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# Arterial Blood Gases

Acid-Base Balance

Components
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## Arterial partial pressure of oxygen (PaO2)

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Measures the amount of oxygen dissolved in the plasma Value is directly dependent upon the alveolar oxygen pressure (PAO2) Measures the amount of CO2 dissolved in the plasma The negative logarithm of the hydrogen ion concentration

## Arterial pressure of carbon dioxide (PaCO2)

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pH
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Components, cont
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Bicarbonate (HCO3-)
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Calculated from the CO2 and pH using the HendersonHasselbach equation Allows assessment of the metabolic component of acidbase balance Reflects A measure of the amount of acid or alkali that must be added to a sample under standard conditions to return the pH to 7.4 Calculated from the pH and PaCO2

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Total CO2
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## Base excess (or deficit)

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Interpreting ABGs
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Assess pH:
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normal, alkalotic, acidotic PaCO2 >45 = respiratory acidosis PaCO2 <35 = respiratory alkalosis HCO3 > 28 = metabolic alkalosis HCO3 < 22 = metabolic acidosis

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## Determine if there is metabolic or respiratory compensation occurring

Anion Gap
The difference between the main positive and negative ions  (Na + K) (Cl + HCO3)  Normal is 10-18  Increased anion gap indicates an accumulation of organic acids (ketoacids, lactic acid, other acids)
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Acid-Base Balance
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Intracellular enzymes function best when the pH is 7.25 7.45 Most metabolic processes produce acids Acid production increases with dx:
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Lactic acid from ischemia/anaerobic metabolism Ketoacids from diabetes Methanol from alcohol ingestion

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Renal/respiratory/liver failure decrease acid removal from the body Loss of acid occurs with vomiting/NG suctioning Loss of bicarb occurs with diarrhea

## Disorders of Acid-Base Balance

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Metabolic acidosis
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## With a normal anion gap

 Renal

bicarb loss  Loss of bicarb from the gut  Decreased renal hydrogen ion secretion
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## Increased anion gap (acid accumulation)

 Lactic
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acidosis

Type A: sepsis, cardiac arrest, hypotension, methanol Type B: insulin deficiency, decreased hepatic metabolism

 Ketoacidosis:

## insulin deficiency, starvation  Exogenous acids: salicylates

Disorders, cont
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Metabolic alkalosis
Hydrogen ion loss: vomiting, renal loss, diuretics, hypokalemia, low Cl states  Bicarb gain: sodium bicarb administration, citrate administration
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Respiratory acidosis
Airway obstruction, pneumonia, ARDS, PE  Respiratory muscle weakness  Trauma  Respiratory depression
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Disorders, cont
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Respiratory alkalosis
High levels of anxiety or pain  Altitude  Excessive mechanical ventilation  Respiratory stimulants/salicylate overdose  Pulmonary embolism, asthma, edema
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## The body prevents pH changes by regulating 2 pathways for eliminating acid

Respiratory  Renal
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100 times more acid equivalents are expired each day in the form of CO2 than are excreted by the kidney  Buffers bind or release hydrogen ion according to the pH to limit the change in pH that occurs when acid is added to the blood
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## Main body buffers

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Bicarbonate
CO2 combines with water to form carbonic acid which dissociates into bicarb and hydrogen ion  CO2 + H2O = H2CO3 = HCO3- + H+  The normal ratio of bicarb to CO2 is 20:1as long as this ratio remains 20:1, the pH will be 7.4
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Hemoglobin
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Especially deoxygenated Hb

## Relationship between pH, PaCO2, HCO3

When CO2 changes persist, pH is slowly corrected by renal compensation (retention or elimination of bicarb)  Metabolic changes can be corrected by respiratory compensation but metabolic alkalosis is not compensated as it would require a drop in ventilation  Mixed conditions (acidosis or alkalosis) can occur
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