Arterial Blood Gas (ABG) Interpretation
Arterial Blood Gases (ABGs) are obtained within the hospital setting by nurses or respiratory therapists, after a physician or advanced practice provider orders them. As the name implies, this arterial blood sample is sent to the lab to evaluate the “gases” within the arterial blood – looking at acid-base disturbances or evaluate adequacy of oxygenation/ventilation. Brace yourselves – this is going to be a long confusing topic but once you understand the concepts, it can really help you manage your patient’s acid-base disturbance like a pro.
Oxygen (O2) and carbon dioxide (CO2) are the main gases within the blood, and these are two of the main components evaluated in an ABG. However, an ABG sample also provides levels of blood pH, as well as bicarbonate. Of all of the measurements, the most important levels to look at are the CO2, the Bicarb, and the pH in determining acid-base balance.
The ability to interpret an ABG is essential for advanced practice providers and physicians, but it is also important for the nurse to be able to have a good understanding of how to interpret ABGs, especially those working in critical care (ER, ICU, etc). This can give you valuable insights into your patient’s medical status and overall condition.
Unfortunately, ABGs can be difficult to understand. Acid-Base balance is exactly that – a balance. A rise in one level will affect other levels – and this can make it difficult to understand the underlying picture. The purpose of this article is to help you be able to master ABG interpretation in order to help you become a better nurse, clinician, or provider.
So… When Should an ABG be Obtained?
As stated above, ABGs are very useful in evaluating acid-base disturbances within a patient. This can come in handy for patients with Diabetic Ketoacidosis (DKA), other forms of metabolic acidosis (kidney failure, sepsis, etc), and CO2 retention (COPD). Patients with active respiratory failure, usually with underlying COPD or CHF, often have an ABG to evaluate their CO2 retention, their O2 saturation, and their acid-base balance – as all of these factors will affect each other.
The pH is the first measurement that will give you the overall picture of the patient: are they acidotic or alkalotic? pH is simply the acidity of the blood. Normal values for arterial blood pH is 7.35-7.45, which is a narrow window where body homeostasis works best.
Low pH (<7.35): Indicates acidosis (metabolic or respiratory), and is termed acidemia.
High pH (>7.45): Indicates alkalosis (metabolic or respiratory), and is termed alkalemia.
pH may be normal or near-normal in the presence of chronic acid-base disturbances from compensation, or the patient can have multiple different acid-base disturbances playing a factor.
Arterial Partial Pressure Carbon Dioxide (PaCO2)
The PaCO2 is the partial pressure of Carbon Dioxide within the arterial blood. Normal values for PaCO2 is 35-45 mmHg.
Did your parent or guardian ever tell you that holding your breath would cause your blood to boil, and that’s why you can’t hold it for long? This tidbit has helped me always remember that hypoventilation (not breathing enough) causes acidosis (boiling blood), and hyperventilation (breathing too much) causes the opposite.
High PaCO2: levels greater than 45mmHg are considered high and termed “hypercapnia”.
A high PaCO2 indicates a primary respiratory acidosis (blood boiling! pH<7.35), but can also indicate compensation for metabolic alkalosis. You see, acid-base is regulating by two organs in your body – your kidneys (metabolic) and your lungs (respiratory). These always hang in balance, and when the scale tips one way (metabolic acidosis), the body will attempt to compensate by increasing production and retention of bicarbonate to act as a buffer to normalize pH (respiratory compensation). This means the compensation will always be in the opposite direction from the primary acid-base disturbance. If one becomes too acidic – the other becomes basic, and vice versa. This is another perfect example of the body performing homeostasis to maintain balance and health. Respiratory compensation tends to occur quickly, as the pt is able to change their ventilation pattern almost instantly.
Low PaCO2: levels less than 35mmHg is considered low and termed “hypocapnia”.
Low PaCO2 indicates a primary respiratory alkalosis, which means the pH must be alkalotic as well (>7.45). Or it could also mean respiratory compensation for metabolic acidosis. If a patient is breathing fast (tachypneic) but doesn’t have a respiratory complaint – you may want to investigate their acid-base to assess for respiratory compensation. This was something I did NOT catch as a new nurse on a telemetry floor. My patient was breathing fast all night and I didn’t know why – by morning her pH was 6.9! A better understanding of acid-base physiology would have helped me recognize the signs of respiratory compensation (Kussmaul respirations), and my patient would have been better off for it.
Arterial Bicarbonate Concentration (HCO3)
HCO3 is the serum bicarb within arterial blood. Bicarb acts as a buffer to make acidity less acidic. Think of it as the opposite of H+. The less bicarb there is, the more acidic the blood is. To get technical, Bicarb reacts with H+ to form carbonic acid, which the body breaks down into CO2 and water – which it breaths out. Normal levels vary but typically are somewhere around 22-26 mEq/L.
High HCO3: Levels greater than 26mEq/L are considered high.
High HCO3 indicates a primary metabolic alkalosis (pH >7.45) – meaning for whatever reason the body is losing its acidity (See specific causes in the next section). However, just as in the case of PaCO2, abnormal HCO3 levels could indicate compensation as well. A high HCO3 level could indicate metabolic compensation for respiratory acidosis – the body is trying to buffer more acid to normalize the pH. Compensation from the kidneys can take a few hours to kick in, but won’t typically reach their peak compensatory effect until a couple of days into the acid-base disturbance.
Low HCO3: Levels less than 22mEq/L are considered low.
Low HCO3 levels indicate primary metabolic acidosis (pH <7.35). This is an acid-base disturbance you will see often – although they are all fairly common. There is an accumulation of acid within the body, and the kidneys are unable to get rid of it quickly enough. Just as with the others, low HCO3 could indicate metabolic compensation for respiratory alkalosis.
Arterial Partial Pressure of Oxygen (PaO2)
PaO2 is the partial pressure of oxygen within arterial blood. This basically measures the actual oxygen content of the blood. Normal values for PaO2 is generally thought to be greater than 80 mmHg.
High PaO2: Usually due to over-oxygenation from supplemental O2 (Think non-rebreather or too high FIO2). This may be better than low PaO2, but don’t forget that too much oxygen can be deleterious as well. Oxygen toxicity can produce reactive oxygen species and cause cellular injury, inflammation, and cell death. It can also accentuate hypercapnia (i.e. COPD).
Low PaO2: Hypoexmia from respiratory disease or anemia
Peripheral Oxygenation (SaO2)
The SaO2 is the peripheral oxygenation, which is equivalent to the Pulse Ox reading.
Normal levels are >96%, whereas levels <92% indicate hypoxia.
The 4 Acid-Base Disturbances
The following 4 categories are the 4 acid-base disturbances that can occur in someone who is sick. The above information will tell you which acid-base disturbance you may be dealing with. The below information is for you to understand what could possibly be causing the underlying disturbance. Don’t forget someone can have multiple acid-base disturbances going on at one time, and this makes clinical interpretation difficult – everything is not black and white in medicine, but this should give you a pretty good idea of what may be causing your patient’s acid-base disturbance.
Respiratory acidosis is due to alveolar hypoventilation. The lungs are NOT able to remove enough carbon dioxide quickly enough, so it builds up in the blood. It also decreases Bicarbonate levels, which decreases pH and causes acidosis.
Hypercapnia tends to occur late in the lung disease or when respiratory muscles are fatigued – this is usually seen in severe respiratory failure. The acidosis can be acute or chronic.
Acute: Could be from CNS disease (think stroke, traumatic brain injury), drug-induced respiratory depression (Opioid or Benzo overdose), Neuromuscular disease (Myasthenia Gravis, ALS, Guillan Barre), or most commonly airway obstruction (asthma/COPD).
Chronic: Chronic respiratory acidosis may occur when the PaCO2 is elevated, but the pH remains normal secondary to renal compensation and elevated serum Bicarb levels. Causes of chronic respiratory acidosis may be Obesity-Hypoventilation syndrome (Pickwickian syndrome), ALS, interstitial fibrosis, and thoracic skeletal deformities.
COPD: Patients with COPD have less responsiveness to hypoxia and hypercapnia. There is also increased dead-space ventilation and decreased diaphragmatic function due to fatigue and hyperinflation.
This acid-base disturbance is due to alveolar hyperventilation. The lungs remove too much carbon dioxide too quickly, so hypocapnia (low PaCO2) and alkalosis occur.
It is commonly found in those who are critically ill including those who are mechanically ventilated, early-intermediate pulmonary disorders (PNA, PTX, aspiration, PE, Asthma, bronchitis), pain, panic/anxiety, psychosis, fevers, high-altitude, sepsis, severe anemia, hepatic failure, CHF
Acute hypocapnia causes a reduction in serum K+ levels (intracellular shifts) and phosphorus, as well as ionized calcium (it increases binding to albumin so there is less calcium in its ionized active form). This explains the common symptoms of numbness/tingling that people having a panic attack may experience.
This acid-base disturbance is due to increased plasma acidity. Metabolic Acidosis is further broken down into whether or not the Anion Gap is normal (termed hyperchloremic metabolic acidosis) or elevated (Elevated gap metabolic acidosis).
Severe HCO3 levels <12 are almost always caused by some degree of metabolic acidosis, instead of just compensation for respiratory alkalosis.
Normal Gap: characterized by hyperchloremia, Bicarb is lost via the GI tract or kidneys. This usually occurs from diarrhea, chronic renal failure, or renal tubular acidosis.
Elevated Gap: Can be from multiple underlying pathologies, but usually caused by Lactic acidosis as in the case of sepsis, ketoacidosis in the case of DKA, acute kidney injury (acute renal failure), and ingestion of certain poisons.
This acid-base disturbance is caused by increased serum bicarb and decreased acidity. The acidity or hydrogen ions (H+) is usually lost in some manner. You know when you throw up and you taste the acid in your throat? This is one way the body loses its acidity – through vomiting. This can also occur in the setting of prolonged NG tube suction. The kidneys can also lose bicarb with the use of diuretics. Sometimes too many alkalotic agents are given and the kidneys aren’t able to excrete them fast enough – this can rarely occur from massive over-consumption of milk products or antacids.
Bicarb (HCO3) levels >35 almost always is caused by some degree of metabolic alkalosis instead of compensation for respiratory acidosis.
And That’s about it for Acid-Base Disturbances. I know – it’s long and hard and I probably lost many of you along the way. Half the battle is remembering which terms have which meanings. Once you establish that – it gets easier understanding the balance that is acid-base homeostasis.
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