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    Abstract
   Introduction
   Case Report
   Discussion
    References

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Table of Contents
CASE REPORT  
Year : 2014  |  Volume : 17  |  Issue : 2  |  Page : 167-169
Use of nitric oxide in thoracic surgery for a high risk cardiac patient


1 Department of Cardiothoracic and Transplant Anaesthesia, Freeman Hospital, Newcastle Upon Tyne, United Kingdom
2 Department of Cardiothoracic Surgery, Freeman Hospital, Newcastle Upon Tyne, United Kingdom

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Date of Submission12-Apr-2013
Date of Acceptance29-Oct-2013
Date of Web Publication1-Apr-2014
 

   Abstract 

Nitric oxide (NO) is a selective pulmonary vasodilator especially in the presence of pulmonary artery hypertension. With right ventricle (RV) dysfunction, inhaled NO may increase RV ejection fraction and cardiac output. The main advantage of NO over intravenous therapy is its inability to decrease systemic pressure thereby maintaining the coronary perfusion pressure and the myocardial perfusion. In this case report, we discuss the use of NO in a routine thoracic surgery patient suffering with severe left ventricular dysfunction and a potential candidate for a very high cardiac risk.

Keywords: Adverse cardiac event; Nitric oxide; Video assisted thoracoscopic surgery

How to cite this article:
Garg V, Ahmed S, Stamenkovic S. Use of nitric oxide in thoracic surgery for a high risk cardiac patient. Ann Card Anaesth 2014;17:167-9

How to cite this URL:
Garg V, Ahmed S, Stamenkovic S. Use of nitric oxide in thoracic surgery for a high risk cardiac patient. Ann Card Anaesth [serial online] 2014 [cited 2018 Sep 18];17:167-9. Available from: http://www.annals.in/text.asp?2014/17/2/167/129882



   Introduction Top


Nitric oxide (NO) is an endogenous molecule with various physiological actions [1] one of which is selective pulmonary vasodilatation in the presence of pulmonary artery hypertension (PAH). [2],[3] In presence of right ventricle (RV) dysfunction, inhaled NO may increase RV ejection fraction (EF) and cardiac output. [4],[5] The main advantage of inhaled NO over intravenous therapy directed at reducing pulmonary vascular resistance (PVR) is its inability to decrease systemic pressure thereby maintaining the coronary perfusion pressure and the myocardial perfusion. In the present patient, we were faced with severe left ventricular (LV) dysfunction (EF-15%), moderate RV dysfunction and elevated pulmonary artery pressures, which we expected to worsen during one lung ventilation (OLV). We present anesthetic management of this patient for video assisted thoracoscopic surgery (VATS).


   Case Report Top


An 80-year-old male patient weighing 78 kg presented with a history of dyspnea (New York Heart Association class III). During evaluation, chest X-ray showed a shadow in the right lower lobe and on investigating further, computed tomography scan showed a nodule in right lower lobe. Patient's past medical history included ischemic heart disease since 3 years with percutaneous intervention to left anterior descending artery, transurethral resection of bladder tumor for carcinoma bladder 2 years ago, total hip replacement 6 months ago, gastroesophageal reflux disease with severe gastritis and chronic atrial fibrillation for which he was receiving warfarin. A transthoracic echocardiogram was done which showed dilated LV, moderate mitral regurgitation and an EF of 15%. RV was moderately dilated and showed moderately impaired function and moderate tricuspid regurgitation. Both the atria were severely dilated. The aortic valve was calcified and showed mild to moderate regurgitation. Pulmonary artery systolic pressure was 42 mmHg. Pulmonary function test revealed forced expiratory volume in one second (FEV1) of 2.13 L (80% of expected), FEV1/vital capacity ratio of 100%. Cardiopulmonary exercise testing (CPET) revealed anaerobic threshold (AT) of 10.4 ml/kg/min and peak oxygen consumption (VO 2 ) of 13.9 ml/kg/min. AT of <11 ml/kg/min and peak VO 2 <20 ml are predictors of significantly high risk surgery. Our main concerns during anesthetic management of this patient were preventing heart failure during the procedure and management of hypoxia during OLV apart from the other concerns associated with this surgery. The issues were discussed with the surgical team and to shorten the duration and magnitude of the procedure, it was decided to conduct a VATS and wedge resection of right lower lobe rather than a thoracotomy lobectomy. We planned for general anesthesia with OLV and paravertebral block for analgesia. In order to manage PAH and reduce the load on the right heart, we decided to use NO during the procedure.

An arterial line was secured before induction for invasive blood pressure monitoring. Arterial blood gas on room air showed pH 7.5, PaO 2 11.2 kPa, PCO 2 4.4 kPa and HCO 3 26 mEq/L. Anesthesia was induced with propofol 100 mg and fentanyl 50 μg. Neuromuscular blockade was achieved with atracurium 30 mg and trachea was intubated with Robertshaw left sided double lumen endobronchial tube, its placement was confirmed by fiberoptic bronchoscopy. A right sided single shot paravertebral block was performed with 0.25% bupivacaine. Right internal jugular vein was cannulated for central venous pressure monitoring and patient was positioned for surgery. Anesthesia was maintained with isoflurane in O 2 and air. NO was introduced once OLV was initiated. Since the duration of surgery was not expected to be very long; titration of NO was considered difficult, hence, we decided to commence NO at 20 ppm in accordance with our institutional practice. In our experience of the use of NO in patients with heart and lung transplantation we have realized that NO 20 ppm gives the best hemodynamic outcome in terms of reducing the PVR without causing any ill-effects. NO was delivered using INOvent delivery system on the Dragger ventilator of the anesthesia machine and the impurities were removed through the scavenging system. There was mild desaturation during OLV, which responded to increase in inspired O 2 (FiO 2 ) from 0.5 to 0.8. The hemodynamic parameters remained stable during the procedure lasting for 60 min. No inotropes were required during the surgery. A catheter was introduced in the paravertebral space by the surgeon for analgesia in the post-operative period. At the end of the procedure, the trachea was extubated. Post-operatively, the patient recovered without any complications and discharged on the 3 rd post-operative day.


   Discussion Top


Anesthetizing a patient with severe cardiac dysfunction is a challenge in itself and when combined with the necessity of providing OLV, the task becomes even more arduous due to the changes in the lung physiology. OLV can result in hypoxia causing decreased myocardial O 2 supply, which can severely compromise LV function especially in a precariously balanced patient with severe ischemic heart disease. Moreover, sudden change in preload in these patients may be poorly tolerated by the LV. Our patient had a severe LV dysfunction (EF-15%), moderate RV dysfunction and PAH. He was also in chronic atrial fibrillation, which was further compromising his cardiac output. Pre-operative CPET showed peak VO 2 of 13.9 ml/kg/min predicting a very low cardiopulmonary reserve of the patient. The cardiac stress in this patient was expected to be tremendous because of physiological changes such as hypoxia, hypercarbia, reduced cardiac output, shunting due to OLV, lateral decubitus position and the surgical stress. Routine measures applied to prevent hypoxia are increasing FiO 2 , positive end expiratory pressure to the ventilated lung and insufflation of oxygen or continuous positive airway pressure to the non-ventilated lung and intermittent inflation of the collapsed lung. Ventilation is adjusted to prevent hypercapnia even though permissive hypercapnia can be allowed to prevent barotrauma. Adequate analgesia is important to minimize the surgical stress. [6] Our goal in the anesthetic management of this patient was to prevent any further worsening of the LV function and acute heart failure. Apart from the routine measures as discussed above, we chose to use inhaled NO during the procedure to selectively decrease the PVR and prevent RV failure. Changes in lung volume increase RV afterload because of alterations of its primary constituent, PVR. [7] We were more concerned about the RV failure even though it was moderate because with the initiation of OLV a sudden increase in PVR is expected, which could result in severe reduction in fractional area change, progressive dilatation of RV both at end systole and end diastole leading to acute RV failure. [8] With a moderately impaired RV, the acute dilatation would result in shifting of inter-ventricular septum toward the LV (ventricular interdependence) causing impaired filling of the LV. [9] This would have then led to biventricular failure. Use of a non-selective pulmonary vasodilator such as milrinone would have resulted in systemic vasodilatation, which could have been detrimental in the presence of severe LV dysfunction. One can argue that we could have used a vasopressor such as vasopressin along with milrinone to counter the systemic vasodilatation. We believed that it would be best if we can avoid drastic changes in the afterload and preload. However, if the hemodynamics would have deteriorated our plan of management was to use combination of these two drugs.

It is suggested that using NO could potentially increase the LV end diastolic pressure (LVEDP) as the reduction in PVR could increase the LV preload. [10],[11] These studies did not measure the LV end-diastolic volume (LVEDV), which is an important limitation. NO has been widely used in cardiac transplantation for preventing RV failure and has been used in post-operative setting for improving PAH to the extent that RV assist device placement has been averted in some cases. [12] In addition, use of vasoactive agents could itself cause increase in LVEDV and LVEDP. We believe the possibility of LV failure due to volume overload after introduction of NO in our patient was probably minimal as the increase in PVR due to lung collapse during OLV was counterbalanced with vasodilation due to inhaled NO. There is no evidence to prove our statement but clinically there were no signs to suggest LV failure. Monitoring the cardiac function using transesophageal echocardiography would have been an ideal tool in this setting to diagnose any worsening and to monitor the therapeutic interventions, but we were limited as the patient suffered with gastroesophageal reflux disease and severe gastritis.

Change in the surgical plan from a conventional lobectomy to VATS and doing a wedge resection helped us to achieve smooth intraoperative and post-operative period. The advantages of VATS over conventional lobectomy were that we were able to minimize the duration of surgery, blood loss, tissue handling and post-operative pain. [13],[14] This reduced the stress on the heart as there were no major fluid shifts, anesthetic time and OLV time were shortened, and post-operative pain was less, and all these benefits resulted in a faster post-operative recovery.

To summarize, there are no guidelines in the literature on use of NO in thoracic surgeries. Our use of NO in such setting is novel and need more number of cases before one can produce definite evidence of its benefit. The concern of withdrawal response to discontinuing NO may not be important in this scenario as NO is given for a short duration and the normal physiology is restored once both lungs are ventilated.

 
   References Top

1.Steudel W, Hurford WE, Zapol WM. Inhaled nitric oxide: Basic biology and clinical applications. Anesthesiology 1999;91:1090-121.  Back to cited text no. 1
    
2.Pepke-Zaba J, Higenbottam TW, Dinh-Xuan AT, Stone D, Wallwork J. Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmonary hypertension. Lancet 1991;338:1173-4.  Back to cited text no. 2
    
3.Rich GF, Murphy GD Jr, Roos CM, Johns RA. Inhaled nitric oxide. Selective pulmonary vasodilation in cardiac surgical patients. Anesthesiology 1993;78:1028-35.  Back to cited text no. 3
    
4.Bhorade S, Christenson J, O'connor M, Lavoie A, Pohlman A, Hall JB. Response to inhaled nitric oxide in patients with acute right heart syndrome. Am J Respir Crit Care Med 1999;159:571-9.  Back to cited text no. 4
    
5.Zwissler B, Welte M, Messmer K. Effects of inhaled prostacyclin as compared with inhaled nitric oxide on right ventricular performance in hypoxic pulmonary vasoconstriction. J Cardiothorac Vasc Anesth 1995;9:283-9.  Back to cited text no. 5
    
6.Eastwood J, Mahajan R. One lung anaesthesia. Br J Anaesth CEPD Rev 2002;2:83-7.  Back to cited text no. 6
    
7.Hakim TS, Michel RP, Chang HK. Effect of lung inflation on pulmonary vascular resistance by arterial and venous occlusion. J Appl Physiol Respir Environ Exerc Physiol 1982;53:1110-5.  Back to cited text no. 7
    
8.Mcmahon CC, Irvine T, Conacher ID. Transoesophageal echocardiography in the management of whole lung lavage. Br J Anaesth 1998;81:262-4.  Back to cited text no. 8
    
9.Kevin L, Barnard M. Right ventricular failure. Continuing education in anaesthesia. Crit Care Pain 2007;7:89-94.  Back to cited text no. 9
    
10.Natori S, Hasebe N, Jin YT, Matsusaka T, Ido A, Matsuhashi H, et al. Inhaled nitric oxide modifies left ventricular diastolic stress in the presence of vasoactive agents in heart failure. Am J Respir Crit Care Med 2003;167:895-901.  Back to cited text no. 10
    
11.Argenziano M, Dean DA, Moazami N, Goldstein DJ, Rose EA, Spotnitz HM, et al. Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure. J Thorac Cardiovasc Surg 1998;115:700-8.  Back to cited text no. 11
    
12.Oz MC, Ardehali A. Collective review: Perioperative uses of inhaled nitric oxide in adults. Heart Surg Forum 2004;7:E584-9.  Back to cited text no. 12
    
13.McKenna RJ Jr, Houck W, Fuller CB. Video-assisted thoracic surgery lobectomy: Experience with 1,100 cases. Ann Thorac Surg 2006;81:421-5.  Back to cited text no. 13
    
14.Solaini L, Prusciano F, Bagioni P, di Francesco F, Solaini L, Poddie DB. Video-assisted thoracic surgery (VATS) of the lung: Analysis of intraoperative and postoperative complications over 15 years and review of the literature. Surg Endosc 2008;22:298-310.  Back to cited text no. 14
    

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Correspondence Address:
Vishal Garg
Department of Cardiothoracic Anaesthesia, Freeman Hospital, Newcastle Upon Tyne, NE7 7DN
United Kingdom
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.129882

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