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CHAPTER 122 Arterial Blood Gas and Placement of A-

line

Joseph J. Miaskiewicz, Jr., MD

Critically ill patients require arterial blood gas (ABG) analysis to assess oxygenation and ventilation due to limitations of noninvasive oximetry measurements. Below a pO2 of 60 mm Hg corresponding to an O2 saturation of 80%, the oxyhemoglobin saturation curve is steep and large changes in oximetry may mean small changes in oxygenation. Below this level oximetry may not correlate with oxygenation, and an arterial blood gas (ABG) should be obtained (Table 122-1).

TABLE 122-1 Obtaining an Arterial Sample and Placement of an Arterial Line

  ABG A-Line Indications In hospitalized medical patients,

an ABG is primarily obtained to confirm the severity and likely cause of the disturbance • Level of oxygenation, especially

in settings when the oximeter measurements are thought to be unreliable or difficult to obtain

• Need for intubation: refractory hypoxemia (pO2 < 55 on 100% O2

Usually in the ICU setting for • Frequent ABG sampling • Continuous blood

pressure monitoring in use of inotropic or vasopressor agents

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NRB mask) or hypercapnic respiratory failure (pCO2 > 55 with acidemia pH < 7.25)

• Severity metabolic acidosis and adequacy of respiratory compensation when ↑ work of breathing

• Contribution of ↑pCO2 versus other causes in somnolent patient

Contraindications Impaired collateral circulation • Raynaud • Thromboangiitis obliterans • Cyanosis

Impaired collateral circulation

Preparation Allen test: occlusion of the radial and ulnar arteries by firm pressure while the fist is clenched followed by opening of the hand and release of the arteries one at a time to assess adequacy of returning blood flow to the hand

Assess collateral circulation with Allen test Avoid brachial and femoral arteries (inadequate collateral supplies)

Technical Tips The radial artery at the wrist best site (near the surface, relatively easy to palpate, and stabilize with good ulnar collateral supply)

Apply local anesthetic with 1% lidocaine in the conscious patient Immobilize hand on a wrist board or towel and dorsiflex wrist

Same as for ABG If lose ability to palpate pulse, likely arterial spasm precluding successful cannulation. Wait until subsides or choose another site If unsuccessful, apply pressure for several minutes to avoid hematoma formation (which will make subsequent attempts more difficult) and consider use of ultrasound to visualize vessel Reassess perfusion of hand after placement

Complications Transient obstruction of blood flow may ↓ arterial flow in distal tissues unless adequate collateral arterial vessels available in the setting of

Remove catheter immediately if any sign of vascular compromise

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• Spasm • Intraluminal clotting • Bleeding and hematoma

formation

Use nondominant hand preferred

By measuring both oxygenation and ventilation ABG analysis assesses the effects of the cardiopulmonary system in oxygen delivery. ABG analysis directly measures the pH, pCO2, and pO2. The normal range for the pH is between 7.36 and 7.44 corresponding to a normal range of 36 to 44 torr for the pCO2. The normal range for the pO2 is between 80 and 100 torr. However, age and the pCO2 also determine alveolar O2.

Oximetry does not measure pCO2 and does not reflect ventilation or acid-base status. Ventilation may be defined in terms of movement of a volume of air into and out of the lungs, removing carbon dioxide from the blood and providing oxygen. Alveolar ventilation is defined in terms of ventilation of CO2. High oxygen saturation may be falsely reassuring in patients whose respiratory drive is compromised by an increase of oxygenation due to supplemental O2. Assessment of alveolar ventilation is the key to determining whether a patient is receiving enough oxygen. A raised PaCO2 reflects reduced alveolar ventilation. See Chapter 238 (Acid Base Disorders). An approach to interpreting arterial blood gases is essential when caring for hospitalized patients (Table 122-3).

Respiratory failure is classified as hypoxemic respiratory failure (hypoxemia without carbon dioxide retention [SaO2 < 95%, PaO2 < 80 on room air]) or hypercarbic respiratory failure (pCO2 > 45 mm Hg). Calculation of the gradient between the alveolar and arterial oxygen tensions (the A-a gradient) in respiratory failure will help to determine whether the patient has associated lung disease or just reduced alveolar ventilation (Table 122-2). See Chapter 138 (Acute Respiratory Failure).

TABLE 122-2 Calculation of the A-a Oxygen Gradient from the ABG

The Alveolar-Arterial Oxygen Gradient The A-a oxygen gradient = PAO2 – PaO2 Estimated normal gradient ∼ (Age/4) + 4

The Alveolar Gas Equation PAO2 = (FiO2 × [Patm – PH2O]) – (PaCO2/R) • Inspired air at sea level, the FiO2 of room air = 0.21 • Atmospheric pressure, Patm = 760 mm Hg • PH2O at 37 F = 47 mm Hg • Respiratory quotient, R = 0.8 Hypoxemic Respiratory Failure with Normal A-a Oxygen Gradient • Alveolar hypoventilation (oversedation, obesity hypoventilation syndrome, muscular

weakness, neurologic disease) • High altitude (low inspired FiO2)

Hypoxemic Respiratory Failure with ↑ A-a Gradient

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• Ventilation-perfusion mismatch (pulmonary embolism, COPD, ARDS, pulmonary artery vasospasm)

• Right-to-left shunt (anatomic: cardiac, pulmonary AVM, hepatopulmonary syndrome; physiologic due to fluid preventing ventilation of perfused alveoli: pneumonia, atelectasis)

Disorders of the lung structure reduce the efficiency of oxygen transfer and widen the A-a gradient. The prolonged respiratory depression may lead to collapse of some areas of lung and an increase in the A-a gradient. Hypercarbic Respiratory Failure, Hypoxemia from Impaired Ventilation with Normal A-a Oxygen Gradient • Inadequate alveolar ventilation (without shunting from fluid or collapse of alveoli) • Ventilatory pump failure (respiratory muscle weakness, neurolgic disease, thoracic cage

issues)

TABLE 122-3 Blood Gas Interpretation

Step 1: Acid-base (ventilation) pH PaCO2 Interpretation

↓ ↑ In acute respiratory failure the change in pH will be accounted for by the high carbon dioxide concentration.

↓ ↓ A severe metabolic acidosis or some limitation on the ability of the respiratory system to compensate.

Normal ↑ Alveolar hypoventilation (raised PaCO2) with a normal pH most likely a primary ventilatory change present long enough for renal mechanisms to compensate. Increased serum bicarbonate may also be a clue of chronic CO2 retention. A similar picture may result from carbon dioxide retention due to reduced ventilation compensating for a metabolic alkalosis, although such compensation is usually only partial.

Normal ↓ A primary metabolic acidosis in which the respiratory system has normalized the pH. Calculate the anion gap.

↑ ↓ Acute alveolar hyperventilation if the pH is appropriately raised for the reduction in PaCO2. Chronic alveolar hyperventilation if the pH is between 7.46 and 7.50 as the renal system seldom compensates completely for an alkalosis.

Step 2: Oxygenation (pO2, %saturation) pO2 PaCO2 pH   Normal Normal ↑ A primary metabolic alkalosis

to which the ventilatory system has not responded.

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↓ Normal ↓ Hypoxemia: when patients with chronic CO2 retention increase usual level of ventilation (acute pulmonary embolism in chronic lung disease).

Step 3: Calculate the A-a gradient to determine whether carbon dioxide retention is related to an intrapulmonary cause A-a Explanation Etiology Gradient Calculating the A-a gradient is

most useful for determining the severity of the underlying disorder and whether there is a component of hypoventilation.

Especially for hospitalized patients who are prescribed medications that may suppress respiration, the A-a gradient is used to determine the relative contribution of hypoventilation to hypoxia due to underlying lung disease.

Normal A normal A-a gradient is ∼10- 15 torr. Advancing age results in increases of the normal A-a gradient. A-a gradient = 2.5 + 0.21 × age in years.

The ABG abnormality is all due to hypoventilation.

Elevated An elevated A-a gradient represents ↑ difficulty in getting O2 from the alveoli to the blood. A higher FiO2 disproportionately increases the PAO2 more than the PaO2.

• Diseases that affect the pulmonary interstitium including interstitial lung disease, pneumonia, and CHF.

• Pulmonary vascular disease: pulmonary emboli, shunts, pulmonary hypertension.

• Ventilation/perfusion mismatches of large vessels (pulmonary or tumor emboli) and small vessels (pulmonary hypertension, vasculitis, interstitial lung disease and emphysema).

• When breathing 100% oxygen, older patients may normally have an A-a gradient as high as 80 torr and younger patients as high as 120 torr.

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Step 4: Does the result correlate with the clinical setting? Possible Source of Error Prevention Presence of heparin in syringe

Express any heparin out of syringe prior to sampling

Air bubbles (resulting in equilibrium between air and arterial blood: ↓PaCO2, ↑PaO2

Inspect sample and remove air bubbles

Inadequate sample Obtain at least 3 mL aterial blood Metabolically active cellular constituents of blood (resulting in changing arterial gas tensions over time)

Cool sample on ice Analyze sample within 1 h

Sampling of venous blood

Pay attention to technique

Neither oximetry nor ABGs will detect the presence of a reduced O2-carrying capacity because anemia, and carbon monoxide (CO) poisoning, and methemoglobinemia do not affect the alveolar pO2. When there is CO poisoning, the oximeter cannot differentiate between hemoglobin molecules with CO attached and those with O2 attached and will report normal O2 saturation. ABGs will also report normal values because the PaO2 is a measurement of the oxygen dissolved in the blood and not the number of O2 molecules attached to hemoglobin molecules. In CO poisoning an elevated carboxyhemoglobin will be required to make the diagnosis. Nonsmokers may have levels up to 3, smokers 10 to 15, and CO poisoning levels above 15. Likewise, the presence of abnormal hemoglobins, such as sickle cell, fetal hemoglobin, and methemoglobin, will not affect the ABG results.

Oximetry may also not correlate with oxygenation with falsely low results when there is poor blood flow and perfusion to the fingertips, vasoconstriction due to hypothermia or sepsis