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CASE REPORT Table of Contents   
Year : 2008  |  Volume : 11  |  Issue : 2  |  Page : 119-122
Perioperative issues due to long-standing lung collapse during repair of a large ascending aortic aneurysm

1 Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India
2 Department of Cardiothoracic and Vascular Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India

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Acute lung collapse during open-heart surgery may potentially lead to problems such as inadequate gas exchange, increased pulmonary vascular resistance, increased afterload to the right ventricle, and difficulty in weaning from cardiopulmonary bypass (CPB). Therefore, expansion of the lungs is ensured prior to separation from CPB. We report the inability to manually expand a chronically collapsed lung during the repair of ascending aortic aneurysm. The collapsed lung did not pose difficulty in separation from CPB and in blood gas management during the perioperative period. We discuss perioperative management issues in such situations.

Keywords: Ascending aorta aneurysm, chronic lung collapse, open-heart surgery

How to cite this article:
Neema PK, Varma PK, Manikandan S, Rathod RC. Perioperative issues due to long-standing lung collapse during repair of a large ascending aortic aneurysm. Ann Card Anaesth 2008;11:119-22

How to cite this URL:
Neema PK, Varma PK, Manikandan S, Rathod RC. Perioperative issues due to long-standing lung collapse during repair of a large ascending aortic aneurysm. Ann Card Anaesth [serial online] 2008 [cited 2022 Dec 2];11:119-22. Available from:

Lung compression and collapse is known in the presence of mediastinal mass, emphysematous bulla, and chronic empyema. The compressed lung may re-expand on manual inflation after the release of compression. We describe the inability to expand a chronically compressed right lung after ascending aortic aneurysm (AAA) repair and discuss its perioperative implications.

   Case Report Top

A 63-year-old female patient weighing 35 kg presented for the repair of AAA. On general examination, the patient was thin-built and emaciated, the blood pressure was 106/70 mmHg, and the heart rate and the respiratory rate were 88 beats and 20 breaths per minute, respectively. Preoperative examination of the respiratory system revealed grossly diminished air entry on the right side of the chest. Computed tomography (CT) scan showed a large, 90 mm x 88 mm, AAA and, compressed and collapsed right lung [Figure 1 A-C]. Fibreoptic bronchoscopy showed normal bronchial tree. Arterial blood gas (ABG) analysis on room air showed - pH 7.41, arterial oxygen tension (PaO 2 ) 62 mmHg, and arterial carbon dioxide tension (PaCO 2 ) 34 mmHg. The patient could not perform pulmonary function tests because of breathlessness. Transthoracic echocardiography examination showed grossly dilated ascending aorta with significant pericardial effusion; and the left ventricular function was normal.

On the day of surgery, the patient was premedicated with inj glycopyrrolate 0.2 mg. In view of significant pericardial effusion, anaesthesia was induced with inj fentanyl 100 g and ketamine 75 mg; pancuronium 4 mg was given to facilitate tracheal intubation with 6 mm ID endotracheal tube. Mechanical ventilation was commenced with a tidal volume of 250 ml and respiratory rate of 15/min, the peak airway pressure (Paw) showed 28-30 cms H 2 O. Anaesthesia was maintained with oxygen, isoflurane (0-1%), fentanyl 200 g, midazolam 2 mg, and intermittent doses of pancuronium. The patient was monitored with electrocardiogram, pulse oximetry, end-tidal carbon dioxide (EtCO 2 ), invasive arterial blood pressure (ABP), central venous pressure, Paw, and tidal volume. ABG at FIO 2 of 1 showed pH 7.38, PaO 2 288 mmHg, PCO 2 36 mmHg, and base excess (BE) -2.8 mEq/L.

Initially, the left femoral artery was exposed and prepared for cannulation, and thereafter midsternotomy was performed. After anticoagulation with heparin 3 mg/kg and ensuring an activated coagulation time (ACT) of >400 seconds, cardiopulmonary bypass (CPB) was initiated with left femoral artery and right atrial cannulation. On CPB, the patient was cooled to 24C, the aorta was clamped proximal to the innominate artery, the aneurysm was opened, and the heart was arrested by cold blood cardioplegic solution administered into the coronary ostia. The diseased ascending aorta was replaced with a 26-mm tube graft. Thereafter, the lungs were manually ventilated for de-airing of the heart and the aortic cross clamp was removed. Cardiac rhythm was spontaneously restored to sinus rhythm. During de-airing, the right pleura was noticed to be not moving on manual ventilation. The mediastinal pleura was widely opened, and the lung was adherent densely to the surrounding tissues. Further manual attempts at ventilation (limited to a Paw of 30 cm H 2O) failed to expand the collapsed right lung. The patient was re-warmed to 35C and weaned off CPB with the support of epinephrine infusion, 0.1 g/kg/min. In the post-CPB period, the Paw decreased marginally to 20-24 cms H 2 O at a tidal volume of 250 ml and ventilatory rate of 15/min; ABG checked with fractional oxygen concentration (FIO 2 ) 1 showed pH 7.41, PaO 2 260 mmHg, PCO 2 35 mmHg, and BE - 3 mEq/L. Two mediastinal drains were inserted before closure of the chest, one in the mediastinum and the other in the chest.

After the surgical procedure, the patient was transferred to the intensive care unit and mechanical ventilation continued with the same ventilator settings, the FIO 2 was decreased to 0.5, and a positive end expiratory pressure (PEEP) of 5 cms H 2 O was applied. The right lung remained collapsed on the first and second postoperative days. On the second postoperative day, the patient was weaned off the ventilator and after fibreoptic bronchoscopy and lavage, the trachea was extubated. Administration of chest physiotherapy and incentive spirometry was continued; however, despite these measures, the air entry remained diminished on the right side of the chest. Repeat CT scan thorax on the ninth postoperative day showed significant expansion of the right lung [Figure 2 A-C]. The patient was discharged on the tenth day after surgery.

   Discussion Top

The collapsed lung can lead to inadequate gas exchange (hypoxaemia) and increased afterload to the right ventricle. [1] It is conceivable that during open-heart surgery, hypoxaemia and increased afterload to the right ventricle may pose difficulty in separation from CPB. Therefore, re-expansion of the lungs is routinely attempted prior to separation from CPB. However, in the presence of long-standing lung collapse, vital capacity manoeuvers to restore lung volume could result in trauma to normal as well as collapsed lung. Earlier, Neema et al. [2] have described fatal endotracheal haemorrhage on manual ventilation of a chronically collapsed lung during repair of AAA. Although in the present case the right lung remained collapsed despite attempts at re-expansion, it did not adversely affect the process of separation from CPB and blood gas management during the postoperative period. However, the appropriate management in such situations is not described.

With chronic lung collapse, the lung parenchyma and its overlying pleura become fibrotic; this may prevent lung re-inflation. [3] Blood gas disturbances due to chronic lung collapse are not significant, since the normal lung usually compensates for the collapsed lung. Under such situations, the normal lung may receive a major portion of the ventilation as well as perfusion. Pulmonary hypoxic vasoconstriction and constriction of extra-alveolar vessels (large pulmonary vessels) divert right ventricular output toward the normal lung. [4] However, chronic lung collapse should be differentiated from acute lung collapse. Acute lung collapse may result in hypoxaemia, while in chronic lung collapse gas exchange may be well compensated.

Fibrotic changes in chronically collapsed lung and compensatory hyperinflation of normal lung result in asymmetric lung compliance. Under such a situation, a greater proportion of tidal volume distributes to the more compliant lung. The PEEP level that may normally maximise the alveolar recruitment in the less compliant lung may over-distend the more compliant lung and lead to increased intra-thoracic pressure, mediastinal shift, and paradoxically, cause compression of the less compliant lung. [5],[6] Under such situations, independent lung ventilation (ILV) may be of value. Various criteria have been used in different studies to change over from conventional ventilation to ILV. [5] Several studies [5],[7] agree on the following requirements for considering a patient for ILV. The patient should have a radiographically apparent unilateral or asymmetrical lung disease with one of the following - (1) Hypoxaemia refractory to high FiO 2 and generalised PEEP, [7] (2) PEEP- induced deterioration in oxygenation, (3) Over-inflation of the non-involved lung, and (4) Significant deterioration of circulatory status in response to PEEP. [7] The critical factor in improvement of oxygenation associated with ILV is related to the ability to deliver differential PEEP to the affected and non-affected lungs. Although AAA repair is not considered an indication of double lumen endobronchial tube (DLT) placement, in the presence of inability to re-expand collapsed lung and refractory hypoxaemia in spite of high FiO 2 and generalised PEEP, DLT placement and ILV should be considered. Although our patient had over-inflation of the left lung, she did not have hypoxaemia, and therefore, we did not use one lung ventilation.

In the present patient, the collapsed lung opened spontaneously over a period of 7 days; however, its volume as shown by repeat CT scan remained considerably less than the left lung. The lung remained collapsed until the patient was on ventilator. Apparently, until the patient was on ventilator, asymmetric compliance may have resulted in asymmetric distribution of ventilation and low volume of the right lung. It is the author's observation that the collapsed lung expanded only after establishment of spontaneous breathing and negative intra-pleural pressure. Chest physiotherapy and incentive spirometry may have further helped in re-expansion of the lung. Logically, in the presence of chronically collapsed lung, early weaning from the ventilator and initiation of normal spontaneous breathing may help in lung expansion. However, one should realise that, because of chronic lung compression, parenchymal fibrosis, and hence restrictive lung disease is a possibility [8] and the altered respiratory mechanics and functional limitations [9] may pose problems during weaning. These changes may lead to respiratory muscle fatigue and failure during weaning from the ventilator. Further, it is important to remember that a collapsed lung may get infected, because of inadequate drainage. Fibreoptic bronchoscopy and lavage may be used in patients who are unable to clear secretions. Regular physical examination and chest X-ray are useful in detecting persistent lung collapse.

To summarise, the management of a patient who underwent replacement of AAA with chronically collapsed right lung is discussed. The collapsed lung did not re-expand on manual ventilation; however, it did not pose difficulty in separation from CPB and blood gas management. Until the patient was on ventilator and received PEEP, the collapsed lung did not expand. It is the author's opinion that because of asymmetric lung compliance, the positive pressure ventilation and PEEP may have resulted in over-inflation of the normal lung. The collapsed lung partially re-expanded over one week; perhaps bronchoscopic lavage before extubation, resumption of normal spontaneous breathing, incentive spirometry, chest physiotherapy, and establishment of negative intra-pleural pressure may have helped in re-expansion of the collapsed right lung.

   References Top

1.Pinsky MR. Heart-lung interactions. In : Ayres SM, Holbrook PR, Shoemaker WC, editors. Text-book of critical care. 4 th ed, Philadelphia: WB Saunders; 2000. p. 1204-21.  Back to cited text no. 1    
2.Neema PK, Varma PK, Manikandan S, Rathod RC. Fatal endotracheal hemorrhage during repair of a large ascending aortic aneurysm. Eur J Anaesthesiol 2007;7:646-7.  Back to cited text no. 2    
3.Corrin B. The lungs. In : Corrin B, editor. Systemic pathology. 1 st ed, New York: Churchill Livingstone; 1990. p. 161-5.  Back to cited text no. 3    
4.West JB. Pulmonary blood flow and metabolism in Best and Taylor's Physiological basis of medical practice. In : West JB, editor. New Delhi: BI Waverly Pvt. Ltd; 1996. p. 529-37.  Back to cited text no. 4    
5.Carlon GC, Ray C Jr, Klein R, Goldiner PL, Miodownik S. Criteria for selective positive end-expiratory pressure and independent synchronized ventilation of each lung. Chest 1978;74:501-7.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Kanarek DJ, Shannon DC. Adverse effect of positive end expiratory pressure on pulmonary perfusion and arterial oxygenation. Am Rev Respir Dis 1975;112:457-9.  Back to cited text no. 6  [PUBMED]  
7.Frame SB, Marshall WJ, Clifford TG. Synchronized independent lung ventilation in the management of pediatric unilateral pulmonary contusion: Case report. J Trauma 1989;29:395-7.  Back to cited text no. 7  [PUBMED]  
8.Hansen JE, Wasserman K. Pathophysiology of activity limitation in patients with interstitial lung disease. Chest 1996;109:1566-76.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Harris-Eze AO, Sridhar G, Clemens RE, Zintel TA, Gallagher CG, Marciniuk DD. Role of hypoxemia and pulmonary mechanics in exercise limitation in interstitial lung disease. Am J Respir Crit Care Med 1996;154:994-1001.  Back to cited text no. 9  [PUBMED]  

Correspondence Address:
Praveen Kumar Neema
B-9, NFH, Sree Chitra Residential Complex, Poonthi Road, Kumarpuram, Trivandrum - 695 011, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.41581

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  [Figure 1 A-C], [Figure 2 A-C]