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Home , Arterial blood, Arterial blood gas test, Blood gas test

ARTERIAL GAS

NOAH CARPENTER, MD Dr. Noah Carpenter is a Thoracic and Peripheral Vascular Surgeon. He completed the Bachelor of Science in chemistry and medical school and training at the University of Manitoba. Dr. Carpenter completed surgical residency and fellowship at the University of Edmonton and Affiliated Hospitals in Edmonton, Alberta, and an additional Adult Cardiovascular and Thoracic fellowship at the University of Edinburgh, Scotland. He has specialized in microsurgical techniques, vascular endoscopy, laser and laparoscopic surgery in Brandon, Manitoba and Vancouver, British Columbia, Canada and in Colorado, Texas, and California. Dr. Carpenter has an Honorary Doctorate of Law from the University of Calgary, and was appointed a Citizen Ambassador to China, and has served as a member of the Native Physicians Association of Canada, the Canadian College of Health Service Executives, the Science Institute of the Northwest Territories, the Canada Science Council, and the International Society of Endovascular Surgeons, among others. He has been an inspiration to youth, motivating them to understand the importance of achieving higher education.

ABSTRACT The gas test (ABG) is one of the most common and useful tests performed by medical professionals. The ABG checks a patient’s arterial blood to determine acidity and levels of and in their blood. It is especially useful to determine whether oxygen is working for a patient or to reveal important information about a patient’s metabolic state. The goal of ABG is to assess the patient’s physiologic condition. Anatomical sites, techniques, and complications of the arterial and ABG interpretation is discussed. Interpretation of gases and detailed discussion of acid-base disturbances are discussed separately.

1 NurseCe4Less.com Policy Statement This activity has been planned and implemented in accordance with the policies of NurseCe4Less.com and the continuing nursing education requirements of the American Nurses Credentialing Center's Commission on Accreditation for registered nurses.

Continuing Education Credit Designation This educational activity is credited for 2.5 hours at completion of the activity.

Statement of Learning Need Health clinicians are often required to analyze respiratory, metabolic and mixed acid-base imbalances through ABG sampling. Clinicians often need to enhance and refresh their knowledge of ABG interpretation to understand cause and treatment of blood gas disorders relative to adult and pediatric conditions.

Course Purpose To provide health clinicians with basic knowledge of the ABG laboratory test and to be able to interpret values.

Target Audience Advanced Practice Registered Nurses, Registered Nurses, and other Interdisciplinary Health Team Members.

Disclosures Noah Carpenter, MD, William Cook, PhD, Douglas Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures. There is no commercial support.

2 NurseCe4Less.com Self-Assessment of Knowledge Pre-Test:

1. Which of the following puncture sites is preferred for obtaining a sample for an arterial blood gas (ABG) test?

a. femoral b. c. brachial artery d. axillary artery

2. Acid is a substance that ______a hydrogen ion.

a. accepts b. rejects c. absorbs d. donates

3. This molecule in the blood binds to and transports oxygen:

a. b. c. d. phosphate

4. A patient’s arterial blood gas (ABG) tests indicate that CO2 levels have decreased while pH levels have increased, which indicates a state of

a. b. c. atelectasis d. fibrosis

5. True or False: A blood sample obtained from a for a blood gas test has a richer of oxygen than a blood samples taken from an artery.

a. True b. False

3 NurseCe4Less.com Introduction

Arterial blood gas levels are often measured in acutely ill patients. ABG sampling is typically obtained to assess the physical state of patients with diabetic , kidney disease, failure, infection, and . The ABG test is not diagnostic by itself and should be used in conjunction with other examinations. The ABG test helps medical clinicians diagnose disorders that may cause acidosis or alkalosis in a patient. ABG laboratory collection may be difficult to perform in some patients, such as those with dehydration and the quality of the patient’s artery must be assessed prior to puncturing an artery for sampling. The indication, procedure and anatomic landmarks of the ABG test will be raised in later sections.

Purpose of the ABG Test

The arterial blood gas (ABG) test is performed to evaluate acid-base balance and function. It involves puncturing a patient’s artery and drawing blood with a thin needle. The most common puncture site is the radial artery; however, the femoral artery and the brachial artery may be used. Blood can also be drawn from an arterial catheter. Regardless of the chosen site, once the blood is drawn it is measured and analyzed for abnormalities in one of the following:1

● Acid-base disturbance identification and ● Partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) measurement ● Therapeutic intervention (i.e., insulin in a case of ) assessment ● Abnormal hemoglobin (i.e., and ) detection and quantification of blood levels ● Procurement of a blood sample in an acute emergency setting when venous sampling is not feasible

4 NurseCe4Less.com During most blood tests, blood is taken from the . However, during the ABG test a blood sample is drawn from the artery prior to it reaching the tissue of the body. Therefore, a blood sample obtained from an has a richer concentration of oxygen.

Arterial blood gas levels are often measured in acutely ill patients who show signs of respiratory distress.1 Other indications for ABG sampling include patients with diabetic ketoacidosis, kidney disease, heart failure, infection, and drug overdose.1,2 Results of the ABG test are not diagnostic and should be used in conjunction with other exams. The ABG sampling may be performed with tests such as BUN, , and measurements to evaluate and kidney function.

In addition to other medical conditions, the ABG test also helps clinicians investigate for disorders that may cause acidosis or alkalosis.1,2 The test uses a complex calculator, known as the A-a Gradient calculator to measure successful and oxygenation. Blood gas analyzers utilized during ABG testing also measure of hemoglobin, oxyhemoglobin, carboxyhemoglobin, methemoglobin, and lactate.1,2

To help understand how the results of the ABG test are interpreted, medical professionals must know basic physiologic principles of how the body maintains a state of homeostasis. By exploring the normal ranges, practitioners will better understand the significance of abnormal ABG results.

Normal Metabolic and Cellular Function

The human body requires a delicate balance between acid and base for normal metabolic and cellular function. This balance is achieved through buffering systems made up of both respiratory and metabolic functions. Any irregularity in one of these functions will result in imbalance.

Acid-Base

Acid is defined as any substance that can donate a hydrogen ion; and base encompasses any substance that can accept a hydrogen ion. Naturally,

5 NurseCe4Less.com acid contributes to an acidic state, while base contributes to an alkaline state.3,4 Three major classes classes of acid include:5

● Approximately 15,000 mmol (is increased with exercise) of carbon dioxide (CO2) is produced each day. When combined with water carbonic acid (H2CO3) is formed. ● Several thousand mmol/day of organic acids, such as and citric acid occur as a result of metabolic processes. Organic acids are metabolized to neutral products (such as glucose) and to CO2 and water. Steady state concentration of these acids in the extracellular fluid is relatively low and stable. ● Approximately 50 to 100 mEq of nonvolatile acid is produced each day (mostly sulfuric acid from sulfur-containing amino acids ).

Acid-base is a reflection of the pH in the body. This is the measurement of the concentration of acid or alkalinity in the body. It is directly influenced by bicarbonate (HCO3) and carbon dioxide (CO2). Normal cellular function in the body is maintained at blood H+ (hydrogen) concentration within a narrow range from typically 37 to 43 nmol/L (pH 7.43 to

7.37, where pH =−log [H+]) and ideally 40 nmol/L (pH = 7.40).3,4 Disturbances of these mechanisms can have serious clinical consequences.

Buffers

The respiratory and renal systems along with buffer mechanisms play an important role in regulating the body’s acid-base balance. The buffer system acts as the first line of defense to counteract fluctuations in pH levels.5 Large amounts of acids are generated that adults must metabolize to non-charged neutral molecules, buffered to avoid fatal acidemia, and expired or excreted.5

Acid-base balance is maintained by normal pulmonary excretion of carbon dioxide, metabolic utilization of organic acids, and renal excretion of nonvolatile acids.5 Renal excretion of acid occurs as a result of hydrogen ions combining with either urinary buffers to form titratable acid, such as

6 NurseCe4Less.com phosphate (HPO4- + H+ → H2PO4-), urate, and creatinine, or with ammonia to form ammonium (NH3 + H+ → NH4+).5

Acid-base status is usually assessed by measuring the components of the bicarbonate-carbon dioxide buffer system in blood:5

Dissolved CO2 + H2O ↔ H2CO3 ↔ HCO3- + H+

In an ABG test the of CO2 (PCO2) and the pH are each measured using analytical electrodes. The bicarbonate (HCO3-) concentration is then calculated with the Henderson-Hasselbalch equation. Generally, the PCO2 is reported in mmHg, and HCO3- in mEq/L.5 There are four blood buffers that combine with bicarbonate and hydrogen ions to help maintain normal blood pH. These buffers include the following values and percentages listed below.

Bicarbonate

Bicarbonate (HCO3) is an essential buffer system for the body and either a positive or negative fluctuation in this acid-base component will result in an imbalance. The normal ratio is twenty-parts HCO3 to one-part carbonic acid. This enzyme is found in intracellular and extracellular fluids and enables the kidneys to excrete H+ ions in the urine while reabsorbing bicarbonate into the blood.5 In this capacity, the kidney eliminates an acid to restore pH. The normal range of HCO3 is 22 to 26 mEq/L.

Hemoglobin

The hemoglobin molecule in the blood binds with and transports oxygen (O2). The total amount of oxygen transported by the blood is known as the oxygen content and the largest quantities are carried in hemoglobin and red blood cells. This is known as the oxygen-hemoglobin saturation 8,9 (SaO2), measured as a percentage. Normal ranges are 94% or greater.

7 NurseCe4Less.com Phosphate

The phosphate compound combines with substances in the body to help stabilize pH. It acts as a buffer in the intercellular fluid and in the urine in a similar manner as bicarbonate.8 Protein

Approximately three-quarters of the chemical buffering is accomplished within intracellular . Proteins are located in the blood and cells of the body and can function as either an acid or a base.6

Respiratory System

The also plays a role in the physiology of acid-base balance. The of oxygen during contributes to the exchange of oxygen and carbon dioxide at the cellular level. Carbon dioxide

(CO2) reacts with water to form carbonic acid, which helps to regulate pH. If

CO2 levels decrease, pH increases, which may result in a state of alkalosis. 5 The normal range pH serum CO2 level is from 35 to 45 mmHG.

Chemical-sensing cells, known as , regulate the respiratory system by monitoring CO2, oxygen (O2) levels, and acid concentration in the blood. If levels in any one of these changes, the chemoreceptors, located in the central nervous system, aorta, and carotid , alert the brain.5 Once these triggers are activated, the brain increases the breathing rate, which helps to restore pH back to normal. This does so by excreting excess CO2 from the blood, while increasing the rate of oxygen. The normal range of CO2 is 60 to 70 mmHg; any rate above this measurement acts as a depressant to the central nervous system and could ultimately result in respiratory arrest if left unchecked.5

Renal System

To maintain homeostasis, for every hydrogen ion secreted in the urine, a sodium ion is reabsorbed into the extracellular fluid. This action occurs in the renal tubes and allows the kidneys to regulate pH. Chloride and

8 NurseCe4Less.com potassium within the renal tubules also play a role in pH balance. A decrease in chloride can cause alkalosis, and elevated potassium levels can cause acidosis. High sodium levels may also contribute toward alkalosis due to the secretion of hydrogen.

Normal ABG Result Values

Partial pressure of oxygen (PaO2): 75 - 100 mmHg Partial pressure of carbon dioxide (PaCO2): 38 - 42 mmHg Arterial blood pH: 7.38 - 7.42 (SaO2): 94 - 100% Bicarbonate (HCO3): 22 - 28 mEq/L

Oxygen Level and Saturation

Along with acid-base balance, the ABG test assesses the patient’s oxygen level and oxygen saturation (SaO2). Oxygen in the pulmonary system is represented as a partial pressure of gas (PaO2). When this oxygen enters the alveoli, its normal concentration range is 80 mmHg to 100 mmHg.5 These alveoli receive oxygen with every breath, and the oxygen is then diffused into the lung. When the oxygen departs the alveoli to the pulmonary , carbon dioxide is exhaled from the .

In healthy patients, the ABG test will reveal normal levels of oxygen and carbon dioxide. The oxygen saturation refers to the percentage of oxygen that binds to hemoglobin. The measurement of oxygen transported through the blood is referred to as the oxygen content of the blood.5 Once the oxygen reaches the tissue level through transportation by hemoglobin, it is unloaded and participates in cellular aerobic metabolism.

Several conditions can affect the attraction of oxygen to hemoglobin. A shift to the left indicates that oxygen is bound too tight to hemoglobin. Decreased levels of carbon dioxide, alkalosis, or hypothermia could cause this to occur. A shift to the right means the hemoglobin is releasing too

9 NurseCe4Less.com much oxygen.6 Increased levels of carbon dioxide, acidosis, or fever could cause this shift.

Common Sites of ABG Sample Collection

A , phlebotomist, physician, or nurse draws the arterial blood for ABG sampling. Planning for the test involves the best selection of a puncture site, which will typically include the radial, femoral, or brachial arteries.6 Assessment of collateral circulation to the hand and wrist must first be performed in cases of radial artery sampling. This can be accomplished by performing what is known as an Allen test. During this procedure, clinicians occlude both the ulnar and radial arteries. The patient then pumps the fist until the blood has drained and the hand appears pale. Pressure is then released from the ulnar artery, while the radial artery remains occluded. If the hand returns to normal, adequate circulation is present. If it fails to return to the normal color within approximately 10 seconds, another site must be used for arterial puncture.6

Radial Artery

Puncture at the radial artery site is the preferred method of obtaining a sample for blood gas analysis due to the artery’s location on the wrist. The procedure is performed as outlined as follows:6,7

● Palpate the patient’s radial pulse with the index and middle finger of the nondominant hand and clean the puncture site with antiseptic.

● Insert the needle at a 45-degree angle, while palpating the radial pulse proximal to the puncture site with the non-dominant hand.

● As the needle slowly advances into the lumen of the radial artery, the arterial blood flow begins to fill the syringe. It is not necessary to pull back the plunger, unless the patient has a weak pulse or an unvented plunger with a small needle is being utilized.

10 NurseCe4Less.com

● The needle can be removed after 2 to 3 mL of arterial blood has been obtained. After the procedure, apply occlusive pressure at the puncture site with a piece of gauze for approximately five minutes prior to applying an adhesive bandage.

Femoral Artery

In cases where radial artery sampling is not feasible, femoral artery sampling may be a viable alternative. However, the deeper the structure, the higher the risk is for damage to nearby nerves. The potential for infection must also be taken into account prior to performing this procedure.

The femoral artery is located midline between the symphysis pubis and the superior iliac crest, and two to four centimeters distal to the inguinal ligament. The procedure is performed as outlined below.

● Palpate the patient’s femoral pulse with the middle and index finger on the non-dominant hand and clean the puncture site with antiseptic.

● Insert the needle at a 60 to 90 degree angle, while palpating the femoral pulse proximal to the puncture site with the non-dominant hand.

● As the needle slowly advances into the lumen of the femoral artery, the arterial blood flow begins to fill the syringe. It is not necessary to pull back the plunger, unless the patient has a weak pulse or an unvented plunger with a small needle is being utilized.

● The needle can be removed after 2 to 3 mL of arterial blood has been obtained. After the procedure, apply occlusive pressure at the puncture site with a piece of gauze for approximately five minutes prior to applying an adhesive bandage.

11 NurseCe4Less.com Brachial Artery

The brachial artery is another option for blood gas sampling; however, because the structures are harder to identify than the other locations, it is the least preferred site. It is located between the medial epicondyle of the humerus and the bicep tendon in the antecubital fossa. It can be identified in the groove between the tricep and bicep tendons. The procedure is performed as outlined as follows:6,7

● Palpate the patient’s brachial pulse with the index and middle finger of the non-dominant hand and clean the puncture site with antiseptic.

● Insert the needle at a 45 to 60-degree angle, while palpating the radial pulse proximal to the puncture site with the non-dominant hand.

● As the needle slowly advances into the lumen of the brachial artery, the arterial blood flow begins to fill the syringe. It is not necessary to pull back the plunger, unless the patient has a weak pulse or an unvented plunger with a small needle is being utilized.

● The needle can be removed after 2 to 3 mL of arterial blood has been obtained. After the procedure, apply occlusive pressure at the puncture site with a piece of gauze for approximately five minutes prior to applying an adhesive bandage.

After the ABG test, patients should be monitored for potential complications, which may include:7

● Local hematoma ● Air or thrombus embolism ● Arterial occlusion ● Infection ● Hemorrhage ● Local anesthetic reaction ● Vessel laceration

12 NurseCe4Less.com Arterial blood gas testing may also be difficult in patients who are cognitively impaired or uncooperative because their pulses may be difficult to locate. Also, in cases of obesity, excess subcutaneous fat may limit access to the vascular area.

Blood Gas Analyzer

Once the blood is drawn through one of the aforementioned methods, it is sent to the blood gas analyzer machine for analysis. There are a variety of manufactures and the technical design has evolved since their inception in the 1950s; however, the function remains fairly straightforward. The blood gas analyzer machine aspirates the blood from the syringe and measures the pH as well as the partial pressures of carbon dioxide, nitrogen, and oxygen and bicarbonate concentration.7

The basic components of the machine include three electrodes that determine pH, PcO2 and Po2.. Each electrode is calibrated at two reference points and measurements are taken based on these points. Once this laboratory analysis is complete, the results are forwarded to the physician for interpretation and potential treatment options.7

ABG Measurement Interpretation

A systematic approach is necessary to properly analyze arterial blood gas results. Using the baseline references as guidance, clinicians assess oxygenation, pH, standard bicarbonate (sHCO3), , and partial 7 pressure of carbon dioxide (PaCO2). Once the arterial blood specimen is taken, the steps outlined below will be taken to analyze the results.

Oxygenation

Arterial oxygen tension (PaO2) is the partial measurement of the partial pressure of oxygen in arterial blood. Arterial oxygen tension is composed of alveolar gas exchange, inspired oxygen concentration, and tissue oxygen consumption.7 During this stage of arterial gas assessment, clinicians record the inspired gas concentration and P/F ratio, which is the

13 NurseCe4Less.com ratio between PaO2 and the inspired oxygen concentration. Hemoglobin saturations should also be assessed during this stage.

Blood pH

As discussed earlier, the normal pH range is between 7.35 and 7.45. Any variation could result in a state of acidosis or alkalinity. Even small changes in pH levels can be clinically significant due to a large fluctuation in hydrogen ion concentration.7

Standard Bicarbonate

Standard bicarbonate (sHCO3) can be used to isolate metabolic causes of acid-base disturbance. Any abnormal sHCO3 reading may indicate primary or compensatory metabolic acid-base issues. During this stage of the testing, the arterial blood gas analyzer software calculates the values of sHCO3 and base excess. A decreased level of sHCO3 indicates acidosis, which is likely to be metabolic in origin, and an increased level of sHCO3 .7

Arterial Partial Pressure of Carbon Dioxide

A low or high arterial partial pressure of carbon dioxide (PaCO2) reading may also indicate or alkalosis respectively. Next, the PaCO2 should be evaluated to identify any ventilatory issue, which may be present in an acid-base disturbance.7 In cases where the respiratory drive is normal, compensatory hypocarbia should be present. Irregular levels of arterial pressure of carbon dioxide could be caused by a variety of conditions, such as chronic obstructive pulmonary disease, incipient ventilator failure, or opioid analgesia.

Additional Analysis

Other considerations may also be useful in determining the cause of any acid-base abnormality. Factors to consider include ,

14 NurseCe4Less.com hemoglobin, glucose, and lactate concentrations. Many arterial blood gas analyzers are now set up to evaluate these additional analysts.

Acid-Base Disorders

After studying the ABG test information, clinicians will be able to identify any potential acid-base disorders. During the interpretation and treatment of abnormal arterial blood values, the disorders commonly present are discussed below.

Respiratory Acidosis

Respiratory acidosis occurs when the body tries to compensate for excessive partial pressure of carbon dioxide. During respiratory acidosis, excess hydrogen in the urine is excreted in exchange for bicarbonate ions. When is impaired during respiratory acidosis, the lungs are unable to excrete carbon dioxide effectively and the accumulation of this carbon dioxide forms an acid in the blood.7 Respiratory acidosis can be caused by any condition that causes a patient to develop a depressed respiratory status, such as chronic obstructive pulmonary disease, infection, asphyxia, central nervous system depression, and hypoventilation.

Respiratory Alkalosis

During excessive of carbon dioxide causes a decrease in blood carbon dioxide concentration. This results in a decrease in hydrogen ions, which leads to an increase in pH.7 Common causes include pulmonary disease, high altitudes, hyperventilation, and stroke.

Metabolic Acidosis

Metabolic acidosis occurs when there is a reduction in bicarbonate, or an accumulation of fixed acid. It is marked by a pH of less than 7.35 and a plasma bicarbonate ion concentration of less than 22 mmol/L.7-10 The bicarbonate level decreases, as the lactic acid accumulates, resulting in a

15 NurseCe4Less.com decrease in pH and bicarbonate levels. Metabolic acidosis may be caused by a failure of the kidneys to excrete hydrogen ions, severe diarrhea, poor infusion induced by , and excessive production of acids caused by diabetic ketoacidosis.

Metabolic Alkalosis

During metabolic alkalosis, there is an increase in pH levels and bicarbonate and a decrease in fixed acid. It is marked by a bicarbonate ion level of greater than 26 mmols. During metabolic alkalosis, the kidneys attempt to conserve hydrogen, which results in the respiratory system decreasing ventilations.7-10 Metabolic alkalosis can be caused by severe loss of gastric acid induced by excessive vomiting, use of steroids or diuretic drugs, and excessive intake of alkaline medications, such as antacids, potassium deficiency, and Cushing’s Syndrome. Symptoms of metabolic alkalosis include slowed breathing, tremors, irritability, and nausea.7-10

Case Studies: Acid-Base Imbalance

The following two case studies provide examples of metabolic disturbances in both pediatric and adult individuals located in a PubMed search on acid-base disturbances and include the types of treatments and health outcomes that followed.

Case Study 1: Pediatric Non-diabetic Ketoacidosis

This first case study obtained through a PubMed search discussed pediatric non-diabetic ketoacidosis in five children.

The authors reported on five children who had been hospitalized three times with signs of dehydration, poor appetite, and Kussmaul breathing. One patient had genetic testing that revealed a genetic mutation and was diagnosed as a case of β-ketothiolase deficiency. He had inherited this disorder in which the body cannot effectively process a protein building block called isoleucine (an amino acid). This disorder also impairs the body's

16 NurseCe4Less.com ability to process ketones (molecules produced during the breakdown of fats).11,12

The patients were reportedly stabilized, and further testing was required to determine the underlying cause of pediatric non-diabetic ketoacidosis. The authors raised the typical causes of non-diabetic ketoacidosis: severe starvation, organic acidemia (such as β-ketothiolase deficiency, and other causes including hyperglycinemia), glycogen storage disease, and gluconeogenesis disorders.

Treatment

Non-diabetic ketoacidosis is treated similarly as diabetic ketoacidosis, but it also requires some unique approaches. The treatment approach mainly consists of the following four components: early glucose supplementation, insulin administration, bicarbonate infusion, and continuous renal replacement therapy. These are discussed next.

Early Glucose Supplementation:

High blood glucose, ketone accumulation, and acidosis are characteristics of non-diabetic ketoacidosis. As a person develops insulin deficiency or insulin resistance, high blood glucose results. Treatment is therefore targeting glucose intake along with insulin supplementation.

Normal or low blood glucose levels develop in individuals with nondiabetic ketoacidosis. Early glucose supplementation helps to maintain a blood glucose level of high-normal and could limit fatty acid oxidation and decrease ketone production.

Insulin Administration:

The authors stated that while insulin is required for glucose metabolism it also inhibits lipolysis and stimulates fat synthesis and storage,

17 NurseCe4Less.com which result in decreased free fatty acid production. Free fatty acids are the main source of ketone production. Insulin supplementation inhibits lipolysis and ketone production, and decreases glucagon secretion, and therefore is considered the main treatment for diabetic ketoacidosis.

In this case study, insulin administration could successfully correct acidosis. One patient was not treated with insulin infusion and took the longest time for acidosis recovery, despite having received the highest amount of bicarbonate infusion. The most severe case of acidosis (serum bicarbonate <3 mmol/L) had received moderate amounts of bicarbonate infusion but prolonged insulin administration, and recovery from acidosis in this patient was brief. Use of insulin can lead to , however the patient raised indicates that insulin treatment in non-diabetic ketoacidosis is effective.

Non-diabetic ketoacidosis in children generally coincides with blood glucose levels that are low to normal. Insulin should be administered together with glucose (ratio of 4–6 g glucose for every 1 unit of insulin), with frequent blood glucose monitoring. A high-normal glucose value is maintained since patients with non-diabetic ketoacidosis carry a significant risk of experiencing hypoglycemia.

Bicarbonate Infusion:

Bicarbonate supplementation is administered in non-diabetic ketoacidosis patients because bicarbonate ions bind with the accumulated ketone bodies and then lost through kidney excretion. The bicarbonate dosing may not correct but actually aggravate acidosis, coinciding with in the central nervous system (CNS), increase hypokalemia, alter the serum concentration, and lead to increase.

The authors explained that bicarbonate infusion increases the blood pCO2, which can cross the blood brain barrier faster than the bicarbonate. “Increased pCO2 in the brain would result in paradoxical fall in cerebral pH. Bicarbonate infusion could increase blood pH, which induces intracellular

18 NurseCe4Less.com shift of potassium and lead to hypokalemia.”11 Calcium binding to proteins is also promoted by alkalosis, hence lowering the free calcium level. Hyponatremia may develop as a result of bicarbonate and sodium combining together. Bicarbonate infusion in these patients is only suggested for patients diagnosed with severe acidosis.

In this case report there were two children who received the highest dose of sodium bicarbonate that coincided with altered mental status and seizures. The child with the highest bicarbonate infusion (85 mL/kg) took the longest to correct acidosis. Conversely, another child with severe acidosis (serum bicarbonate <3 mmol/L) and the lowest amount of bicarbonate infusion had shorter recovery time from the acidosis.

Treatment of non-diabetic ketoacidosis with bicarbonate infusion should be decided with caution. Only in severe acidosis and unstable hemodynamic signs after initial fluid should bicarbonate be considered. Bicarbonate administration may be as 5% sodium bicarbonate solution (1~2 mL/kg) over 1 hour.

Continuous Renal Replacement Therapy:

Continuous Renal Replacement Therapy (CRRT) has not been well researched in diabetic ketoacidosis, however the authors stated that a few cases have been reported. Ketones are small enough molecules that they are eliminated through CRRT.

In two of the mentioned cases, CRRT resulted in only partial correction of acidosis, and acidosis corrected 10–36 hour after stopping CRRT. The authors suggested that CRRT was not effective in these cases. CRRT can only eliminate existing ketones and does not have any effect on the production of ketones. Once CRRT stops, ketone concentration is expected to increase with the occurrence of acidosis.

19 NurseCe4Less.com Discussion11

The authors reported on pediatric non-diabetic ketoacidosis and their treatment approach to correct metabolic disorders in the children. Laboratory testing had confirmed non-diabetic ketoacidosis, and a normal or low blood glucose level, low bicarbonate, high metabolic acidosis, and ketone found in the blood or urine are characteristic findings of non- diabetic ketoacidosis.

One child had a genetic mutation and was diagnosed with β- ketothiolase deficiency and was expected to have impaired ketone metabolism and ketone accumulation in the body. Ketoacidosis in this child had occurred three times, and seizures had occurred during the first episode. A brain MRI study showed an abnormal finding and suggested local edema. Treatment was described as intravenous fluid resuscitation, insulin, glucose supplementation, bicarbonate infusion, and continuous renal replacement therapy (CRRT).

The authors concluded that all children survived till hospital discharge. No severe electrolyte disturbances of their potassium and of glucose levels dropping were seen. Early identification of potential ketoacidosis as evidenced by poor appetite, Kussmaul respiration, and rotten apple smell in the breath in children should prompt laboratory analysis, and early insulin administration with glucose supplementation to reverse the ketoacidosis. Bicarbonate administration and CRRT should be determined cautiously according to the authors due to the limited clinical efficacy known to date. The optimal therapeutic approach to pediatric non-diabetic ketoacidosis is an area that requires ongoing studies.

Case Study 2: Caffeine Overdose and Electrolyte Disturbance

This second case study obtained through a PubMed search discussed a case of caffeine overdose and the potential life-threatening outcomes that could occur with excessive caffeine use.13

20 NurseCe4Less.com The authors reported on a A 32-year-old woman who arrived to the (ED) reporting symptoms of malaise, anxiety, dizziness and nausea. The patient had no significant medical and family history and denied experiencing chest pain, syncope, palpitations or fever.

Physical evaluation of the patient on an initial assessment revealed her to be awake and oriented, with a of 19 breaths/min, 100% oxygen saturation on room air, blood pressure of 112/70 mmHg, pulse 80 beats/min and she was afebrile. A blood sugar was obtained and showed 147 mg/dL.

While in the ED the patient had presyncopal episode followed by symptoms of agitation and vomiting, and she became pale, sweaty and distracted mental status however could open her eyes, respond verbally and showed good motor response. Her pupils were equally round and reactive to light, and she had no muscle weakness or sensory deficits. The blood pressure remained stable at 115/75 mmHg, and she developed tachycardia (160 beats/min). Her oxygen saturation on room air was 99%.

An ECG was obtained that showed a polymorphic broad QRS tachycardia and an arterial blood gas was taken that revealed metabolic acidosis with severe hypokalemia. A dysrhythmia was successfully treated with propranolol 5 mg intravenously. The patient’s acid–base and electrolyte disorders were corrected.

Once the patient had stabilized, she reported recent use of a preworkout supplement, a proteic supplement for anhydrous caffeine, however instead of a recommended dose dose of 300 mg (6 mg/kg) of anhydrous caffeine, a total of 5000 mg (89 mg/kg),30 min before going to the ED had been consumed. The patient also reported occasional use of one espresso (60 mg of caffeine) and denied alcohol or any recreational drugs.

21 NurseCe4Less.com The patient’ initial exams are shown here:13

● Electrocardiogram: showing broad QRS polymorphic tachycardia. ● Arterial blood gas: showed metabolic acidosis with pH of 7.296 (7.35– 7.45), pCO2 of 29.9 mm Hg, pO2 of 117 mm Hg, HCO3 of 16.1 mmol/L (22–26) and severe lactatemia with serum lactate level of 5.3 mmol/L (0.5–1.6). ● Laboratory findings included: ❏ mild leucocytosis of 13.50×109/l (4.0–10.0) with 68.3% neutrophils ❏ hyperglycaemia of 254 mg/dL (70–105), ❏ hypocalcaemia of 2.5 mmol/L (3.5–5.1) ❏ hypophosphataemia of 1.8 mg/dL (2.3–4.7). ❏ Magnesium and calcium serum values were within normal range as well as thyroid, renal and . ❏ Urinalysis was positive for ketones and glucose and negative for cocaine and opioid drugs. Unfortunately, a blood sample for caffeine analysis was not taken. ❏ Plain chest X-ray was normal. ❏ Echocardiogram revealed a structurally normal heart.

Therapy was supportive and involved intravenous fluids, propranolol, potassium and phosphorus supplementations. Because the medical team was initially unaware of a dietary supplement there was no activated charcoal administered. The patient was observed for 48 hours of observation in the intermediate care unit, then transferred to the general ward as stable with asymptomatic sinus tachycardia (maximum of 120 beats/min) and other vital signs were stable. A normal serum pH, lactate and glucose levels were notable in the laboratory testing. A blood sample to assess the caffeine level was not taken. The dietary product consumed was not sent out for chemical analysis to determine the amount of caffeine in it.

After 2 days of remaining in intermediate care the patient’s status was evaluated as having a normal level of consciousness, arterial blood gas values were normal, and there had been no recurrence of presyncope episodes. A persistent sinus tachycardia was reported, which resulted in a 3-

22 NurseCe4Less.com day course of Propranolol 30 mg/day orally for heart rate control. The patient remained clinically stable and was discharged asymptomatic after 5 days and referred to internal medicine for follow-up.

A treadmill exercise stress test was done and returned a negative result for myocardial . Six months after the episode, at follow-up evaluation, the patient remained asymptomatic.

Discussion13

The authors stated that caffeine is a natural product commonly found in food, beverages and medication. Caffeine consumed in low doses rarely lead to side effects, however, in large amounts it can lead to higher level of endurance. According to the authors patients will take energy drinks or dietary supplements that contains anhydrous caffeine to improve energy, concentration and athletic performance.

A caffeine dosage of 0.05–0.2 g will result in mild stimulation generally. Fatal caffeine intoxication is rare, however acute ingestion >5 g can be lethal. After oral intake, an approximate 90% of the product is rapidly absorbed from the gastrointestinal tract and within 15 minutes the clinical effects are observed that includes a peak effect within 1–1.5 hours following use. Caffeine half-life elimination varies between 3 and 7 hours and can be influenced by sex, age, use of oral contraceptives, pregnancy and smoking. There is significant variability regarding ingested amounts and the drug’s toxic effects. Caffeine is structurally similar to adenosine and acts as a competitive antagonist on adenosine receptors. Adenosine receptors are found throughout the human body but are specifically found in the brain and heart.

By blocking the adenosine receptors, at high doses, caffeine intensifies beta-receptor activation which can trigger arrhythmia. In toxic doses, caffeine directly releases calcium from intracellular stores, which also may increase the susceptibility for arrhythmias. Symptoms of caffeine intoxication may include headache, fever, nausea, vomiting, tachycardia, dizziness,

23 NurseCe4Less.com tinnitus, anxiety, irritability, insomnia and seizures. At toxic levels, severe hypokalemia, , rhabdomyolysis, renal failure and hyperlactacidemia have also occurred. Leukocytosis, mild metabolic acidosis, ketonuria, hypophosphatemia and hypocalcemia are also possible with caffeine intoxication.

Hypertension followed by hypotension and cardiac dysrhythmias, including supraventricular and ventricular tachyarrhythmias are reportedly common cardiovascular effects of caffeine intoxication. The authors raised that the most common cause of caffeine-related death is arrhythmia and a blood caffeine concentration would help confirm diagnosis.

Treatment of caffeine toxicity generally involves careful and immediate assessment of the patient’s airway, breathing and circulation. Continuous cardiac monitoring, and fingerstick glucose levels need to be started as well as intravenous access.

Activated charcoal and intravenous lipid emulsion will help to reduce systemic effects/ Hypotension is treated by intravenous fluid therapy with isotonic fluid and when patients are hemodynamically unstable then dysrhythmia should be treated by advanced cardiac life support protocols.

Combination short-acting beta-blocker drugs, procainamide or lidocaine with electrolyte correction successfully treated the cardiac arrhythmias in this case report. Dialysis has been reported in some cases to successfully treat caffeine toxicity.

The authors summarized that this case of severe caffeine intoxication due to an accidental high dosage of a dietary supplement for sport enhancement serves as an example of clinical importance in young individuals at risk of caffeine toxicity. Because cardiac arrhythmias are the most frequent cause of death by caffeine overdose, they suggest clinicians contact poison control centers for guidance on treatment to prevent a potentially lethal outcome. Caffeine overdose can be fatal due to cardiac arrhythmia, and clinical awareness of caffeine toxicity needs to be increased.

24 NurseCe4Less.com Summary

Health providers may have difficulty with the interpretation of an arterial blood gas (ABG) test. The best approach to ABG interpretation is a systematic one. Primary aspects of ABG analysis involve the blood pH, whether it is normal, acidotic or alkalotic, and the pO2 level indicating whether the patient is hypoxic. It’s also necessary to understand compensatory mechanisms, such as with the rise and fall to maintain pH balance in the setting of respiratory or renal failure.

To be proficient in ABG interpretation health providers need to understand the body systems involved to maintain adequate oxygenation and acid-base balance, and to practice ABG analysis. By understanding the various aspects of ABG testing and interpretation, medical and nursing professionals are able to better treat any underlying conditions related to respiratory and metabolic (acid-base) disturbances. The systematic approach to ABG analysis can help determine the differential diagnoses, which will help to ensure the best possible outcomes for patients.

25 NurseCe4Less.com Self-Assessment of Knowledge Post Test:

Please take time to help NurseCe4Less.com course planners evaluate the nursing knowledge needs met by completing the self-assessment of Knowledge Questions after reading the article, and providing feedback in the online course evaluation. Completing the study questions is optional and is NOT a course requirement.

1. Which of the following puncture sites is preferred for obtaining a sample for an arterial blood gas (ABG) test?

a. femoral artery b. radial artery c. brachial artery d. axillary artery

2. Acid is a substance that ______a hydrogen ion.

a. accepts b. rejects c. absorbs d. donates

3. This molecule in the blood binds to and transports oxygen:

a. protein b. bicarbonate c. hemoglobin d. phosphate

4. A patient’s arterial blood gas (ABG) tests indicate that CO2 levels have decreased while pH levels have increased, which indicates a state of

a. alkalosis. b. acidosis. c. atelectasis. d. fibrosis.

26 NurseCe4Less.com 5. True or False: A blood sample obtained from a vein for a blood gas test has a richer concentration of oxygen than a blood samples taken from an artery.

a. True b. False

6. An arterial blood gas (ABG) measures ______to determine the percentage of oxygen that is binding to hemoglobin in the arteries.

a. exhaled carbon dioxide (CO2) b. extracorporeal circulation c. cellular aerobic metabolism d. oxygen saturation (SaO2)

7. A patient’s arterial blood gas (ABG) report shows a pH of less than 7.35 and a plasma bicarbonate ion concentration of less than 22 mmol/L, which indicates a condition known as

a. metabolic alkalosis. b. respiratory alkalosis. c. metabolic acidosis. d. respiratory acidosis.

8. Carbon dioxide (CO2) reacts with water to form ______, which helps to regulate pH.

a. carbonic acid b. bicarbonate c. oxygen d. chloride

9. Bicarbonate (HCO3) is an essential buffer system for the body and ______fluctuation in this acid-base component will result in an imbalance

a. a positive b. a negative c. a positive or negative d. elevated

27 NurseCe4Less.com 10. Metabolic acidosis may be caused by

a. an increase in bicarbonate levels. b. a decrease in chloride concentration. c. a failure of the kidneys to excrete hydrogen ions. d. a failure of the kidneys to excrete phosphate.

11. A decrease in chloride within the renal tubules can cause

a. elevated potassium levels. b. hydrogen secretion. c. acidosis. d. alkalosis.

12. In a patient’s arterial blood gas (ABG) test, a “shift to the left” of the normal levels of oxygen content in the blood indicates

a. that the hemoglobin is releasing too much oxygen. b. that oxygen is bound too tight to hemoglobin. c. an increased level of carbon dioxide. d. a condition called metabolic acidosis.

13. After an arterial blood gas (ABG) test, the patient should be monitored for potential complications, which may include:

a. air or thrombus embolism. b. infection. c. arterial occlusion. d. All of the above

14. True or False: Small changes in pH levels are not clinically significant since pH levels fluctuate all the time in a healthy patient.

a. True b. False

15. During ______, excess hydrogen in the urine is excreted in exchange for bicarbonate ions.

a. metabolic acidosis b. respiratory alkalosis c. cellular aerobic metabolism d. respiratory acidosis

28 NurseCe4Less.com CORRECT ANSWERS:

1. Which of the following puncture sites is preferred for obtaining a sample for an arterial blood gas (ABG) test? b. radial artery

“Puncture at the radial artery site is the preferred method of obtaining a sample for blood gas analysis due to the artery’s location on the wrist.”

2. Acid is a substance that ______a hydrogen ion. d. donates

“Acid” is defined as any substance that can donate a hydrogen ion; and “base” encompasses any substance that can accept a hydrogen ion.”

3. This molecule in the blood binds to and transports oxygen: c. hemoglobin

“The hemoglobin molecule in the blood binds with and transports oxygen (O2).”

4. A patient’s arterial blood gas (ABG) tests indicate that CO2 levels have decreased while pH levels have increased, which indicates a state of a. alkalosis.

“If CO2 levels decrease, pH increases, which may result in a state of alkalosis. The normal range pH serum CO2 level is from 35 to 45 mmHG.”

5. True or False: A blood sample obtained from a vein for a blood gas test has a richer concentration of oxygen than a blood samples taken from an artery. b. False

“During most blood tests, blood is taken from the veins. However, during the ABG test a blood sample is drawn from the artery prior to it reaching the tissue of the body. Therefore, a blood sample obtained from an arterial blood gas test has a richer concentration of oxygen.”

29 NurseCe4Less.com 6. An arterial blood gas (ABG) measures ______to determine the percentage of oxygen that is binding to hemoglobin in the arteries.

d. oxygen saturation (SaO2)

“The oxygen saturation refers to the percentage of oxygen that binds to hemoglobin. The measurement of oxygen transported through the blood is referred to as the oxygen content of the blood. Once the oxygen reaches the tissue level through transportation by hemoglobin, it is unloaded and participates in cellular aerobic metabolism.”

7. A patient’s arterial blood gas (ABG) report shows a pH of less than 7.35 and a plasma bicarbonate ion concentration of less than 22 mmol/L, which indicates a condition known as

d. metabolic acidosis.

“Metabolic acidosis occurs when there is a reduction in bicarbonate, or an accumulation of fixed acid. It is marked by a pH of less than 7.35 and a plasma bicarbonate ion concentration of less than 22 mmol/L.”

8. Carbon dioxide (CO2) reacts with water to form ______, which helps to regulate pH.

a. carbonic acid

“Carbon dioxide (CO2) reacts with water to form carbonic acid, which helps to regulate pH.”

9. Bicarbonate (HCO3) is an essential buffer system for the body and ______fluctuation in this acid-base component will result in an imbalance

c. a positive or negative

30 NurseCe4Less.com 10. Metabolic acidosis may be caused by c. a failure of the kidneys to excrete hydrogen ions.

“The bicarbonate level decreases, as the lactic acid accumulates, resulting in a decrease in pH and bicarbonate levels. Metabolic acidosis may be caused by a failure of the kidneys to excrete hydrogen ions, severe diarrhea, poor infusion induced by shock, and excessive production of acids caused by diabetic ketoacidosis.”

11. A decrease in chloride within the renal tubules can cause d. alkalosis.

“Chloride and potassium within the renal tubules also play a role in pH balance. A decrease in chloride can cause alkalosis, and elevated potassium levels can cause acidosis. High sodium levels may also contribute toward alkalosis due to the secretion of hydrogen.”

12. In a patient’s arterial blood gas (ABG) test, a “shift to the left” of the normal levels of oxygen content in the blood indicates b. that oxygen is bound too tight to hemoglobin.

“In healthy patients, the ABG test will reveal normal levels of oxygen and carbon dioxide. The oxygen saturation refers to the percentage of oxygen that binds to hemoglobin. The measurement of oxygen transported through the blood is referred to as the oxygen content of the blood. Once the oxygen reaches the tissue level through transportation by hemoglobin, it is unloaded and participates in cellular aerobic metabolism. Several conditions can affect the attraction of oxygen to hemoglobin. A ‘shift to the left’ indicates that oxygen is bound too tight to hemoglobin. Decreased levels of carbon dioxide, alkalosis, or hypothermia could cause this to occur. A ‘shift to the right’ means the hemoglobin is releasing too much oxygen. Increased levels of carbon dioxide, acidosis, or fever could cause this shift.”

31 NurseCe4Less.com 13. After an arterial blood gas (ABG) test, the patient should be monitored for potential complications, which may include: a. air or thrombus embolism. b. infection. c. arterial occlusion. d. All of the above [correct answer]

“After the ABG test, patients should be monitored for potential complications, which may include: Local hematoma; Air or thrombus embolism; Arterial occlusion; Infection; Hemorrhage; Local anesthetic reaction; Vessel laceration.”

14. True or False: Small changes in pH levels are not clinically significant since pH levels fluctuate all the time in a healthy patient. b. False

“As discussed earlier, the normal pH range is between 7.35 and 7.45. Any variation could result in a state of acidosis or alkalinity. Even small changes in pH levels can be clinically significant due to a large fluctuation in hydrogen ion concentration.”

15. During ______, excess hydrogen in the urine is excreted in exchange for bicarbonate ions. d. respiratory acidosis

“During respiratory acidosis, excess hydrogen in the urine is excreted in exchange for bicarbonate ions.”

32 NurseCe4Less.com Reference Section

The References below include published works and in-text citations of published works that are intended as helpful material for further reading.

1. Theodore, A (2019). Arterial blood gases. UpToDate. Retrieved from https://www.uptodate.com/contents/arterial-blood- gases?search=arterial%20blood%20gas&source=search_result&select edTitle=1~150&usage_type=default&display_rank=1 2. Rogers, M., McCutcheon, K. (2013). Understanding arterial blood gases. J Perio Prac; 23(9):191-197 3. DeBerardinis, RJ and Thompson, CB (2012). Cellular metabolism and disease: what do metabolic outliers teach us? Cell; 128(6):1132-1144. 4. Lewis, J (2019). Acid Base Physiology. Merck Manual, Professional Version. Retrieved from https://www.merckmanuals.com/professional/endocrine-and- metabolic-disorders/acid-base-regulation-and-disorders/acid-base- regulation?query=acid%20base 5. Emmett, M and Palmer, B (2019). Simple and mixed acid-base disorders. UpToDate. Retrieved from https://www.uptodate.com/contents/simple-and-mixed-acid-base- disorders?search=blood%20buffers&source=search_result&selectedTitl e=4~150&usage_type=default&display_rank=4 6. Wood, K (2019). Measurement of Gas Exchange. Merck Manual, Professional Version. Retrieved from https://www.merckmanuals.com/professional/pulmonary- disorders/tests-of-pulmonary-function-pft/measurement-of-gas- exchange?query=abg 7. Arthur, Theodore (2019). Arterial Blood Gases. UpToDate. Retrieved from https://www.uptodate.com/contents/arterial-blood- gases?search=ABG&source=search_result&selectedTitle=1~150&usag e_type=default&display_rank=1 8. Sutton, R (2019). Inborn errors of metabolism: Classification. UpToDate. Retrieved from https://www.uptodate.com/contents/inborn-errors-of-metabolism- classification?search=metabolism&source=search_result&selectedTitle =3~150&usage_type=default&display_rank=3 9. Lewis, J (2019). Metabolic Acidosis. Merck Manual, Professional Version. Retrieved from https://www.merckmanuals.com/professional/endocrine-and- metabolic-disorders/acid-base-regulation-and-disorders/metabolic- acidosis

33 NurseCe4Less.com 10. Djouadi, F and Bastin, J (2019). Mitochondrial Genetic Disorders: Cell Signaling and Pharmacological . Cells; 8(4). pii: E289. doi: 10.3390/cells8040289. 11. Bai, F, Fu, Y, Liu, C, Xy, F, Zhu, M (2017). Pediatric non-diabetic ketoacidosis: a case-series report. BMC Pediatr; 17(1):209. doi: 10.1186/s12887-017-0960-3. 12. US National Libraroy of Medicine (2019). Beta-ketothiolase deficiency. Genetics Home Reference. NIH. Retrieved from https://ghr.nlm.nih.gov/condition/beta-ketothiolase-deficiency] 13. Andrade, A, Sousa, C, Pedro, M and Fernandes, M (2018). Dangerous mistake: an accidental caffeine overdose. BMJ Case Rep; bcr2018224185. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6011436/

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