Contact Hours: 3
This online independent study activity is credited for 3 contact hours at completion.
The purpose of this course is to provide healthcare providers with an overview of arterial blood gas interpretation, and acidosis and alkalosis conditions.
Arterial blood gas (ABG) analysis is a commonly used diagnostic tool to evaluate the partial pressure of gas in blood and acid-base content. It is especially important for critically ill patients and helps interpret respiratory, circulatory, and metabolic disorders. This course will discuss the step-by-step approach of ABG interpretation for nurses and other healthcare providers.
By the end of this learning activity, the learner will be able to:
- Review normal values for arterial blood gas interpretation.
- Describe indications and contraindications for obtaining an arterial blood gas.
- Identify causes of acidosis and alkalosis.
- Recognize the differences between metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis.
- Interpret an arterial blood gas through worked example.
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|ABG||The sampling of the blood levels of oxygen and carbon dioxide within the arteries.|
|Acidemia||A decrease in the arterial blood pH below 7.35. The hydrogen ion concentration of the blood increases, as reflected by a lowering of serum pH values.|
|Alkalemia||An abnormal pathophysiological condition that is characterized by a buildup of excess base or alkali in the body.|
|Allen Test||A standard test used to assess the arterial blood supply of the hand.|
|Anion Gap||(AG), A test that checks the acid-base balance and the balance of electrolytes in blood.|
|Anticholinergic Drugs||Drugs that block the action of acetylcholine.|
|Beta-Agonists||Medicine that opens the airways by relaxing the muscles around the airways.|
|Blood Gas Analysis||A commonly used diagnostic tool to evaluate the partial pressure of gas in blood and acid-base content.|
|Cl-||Chloride (chemical formula Cl-) is an electrolyte that helps keep a proper fluid and acid-base balance in the body.|
|Co2||Carbon dioxide (chemical formula CO2) is a chemical compound made up of molecules that each have one carbon atom covalently double bonded to two oxygen atoms.|
|Collateral Circulation||Alternate blood vessels in the body that can take over when another artery or vein becomes blocked or damaged.|
|Conn Syndrome||Primary aldosteronism (also called Conn’s syndrome) is a rare condition caused by overproduction of the hormone aldosterone that controls sodium and potassium in the blood.|
|HCO3||Bicarbonate, (chemical formula HCO3) is a byproduct of metabolism.|
|Hypercapnia||Arises from having too much carbon dioxide in the blood, usually resulting from not having enough oxygen in the body.|
|Metabolic Acidosis||A condition in which there is too much acid in the body fluids.|
|Metabolic Alkalosis||A condition in which the body produces too much bicarbonate, raising to pH to a level above normal.|
|Methylxanthines||A purine-derived group of pharmacologic agents that cause bronchodilation and stimulation.|
|PaCO2||The partial pressure of carbon dioxide in arterial blood.|
|Peripheral Vascular Disease||A slow and progressive circulation disorder that causes narrowed blood vessels, reducing blood flow in the arms or legs.|
|pH||The acid-base balance of the blood.|
|PO2||The concentration of oxygen in the blood.|
|Renin-Angiotensin-Aldosterone System||A physiological system that regulates blood pressure.|
|Respiratory Acidosis||A condition that occurs when the lungs cannot remove all the carbon dioxide the body produces.|
|Respiratory Alkalosis||Occurs when high levels of carbon dioxide disrupt the blood’s acid-base balance. It often occurs in people who experience rapid, uncontrollable breathing.|
|SpO2||Also known as oxygen saturation, is a measure of the amount of oxygen-carrying hemoglobin in the blood relative to the amount of hemoglobin not carrying oxygen.|
|Venous Blood Gas||An alternative method of estimating systemic carbon dioxide and pH that does not require arterial blood sampling.|
|∆||Symbol meaning change in a variable.|
ABG (arterial blood gas) interpretation is important for physicians, respiratory therapists, nurses, and other healthcare providers.1 Blood gas analysis is a commonly used diagnostic tool to evaluate the partial pressure of gas in blood and acid-base content.2 It is especially important for critically ill patients and helps interpret respiratory, circulatory, and metabolic disorders.2
For an ABG interpretation, the blood sample is explicitly taken from the artery and helps assess a patient’s partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2).2 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.2
Understanding the significance of the findings for arterial blood gases (ABG) is the first step in interpreting them. Without this understanding, the nurse cannot be expected to realize the implication of the results.3
This course will discuss the step-by-step approach of ABG interpretation for nurses and other healthcare providers.
Analyzing and monitoring the arterial blood gas (ABG) is essential in diagnosing and managing the oxygenation status and acid-base balance of high-risk patients and the care of those who are critically ill.4 Nurses must be able to analyze arterial blood gas competently, determine blood gas exchange levels, and assess renal, metabolic, and respiratory function.3
Before we move on to the process of ABG interpretation, it is important to review the normal values for ABG, indications, and contraindications for sampling.
Normal Values For ABG
Normal values for ABG may vary slightly between analyzers. Be sure to know the normal ranges and units for the analyzer you will use.5
- pH: 7.35 – 7.45
- pO2: 80-100 mmHg
- pCO2: 35-45 mmHg
- Base excess (BE): -2 – 3 mEq/L
- HCO3: 22 – 26 mEq/L
- SpO2: 95-99%
The following are indications for ABG interpretation3:
- Determine the partial pressure of respiratory gases
- Evaluate arterial respiratory gases during diagnostic workup
- Evaluate the effectiveness of mechanical ventilation in a patient with respiratory failure
- Monitor acid-base status
- Monitor metabolic, respiratory, and mixed acid-base disorders
- Venous sampling is not a viable option
The following are contraindications that may affect the analysis of ABG interpretation3:
- Abnormal Allen test
- Arteriovenous fistula
- Distorted anatomy
- Local infection
- Severe coagulopathy
- Severe peripheral vascular disease in the limb being tested
- Use of blood thinners
- Use of thrombolytic agents
- Vascular grafts
Factors That Affect ABG Interpretation
The following are factors that may make ABG interpretation difficult3:
- Difficulty in positioning the patient
- Obesity, as it obscures landmarks of access areas
- Poor distal perfusion from heart failure, hypovolemia, vasopressor therapy, etc.
- Pulses that cannot be easily identified
- Uncooperative patient
- Vascular disease leading to rigidity in vessel walls
ABG interpretation is used to analyze the patient’s physiologic state at the time of the test.3 The radial artery is typically the preferred site because it has collateral circulation and is accessible, but when it is not a viable option, the femoral or brachial artery can be used.3
Although there are many guides and methods available to interpret an ABG, we will discuss a 6-step approach based on the anion gap.1 The anion gap is an artificial measure that is calculated by subtracting the total number of anions (Cl- + HCO3–) from the total number of cations (Na+).6
This step involves assessing the internal consistency of the values using the Henderson-Hasselbalch equation1:
[H+] = 24(PaCO2)
The ABG is not valid if the pH and the [H+] are inconsistent.1
Table 1: pH and the appropriate [H+] values1
|pH||Approximate [H+] (nmol/L)|
Next, you need to check if there is alkalemia or acidemia present.1 The normal pH is 7.35-7.45. If a pH is less than 7.40, acidosis may be present. If the pH is greater than 7.40, alkalosis may be present. For example, a pH of 7.37 would be categorized as acidosis, and a pH of 7.42 would be categorized as alkalemia.2
Remember, this is usually a primary disorder, and alkalemia or acidemia might be present even if the pH is in the normal range (7.35 – 7.45).1
Now, you need to determine if the disturbance is respiratory or metabolic.1 For this, you can evaluate the respiratory and metabolic components of the ABG results, the PaCO2 and HCO3, respectively.2
What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders, the pH and PaCO2 change in the same direction.1 We have summarized the relationships in the table below.
Table 2: Relationship between pH and PaCO21:
|Acidosis||Respiratory||pH ↓||PaCO2 ↑|
|Acidosis||Metabolic||pH ↓||PaCO2 ↓|
|Alkalosis||Respiratory||pH ↑||PaCO2 ↓|
|Alkalosis||Metabolic||pH ↑||PaCO2 ↑|
Next step is used to determine if there is appropriate compensation for the primary disturbance.1 Usually, compensation does not return the pH to normal (7.35 – 7.45).1 Also, If the observed compensation is not the expected compensation, more than one acid-base disorder is likely present.1
Table 3: Disorders and expected compensation1
|Disorder||Expected Compensation||Correction Factor|
|Metabolic acidosis||PaCO2 = (1.5 x [HCO3-]) +8||± 2|
|Acute respiratory acidosis||Increase in [HCO3-] = ∆ PaCO2/10||± 3|
|Chronic respiratory acidosis||Increase in [HCO3-] = 3.5(∆ PaCO2/10)|
|Metabolic alkalosis||Increase in PaCO2 = 40 + 0.6(∆HCO3-)|
|Acute respiratory alkalosis||Decrease in [HCO3-] = 2(∆ PaCO2/10)|
|Chronic respiratory alkalosis||Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆ PaCO2/10)|
Next, if a metabolic acidosis exists, you need to calculate the anion gap.1 A normal anion gap is approximately 12 meq/L, but it can vary in patients with hypoalbuminemia.1 In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the “normal” anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration.1
If the anion gap increases, consider calculating the osmolal gap in compatible clinical situations.1 An elevation in the anion gap may not be explained by an obvious case (diabetic ketoacidosis, lactic acidosis, renal failure), moreover, toxic ingestion should also be suspected.1
If an increased anion gap is present, assess the relationship between the increase in the anion gap and the decrease in [HCO3-].1 The ratio of the change should be between 1.0 and 2.0 if an uncomplicated anion gap metabolic acidosis is present.1
But if the ratio falls outside this range, another metabolic disorder is present.1 For instance, if ∆AG/∆[HCO3-] < 1.0, then a concurrent non-anion gap metabolic acidosis is likely to be present and if ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic alkalosis is likely to be present.1
To better understand the 6-step approach, consider the worked example below.
Example2: ABG: pH = 7.39, PaCO2 = 51 mm Hg, PaO2 = 59 mm Hg, HCO3 = 30 mEq/L and SaO2 = 90%, on room air.
- pH is in the normal range, so use 7.40 as a cutoff point, in which case it is <7.40, acidosis is present.
- The PaCO2 is elevated, indicating respiratory acidosis, and the HCO3 is elevated, indicating metabolic alkalosis.
- The value consistent with the pH is PaCO2. Therefore, this is a primary respiratory acidosis. The acid base that is inconsistent with the pH is the HCO3, as it is elevated, indicating a metabolic alkalosis, so there is compensation signifying a non-acute primary disorder because it takes days for metabolic compensation to be effective.
- Last, the PaO2 is decreased, indicating an abnormality with oxygenation. However, history and physical will help delineate the severity and urgency of required interventions, if any.
Arterial blood gas (ABG) analysis is a key step in assessing the adequacy of oxygenation and ventilation while diagnosing and monitoring acid-base disturbances.7 But an arterial puncture is required for the blood sample. It can lead to complications like pain, hematoma, nerve injury, etc.7 In contrast, central venous blood gas (VBG) analysis may allow an estimate of ABG values. It can be obtained from an indwelling central venous catheter.7
It has been researched that an arterial access can cause more pain than venous access and may also be difficult due to patient position or diminished pulses, which may delay care and results.7 But there are some drawbacks of VBG as well.7 Venous blood PO2 cannot estimate arterial PO2, and pulse oximetry is more commonly used for monitoring oxygenation.7
However, multiple studies have examined the utility of peripheral VBG in assessing ventilation and acid-base status and concluded that pH and PCO2 in peripheral venous blood closely approximate arterial levels.7
In a review of seven studies, findings suggest that measuring blood gas values from centrally obtained venous blood is a good substitute for estimating arterial pH and PCO2 values in critically ill patients who are hemodynamically stable.7
There are four major acid-base disorders, namely, respiratory acidosis, metabolic acidosis, respiratory alkalosis, and metabolic alkalosis.3
Respiratory acidosis is caused by inadequate alveolar ventilation leading to CO2 retention.6 Simply put, in this condition, the lungs cannot eliminate enough of the carbon dioxide made by the body.3 As a result, the body excretes the extra hydrogen in the urine and exchanges it for bicarbonate ions.3 HCO3 rises to restore the body to a normal pH when this happens. Until the pH returns to normal, the PaCO2 may stay elevated.3 It can be subcategorized as acute, chronic, or acute and chronic.8
A respiratory acidosis would have the following characteristics on an ABG3,6:
- ↓ pH
- ↑ CO2
There are multiple causes and situations that can lead to a patient having a depressed respiratory status, such as hypoventilation, asphyxia, asthma, central nervous system depression, chronic obstructive pulmonary disease, infection, Guillain-Barre, and drug-induced respiratory depression.3,6
Once the diagnosis has been made, the underlying cause of respiratory acidosis must be treated.8 The hypercapnia should be corrected gradually because rapid alkalization of the cerebrospinal fluid (CSF) may lead to seizures.8
To improve ventilation, pharmacologic therapy can also be used. Bronchodilators like beta-agonists, anticholinergic drugs, and methylxanthines can be used in treating patients with obstructive airway diseases.8 Naloxone can be used in patients who overdose on opioid use.8
Metabolic acidosis is not a benign condition and signifies an underlying disorder that needs immediate attention to minimize morbidity and mortality.9 It can occur because of either increased acid production or acid ingestion, decreased acid excretion, or increased rate of gastrointestinal and renal HCO3– loss.6
When patients demonstrate metabolic acidosis, their bodies pull the HCO3 into the cells as a buffer and deplete the plasma level. The body begins compensating by increasing ventilation; thus, renal retention of the HCO3 occurs.3
A metabolic acidosis would have the following characteristics on an ABG:3,6
- ↓ pH
- ↓ HCO3-
- ↓ BE
The type of metabolic acidosis helps determine the cause of the disturbance. For instance, the classification of metabolic acidosis is based on the presence or absence of an anion gap or concentration of unmeasured serum anions.9
A few conditions can cause metabolic acidosis. For instance, HCO3 loss from diarrhea, shock, renal tubular acidosis, drug intoxication, salicylate poisoning, renal failure, diabetic ketoacidosis, and circulatory failure producing lactic acid can all cause metabolic acidosis.3
We can also categorize the causes based on the epidemiology:3
- Increased acid production – increased anion gap
- Lactic acidosis
- Ingestions – aspirin, methanol, ethylene glycol
- Loss of bicarbonate – generally, a normal anion gap
- Intestinal tube drainage
- Carbonic anhydrase inhibitor
- Renal tubular acidosis Type 2
- Decreased renal acid secretion
- Chronic kidney disease
- Renal tubular acidosis Type 1 and 4
Treatment of metabolic acidosis depends on the cause and whether it is acute or chronic.3 For instance, adequate fluid resuscitation and correction of electrolyte abnormalities are necessary for sepsis and diabetic ketoacidosis.9
In severe metabolic acidosis, sodium bicarbonate is sometimes used.3 Other therapies to consider include antidotes for poisoning, dialysis, and antibiotics.9
Respiratory alkalosis is caused by excessive alveolar ventilation (hyperventilation), resulting in more than normal CO2 exhaling. As a result, PaCO2 is reduced, and pH increases, causing alkalosis.6 It can be acute or chronic and is mainly based on the level of metabolic compensation for the respiratory disease.10 For instance, acute respiratory alkalosis is associated with high bicarbonate levels resulting from inadequate time to lower the HCO3 levels. Chronic respiratory alkalosis is associated with low to normal HCO3 levels.10
A respiratory alkalosis would have the following characteristics on an ABG:3,6
- ↑ pH
- ↓ CO2
The primary cause of all respiratory alkalosis etiologies is hyperventilation.10 These include central causes, hypoxemic causes, pulmonary causes, and iatrogenic causes.10
- Head injury
- Hypoxic stimulation leads to hyperventilation to correct hypoxia at the expense of CO2 loss.
- Acute asthma
- COPD exacerbations
- Pulmonary embolisms
- iatrogenic causes are primarily due to hyperventilation in intubated patients on mechanical ventilation.
Treatment for respiratory alkalosis is focused on treating the underlying problems, such as 10:
- In anxious patients, anxiolytics may be necessary.
- In infectious diseases, antibiotics targeting sputum or blood cultures are appropriate.
- In embolic disease, anticoagulation is necessary.
Patients with acute respiratory failure, acute asthma, or acute, chronic obstructive pulmonary disease (COPD) exacerbation may need ventilator support.10
In ventilator-controlled patients, it may be necessary to reevaluate their ventilator settings to reduce the respiratory rate. If hyperventilation is intentional, monitor the arterial or venous blood gas values closely. In severe cases, the pH may be directly reduced by using acidic agents. However, this is not a routine clinical practice.10
Metabolic alkalosis occurs due to decreased hydrogen ion concentration, leading to increased bicarbonate or increased bicarbonate concentrations.6 The kidneys will increase the HCO3 excretion trying to conserve the hydrogen. As a result, the respiratory system will compensate by decreasing ventilation, conserving CO2, and raising PaCO2.3
A metabolic alkalosis would have the following characteristics on an ABG:6
- ↑ pH
- ↑ HCO3-
- ↑ BE
Multiple causes and diseases induce metabolic alkalosis.11 In general, the causes can be narrowed down to an intracellular shift of hydrogen ions, gastrointestinal (GI) loss of hydrogen ions, excessive renal hydrogen ion loss, retention or addition of bicarbonate ions, or volume contraction around a constant amount of extracellular bicarbonate known as contraction alkalosis. All of which leads to the net result of increased levels of bicarbonate in the blood.11
Before considering treatment, we need to know the types of metabolic alkalosis. Metabolic alkalosis is split into 2 main categories11:
- Chloride responsive with urine chloride less than 10 mEq/L
- Chloride resistant with urine chloride greater than 20 mEq/L
The treatment of chloride-resistant metabolic alkalosis focuses on treating the underlying condition that triggered the alkalotic event.11 Since many of these pathologies result from the effect on the renin-angiotensin-aldosterone system, treatment includes11:
- Inhibiting the effect of aldosterone on the nephron using potassium-sparing diuretics such as amiloride and triamterene.
- Investigating a malignant source, such as primary hyperaldosteronism and Conn syndrome.
In chloride-responsive metabolic alkalosis, this includes the repletion of electrolytes, specifically chloride and potassium, and fluid replenishment.11 In scenarios such as congestive heart failure (CHF) or edematous states, diuresis is essential using potassium-sparing diuretics.11
In addition to the four major acid-base disturbances, there are multiple mixed and complex disorders.
Table 4: Selected mixed and complex acid-base disturbances1
|Respiratory acidosis with metabolic acidosis||↓in pH ↓ in HCO3 ↑ in PaCO2||Cardiac arrest Intoxications Multi-organ failure|
|Respiratory alkalosis with metabolic alkalosis||↑in pH ↑ in HCO3- ↓ in PaCO2||Cirrhosis with diuretics Pregnancy with vomiting Over ventilation of COPD|
|Respiratory acidosis with metabolic alkalosis||pH in normal range ↑ in PaCO2, ↑ in HCO3-||COPD with diuretics, vomiting, NG suction Severe hypokalemia|
|Respiratory alkalosis with metabolic acidosis||pH in normal range ↓ in PaCO2 ↓ in HCO3||Sepsis Salicylate toxicity Renal failure with CHF or pneumonia Advanced liver disease|
|Metabolic acidosis with metabolic alkalosis||pH in normal range HCO3- normal||Uremia or ketoacidosis with vomiting, NG suction, diuretics, etc.|
Acid-base disorders are typically associated with a compensatory response that lessens the HCO3/ PaCO2 ratio change and, consequently, the pH.3 Remember that pH is closely controlled in the human body, and there are various mechanisms to maintain it at a constant value.5
It is important to note that the body will never overcompensate as the drivers for compensation cease as the pH returns to normal. In essence, compensation for an acidosis will not cause an alkalosis or vice versa.5
Respiratory compensation is a rapid adjustment. In metabolic acidosis, the respiratory compensation starts within 30 minutes and is usually done in 12-24 hours.3
If metabolic acidosis develops, the change is sensed by chemoreceptors centrally in the medulla oblongata and peripherally in the carotid bodies.5 The body responds by increasing the depth and rate of respiration, increasing the excretion of CO2 to try to keep the pH constant.5
If respiratory acidosis develops, for example, in CO2 retention secondary to COPD, the kidneys will start to retain more HCO3 to correct the pH.5 The result is a low normal pH with a high CO2 and high bicarbonate, and this process can take over days.5
Compensation effects are only seen in chronic conditions.3 If the compensating effect is inappropriate, then a complex acid-base disorder may be present.5
Table 5: Overview of compensating effect3
|Disorder||pH||Initiating Event||Compensating Effect|
|Respiratory Acidosis||↓||↑ PaCO2||↑ HCO3|
|Respiratory Alkalosis||↑||↓ PaCO2||↓ HCO3|
|Metabolic Acidosis||↓||↓ HCO3||↓ PaCO2|
|Metabolic Alkalosis||↑||↑ HCO3||↑ PaCO2|
You are assessing a 60-year-old male in the intensive care unit. He has just arrived from surgery and per the report, he was administered pain medication prior to being transported. The results of the ABG values include pH 7.21, PaCO2 64 mm Hg, HCO3 = 24 mm Hg. What does the ABG reflect?
- Respiratory acidosis
- Metabolic alkalosis
- Respiratory alkalosis
- Metabolic acidosis
*The ABG shows respiratory acidosis, which is likely caused by hypoventilation because of pain medication administration.
The condition of severe trauma is a major global issue as it accounts for one in ten mortalities.12 The pre-hospital resuscitation and monitoring of trauma patients rely on clinical experience and a few basic parameters, including consciousness, breathing quality and rate, heart rate, and blood pressure.12 But even when these parameters are normal or close to normal, the risks of shock are high at cellular and organ levels.12 Thus, the complete resuscitation from shock is indicated through the successful reversal of anaerobic metabolism and tissue acidosis.12
Here is where ABG is helpful. Abnormal arterial blood gas (ABG) is known to be an essential marker for poor outcomes along with occult malperfusion.12 Because of this, ABG is used as a screening tool among patients sustaining trauma for occult injury.12
A study investigated the association between arterial blood gases and the coagulation profile of multiple trauma patients. The findings showed that decreased bicarbonate serves as a predictor for the high risk of multiple traumas among patients.12 Moreover, PCO2 was also demonstrated to lead to worse outcomes concerning multiple trauma patients, which was linked to high-risk trauma patients.12
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 helpful in confirming and calibrating non-invasive monitoring techniques.2
ABG analysis is also used to evaluate a patient’s response to therapeutic treatments and for monitoring the severity and progression of documented cardiopulmonary disease processes.2 Despite its clinical value, erroneous or discrepant values represent a potential drawback of blood gas analysis, so eliminating potential sources of error is paramount. Therefore, nurses should provide attention to detail in the sampling and processing technique.2
The American Association for Respiratory Care has published Clinical Care Guidelines for Blood Gas Analysis and Hemoximetry that provide current best practices for sampling, handling, and analyzing ABGs.2
- Kaufman D. American Thoracic Society – Interpretation of Arterial Blood Gases (ABGs). Thoracic.org. Published 2019. https://www.thoracic.org/professionals/clinical-resources/critical-care/clinical-education/ABGs.php
- Castro D, Keenaghan M. Arterial blood gas. National Library of Medicine. Published 2021. https://www.ncbi.nlm.nih.gov/books/NBK536919/
- Edu, N. (2020). ABG interpretation for nurses.
- Safwat AM, Khorais AM. Effectiveness of a computer-based learning module on arterial blood gas interpretation among staff nurses in critical care units. International journal of Nursing Didactics. 2018;8(03). doi:10.15520/ijnd.v8i03.2087
- Oxford Medical Education. Arterial Blood Gas (ABG) interpretation for medical students, OSCEs and MRCP. Oxford Medical Education. Published July 29, 2014. https://oxfordmedicaleducation.com/ABGs/ABG-interpretation/
- Zaininger. ABG Interpretation | A guide to understanding ABGs | Geeky Medics. Geeky Medics. Published June 12, 2016. https://geekymedics.com/ABG-interpretation/
- Chong WH, Saha BK, Medarov BI. Comparing Central Venous Blood Gas to Arterial Blood Gas and Determining Its Utility in Critically Ill Patients: Narrative Review. Anesthesia & Analgesia. Published online March 29, 2021. doi:10.1213/ane.0000000000005501
- Shivani Patel, Sandeep Sharma. Physiology, Respiratory Acidosis. Nih.gov. Published June 24, 2021. https://www.ncbi.nlm.nih.gov/books/NBK482430/
- Burger, M., & Schaller, D. J. (2019, June 4). Metabolic Acidosis. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482146/
- Brinkman, J. E., & Sharma, S. (2019, June 23). Physiology, Respiratory Alkalosis. Nih.gov; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482117/
- Brinkman, J. E., & Sharma, S. (2020). Physiology, Metabolic Alkalosis. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482291/
- Raffee, L. A., Oteir, A. O., Alawneh, K. Z., & Alustath, A. M. (2020). Relationship Between Initial Arterial Blood Gases and Coagulation Profiles – Analyzing the Prognosis and Outcomes in Patients with Multiple Injuries/Trauma. Open Access Emergency Medicine, Volume 12, 87–92. https://doi.org/10.2147/oaem.s244941