Arterial Blood Gas Analysis Learning Objectives:

After completing this lecture, the nurses should be able to: Identify normal arterial blood gas values and interpret the meaning of abnormal values. Compare the roles of PaO2, pH, PaCO2, and Bicarbonate in maintaining acid/base balance. Interpret the oxygenation state of a patient using the reported arterial blood gas PaO2 value.

Introduction/ Overview:
Many critical illnesses can upset a patients acid-base balance, and a disturbance in acid-base equilibrium may indicate other underlying diseases or organ damage. Accurately interpreting acid-base balance requires simultaneously measurements of arterial pH and plasma electrolytes, as well as knowledge of compensatory physiologic mechanisms. ABG analysis must be done by a written physician order. Body acids are formed as end products of cellular metabolism. Under normal physiologic conditions, a person generates 50 to 100 mEq/day of acid from metabolism of carbohydrates, proteins and fats. The body loses base in the stool. Acid production must balance the neutralization or excretion. The lungs and kidneys are the main regulators of acid-base homeostasis. The lungs release CO2, an end product of carbonic acid (H2CO3). The renal tubules, with the regulation of bicarbonate (HCO3), excrete other acids produced from the metabolism of proteins, carbohydrates and fats. Acidosis is described as a physiologic condition caused by the bodys inability to buffer excess H+ ions. Alkalosis results from deficiency in H+ ion concentration.

Definition of terms:
1. ABG- arterial blood gas- analysis evaluates gas exchange in the lungs by measuring the PaO2 and the pH of an arterial blood sample. 2. Acidosis- when pH value of body fluids is below 7.35 3. Alkalosis- when pH value of body fluids above 7.45 4. pH- normal pH values body fluids between pH 7.35- 7.45 - refers to German word Poten2(power) so pH means power of Hydrogen 5. - (Arterial tension)- symbol for partial pressure of carbon dioxide in the arterial blood . 6. PaO2- (arterial O2 tension)- symbol for partial pressure of oxygen in arterial blood. 7. HCO3- Bicarbonate- main body buffer for acid-base balance. 8. SBE- (standard base excess) (deficit) - amount of strong acid or base required to titrate 1 liter of blood back to a pH of 7.4 at temperature of 37C and PCO2 of 40mmHg. 9. B.E- another measure of the metabolic (renal) component, normal range of B.E (-2 to +2). 10. Acid- compound that forms hydrogen ions 9 (proton donor).

11. Base- compound that combines with hydrogen ions in solution. The body has three compensatory mechanisms to handle changes in serum pH: Physiologic buffer, consisting of a weak acid (which can easily be broken down) and its base salt or of a weak base and its acid salt. These buffers are the bicarbonate-carbonic acid buffering system, intracellular protein buffers, and phosphate buffers in the bone. Pulmonary compensation, in which changes in ventilation work to change the partial pressure of arterial carbon dioxide and drive the pH toward the normal range. Renal compensation, which kicks in when the other mechanism have been ineffective, generally after about 6 hours of sustained acidosis or alkalosis. Metabolism- produces acidic products that lower the pH of body fluids. Example 1. Carbon dioxide- by product of metabolism - Combines with water to form carbonic acid 2. Lactic Acid- product of an aerobic metabolism; protein metabolism produces phosphoric and sulfuric acid, lipid metabolism produces fatty acids - These acidic substances must continuously be eliminated from our body to maintain pH homeostasis. - When rapid elimination of acidic products of metabolism results in alkalosis. - Failure to eliminate acidic products of metabolism results in acidosis. Major effect of acidosis- depression of central nervous system, when pH blood falls below 7.35 malfunctions the individual becomes disoriented or possibly comatose as condition worsens. Major effects of alkalosis- hyper excitability of the nervous system. Peripheral nerves are affected first resulting in spontaneous nervous stimulation of muscles. Spasms/ tetanic contractions and possibly extreme nervousness or convulsion result. Severe alkalosis can cause death as result of tetany of the respiratory muscles. Buffers- body fluids helps resist changes in pH of body fluids. The respiratory system and kidneys regulate the ph body fluids. Malfunction of either respiratory or kidneys can result to acidosis or alkalosis.

Most common acid-base derangements

1. Metabolic acidosis Increase in amount of absolute body acid either excess production of acids or excessive loss of bicarbonate, sodium and potassium. Causes include lactic acidosis, ketoacidosis, and loss of bicarbonate through severe diarrhea or bicarbonate wasting through kidneys or G.I tract. Kidneys attempts to preserved sodium by exchanging it for excreted H+ or potassium. Presence of H+ load, H+ ions move from extra cellular fluid into intracellular fluid. Potassium moves outside the cell into extracellular fluid to maintain electro neutrality. Severe acidosis, significant overall depletion of total body potassium stores can occur despite severe hyperkalemia.

2.

Treatment- Intravenous (IV) potassium given to patient with diabetic ketoacidosis, early treatment. pH is low, PaCO2 normal, HCO3 is low

Metabolic alkalosis - When HCO3 is increased, usually as result of excessive loss of metabolic acids. Causes include diuretics, secretory adenoma of colon, emesis, hyper aldosteronism, Cushing syndrome and exogenous steroids. - Some cause respond to treatment with 0.9% sodium chloride solution. Example; urine chloride concentration is less than 15mmol/L- Saline responsive. Includes G.I loss, dieresis, or renal compensation for hypercapnea. Results mineralo corticoid excess or potassium depletion. - Urine chloride concentration level above 25 mmol/L non saline responsive. - Treatment- fluid administration- foundation of treatment for saline responsive metabolic alkalosis. In case of extreme alkalosis, the patient may be given dilute hydrochloric acid. Saline-resistant alkalosis is treated by addressing the underlying etiology. - pH is high, PaCO2 normal, HCO3 is high

3. Respiratory Acidosis - Rate at which carbon dioxide is eliminated from the body fluids through the lungs falls. This increases the concentration of carbon dioxide in the body fluids. pH less than 7.35 and his PaCO2 is above 45 mmHg. - Alveolar hypoventilation is the only mechanism that causes hypercabia, PaCO2 above normal amount alveolar ventilation necessary to maintain PaCO2 varies depending upon CO2 produced. - Relationship between PaCO2 and plasma HCO3 determines arterial pH. Generally acute increases in PaCO2 are accompanied by only minimal changes in serum HCO3. However, over a period of 1 to 3 days renal conservation of HCO3 results in the increased in pH. - Chronic respiratory acidosis- occurs secondary to chronic reduction in alveolar ventilation. In chronic diseases such as chronic obstructive pulmonary disease. Acute respiratory acidosis is caused by an acute change in alveolar ventilation; respiratory depression from acute opioid ingestion is one cause. - Treatment for respiratory acidosis is largely supportive, but if opioid is ingestion is suspected, IV naloxone may be given as an antidote. - pH is low, PaCO2 high, HCO3 is normal

4. Respiratory alkalosis - Results from hyperventilation of the lungs. Increases rate at which carbon dioxide is eliminated from the body fluids and results in a decrease in the concentration of carbon dioxide in the body fluids. Occurs when PaCO2 is reduced causing an increase in pH. Common causes increase alveolar ventilation, which can happen in hyperventilation, mechanical over ventilation, hepatic disease, pregnancy, and septicemia. - Treatment- directed at discovering and correcting the underlying etiology.

Example: patient hyperventilating from anxiety have him breath into a paper bag. Mechanical ventilated patients with mechanical over ventilation reducing the minute ventilation or tidal volume will increase PaCO2 and reduce pH. Monitor closely rapid reduction of PaCO2 in a patient with chronic respiratory alkalosis may cause acute metabolic acidosis. pH is high, PaCO2 low, HCO3 is normal

Implementation Arterial 7.35- 7.36 80-100 mmHg 35-45 mmHg 22-26 mEq/L or mmol/L -2 to +2 mEq/L or mmol/L 95% - 100% Blood Gas Components pH pO2 pCO2 HCO3 Base Excess (BE) O2 Saturation Venous 7.31-7.41 35-40 mmHg 41-51 mmHg 22-26 mEq/L or mmol/L -2 to +2 mEq/L or mmol/L 68% - 77%

Steps how to determine acidosis and alkalosis

Step 1 use pH to determine acidosis or alkalosis

Acidosis

Normal or Compensated

Alkalosis

7.35 35
Tends toward alkalosis Causes high pH Neutralizes low pH

7.35-7.45 35-45
Normal or compensated

7.45 45
tends toward acidosis causes low pH neutralizes high pH

Step 2 - Use PaCO2 to determine respiratory effect

Step 3 Assume metabolic cause when respiratory is ruled out. High pH Low pH

Alkalosis High PaCO2 Metabolic Low PaCO2 Respiratory

Acidosis High PaCO2 Respiratory Low PaCO2 Metabolic

If PaCO2 is abnormal and pH is normal, it indicates compensation. pH 7.4 would be a compensated alkalosis pH < 7.4 would be a compensated acidosis.

Step 4 Use HCO3 to verify metabolic effect Normal HCO3 is 22-26

Please note:
Remember, the first three steps apply to the majority of cases, but do not take into account: the possibility of complete compensation, but those cases are usually less serious, and Instances of combined respiratory and metabolic imbalance, but those cases are pretty rare. . Combined disturbance means HCO3 alters the pH in the same direction as the PaCO2 . High PaCO2 and low HCO3 (acidosis) . Low HCO3 and high HCO3 (alkalosis)

Patient and Family Education

1. Explain the purpose and tell the watcher/ mother that the arterial blood gas analysis requires blood sample. 2. Explain who will perform the arterial puncture, when it will occur, and where the puncture will be: radial, brachial or femoral artery.