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Ann Thorac Surg 1997;63:533-535
© 1997 The Society of Thoracic Surgeons

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Case Report

ECMO and Inhaled Nitric Oxide for Cardiopulmonary Failure After Heart Retransplantation

Department of Anesthesiology and Biotechnology and Biomedical Technologies Laboratory, IRCCS Policlinico San Matteo, and Charles Dubost Center of Cardiac Surgery, University of Pavia and IRCCS Policlinico San Matteo, Pavia, Italy

Accepted for publication July 19, 1996.

	Abstract

Top Footnotes Abstract Introduction Comment References

 
Cardiopulmonary failure occurred in a 62-year-old patient a few hours after emergency cardiac retransplantation. Venoarterial extracorporeal membrane oxygenation was required to support biventricular dysfunction; thereafter, inhaled nitric oxide was given for residual hypoxemia and pulmonary hypertension. We report survival after venoarterial extracorporeal membrane oxygenation and inhaled nitric oxide treatment for both heart and lung failure in a heart recipient.

	Introduction

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Cardiopulmonary failure after heart transplantation is a life-threatening condition that dictates urgent intervention to support oxygenation and circulation. However, to date successful extracorporeal membrane oxygenation (ECMO) after cardiac transplantation has been reported only in 5 adult recipients [1, 2]. The selective pulmonary vasodilator inhaled nitric oxide (i-NO) has been found to increase arterial oxygenation in adult respiratory distress syndrome [3] and to provide adequate support to the failing right ventricle after transplantation [4]. Therefore, i-NO may represent an additional strategy to treat posttransplantation right ventricular dysfunction secondary to pulmonary hypertension and hypoxemia.

We describe an adult patient with cardiopulmonary failure complicating orthotopic cardiac transplantation, successfully treated with ECMO and i-NO.

In October 1995, a 62-year-old man was referred to the Cardiac Surgery Department for orthotopic transplantation of a heart from a 47-year-old female donor. Recipient preoperative transpulmonary gradient was 7 mm Hg, and pulmonary vascular resistance was 1.8 Wood units. The ischemic time of the donor heart was 215 minutes. Weaning from extracorporeal circulation repeatedly failed because of postcardiotomy cardiogenic shock refractory to counterpulsation and maximal-dose inotropes. While the patient was on cardiopulmonary bypass, a second heart became available and the patient underwent successful retransplantation. The ischemic time of the second heart was 155 minutes. The cumulative extracorporeal circulation time was 580 minutes. Coagulopathy occurred, and 23 units of blood derivatives were required intraoperatively.

At intensive care unit admission, respiratory failure developed. An inspired oxygen fraction (FiO₂) up to 0.8 with a positive end-expiratory pressure up to 15 cm H₂O was required to maintain acceptable arterial oxygenation. Bilateral infiltrates were present on the chest roentgenogram. Ten hours after intensive care unit admission, catecholamine-unresponsive cardiocirculatory failure occurred. At emergency reoperation, biventricular failure was demonstrated and the patient was started on venoarterial ECMO without systemic heparinization, using a heparin-coated circuit. Within 30 minutes cardiac contractility improved and inotrope doses were reduced to 6 µg • kg^-1 • min^-1 for dopamine and 0.012 µg • kg^-1 • min^-1 for isoproterenol. On ECMO, the ventilator was set to minimize barotrauma and oxygen toxicity. Weaning off was accomplished after 108 hours by progressive reduction of pump flows under visual inspection of the heart and serial blood gas analysis. The procedure required 10 µg • kg^-1 • min^-1 dopamine, 0.014 µg • kg^-1 • min^-1 isoproterenol, and 0.1 µg • kg^-1 • min^-1 norepinephrine. At ECMO removal, the arterial oxygen tension (PaO₂)/FiO₂ ratio was 125 mm Hg.

About 3 hours after weaning, arterial oxygenation worsened. The PaO₂ did not increase to more than 70 mm Hg despite FiO₂ up to 0.80 and a peak airway pressure/positive end-expiratory pressure ratio of 31/6 cm H₂O. Respiratory compliance was 30 mL/cm H₂O, and the Murray adult respiratory distress syndrome score was 2.75. The patient underwent a trial of nitric oxide (NO) inhalation at doses of 10 and 20 ppm. Nitric oxide (900 ppm in N₂) was delivered into the inspiratory limb of the external circuit of the ventilator with a recently developed system (Pulmonox mini; Messer-Griesheim, Gumpoldskirchen, Austria) allowing control of the NO-N₂ mixture administration and continuous monitoring of the delivered NO-NO₂ doses. Within 5 minutes of i-NO administration at 10 ppm, the PaO₂/FiO₂ ratio increased from 68 to 130 mm Hg and the mean pulmonary artery pressure and transpulmonary gradient decreased from 35 to 28 mm Hg and from 20 to 15 mm Hg, respectively, while systemic hemodynamics did not change (cardiac index, 4.4 and 4.3 L • min^-1 • m^-2, respectively; mean arterial pressure, 70 and 69 mm Hg, respectively). The changes in these parameters were maximal at the 10 ppm dose. Prolonged low-dose (7 ± 3 ppm) i-NO administration was started. Brief daily discontinuations of i-NO administration were associated with a nearly 50% decrease in PaO₂/FiO₂ ratio together with a 20% and 25% increase in mean pulmonary artery pressure and transpulmonary gradient, respectively. Although the patient remained responsive and i-NO was well tolerated, administration of the gas was discontinued after 10 days, when residual lung injury was markedly reduced (clear chest roentgenogram and a PaO₂/FiO₂ of 240 mm Hg at an FiO₂ of 0.40 without i-NO) (Fig 1). On day 72, the patient was transferred to a rehabilitation facility.

View larger version (21K): [in this window] [in a new window]   Fig 1. . Changes in transpulmonary gradient (TPG), cardiac index (CI), and arterial oxygen tension/inspired oxygen fraction (PaO2/FiO2) 5 minutes before inhaled nitric oxide (i-NO) administration, during i-NO treatment, and 5 minutes after discontinuation of i-NO treatment.

	Comment

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This case has several interesting features. Coronary artery disease in the graft should be considered in the differential diagnosis of postcardiotomy cardiogenic shock, especially in a clinical setting of otherwise unexplained cardiac failure immediately after transplantation. In the present case, the lack of information about the coronary lesions and the acute, unresponsive, global cardiac failure prevented revascularization.

The heart dysfunction after retransplantation was likely to have been determined by an acute adult respiratory distress syndrome, with consequent hypoxemia and hypoxic pulmonary vasoconstriction. If the transient nature of the left ventricular dysfunction could have been anticipated, it would have been interesting to evaluate the effect of i-NO administration on arterial oxygenation and pulmonary vascular resistance. In fact, i-NO treatment is a valuable alternative to ECMO support in critically ill hypoxic near-term infants [5], and it may represent a therapeutic option in acute reperfusion injury after lung transplantation [6] and in right ventricular dysfunction after cardiac transplantation [4]. However, it is definitely contraindicated when a left heart failure exists [7].

Extracorporeal membrane oxygenation was discontinued as soon as the patient could be managed with noninvasive support. We have no explanation for the worsening of arterial oxygenation that occurred soon after ECMO removal. Because lung function test results were consistent with a residual adult respiratory distress syndrome, NO inhalation was considered the treatment of choice to relieve hypoxemia in view of the evidence that it may increase arterial oxygenation in patients with adult respiratory distress syndrome [3]. Nitric oxide may also exert additional beneficial effects on the right ventricle by reducing mean pulmonary artery pressure and improving right ventricular ejection fraction [8]. In our patient, right ventricular ejection fraction was not measured, but cardiac output did not change after NO administration. Therefore, a positive effect of i-NO on right heart contractility (in terms of right ventricular ejection fraction but not cardiac index) could only be inferred on the basis of mean pulmonary artery pressure reduction during NO treatment. In contrast, NO treatment was associated with a marked reduction in transpulmonary gradient, the values of which are directly related to the risk of right ventricular failure after cardiac transplantation.

Prospective studies are required to define the role of i-NO therapy in the early postoperative management of heart recipients, in whom i-NO, because of the lack of systemic vasodilation, could be more advantageous than prostacyclin and prostaglandin E_1.

	Footnotes

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Address reprint requests to Dr Barzaghi, Servizio di Anestesia e Rianimazione I - Direzione, IRCCS Policlinico San Matteo, Piazzale Golgi, 2, 27100 Pavia, Italy.

	References

Top Footnotes Abstract Introduction Comment References

 

1. Aranki SF, Adams DH, Rizzo RJ, et al. Femoral veno-arterial extracorporeal life support with minimal or no heparin. Ann Thorac Surg 1993;56:149–55.
2. Whyte RI, Deeb GM, McCurry KR, Anderson HL III, Bolling SF, Bartlett RH. Extracorporeal life support after heart or lung transplantation. Ann Thorac Surg 1994;58:754–9.[Abstract/Free Full Text]
3. Bigatello LM, Hurford WE, Kacmarek RM, Roberts JD, Zapol WM. Prolonged inhalation of low concentrations of nitric oxide in patients with severe adult respiratory distress syndrome. Anesthesiology 1994;80:761–70.[Medline]
4. Girard C, Durand PG, Vedrinne C, et al. Inhaled nitric oxide for right ventricular failure after heart transplantation. J Cardiothorac Vasc Anesth 1993;7:481–5.[Medline]
5. Finer NN, Etches PC, Kamstra B, Tierney AJ, Pellowski A, Ryan CA. Inhaled nitric oxide in infants referred for extracorporeal membrane oxygenation: dose response. J Pediatr 1994;124:302–8.[Medline]
6. Adatia I, Lillehei C, Arnold JH, et al. Inhaled nitric oxide in the treatment of postoperative graft dysfunction after lung transplantation. Ann Thorac Surg 1994;57:1311–8.[Abstract/Free Full Text]
7. Girard C, Arvieux C. Inhaled nitric oxide and cardiac surgery. Curr Opin Anesthesiol 1996;9:71–5.
8. Rossaint R, Slama K, Steudel W, et al. Effects of inhaled nitric oxide on right ventricular function in severe acute respiratory distress syndrome. Intensive Care Med 1995;21:197–203.[Medline]

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Mario Viganò Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Barzaghi, N. Articles by Viganò, M. Search for Related Content PubMed PubMed Citation Articles by Barzaghi, N. Articles by Viganò, M.