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Two-Lung and One-Lung Ventilation in Patients - Anesthesia ...

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ANESTH ANALG CARDIOVASCULAR ANESTHESIA BARDOCZKY ET AL. 39<br />

2000;90:35–41 POSITION AND Fio 2 DURING OLV<br />

Figure 2. Values of arterial oxygen tension <strong>in</strong>creases between lateral <strong>and</strong> sup<strong>in</strong>e positions, dur<strong>in</strong>g TLV <strong>and</strong> OLV <strong>in</strong> the three groups of<br />

patients. The bold l<strong>in</strong>es represent the median values. TLV two-lung ventilation, OLV one-lung ventilation.<br />

to the dependent lung (7,8). As a result of anesthesia<br />

<strong>and</strong> muscle relaxation, the distribution of ventilation<br />

also changes <strong>in</strong> the lateral position because the applied<br />

positive-pressure ventilation displaces the diaphragm<br />

preferentially at the nondependent part. Traditionally,<br />

this discrepancy is thought to be disadvantageous (7).<br />

However, <strong>in</strong> our patients, the change <strong>in</strong> position from<br />

the sup<strong>in</strong>e to lateral decubitus position resulted <strong>in</strong> a<br />

modest change <strong>in</strong> Pao 2 dur<strong>in</strong>g TLV (124 [81–240] <strong>and</strong><br />

132 [102–296] mm Hg <strong>in</strong> Group 0.4; 256 [172–391] <strong>and</strong><br />

289 [225–353] mm Hg <strong>in</strong> Group 0.6; <strong>and</strong> 472 [232–591]<br />

<strong>and</strong> 492 [336–600] mm Hg <strong>in</strong> Group 1.0, respectively).<br />

This is <strong>in</strong> agreement with the f<strong>in</strong>d<strong>in</strong>gs of Boldt et al.<br />

(16) <strong>and</strong> Rehder et al. (17), who also reported no<br />

difference <strong>in</strong> Pao 2 between the lateral <strong>and</strong> the sup<strong>in</strong>e<br />

positions with TLV.<br />

Induc<strong>in</strong>g OLV when the patient is <strong>in</strong> the lateral<br />

position activates HPV <strong>and</strong> reduces the further perfusion<br />

of the collapsed lung. Hence, we found that Pao 2<br />

was significantly greater when OLV was <strong>in</strong>itiated after<br />

turn<strong>in</strong>g the patients <strong>in</strong>to the lateral decubitus position<br />

(Tables 2–4 <strong>and</strong> Figures 1 <strong>and</strong> 2).<br />

Fiser et al. (9) studied the period of OLV <strong>in</strong> both the<br />

sup<strong>in</strong>e <strong>and</strong> the lateral positions <strong>and</strong> did not f<strong>in</strong>d<br />

changes <strong>in</strong> arterial oxygen tension after 10 to 20 m<strong>in</strong>utes<br />

of OLV when the patients were turned <strong>in</strong>to the<br />

lateral position. However, <strong>in</strong> the study of Fiser et al.<br />

(9), OLV was <strong>in</strong>itiated <strong>in</strong> the sup<strong>in</strong>e position <strong>and</strong><br />

ma<strong>in</strong>ta<strong>in</strong>ed cont<strong>in</strong>uously, even dur<strong>in</strong>g the period of<br />

position<strong>in</strong>g <strong>and</strong> turn<strong>in</strong>g the patient, with an Fio 2 of<br />

1.0.<br />

The most important mechanism for reduc<strong>in</strong>g blood<br />

flow of an atelectatic lung is HPV (6,14). When OLV is<br />

<strong>in</strong>duced <strong>in</strong> the lateral position, the blood flow of the<br />

nondependent lung is already reduced by gravitational<br />

forces, <strong>and</strong> HPV further reduces blood flow. In<br />

contrast, <strong>in</strong> the sup<strong>in</strong>e position, both lungs are equally<br />

exposed to an identical gravitational force; thus dur<strong>in</strong>g<br />

OLV, the reduction of blood flow depends solely<br />

on the strength of the HPV.<br />

Here, consideration should be given to possible limitations<br />

<strong>in</strong> our experimental methods.<br />

First, concern<strong>in</strong>g the patients <strong>in</strong>cluded <strong>in</strong> the study,<br />

the presence of chronic airflow obstruction may be<br />

associated with better Pao 2 dur<strong>in</strong>g OLV possibly because<br />

of dynamic hyper<strong>in</strong>flation result<strong>in</strong>g <strong>in</strong> an <strong>in</strong>creased<br />

functional residual capacity <strong>and</strong> <strong>in</strong>tr<strong>in</strong>sic positive<br />

end-expiratory pressure <strong>in</strong> the dependent lung<br />

(18). In contrast, <strong>in</strong> patients with severe COPD, HPV<br />

may not be an important protective mechanism, as<br />

these patients already have an <strong>in</strong>creased pulmonary<br />

arterial pressure <strong>and</strong> reduced pulmonary vascular<br />

bed. The amount of disease <strong>in</strong> the nondependent lung<br />

is also a significant determ<strong>in</strong>ant of the amount of<br />

blood flow to the nondependent lung. If the nondependent<br />

lung is severely diseased, there may be a<br />

fixed reduction <strong>in</strong> blood flow to this lung preoperatively,<br />

<strong>and</strong> the collapse of such a diseased lung may

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