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Ann Thorac Surg 2002;73:1299-1301
© 2002 The Society of Thoracic Surgeons

Case report

Successful treatment of pulmonary hypertension with inhaled nitric oxide after pulmonary embolectomy

Georg Trummer, MD*a, Michael Berchtold-Herz, MDa, Jürgen Martin, MDa, Friedhelm Beyersdorf, MDa

a Department of Cardiovascular Surgery, Albert-Ludwigs-University Freiburg, Freiburg, Germany

Accepted for publication August 14, 2001.

* Address reprint requests to Dr Trummer, Department of Cardiovascular Surgery, Albert-Ludwigs-University Freiburg, Hugstetter Straße 55, D-79106 Freiburg, Germany
e-mail: georg_trummer{at}yahoo.com


   Abstract
Top
 Abstract
Introduction
 Comment
 References
 
Inhaled nitric oxide is an agent known to reduce pulmonary vascular resistance and prevent right heart failure. Pulmonary embolism is frequently followed by right heart failure and cardiogenic shock. Although successful treatment of patients with right ventricular failure caused by pulmonary embolism has been reported, clinical use of inhaled nitric oxide as an adjunct to surgical treatment is not in widespread use. We present a case of a 69-year-old woman with massive pulmonary embolism followed by right ventricular failure. After emergency operation, weaning from ventilation was prolonged. Pulmonary hypertension was decreased with low-dose inhaled nitric oxide, although pulmonary gas exchange did not improve. The patient was weaned successfully from ventilation 52 hours after operation and recovered completely. In a follow-up examination after 9 months, the patient is in healthy constitution with good cardiopulmonary function.


   Introduction
Top
 Abstract
 Introduction
Comment
 References
 
Massive pulmonary embolism is still associated with a high early mortality [1], and emergency surgical treatment before cardiac arrest occurs is mandatory [2, 3]. Postoperatively right heart failure is one of the main causes of death in the perioperative period [2, 4]. Pulmonary emboli result in active pulmonary vasoconstriction caused by release of vasoactive humoral factors from activated platelets [5]. Serotonin and thromboxane A2 are considered to be most important vasoactive factors [6]. In addition, incomplete embolectomy and cardiopulmonary bypass itself can cause pulmonary hypertension. Inhaled nitric oxide (iNO) acts as a powerful selective pulmonary vasodilator and can reduce pulmonary hypertension and improve gas exchange [7, 8]. Inhaled nitric oxide has been successfully used to treat other causes of pulmonary hypertension, such as that occurring after mitral valve replacement [9], pulmonary thromboendarterectomy [10], implantation of left ventricular assist systems [11], and cardiac transplantation [12]. Furthermore, investigations in pigs showed a beneficial effect of iNO owing to an inhibitory effect on platelet aggregation [13]. However, use of iNO after pulmonary embolectomy is not very common. We report a case of fulminant pulmonary emboli in which iNO was used as an adjunct to pulmonary embolectomy.

A 69-year-old woman with coronary heart disease underwent uneventful percutaneous transluminal coronary angioplasty. To prevent bleeding from the puncture site of the femoral artery, a pressure dressing was applied. The next day, the dressing was removed and bed rest was abolished. While the patient was mobilized, signs of circulatory collapse were obvious. Echocardiography showed a dilated right atrium and an enlarged right ventricle with good left ventricular function. Furthermore, a large floating mass in the right atrium was detected. This mass prolapsed through the tricuspid valve in the right ventricle. Duplex sonography showed a deep vein thrombosis of the lower leg. Following the standardized protocol for acute pulmonary emboli and deep vein thrombosis, a bolus of 10,000 IU heparin was administered intravenously at the time of admission to the hospital. A continuous venous infusion of 20,000 IU heparin for the next 24 hours was established, and no vena cava filter was inserted. To prevent further embolization an emergency operation was performed.

Surgical thrombectomy of the right atrium, right ventricle, superior and inferior venae cavae, and the pulmonary mainstem artery, including the right and left pulmonary arteries, was performed. Weaning from cardiopulmonary bypass was only possible with moderate inotropic agents (epinephrine, 0.2 µg · kg-1 · min-1; dobutamine, 3 µg · kg-1 · min-1). Hemodynamic monitoring was performed with a Swan-Ganz catheter.

Immediately after the patient was transferred to the intensive care unit, her hemodynamics were poor with a cardiac index (CI) of 1.1 L · min-1 · m-2 and a pulmonary vascular resistance of 520 dyne · s · cm-5. To prevent right ventricular failure we started to administer iNO in the inspiratory limb of the ventilator (Evita 4, Dräger, Lübeck, Germany). A gas mixture that contained nitric oxide in a concentration of 600 ppm (Messer Spezialgase, Griesheim, Germany) was used. Administration was controlled with a flowmeter (Rota Yokogawa, Lörrach, Germany) that was calibrated for nitrogen. The administered flow was calculated based on the current breathing volume per minute and the required nitric oxide concentration in the inspiratory limb. Nitric oxide concentration was controlled daily using a gas analyzer (Ecophysics AL 300 med, Munich, Germany).

Low doses of iNO (20 ppm) were necessary to reduce the pulmonary vascular resistance to 220 dyne · s · cm-5 (CI, 2.4 L · min-1 · m-2) within 1 hour after operation. Pulmonary vascular resistance remained low during the subsequent hours. For this reason we started weaning from iNO 7 hours later; iNO was reduced to 10 ppm, and 1 hour later, to 5 ppm. As hemodynamics were stable at this time (CI, 2.5 L · min-1 · m-2) and pulmonary vascular resistance remained low (144 dyne · s · cm-5), iNO was discontinued after a total time of 10 hours.

Pulmonary vascular resistance increased again to 295 dyne · s · cm-5 24 hours later. Although epinephrine and dobutamine were increased to medium doses, CI remained low at 2.1 L · min-1 · m-2. Echocardiography showed an enlarged right atrium and ventricle, although left ventricular function was good. To prevent right heart failure because of an increased pulmonary vascular resistance, iNO was started again with 10 ppm. Two hours later CI increased to 2.4 L · min-1 · m-2, whereas pulmonary vascular resistance decreased to 240 dyne · s · cm-5. Five hours later CI was at 3.0 L · min-1 · m-2 and pulmonary vascular resistance at a low level (188 dyne · s · cm-5). Inhaled nitric oxide was stopped again after a second total period of 10 hours. Echocardiography showed a better function of the right ventricle, and the right atrium was not enlarged anymore. Twelve hours after iNO was stopped, extubation was performed. According to stable hemodynamics, inotropic agents were reduced and stopped after another 48 hours.

The patient was ventilated (Evita 4, Dräger) for a total time of 52 hours. Biphasic positive airway pressure ventilation was used with the fraction of inspired oxygen between 0.4 and 0.7 and a positive end-expiratory pressure of 5 cm H2O. Inspiratory to expiratory time ratio was 1:1.5. Because of the massive pulmonary embolism, gas exchange was restricted. To reach a minimum arterial oxygen pressure of 80 mm Hg, reduction of the inspired oxygen fraction lower than 0.5 was not possible within the first 28 hours. Arterial carbon dioxide pressure was always in the physiologic range. After onset of iNO there was no improvement in pulmonary gas exchange. After extubation was performed there was a demand of 5 L of oxygen by face mask for another 4 days to prevent hypoxemia. During the whole stay in the intensive care unit, methemoglobin concentration never exceeded 1.3%.

Once oral anticoagulation with coumarin was established as sufficient, the continuous intravenous heparin infusion with 20,000 IU heparin per day was stopped. No long-term vena cava filter to prevent further emboli was inserted.

Further postoperative course was without complications, and the patient was discharged 14 days later from the hospital. During a follow-up examination after 9 months, the patient is in healthy constitution with good cardiopulmonary function.


   Comment
Top
 Abstract
 Introduction
 Comment
References
 
The patient was admitted to the hospital because of suspicion of acute pulmonary emboli (grade III to IV) after a deep venous thrombosis after percutaneous transluminal coronary angioplasty. For this grade of pulmonary emboli, a therapeutic decision has to be made between thrombolysis or pulmonary embolectomy [14]. Depending on the grade of pulmonary emboli and the used agent of thrombolysis, hemodynamic stabilization is described in many randomized trials [15, 16]. Because of the large masses of thrombi in the right atrium, the critical hemodynamic situation, and the existing contraindication for thrombolysis after arterial puncture, an emergency operation was indicated.

In cardiac operation, iNO is used routinely for pulmonary hypertension after mitral valve replacement, pulmonary thromboendarterectomy, implantation of left ventricular assist devices, or cardiac transplantation [9–11]. However, there are only a few reports about the use of iNO after emergency pulmonary embolectomy [10, 13, 17], and our case report underscores the importance of reducing pulmonary vascular resistance by iNO and thereby preventing right heart failure.

Although thrombotic masses were removed from the pulmonary arteries in an emergency surgical procedure, pulmonary vascular resistance remained high despite removal of emboli from the main truncus and the larger pulmonary branches. Besides residual emboli in peripheral pulmonary arteries, vasoconstriction could have been caused by release of vasoconstrictors from the thrombus and the cardiopulmonary bypass [5]. Using iNO, a sudden decrease of pulmonary vascular resistance in combination with improved hemodynamics was observed. This enabled us to reduce inotropic agents and start weaning from ventilation.

In the literature there is evidence of improved pulmonary gas exchange after iNO treatment [5, 17]; however, other authors describe no improvement in gas exchange owing to reduced pulmonary vascular tone. In our case, gas exchange was restricted. Although the arterial partial pressure of oxygen was lowered constantly, requiring a higher inspired fraction of oxygen, the arterial partial pressure of carbon dioxide was in the regular range. There was no difference whether iNO was administered or not.

We conclude that low-dose iNO is an easy and safe way to prevent right heart failure in patients after pulmonary embolism. In our case pulmonary gas exchange did not improve, but pulmonary vascular resistance decreased within 1 hour to the normal range. Although surgical therapy is preferred in cases with thrombotic masses in the right atrium or ventricle, iNO can be useful in the preoperative or postoperative period. Furthermore, platelet aggregation is an important factor in the genesis of thrombotic masses, and iNO inhibits platelet aggregation. This additional effect may reduce platelet thrombi in pulmonary resistance vessels [12].


   References
Top
 Abstract
 Introduction
 Comment
 References
 

  1. Anderson F.A., Wheeler H.B., Goldberg R.J. A population based perspective of the hospital incidence and case fatality rates of venous thrombosis and pulmonary embolism: the Worcester DVT study. Ann Intern Med 1991;151:933-938.
  2. Jakob H., Vahl C., Lange R., Micek M., Tanzeem A., Hagl S. Modified surgical concept for fulminant pulmonary embolism. Eur J Cardiothorac Surg 1995;9:557-561.[Abstract]
  3. Satter P. Medikamentöse oder invasive Behandlung der Lungenarterienembolie-Operation. Verh Dtsch Ges Inn Med 1991;96:364-371.
  4. Doerge H.C., Schoendube F.A., Loeser H., Walter M., Messmer B.J. Pulmonary embolectomy: review of a 15 year experience and role in the age of thrombolytic therapy. Eur J Cardiothorac Surg 1996;10:952-957.[Abstract]
  5. Schenk P., Mittermayer C., Ratheiser K. Inhaled nitric oxide in a patient with severe pulmonary embolism. Ann Emerg Med 1999;33:710-714.[Medline]
  6. Manny J., Hechtmann H.B. Vasoactive humoral factors. In: Goldhaber S.Z., ed. Pulmonary embolism and deep venous thrombosis. Philadelphia: WB Saunders, 1985:283.
  7. Rossaint R., Falke K.J., Lopez F., et al. Inhaled nitric oxide for the adult respiratory distress syndrome. N Engl J Med 1993;328:399-405.[Abstract/Free Full Text]
  8. Melot C., Vermeulen F., Maggiorini M., Gilbert E., Naeije R. Site of pulmonary vasodilatation by inhaled nitric oxide in microembolic lung injury. Am J Respir Crit Care Med 1997;156:75-85.[Abstract/Free Full Text]
  9. Girard C., Lehot J.J., Pannetier J.C., et al. Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension. Anesthesiology 1992;77:880-883.[Medline]
  10. Pinelli G., Mertes P.M., Carteaux J.P., et al. Inhaled nitric oxide as an adjunct to pulmonary thromboendarterectomy. Ann Thorac Surg 1996;61:227-229.[Abstract/Free Full Text]
  11. Mertes P.M., Pinelli G., Hubert T., et al. Impact of nitric oxide inhalation on right ventricular failure after implantation of Novacor left ventricular assist system. J Thorac Cardiovasc Surg 1995;109:1251.
  12. Girard C., Durand P.G., Vedrinne C., et al. Inhaled nitric oxide for right ventricular failure after heart transplantation. J Cardiothoracic Vasc Anesth 1993;7:481-485.[Medline]
  13. Gries A., Bott B.W., Dorsam J., et al. Inhaled nitric oxide inhibits platelet aggregation after pulmonary embolism in pigs. Anesthesiology 1997;86:387-393.[Medline]
  14. Seifried E., Heinrich F. Lungenembolie. Stuttgart: Georg Thieme Verlag, 2000:82-85.
  15. Goldhaber S.Z., Haire W.D., Feldstein M.L., et al. Alteplase versus heparin in acute pulmonary embolism: randomized trial assessing right ventricular function and pulmonary perfusion. Lancet 1993:507-511.
  16. Meneveau N., Schiele F., Vuillemenot A., et al. Streptokinase vs alteplase in massive pulmonary embolism. A randomized trial assessing right heart hemodynamics and pulmonary vascular obstruction. Eur Heart J 1997:1141-1148.
  17. Capellier G., Jacques T., Balvay P., et al. Inhaled nitric oxide in patients with pulmonary embolism. Intensive Care Med 1997;23:1089-1092.[Medline]




This Article
Right arrow Abstract Freely available
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Right arrow Author home page(s):
Friedhelm Beyersdorf
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Right arrow Articles by Trummer, G.
Right arrow Articles by Beyersdorf, F.
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Right arrow Articles by Trummer, G.
Right arrow Articles by Beyersdorf, F.
Related Collections
Right arrow Lung - other

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