechanism for alterations in pH is the activity of the renal system. The kidney works in two ways: the first is a ‘‘buy one, get one free’’ manner when dealing with volatile acid. Because of the action of carbonic anhydrase (CA), an enzyme found in both intracellular and extracellular fluids (Fig 1), CO2 can be manipulated so that it is separated into an acid (H1) and a buffer (HCO3–). This enzyme enables the kidney to excrete H1 in the urine while reabsorbing HCO3– back into the bloodstream. This is a ‘‘buy one, get one free’’ because in the same mechanism, the kidney eliminates an acid to restore pH as well as recycles a buffer, which further restores pH. The kidney also excretes fixed acids into the urine, as would be present with the elimination of ketones with dieting or starvation. Finally, the kidney reabsorbs or recycles filtered bicarbonate from the renal tubule back into the venous circulation. The kidney is responsible for the long-term compensation for abnormalities in pH homeostasis, but it takes time for these mechanisms to become active.
PATHO CORNER
Arterial Blood Gas Abnormalities Metabolic Acidosis Metabolic acidosis occurs whenever there is a reduction of bicarbonate or an increased production or accumulation of fixed acid. One of the most common types of metabolic acidosis is lactic acidosis after decreased tissue perfusion and anaerobic metabolism. Lactic acid accumulates because of limited processing of glucose as a fuel by the lack of an adequate oxygen supply. As lactic acid accumulates, the bicarbonate level decreases. This results in a decrease in both the pH and the bicarbonate levels on ABG analysis. A second method of increasing the production of acid is present in any disorder where fat is being broken down by the liver as a fuel. The byproduct of fat metabolism is ketoacids that can accumulate, decrease available bicarbonate, and lead to metabolic acidosis. Diabetic ketoacidosis (DKA) is a common disorder that leads to the development of metabolic acidosis from the increased production of ketoacids as fat is used to produce ATP because of a lack of insulin. Ketoacidosis may also be seen in malnutrition or with the elimination of carbohydrates from the diet. Metabolic acidosis may follow the ingestion of acid as would be seen in salicylate toxicity from aspirin overdosage. It may also be present in renal failure from the loss of the renal excretion of acid and reabsorption of bicarbonate. Finally, metabolic acidosis may be present in disorders where bicarbonate-rich fluids are lost, as would be seen in severe diarrhea, small bowel disease, fistula formation in the biliary system, pancreatic disease, or prolonged intestinal suction.3 With acidotic disorders, the H1/K1 exchange mechanism (the first compensatory mechanism) is active immediately and leads to the intracellular movement of the accumulating lactic acid (H1) in exchange for intracellular potassium (K1). This leads to an increase in the extracellular potassium and a rise in the serum K1. Metabolic Alkalosis Metabolic alkalosis is caused by any disorder that leads to a loss of fixed acid or increases bicarbonate and pH levels. A common cause of temporary metabolic alkalosis is the ingestion of bicarbonate-containing antacids. The kidney rapidly compensates for the increased buffer by increasing the excretion of bicarbonate in the urine.3 A second cause of metabolic alkalosis is gastrointestinal suction, leading to the loss of gastric hydrochloric acid (HCl). This disorder would follow any condition, which would cause prolonged vomiting or nasogastric suction.
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As with acidotic disorders, in alkalosis the H1/K1 exchange mechanism is active immediately and H1 is scavenged from the intracellular space to the extracellular space in exchange for intracellular potassium (K1). The loss of K1 from the extracellular compartment would lead to a decrease in the extracellular potassium and hypokalemia or decreased serum K1. Respiratory Acidosis Respiratory acidosis follows any disorder that interferes with oxygen (O2) and carbon dioxide (CO2) movement in the lung. This classification of acid-base derangement can be further divided into two disorders: acute disorders, which occur rapidly and do not allow the kidney the time needed for a compensatory response; or chronic disorders, where the kidney is able to compensate for the decreased pH by excreting H1 in the urine and reabsorbing HCO3–. In renal compensation, the pH would normalize and the bicarbonate levels would increase to compensate for the increased CO2 levels seen in longstanding lung disease. Respiratory acidosis and hypoventilation is common in patients emerging from anesthesia. As mentioned before, because of the activity of the H1/ K1 exchange mechanism in acidosis, hyperkalemia, or a rise in K1, should be anticipated. Respiratory Alkalosis Respiratory alkalosis may be seen in any disorder characterized by an increase in ventilatory rate, leading to a reduction in CO2 and an increase in pH. A common cause of the acid-base imbalance could be seen in anxiety attacks, causing an increase in the rate and depth of breathing. Respiratory alkalosis could also be seen in high altitudes or increased tidal volume or ventilatory rate of mechanical ventilation.3 As mentioned before, because of the activity of the H1/K1 exchange mechanism in alkalosis, hypokalemia, or a decrease in K1, should be anticipated.
Arterial Blood Gas Analysis A simplistic approach to acid-base interpretation will help ease the analysis of the many involved factors. I suggest first analyzing the pH. The normal range for the pH is between 7.35 and 7.45. If the pH is , 7.35, the patient is experiencing acidosis; if it is between 7.35 and 7.45, the acid-base relationship is in balance; if the pH is .7.45 the patient is alkalotic. By first giving the disorder a last name, you narrow the possibilities by half and refine your analysis. I advise using arrows to indicate the direction of the abnormality of the pH and to make further analysis easier. The arrow technique is also very useful to identify compensatory changes in the ABG values because the arrows identify the change caused by disease or because of compensation.
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Figure 2. Respiratory acidosis. This figure is available in color online at www.jopan.org.
My second step is to look at the PCO2 as the lungs become involved in compensation before the kidney. If the acidbase derangement has a respiratory cause, the arrows will appear in different directions. For example, if the pH arrow decreases, indicating acidosis, it would be a respiratory cause when the PCO2 is increased (Fig 2). If the pH arrow indicates an increase—alkalosis—it is a respiratory cause when the PCO2 is decreased. The next step in ABG analysis is to look at the HCO3– to determine whether the cause of the derangement is metabolic. In this instance, the arrows point in the same direction or, as the pH decreases in metabolic acidosis, the HCO3– also decreases (Fig 3). Confusion arises when there is compensation by the body to normalize the pH. This is the status quo in chronic respiratory acidosis because the compensation by the kidney balances the increased CO2 so the pH is in a more normal range. Again, the arrows will help you to identify the compensation because you will be able to identify which is disease and which is compensation by their direction (Fig 4).
Implications for the PACU Patient The admission of a critically ill patient into the Phase I PACU can be very challenging and may require many hands. The analysis of received laboratory measurement data adds to the workload of the perianesthesia nurse. Rapid analysis and consultation with the anesthesia care provider is required if indicated by the analysis. A thorough understanding of the physiologic mechanisms that govern acid-base balance can help the perianesthesia nurse with the analysis and interpretation of ABG values, ensuring rapid communication and treatment of developing disorders. Alteration in Respiratory Function A rapid respiratory assessment is completed upon admission to the Phase I PACU for patients with artificial airways
Figure 3. Metabolic acidosis. This figure is available in color online at www.jopan.org.
KIM A. NOBLE
Figure 4. Compensated chronic respiratory acidosis.This figure is available in color online at www.jopan.org.
in place. Ventilation, bilateral expansion, and auscultation of breath sounds is a first priority to determine whether there has been any misplacement of the ETT upon transfer from the operating room and the PACU. The ETT should be well-secured and the exact placement noted by the placement of the incremental markings on the ETT and the patient’s lip. A portable chest x-ray should be obtained for ETT placement if it has not already been completed. Preparation for an intubated patient should include the set-up of a mechanical ventilator using the settings received from the anesthesia care provider. The patient should be placed on the ventilator after auscultation of breath sounds using the bag-mask-valve ventilation device. Suction should be immediately available and used as indicated to clear airway secretions. Continuous measurement of oxygen saturation (SaO2) is indicated and any noted abnormalities should be reported immediately to the anesthesia care provider. ABG samples should be obtained, results received and reported to the anesthesia care provider, and changes in mechanical ventilation made as ordered. If the blood pressure is stable, the head of the bed should be elevated to facilitate improved gas exchange. Alteration in Cardiovascular Function Continuous cardiac monitoring is used for any patient recovering from general anesthesia. Rare ventricular ectopy warrants attention, but may be caused by many factors and is only concerning if the frequency of ectopy increases. Maintenance of blood pressure is imperative in vascular surgery patients to ensure perfusion and adequate blood flow through the grafts and to prevent clotting. Parameters for treatment should be received from the anesthesia care provider and fluid challenges or vasoactive medications used as indicated. Peripheral pulses should be noted at admission and monitored hourly, and any changes reported to the anesthesia care provider and the surgeon. A visual assessment of the skin should also be completed for any areas of pressure or swelling. The condition of dressings and presence of drains should be noted, with documentation of the character, quantity, and consistency of drainage per policy. Postoperative electrocardiogram or troponin levels may be ordered because of the stress and increased workload cross-clamping the aorta places on the heart.4
PATHO CORNER
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Alteration in Temperature Balance Mr. AA’s hypothermia is a common finding after an open abdominal repair of an aortic aneurysm.4 Slow, active rewarming should be initiated and carefully monitored for improvement. AA’s metabolic acidosis may worsen as the vasculature dilates with rewarming and moves lactic acid that has been trapped in tissues because of vasoconstriction into the core circulation. Alteration in Acid-Base Balance AA’s ABG results (pH 7.31; PCO2 41 mm Hg; PO2 212 mm Hg, CO3– 18 mmol/L; saturation 100%) indicate a metabolic acidosis most likely a result of the length of time of cross clamping, hypotension, hypothermia, and embolization of the left leg. All of these factors would decrease tissue perfusion, leading to a switch from aerobic to anaerobic metabolism and the increased production of lactic acidosis. There is no respiratory compensation because AA is paralyzed and mechanically ventilated. With AA’s past medical history of long-term smoking, a baseline ABG analysis would be expected to reveal compensated chronic respiratory acidosis. The incremental administration of sodium bicarbonate (Na1HCO3–) may be indicated for the short-term correction of the lactic acidosis as AA rewarms. This will be governed by serial ABG analysis. Alteration in Fluid and Electrolyte Balance Mr. AA has had a major blood loss and received replacement fluids. Laboratory measurement of hemoglobin and hematocrit should be obtained quickly and the patient should receive additional blood products and fluid replenishment as indicated. Blood replacement orders have already been received for AA and should be initiated as soon as the blood products are available. Cross-clamping the aorta may cause renal ischemia and predispose the patient to acute renal failure.4 The need for hourly urine outputs is imperative and the effects of fluid mobilization monitored and interventions initiated as ordered. AA has abnormal electrolyte values, indicating a need for replacement of calcium and magnesium. Although his potassium is within a normal range because of the extracel-
lular exchange of K1 associated with acidotic abnormalities, his serum potassium may decline as his acidosis improves. This may necessitate the replacement of potassium and may be the cause of the rare ventricular ectopy present on continuous cardiac monitoring. Alteration in Hemostasis Careful assessment should be made of incisional sites for signs of bleeding or hematoma. Patients may receive heparin, an anticoagulant for embolectomy, and may be at risk for bleeding. Coagulation studies should be obtained and blood products should be administered as ordered. AA’s abnormal coagulation studies (platelets 130,000; PT 14.3 seconds; INR 1.0; PTT 50 sec) place him at increased risk for bleeding, and replacement of platelets or fresh frozen plasma (FFP) should be anticipated and initiated as ordered. Potential for Pain Although AA was not reversed, he may experience surgical pain because paralytic agents do not have any analgesic qualities. A ventilatory plan should be obtained from the anesthesia care provider. If the patient is to remain mechanically ventilated, incremental doses of an opioid should be provided. If the plan is to wean and extubate AA, effective pain relief will facilitate respiratory function in a patient with a large abdominal incision. Alteration in Gastrointestinal Function As with any patient undergoing abdominal surgery, AA’s Phase I care needs to include ongoing assessment of his abdominal and femoral dressings and NGT placement and drainage. Any abnormalities should be quickly reported to the anesthesia care provider and the surgical team. In conclusion, the skills needed for rapid assessment of ABG analysis mimic many other skills, where practice makes perfect. A comprehensive understanding of the physiologic mechanisms in place to facilitate acid-base balance is important for the rapid analysis of laboratory results, which is required when caring for a critically ill patient.
References 1. Diby M, Merlani M, Garnerin P, et al. Harmonization of practice among different groups of caregivers: A guideline on arterial blood gas utilization. J Nurs Care Qual. 2005;20:327-334. 2. Ruholl L. Arterial blood gases: Analysis and nursing responsibilities. MEDSURG Nurs. 2006;15:343-350.
3. Porth CM, Mattison G. Pathophysiology: Concepts of Altered Health States. 8th ed. Philadelphia: Lippincott Williams & Wilkins; 2009. 4. Drain CB, Odom-Forren J. PeriAnesthesia Nursing: A Critical Care Approach. 5th ed. St. Louis, MO: Saunders; 2009.
THE ABCs of Arterial Blood Gasses Kim A. Noble, PhD, RN, CPAN
THE RAPID ANALYSIS, interpretation, and treatment of abnormal lab values is imperative for all perioperative patients, and this is especially true for the critically ill patient in the Phase I PACU. Because arterial blood gas (ABG) analysis is the most frequently performed laboratory testing in critically ill patients,1 the ability to accurately interpret and report abnormal results is required by the PACU nurse. This column begins with a case study of a fictitious patient with abnormal ABG results, followed by a description of normal acid base balance, forms of compensation, and common abnormalities associated with blood gas derangement.
100% oxygen, 2 mg midazolam, 100 mcg fentanyl, 200 mg propofol, and succinylcholine. Surgical anesthesia was maintained with nitrous oxide, sevoflurane, and vecuronium, and 10 mg of morphine sulfate was given in divided doses during the final hour of the procedure. He was not reversed and is planned for overnight ventilation. AA’s blood pressure was slightly labile during the procedure, and he was treated with intermittent fluid boluses. His estimated blood loss was 1,800 mL; he received 4,000 mL of normal saline solution (NSS), 1,500 mL of lactated Ringer’s, and 3 units of packed red blood cells (1,075 mL).
Arnold Aneurysm (AA) is a 62-year-old male who was emergently admitted to the hospital after reporting approximately 45 minutes of severe, midline ‘‘tearing’’ abdominal pain. He was taken for a computerized axial tomography (CAT/CT) scan and was found to have a 7-cm dissecting abdominal aneurysm. He was transferred immediately to the operating room.
Kim A. Noble, PhD, RN, CPAN, is an Assistant Professor at Temple University, Philadelphia, PA, USA. Address correspondence to Dr Kim A. Noble, Department of Nursing, Temple University, 3307 Broad St, Philadelphia, PA 19140; e-mail address: [email protected]. Ó 2009 by American Society of PeriAnesthesia Nurses 1089-9472/09/2406-0010$36.00/0 doi:10.1016/j.jopan.2009.08.005
Mr. AA has a past medical history of smoking approximately 112⁄ packs per day for 40 years, hypertension treated daily with losartan, high serum cholesterol controlled with simvastatin, angina, and prostatic hypertrophy. AA’s surgical history includes only a tonsillectomy at age 8. His preoperative lab work was minimal because of the emergent need for surgery, and it included a type and screen, hemoglobin 14.9 g/dL and hematocrit 46%, Na1 141 mEq/L; Cl2 98 mEq/L; K1 3.1 mEq/L. Your admission assessment includes the following: unresponsive, overweight adult male; sinus tachycardia, rate 112 beats/ minute with rare unifocal premature ventricular contractions; BP 102/61; femoral pulse present on the left femoral area. Right popliteal pulse is palpable and distal pulses present with use of Doppler only. Feet are cool to the touch with decreased refill. AA is intubated orally with an 8.0 endotracheal tube (ETT) taped at the 12-cm lip mark. Ventilator settings include 70% FIO2, assist/control at a rate of 14 breaths/minute, tidal volume 650 mL. Bilateral breath sounds are present with rhonchi scattered throughout. A large midline abdominal dressing is dry and intact. He has a nasogastric tube (NGT) that is connected to low suction and is draining scanty dark bilious fluid. Mr. AA has a urinary catheter in place that is draining clear light yellow urine. He has bilateral large-bore intravenous lines and has NSS infusing rapidly into each one. He is noted to have very cool skin and a tympanic temperature of 93.2 F. A forced-air warming device is applied. After 30 minutes in the PACU, the following lab results are obtained: Na1 146 mEq/L; Cl2 101 mEq/L; K1 4.0 mEq/ L; Ca11 7.2 mg/dL; Mg11 1.2 mg/dL; Hgb. 7.1; Hct 29%; platelets 130,000; PT 14.3 seconds; International
Journal of PeriAnesthesia Nursing, Vol 24, No 6 (December), 2009: pp 401-405
401
You are post-call and arrive for work as scheduled at 1600 hours. You assume care, receive report on several patients, and are told of the difficult abdominal aortic aneurysm (AAA) repair that is underway. At 1830 you are notified of the impending arrival of Mr. AA to the Phase I PACU, and a ventilator is requested. You currently do not have a patient assignment, so you are assigned to set up a critical care bay for AA’s arrival. Mr. AA arrives at 1910 with a fanfare of personnel and equipment. He has undergone an open AAA repair with cross-clamping of the aorta above the renal arteries, lasting 95 minutes. The procedure took over 4 hours and was complicated by blood loss and a left femoral embolectomy. Mr. AA received a rapid-sequence induction with
402
Normalized Ratio (INR) 1.0; PTT 50 seconds; pH 7.31; PCO2 41 mm Hg; PO2 212 mm Hg, HCO3– 18 mmol/L; saturation 100%. Lab results reported an additional 4 units of PRBCs are to be crossed and 2 units infused; 10 units of platelets are to be infused and the FIO2 on the ventilator reduced to 50% and repeat ABG labs 30 minutes after the change in ventilator settings.
The Physiology of Acid-Base Balance A delicate balance between acid and base is closely maintained in the human body and if the scale tips with changes in metabolism, mechanisms are built in to again balance the scale. The measurement of the concentration acid or H1 ions is termed pH and the amount of acid in the body is inversely proportional to the pH; as acid accumulates, the pH declines in an inverse fashion and losses of acid lead to an increased pH. The process of metabolism leads to the production of acidic byproducts both in the production of adenosine triphosphate (ATP) from glucose and fat, termed fixed acids, and again as ATP is degraded, to provide energy for body processes,2 termed volatile acids. Fixed acids, such as ketone bodies, released when fat is broken down or lactic acid produced by anaerobic metabolism are strong acids and are usually produced in relatively small amounts. Carbonic acid (H2CO3) is a volatile acid produced when CO2 is combined with water to form the weak carbonic acid (Fig 1). Volatile acids are produced in large quantities by cellular metabolism from the break-down of ATP. The balance between acid and buffers in the body is pH homeostasis, maintained in a narrow range of 7.35 to 7.45. Acidosis is seen if the pH declines below 7.35 and alkalosis if the pH rises above 7.45. Finally, the scale can be tipped by altering either substance in balance. For instance, acidosis or a decrease in pH can follow either an increase in the production of acid or a loss of buffer from the body.
Acid-Base Compensation Three mechanisms are found in the body to maintain the pH within its normal, narrow range. These compensatory mechanisms differ in their action and timing, but their final outcome of a normalized pH in consistent. The goal of a compensatory mechanism is not to correct the original problem but to do whatever is necessary to normalize the pH homeostasis. The three mechanisms will be described briefly in the sequence based on the timing of their response. When metabolic changes affect pH, the protein buffer system is immediately put to use. Proteins, present in all body cells and in the blood, are amphoteric and can function as either an acid or a base.3 These proteins have a variety of functions based on location and provide a tremendous source of ‘‘hidden’’ buffer, immediately accessible for alterations in pH. For instance, as H1 begins to accumulate in the body or HCO3– or bicarbonate is lost,
KIM A. NOBLE
Figure 1. Production of carbonic acid from CO2 and water. This figure is available in color online at www.jopan.org.
a hydrogen-potassium (H1/K1) exchange mechanism immediately shuttles the excess H1 into the cell in exchange for K1. The addition of acid is accommodated by the intracellular protein acting as a buffer. The movement of K1 from the intracellular to extracellular space leads to the rise in serum K1 associated with an acidotic pH. This first compensation is very efficient—limited because only so much acid can move into the cell before it will affect intracellular pH homeostasis. The second compensatory mechanism, mobilized with alterations in pH, is the respiratory system. Carbon dioxide (CO2) is enzymatically combined with water to form carbonic acid, a weak acid (Fig 1). Manipulating the amount of CO2 by changing ventilation is the second mechanism to compensate for changes in pH. For example, as the pH increases or becomes alkalotic, ventilation decreases, retaining CO2 and therefore forming carbonic acid, which in turn leads to normalization of the pH. In diabetic ketoacidosis, characteristic increases in ventilatory rate and depth, termed Kussmal respirations, are used to eliminate CO2 and normalize the pH. Compensation for pH abnormalities with the manipulation of CO2 levels begins within minutes of pH abnormalities, but is limited to approximately 12 to 24 hours because of the impact on respiration. Although respiratory compensation has only approximately 50% to 75% efficiency as a buffer system,3 large swings in pH are prevented until the third, much more efficient compensation is activated. The third compensatory mechanism for alterations in pH is the activity of the renal system. The kidney works in two ways: the first is a ‘‘buy one, get one free’’ manner when dealing with volatile acid. Because of the action of carbonic anhydrase (CA), an enzyme found in both intracellular and extracellular fluids (Fig 1), CO2 can be manipulated so that it is separated into an acid (H1) and a buffer (HCO3–). This enzyme enables the kidney to excrete H1 in the urine while reabsorbing HCO3– back into the bloodstream. This is a ‘‘buy one, get one free’’ because in the same mechanism, the kidney eliminates an acid to restore pH as well as recycles a buffer, which further restores pH. The kidney also excretes fixed acids into the urine, as would be present with the elimination of ketones with dieting or starvation. Finally, the kidney reabsorbs or recycles filtered bicarbonate from the renal tubule back into the venous circulation. The kidney is responsible for the long-term compensation for abnormalities in pH homeostasis, but it takes time for these mechanisms to become active.
PATHO CORNER
Arterial Blood Gas Abnormalities Metabolic Acidosis Metabolic acidosis occurs whenever there is a reduction of bicarbonate or an increased production or accumulation of fixed acid. One of the most common types of metabolic acidosis is lactic acidosis after decreased tissue perfusion and anaerobic metabolism. Lactic acid accumulates because of limited processing of glucose as a fuel by the lack of an adequate oxygen supply. As lactic acid accumulates, the bicarbonate level decreases. This results in a decrease in both the pH and the bicarbonate levels on ABG analysis. A second method of increasing the production of acid is present in any disorder where fat is being broken down by the liver as a fuel. The byproduct of fat metabolism is ketoacids that can accumulate, decrease available bicarbonate, and lead to metabolic acidosis. Diabetic ketoacidosis (DKA) is a common disorder that leads to the development of metabolic acidosis from the increased production of ketoacids as fat is used to produce ATP because of a lack of insulin. Ketoacidosis may also be seen in malnutrition or with the elimination of carbohydrates from the diet. Metabolic acidosis may follow the ingestion of acid as would be seen in salicylate toxicity from aspirin overdosage. It may also be present in renal failure from the loss of the renal excretion of acid and reabsorption of bicarbonate. Finally, metabolic acidosis may be present in disorders where bicarbonate-rich fluids are lost, as would be seen in severe diarrhea, small bowel disease, fistula formation in the biliary system, pancreatic disease, or prolonged intestinal suction.3 With acidotic disorders, the H1/K1 exchange mechanism (the first compensatory mechanism) is active immediately and leads to the intracellular movement of the accumulating lactic acid (H1) in exchange for intracellular potassium (K1). This leads to an increase in the extracellular potassium and a rise in the serum K1. Metabolic Alkalosis Metabolic alkalosis is caused by any disorder that leads to a loss of fixed acid or increases bicarbonate and pH levels. A common cause of temporary metabolic alkalosis is the ingestion of bicarbonate-containing antacids. The kidney rapidly compensates for the increased buffer by increasing the excretion of bicarbonate in the urine.3 A second cause of metabolic alkalosis is gastrointestinal suction, leading to the loss of gastric hydrochloric acid (HCl). This disorder would follow any condition, which would cause prolonged vomiting or nasogastric suction.
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As with acidotic disorders, in alkalosis the H1/K1 exchange mechanism is active immediately and H1 is scavenged from the intracellular space to the extracellular space in exchange for intracellular potassium (K1). The loss of K1 from the extracellular compartment would lead to a decrease in the extracellular potassium and hypokalemia or decreased serum K1. Respiratory Acidosis Respiratory acidosis follows any disorder that interferes with oxygen (O2) and carbon dioxide (CO2) movement in the lung. This classification of acid-base derangement can be further divided into two disorders: acute disorders, which occur rapidly and do not allow the kidney the time needed for a compensatory response; or chronic disorders, where the kidney is able to compensate for the decreased pH by excreting H1 in the urine and reabsorbing HCO3–. In renal compensation, the pH would normalize and the bicarbonate levels would increase to compensate for the increased CO2 levels seen in longstanding lung disease. Respiratory acidosis and hypoventilation is common in patients emerging from anesthesia. As mentioned before, because of the activity of the H1/ K1 exchange mechanism in acidosis, hyperkalemia, or a rise in K1, should be anticipated. Respiratory Alkalosis Respiratory alkalosis may be seen in any disorder characterized by an increase in ventilatory rate, leading to a reduction in CO2 and an increase in pH. A common cause of the acid-base imbalance could be seen in anxiety attacks, causing an increase in the rate and depth of breathing. Respiratory alkalosis could also be seen in high altitudes or increased tidal volume or ventilatory rate of mechanical ventilation.3 As mentioned before, because of the activity of the H1/K1 exchange mechanism in alkalosis, hypokalemia, or a decrease in K1, should be anticipated.
Arterial Blood Gas Analysis A simplistic approach to acid-base interpretation will help ease the analysis of the many involved factors. I suggest first analyzing the pH. The normal range for the pH is between 7.35 and 7.45. If the pH is , 7.35, the patient is experiencing acidosis; if it is between 7.35 and 7.45, the acid-base relationship is in balance; if the pH is .7.45 the patient is alkalotic. By first giving the disorder a last name, you narrow the possibilities by half and refine your analysis. I advise using arrows to indicate the direction of the abnormality of the pH and to make further analysis easier. The arrow technique is also very useful to identify compensatory changes in the ABG values because the arrows identify the change caused by disease or because of compensation.
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Figure 2. Respiratory acidosis. This figure is available in color online at www.jopan.org.
My second step is to look at the PCO2 as the lungs become involved in compensation before the kidney. If the acidbase derangement has a respiratory cause, the arrows will appear in different directions. For example, if the pH arrow decreases, indicating acidosis, it would be a respiratory cause when the PCO2 is increased (Fig 2). If the pH arrow indicates an increase—alkalosis—it is a respiratory cause when the PCO2 is decreased. The next step in ABG analysis is to look at the HCO3– to determine whether the cause of the derangement is metabolic. In this instance, the arrows point in the same direction or, as the pH decreases in metabolic acidosis, the HCO3– also decreases (Fig 3). Confusion arises when there is compensation by the body to normalize the pH. This is the status quo in chronic respiratory acidosis because the compensation by the kidney balances the increased CO2 so the pH is in a more normal range. Again, the arrows will help you to identify the compensation because you will be able to identify which is disease and which is compensation by their direction (Fig 4).
Implications for the PACU Patient The admission of a critically ill patient into the Phase I PACU can be very challenging and may require many hands. The analysis of received laboratory measurement data adds to the workload of the perianesthesia nurse. Rapid analysis and consultation with the anesthesia care provider is required if indicated by the analysis. A thorough understanding of the physiologic mechanisms that govern acid-base balance can help the perianesthesia nurse with the analysis and interpretation of ABG values, ensuring rapid communication and treatment of developing disorders. Alteration in Respiratory Function A rapid respiratory assessment is completed upon admission to the Phase I PACU for patients with artificial airways
Figure 3. Metabolic acidosis. This figure is available in color online at www.jopan.org.
KIM A. NOBLE
Figure 4. Compensated chronic respiratory acidosis.This figure is available in color online at www.jopan.org.
in place. Ventilation, bilateral expansion, and auscultation of breath sounds is a first priority to determine whether there has been any misplacement of the ETT upon transfer from the operating room and the PACU. The ETT should be well-secured and the exact placement noted by the placement of the incremental markings on the ETT and the patient’s lip. A portable chest x-ray should be obtained for ETT placement if it has not already been completed. Preparation for an intubated patient should include the set-up of a mechanical ventilator using the settings received from the anesthesia care provider. The patient should be placed on the ventilator after auscultation of breath sounds using the bag-mask-valve ventilation device. Suction should be immediately available and used as indicated to clear airway secretions. Continuous measurement of oxygen saturation (SaO2) is indicated and any noted abnormalities should be reported immediately to the anesthesia care provider. ABG samples should be obtained, results received and reported to the anesthesia care provider, and changes in mechanical ventilation made as ordered. If the blood pressure is stable, the head of the bed should be elevated to facilitate improved gas exchange. Alteration in Cardiovascular Function Continuous cardiac monitoring is used for any patient recovering from general anesthesia. Rare ventricular ectopy warrants attention, but may be caused by many factors and is only concerning if the frequency of ectopy increases. Maintenance of blood pressure is imperative in vascular surgery patients to ensure perfusion and adequate blood flow through the grafts and to prevent clotting. Parameters for treatment should be received from the anesthesia care provider and fluid challenges or vasoactive medications used as indicated. Peripheral pulses should be noted at admission and monitored hourly, and any changes reported to the anesthesia care provider and the surgeon. A visual assessment of the skin should also be completed for any areas of pressure or swelling. The condition of dressings and presence of drains should be noted, with documentation of the character, quantity, and consistency of drainage per policy. Postoperative electrocardiogram or troponin levels may be ordered because of the stress and increased workload cross-clamping the aorta places on the heart.4
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Alteration in Temperature Balance Mr. AA’s hypothermia is a common finding after an open abdominal repair of an aortic aneurysm.4 Slow, active rewarming should be initiated and carefully monitored for improvement. AA’s metabolic acidosis may worsen as the vasculature dilates with rewarming and moves lactic acid that has been trapped in tissues because of vasoconstriction into the core circulation. Alteration in Acid-Base Balance AA’s ABG results (pH 7.31; PCO2 41 mm Hg; PO2 212 mm Hg, CO3– 18 mmol/L; saturation 100%) indicate a metabolic acidosis most likely a result of the length of time of cross clamping, hypotension, hypothermia, and embolization of the left leg. All of these factors would decrease tissue perfusion, leading to a switch from aerobic to anaerobic metabolism and the increased production of lactic acidosis. There is no respiratory compensation because AA is paralyzed and mechanically ventilated. With AA’s past medical history of long-term smoking, a baseline ABG analysis would be expected to reveal compensated chronic respiratory acidosis. The incremental administration of sodium bicarbonate (Na1HCO3–) may be indicated for the short-term correction of the lactic acidosis as AA rewarms. This will be governed by serial ABG analysis. Alteration in Fluid and Electrolyte Balance Mr. AA has had a major blood loss and received replacement fluids. Laboratory measurement of hemoglobin and hematocrit should be obtained quickly and the patient should receive additional blood products and fluid replenishment as indicated. Blood replacement orders have already been received for AA and should be initiated as soon as the blood products are available. Cross-clamping the aorta may cause renal ischemia and predispose the patient to acute renal failure.4 The need for hourly urine outputs is imperative and the effects of fluid mobilization monitored and interventions initiated as ordered. AA has abnormal electrolyte values, indicating a need for replacement of calcium and magnesium. Although his potassium is within a normal range because of the extracel-
lular exchange of K1 associated with acidotic abnormalities, his serum potassium may decline as his acidosis improves. This may necessitate the replacement of potassium and may be the cause of the rare ventricular ectopy present on continuous cardiac monitoring. Alteration in Hemostasis Careful assessment should be made of incisional sites for signs of bleeding or hematoma. Patients may receive heparin, an anticoagulant for embolectomy, and may be at risk for bleeding. Coagulation studies should be obtained and blood products should be administered as ordered. AA’s abnormal coagulation studies (platelets 130,000; PT 14.3 seconds; INR 1.0; PTT 50 sec) place him at increased risk for bleeding, and replacement of platelets or fresh frozen plasma (FFP) should be anticipated and initiated as ordered. Potential for Pain Although AA was not reversed, he may experience surgical pain because paralytic agents do not have any analgesic qualities. A ventilatory plan should be obtained from the anesthesia care provider. If the patient is to remain mechanically ventilated, incremental doses of an opioid should be provided. If the plan is to wean and extubate AA, effective pain relief will facilitate respiratory function in a patient with a large abdominal incision. Alteration in Gastrointestinal Function As with any patient undergoing abdominal surgery, AA’s Phase I care needs to include ongoing assessment of his abdominal and femoral dressings and NGT placement and drainage. Any abnormalities should be quickly reported to the anesthesia care provider and the surgical team. In conclusion, the skills needed for rapid assessment of ABG analysis mimic many other skills, where practice makes perfect. A comprehensive understanding of the physiologic mechanisms in place to facilitate acid-base balance is important for the rapid analysis of laboratory results, which is required when caring for a critically ill patient.
References 1. Diby M, Merlani M, Garnerin P, et al. Harmonization of practice among different groups of caregivers: A guideline on arterial blood gas utilization. J Nurs Care Qual. 2005;20:327-334. 2. Ruholl L. Arterial blood gases: Analysis and nursing responsibilities. MEDSURG Nurs. 2006;15:343-350.
3. Porth CM, Mattison G. Pathophysiology: Concepts of Altered Health States. 8th ed. Philadelphia: Lippincott Williams & Wilkins; 2009. 4. Drain CB, Odom-Forren J. PeriAnesthesia Nursing: A Critical Care Approach. 5th ed. St. Louis, MO: Saunders; 2009.