Annals of Cardiac AnaesthesiaAnnals of Cardiac AnaesthesiaAnnals of Cardiac Anaesthesia
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LETTER TO EDITOR Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 3  |  Page : 263-264
Anesthetic management of patent ductus arteriosus - Not always an easy option


Department of Cardiac Anaesthesia, AIIMS, New Delhi, India

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Date of Web Publication6-Sep-2010
 

How to cite this article:
Singh SP, Chauhan S, Kiran U. Anesthetic management of patent ductus arteriosus - Not always an easy option. Ann Card Anaesth 2010;13:263-4

How to cite this URL:
Singh SP, Chauhan S, Kiran U. Anesthetic management of patent ductus arteriosus - Not always an easy option. Ann Card Anaesth [serial online] 2010 [cited 2014 Apr 16];13:263-4. Available from: http://www.annals.in/text.asp?2010/13/3/263/69061


The Editor,

Congenital cardiac diseases like isolated patent ductus arteriosus (PDA) and, atrial septal defect (left to right shunts) may lead to an increase in pressure of end tidal carbon dioxide (PEtCO 2 ) and partial pressure of carbon dioxide in arterial blood (PaCO 2 ). However, this occurs only if the pulmonary blood flow (PBF) is high enough to cause alveolar congestion and transudation into the alveolar spaces, compromising gas exchange. In infants and children with a left to right cardiac shunt, (a-Et) PCO 2 gradient is not significantly different from children with normal circulation. Several studies have demonstrated the usefulness of EtCO 2 pressures in assessing pulmonary blood flow in a variety of scenarios. [1],[2]

We hereby report a case of an 8 month old female child, weighing 3.75 kg, diagnosed with PDA and bicuspid aortic valve. The patient was taken for ligation of PDA under general anesthesia. Anesthesia was induced with sevoflurane (8%) and fentanyl (5 micg/kg) and muscle relaxation was achieved with rocuronium (1 mg/kg). The trachea was intubated with a 4 mm internal diameter uncuffed endotracheal tube. The child was ventilated with pressure control mode of ventilation using air oxygen 50-50%, with the inspiratory pressure set at 25 cm H 2 O and ventilatory rate at 35 breaths per minute; generating a tidal volume of 30 ml. Anesthesia was maintained with fentanyl, midazolam and vecuronium bromide.

After intubation, initially, the PEtCO 2 was 53 mmHg, as expected. The patient was positioned in right lateral position for surgery. Following positioning, at the time of thoracotomy, the PEtCO 2 suddenly rose to 82 mmHg and the oxygen saturation of hemoglobin decreased to 93% (on 50% FiO 2 ). All probable causes of increased PEtCO 2 , like endobronchial intubation, leak in ventilatory circuit, bronchospasm, obstruction of endotracheal tube and rise in temperature, were ruled out. Intraoperatively, the surgeon discovered a tense left pulmonary artery (LPA), which is an unusual finding during this surgery. During dissection of PDA, suddenly, the PEtCO 2 dropped from 82 mmHg to 41 mmHg even when the PDA was patent and flowing. On close inspection of the surgical field, it appeared that the surgeon has retracted the LPA and it was being compressed. The reduced blood flow through the LPA caused a fall in PEtCO 2 but the LPA could only be released after the ligation of PDA. Following ligation of PDA, the PEtCO 2 was still high, at 63 mmHg, which, in normal circumstances, drops to 35-40 mmHg after the PBF is normalized following PDA ligation. When the patient was turned to supine position, the PEtCO 2 was still 56 mmHg. A provisional diagnosis of compromised ventilation of lung due to atelectasis was hypothesized and lung recruitment maneuvers were undertaken. A chest X-ray in the intensive care unit showed upper lobe collapse of the right lung.

In the present case, the main cause of hypoventilation of the dependent right lung was compression of a compliant pediatric thorax by rolls and drapes used for positioning of the patient. A large roll of the entire width of the thorax must have caused the compression of the dependent lung due to suboptimal positioning. [3] This premise was further confirmed by the intraoperative finding of a tense LPA, as most of the pulmonary blood was being shunted through the LPA because of hypoxic vasoconstriction occurring in the dependent collapsed upper lobe of the right lung. [4],[5] Moreover, when the LPA was occluded accidentally during dissection of the PDA, the blood flow to the functional part of the left lung dropped exponentially and so did the PEtCO 2 . If the right lung would have been functioning properly, the PEtCO 2 should have risen instead of falling, as the blood flow would have been diverted to the normally ventilated lung and the alveoli necessarily have eliminated the CO 2 efficiently. Furthermore, once the PDA was ligated, the PEtCO 2 should have decreased to normal values, but it remained in a higher range because of ventilatory compromise of the right lung.

Thus, congenital heart diseases with shunting of blood and lateral decubitus position along with pediatric physiology of respiratory mechanics all pose a great challenge to the working anesthesiologist. The interpretation of observed values should be carried out in the context of the clinical situation of the patient.

 
   References Top

1.Shibutani K, Muraoka M, Shirasaki S, Kubal K, Sanchala VT, Gupte P. Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output? Anesth Analg 1994;79:829-33.   Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Domsky M, Wilson RF, Heins J. Intraoperative end-tidal carbon dioxide values and derived calculation correlated with outcome: Prognosis and capnography. Crit Care Med 1995;23:1497-503.   Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Wilson WC, Benumof JL. Anesthesia for thoracic surgery. In: Miller RD, editor. Anesthesia. 6 th ed. Philadelphia, Pa: Churchill Livingstone; 2005. p. 1872.  Back to cited text no. 3      
4.Benumof JL. Mechanism of decreased blood flow to atelectatic lung. J Appl Physiol 1978;46:1047-53.  Back to cited text no. 4      
5.Pirlo AF, Benumof JL, Trousdale FR. Atelectatic lobe blood flow: Open vs. closed chest, positive pressure vs. spontaneous ventilation. J Appl Physiol 1981;50:1022-6.  Back to cited text no. 5      

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Correspondence Address:
Sarvesh P Singh
112, Doctors Hostel, J P N A Trauma Centre, AIIMS, New Delhi - 110 029
India
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DOI: 10.4103/0971-9784.69061

PMID: 20826973

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