 Arterial Blood Gas interpretation is an easy skill to master. It simply requires an understanding of pH, the respiratory component (pCO2), a metabolic component (HCO3 and/or Base Excess), what they represent, and what the normal ranges are.

 In chemistry class we learned that pH describes the concentration of hydrogen ions, and that a pH of 7.0 is perfectly neutral  The acceptable pH range of our blood is 7.35 – 7.45, which is slightly alkaline  The body needs to maintain the pH of its chemical broth within fairly narrow limits for proper body functioning  The body’s own regulatory mechanisms usually maintain this balance, but certain disease processes, illnesses, and treatments can cause imbalances that may become life threatening unless appropriate interventions are implemented  A pH that is less than 7.0 or greater than 7.7 is not compatible with life

 The body has several buffer systems that work to maintain the pH within acceptable limits  Of these, the bicarbonate-carbonic acid buffer system is the most important, and is controlled by the lungs and kidneys  Normal (aerobic) metabolism produces two forms of acid  respiratory acid (carbonic acid)  metabolic acids  In order to maintain proper pH balance, the body attempts to maintain a ratio of 20:1 (bicarbonate to carbonic acid.) A wide variety of pulmonary and metabolic problems can create an imbalance, so it is necessary to look carefully at the respiratory and metabolic components of ABG interpretation

 Carbon dioxide is an end product of metabolism, and when dissolved in blood becomes carbonic acid  Carbonic acid is termed a volatile acid because it dissociates into water and a gas, CO2 which is exhaled by the lungs  The pCO2 or PaCO2 represents the partial pressure of carbon dioxide dissolved in arterial blood, and provides an important measure of the adequacy of a patient’s ventilation  The lungs normally maintain an acceptable balance of CO2 in the bloodstream  The normal range for this respiratory component of ABG’s, the pCO2, is 35 – 45 mmHg, and is maintained by ventilation

 PO2 is the partial pressure of oxygen and determines the amount of oxygen available to bind with hemoglobin.  The pH affects the combining power of oxygen in hemoglobin and with a low pH, there is less O2 to bind to hemoglobin.  PO2 is decreased in emphysema, pneumonia, pulmonary edema.  C02 retainers

 When the patient is moving a normal volume of air in and out of the lungs, the pCO2 will stay within the normal range  Hypoventilation will prevent sufficient removal of CO2 from the bloodstream, causing a respiratory acidosis  Some causes of respiratory acidosis include obstructive lung disease, restrictive lung disease and hypoventilation as a result of oversedation, anesthesia or improper ventilator settings (e.g., tidal volume too low.) Respiratory acidosis could also result from a drug overdose and neuromuscular diseases such as Guillain-Barre syndrome or myasthenia gravis

 Hyperventilation, on the other hand, causes CO2 to be “blown off” or removed, causing a respiratory alkalosis  The pCO2 falls below 35, and the acid-load decreases, causing an alkalosis  Some possible causes of respiratory alkalosis include pain, panic attacks, anxiety, pulmonary embolism, pregnancy, and a tidal volume that is too high for a ventilator patient

 Notice that a high value in pCO2 actually represents an acidosis (retention of CO2), whereas a high value in pH represents an alkalosis  Do not try to memorize, but rather to understand the concept of what the components represent  A high level of pCO2 simply means there is retention of CO2 or hypoventilation  CO2 is acidotic in the blood, and too much causes respiratory acidosis.

 HCO3 represents the metabolic component of ABG interpretation, with a normal range of mEq/L  Bicarbonate (HCO3) is a weak base that is regulated by the kidneys  When there is a loss of acid in the body, or an excess of base, the HCO3 will be greater than 26, resulting in metabolic alkalosis  Some causes of metabolic alkalosis include loss of stomach acid and potassium from vomiting or gastric suction, and ingestion of large amounts of bicarbonate. Prolonged therapy with potassium- wasting diuretics, steroid therapy, Cushing's disease, and aldosteronism can also deplete potassium, chloride, and hydrogen levels, resulting in metabolic alkalosis

 When there is an excess of metabolic acid, or not enough base, the HCO3 will be less than 22, causing metabolic acidosis  Conditions that increase acid-load include diabetic ketoacidosis or prolonged fasting, lactic acidosis, and renal failure. Actual loss of bicarbonate ions through severe diarrhea leads to metabolic acidosis. During cardiac arrest, or when low cardiac output states (as in external cardiac compression) are present, anaerobic metabolism occurs and there is an increase in the production of lactic acid. Metabolism of lactic acid is normally effected through the Krebs cycle, and oxygen is the essential element for this metabolic process. In the absence of adequate tissue oxygenation, lactic acid cannot be metabolized; its quantity increases and the result is metabolic acidosis.

pH 7.35 – 7.45 pCO mmHg HCO mEq/L pO 2 75 – 100mmHg How do we treat these problems? Treat your patient, not the lab values.

 Mrs. Puffer is a 35-year-old single mother, just getting off the night shift. She reports to the ED in the early morning with shortness of breath. She has cyanosis of the lips. She has had a productive cough for 2 weeks. Her temperature is 38.5, blood pressure 110/76, heart rate 108, respirations 32, rapid and shallow. Breath sounds are diminished in both bases, with coarse rhonchi in the upper lobes. Chest X-ray indicates bilateral pneumonia.  ABG results are:  pH= 7.44  PaCO2= 28  HCO3= 24  PaO2= 54  Problems:  PaCO2 is low  pH is on the high side of normal, therefore compensated respiratory alkalosis.  Also, PaO2 is low, probably due to mucous displacing air in the alveoli affected by the pneumonia  Solutions:  The alkalosis need not be treated directly. Mrs. Puffer is hyperventilating to increase oxygenation, which is incidentally blowing off CO2. Improve PaO2 and a normal respiratory rate should normalize the pH. (get her to deep breath and cough – assist in her comfort, apply O2 if needed)

 Mr. Worried is a 52-year-old widow. He is retired and living alone. He enters the ED complaining of shortness of breath and tingling in fingers. His breathing is shallow and rapid. He denies diabetes; blood sugar is normal. There are no EKG changes. He has no significant respiratory or cardiac history. He takes several antianxiety medications. He says he has had anxiety attacks before. While being worked up for chest pain an ABG is done:  ABG results are:  pH= 7.48  PaCO2= 28  HCO3= 22  PaO2= 85  Problem:  pH is high,  PaCO2 is low  respiratory alkalosis  Solution:  If he is hyperventilating from an anxiety attack, the simplest solution is to have him breathe into a paper bag. He will rebreathe some exhaled CO2.This will increase PaCO2 and trigger his normal respiratory drive to take over breathing control.  * Please note this will not work on a person with chronic CO2 retention, such as a COPD patient. These people develop a hypoxic drive, and do not respond to CO2 changes.

 Carbon dioxide levels are chronically elevated (like in the patient with COPD)  The respiratory center becomes less sensitive to CO2 as a stimulant of the respiratory drive  Therefore the PaO2 provides the primary stimulus for respirations  Administering excess supplemental oxygen can potentially suppress the respiratory center  However, it is unclear whether such a hypoxic drive exists in the first place

 pH: 7.46  PaCO 2 : 43 mmHg  [HCO 3 - ]: 27 mEq/L  PaO2: 80 mmHg

 Met alk

 pH: 7.34  PaCO 2 : 43 mmHg  [HCO 3 - ]: 20 mEq/L  PaO2: 80 mmHg

 met acid

 pH: 7.38  PaCO 2 : 40 mmHg  [HCO 3 - ]: 25 mEq/L  PaO2: 80 mmHg

 Everything is fine

 pH: 7.28  PaCO 2 : 48 mmHg  [HCO 3 - ]: 22 mEq/L  PaO2: 86 mmHg

 Resp acid

 pH: 7.50  PaCO 2 : 38 mmHg  [HCO 3 - ]: 18 mEq/L  PaO2: 86 mmHg

 Met alk

 pH: 7.46  PaCO 2 : 50 mmHg  [HCO 3 - ]: 26 mEq/L  PaO2: 86 mmHg

 Resp alk

 pH: 7.32  PaCO 2 : 49 mmHg  [HCO 3 - ]: 30 mEq/L  PaO2: 90 mmHg

 Met acidosis with respiratory compensation (respiratory system is compensating by adding some alkalitity)

 pH: 7.52  PaCO 2 : 50 mmHg  [HCO 3 - ]: 28 mEq/L  PaO2: 90 mmHg

 Met alk with respiratory compensation (adding some acid)

 pH: 7.33  PaCO 2 : 50 mmHg  [HCO 3 - ]: 28 mEq/L  PaO2: 92 mmHg

 Resp acidosis with metabolic compensation