Blood Gas, Acid–Base Analysis and Electrolyte Abnormalities



Blood Gas Analysis


Blood gas analysis gives us information about both pulmonary function and acid–base status and is essential in order to make a diagnosis, provide treatment and monitor the progress of patients with either respiratory or metabolic abnormalities. Acid–base status can be evaluated on arterial blood gas (ABG) or venous blood gas (VBG) samples. In order to evaluate oxygenation, however, an arterial sample is mandatory. Four key pieces of in­­formation are provided from the ABG: partial pressures of both oxygen (PaO2) and carbon dioxide (PaCO2), blood pH and bicarbonate concentration (HCO3). It is vital to know the normal values in order to evaluate samples accurately (see Table 5.1).


Table 5.1 Normal arterial blood gas values


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Assessing Ventilation


PaO2 (measured in mmHg or kPa) is an accurate reflection of the ability of the lungs to transfer oxygen to the blood. A low PaO2 represents hypoxaemia and can initiate hyperventilation. The SaO2 (pulse oximeter) measures the percentage of haemoglobin actually carrying oxygen, which is why 95–100% is normal. These two values are crucial to optimise the oxygen concentration delivered during mechanical ventilation.


PaCO2 (in mmHg or kPa) indicates the effectiveness of alveolar ventilation. Alveolar ventilation determines PaCO2. Hyperventilation results in a decreased PaCO2 (hypocapnia), whereas hypoventilation increases PaCO2 (hypercapnia). Changes in ventilation may occur in patients with primary pulmonary disease, central nervous system (CNS) impairment, or may occur as a compensatory change in patients with metabolic disturbances.


Assessing Acid–Base Status


Changes in ventilation may occur as a response to a metabolic disorder causing an abnormal pH. Respiratory compensation occurs when the body attempts to correct an acidosis or alkalosis by altering ventilation in order to either increase or decrease the level of CO2 within the body. For example, a decrease in the blood pH and HCO3 indicate a primary metabolic acidosis; in response, the respiratory rate would increase in order to reduce the PaCO2 and therefore try to self-correct the imbalance.






Definitions


Acid – a substance that can donate hydrogen ions (H+)

Acidaemia/alkalaemia – describes the actual pH of the blood. Acidaemia is present if the pH is <7.4 and alkalaemia is present if the pH is >7.4

Acidosis – refers to processes in the body that result in increased acidity (decrease pH)

Alkalosis – refers to processes in the body that result in decreased acidity (increase pH)

Base – a substance that can accept hydrogen ions (H+)

Base excess – a measurement used to assess the metabolic contribution to an acidosis or alkalosis. A positive value indicates an excess of base (metabolic alkalosis) and a negative value indicates a deficit of base (metabolic acidosis)

Buffers – systems that offer immediate cushioning (buffering) to sudden changes in pH

FiO2 – fraction of inspired oxygen is the measured concentration of oxygen delivered to the patient. Room air is 21% (FiO2 = 0.21)

Metabolic acid – body acids that cannot be converted to a gas (lactic acid, ketones, glycolic acid, acetoacetic acid)

pH – determines the acid–base status by measuring hydrogen ions (H+)

PaCO2 – the partial pressure of CO2 dissolved in arterial blood as the result of cellular metabolism, and is a direct reflection of the adequacy of alveolar ventilation. PaCO2 is controlled through the lungs via either hyperventilation or hypoventilation and changes can occur within minutes. Measured in mmHg or kPa

PaO2 – the partial pressure of oxygen dissolved in arterial blood, representing the lungs’ ability to oxygenate blood. A decrease in PaO2 is defined as hypoxaemia. Measured in mmHg or kPa

Respiratory acid – carbon dioxide (CO2)




Metabolic Assessment


Serum bicarbonate levels provide information about the metabolic aspect of acid–base balance. HCO3 is controlled by renal retention and excretion; this can be accurately measured in either venous or arterial samples. An increase in HCO3 results in a metabolic alkalosis, whilst an abnormally low HCO3 results in a primary metabolic acidosis. Primary metabolic acid–base disorders are predominantly corrected by treating the underlying disease. The kidneys respond to respiratory acid–base disturbance by retaining or excreting increased amounts of HCO3. This compensatory response occurs far more slowly than respiratory changes.


Step by Step Blood Gas Analysis


As previously stated, the body functions best at a pH of 7.4. Any physiological event that causes a change in blood pH is called a primary disorder. A primary disorder will stimulate a compensatory response in an attempt to restore the pH to normal.



Step 1. Examine the PaO2 and determine if the patient is hypoxaemic – administer oxygen if necessary.

Step 2. Examine the pH. If the pH is <7.35 an acidaemia exists; if the pH is >7.45 an alkalaemia exists.

Step 3. Is there a respiratory component? Ex­­amine the PaCO2. If it is high or low, a respiratory component exists (could be primary or secondary/compensatory); if it is normal, no respiratory component is present. For example, increased PaCO2 will result in a respiratory acidosis, and a decreased PaCO2 a respiratory alkalosis.

Step 4. Is there a metabolic component? Examine the HCO3−, if it is high or low, a metabolic component exists (could be primary or secondary/compensatory); if it is normal, no metabolic component is detected. If the HCO3− is high, a metabolic alkalosis exists; if low, a metabolic acidosis exists.

Step 5. Determine which component is the primary disorder. In simple acid–base disturbances, the primary disorder is the component that has changed in the same manner as the pH. If an acidaemia exists, the primary disorder will be the component that corresponds to an acidosis. For example, if the pH and the HCO3− are low, the primary disorder is metabolic (a metabolic acidosis). Conversely, if the pH is low, and the pCO2 is elevated (respiratory acidosis), the primary disorder is respiratory. If both the metabolic and respiratory components have changed, in the manner of the pH, then a mixed acid–base disturbance exists.

Step 6. Determine if there is a compensatory response. Compensatory responses will cause the component to move in an opposite manner from the pH. That is, if an acidaemia exists, the compensatory response to an acidaemia would be an alkalosis. Thus, a compensatory response to an acidaemia wound be an elevated HCO3−, or a decreased pCO2; a compensatory response to an alkalaemia would be a decreased HCO3− or increased pCO2. For example, if the pH HCO3− and pCO2 are low, then a primary metabolic acidosis with respiratory compensation exists. If the pH is low, and the HCO3− and pCO2 are high, a primary respiratory acidosis, with metabolic compensation exists.

Step 7. Always remember the body can never fully compensate to a normal pH, and it will never over-compensate.

Treating Acid–Base Disorders


Acid–base disorders are best treated by address­ing and correcting the underlying problem. Occasionally, however, intervention to directly adjust pH must be initiated, usually if the pH becomes life-threatening.


Metabolic Acidosis


Causes:



  • Diabetic ketoacidosis
  • Renal insufficiency
  • Excessive lactic acid production
  • Exogenous toxins (ethylene glycol)
  • Diarrhoea.

Acidaemia should be treated with intravenous sodium bicarbonate, but only when the pH is <7.05. To calculate the amount of sodium bicarbonate to administer it is necessary to first calculate the bicarbonate deficit:


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Administer one-quarter of the bicarbonate deficit intravenously over 5–10 minutes, and then re-check the patient’s pH. If the pH returns to a more acceptable range >7.2, discontinue bicarbonate administration and continue treating the underlying disorder. There are potentially several adverse complications associated with the administration of sodium bicarbonate. The most common are the following:



1) Rebound alkalaemia.

2) Hypernatraemia.

3) Hypokalaemia – rapid correction of the pH drives potassium intracellularly. This is most important with severe metabolic acidosis secondary to diabetic ketoacidosis. This is an advantage when treating severe hyperka­laemia and acidosis secondary to urethral obstruction.

4) Seizures secondary to hypocalcaemia. If there is a rebound alkalaemia, this will cause in­­creased protein binding of calcium, which lowers ionised calcium.

5) Paradoxical cerebrospinal fluid (CSF) acidosis. Increasing plasma HCO3 can increase PaCO2. Increased amounts of CO2 can then cross the blood–brain barrier readily and lower the pH of the CSF.

Respiratory Acidosis (Hypoventilation)


The most common cause of respiratory acidosis is respiratory depression caused by the following:



1) Drugs – general anaesthetics, opioids, etc.

2) Central nervous system trauma

3) Space occupying lesions in the brain

4) Respiratory disease/trauma – pneumothorax, airway obstruction, pulmonary oedema, etc.

Treatment depends on the underlying cause and the severity of the hypercapnia. Acute, severe respiratory acidosis usually requires intubation and positive pressure ventilation.


Metabolic Alkalosis


The most common causes of metabolic alkalosis are the following:



1) Vomiting (loss of H+ in the stomach contents)

2) Hyperadrenocorticism

3) Exogenous steroid therapy

4) Potassium depleting diuretic therapy leading to hypokalaemia and ‘contraction alkalosis’

5) Bicarbonate therapy.

It is very rare for any patient to require the administration of acid to correct a severe meta­bolic alkalaemia (pH >7.8). Nearly all patients will respond when 0.9% saline is administered because it is an acidifying solution.


Respiratory Alkalosis (Hyperventilation)


Respiratory alkalosis is the result of hyperventilation. The most common causes in animals are pain, fever and anxiety. Other conditions include CNS disorders, exogenous drug administration and over-zealous ventilation. Treatment is based on identification and treatment of the underlying cause.


Placement of an Arterial Catheter


Arterial catheterisation is technically more difficult than placing a catheter into a vein, as arteries are less superficial and much smaller. Arterial catheters are used for measuring blood pressure directly and to collect blood samples for blood gas analysis, particularly if repeated samples are likely to be required. The commonly used artery for both these procedures is the dorsal metatarsal artery, but the femoral, auricular, radial, brachial and coccygeal arteries can also be used.


Catheterisation of the Dorsal Metatarsal Artery


This artery is relatively superficial. It can be located in the proximal area of the metatarsus, medial to the extensor tendon and between the second and third metatarsal bones. Catheters of 20–24 gauge are used:



  • The patient should be in lateral recumbency with the limb to be used for catheterisation placed dependently.
  • The skin over the proposed site should be clipped and briefly prepped (the author places a Hibitane solution soaked swab over this site whilst carrying out hand washing) and then wiped with Hibitane solution. The area should not be scrubbed as this will often result in muscular spasm in the artery, making catheterisation impossible.
  • The pulse should be palpated on the dorsal metatarsal, a small bleb of 2% lidocaine can be used in the area in order to desensitise it (see Figure 5.2).
  • Whilst still palpating the artery the catheter should be inserted directly, using the other hand, above the vessel (between the second and third metatarsus) (see Figure 5.3). The catheter should be inserted, through the skin, at an angle of 45–60°, depending on operator preference.
  • Once through the skin, the angle of the catheter should be reduced. Care should be taken to approach the artery at an angle of 10–30° to ensure the catheter is correctly aligned to the artery, which will facilitate feeding.
  • Arterial walls are much thicker than venous walls, so a purposeful directed motion may be required once the tip of the inner stylet is resting just over the arterial wall.
  • Once a flashback of blood is seen in the hub of the catheter, the catheter and stylet should then be advanced together for approximately 1–2 mm (to ensure the catheter itself lies within the arterial lumen and not just the tip of the stylet) and then pushed off the needle and into the artery; as this is performed the angle of the catheter can also be reduced (see Figure 5.4).
  • The catheter should then be flushed with heparinised saline solution, taped into place and labelled as arterial (see Figure 5.5).
  • Arterial lines should be flushed every 15 min­utes or continually via a pressure bag and microtubing.

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Jul 30, 2017 | Posted by in GENERAL | Comments Off on Blood Gas, Acid–Base Analysis and Electrolyte Abnormalities

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