Arterial Blood Gases

Alveolar hypoventilation during wakefulness is defined as an arterial partial pressure of carbon dioxide (PaCO₂) of 45 mm Hg or higher. If the sleeping PaCO₂ is ≥10 mm Hg above the awake value, nocturnal hypoventilation is said to be present. Hypoxemia is defined as a low arterial partial pressure of oxygen (PaO₂) relative to predicted values. A PaO₂ less than 55 mm Hg while breathing room air is considered severe and an indication for chronic 24-hour supplemental oxygen therapy. Milder degree of hypoxemia can be identified by comparing a PaO₂ with a predicted value for age. A simple estimate of a normal predicted PaO₂ is 105 – age (yr).

The alveolar gas equation¹ (Equation 10–1) allows one to compute the alveolar (ideal) partial pressure of oxygen (PAO₂) from the fractional concentration of oxygen in inspired gas (FiO₂), which is 0.21 when breathing room air, and the PaCO₂. The respiratory exchange ratio (R) is the CO₂ elimination divided by the O₂ uptake. At steady state, R is equal to the respiratory quotient (RQ), which equals the CO₂ production/O₂ consumption (). R is usually assumed to be 0.8.¹ In Equation 10–1, FiO₂ = 0.21 (breathing room air), P_B is the barometric pressure (760 mm Hg at sea level), and PH₂O is the partial pressure of water vapor (47 mm Hg at 37°C).

Breathing room air, Equation 10–1 becomes Equation 10–2. The A-a gradient (Equation 10–3) is the difference between the ideal PAO₂ and the actual (measured) PaO₂. Equation 10–4 gives the predicted A-a gradient (usually <25 mm Hg).

(room air)PAO2=0.21(760−47)−PaCO2/0.8=150−PaCO2/0.8 Equation 10–2

Equation 10–2

A-a gradient=PAO2−PaO2 Equation 10–3

Equation 10–3

Predicted estimate of normal A-a gradient=4+age (yr)/4For example,for a 48-year-old,A-a gradient=16 Equation 10–4

Equation 10–4

The major causes of hypoxemia are listed in Table 10–1. Causes of hypoxemia include a low FiO₂, a low P_B (high altitude), hypoventilation (increased PaCO₂), and incomplete oxygenation of the blood by the lung (ventilation-perfusion [] mismatch or shunt). In mismatch, some alveoli are underventilated for their blood flow (low ) and blood is incompletely oxygenated. This can be overcome by increasing the FiO₂, thereby increasing the effective oxygen flow to underventilated alveoli. If shunt is causing hypoxemia, blood completely bypasses the alveoli. The deoxygenated blood mixes with oxygenated blood to give a lower than ideal PaO₂. Raising the FiO₂ has no effect on shunted blood. Most patients with lung disease also have defects in CO₂ excretion. This may not result in alveolar hypoventilation because the patient may compensate by increasing the minute ventilation (discussed later).

TABLE 10–1

Major Causes of Hypoxemia

	A-a GRADIENT	RESPONDS TO SUPPLEMENTAL OXYGEN
Low FiO2, low PB	Normal	Yes
Hypoventilation	Normal	Yes
mismatch	Increased	Yes
Shunt	Increased	No

A-a = alveolar-arterial; FiO₂ = fractional concentration of oxygen in inspired gas; P_B = barometric pressure; = ventilation-perfusion (ratio).

Hypoxemia can occur simply as a consequence of hypoventilation. For example, a patient with normal lungs may have an increased PaCO₂ due to muscle weakness or abnormal ventilatory control. In this case, the PaO₂ is fairly close to the ideal (PAO₂) computed from the alveolar gas equation (Equation 10–1) using the known PaCO₂. The A-a gradient (Equation 10–3) in such patients is normal. Lung disease severe enough to cause an increased PaCO₂ is always associated with an increased A-a gradient.

Box 10–1 presents examples of use of the alveolar gas equation (Equation 10–1). In a patient with amyotrophic lateral sclerosis (ALS; Example 1), an arterial blood gas reveals a PaO₂ of 60 and PaCO₂ of 65 mm Hg. The computed A-a gradient is 8.7 mm Hg (normal). Hypoxemia is due to hypoventilation. In Example 2, a patient with chronic obstructive pulmonary disease has evidence of both hypoxemia and hypercapnia and the A-a gradient is increased. The hypoxemia is due to both mismatch and hypoventilation. In patients with hypoventilation of unclear etiology, calculating an A-a gradient can provide an important clue as to whether the hypoventilation is due to lung disease or due totally to hypoventilation. A normal A-a gradient in a patient with hypoventilation would suggest a disorder of ventilatory control or muscle weakness.

Box 10–1   Examples of Computation of the Alveolar Partial Pressure of Oxygen and the A-a Gradient

Example 1: Hypoventilation Due to Amyotrophic Lateral Sclerosis (normal A-a gradient)

Laboratory: PaO₂ = 60 mm Hg and PaCO₂ = 65 mm Hg (breathing room air)

PAO2=150−65/0.8=68.7

A-a gradient=PAO2−PaO2=68.7−60=8.7(normal)

Example 2: Hypoventilation Due to Chronic Obstructive Pulmonary Disease (INCREASED A-a GRADIENT)

Laboratory: PaO₂ = 50 mm Hg and PaCO₂ = 55 mm Hg

PAO2=150−55/0.8=81

A-a gradient=PAO2−PaO2=81−50=31(increased)

A-a = alveolar-arterial; PaCO₂ = arterial partial pressure of carbon dioxide; PAO₂ = alveolar partial pressure of oxygen; PaO₂ = arterial partial pressure of oxygen.

Oxygen Transport and Saturation

The majority of the oxygen-carrying capacity of the blood is due to oxygen bound to hemoglobin (Hb) with a small fraction of dissolved oxygen (Equation 10–5).¹ When fully saturated, a gram of Hb carries about 1.34 mL/dL of oxygen (1 dL = 100 mL).

Oxygen content of arterial blood (CaO₂ [mL O₂/100 mL])

CaO2=1.34 mL/g×Hb(g/100mL)×SaO2+0.003 PaO2 Equation 10–5

Equation 10–5

SaO2=100×O2Hb/(O2Hb+RHb) Equation 10–6

Equation 10–6

The arterial oxygen saturation (SaO₂) is usually expressed as the ratio of oxygenated hemoglobin (O₂Hb) to the total amount of Hb that can bind oxygen (Equation 10–6). The amount of hemoglobin that can bind oxygen is the sum of O₂Hb and deoxygenated (reduced) hemoglobin (RHb). The SaO₂ value for a given PaO₂ depends on the position of the oxygen-hemoglobin saturation curve (also called the oxygen-hemoglobin dissociation curve)¹ (Fig. 10–1). At the usual body temperature and pH, a PaO₂ of 60 mm Hg corresponds to approximately an SaO₂ of 90%. A left shift results in a lower PaO₂ being associated with a given SaO₂ and vice versa. A shift to the left can occur with decreasing temperature, hydrogen ion concentration [H⁺], PaCO₂, or level of 2,3-diphosphoglycerate (2,3-DPG). Abnormal Hbs can also result in a different relationship between the SaO₂ and the PaO₂. For example, in patients with sickle cell disease (SCD), the PaO₂ for a given SaO₂ is higher due to the rightward shift of the O₂Hb saturation curve for hemoglobin S (HbS) compared with hemoglobin A (HbA).² The position of the O₂Hb dissociation curve is often defined by the P₅₀, which is the PaO₂ corresponding to an SaO₂ of 50%. For HbA, the P₅₀ is 26 mm Hg but is 42 to 56 mm Hg in SCD patients.² The net effect is a rightward shift in the O₂Hb dissociation curve for HbS. This means that for a given SaO₂, the PaO₂ is higher in SCD patients than would be expected based on the normal O₂Hb dissociation curve. The amount of right shift varies considerably between SCD patients and can be influenced by transfusion with blood (HbA) (Fig. 10–2).

Table 10–2 presents some useful PaO₂ and associated saturations. For PaO₂ values of 30, 40, and 60 mm Hg, the corresponding SaO₂ is 60%, 75%, and 90% values, respectively. The SaO₂ is measured noninvasively during sleep studies by pulse oximetry³ (SpO₂) to detect arterial oxygen desaturation and hypoxemia.

At normal PaO₂ levels, only a small amount of oxygen is dissolved in the blood and most of the oxygen-carrying capacity depends on the amount of Hb bound to oxygen. However, determining the oxygen-carrying capacity of Hb is complicated by the fact that both carboxyhemoglobin (COHb) and methemoglobin (MetHb) are forms of circulating Hb that do not bind oxygen. Carboxyhemoglobin occurs when carbon monoxide (CO) binds to Hb. Smokers have increased carboxyhemoglobin. MetHb occurs when the normal ferrous state (Fe²⁺) of the iron moiety in Hb is oxidized to the ferric stage (Fe³⁺). Significant methemoglobinemia can occur after exposure to certain medications but is uncommon in the sleep center. The sum of the fractional concentrations of O₂Hb, RHb, COHb, and MetHb equal 100% (Equation 10–7). The true fraction of hemoglobin bound to oxygen (FO₂Hb) is given by Equation 10–8 and depends on the fraction (%) of carboxyhemoglobin (FCOHb) and methemoglobin (FMetHb) as well as the fraction of reduced hemoglobin (FRHb).⁴–⁶

FO2Hb+FRHb+FCOHb+FMetHb=100% Equation 10–7

Equation 10–7

or

FO2Hb=O2Hb×100/(O2Hb+RHb+COHb+MetHb)FO2Hb=O2Hb×100/Hbt Equation 10–8

Equation 10–8

where O₂Hb, RHb, COHb, and MetHb are the concentrations of the types of Hb and equal the total Hb concentration (Hb_t). For example, if the FO₂Hb = 85%, FCOHb = 8%, FMetHb = 1%, then the FRHb is 6%. Using these numbers and Equation 10–6, the SaO₂ equals 85 × 100/(85 + 6) or 93%, which is considerably higher than FO₂Hb of 85%. The FO₂Hb and the amount of Hb are the main determinants of the blood’s oxygen-carrying capacity. When significant COHb or MetHb is present, Equation 10–5 should have SaO₂ replaced by FO₂Hb. The difference between the SaO₂ and the FO₂Hb (in %) at normal PO₂ values is approximately equal to the sum of FCOHb and FMetHb.⁴ The FO₂Hb is sometimes called the fractional saturation and the SaO₂ the functional or effective saturation. Of note, the PaO₂ depends on the SaO₂, not the FO₂Hb. That is, the oxyhemoglobin saturation curve expresses the ratio of oxygenated Hb to the total Hb available for oxygen binding. Neither COHb nor MetHb binds oxygen. However, the position of the oxyhemoglobin saturation curve is shifted to the left by the presence of COHb or MetHb.^4,7

The previous four fractions of Hb can be accurately measured by co-oximeters that measure the absorption of 4 or more wavelengths of electromagnetic radiation by blood.1,5 This is possible because the four forms of Hb differ in their absorption for the different wavelengths of radiation. In contrast, pulse oximetry³ uses only two wavelengths: 660 nm (red) and 940 nm (infrared) to measure the O₂Hb and RHb. The absorption of radiation at 660 nm is much greater with RHb than O₂Hb, whereas O₂Hb absorbs more radiation at 940 nm (Fig. 10–3A). SpO₂ is based on the empirical observation that the ratio (R) of absorbance at the 2 wavelengths is related to the oxygen saturation (see Fig. 10–3B). This relationship (calibration curve) is calculated experimentally by determining R at varying oxygen saturations. To specifically determine the absorbance of arterial blood, the AC (pulse added absorbance) at each wavelength is divided by the DC (background absorbance) to account for the effect of the absorption of the radiation by venous blood and tissue. COHb has about the same absorbance at 660 as O₂Hb and, if present, increases the measured SpO₂ value. In normal individuals, FCOHb is 2% or less but can be 8% or more in cigarette smokers. Patients with SCD often have FCOHb values of 4% or more due to production of CO from chronic hemolysis. Based on a canine experiment,³ it has been estimated that a pulse oximeter sees COHb as 90% O₂Hb and 10% RHb. For example, from the values FO₂Hb = 85%, COHb = 4%, MetHb = 0%, RHb = 11%, one can estimate the SpO₂ as 88.6% (85 + 0.9 × 4). This is essentially the same as the SaO₂ computed from Equation 10–6 for these values. Thus, the SpO₂ is a much better estimate of the SaO₂ than the FO₂Hb is. In patients who are heavy smokers, it is important to remember that the SpO₂ may overestimate the FO₂Hb.

If a patient has a lower than expected SpO₂ while awake in the sleep center, a number of possibilities should be considered including a faulty oximetry probe, poor signal quality due to poor perfusion, a shift in the O₂Hb saturation curve due to the factors illustrated in Figure 10–1 or an abnormal Hb. If oximetry issues are ruled out, an arterial blood gas is needed to determine whether hypoxemia is really present. In this situation, co-oximetry analysis could also determine whether significant COHb or MetHb is present and determine a true SaO₂ and the fraction of Hb that is oxygenated. Sometimes, the SaO₂ reported with an arterial blood gas is simply determined from the measured PaO₂ and a nomogram. If clinically indicated, analysis with a co-oximeter will provide more accurate information.

Determinants of PaCO₂

The PaCO₂ is related to the and the alveolar ventilation () (Equation 10–9). For a given , if the doubles, the PaCO₂ decreases by half. The PaCO₂ will increase if the decreases or the increases (Equation 10–9). The equals the minute ventilation () minus the dead space ventilation (). The is “wasted ventilation”. The = the respiratory rate (RR) Ö tidal volume (V_T) (Equation 10-10). The can be written as the product of the RR and the dead space (V_D). The dead space includes the anatomic dead space (no alveoli) and overventilated areas of the lung (high units). The equation for PaCO₂ can be written so that PaCO₂ depends on the minute ventilation (V_T × RR) and the V_D/V_T ratio (Equation 10–11).

PaCO2=KV˙CO2V˙AK=constant Equation 10–9

Equation 10–9

V˙A=V˙E−V˙D=RR×VT−RR×VD Equation 10–10

Equation 10–10

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