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ABG Interpretation - 2 Contact Hours

This course is approved through the California Board of Registered Nursing Provider #CEP 13509.

 

Authors: Raymond Lengel (MSN, FNP-BC, RN)

Outcomes

The course will provide an overview of arterial blood gas interpretation, raise awareness and understanding of the various aspects of arterial blood gases, and increase the healthcare provider's knowledge base.

Objectives

After completion of this course, the learner will be able to:

  1. List the steps in obtaining an arterial blood gas (ABG) sample.

  2. Compare and contrast metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis.

  3. List common causes of metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis.

  4. Interpret ABGs given a clinical scenario.

  5. Identify compensation of ABGs given a clinical scenario.

Introduction

Understanding the significance of the findings of arterial blood gases (ABGs) is the first step in interpreting them. Without this understanding, the healthcare provider cannot be expected to realize the implications of the results.

Adult students demonstrate various methods of learning to enhance their knowledge base. Finding the best education method for the individual is the first step to success in clinical competence. Short educational modules for healthcare providers in ABG analysis can significantly impact improving knowledge. Therefore, this course will use case studies to help learners understand ABGs.

Many disorders can cause acid-base imbalances. Acid-base imbalances can be life-threatening, so managing them is critical. In order to manage the underlying cause of the acid-base imbalance, the cause must be established. Prior to determining the cause, the specific acid-base imbalance must be confirmed. Determining the type of imbalance can be challenging. Therefore, this course will discuss the characteristics of each acid-base imbalance and then help the learner determine which imbalance is present.

photo of abg analysis

ABG Analysis

Arterial Blood Gas Sampling

ABG sampling involves the direct puncture of an artery. It is associated with a low incidence of complications, determines blood gas exchange levels, and assesses renal, metabolic, and respiratory function.

The purpose of ABGs includes:

  • Determining the partial pressure of respiratory gases that are involved in ventilation and oxygenation
  • Evaluating arterial respiratory gases during diagnostic workups
  • Monitoring acid-base status
  • Monitoring for metabolic, respiratory, and mixed acid-base disorders
  • Evaluating the effectiveness of mechanical ventilation in a patient with respiratory failure
  • Getting a blood sample when venous sampling is not feasible

Absolute contraindications to ABGs include the following:

  • Local infection
  • Distorted anatomy
  • Abnormal Allen test – at the radial site
  • Severe peripheral vascular disease in the limb being tested
  • Arteriovenous fistulas
  • Vascular grafts

Relative contraindications to ABGs include the following:

  • Severe coagulopathy
  • Currently taking blood thinners (warfarin, heparin, direct thrombin inhibitors, or factor X inhibitors)
  • Use of thrombolytic agents

Factors that make ABGs difficult include the following:

  • Uncooperative patient
  • Pulses that cannot be identified easily
  • Difficulty in positioning the patient
  • Obesity – because subcutaneous fat over access areas obscures landmarks
  • Vascular disease leading to rigidity in vessel walls
  • Poor distal perfusion – e.g., heart failure, dehydration

Sources of errors include:

  • Air bubbles can increase the partial pressure of oxygen in arterial blood (PaO2) and lower the partial pressure of carbon dioxide in arterial blood PaCO2
  • Excessive heparin can distort values
  • Delay in analyzing the specimen
  • Gas may diffuse through a plastic syringe
  • Acid-base balance may be inaccurate in arterial blood in those with reduced cardiac output (cardiopulmonary resuscitation [CPR]/circulatory failure)

ABGs reflect the patient's physiologic state when the test is done. The radial artery is typically the preferred site because it has collateral circulation and is accessible. When the radial artery is not feasible, the femoral or brachial artery can be used. The femoral artery is deeper, and there is a greater risk of damage to adjacent structures. It is close to the femoral vein and nerve. When the femoral artery is sampled, it requires monitoring and is often only done in an inpatient setting.

The brachial artery is also deep and is more difficult to identify. There are multiple obstacles to the brachial artery. It is a small-caliber vessel with poor collateral circulation, and attaining hemostasis is more difficult.

Repeated punctures increase the risk of artery laceration, inadvertent venous sampling, hematoma, and scarring. When frequent sampling is needed, an indwelling arterial catheter may be beneficial.

When it is difficult to identify sampling sites, such as those with weak pulses, distorted anatomic landmarks, or when a deep vascular artery is being accessed, ultrasound-guided ABG sampling may be used. Ultrasound allows for more accurate needle placement and reduces the risk of damage to the surrounding structures.

Table 1: Key Points to ABG Sampling
  • A vein is likely punctured if there is a lack of pulsatile flow or the blood is very dark.
  • Pulling the needle back may help when no blood is obtained, as the needle may have gone through the artery.
  • If air bubbles are not removed, the partial pressure of oxygen may be increased.
  • For those with a lot of soft tissue or extra skin over the puncture site, the non-dominant hand can be used to smooth the skin.
  • An ultrasound may be used to find the femoral or brachial artery.
  • If no arterial blood flow occurs when the needle is inserted, the pulse should be found again, and the needle should be repositioned and redirected to the pulse.
  • When there is poor distal perfusion, the plunger is often pulled back to get a blood sample; this increases the risk of getting a venous sample, which occurs in those with advanced heart failure or dehydration.
  • Do not puncture the femoral or brachial artery if there is poor perfusion distally.
(Danckers, 2022)

Allen Test

Before getting a blood sample from the radial artery, collateral circulation should be assessed, commonly done with the Allen or modified Allen test. The modified Allen test ensures ulnar artery collateral circulation and palmar arch patency.

In the modified Allen test, the patient flexes their arm and clenches the fist to exsanguinate the hand. At the same time, the clinician compresses the radial and ulnar arteries. The arm is then extended (to no more than 180 degrees; the patient should not overextend the hand or spread the fingers wide, leading to false-normal results), the fist is opened, and pressure is removed from the ulnar artery. Within 5-15 seconds, the color should return to the hand, which suggests that the ulnar artery and the superficial palmar arch are open. If it takes more than 15 seconds, the test is abnormal.

graphic showing modified allen test

Modified Allen Test

Another method to assess circulation includes using a pulse oximeter. The oximeter is placed on the thumb, and a baseline saturation is obtained. Then, the ulnar and radial arteries are compressed until saturation reaches zero. Next, the pressure on the ulnar artery is released, and the saturation should return to baseline, suggesting adequate collateral blood flow.

The Allen test (from which the modified Allen test evolved) is performed similarly. The patient raises both arms above the head for thirty seconds, then clenches their fists while the clinician occludes both radial arteries. The hands are opened rapidly, and the initial pallor should transition to normal color as the ulnar arteries return blood flow. The test is done again while occluding the ulnar arteries. Normal color should return.

Much debate has been held regarding obtaining a modified Allen test before obtaining ABGs. Many believe the modified Allen test is a standard of care and should be written into policy at facilities nationwide. Unfortunately, it is not definitely known if it can predict ischemic complications when radial artery occlusion is present (Danckers, 2022).

Determining abnormality is challenging because the definition of an abnormal Allen test is difficult to describe. In a study by Jarvis et al. (2000), the conclusion was that the Allen test was only accurate about 80% of the time.

A recent study examined the modified Allen test and its ability to determine adequate collateral circulation in the palm. The study concluded that the modified Allen test is not valid as a screening tool for collateral circulation of the hand. It also cannot predict ischemia in the hand after an ABG measurement. It was concluded that inadequate evidence supports its use before arterial puncture (Romeu-Bordas & & Ballesteros-Peña, 2017).

Golamari and Gilchrist (2021) agree with the lack of evidence to support the Allen test's use. The authors suggest that the test depends on the clinician's skill; abnormal findings are not standardized, and observational bias can occur. In addition, the transformation of abnormal testing into a clinical outcome is unknown. Even though the Allen test is controversial, hospital policy must always be followed.

Performing Arterial Blood Gas Sampling

Technique

  • Determine the site to be sampled.
  • The site is prepped in a sterile fashion.
  • Consider local anesthesia before arterial puncture, as it reduces pain without negatively impacting the procedure.
  • Use an ABG kit.
  • Palpate the artery with the non-dominant hand.
  • Puncture the artery with the needle at a 45-degree angle relative to the skin.
  • The syringe should fill on its own – get 2-3 mL of blood.
  • Hold pressure on the site for 5-10 minutes.

Before performing ABGs, the patient should be educated about the procedure, including the risks and benefits. The patient should inform the health care provider if there is new/worsening pain, reduced movement, numbness/tingling in the limb, or active bleeding after the procedure.

The patient should lie supine with the forearm supinated on a hard surface to get a sample from the radial artery. The wrist is extended 20-30 degrees; a small roll may be put under the wrist to make the radial artery more superficial. If a sample is taken from the femoral artery, the patient is supine with the leg in a neutral position. Place the arm on a firm surface if blood is taken from the brachial artery. The shoulder is abducted with the forearm supinated and the elbow extended.

The provider should wear gloves and eye protection when performing ABG sampling. The site should be cleaned with an antiseptic solution. The non-dominant hand locates the arterial pulse with the second and third fingers, with both fingers proximal to the desired puncture site.

The needle is inserted at a 45-degree angle aiming at the artery, with the bevel facing upwards. When the needle is angled, it reduces vessel trauma. It allows the muscle fibers to seal the puncture site after the puncture.

When the blood starts filling the syringe, remove the non-dominant hand. After 2-3 ml is obtained, the needle is removed, and gauze is placed over the site with the non-dominant hand to hold pressure for five minutes. Pressure may need to be held longer for those at risk for bleeding. Afterward, an adhesive dressing should be placed over the puncture site.

The excess air should be removed from the syringe, capped, and placed in ice while awaiting analysis. No air bubbles should be present as this may underestimate the PaCO2 and overestimate the PaO2.

The nurse must monitor for complications. Active profuse bleeding from the puncture site suggests a vessel laceration. Compartment syndrome may result from an expanding hematoma that compromises circulation. Compartment syndrome is suggested by the six P's: pain, pallor, paresthesia, paralysis, poikilothermia, and pulselessness. Ischemia from a thrombus, vasospasm, or arterial occlusion presents as pulselessness, color change, and distal coldness. A nerve injury may present with paresis and persistent pain. Infection presents with fever and local erythema.

Arterial Blood Gas Interpretation

When interpreting the ABG results, one must first know the five major components of the ABG to be addressed: oxygen saturation (SaO2), PaO2, acidity or alkalinity (pH), PaCO2, and bicarbonate ion concentration (HCO3).

  • Acidemia – arterial pH less than 7.35
  • Acidosis – lowering of the extracellular fluid pH caused by an elevated PaCO2 or a reduced HCO3
  • Metabolic acidosis – reduction in pH and serum HCO3
  • Respiratory acidosis – reduction in pH with an elevation of the PaCO2
  • Alkalemia – arterial pH above 7.45
  • Alkalosis – elevation of the extracellular fluid pH caused by a fall in PaCO2 or a rise in HCO3
  • Metabolic alkalosis - elevation in pH and serum HCO3
  • Respiratory alkalosis – elevation of the pH with a reduction in the PaCO2
  • Mixed acid-base disorder – more than one acid-base disorder at the same time
  • Anion gap = (Sodium [Na]) - (Chloride [Cl] + HCO3)
    • The normal range is 8-16 milliequivalents per liter (mEq/L)
(Sood et al., 2010)
Table 2: Key Definitions for Interpreting ABGs

The four main acid-base disorders are respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis.

The acid-base balance of the blood is maintained by two areas of the body: the lungs and the kidneys. The lower pH represents acidosis, and the higher pH represents alkalosis, with the normal pH ranging from 7.35 to 7.45.

PaO2 evaluates the oxygen in plasma and has an 80-95 millimeters of mercury (mm Hg) normal range. PaO2 does not measure the amount of oxygen attached to the hemoglobin. SaO2 measures the amount of oxygen attached to the hemoglobin. The normal range is 95-100% and generally should be above 90%.

PaCO2 evaluates the ventilation component. The normal range is 35-45 mm Hg. The value is inversely related to ventilation. For example, decreased ventilation is associated with a higher value, and increased ventilation is associated with a lower value. Therefore, hyperventilation can lead to alkalosis because the patient is blowing off carbon dioxide, and hypoventilation can lead to acidosis because the patient is retaining carbon dioxide. The body adjusts to these conditions by changing the respiratory rate.

The kidneys regulate HCO3 (bicarbonate) and evaluate the metabolic component. The normal bicarbonate range is 22-26 mEq/L. Below 22 mEq/L is considered acidotic, and above 26 mEq/L is alkalotic. The kidneys compensate for respiratory alkalosis and acidosis, but it takes up to five days for the renal system to compensate for respiratory disorders. The kidneys compensate for respiratory acidosis by increasing bicarbonate resorption and excretion of hydrogen ions. The kidneys compensate for respiratory alkalosis by excreting bicarbonate and lowering newly generated bicarbonate.

Table 3: Normal ABG Values
Test Normal Values
pH 7.35-7.45
HCO3 22-26 mEq/L
PaCO2 35-45 mm Hg
PaO2 80-95 mm Hg
SaO2 95-100%
*Note: These ranges can differ slightly depending on the facility/scale used.
(Castro et al., 2022)

Four abnormal conditions can be identified based on the ABGs: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. We will better understand what is happening within the body as we explore these conditions, the potential causes, the ABG values, and the compensatory mechanisms.

Respiratory Acidosis

Respiratory acidosis occurs when the lungs cannot eliminate enough of the carbon dioxide made by the body. In order to compensate, the kidneys work to normalize the pH. The kidneys attempt to excrete hydrogen in the urine and reabsorb bicarbonate ions. When this happens, the bicarbonate rises to restore the body to a normal pH.

Any situation that can cause the patient to develop a depressed respiratory status can cause respiratory acidosis. Examples include hypoventilation, asphyxia, central nervous system depression, chronic obstructive pulmonary disease, infection, and drug-induced respiratory depression (Table 10).

The ABG values one would see with respiratory acidosis would be pH < 7.35, PaCO2 > 45 mm Hg, and HCO3 > 26 mEq/L if compensating.

In acute respiratory acidosis, the HCO3 increases by approximately 1 mEq/L for each 10 mm Hg in PaCO2 to compensate. In chronic respiratory acidosis (after 3-5 days), the HCO3 will increase by 3-5 mEq/L per 10 mm Hg of PaCO2. If there is a mild-to-moderate chronic respiratory acidosis, suggested by a PaCO2 of less than 70 mm Hg, the pH may be in the low-normal range or slightly reduced. If the pH is significantly acidic in chronic respiratory acidosis, there may be a co-existent metabolic acidosis or acute respiratory acidosis. If the pH is 7.40 or more, there is likely a co-existent acute respiratory alkalosis or a metabolic alkalosis.

Table 4: Respiratory Acidosis
pH Decreased
PaCO2 Increased
HCO3 Normal (increased if compensating)
(Castro et al., 2022)

Respiratory Alkalosis

Respiratory alkalosis is an increased pH due to a respiratory process. Conditions that cause the respiratory system to be overstimulated can be causative factors in respiratory alkalosis, such as hyperventilation (see Table 10). In addition, respiratory alkalosis can be seen in critically ill patients, such as those on ventilators (mechanical overventilation) and those who have pulmonary embolism, asthma exacerbation, sepsis, salicylic acid poisoning, and pneumonia.

The ABG values one would see with respiratory alkalosis would be pH > 7.45, PaCO2 < 35 mm Hg, and HCO3 < 22 mEq/L if compensating.

In acute respiratory alkalosis, the compensation is to lower the serum HCO3 by 2 mEq/L for every 10 mm Hg reduction in PaCO2. In chronic respiratory alkalosis (after 3-5 days), the serum HCO3 falls about 4-5 mEq/L for every 10 mm Hg reduction in PaCO2.

Table 5: Respiratory Alkalosis
pH Increased
PaCO2 Decreased
HCO3 Normal (decreased if compensating)
(Castro et al., 2022)

Metabolic Acidosis

Metabolic acidosis occurs when too much acid builds up in the body, and it results from one of the following: increased acid production, reduced ability of the kidneys to excrete acids, or bicarbonate loss.

Calculation of the serum anion gap should be determined in metabolic acidosis. Online calculators can help with this calculation. The anion gap is typically classified as high or normal, and determining the anion gap will help determine the cause of metabolic acidosis. The anion gap is affected by albumin levels. If the albumin levels drop by one point, the anion gap drops by 2.5.

When patients present with the following conditions, one must consider metabolic acidosis: profuse diarrhea, shock, renal tubular acidosis, drug intoxication, salicylate poisoning, renal failure, diabetic ketoacidosis, and circulatory failure.

ABG values one would see with metabolic acidosis would be pH < 7.35, HCO3 < 22 mEq/L, and PaCO2 < 35 mm Hg if compensating. Symptoms present in metabolic acidosis include anxiety, headache, nausea, vomiting, low blood pressure, and hyperventilation.

Respiratory compensation for metabolic acidosis causes a reduction in the arterial PaCO2 by about 1.2 mm Hg for every 1 mEq/L reduction in the serum HCO3. The response starts in about thirty minutes and is typically complete within 24 hours.

Winter's formula [Expected CO2 = (Bicarbonate x 1.5) + (8 +/- 2)] predicts the expected carbon dioxide in metabolic acidosis. The expected carbon dioxide should align with the measured carbon dioxide in normal compensation. If the predicted carbon dioxide is higher than expected, there is an additional respiratory acidosis. If it is less than expected, an additional respiratory alkalosis is present.

Table 6: Metabolic Acidosis
pH Decreased
PaCO2 Normal (decreased if compensating)
HCO3 Decreased
(Castro et al., 2022)

If there is an increased anion gap, one can use the mnemonic MUDPILES to predict the cause of acidosis. MUDPILES stands for: Methanol, Uremia, Diabetic ketoacidosis, Propylene Glycol, Isoniazid, Lactic acidosis, Ethylene Glycol (anti-freeze), and Salicylates. Normal anion gap metabolic acidosis is caused by chronic renal failure, renal tubular acidosis, ureteroureterostomy, gastrointestinal loss, laxative overuse, ammonium chloride, carbonic anhydrase inhibitors, aldosterone deficiency, and excessive chloride administration.

Treatment of metabolic acidosis depends on the cause and whether it is acute or chronic. In severe metabolic acidosis, sodium bicarbonate is sometimes used.

Metabolic Alkalosis

With metabolic alkalosis, one will see an increased level of HCO3, which could be caused by several factors such as too much bicarbonate during a code, excess hydrogen loss during vomiting or suctioning, chronic diuresis, excessive mineralocorticoids, or excessive alkali ingestion.

ABG values one would see with metabolic alkalosis would be pH > 7.45, HCO3 > 26 mEq/L, and PaCO2 > 45 mm Hg if compensating. An example of metabolic alkalosis would include a 70-year-old with heart failure who is on daily furosemide therapy and presents after returning from a trip to Mexico, where he contracted a gastrointestinal virus that resulted in 3 days of vomiting. In the emergency department, ABGs showed a pH of 7.51, HCO3 of 33 mEq/L, and PaCO2 of 43 mm Hg.

The respiratory system will compensate by decreasing ventilation and raising PaCO2, lowering arterial pH toward normal. Respiratory compensation of metabolic alkalosis typically raises the PaCO2 by approximately 0.7 mm Hg for every 1 mEq/L increase in HCO3. Arterial PaCO2 rarely goes above 55 mm Hg. Compensation is calculated by determining the expected CO2 = 0.7 X HCO3 + 20 (+/-5). In the above example, the expected CO2 would be 43 (38-48), so compensation is occurring.

Table 7: Metabolic Alkalosis
pH Increased
PaCO2 Normal (increased if compensating)
HCO3 Increased
(Castro et al., 2022)

Compensation

Acid-base disorders are typically associated with a compensatory response to correct the imbalance and normalize the pH. For example, if there is metabolic acidosis (a low serum HCO3), there should be respiratory compensation by moving the PaCO2 in the same direction as the serum HCO3 (falling). The respiratory compensation works to normalize the pH. Respiratory compensation is a rapid adjustment. In metabolic acidosis, the respiratory compensation starts within 30 minutes and is done in 12-24 hours.

Generally, after the primary acid-base disorder, there is compensation in an attempt to normalize the pH. In primary metabolic acidosis, the compensation involves respiratory alkalosis. In primary metabolic alkalosis, the compensation is respiratory acidosis. In primary respiratory acidosis, the compensation is metabolic alkalosis. If the primary disorder is respiratory alkalosis, the compensation is metabolic acidosis.  

Compensation is associated with many key factors. Overcompensation does not occur. For example, in a patient with respiratory acidosis who compensates with metabolic alkalosis, the body will not push the pH to the alkalemia side of normal. If the body overcompensates, there is likely a mixed acid-base disorder. Respiratory compensation tends to occur quickly, whereas metabolic compensation occurs more slowly. In addition, the pH may not return to the normal range despite compensation.

Figure 1: Example of Compensation
An example of full compensation would be pH of 7.37, PaCO2 of 26 mm hg, and HCO3 of 16 mEq/L. The pH is closer to an acidotic state (normal pH range 7.35-7.45), with low bicarbonate (which is acidotic – representing the initial disorder), and the carbon dioxide compensates by being in the alkalotic range. The example represents a fully compensated metabolic acidosis.

Table 8 discusses what happens in each disorder regarding the pH, the initiating event causing the disorder, and the compensatory effect.

Table 8: Overview of Acid-Base Disorder
Disorder pH Initiating Event Compensating Effect
Respiratory Acidosis ↓ ↑ PaCO2 ↑ HCO3
Respiratory Alkalosis ↑ ↓ PaCO2 ↓ HCO3
Metabolic Acidosis ↓ ↓ HCO3 ↓ PaCO2
Metabolic Alkalosis ↑ ↑ HCO3 ↑ PaCO2
(Hamilton et al., 2017)

Case Study 1

A 50-year-old female arrives in the emergency department via ambulance. She was the vehicle driver that ran head-on into the median underpass on the interstate. She wore a seat belt but hit the steering wheel before the airbag deployed. When she arrived in the emergency department, she had a Glasgow Coma Scale (GCS) of 15 and was anxious. She had bruising to her chest from the seat belt, with no visible head injury noted. 

Along with other indicators, such as the GCS, the ABG results can strongly indicate a patient's mortality during the hospital course. A recent study showed that acid-base disturbances were predictors of death in major trauma patients (Mohsenian et al., 2018).

Addressing the GCS of each trauma patient arriving in the emergency department is an important step in the assessment process. The nurse can assess eye-opening, motor, and verbal responses using the information included in the GCS (Table 9).

Patients arriving in the emergency department post-trauma receive a head-to-toe trauma assessment, including the GCS. A GCS of < 8 indicates a severe head injury and generally has a poor outcome in head trauma. 

However, a patient can arrive with a GCS of 15, indicating they have spontaneous eye-opening, obey verbal commands, and are oriented and conversing. This patient can suffer from respiratory distress caused by a traumatic lung injury; therefore, when used alone, the GCS may be a poor indicator of the patient's condition.

Upon arrival in the emergency department, her vital signs were within normal limits. Shortly after arriving, she complained of needing to have a bowel movement and difficulty breathing. Her oxygen saturation dropped to 88% on room air. An ABG was obtained with the following results: pH 7.47, PaCO2 23 mm Hg, and HCO3 22 mEq/L, and now her vital signs have slightly changed from within normal limits to blood pressure 120/70 mm Hg, heart rate 112, and respiratory rate 30.

Understanding the patient's blood gas reveals a respiratory alkalosis; preparations begin to treat the cause when the x-ray results reveal a left-side pneumothorax.

Table 9: Glasgow Coma Scale
Eyes Open Spontaneous 4
To verbal command 3
To pain 2
No response 1
Best Motor Response Obeys commands 6
Localizes pain 5
Withdrawals from pain 4
Abnormal flexion 3
Abnormal extension 2
No response 1
Best Verbal Response Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
(Jain & Iverson, 2023)
Table 10: Causes of Acid-Base Disturbances
Causes of Respiratory Acidosis
  • COPD
  • Severe asthma
  • Obstructive sleep apnea
  • Chest wall disorders
    • Kyphoscoliosis
    • Fail chest
    • Ankylosing spondylitis
  • Obesity
  • Sedative/narcotic overdose
  • Neuromuscular disease
    • Myasthenia gravis
    • Amyotrophic lateral sclerosis
    • Guillain-Barré syndrome
  • CNS depression
    • Encephalitis
    • Trauma
Causes of Respiratory Alkalosis
  • Hyperventilation
  • Fever
  • Anxiety
  • Hypoxemia
  • Pregnancy
Causes of Metabolic Acidosis
  • Increased acid production – generally increased anion gap
    • Ketoacidosis
    • Lactic acidosis
    • Ingestions – aspirin, methanol, ethylene glycol
  • Loss of bicarbonate – generally normal anion gap
    • Diarrhea
    • 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
Causes of Metabolic Alkalosis
  • Renal hydrogen loss
    • Diuretics
    • Primary mineralocorticoids excess
  • Gastrointestinal hydrogen loss
    • Chronic diarrhea
    • Vomiting
    • Nasogastric tube suctioning
  • Contraction alkalosis
    • Diuresis
    • Sweat loss in cystic fibrosis
    • Vomiting/nasal gastric tube suctioning in achlorhydria
  • Intracellular shift of hydrogen
    • Low serum potassium
  • Alkali administration
(Hamilton et al., 2017)
Table 11: ABG Cheat Sheet
  pH PaCO2 HCO3  
Metabolic Acidosis < 7.35 35-45 < 22  
Metabolic Alkalosis > 7.45 35-45 > 26  
Respiratory Acidosis < 7.35 > 45 22-26  
Respiratory Alkalosis > 7.45 < 35 22-26  
Fully Compensated Metabolic Acidosis 7.35-7.45 < 35 < 22 pH usually < 7.4
Fully Compensated Metabolic Alkalosis 7.35-7.45 > 45 > 26 pH usually > 7.4
Fully Compensated Respiratory Acidosis 7.35-7.45 > 45 > 26 pH usually < 7.4
Fully Compensated Respiratory Alkalosis 7.35-7.45 < 35 < 22 pH usually > 7.4
(Castro et al., 2022; Sood et al., 2010)

Case Study 3

A 42-year-old female presents to the emergency department via ambulance. The patient reports that she was driving home from work and started sweating profusely but attributed the sweating to the lack of air conditioning in the car. When she got home, she noticed she was experiencing shortness of breath, followed by her heart racing and chest pain. She sat down to drink some cold water, then developed dizziness and felt like she would pass out. In addition, she experienced numbness and tingling in both arms.

She then called an ambulance and was brought to the emergency room. After taking a good history, the emergency room physician performed a complete physical exam, which showed a female who appeared of her stated age in mild distress but could speak in full sentences with no major abnormalities on exam except slightly elevated blood pressure and heart rate.

The diagnostic workup was reasonably unremarkable and included a normal complete blood count, normal liver and kidney function, electrolytes within normal limits, negative cardiac enzymes, and a negative d-dimer. The chest x-ray was unremarkable, and an EKG showed no ischemic changes and sinus tachycardia at 110 beats per minute.

About ten minutes after all her results returned, her heart rate, blood pressure, and respiratory rate increased, and ABGs were drawn. They revealed a pH of 7.5, PaCO2 of 28 mm Hg, and an HCO3 of 23 mEq/L.

The patient's presentation reveals a respiratory alkalosis, and her negative workup suggests the presentation likely represents a panic attack. The patient was given a beta-blocker and lorazepam and monitored overnight with complete normalization of all signs and symptoms.

Conclusion

Appropriate use of ABGs is an important aspect of good clinical care. Clinicians must interpret the ABGs and determine the acid-base disturbance to help assess and treat the patient. Competent and accurate determination of acid-base disturbances takes practice. Still, the clinician who takes the time to understand the appropriate use of acid-base disturbances improves their clinical ability and helps enhance patient outcomes.

References

  • Castro, D., Patil, S. M., & Keenaghan, M. (2022). Arterial Blood Gas. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
  • Danckers, M. (2022). Arterial Blood Gas Sampling Technique. Medscape. Visit Source.
  • Golamari, R., & Gilchrist, I. C. (2021). Collateral circulation testing of the hand- Is it relevant now? A narrative review. The American Journal of the Medical Sciences, 361(6), 702–710. Visit Source.
  • Hamilton, P. K., Morgan, N. A., Connolly, G. M., & Maxwell, A. P. (2017). Understanding Acid-Base Disorders. The Ulster medical journal, 86(3), 161–166.
  • Jain, S., & Iverson, L. M. (2023). Glasgow Coma Scale. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Visit Source.
  • Jarvis, M. A., Jarvis, C. L., Jones, P. R., & Spyt, T. J. (2000). Reliability of Allen's test in selection of patients for radial artery harvest. The Annals of Thoracic Surgery, 70(4), 1362–1365. Visit Source.
  • Mohsenian, L., Khoramian, M. K., & Sadat Mazloom, S. (2018). Prognostic value of arterial blood gas indices regarding the severity of traumatic injury and fractures of the femur and Pelvis. Bulletin of Emergency and Trauma, 6(4), 318–324. Visit Source.
  • Romeu-Bordas, Ó., & Ballesteros-Peña, S. (2017). Validez y fiabilidad del test modificado de Allen: una revisión sistemática y metanálisis [Reliability and validity of the modified Allen test: a systematic review and metanalysis]. Emergencias : revista de la Sociedad Espanola de Medicina de Emergencias, 29(2), 126–135.
  • Sood, P., Paul, G., & Puri, S. (2010). Interpretation of arterial blood gas. Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine, 14(2), 57–64. Visit Source.

Case Study 2

A 45-year-old female presented to the emergency department with severe diarrhea for the last two days. She has the following ABG results:

  • Arterial pH - 7.26
  • HCO3 - 12 mEq/L
  • PaCO2 - 26 mm Hg

The pH is low. Therefore, the patient has acidemia. The low HCO3 suggests metabolic acidosis. The HCO3 is 12 mEq/L below the normal (24 mEq/L), which should (and did) lead to respiratory compensation with a 14 mm Hg fall in PaCO2 (the normal PaCO2 is 40 mm Hg). Respiratory compensation for metabolic acidosis is when the arterial PaCO2 falls about 1.2 mm Hg per 1 mEq/L reduction in the serum HCO3 concentration.

This patient has a partially compensated metabolic acidosis (the pH is not in the normal range, so it is only partially compensated). If the PaCO2 were significantly higher (above 26 mmHg) than expected, there would be a concurrent respiratory acidosis (e.g., an obtunded patient).

A concurrent respiratory alkalosis might be present if the PaCO2 was significantly lower than expected (below 26 mmHg). Respiratory alkalosis with metabolic acidosis is often seen in salicylate intoxication or septic shock.

The patient is noted to have a normal anion gap, consistent with a metabolic acidosis caused by diarrhea.

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