Technique

V_T can be measured directly by simple spirometry (see Figure 2-1). The patient breathes into a volume-displacement or flow-sensing spirometer (see Chapter 11). Volume change may be measured directly from the excursions of a volume spirometer. V_T may also be measured from an integrated flow signal (see Chapter 11). A graphic representation of tidal breathing can be displayed on a computer screen. Because no two breaths are the same, inhaled or exhaled tidal breaths should be measured for at least 1 minute and then divided by the rate to determine an average volume:

< ?xml:namespace prefix = "mml" />VT=V·fb

where:

   = volume expired or inspired per minute (usually the _E )

f_b = number of breaths for the same interval (i.e., the respiratory rate)

The inspired minute volume (_I ) and V_T are normally slightly greater than the _E because at rest the body produces a slightly lower volume of CO₂ than the volume of O₂ consumed. This exchange difference is termed the respiratory exchange ratio (RER). It is calculated as the co₂/o₂, where co₂ is the volume of CO₂ produced and o₂ is the volume of O₂ consumed per minute. It is assumed that RER is approximately 0.8 in resting patients. For most clinical purposes, expired volume is measured to calculate V_T.

V_T may also be estimated by means of a respiratory inductive plethysmography (RIP). The RIP uses coils of wire as transducers that respond to changes in the cross-sectional area of the rib cage and abdominal compartments. With appropriate calibration, inductive plethysmography can be used to measure V_T. This method allows the measurement of V_T and minute ventilation without a direct connection to the patient’s airway.

Respiratory frequency (f_b) may be determined by counting chest movements, noting the excursions of a volume displacement spirometer (Criteria for Acceptability 5-1), or most commonly by measuring flow changes while the subject breathes through a flow-sensing spirometer. Counting the rate for several minutes and taking an average produces a more accurate value than shorter measurements. Prolonged measurement of V_T and rate with a volume-displacement spirometer requires a means of removing CO₂. This is called a rebreathing system and uses a chemical CO₂ absorber (see Figure 4-1, B). Sodium hydroxide crystals (Sodasorb) or barium hydroxide crystals (Baralyme) are commonly used to scrub CO₂ from rebreathing systems. Flow-sensing spirometers usually do not require a chemical absorber.

The _E may be measured by allowing the patient to breathe into or out of a volume-displacement or flow-sensing spirometer for at least 1 minute. A shorter breathing interval can be used with minute volume extrapolated but may give a misleading estimate of ventilation if the patient’s breathing rate is irregular. If a rebreathing system is used, a CO₂ absorber must be included, as well as a means of replenishing O₂. Measuring expired gas volume for several minutes and dividing by the time gives an average _E. _E, measured from expired gas, is usually slightly smaller than _I because of the RER, as described previously. For most clinical purposes, this difference is negligible. BTPS corrections should be made.

Significance and Pathophysiology

See Interpretive Strategies 5-1. Average V_T for healthy adults at rest ranges between 400 and 700 mL, but there is considerable variation. Decreased V_T occurs in many types of pulmonary disorders, particularly those that cause severe restrictive patterns. Pulmonary fibrosis and neuromuscular diseases (e.g., myasthenia gravis) often cause reduced V_T. Decreased tidal breathing usually accompanies changes in the mechanical properties of the lungs or chest wall (i.e., compliance and resistance). These changes usually produce an increased respiratory rate (f_b) required to maintain an adequate _A. Decreases in both V_T and respiratory rate are often associated with respiratory center depression because of drugs or pathologic conditions affecting the brain stem. Low V_T and rate usually result in alveolar hypoventilation.

Some patients who have pulmonary disease may exhibit increased V_T, particularly at rest. The V_T alone is not a good indicator of the adequacy of alveolar ventilation ( _A). Tidal volume should always be considered in conjunction with respiratory rate and _E. Many healthy patients display increased V_T simply because of breathing into the pulmonary function apparatus with the nose occluded. Estimates of resting ventilation may be artifactually increased when measured during pulmonary function testing. Some subjects adopt unusual breathing strategies (e.g., large tidal volumes with slow respiratory rate or small tidal volumes with rapid breathing rates) during exercise or stress for nonphysiologic reasons.

The normal respiratory rate (f_b) ranges from 10–20 breaths/min in adults. Increased demand for ventilation, such as during exercise, usually results in increases in both the rate and depth of breathing (i.e., the tidal volume). Increases or decreases in the respiratory rate are indications of a change in the ventilatory status. Breathing frequency, when evaluated with the V_T, may be used as an index of ventilation. Hypoxia, hypercapnia, metabolic acidosis, decreased lung compliance, and exercise can all result in increased respiratory rate. Rapid breathing rates and small tidal volumes may suggest increased V_D or hypoventilation but must be correlated with arterial pH and Pco₂ values to confirm those conditions. Decreased breathing frequency is common in central nervous system depression and in CO₂ narcosis. Respiratory rate may be falsely elevated in patients connected to unfamiliar breathing circuits, with or without a noseclip.

Normal _E ranges from 5–10 L/min in healthy adults with wide variations in normal patients. The _E, when used in conjunction with blood gas values, indicates the adequacy of ventilation. _E is the sum of the _D (dead space ventilation per minute) and _A. Because the relative proportions of these components can change, absolute values for _E do not necessarily indicate either hypoventilation or hyperventilation. In other words, low minute ventilation does not necessarily indicate hypoventilation. Similarly, elevated _E does not indicate hyperventilation. To make these diagnoses, arterial pH and Pco₂ must be measured.

A large _E at rest (greater than 20 L/min) may result from an enlarged V_D because an increase in total ventilation is required to maintain adequate _A. _E increases in response to hypoxia, hypercapnia, metabolic acidosis, anxiety, and exercise. Hyperventilation is ventilation in excess of that needed to adequately remove CO₂, resulting in respiratory alkalosis.

Decreased ventilation may result from hypocapnia, metabolic alkalosis, respiratory center depression, or neuromuscular disorders that involve the ventilatory muscles. Hypoventilation is defined as inadequate ventilation to maintain a normal arterial Pco₂, with respiratory acidosis as the result. The diagnosis of either hyperventilation or hypoventilation requires blood gas analysis (see Chapter 6).

Anatomic dead space is sometimes estimated from an individual’s body size as 1 mL/lb of ideal body weight. The actual respiratory dead space, however, is of greater clinical importance. V_D can be calculated in two ways. The first uses the Enghoff modification of the Bohr equation defining V_D:

VD=FACO2−F E¯CO2FACO2×VT

where:

V_T   = tidal volume

F_Aco₂  = fraction of CO₂ in alveolar gas

Fco₂ = fraction of CO₂ in mixed expired gas

Because the fractional concentration of alveolar CO₂ is difficult to measure, partial pressure of CO₂ may be substituted and the equation written as follows:

VD=(PaCO2−P E¯CO2)PaCO2×VT

where:

Paco₂ = arterial Pco₂

PE¯co₂ = Pco₂ of mixed expired gas sample

Note that the Paco₂ is substituted for the alveolar Pco₂. This substitution presumes perfect equilibration between alveoli and pulmonary capillaries. This may not be true in certain diseases. The test also assumes that little CO₂ is in the atmosphere. Therefore, the Pco₂ in expired gas is inversely proportional to the V_D. Exhaled gas is collected over a short interval, and arterial blood is obtained simultaneously to measure Paco₂. V_D is calculated by applying the previous equation. The estimate usually becomes more representative as more expired gas is collected. Accuracy depends on measurement of V_T (usually derived from _E and f_b) and on the precision of the partial pressures of CO₂ measured in expired gas and arterial blood. The mixed expired gas sample is usually collected in a bag or balloon after filling and emptying it several times with expired gas to wash out room air from the valves, tubing, and bag itself. The volume of gas in the bag can be measured during collection by including a flow-sensing spirometer in the circuit. If _E and respiratory rate are recorded, the volumes of V_D and V_T can be determined. If expired volume is not measured, only a dilution ratio can be determined; this is called the V_D/V_T ratio.

The V_D/V_T ratio can be calculated if arterial and mixed-expired Pco₂ values are known. It can also be estimated noninvasively. End-tidal Pco₂ (see the section on capnography in Chapter 6) can be used to estimate Paco₂. The main advantage of this method is that it is not necessary to obtain an arterial blood sample. This technique is often used in systems that monitor expired CO₂ continuously and in breath-by-breath metabolic measurement devices. V_D/V_T may be calculated as follows:

VDVT=PETCO2−PE¯CO2PETCO2

where:

Petco₂ = end-tidal Pco₂

Pco₂= Pco₂ of mixed-expired gas sample

In some patients, particularly those with severe obstruction, Petco₂ may not accurately reflect Paco₂. Consequently, the V_D/V_T ratio may be estimated incorrectly. Paco₂ should be used in the V_D calculation whenever possible.

Alveolar Ventilation

_A can be calculated in two ways:

V·A=fb(VT−VD)

where:

V_T = tidal volume

V_D = respiratory dead space

f_b = respiratory rate

For convenience, V_D is often estimated as equal to anatomic dead space. This method is valid only when there is little or no alveolar dead space, as in individuals who do not have pulmonary disease.

Because atmospheric gas contains almost no CO₂, _A can be calculated on the basis of CO₂ elimination from the lungs. A volume of expired gas may be collected in a bag, balloon, or spirometer and analyzed to determine the volume of CO₂ (see Chapter 7). The following equation can then be used:

V·A=V·CO2FACO2

where:

co₂= volume of CO₂ produced in liters per minute (STPD)

F_Aco₂= fractional concentration of CO₂ in alveola

If an end-tidal CO₂ monitor (i.e., a capnograph) is used, a close approximation of the concentration of alveolar CO₂ is easily obtained, and the equation is simplified as follows:

V·A=V·CO2% alveolar CO2×100

End-tidal CO₂ may not equal alveolar CO₂ in patients with grossly abnormal patterns of ventilation-perfusion (see Chapter 6).

The same equation can be used substituting Paco₂ for the alveolar Pco₂ (i.e., P_Aco₂), again presuming that arterial blood and alveolar gas are in equilibrium. The equation is then as follows:

V·A=V·CO2PaCO2×0.863

where:

co₂= CO₂ production in mL/min (STPD)

Paco₂= partial pressure of arterial CO₂

0.863= conversion factor (concentration to partial pressure, correcting co₂ to BTPS)

Significance and Pathophysiology

See Interpretive Strategies 5-2. Measurement of V_D yields important information regarding the ventilation-perfusion characteristics of the lungs. Anatomic dead space is larger in men than in women because of differences in body size. It increases along with the V_T