Arterial blood gases (ABGs) are diagnostic tests performed on blood taken from an artery which contains oxygen

and carbon dioxide. also measure blood pH and the integrity of the body's acid-base balance.

Arterial Blood Gas analysis typically measures:

pH (Acidity) pCO2 (Partial Pressure of Carbon Dioxide) pO2 (Partial Pressure of Oxygen) CO2 (Carbon Dioxide Content) Base Excess (The loss of Buffer Base to neutralize acid)

And may include: Oxygen Saturation

These measurements are often used to evaluate oxygenation of the tissues and pulmonary function.

pH is a measurement of the acidity of the blood, reflecting the number of hydrogen ions present. Lower numbers mean more acidity; higher number mean more alkalinity. pH is Elevated (more alkaline, higher pH) with: Hyperventilation Anxiety, pain Anemia Shock Some degrees of Pulmonary disease Some degrees of Congestive heart failure Myocardial infarction Hypokalemia (decreased potassium) Gastric suctioning or vomiting Antacid administration Aspirin intoxication

pH is Decreased (more acid, lower pH) with: Strenuous physical exercise Obesity Starvation Diarrhea Ventilatory failure More severe degrees of Pulmonary Disease More severe degrees of Congestive Heart Failure Pulmonary edema Cardiac arrest Renal failure Lactic acidosis

Ketoacidosis in diabetes

pCO2 (Partial Pressure of Carbon Dioxide) reflects the the amount of carbon dioxide gas dissolved in the blood. Indirectly, the pCO2 reflects the exchange of this gas through the lungs to the outside air. Two factors each have a significant impact on the pCO2. The first is how rapidly and deeply the individual is breathing: Someone who is hyperventilating will "blow off" more CO2, leading to lower pCO2 levels Someone who is holding their breath will retain CO2, leading to increased pCO2 levels

The second is the lungs capacity for freely exchanging CO2 across the alveolar membrane: With pulmonary edema, there is an extra layer of fluid in the alveoli that interferes with the lungs' ability to get rid of CO2. This leads to a rise in pCO2. With an acute asthmatic attack, even though the alveoli are functioning normally, there may be enough upper and middle airway obstruction to block alveolar ventilation, leading to CO2 retention.

Increased pCO2 is caused by: Pulmonary edema Obstructive lung disease

Decreased pCO2 is caused by: Hyperventilation Hypoxia Anxiety Pregnancy Pulmonary Embolism (This leads to hyperventilation, a more important consideration than the embolized/infarcted areas of the lung that do not function properly. In cases of massive pulmonary embolism, the infarcted or non-functioning areas of the lung assume greater significance and the pCO2 may increase.)

PO2 (Partial Pressure of Oxygen) reflects the amount of oxygen gas dissolved in the blood. It primarily measures the effectiveness of the lungs in pulling oxygen into the blood stream from the atmosphere. Elevated pO2 levels are associated with: Increased oxygen levels in the inhaled air Polycythemia

Decreased PO2 levels are associated with: Decreased oxygen levels in the inhaled air

Anemia Heart decompensation Chronic obstructive pulmonary disease Restrictive pulmonary disease Hypoventilation

CO2 Content is a measurement of all the CO2 in the blood. Most of this is in the form of bicarbonate (HCO3), controlled by the kidney. A small amount (5%) of the CO2 is dissolved in the blood, and in the form of soluble carbonic acid (H2CO3). For this reason, changes in CO2 content generally reflect such metabolic issues as renal function and unusual losses (diarrhea). Respiratory disease can ultimately effect CO2 content, but only slightly and only if prolonged. Elevated CO2 levels are seen in: Severe vomiting Use of mercurial diuretics COPD Aldosteronism

Decreased CO2 levels are seen in: Renal failure or dysfunction Severe diarrhea Starvation Diabetic Acidosis Chlorthiazide diuretic use

Base Excess or Base Deficit Whenever there is an accumulation of metabolically-produced acids, the body attempts to neutralize those acids to maintain a constant acid-base balance. This neutralizing is achieved by using up various "buffering" compounds in the blood stream, to bind the acids, disallowing them from contributing to more acidity. About half of these buffering compounds come from HCO3, and the other half from plasma and red blood cell proteins and phosphates. The words "base deficit" and "base excess" are equivalent and are generally used interchangeably. The only difference is that base deficit is expressed as a positive number and base excess is expressed as a negative number. A "Base Deficit" of 10 means that 10 mEqu/L of buffer has been used up to neutralize metabolic acids (like lactic acid). Another way to say the same thing would be the "Base Excess is minus 10."

More Negative Values of Base Excess may Indicate: Lactic Acidosis Ketoacidosis Ingestion of acids Cardiopulmonary collapse Shock

More Positive Values of Base Excess may Indicate: Loss of buffer base Hemorrhage Diarrhea Ingestion of alkali

Oxygen Saturation (SO2) measures the percent of hemoglobin which is fully combined with oxygen. While this measurement can be obtained from an arterial or venous blood sample, it's major attractive feature is that it can be obtained non-invasively and continuously through the use of a "pulseoximeter." Normally, oxygen saturation on room air is in excess of 95%. With deep or rapid breathing, this can be increased to 98-99%. While breathing oxygen-enriched air (40% - 100%), the oxygen saturation can be pushed to 100%. Oxygen Saturation will fall if: Inspired oxygen levels are diminished, such as at increased altitudes. Upper or middle airway obstruction exists (such as during an acute asthmatic attack) Significant alveolar lung disease exists, interfering with the free flow of oxygen across the alveolar membrane.

Oxygen Saturation will rise if: Deep or rapid breathing occurs Inspired oxygen levels are increased, such as breathing from a 100% oxygen source

 pH pCO2 pO2 CO2 Base Excess/Deficit SO2

Normal Adult Arterial Values* 7.35-7.45 35-45 torr >79 torr 23-30 mmol/L 3 mEq/L >94%

pH pCO2 pO2 CO2 Base Excess/Deficit SO2 BE HCO3 H2CO3 PO2 PaO2 PvO2 PCO2 PaCO2 PvCO2 SO2 SaO2 SvO2 TCO2

Normal Adult Venous Values* 7.31-7.41 41-51 torr 30-40 torr 23-30 mmol/L 3 mEq/L 75% Blood Gas Abbreviations

Base Excess (positive number) or Base Deficit (negative number) Bicarbonate Carbonic Acid Partial Pressure of Oxygen Partial Pressure of Oxygen in Arterial Blood Partial Pressure of Oxygen in Venous Blood Partial Pressure of Carbon Dioxide Partial Pressure of Carbon Dioxide in Arterial Blood Partial Pressure of Carbon Dioxide in Venous Blood Oxygen Saturation Oxygen Saturation in Arterial Blood Oxygen Saturation in Venous Blood Total Carbon Dioxide Content

Normal Values (At sea level):

pH 7.35--7.45 pCO2 35--45mmHg pO2 80--100mmHg O2Saturation95--100% HCO3--22--26mEq/L BaseExcess+or--2

The 6 Easy Steps to ABG Analysis:

1. Is the pH normal? 2. Is the CO2 normal? 3. Is the HCO3 normal? 4. Match the CO2 or the HCO3 with the pH 5. Does the CO2 or the HCO3 go the opposite direction of the pH? 6. Are the pO2 and the O2 saturation normal?

Test Normal Value Value

pH 7.35-7.45 Acidosis Alkalosis pCO2 35-45 Alkalosis Acidosis HCO3 22-26 Acidosis Alkalosis pO2 80-100 Hypoxemia O2 Therapy SaO2 95-100% Hypoxemia

Acid-Base Regulation

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Metabolic processes continually produce acid and, to a lesser degree, base. Hydrogen ion (H+) is especially reactive; it can attach to negatively charged proteins and, in high concentrations, alter their overall charge, configuration, and function. To maintain cellular function, the body has elaborate mechanisms that maintain blood H+ concentration within a narrow rangetypically 37 to 43 nmol/L (pH 7.43 to 7.37, where pH = log [H+]) and ideally 40 nmol/L (pH = 7.40). Disturbances of these mechanisms can have serious clinical consequences. Acid-base equilibrium is closely tied to fluid and electrolyte balance, and disturbances in one of these systems often affect another. Fluid metabolism is discussed in discussed in Fluid Metabolism, and electrolytes are discussed in see Electrolyte Disorders. Acid-Base Physiology Most acid comes from carbohydrate and fat metabolism, which generates 15,000 to 20,000 mmol of CO2 daily. CO2 is not an acid itself but combines with water (H2O) in the blood to create carbonic acid (H2CO3), which in the presence of the enzyme carbonic anhydrase dissociates into H+ and HCO3. The H+ binds with Hb in RBCs and is released with oxygenation in the alveoli, at which time the reaction is reversed, creating H2O and CO2, which is exhaled in each breath. Lesser amounts of organic acid derive from the following:

Incomplete metabolism of glucose and fatty acids into lactic acid and ketoacids Metabolism of sulfur-containing amino acids (cysteine, methionine) into sulfuric acid Metabolism of cationic amino acids (arginine, lysine) Hydrolysis of dietary phosphate

This fixed or metabolic acid load cannot be exhaled and therefore must be neutralized or excreted. Most base comes from metabolism of anionic amino acids (glutamate and aspartate) and from oxidation and consumption of organic anions such as lactate and citrate, which produce HCO3. Acid-Base Balance Acid-base balance is maintained by chemical buffering and by pulmonary and renal

elimination. Chemical buffering: Chemical buffers are solutions that resist changes in pH. Intracellular and extracellular buffers provide an immediate response to acid-base disturbances. Bone also plays an important buffering role. A buffer is made up of a weak acid and its conjugate base. The conjugate base can accept H+ and the weak acid can relinquish it thereby minimizing changes in free H+ concentration. The most important extracellular buffer is the HCO3/CO2 system, described by the equation: H+ + HCO3 H2CO3 CO2 + H2O An increase in H+ drives the equation to the right and generates CO2. This important buffer system is highly regulated; CO2 concentrations can be finely controlled by alveolar ventilation, and H+ and HCO3 concentrations can be finely regulated by renal excretion. The relationship between HCO3 and CO2 in the system can be described by the Kassirer-Bleich equation, derived from the Henderson-Hasselbalch equation: H+ = 24 Pco2/HCO3 This equation illustrates that acid-base balance depends on the ratio of Pco2 and HCO3, not on the absolute value of either one alone. With this formula, any 2 values (usually H+ and Pco2) can be used to calculate the other (usually HCO3). Other important physiologic buffers include intracellular organic and inorganic phosphates and proteins, including Hb in RBCs. Less important are extracellular phosphate and plasma proteins. Bone becomes an important buffer after consumption of extracellular HCO3. Bone initially releases sodium carbonate (NaHCO3) and potassium carbonate (KHCO3) in exchange for H+. With prolonged acid loads, bone releases calcium carbonate (CaCO3) and calcium phosphate (CaPO4). Long-standing acidemia therefore contributes to bone demineralization and osteoporosis. Pulmonary regulation: CO2 concentration is finely regulated by changes in tidal volume and respiratory rate (minute ventilation). A decrease in pH is sensed by arterial chemoreceptors and leads to increases in tidal volume or respiratory rate; CO2 is exhaled and blood pH increases. In contrast to chemical buffering, which is immediate, pulmonary regulation occurs over minutes to hours. It is about 50 to 75% effective; it does not completely normalize pH. Renal regulation: The kidneys control pH by adjusting the amount of HCO3 that is reabsorbed and the amount of H+ that is excreted; increase in HCO3 is equivalent to removing free H+. Changes in renal acid-base handling occur hours to days after

changes in acid-base status. HCO3 reabsorption occurs mostly in the proximal tubule and, to a lesser degree, in the collecting tubule. H2O within the tubular cell dissociates into H+ and hydroxide (OH); in the presence of carbonic anhydrase, the OH combines with CO2 to form HCO3, which is transported back into the peritubular capillary, while the H+ is secreted into the tubular lumen and joins with freely filtered HCO3 to form CO2 and H2O, which are also reabsorbed. Thus, reabsorbed HCO3 ions are newly generated and not the same as those that were filtered. Decreases in effective circulating volume (such as occur with diuretic therapy) increase HCO3 reabsorption, while increases in parathyroid hormone in response to an acid load decrease HCO3 reabsorption. Also, increased Pco2 leads to increased HCO3 reabsorption, while Cl depletion (typically from volume depletion) leads to increased Na+ reabsorption and HCO3 generation by the proximal tubule. Acid is actively excreted into the proximal and distal tubules where it combines with urinary buffersprimarily freely filtered HPO42, creatinine, uric acid, and ammoniato be transported outside the body. The ammonia buffering system is especially important because other buffers are filtered in fixed concentrations and can be depleted by high acid loads; by contrast, tubular cells actively regulate ammonia production in response to changes in acid load. Arterial pH is the main determinant of acid secretion, but excretion is also influenced by K+, Cl, and aldosterone levels. Intracellular K+ concentration and H+ secretion are reciprocally related; K+ depletion causes increased H+ secretion and hence metabolic alkalosis.

pH 7.27 acidotic CO2 53 Acidotic pO2 50 low O2 sat. 79% low HCO3 24 normal

pH7.52alkalotic CO229alkalotic pO2100normal O2sat.98%normal HCO323normal