Relationship between alveolar ventilation and arterial blood gases

Arterial Blood Gases - Clinical Methods - NCBI Bookshelf

relationship between alveolar ventilation and arterial blood gases

Nonuniform pulmonary blood flow alveolar-arterial oxygen difference. . dead space, differences between the alveolar and arterial Image not available. The alveolar gas equation is used to calculate the alveolar oxygen partial pressure: Furthermore, by understanding the alveolar gas equation we can see how hypoventilation (resulting in Interpretation of Arterial Blood Gases The alveolar-to-arterial (A − aO2) oxygen gradient is the difference between the amount of. The level of minute ventilation (VE) is the product of tidal volume (Vt) and (VD) in which gas exchange cannot occur; the alveolar space (VA) in which gas exchange The PaCO2 reflects the balance between CO2 production by tissues (VCO2) and to VA) as given by the following relationship: ; PaCO2 = VCO2/VA x K.

The Pco2 electrode Severinghaus electrode employs an adaptation of the pH measurement. The Pco2 of the sample is determined indirectly by sensing the pH change in this solution.

The Po2 electrode Clark electrode determines Po2 amperometrically. Oxygen from the blood sample diffuses across a semipermeable membrane and is reduced at the cathode of a polarographic electrode. This reaction produces a measurable current that is directly proportional to the sample Po2. Each electrode is calibrated at two reference points in the typical operational range. After calibration, the accuracy and reliability of measurements may be checked by analyzing commercially available quality-control samples with known values of pH, Pco2 and Po2 that span the range of common clinical values.

The Po2 electrode is not linear and therefore may be inaccurate at values far beyond its calibration points 0 mm Hg and mm Hg at sea level for the reference gases above.

Consequently, the precision of Pao2 values exceeding mm Hg is uncertain unless the electrode has been recalibrated in an appropriate range, and this is not generally feasible in an automated analyzer. Nonetheless, pH, Paco2, and Pao2 are all temperature dependent because gas solubilities are a function of temperature. The equations, however, are too complex for easy calculation.

The effect of varying temperature on a "normal" set of ABGs is illustrated in Table There is no uniform practice regarding Pao2, and the clinician must be familiar with local policy. As shown in Table The issue is clinically relevant primarily in hypothermia and hyperthermia. The normal range of blood pH is 7.

Alveolar Ventilation

The Pao2 is the partial pressure of oxygen in arterial blood. The normal range for Pao2 is affected by age and altitude. As a result of changes in overall matching of ventilation with perfusion, normal Pao2 declines with advancing age.

relationship between alveolar ventilation and arterial blood gases

Regression equations have been published to estimate this decrease; however, there is some disparity in the results, probably attributable to heterogeneous study populations and nonuniform study conditions. Hence, these equations are only guidelines. For example, Sorbini et al. Based on this equation, the lower limit of normal for Pao2 at age 70 would be approximately 70 mm Hg. At elevations above sea level, the partial pressure of inspired oxygen falls with the barometric pressure, and the normal Pao2 decreases concomitantly.

For example, at m barometric pressure mm Hgthe predicted normal Pao2 in a healthy, young subject is approximately 80 mm Hg; this contrasts with a value close to 95 mm Hg at sea level. Therefore, at locations substantially above sea level, local normal values that correct for altitude must be utilized in ABG interpretation. The Paco2 is the partial pressure of carbon dioxide in arterial blood.

The normal range is 35 to 45 mm Hg and does not vary significantly with age. Nevertheless, normal Paco2, tends to be lower at high altitudes because ventilation is stimulated, and local norms must be established. Cellular metabolism and whole organ function are optimum over a relatively narrow range of pH. Hence, the acid—base status of the blood is closely regulated.

Homeostasis is maintained by three mechanisms: The central relationship among these is the following reaction: Therefore, the lungs effectively regulate the H2CO3 concentration. Acidosis and alkalosis refer to pathophysiologic disturbances that tend to increase or decrease hydrogen ion concentration respectively. Primary disturbances in Paco2 cause the respiratory acid—base disorders, whereas primary alterations in bicarbonate are responsible for the metabolic derangements.

Each primary disturbance elicits a compensatory response, which is usually incomplete, but returns the pH toward normal.

Arterial Blood Gases

The simple acid—base disorders are illustrated in Table Mixed acid—base disturbances are the result of two or more simple disorders occurring together. While these are more complex, their recognition and analysis are predicated on a thorough understanding of the primary disorders.

The primary purposes of respiration are to provide oxygen to the cells for aerobic metabolism and to excrete the carbon dioxide produced by this metabolic activity.

This requires the integrated function of both the respiratory system for gas exchange between alveolar air and pulmonary capillary blood, and the cardiovascular system for gas transport to and from the metabolizing tissues.

The respiratory system may be divided into two parts: The respiratory pump includes the thoracic cage and abdomen, the respiratory muscles, the respiratory control centers, and the neural interconnections. The major function of the respiratory pump is ventilation of the lung, whereas the primary role of the lung itself is gas transfer. Factors that influence gas exchange in the lung include 1 movement of gas into and out of the lung ventilation ; 2 blood flow through the lung perfusion ; 3 the regional distributions of ventilation and perfusion ventilation—perfusion matching ; and 4 diffusion across the alveolar—capillary membrane.

The overall adequacy of gas exchange for oxygen and carbon dioxide is reflected by the Pao2 and Paco2.

relationship between alveolar ventilation and arterial blood gases

Carbon dioxide, the major by-product of oxidative metabolism, is transported to the lung in venous blood and eliminated through alveolar ventilation. The Paco2 is directly proportional to carbon dioxide excretion rate co2 and inversely proportional to alveolar ventilation A.

It will rise if CO2 production increases and is not balanced by an appropriate rise in alveolar ventilation, or if alveolar ventilation decreases at a given CO2 production. Therefore, the Paco2 is an index of the adequacy of alveolar ventilation in relation to carbon dioxide production. Alveolar ventilation is that portion of the total minute ventilation E that participates effectively in gas exchange.

The remainder of minute ventilation reaches only anatomic or physiologic dead space; it does not participate in gas exchange and is called dead space ventilation D. Alveolar ventilation, then, is total minute ventilation minus dead space ventilation. Alveolar ventilation may fall due to a decrease in minute ventilation with a normal dead space, or due to an increase in dead space ventilation without a compensatory increase in minute ventilation.

Oxygen is essential for aerobic metabolism. The transfer of oxygen from alveolar air to pulmonary capillary blood is affected by the partial pressure of oxygen in the alveoli, its diffusion across the alveolar—capillary membrane, and the matching of alveolar ventilation to capillary perfusion. There are five possible causes of a reduction in Pao2: In addition, a low mixed venous oxygen tension will magnify the reduction in Pao2 due to ventilation—perfusion mismatching and shunt.


The partial pressure of oxygen in the alveoli PAo2 may be determined from the ideal alveolar gas equation, where PB is barometric pressure, PH2O the partial pressure of water vapor 47 mm HgFIo2 the fractional concentration of inspired oxygen, and R the respiratory exchange ratio usually 0. The alveolar—arterial oxygen tension gradient, P A-a o2, is the difference between calculated PAo2 and measured Pao2.

The normal gradient increases with age, but is usually in the range of 5 to 20 mm Hg. If either alveolar hypoventilation or a low inspired oxygen tension is the cause of a decreased Pao2, this gradient remains normal. In contrast, an abnormality in either diffusion or ventilation—perfusion matching will increase P A-a o2. Diffusion, however, is rarely the cause of a low Pao2 at rest.

Arterial oxygen content Cao2 is the sum of hemoglobin-bound oxygen and dissolved oxygen where Hb is the hemoglobin concentration and Sao2 the arterial O2 saturation. The contribution of dissolved oxygen is very small, and the major impact of Pao2 on oxygen content is through its effect on hemoglobin saturation Figure Above a Pao2 of 60 mm Hg, the dissociation curve is relatively flat and Sao2 increases very little even with a large increment in Pao2.

A close approximation of the dead space in ml is a subject's weight in pounds.

Hypoxia and Hypoxemia: Mechanisms and Etiologies (ABG Interpretation - Lesson 18)

Under some pathological conditions a certain amount of inspired air, although reaching the respiratory zone, does not take part in the gas exchange. Figure 5 illustrates two examples B and C of these pathologies. In these circumstances, i. The sum of alveolar and anatomical dead spaces is called the physiological dead space.

Types of respiratory dead space. Air in the conducting airways does not contribute to gas exchange.

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Air in alveoli witout blood supply does not contribute to gas exchange "wasted" ventilation. Therefore, some air in these alveoli is also "wasted" and adds to the alveolar dead space. The sume of the anatomical and alveolar dead space represent the physiological dead space. Arrows indicate direction of blood flow. The alveolar ventilation equation describes the exact relation between alveolar ventilation and PACO2 for any given metabolic rate VCO2.

Alveolar hyperventilation occurs when more O2 is supplied and more CO2 removed than the metabolic rate requires: A fall in the overall level of ventilation can reduce alveolar ventilation below that required by the metabolic activity of the body.

Under the condition of alveolar hypoventilation, the rate at which oxygen is added to the alveolar gas, and CO2 is eliminated, is lowered, so that the alveolar partial pressure of O2 PAO2 falls and PACO2 rises.