An Overview of Arterial Blood Gases

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.

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 nurses in arterial blood gas analysis can have a significant impact on improving the knowledge of the nurse

Whatever the underlying cause for the acid-base disturbance, one must gain knowledge for interpretation of the ABG to establish the best course of treatment. Therefore, the healthcare provider will determine the limitations of therapy based on the results of the ABG.

Another recent analysis showed that teaching a stepwise approach to evaluating arterial blood gases and using case studies, along with tables and figures, could enhance the ability of the nurse to interpret arterial blood gases.

Arterial blood gas sampling is a procedure that involves the direct puncture of an artery. It is associated with a low incidence of complications. It is used to determine blood gas exchange levels and assess renal, metabolic and respiratory function.

Indications for ABG include:

• Determining the partial pressure of respiratory gases that are involved in ventilation and oxygenation
• Evaluating arterial respiratory gases during diagnostic workups
• Monitoring acid-bases 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 ABG include:

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

Relative contraindications to ABG include:

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

Factors that make ABG difficult:

• Uncooperative patient
• Pulses that cannot be identified easily
• Difficult to position the patient
• Obesity – because subcutaneous fat over access areas obscures landmarks
• Vascular disease leading to rigidity in vessel walls
• Poor distal perfusion – heart failure, hypovolemia, vasopressor therapy

Sources of errors include:

• Air bubbles can increase PaO² and lower PaCO₂
• Heparin may lower PaCO₂
• Gas may diffuse through a plastic syringe
• Acid-base balance may be inaccurate in arterial blood in those with reduced cardiac output (CPR/circulatory failure)

ABG reflects the patient's physiologic state at the time the test was done. The radial artery is typically the preferred site because it has a 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 problems with the brachial artery. It is a small-caliber vessel. It does not have good collateral circulation, and attaining hemostasis is more difficult.

Repeated punctures increase the risk of artery laceration, inadvertent venous sampling, hematoma, and scaring. When frequent sampling is needed, the use of 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. This allows for more accurate needle placement and reduces the risk of damage to the surrounding structures.

Technique

• Determine the site to be sampled
• The site is prepped in a sterile fashion
• Consider local analgesia before arterial puncture as it reduces pain without negatively impacting the procedure
• Use an ABG kit
• Palpate the artery with the nondominant 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 ABG, the patient should be educated about the procedure, including the risks and benefits. The patient should let the health care provider know if there is new/worsening pain, reduced movement, numbness/tingling in the limb, or active bleeding after the procedure is performed.

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. If blood is taken from the brachial artery, place the arm on a firm surface. The shoulder is abducted with the forearm supinated and the elbow extended.

When performing an ABG sampling, the provider should wear gloves and eye protection. The site should be cleaned with an antiseptic solution. The non-dominate 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 nondominant hand. After 2-3 ml is obtained, the needle is removed, and gauze is placed over the site with the nondominant hand to hold pressure for five minutes. Pressure may need to be held for longer periods 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 PaC0₂ and overestimate the PaO₂.

The nurse must monitor for complications. Active profuse bleeding from the puncture site suggests that there is 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.

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

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

Respiratory alkalosis and acidosis may be classified as acute or chronic. It takes up to five days for the renal system to compensate for respiratory disorders.

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

The PaO₂ evaluates the oxygen in plasma and has an 80-95 mm Hg normal range. The 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 95-99% and generally should be above 90%.

PaCO₂ evaluates the ventilation component. The normal range is 35-45 mm Hg. However, the value is inversely related to ventilation. For example, decreased ventilation has a higher value, and increased ventilation has a lower value. Therefore, hyperventilation causes alkalosis because the patient is blowing off carbon dioxide, and hypoventilation causes acidosis because the patient is retaining carbon dioxide. The body adjusts for these conditions by changing the respiratory rate (Romeu-Bordas et al., 2017).

HCO₃ (bicarbonate) is regulated by the kidneys and evaluates the metabolic component. The normal range is 22-26 mEq/L. Below 22 mEq/L is considered acidosis, and above 26 mEq/L is alkalosis. The body can adjust to the abnormalities in the HCO₃ levels but not as quickly as it can to the abnormal PaCO₂ levels. Several days could be required to make the necessary adjustments to bring the HCO₃ levels to a normal range (Byrd, 2018).

Four conditions are evaluated based on the ABG: respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. As we explore these conditions, the potential causes, the ABG values, and the compensatory mechanisms, we will better understand what is happening within the body.

Respiratory acidosis is a condition that happens when the lungs cannot eliminate enough of the carbon dioxide made by the body. The body excretes the extra hydrogen in the urine and exchanges it for bicarbonate ions. HCO₃ rises to restore the body to a normal pH when this happens. Until the pH returns to normal, the PaCO₂ may stay elevated.

Any situation that can cause the patient to develop a depressed respiratory status can cause this medical condition. Examples of these situations could be hypoventilation, asphyxia, central nervous system depression, chronic obstructive pulmonary disease, infection, and drug-induced respiratory depression (Table 9). 

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

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

Respiratory alkalosis is a compensatory mechanism of the body aimed to increase the excretion of HCO₃ and retention of the hydrogen ions. Respiratory alkalosis lowers the HCO₃ and restores pH to normal. Conditions that cause the respiratory system to be overstimulated can be extenuating factors in respiratory alkalosis such as hyperventilation (see Table 9). In addition, respiratory alkalosis can be seen in those who are critically ill, such as those who are on ventilators or those with lung or heart disease (Byrd, 2018).

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 mmHg reduction in PaCO₂. In chronic respiratory alkalosis (after 3-5 days) the serum HCO₃ falls about 4-5 mEq/L for every 10 mmHg reduction in PaCO₂ (Emmett & Palmer, 2018).

When a patient demonstrates metabolic acidosis, their body pulls the HCO₃ into the cells as a buffer and depletes the plasma level. The body begins compensating by increasing the ventilation, and thus, renal retention of the HCO₃ takes place.

When patients present with the following conditions, one must consider the patient could be a candidate for metabolic acidosis: HCO3 loss from diarrhea, shock, renal tubular acidosis, drug intoxication, salicylate poisoning, renal failure, diabetic ketoacidosis, and circulatory failure producing lactic acid.

ABG values one would see with metabolic acidosis would be: pH < 7.35; HCO₃ < 22 mEq/L; and PaCO₂ < 35 mm Hg if compensating.

Respiratory compensation for metabolic acidosis causes a reduction in the arterial PaCO₂ by about 1.2 mmHg for every 1 mEq/L reduction in the serum HCO₃. There is a likely underlying neurologic or respiratory disease (Emmett & Palmer, 2018).

Calculation of the serum anion gap should be determined in metabolic acidosis. The anion gap may be high in metabolic acidosis, normal or combined. Determining the anion gap will help determine the cause of metabolic acidosis.

One generally considers the ABG a test for respiratory conditions; however, a study of ABGs in Brazil to test patients for metabolic acidosis about sepsis and shock was conducted. The study revealed that a group that could not clear their inorganic ions had a higher morbidity rate, whereas those who could correct their acidosis survived.

The severely septic patient who developed acute renal failure upon arrival to the intensive care unit (ICU) had many tests, including ABG. Results of the ABG revealed: a pH of 7.32, PaCO₂ of 45 mmHg, and an HCO₃ of 21mEq/L. Without treatment, metabolic acidosis will worsen; steps need to be taken to bring the patient into a compensatory mode to recovery.

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

With metabolic alkalosis, one will see an increased level of HCO₃. This could be caused by several factors such as too much bicarbonate during a code, excess hydrogen loss during vomiting or suctioning, potassium loss from diuretics or steroids, or excessive alkali ingestion. The kidneys will increase the HCO₃ excretion trying to conserve the hydrogen. The respiratory system will compensate by decreasing the ventilation, conserving CO₂, and raising PaCO₂. Patients with normal kidney function can excrete excess bicarbonate in the urine, so if metabolic alkalosis is maintained, there is an inability to excrete bicarbonate in the urine.

ABG values one would see with metabolic alkalosis would be: pH > 7.45; HCO₃ > 26 mEq/L and PaCO₂ > 45 Hg if compensating.

Respiratory compensation of metabolic alkalosis typically raises the PaCO2 approximately 0.7 mmHg for every 1 mEq/L increase in HCO₃. The arterial PaCO₂ rarely goes above 55 mmHg.

Acid-base disorders are typically associated with a compensatory response that lessens the HCO₃/ PaCO₂ ratio change and, consequently, in pH. For example, if there is metabolic acidosis (a reduction in the serum HCO₃), there should be respiratory compensation by moving the PaCO₂ in the same direction as the serum HCO₃ (falling). The respiratory compensation lessens the change in the serum HCO₃ to PaCO₂ and consequently 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.

A respiratory acid-base disorder leads to compensation in two phases: immediate and delayed. The immediate change is small in serum HCO₃ in the same direction as the PaCO₂. If the respiratory condition persists, the kidneys produce larger changes in the HCO₃. This is meant to stabilize the pH.

In respiratory alkalosis, urinary HCO₃ and hydrogen ion secretion are reduced. In respiratory acidosis, hydrogen ion secretion and HCO₃ are increased to compensate. Renal compensation takes longer than respiratory compensation; it takes three to five days to complete compensation.

A glance at the four disorders demonstrates what happens with the pH, the initiating event causing the disorder, and the compensatory effect shown in the following table (Table 8). It is important to remember that compensating effects are seen in chronic conditions.

Studies have shown that along with other indicators such as the Glasgow Coma Scale (GCS), the ABG results can serve as a strong indicator of a patient's mortality during the hospital course. A recent study showed that acid-base disturbances were predictors of death in major trauma patients.

Addressing the GCS of each trauma patient arriving in the ED is an important step in the assessment process. Using the information included in the following Glasgow Coma Scale, the nurse can assess eye-opening, motor response, and verbal response.

Patients arriving in the Emergency Department (ED) post-trauma receive a head-to-toe trauma assessment, including the GCS. When head trauma, a GCS of < 8 indicates a severe head injury and generally has a poor outcome. The low GCS coupled with a strong ion gap is a strong predictor of hospital mortality. Therefore, a vascular injury must be assessed along with other areas of assessment and fluid resuscitation initiated to prevent further decline.

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

A 50-year-old female arrives in the ED 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 GCS of 15 and was anxious. She had bruising to her chest from the seat belt at the inspection, with no visible head injury noted. Her vital signs were within normal limits. Shortly after arriving in the ED, she complained of needing a bowel movement and difficulty breathing. Her oxygen saturation dropped to 88% on room air. An ABG was obtained with the following results: pH 7.32, PaCO₂ 47 mmHg, and HCO₃ 28 mEq/L. Vital signs have slightly changed from being within normal limits to blood pressure 120/70 mm Hg, HR 102, and respiratory rate 30.

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

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

• Arterial pH - 7.25
• HCO₃ – 12 mEq/L
• PaCO₂ - 26 mmHg

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). This should (and did) lead to respiratory compensation with a 14 mmHg fall in PaCO₂ (the normal PaCO₂ is 40 mmHg). Respiratory compensation for metabolic acidosis is when the arterial PaCO₂ falls about 1.2 mmHg 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 was 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, which is consistent with a metabolic acidosis caused by diarrhea.

Regardless of the patient's condition, an important aspect of the ABG is to take a systematic approach to the interpretation of the ABG and determine between the differential diagnoses. Know the patient history and begin treatment as soon as feasible to ensure the best possible outcomes. Placing the patient at the top of the pyramid is the most significant step in the process.

• Byrd RB. Respiratory Alkalosis. Updated October 3, 2018. Accessed August 14, 2019. Visit Source.
• Emmett M, Palmer BF. Simple and mixed acid-base disorders. www.uptodate.com Updated October 8, 2018. Accessed August 13, 2019.
• Romeu-Bordas, Ballesteros-Pena S. Reliability and validity of the modified Allen test: a systematic review and meta-analysis Emergencias. 2017;29(2):126-135.
• Theodore AC. Arterial blood gasses. www.uptodate.com Updated February 27, 2019. Accessed August 13, 2019.