Fast breathing (due to anxiety, pain, shock) Severe infection or fever Liver failure Pneumonia, pulmonary congestion or embolism
Alcoholic ketoacidosis Diabetic ketoacidosis Kidney failure Lactic acidosis Toxins – overdose of salicylates (aspirin), methanol, ethylene glycol, toluene Gastrointestinal bicarbonate loss, such as from prolonged diarrhoea
Diuretics Prolonged vomiting Severe dehydration
Most acid-base disorders do not require treatment of the abnormal pH. The aim of diagnosis is to identify what has caused the acid-base disorder and, when necessary, treat this cause. Occasionally, doctors may give intravenous bicarbonate to patients with dangerously low blood pH levels. Blood gas analysis is a commonly used diagnostic tool to evaluate the partial pressures of gas in blood and acid-base content. Understanding and use of blood gas analysis enable providers to interpret respiratory, circulatory, and metabolic disorders. [1] A "blood gas analysis" can be performed on blood obtained from anywhere in the circulatory system (artery, vein, or capillary). An arterial blood gas (ABG) tests explicitly blood taken from an artery. ABG analysis assesses a patient's partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2). PaO2 provides information on the oxygenation status, and PaCO2 offers information on the ventilation status (chronic or acute respiratory failure). PaCO2 is affected by hyperventilation (rapid or deep breathing), hypoventilation (slow or shallow breathing), and acid-base status. Although oxygenation and ventilation can be assessed non-invasively via pulse oximetry and end-tidal carbon dioxide monitoring, respectively, ABG analysis is the standard. When assessing the acid-base balance, most ABG analyzers measure the pH and PaCO2 directly. A derivative of the Hasselbach equation calculates the serum bicarbonate (HCO3) and base deficit or excess. This calculation frequently results in a discrepancy from the measured due to the blood CO2 unaccounted for by the equation. The measured HCO3 uses a strong alkali that liberates all CO2 in serum, including dissolved CO2, carbamino compounds, and carbonic acid. The calculation only accounts for dissolved CO2; this measurement using a standard chemistry analysis will likely be called a "total CO2". For that reason, the difference will amount to around 1.2 mmol/L. However, a larger difference may be seen on the ABG, compared to the measured value, especially in critically ill patients. [2] The calculation has been disputed as both accurate and inaccurate based on the study, machine, or calibration used and must be interpreted appropriately based on your institutional standards.[3] Arterial blood gases are frequently ordered by emergency medicine, intensivist, anesthesiology, and pulmonology clinicians but may also be needed in other clinical settings. Many diseases are evaluated using an ABG, including acute respiratory distress syndrome (ARDS), severe sepsis, septic shock, hypovolemic shock, diabetic ketoacidosis, renal tubular acidosis, acute respiratory failure, heart failure, cardiac arrest, asthma, and inborn errors of metabolism. By obtaining an ABG and analyzing the pH, partial pressures, comparing it to measured serum bicarbonate in a sick patient, multiple pathological conditions can be diagnosed. The alveolar-arterial oxygen gradient is a useful measure of lung gas exchange, which can be abnormal in patients with a ventilation-perfusion mismatch. Whole blood is the required specimen for an arterial blood gas sample. The specimen is obtained through an arterial puncture or acquired from an indwelling arterial catheter. A description of these procedures is beyond the scope of this article; please refer to the StatPearls article “arterial lines” and other references for more information.[4] Once obtained, the arterial blood sample should be placed on ice and analyzed as soon as possible to reduce the possibility of erroneous results. Automated blood gas analyzers are commonly used to analyze blood gas samples, and results are obtained within 10 to 15 minutes. Automated blood gas analyzers, directly and indirectly, measure specific components of the arterial blood gas sample (see above). ABG Components:
A modified Allen test is a must before an ABG is drawn from either of the upper extremities to check for adequate collateral flow. Alternatively, pulse oximetry and duplex ultrasound can be used too. The arterial site commonly used is the radial artery, as it is superficial and easily palpable over the radial styloid process. The next most common site is the femoral artery. The test is performed on the unilateral upper extremity chosen for the procedure (Please look at the attached image for graphical illustration). The selected upper extremity is flexed at the elbow, and the patient requested to clench the raised fist for 30 seconds. Then pressure is applied over the ulnar and radial arteries with the intent to occlude the blood flow. After five seconds, unclench the raised fist. The palm will now appear pale, white, or blanched. Then pressure over the ulnar artery is released while the radial artery compression is maintained. In 10 to 15 seconds, the palm returns to its original color, indicating adequate Ulnar collateral blood flow. If the palm does not return to its actual color, it is an abnormal test and unsafe to puncture the radial artery. Similarly, the radial collateral blood flow is assessed by maintaining ulnar artery pressure and releasing the radial artery pressure. [5] An acceptable normal range of ABG values of ABG components are the following,[6][7] noting that the range of normal values may vary among laboratories and in different age groups from neonates to geriatrics:
Arterial blood gas interpretation is best approached systematically. Interpretation leads to an understanding of the degree or severity of abnormalities, whether the abnormalities are acute or chronic, and if the primary disorder is metabolic or respiratory in origin. Several articles have described simplistic ways to interpret ABG results. However, the Romanski method of analysis is most simplistic for all levels of providers.[8][6][7][9] This method helps determine the presence of an acid-base disorder, its primary cause, and whether compensation is present. The first step is to look at the pH and assess for the presence of acidemia (pH < 7.35) or alkalemia (pH > 7.45). If the pH is in the normal range (7.35-7.45), use a pH of 7.40 as a cutoff point. In other words, a pH of 7.37 would be categorized as acidosis, and a pH of 7.42 would be categorized as alkalemia. Next, evaluate the respiratory and metabolic components of the ABG results, the PaCO2 and HCO3, respectively. The PaCO2 indicates whether the acidosis or alkalemia is primarily from a respiratory or metabolic acidosis/alkalosis. PaCO2 > 40 with a pH < 7.4 indicates a respiratory acidosis, while PaCO2 < 40 and pH > 7.4 indicates a respiratory alkalosis (but is often from hyperventilation from anxiety or compensation for a metabolic acidosis). Next, assess for evidence of compensation for the primary acidosis or alkalosis by looking for the value (PaCO2 or HCO3) that is not consistent with the pH. Lastly, assess the PaO2 for any abnormalities in oxygenation. Example 1[7]: ABG : pH = 7.39, PaCO2 = 51 mm Hg, PaO2 = 59 mm Hg, HCO3 = 30 mEq/L and SaO2 = 90%, on room air.
Example 2[7]: ABG : pH = 7.45, PaCO2 = 32 mm Hg, PaO2 = 138 mm Hg, HCO3 = 23 mEq/L, the base deficit = 1 mEq/L, and SaO2 is 92%, on room air.
When evaluating a patient's acid-base status, it is important to include an electrolyte imbalance or anion gap in your synthesis of the information. For example: In a patient who presents with Diabetic Ketoacidosis, they will eliminate ketones, close the anion gap but have persistent metabolic acidosis due to hyperchloremia. This is due to the strong ionic effect, which is beyond the scope of this article. Arterial blood gas monitoring is the standard for assessing a patient’s oxygenation, ventilation, and acid-base status. Although ABG monitoring has been replaced mainly by non-invasive monitoring, it is still useful in confirming and calibrating non-invasive monitoring techniques. In the intensive care unit (ICU) and emergency room settings, evaluation of oxygenation is frequently done in the context of severe sepsis, acute respiratory failure, and ARDS. Calculating an alveolar-arterial (A-a) oxygen gradient can aid in narrowing down the hypoxemia cause. For example, a gradient's presence or absence can help determine whether the abnormality in oxygenation is potentially due to hypoventilation, a shunt, V/Q mismatch, or impaired diffusion. The equation for the expected A-a gradient assumes the patient is breathing room air; therefore, the A-a gradient is less accurate at higher percentages of inspired oxygen. Determining the intrapulmonary shunt fraction, the fraction of cardiac output flowing through pulmonary units that do not contribute to gas exchange is the best estimate of oxygenation status. Calculating the shunt fraction is traditionally done at a delivered FiO2 of 1.0, but if performed at a FiO2 lower than 1.0, then venous admixture would be the more appropriate term.[1] For simplicity, assessing oxygenation is more commonly performed by computing the ratio of PaO2 and fraction of inspired oxygen (PaO2/FiO2 or P/F ratio). However, there are limitations in using the P/F ratio in assessing oxygenation, as the discrepancy between venous admixture and the P/F ratio at a given shunt fraction depends on the delivered FiO2.[1] For research purposes, the P/F ratio has also been used to categorize disease severity in ARDS.[10] Another parameter commonly used in ICUs to assess oxygenation is the oxygenation index (OI). This index is considered a better indicator of lung injury, particularly in the neonatal and pediatric population, compared to the P/F ratio. It includes the level of invasive ventilatory support required to maintain oxygenation.[11] The OI is the product of the mean airway pressure (Paw) in cm H2O, as measured by the ventilator, and the FiO2 as the percentage divided by the PaO2. The OI is commonly used to guide management, such as initiating inhaled nitric oxide, administering surfactant, and defining the potential need for extracorporeal membrane oxygenation.[12] The presence of a normal PaO2 value does not rule out respiratory failure, particularly in the presence of supplemental oxygen. The PaCO2 reflects pulmonary ventilation and cellular CO2 production. It is a more sensitive marker of ventilatory failure than PaO2, particularly in the presence of supplemental oxygen, as it has a close relationship with the depth and rate of breathing.[6] Calculation of the pulmonary dead space is a good indicator of overall lung function. Pulmonary dead space is the difference between the PaCO2 and mixed expired PCO2 (physiological dead space) or the end-tidal PCO2 divided by the PaCO2. Pulmonary dead space increases when the pulmonary units' ventilation increases relative to their perfusion and when shunting increases. Hence, pulmonary dead space is an excellent bedside indicator of lung function and one of the best prognostic factors in ARDS patients.[1] The pulmonary dead space fraction may also help diagnose other conditions such as pulmonary embolism.[13] Acid-base balance can be affected by the aforementioned respiratory system abnormalities. For instance, acute respiratory acidosis and alkalemia result in acidemia and alkalemia, respectively. Additionally, hypoxemic hypoxia leads to anaerobic metabolism, which causes metabolic acidosis that results in acidemia. Metabolic system abnormalities also affect acid-balance as acute metabolic acidosis and alkalosis result in acidemia and alkalemia, respectively. Metabolic acidosis is seen in patients with diabetic ketoacidosis, septic shock, renal failure, drug or toxin ingestion, and gastrointestinal or renal HCO3 loss. Metabolic alkalosis is caused by conditions such as kidney disease, electrolyte imbalances, prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. An arterial blood gas can be analyzed as a point-of-care test, along with electrolytes (often called a Shock panel). It is essential that these machines are calibrated/standardized appropriately to ensure accurate and precise readings for clinical decisions. Please refer to the appropriate user manuals to ensure the appropriate device calibration at all times in discussion with the clinical laboratory team. ABG is recommended for evaluating a patient’s ventilatory, acid-base, and oxygenation status.[14] [Level 1A] Blood gas analysis is also recommended to evaluate a patient’s response to therapeutic interventions. [Level 2B] and for monitoring the severity and progression of documented cardiopulmonary disease processes.[14] [Level 1A] Despite its clinical value, erroneous or discrepant values represent a potential drawback of blood gas analysis, so eliminating potential sources of error is paramount.[6] Therefore, attention to detail in the sampling technique and processing is essential. Rigorous quality control of the automated blood gas analyzers is also necessary for accurate results. However, advances in machine performance and quality assurance have now made most errors, in point of care analysis, of ABG’s attributable to clinical providers.[6] Several necessary pre-analytic steps must be followed to obtain a valid, interpretable ABG.[6] In most hospital settings, ABG analysis is a process that involves multiple healthcare providers (e.g., physicians, respiratory therapists, and nurses). Hence, interprofessional coordination, cooperation, and communication are vitally important. The American Association for Respiratory Care has published Clinical Care Guidelines for Blood Gas Analysis and Hemoximetry that provides current best practices for sampling, handling, and analyzing ABG’s.[14] Notable sources of erroneous values at the time of blood draw include abnormal or misstated FiO2, barometric pressures, or temperatures. Temperature is a significant variable as it leads to PaO2 and O2 saturation discrepancies, as do acid-base disturbances. Several physiological and clinical conditions, such as hyperleukocytosis and dyshemoglobinemias, can also lead to PaO2 and O2 saturation discrepancies. Sample dilution can be an additional error source, with both liquid heparin and saline as potential culprits.[15] The mode of sample transportation is also of significance as discrepant values can result from air contamination after pneumatic tube system transport, compared with manual transport of the specimen, especially in the presence of inadvertent air bubbles.[15] Therefore, procuring samples using suitable syringes filled with adequate amounts of blood without air bubbles, maintaining them at correct temperatures, and transporting them appropriately and promptly for rapid analysis can minimize erroneous values.[15] Review Questions Modified Allen test. Illustration by Katherine Humphreys 1. Gattinoni L, Pesenti A, Matthay M. Understanding blood gas analysis. Intensive Care Med. 2018 Jan;44(1):91-93. [PubMed: 28497267] 2.Kim Y, Massie L, Murata GH, Tzamaloukas AH. Discrepancy between Measured Serum Total Carbon Dioxide Content and Bicarbonate Concentration Calculated from Arterial Blood Gases. Cureus. 2015 Dec 07;7(12):e398. [PMC free article: PMC4725444] [PubMed: 26824002] 3.Kumar V, Karon BS. Comparison of measured and calculated bicarbonate values. Clin Chem. 2008 Sep;54(9):1586-7. [PubMed: 18755915] 4.Dev SP, Hillmer MD, Ferri M. Videos in clinical medicine. Arterial puncture for blood gas analysis. N Engl J Med. 2011 Feb 03;364(5):e7. [PubMed: 21288091] 5.Zisquit J, Velasquez J, Nedeff N. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Oct 2, 2021. Allen Test. [PubMed: 29939593] 6.Cowley NJ, Owen A, Bion JF. Interpreting arterial blood gas results. BMJ. 2013 Jan 16;346:f16. [PubMed: 23325867] 7.Larkin BG, Zimmanck RJ. Interpreting Arterial Blood Gases Successfully. AORN J. 2015 Oct;102(4):343-54; quiz 355-7. [PubMed: 26411819] 8.Rogers KM, McCutcheon K. Four steps to interpreting arterial blood gases. J Perioper Pract. 2015 Mar;25(3):46-52. [PubMed: 26016282] 9.Romanski SO. Interpreting ABGs in four easy steps (continuing education credit). Nursing. 1986 Sep;16(9):58-64. [PubMed: 3638536] 10.ARDS Definition Task Force. Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012 Jun 20;307(23):2526-33. [PubMed: 22797452] 11.Pediatric Acute Lung Injury Consensus Conference Group. Pediatric acute respiratory distress syndrome: consensus recommendations from the Pediatric Acute Lung Injury Consensus Conference. Pediatr Crit Care Med. 2015 Jun;16(5):428-39. [PMC free article: PMC5253180] [PubMed: 25647235] 12.Rawat M, Chandrasekharan PK, Williams A, Gugino S, Koenigsknecht C, Swartz D, Ma CX, Mathew B, Nair J, Lakshminrusimha S. Oxygen saturation index and severity of hypoxic respiratory failure. Neonatology. 2015;107(3):161-6. [PMC free article: PMC4405613] [PubMed: 25592054] 13.Kurt OK, Alpar S, Sipit T, Guven SF, Erturk H, Demirel MK, Korkmaz M, Hayran M, Kurt B. The diagnostic role of capnography in pulmonary embolism. Am J Emerg Med. 2010 May;28(4):460-5. [PubMed: 20466226] 14.Davis MD, Walsh BK, Sittig SE, Restrepo RD. AARC clinical practice guideline: blood gas analysis and hemoximetry: 2013. Respir Care. 2013 Oct;58(10):1694-703. [PubMed: 23901131] 15.Albert TJ, Swenson ER. Circumstances When Arterial Blood Gas Analysis Can Lead Us Astray. Respir Care. 2016 Jan;61(1):119-21. [PubMed: 26682966] |
What is the difference between respiratory acidosis alkalosis and metabolic acidosis alkalosis?
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