This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Jiang, Y. Articles by Xie, Z. Search for Related Content PubMed PubMed Citation Articles by Jiang, Y. Articles by Xie, Z. Related Collections Cardiovascular Monitoring (Non-cardiac) Pharmacology

---

CARDIOVASCULAR ANESTHESIA

Differential Changes of Alveolar Gas Concentrations During Anesthetic Induction of a Patient with an Absent Right Pulmonary Artery

Yandong Jiang, MD, PhD^*, John C. Wain, MD, August W. Chang, MD^*, Warren M. Zapol, MD^*, and Zhongcong Xie, MD, PhD^*

From the *Department of Anesthesia and Critical Care, Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA.

Address correspondence and reprint requests to Zhongcong Xie, MD, PhD, Department of Anesthesia and Critical Care, 55 Fruit Street, CLN 309, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114. Address e-mail to zxie{at}partners.org.

	Abstract

Top Abstract Introduction CASE REPORT DISCUSSION REFERENCES

 
A 38-yr-old man with congenital right pulmonary artery agenesis, whose right lung was perfused with collateral systemic arterial blood, presented for right pneumonectomy. Because of a likely difference in gas exchange between the two lungs, we sampled end-tidal gases from each lung individually, as well as from the common gas outlet of a double-lumen endobronchial tube. Our results indicated a higher end-tidal CO₂ from the left, normally perfused, lung than from the right, systemically perfused, lung. We also determined uptake of sevoflurane from each lung, demonstrating a more rapid uptake in the left lung than in the right. In conclusion, we report the rare case of unilateral pulmonary artery agenesis with systemic arterial collateralization and characterize the differences in gas exchange.

	Introduction

Top Abstract Introduction CASE REPORT DISCUSSION REFERENCES

 
Unilateral pulmonary artery agenesis is a rare congenital anomaly, with only 108 known reported cases (1). It is a unique developmental error that illustrates the pharmacokinetics of inhaled volatile anesthetics and gas exchange in a combined normal and pathologic scenario. In this case report, we present the unusual kinetics of sevoflurane uptake as well as the significant differences in the end-tidal CO₂ (ETco₂) levels from the right and left lungs of a patient with congenital isolated absence of the right pulmonary artery.

	CASE REPORT

Top Abstract Introduction CASE REPORT DISCUSSION REFERENCES

 
A 38-yr-old man presented with a 3-mo history of intermittent hemoptysis found on bronchoscopy to be the result of active bleeding from the right lung. Further diagnostic evaluation included a computed tomography scan that demonstrated complete absence of the right pulmonary artery. The patient underwent embolization of the right inferior phrenic artery with coils and Gelfoam. Four days later he was admitted for elective right pneumonectomy. His physical examination was unremarkable except for diminished breathing sounds bilaterally. His Spo₂ was 94% while breathing room air and arterial blood gas revealed pH 7.42, Paco₂ 42, and Pao₂ 72. The chest radiograph showed a small right lung field compared with the left lung. Aortic angiography demonstrated systemic blood supplying the right lung via hypertrophied right bronchial arteries, right intercostal arteries, right internal mammary artery, branches of the right thyrocervical trunk, and the right inferior phrenic artery. A ventilation/perfusion scan revealed complete absence of perfusion in the right lung but relatively normal ventilation. The left lung demonstrated normal ventilation and perfusion. Pulmonary function testing showed a reduced forced expiratory volume (FEV₁), forced vital capacity (FVC), and FEV₁/FVC, with normal total lung capacity and residual volume/total lung capacity ratio. Airway resistance was increased but specific conductance was normal. The single breath diffusing capacity of the lung for carbon monoxide test and the diffusing capacity adjusted for alveolar volume were normal.

After administration of oxygen, a rapid sequence anesthetic induction was performed using propofol 200 mg and succinylcholine 120 mg. A 39F left-sided double-lumen tube (Tyco Healthcare Group, Pleasanton, CA) was placed and positioning was confirmed by fiberoptic bronchoscopy. Successful lung isolation was further ensured by auscultation.

Because we were unsure how to interpret expired gas concentrations during surgery, we sampled from both lungs individually, as well as from the usual distal end of the endotracheal tube (Fig. 1). The patient's lungs were ventilated through both lumens of the double-lumen tube with a Fio₂ 1.0 at 14 breaths/min. His exhaled tidal volume was 570 mL, peak airway pressure of 26 cm H₂O, at an O₂ flow of 3 L/min. Inspired sevoflurane was administered at 4% for 10 min and then reduced to 2%. Gas was first sampled through the common gas sampling port for 30 s, then through the left side sampling port for 30 s, and thereafter from the right-side sampling port for another 30 s (Fig. 1). This monitoring sequence was repeated for 10 min. Exhaled sevoflurane and CO₂ were measured using infrared spectrum (SAM-80 Module; GE Healthcare, Piscataway, NJ). These concentrations were manually recorded before and after each of the above measurement periods. The patient was then placed in the left lateral decubitus position and data collection was repeated after first reconfirming correct positioning of the double-lumen tube with fiberoptic bronchoscopy.

View larger version (9K): [in this window] [in a new window]   Figure 1. Schematic of the three gas-sampling ports. The gas sampling port from the right, left, and common lumens of the endobronchial tube are illustrated.

As shown in Table 1, the ETco₂ levels in gas sampled from the left lung (with blood supply from both pulmonary and bronchial arteries) were higher than those sampled from the right lung (without pulmonary artery blood supply) (55 mm Hg versus 27 mm Hg). Further, the ETco₂ concentration in gas sampled from the common port (45 mm Hg) was not the mean value of gas sampled from the left lung and the right lung. The alveolar to arterial Pco₂ gradient from the left lung was +13 mm Hg (55–42 mm Hg), whereas that from the right lung was –15 mm Hg (27–42 mm Hg). Interestingly, we found that the Pao₂ levels increased from 127 mm Hg to 161 mm Hg when only the left lung was ventilated. Assessment of the uptake of sevoflurane from the left and right lung respectively is shown in Figure 2. We found a greater uptake rate of sevoflurane in gas sampled from the left lung than that sampled from the right lung.

View larger version (3K): [in this window] [in a new window]   Figure 2. Sevoflurane uptake by the left and right lungs. The diamonds represent the ratio (FA:FI) of inspired concentration to expired concentration of sevoflurane from the left lung measured from the left lung port; the squares represent the FA:FI of sevoflurane from the right lung measured from the right lung port. The FA:FI of sevoflurane was plotted against time. These results indicate that the uptake of sevoflurane from the right lung (without a pulmonary artery) is far slower than that from the left lung (with a pulmonary artery).

A right pneumonectomy was performed uneventfully using the combination of epidural and general anesthesia. The patient had an uneventful recovery and was discharged from the hospital on postoperative day 7. Postoperative pathologic findings revealed right pulmonary artery agenesis with interstitial fibrosis as well as marked and extensive hypertrophy of intrapulmonary systemic arteries including bronchial arteries.

	DISCUSSION

Top Abstract Introduction CASE REPORT DISCUSSION REFERENCES

 
We report differential measurements of ETco₂ levels and exhaled sevoflurane from a patient with congenital absence of the right pulmonary artery. We found that the ETco₂ (Table 1) was greater in gas sampled from the left lung than gas sampled from the right lung. These findings confirmed the expected physiologic changes in a patient with this congenital abnormality. Simultaneous measurement of Paco₂ combined with ETco₂ measurements (left lung was + 13 mm Hg versus right lung –15 mm Hg) indicates that a single mixed ETco₂ concentration sampled from both lungs (common port) cannot be used to estimate the ETco₂, when there is such an abnormal pulmonary circulation. These findings suggest that frequent measurement of pHa and Paco₂ are indicated during one-lung ventilation to adequately assess ventilation for patients with this abnormality.

We also found that the uptake of sevoflurane from the right lung was far slower than that from the left lung (Fig. 2). This observation confirmed our expectation that sevoflurane concentrations of expired gas from each lung and sevoflurane uptake rates of each lung are different. Although there are many models that predict the rate of inhaled anesthetic uptake from the alveolus to arterial blood (2–12), these models would not apply to the right lung receiving systemic rather than mixed venous perfusion. That is, systemic blood perfusing the right lung would have larger blood sevoflurane concentrations than mixed venous blood because the former more closely reflects pulmonary venous effluent before organ perfusion and thus tissue uptake of the anesthetic. This resulted in the slower rate of uptake of sevoflurane from the right than the left lung, as the gradient of sevoflurane concentration from the alveolus to pulmonary capillary blood containing systemic arterial blood was less than that between the alveoli in the left lung and mixed venous blood. Thus, the end-tidal concentration obtained from the right lung over-estimated the systemic arterial concentration before reaching equilibrium. In contrast, the end-tidal concentration obtained from the left lung under-estimated the arterial concentration. For this particular patient, because the arterial blood was approximately a 50% mix of pulmonary venous blood from the left and right lungs, the arterial sevoflurane partial pressure should be close to the mean of the mixed end-tidal sevoflurane from the right and left lung. However, arterial sevoflurane partial pressure cannot be accurately estimated from end-tidal sevoflurane partial pressure from either lung, if there is an unknown ratio of blood flow to each lung in a given patient with a similar anomaly.

We believe that the alveolar surface area of the right lung was close to normal and provided adequate gas exchange because the CO diffusion test was within the normal range and the diffusing capacity adjusted for alveolar volume was 103% of the predicted value. The right lung, however, may not have significantly contributed to O₂ uptake, as perfusion through the alveolar capillaries in the right lung was arterial blood. In addition, because there was no mixed venous blood supply to the right lung, there should have been minimal shunting when solely ventilating the left lung and allowing the right lung to collapse. Therefore, it was not surprising to observe not only no decrement in Pao₂ levels during one-lung ventilation via the left lung but an actual increase in Pao₂ levels from 127 mm Hg to 161 mm Hg. Theoretically, the Pao₂ levels should have been higher than what we observed if there had been no ventilation/perfusion mismatch in his left lung. Thus, an explanation for the lower than predicted increase in Pao₂ was that the left lung received 100% of the right ventricular mixed venous output, but participated in less than 100% of ventilation. This ventilation-perfusion mismatch could have been further exacerbated by his obesity.

Although we did not directly measure blood flow to the right lung or right ventricular output to the left lung, it appears that the right lung was still well perfused despite preoperative embolization. This assumption is based on the following calculations. We know that the CO₂ content in the blood is roughly linearly proportional to its partial pressure in the range between 27 and 55 mm Hg (13). If one assumes that a) the Pco₂ in the left pulmonary vein is equal to the ETco₂ from the left lung (55 mm Hg), b) the ETco₂ from the right lung is equal to that of the right pulmonary venous blood (27 mm Hg), and c) the Pco₂ in the left atrium, left ventricle, and arterial blood are the same (42 mm Hg), then:

(Flpv x 55) + (Frpv x 27) = (Flpv + Frpv) x 42,

then Flpv x 13 = Frpv x 15,

then Flpv/Frpv = 15/13 = 1.15.

where "F" represents blood flow and "lpv" and "rpv" represent left and right pulmonary vein, respectively. Left pulmonary venous blood flow contributes 54% (15/[15 + 13]) and the right pulmonary venous blood flow contributes 46% (13/[15 + 13]) to the left ventricular output. However, we know that his right lung was smaller than his left lung based on preoperative chest radiograph.

It is also possible to calculate relative distribution of each lung to the total alveolar tidal volume, even in the absence of a measurement of anatomic dead-space. The calculation is based on an assumption that a) the ETco₂ from right lung (27 mm Hg), left lung (55 mm Hg) and from the common port (45 mm Hg) are homogeneous in supine position, and b) the level of ETco₂ is the same of alveolar CO₂ level. If so, then:

(Vll x 55) + (Vrl x 27) = (Vll + Vrl) x 45,

then [(Vll/Vrl) x 55)] + 27 = (Vll/Vrll) x45 + 45,

then (Vll/Vrl) x 10 = 18,

then Vll/Vrl = 18/10 or Vll/Vrl = 1.8.

where "V" represents alveolar tidal volume and "ll" and "rl" represent the left and right lungs, respectively. The right lung then contributes 36% (10/[10 + 18]) and left lung 64% (18/[10 + 18]) to total alveolar ventilation. The ratio of alveolar ventilation to blood flow is 0.78 (35%/46%) for the right lung and 1.19 (64%/54%) for the left lung. The right lung is relatively hyperperfused compared with the left lung or the left lung is relatively hyperventilated compared with the right lung.

It is interesting to note that changing the patient's position from supine to the left lateral decubitus in the setting of constant minute ventilation and airway pressure enhanced the difference between the ETco₂ level from the right and left lungs (Table 1). This may have been a result of the dependent (left) lung receiving less ventilation and the nondependent (right) lung receiving more ventilation in the left lateral position. The blood flow to the left lung may not have changed significantly because it already received the entire cardiac output from the right ventricle. Perfusion to the right lung of this patient may have been less sensitive to a positional change, as it was perfused from the high-pressure systemic arterial circulation and not from the low-pressure pulmonary arterial circulation.

In summary, unilateral agenesis of the pulmonary artery with significant systemic collateral blood flow is a rare congenital anomaly. The capillaries in the abnormal lung are perfused with systemic arterial blood and participate in gas exchange, but in a unique way. The lung without a pulmonary artery blood supply has a slower uptake rate of inhaled anesthetic and produces lower ETco₂ levels than the lung perfused with mixed venous blood via a normal pulmonary arterial circulation. This anomaly greatly affects the kinetics of volatile anesthetic uptake in both lungs individually and ETco₂ monitoring.

	ACKNOWLEDGMENTS

 
The authors thank Drs. Edward Lowenstein and William R. Kimball for their helpful comments and suggestions during our preparation of this manuscript.

	Footnotes

 
Accepted for publication April 20, 2006.

Supported, in part, by the Departments of Anesthesia and Critical Care and Surgery at Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USPHS grant HL 42397 (WMZ), and USPHS grant AG 000294-17, NS048140-01, and AG008812-15 (ZX).

	REFERENCES

Top Abstract Introduction CASE REPORT DISCUSSION REFERENCES

 

1. Ten Harkel AD, Blom NA, Ottenkamp J. Isolated unilateral absence of a pulmonary artery: a case report and review of the literature. Chest 2002;122:1471–7.[Abstract/Free Full Text]
2. Wissing H, Kuhn I, Rietbrock S, et al. Pharmacokinetics of inhaled anaesthetics in a clinical setting: comparison of desflurane, isoflurane and sevoflurane. Br J Anaesth 2000;84:443–9.[Abstract/Free Full Text]
3. Beams DM, Sasse FJ, Webster JG, et al. Model for the administration of low-flow anaesthesia. Br J Anaesth 1998;81:161–70.[Abstract/Free Full Text]
4. Cowles AL, Borgstedt HH, Gillies AJ. The uptake and distribution of four inhalation anesthetics in dogs. Anesthesiology 1972;36:558–70.[Web of Science][Medline]
5. Heffernan PB, Gibbs JM, McKinnon AE. Evaluation of a computer simulation program for teaching halothane uptake and distribution. Anaesthesia 1982;37:43–6.[Web of Science][Medline]
6. Heffernan PB, Gibbs JM, McKinnon AE. Teaching the uptake and distribution of halothane: a computer simulation program. Anaesthesia 1982;37:9–17.[Web of Science][Medline]
7. Kennedy RR, Baker AB. The effect of cardiac output changes on end-expired volatile anaesthetic concentrations: a theoretical study. Anaesthesia 2001;56:1034–40.[Web of Science][Medline]
8. Kennedy RR, French RA, Spencer C. Predictive accuracy of a model of volatile anesthetic uptake. Anesth Analg 2002;95:1616–21.[Abstract/Free Full Text]
9. Lerou JG, Dirksen R, Beneken Kolmer HH, et al. A system model for closed-circuit inhalation anesthesia. I. Computer study. Anesthesiology 1991;75:345–55.[Web of Science][Medline]
10. Lerou JG, Booij LH. Model-based administration of inhalation anaesthesia: developing a system model. Br J Anaesth 2001;86:12–28.[Abstract/Free Full Text]
11. Mapleson WW. Mathematical aspects of the uptake, distribution and elimination on inhaled gases and vapours. Br J Anaesth 1963;36:129–39.
12. Mapleson WW. Circulation-time models of the uptake of inhaled anaesthetics. Br J Anaesth 1978;50:731.[Free Full Text]
13. Lumb AB. Nunn's applied respiratory physiology, 5th ed. Oxford: Butterworth-Heinemann, 2000:227.

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Jiang, Y. Articles by Xie, Z. Search for Related Content PubMed PubMed Citation Articles by Jiang, Y. Articles by Xie, Z. Related Collections Cardiovascular Monitoring (Non-cardiac) Pharmacology