One-Lung Ventilation Can Alter the Severity of Aortic Regurgitation

Aortic regurgitation (AR) is mainly affected by changes in the systemic vascular resistance (SVR) and left ventricular (LV) diastolic pressures. There are no previous reports describing the effects of one-lung ventilation (OLV) on the magnitude of AR.

An 82-year-old man (157 cm and 45 kg) presented to our institution for the repair of a type-V descending thoracoabdominal aortic aneurysm (TAAA). The modified Crawford type-V TAAA extends from the level of the left atrium to just above the origin of the celiac axis. There was associated mild (2+)–to–moderate (3+) AR without dilatation of the aortic annulus or root. The LV function was reported to be good. The patient underwent repair of the TAAA in the modified right lateral decubitus position (hip rotated and left leg straightened for femoral artery cannulation).

Anesthetic management consisted of general anesthesia with isoflurane in a mixture of air-oxygen supplemented with continuous thoracic epidural analgesia (5-6 mL/h of bupivacaine 0.125% plus 5 μg/mL of fentanyl). OLV was achieved after left thoracotomy with a Mallinckrodt Bronchocath 35F left-sided double-lumen tube (Mallinckrodt Medical, Athlone, Ireland) to facilitate the surgical exposure. Cerebrospinal fluid was drained intermittently using a small-bore catheter in the intrathecal space. The cerebrospinal fluid pressure was kept below 10 mmHg during aortic cross-clamping. A descending thoracic aorta to the left femoral artery bypass was used along with a roller pump blood retrieval system to transfuse and replace operative site blood loss.

Intraoperative transesophageal echocardiography was used to confirm the preoperative findings. In addition, a central jet of mild-to-moderate AR was seen in the midesophageal aortic valve short- and long-axis views (Fig 1) during two-lung ventilation. However, after the institution of OLV (with the same tidal volume of 450 mL and respiratory rate of 10/minute), the regurgitant jet almost completely disappeared (Fig 2). It reappeared with the application of a cross-clamp on the descending thoracic aorta (Fig 3A), persisting after reinstitution of two-lung ventilation following repair of the aneurysm (Fig 3B). The rest of the perioperative period was uneventful, and the patient's trachea was extubated on the first postoperative day.

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Fig 1. A midesophageal view of the aortic valve before the institution of OLV showing a central jet of mild-to-moderate aortic regurgitation. (A) Short-axis view and (B) long-axis view. LA, left atrium; RA, right atrium; AO, aortic root. (Color version of figure is available online.)

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Fig 2. A midesophageal view of the aortic valve after the institution of OLV showing almost complete disappearance of the regurgitant jet. (A) Short-axis view and (B) long-axis view. LA, left atrium; RA, right atrium; AO, aortic root; RVOT, right ventricular outflow tract. (Color version of figure is available online.)

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Fig 3. A midesophageal long-axis view of the aortic valve showing reappearance of the regurgitant jet. (A) After application of the aortic cross-clamp and (B) after the reinstitution of two-lung ventilation following aneurysm repair. LA, left atrium; LV, left ventricle; AO, aortic root. (Color version of figure is available online.)

During OLV, the total tidal volume is applied to the dependent lung. This, in turn, affects the respiratory mechanics resulting in an increase in peak (Ppeak) as well as plateau (Pplat) airway pressures.1 Other important changes that occur with the institution of OLV are increases in both pulmonary vascular resistance (secondary to hypoxic pulmonary vasoconstriction in the nondependent lung) and pulmonary artery pressure. Thus, the net increase in intrathoracic pressure is secondary to changes in both respiratory and vascular mechanics.

The increases in Ppeak and Pplat in the dependent lung are sustained even when the thorax is opened.2 Increased intrathoracic pressure affects LV preload as well as afterload. The LV preload is decreased secondary to a decrease in right ventricular (RV) output and interventricular septal shifts. Although increased intrathoracic pressure increases RV afterload, it has the opposite effect on the LV (ie, it reduces LV afterload).3, 4, 5

The main cause of reduction in LV afterload is an increase in pressure in the thoracic and abdominal cavities relative to the atmospheric pressure. Because the systemic circulation is at atmospheric pressure, it results in a pressure differential.3 Thus, the systemic circulation is at a lower pressure than either the LV or the thoracic aorta, thereby reducing the LV afterload. Overall, the heart rate or contractility is unaffected by changes in the intrathoracic pressure.3 Therefore, the net effect of raised intrathoracic pressure secondary to the institution of OLV decreases in both LV preload and afterload without change in either heart rate or contractility. Additionally, an increase in intrathoracic pressure also leads to sympathetic stimulation resulting in reflex vasodilation,3 which could have been a further cause of reduction in the magnitude of AR observed in our patient. The reappearance of the AR jet with the application of a cross-clamp on the descending thoracic aorta was probably caused by the increase in afterload.

In our patient, the Ppeak increased from 22 mmHg to 35 mmHg with the institution of OLV. However, because we did not use a pulmonary artery catheter, we cannot comment on the change of SVR with the institution of OLV. Furthermore, heart rate and the Doppler color scale with which the changes in the magnitude of AR were observed were unchanged. Similarly, the systemic blood pressure was unchanged during the initiation of OLV although it did increase transiently when the clamp was applied on the descending thoracic aorta, proximal to the aneurysmal segment.

In conclusion, we observed a decrease in the magnitude of AR with the initiation of OLV in a patient undergoing repair of a TAAA, probably because of a reduction in the LV afterload secondary to an increase in the intrathoracic pressure. However, further studies are required to determine the effects of raised intrathoracic pressure (eg, maneuvers like positive end-expiratory pressure) on the magnitude of AR, especially in the closed chest.