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Measurement of Gas Exchange
Gas exchange is measured through several means, including diffusing capacity for carbon monoxide, pulse oximetry, and arterial blood gas sampling.
The diffusing capacity for carbon monoxide (DL co ) is a measure of the ability of gas to transfer from the alveoli across the alveolar epithelium and the capillary endothelium to the RBCs. The DL co depends not only on the area and thickness of the blood-gas barrier but also on the volume of blood in the pulmonary capillaries. The distribution of alveolar volume and ventilation also affects the measurement.
DL co is measured by sampling end-expiratory gas for carbon monoxide (CO) after patients inspire a small amount of CO, hold their breath, and exhale. Measured DL co should be adjusted for alveolar volume (which is estimated from dilution of helium) and the patient’s Hct. DL co is reported as mL/min/mm Hg and as a percentage of a predicted value.
Conditions that primarily affect the pulmonary vasculature, such as primary pulmonary hypertension and pulmonary embolism, decrease DL co . Conditions that affect the lung diffusely, such as emphysema and pulmonary fibrosis, decrease both DL co and alveolar ventilation (V A ). Reduced DL co also occurs in patients with previous lung resection because total lung volume is smaller, but DL co corrects to or even exceeds normal when adjusted for V A because increased additional vascular surface area is recruited in the remaining lung. Anemic patients have lower DL co values that correct when adjusted for Hb.
DL co may be higher than predicted in patients with heart failure, presumably because the increased pulmonary venous and arterial pressure recruits additional pulmonary microvessels. DL co is also increased in patients with erythrocythemia, in part because of increased Hct and because of the vascular recruitment that occurs with increased pulmonary pressures due to increased viscosity. DL co is increased in patients with alveolar hemorrhage because RBCs in the alveolar space can also bind CO. DL co is also increased in patients with asthma. Although this increase is attributed to presumed vascular recruitment, some data suggest it may also be due to growth factor–stimulated neovascularization.
Transcutaneous pulse oximetry estimates O 2 saturation (Sp o 2 ) of capillary blood based on the absorption of light from light-emitting diodes positioned in a finger clip or adhesive strip probe. The estimates are generally very accurate and correlate to within 5% of measured arterial O 2 saturation (Sa o 2 ). Results may be less accurate in patients with highly pigmented skin; patients wearing nail polish; and patients with arrhythmias, hypotension, or profound systemic vasoconstriction, in whom the amplitude of the signal may be dampened. Also, pulse oximetry is able to detect only oxyhemoglobin or reduced Hb but not other types of Hb (eg, carboxyhemoglobin, methemoglobin); those types are assumed to be oxyhemoglobin and falsely elevate the Sp o 2 measurement.
ABG sampling is done to obtain accurate measures of Pa o 2 , Pa co 2 , and arterial pH; these variables adjusted for the patient’s temperature allow for calculation of HCO 3 level (which can also be measured directly from venous blood) and Sa o 2 . ABG sampling can also accurately measure carboxyhemoglobin and methemoglobin.
The radial artery is usually used. Because arterial puncture in rare cases leads to thrombosis and impaired perfusion of distal tissue, Allen test may be done to assess adequacy of collateral circulation. With this maneuver, the radial and ulnar pulses are simultaneously occluded until the hand becomes pale. The ulnar pulse is then released while the pressure on the radial pulse is maintained. A blush across the entire hand within 7 sec of release of the ulnar pulse suggests adequate flow through the ulnar artery.
Under sterile conditions, a 22- to 25-gauge needle attached to a heparinized syringe is inserted just proximal to the maximal impulse of the radial arterial pulse and advanced slightly distally into the artery until pulsatile blood is returned. Systolic BP is usually sufficient to push back the syringe plunger. After 3 to 5 mL of blood is collected, the needle is quickly withdrawn, and firm pressure is applied to the puncture site to facilitate hemostasis. Simultaneously, the ABG specimen is placed on ice to reduce O 2 consumption and CO 2 production by WBCs and is sent to the laboratory.
Hypoxemia is a decrease in P o 2 in arterial blood; hypoxia is a decrease in the P o 2 in the tissue. ABGs accurately assess the presence of hypoxemia, which is generally defined as a Pa o 2 low enough to reduce the Sa o 2 below 90% (ie, Pa o 2 < 60 mm Hg). Abnormalities in Hb (eg, methemoglobin), higher temperatures, lower pH, and higher levels of 2,3-diphosphoglycerate reduce Hb O 2 saturation despite an adequate Pa o 2 , as indicated by the oxyhemoglobin dissociation curve (see Figure: Oxyhemoglobin dissociation curve.).
Oxyhemoglobin dissociation curve.
Causes of hypoxemia can be classified based on whether the alveolar-arterial P o 2 gradient [(A-a)D o 2 ], defined as the difference between alveolar O 2 tension (P Ao 2 ) and Pa o 2 , is elevated or normal. P Ao 2 is calculated as follows:
where F io 2 is the fraction of inspired O 2 (eg, 0.21 at room air), P atm is the ambient barometric pressure (eg, 760 mm Hg at sea level), P H 2 O is the partial pressure of water vapor (eg, usually 47 mm Hg), Pa co 2 is the measured partial pressure of arterial CO 2 , and R is the respiratory quotient, which is assumed to be 0.8 in a resting patient eating a normal diet.
For patients at sea level and breathing room air, F io 2 = 0.21, and the (A-a)D o 2 can be simplified as follows:
where (A-a)D o 2 is typically < 20 but increases with age (because of age-related decline in pulmonary function) and with increasing F io 2 (because, although Hb becomes 100% saturated at a Pa o 2 of about 150 mm Hg, O 2 is soluble in blood, and the O 2 content of plasma continues to increase at increasing F io 2 ). Estimations of normal (A-a)D o 2 values as < (2.5 + [F io 2 × age in years]) or as less than the absolute value of the F io 2 (eg, < 21 on room air; < 30 on 30% F io 2 ) correct for these effects.
This situation is caused by
Low V/Q ratio is one of the more common reasons for hypoxemia and contributes to the hypoxemia occurring in COPD and asthma. In normal lungs, regional perfusion closely matches regional ventilation because of the arteriolar vasoconstriction that occurs in response to alveolar hypoxia. In disease states, dysregulation leads to perfusion of alveolar units that are receiving less than complete ventilation (V/Q mismatch). As a result, systemic venous blood passes through the pulmonary capillaries without achieving normal levels of Pa o 2 . Supplemental O 2 can correct hypoxemia due to low V/Q ratio by increasing the Pa o 2 , although the increased (A-a)D o 2 persists.
Right-to-left shunting is an extreme example of low V/Q ratio. With shunting, deoxygenated pulmonary arterial blood arrives at the left side of the heart without having passed through ventilated lung segments. Shunting may occur through lung parenchyma, through abnormal connections between the pulmonary arterial and venous circulations, or through intracardiac communications (eg, patent foramen ovale). Hypoxemia due to right-to-left shunting does not respond to supplemental O 2 .
Impaired diffusing capacity only rarely occurs in isolation; usually it is accompanied by low V/Q ratio. Because O 2 completely saturates Hb after only a fraction of the time that blood is in contact with alveolar gas, hypoxemia due to impaired diffusing capacity occurs only when cardiac output is increased (eg, with exercise), when barometric pressure is low (eg, at high altitudes), or when > 50% of the pulmonary parenchyma is destroyed. As with low V/Q ratio, the (A-a)D o 2 is increased, but Pa o 2 can be increased by increasing the F io 2 . Hypoxemia due to impaired diffusing capacity responds to supplemental O 2 .
This situation is caused by
Hypoventilation (reduced alveolar ventilation) decreases the P ao 2 and increases the Pa co 2 , thereby decreasing Pa o 2 . In cases of pure hypoventilation, the (A-a)D o 2 is normal. Causes of hypoventilation include decreased respiratory rate or depth (eg, due to neuromuscular disorders, severe obesity, or drug overdose, or in compensation for metabolic alkalosis) or an increase in the fraction of dead space ventilation in patients already at their maximal ventilatory limit (eg, an exacerbation of severe COPD). Hypoventilatory hypoxemia responds to supplemental O 2 .
Decreased Pio 2 is a final uncommon cause of hypoxemia that in most cases occurs only at high altitude. Although F io 2 does not change with altitude, ambient air pressure decreases exponentially; thus, P io 2 decreases as well. For example, P io 2 is only 43 mm Hg at the summit of Mt. Everest (altitude, 8848 m [29,028 ft]). The (A-a)D o 2 remains normal. Hypoxic stimulation of respiratory drive increases alveolar ventilation and decreases Pa co 2 level. This type of hypoxemia responds to supplemental O 2 .
P co 2 normally is maintained between 35 and 45 mm Hg. A dissociation curve similar to that for O 2 exists for CO 2 but is nearly linear over the physiologic range of Pa co 2 . Abnormal P co 2 is almost always linked to disorders of ventilation (unless occurring in compensation for a metabolic abnormality) and is always associated with acid-base changes.
Hypercapnia is P co 2 > 45 mm Hg. Causes of hypercapnia are the same as those of hypoventilation (see Tests of Pulmonary Function (PFT):Hypoxemia with normal (A-a)Do 2). Disorders that increase CO 2 production (eg, hyperthyroidism, fever) when combined with an inability to increase ventilation also cause hypercapnia.
Hypocapnia is P co 2 < 35 mm Hg. Hypocapnia is always caused by hyperventilation due to pulmonary (eg, pulmonary edema or embolism), cardiac (eg, heart failure), metabolic (eg, acidosis), drug-induced (eg, aspirin, progesterone), CNS (eg, infection, tumor, bleeding, increased intracranial pressure), or physiologic (eg, pain, pregnancy) disorders or conditions. Hypocapnia is thought to directly increase bronchoconstriction and lower the threshold for cerebral and myocardial ischemia, perhaps through its effects on acid-base status.
CO binds to Hb with an affinity 210 times that of O 2 and prevents O 2 transport. Clinically toxic carboxyhemoglobin levels are most often the result of exposure to exhaust fumes or from smoke inhalation, although cigarette smokers have detectable levels. Patients with CO poisoning (see Carbon Monoxide Poisoning) may present with nonspecific symptoms such as malaise, headache, and nausea. Because poisoning often occurs during colder months (because of indoor use of combustible fuel heaters), symptoms may be confused with a viral syndrome such as influenza. Clinicians must be alert to the possibility of CO poisoning and measure levels of carboxyhemoglobin when indicated; COHb can be directly measured from venous blood—an arterial sample is unnecessary.
Treatment is the administration of 100% O 2 (which shortens the half-life of carboxyhemoglobin) and sometimes the use of a hyperbaric chamber.
Methemoglobin is Hb in which the iron is oxidized from its ferrous (Fe 2+ ) to its ferric (Fe 3+ ) state. Methemoglobin does not carry O 2 and shifts the normal HbO 2 dissociation curve to the left, thereby limiting the release of O 2 to the tissues. Methemoglobinemia is caused by certain drugs (eg, dapsone, local anesthetics, nitrates, primaquine, sulfonamides) or, less commonly, by certain chemicals (eg, aniline dyes, benzene derivatives). Methemoglobin level can be directly measured by co-oximetry (which emits 4 wavelengths of light and is capable of detecting methemoglobin, COHb, Hb, and HbO 2 ) or may be estimated by the difference between the O 2 saturation calculated from the measured Pa O 2 and the directly measured Sa O 2 . Patients with methemoglobinemia most often have asymptomatic cyanosis. In severe cases, O 2 delivery is reduced to such a degree that symptoms of tissue hypoxia result, such as confusion, angina, and myalgias. Stopping the causative drug or chemical exposure is often sufficient. Rarely, methylene blue (a reducing agent; a 1% solution is given 1 to 2 mg/kg slowly IV) or exchange transfusion is needed.
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