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Canadian Journal of Anesthesia 48:924-929 (2001)
© Canadian Anesthesiologists' Society, 2001
Neuroanesthesia and Intensive Care

Inhaled prostacyclin (PGI2) is an effective addition to the treatment of pulmonary hypertension and hypoxia in the operating room and intensive care unit

[L'inhalation de prostacycline (PGI2) est un traitement complémentaire efficace de l'hypertension pulmonaire et de l'hypoxie observées en salle d'opération et à l'unité des soins intensifs]

Manon Haché, MD*, André Y. Denault, MD FRCPC*, Sylvain Bélisle, MD FRCPC*, Pierre Couture, MD FRCPC*, Denis Babin, MSc*, Francine Tétrault, pharm MSc{dagger} and Jean-Gilles Guimond, MD FRCPC{ddagger}

* From the Department of Anesthesiology, Montreal Heart Institute, and the
{dagger} Departments Of Pharmacy, and
{ddagger} Medicine Centre Hospitalier de l'Université de Montréal (CHUM), Campus Notre-Dame, Montreal, Quebec, Canada.

Address correspondence to: Dr. A.Y. Denault, Department of Anesthesiology, Montreal Heart Institute, 5000 Belanger Street East, Montreal, Quebec H1T 1C8, Canada. Phone: 514-376-3330, ext. 3732; Fax: 514-376-8784; E-mail: denault{at}videotron.ca


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Purpose: There is a growing interest in the intraoperative and intensive care use of inhaled epoprostenol (PGI2) for the treatment of pulmonary hypertension (PHT) and hypoxia of cardiac or non-cardiac origin. We report our experience with this form of therapy.

Methods: A retrospective chart review of all patients who received inhaled PGI2 over a one-year period was undertaken. Demographic, hemodynamic, oxygenation status, mode of administration, side effects, duration of hospital stay, and mortality were noted.

Results: Thirty-five patients, of which 33 (92%) were in the intensive care unit, received inhaled PGI2. Of the 27 patients whose pulmonary artery pressure (PAP) was monitored, a significant decrease in mean PAP from 34.8 ± 11.8 mmHg to 32.1 ± 11.8 mmHg was observed within one hour after the start of therapy (P=0.0017). Selective pulmonary vasodilatation occurred in 77.8% of the patients. Thirty-three patients had arterial blood gases before and after therapy. There was an improvement in the PaO2/FIO2 ratio in 88% of these with a 175% improvement on average. The ratio of PaO2/FIO2 improved from 108 ± 8 to 138 ± 105 (P=0.001). Six patients (17%) presented hypotension, two had subsequent pneumothorax, one had bronchospasm and in one patient PGI2 inhalation was stopped because of increasing peak pulmonary pressures from the secondary flow coming from the nebulizer. Mortality of the cohort was 54%.

Conclusion: Inhaled PGI2 can be useful in the treatment of patients with PHT and severe hypoxia. It can however be associated with systemic side effects.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
PROSTACYCLIN (PGI2, epoprostenol) is an endogenously produced prostaglandin.1 It is formed by the cyclo-oxygenase pathway of arachidonic acid metabolism. At physiologic pH, it is spontaneously hydrolyzed to 6-keto-prostaglandin-F1{alpha} (6-ketoPGF1{alpha})2 and has a half-life of two to three minutes. Over the years, it has been used for many indications including long-term management of PHT. When given systemically, its use is limited by adverse effects including systemic hypotension and worsening of intrapulmonary shunt.3 Administration by inhalation has been used to improve its pulmonary selectivity. Hence, it reduces pulmonary hypertension (PHT) and improves oxygenation by matching perfusion and ventilation of lung units.4

With approval of our Research and Ethics Committee, we present our one-year experience with nebulized PGI2, including its utilization in the intensive care unit (ICU) and the operating room (OR).


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
We reviewed the medical charts of all patients who received off-protocol nebulized PGI2 from December 1999 to November 2000 in two different hospitals (Notre-Dame Hospital of the Centre Hospitalier de l'Université de Montréal (CHUM) and the Montreal Heart Institute). Demographic data obtained included age, sex and medical history of the patients. We also noted medical conditions that warranted the administration of PGI2, previous or concurrent inhaled nitric oxide (NO) administration, location of use (OR or ICU), method of administration (continuous or bolus) and total dose given. Acute respiratory distress syndrome (ARDS) was defined according to the American European Consensus Conference on ARDS.5 PHT was defined as systolic pulmonary artery pressure superior to 30 mmHg or mean pulmonary artery pressure (MPAP) above 25 mmHg. We noted the response of inhaled PGI2 on the systemic arterial pressure (SAP) and the pulmonary artery pressure (PAP) or central venous pressure (CVP) if no PAP monitoring was installed. We calculated the MPAP and the mean SAP (MSAP) by adding the diastolic pressure to the third of pulse pressure. To better evaluate the selective action of PGI2 on pulmonary hemodynamics, we calculated the ratio of MSAP over MPAP. Gas exchange variables (ratio of arterial partial oxygen pressure to fraction of inspired oxygen (PaO2/FIO2) or arterial oxygen saturation (SaO2) if no arterial blood gases (ABG) were available) were recorded. The pulmonary and systemic hemodynamics as well as gas exchange variables were noted before and after the first dose of medication as well as after the best response achieved during treatment. A positive response to PGI2 was defined as a 10% decrease in MPAP or an increase in PaO2/FIO2 >10%.6 Finally, we noted side effects, length of stay in the hospital and mortality. Patient charts were reviewed until discharge. Those in which the method of administration or the side effects were unexpected, will be described in more detail.

PGI2 (Flolan, Glaxo Wellcome Inc, Mississauga, ON, Canada) was given as epoprostenol salt 1.5 mg dissolved in 100 mL of sterile glycine buffer diluent for a concentration of 15 µg•mL–1. The drug is administered through a conventional in-line nebulizer kit (Ref 8901, Salter Labs, Arvin, CA, USA) with an oxygen flow of 6 L•min–1 connected to the inspiratory limb of the ventilator. For continuous administration, the bag containing the drug is attached to an ice pack and delivered directly in the nebulizer through a volumetric pump.

Statistical analysis
Paired Student's t tests were used to evaluate changes in hemodynamic and oxygenation variables. To determine independent predictors of death, we used unpaired Student' t tests to compare means and chi-square tests for proportions. P <0.05 was considered statistically significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
A total of 37 charts were reviewed. Two were excluded because of insufficient information. Of the 35 remaining patients, 21 (60%) of them were male and 14 (40%) were female. The average age was 56.8 ± 16.5 yr. Inhaled PGI2 was administered to 27 patients (77.1%) for hypoxemia and to eight patients (22.9%) for PHT of various etiologies (TableGo). Most of the patients were treated in the ICU with only two of them treated in the OR. One was treated both in the ICU and the OR. Twenty-two patients (62.9%) received boluses only (60–120 µg) and four patients (11.4%) were treated with continuous inhalation only (60–210 µg•hr–1). Nine patients (25.7%) received a combination of the two. One patient received direct intratracheal boluses without prior nebulization (60 and 105 µg). One patient was treated before intubation with nebulization via face mask. Nine (25.7%) had NO administration before PGI2 administration. Inhaled PGI2 was added when NO was ineffective and the measures were recorded without any changes in the NO concentration.


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  		TABLE
 
Twenty-seven patients (77.8%) were monitored with a PAP catheter while six (17%) had CVP monitoring only. The remaining two patients (6%) had no invasive hemodynamic monitoring. Of the 27 patients whose PAP was monitored, there was a statistically significant decrease in MPAP from before the start of therapy to the first measurement from 34.8 ± 11.8 mmHg to 32.1 ± 11.8 mmHg (P=0.0017) and to the best response 27.5 ± 11.1 mmHg (P <0.0001). Twenty-five (93%) of these patients showed a decrease in MPAP after inhaled PGI2 administration. Twenty-one patients (77.8%) had lowered their MPAP within one hour with a 22% decrease in MPAP on average. The ratio of MSAP to MPAP increased from 2.33 ± 0.87 to 2.53 ± 1.05 (P=0.01) after initial treatment and to 2.86 ± 1.22 (P=0.003) after the best response was noted. The ratio increased in 77.8% of patients. Of the six patients who had only CVP monitoring, there was an initial lowering from 13.4 ± 5.2 mmHg to 11.6 ± 4.4 mmHg (P=0.15) and further to 7.2 ± 5.1 mmHg (P=0.008).

Thirty-three patients (94.3%) had ABG analyzed before and after inhaled PGI2 administration. The ratio of PaO2/FIO2 improved from 108 ± 81 to 138 ± 105 (P=0.001) initially and to 224 ± 134 (P 0.0001) after best improvement. In total, 87.9% of these patients improved their PaO2/FIO2 ratio with a 174.7% improvement on average observed in responders. Two patients did not have ABG either before or after treatment. One was a patient treated in the OR who had a SaO2 of 100% before and after treatment with a FIO2 of 50% and the other was treated in the ICU and improved his SaO2 from 95 to 100% with a FIO2 of 70%.

Six patients (17%) presented hypotension, two had subsequent pneumothoraces, one had bronchospasm and in one patient PGI2 inhalation was stopped because of increasing peak pulmonary pressures from the secondary flow coming from the nebulizer. Nineteen patients died. On average, the patients who died were older than those who survived (49.35 ± 19.2 yr vs 63.2 ± 10.7 yr, P=0.02).


   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
In December 1999, inhalation of PGI2 or epoprostenol was added to our therapeutic armamentarium for treatment of PHT and severe hypoxemia of various etiologies. We believe our experience represents the largest published case series of consecutive patients receiving inhaled PGI2 in the OR and in the ICU. The results presented confirm that this medication can improve oxygenation in patients suffering from hypoxemia in acute pulmonary edema of cardiac or non-cardiac origin, pneumonia, after lung transplant, and in one patient after pulmonary artery thrombectomy following massive pulmonary embolism. It also helped reduce PHT in patients suffering from ARDS, Pickwick's syndrome, massive pulmonary embolism, and after cardiac surgery. Although 92.6% of patients monitored responded with decreasing MPAP, this was associated with an increase in MAP/MPAP in only 74.1% of these, which suggests pulmonary selectivity in most, but not all, cases. It was ineffective in improving oxygenation in four patients including one who had pulmonary edema of neurogenic origin with superimposed pneumonia, one who had pulmonary edema of cardiac origin, one who suffered from massive pulmonary embolism and one who presented with PHT after cardiac surgery with no concomitant hypoxemia. In two patients, PGI2 had no effect on pulmonary hemodynamics. One had lung transplantation and did not have PHT and the other had pulmonary edema of cardiac origin and superimposed pneumonia as well as severe PHT secondary to pulmonary fibrosis and CREST syndrome (Calcinosis, Raynaud's phenomenon, Esophageal motility disorder, Sclerodactyly and Telangiescasia of scleroderma). Recently, Domenighetti suggested that patients with ARDS of pulmonary origin (primary ARDS) will tend to have no response to PGI2 as opposed to those with ARDS from an extrapulmonary origin (secondary ARDS).6 They observed that the computed tomographic appearance of patients with primary ARDS showed more extensive consolidation. Their study however was limited to 15 patients. Also, Walmrath et al. noted that patients with underlying pulmonary fibrosis complicated by pneumonia tended to have a diminished response to inhaled PGI2 compared with those having pneumonia without underlying pulmonary pathology.7

Prostacyclin is known to be a powerful vasodilator through an increase in intracellular cyclic adenosine monophosphate (cAMP). When given systemically, it can have adverse effects such as hypotension and worsening of intrapulmonary shunt. Recently, it has been given by inhalation after nebulization both in animals and humans and this has been shown to increase pulmonary selectivity. PGI2 is not inactivated in the lung like other prostaglandins but is spontaneously hydrolyzed at physiologic pH to an inactive metabolite, 6-ketoPGF1{alpha}. Therefore, when given by inhalation, it tends to be absorbed locally in ventilated areas and is inactivated by the time it reaches the systemic circulation in significant amounts. Many animal models7–13 of hypoxemia and PHT and human studies have confirmed that inhaled PGI2 can improve oxygenation and decrease PHT in many subjects including those suffering from ARDS and PHT of various causes.

Case series are predominant in the literature on PGI2. Pappert et al.14 suggested that side effects and toxicity should be studied more extensively. One of our patients had bronchospasm on two occasions after receiving inhaled prostacyclin. She had a history of CREST syndrome, PHT secondary to lung fibrosis, coronary artery disease, hypertension and diabetes but was not a known asthmatic. A study by Hardy et al.15 demonstrated that PGI2 could exhibit both bronchoconstrictor and antibronchoconstrictor properties when inhaled. They demonstrated that, in asthmatics, inhaled PGI2 can prevent metacholine or PGD2 induced bronchospasm. On the other hand, small airway resistance as measured by forced expiratory volume in one second (FEV1) and maximum expiratory flow at 30% vital capacity (Vmax30) was increased while larger airway resistance, measured by specific airway conductance remained unchanged. They hypothesized that pulmonary vasodilation could enhance the clearance of inhaled bronchoconstrictors while causing engorgement of small airways, thereby increasing resistance. On the other hand, Burghuber did not observe any changes in pulmonary function tests in normal volunteers receiving inhaled PGI2.16

Six patients had hypotension after treatment with inhaled PGI2. It is noteworthy that these patients were suffering from hypotension before the start of therapy. There was a patient with postmyocardial infarction persisting ventricular septal defect who had an intra-aortic balloon pump, a postoperative cardiac surgical patient on vasoactive support, a patient who had dilated cardiomyopathy and suspected septic shock and two patients with septic shock. Hypotension has rarely been encountered after inhaled PGI2 as opposed to iv PGI2 treatment.17 It is possible that ventricular dysfunction in these patients was associated with an improvement in cardiac output through a reduction in afterload, which has been reported with PGI2. Such a reduction in afterload could be associated with a fall in blood pressure but not in cardiac output. This is what we observed in one patient who had hypotension while receiving direct intratracheal boluses. The hypotension was associated with a 25% increase in cardiac index. It is also possible that with direct intratracheal administration or with relatively large nebulized doses that systemic absorption occurred because PGI2 is not inactivated by pulmonary epithelium. This "spillover" into the systemic circulation has been described.18

Inhaled NO has received a fair amount of interest in the last few years as a treatment of ARDS and PHT because of its ability to provoke selective pulmonary vasodilation.19 Its effect remains localized because it is inactivated by hemoglobin as soon as it reaches the circulation. It may, however, have toxic metabolites and can cause methemoglobinemia, especially when given at high concentrations for a long period of time and necessitates specialized and costly equipment to administer. Prostacyclin, on the other hand, has no known toxic metabolites and very few side effects. It can be administered easily by simple nebulization with minimal extra equipment, which is interesting for utilization in the OR. A full 24-hr of treatment, is estimated to cost $115.00 CDN. Several studies have compared NO and PGI2. Some authors have observed a better reduction in PAP with inhaled PGI217,20,21 while some show no significant difference between the two agents.18,22 Improvement in oxygenation sometimes appears to be better with NO,20 or with inhaled PGI2.23 Others showed no differences between the two agents.22 It should be noted that in all these studies, the administration of inhaled PGI2 was not controlled or randomized and that the doses used are not necessarily equipotent to NO.

Our study has several limitations. First, it is a retrospective study. Second, patients had very different pathologies bringing about the use of inhaled prostacyclin. This may explain why some responded sooner than others and why others required escalating doses of prostacyclin, becoming somewhat resistant to the drug. Some authors have reported inhaled PGI2 to be associated with in vitro hemostatic disturbances16,23 but this remains controversial. We did not explore this aspect. In addition, we could not determine the aerosol fraction that was deposited in the lung. This has been estimated to be less than 5% in mechanically ventilated patients.24,25

In summary, inhaled prostacyclin is a useful and affordable addition to anesthesiologists and intensivists in the treatment of PHT and hypoxia of various origins. Systemic absorption can occur despite administration by the inhaled route. Further studies are required to determine dose-responsiveness, optimal condition of utilization and impact on survival.


   Footnotes
 
This study was supported by the "Plan de Pratique des Anesthésistes" of the Montreal Heart Institute.

Revision received July 11, 2001. Accepted for publication May 18, 2001.


   References
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Moncada S, Korbut R, Bunting S, Vane JR. Prostacyclin is a circulating hormone. Nature 1978; 273: 767–8.[Medline]

2 Kerins DM, Murray R, FitzGerald GA. Prostacyclin and prostaglandin E1: molecular mechanisms and therapeutic utility. Prog Hemost Thromb 1991; 10: 307–37.[Medline]

3 Olschewski H, Ghofrani HA, Walmrath D, et al. Inhaled prostacyclin and iloprost in severe pulmonary hypertension secondary to lung fibrosis. Am J Respir Crit Care Med 1999; 160: 600–7.[Abstract/Free Full Text]

4 Walmrath D, Schneider T, Pilch J, Grimminger F, Seeger W. Aerosolised prostacyclin in adult respiratory distress syndrome. Lancet 1993; 342: 961–2.[Medline]

5 Bernard GR, Artigas A, Brigham KL, et al. Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Consensus Committee. J Crit Care 1994; 9: 72–81.[Medline]

6 Domenighetti G, Stricker H, Waldispuehl B. Nebulized prostacyclin (PGI2) in acute respiratory distress syndrome: impact of primary (pulmonary injury) and secondary (extrapulmonary injury) disease on gas exchange response. Crit Care Med 2001; 29: 57–62.[Medline]

7 Walmrath D, Schermuly R, Pilch J, Grimminger F, Seeger W. Effects of inhaled versus intravenous vasodilators in experimental pulmonary hypertension. Eur Respir J 1997; 10: 1084–92.[Abstract]

8 Welte M, Zwissler B, Habazettl H, Messmer K. PGI2 aerosol versus nitric oxide for selective pulmonary vasodilation in hypoxic pulmonary vasoconstriction. Eur Surg Res 1993; 25: 329–40.[Medline]

9 Zobel G, Dacar D, Rodl S, Friehs I. Inhaled nitric oxide versus inhaled prostacyclin and intravenous versus inhaled prostacyclin in acute respiratory failure with pulmonary hypertension in piglets. Pediatr Res 1995; 38: 198–204.[Medline]

10 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.[Medline]

11 Booke M, Bradford DW, Hinder F, et al. Effects of inhaled nitric oxide and nebulized prostacyclin on hypoxic pulmonary vasoconstriction in anesthetized sheep. Crit Care Med 1996; 24: 1841–8.[Medline]

12 Kleen M, Habler O, Hofstetter C, et al. Efficacy of inhaled prostanoids in experimental pulmonary hypertension. Crit Care Med 1998; 26: 1103–9.[Medline]

13 Hill LL, Pearl RG. Combined inhaled nitric oxide and inhaled prostacyclin during experimental chronic pulmonary hypertension. J Appl Physiol 1999; 86: 1160–4.[Abstract/Free Full Text]

14 Pappert D, Busch T, Gerlach H, Lewandowski K, Radermacher P, Rossaint R. Aerosolized prostacyclin versus inhaled nitric oxide in children with severe acute respiratory distress syndrome. Anesthesiology 1995; 82: 1507–11.[Medline]

15 Hardy CC, Bradding P, Robinson C, Holgate ST. Bronchoconstrictor and antibronchoconstrictor properties of inhaled prostacyclin in asthma. J Appl Physiol 1988; 64: 1567–74.[Abstract/Free Full Text]

16 Burghuber OC, Silberbauer K, Haber P, Sinzinger H, Elliott M, Leithner C. Pulmonary and antiaggregatory effects of prostacyclin after inhalation and intravenous infusion. Respiration 1984; 45: 450–4.[Medline]

17 Olschewski H, Walmrath D, Schermuly R, Ghofrani A, Grimminger F, Seeger W. Aerosolized prostacyclin and iloprost in severe pulmonary hypertension. Ann Intern Med 1996; 124: 820–4.[Abstract/Free Full Text]

18 Walmrath D, Schneider T, Pilch J, Schermuly R, Grimminger F, Seeger W. Effects of aerosolized prostacyclin in severe pneumonia. Impact of fibrosis. Am J Respir Crit Care Med 1995; 151: 724–30.[Abstract]

19 Troncy E, Francoeur M, Blaise G. Inhaled nitric oxide: clinical applications, indications, and toxicology. Can J Anaesth 1997; 44: 973–88.[Abstract/Free Full Text]

20 Zwissler B, Kemming G, Habler O, et al. Inhaled prostacyclin (PGI2) versus inhaled nitric oxide in adult respiratory distress syndrome. Am J Respir Crit Care Med 1996; 154: 1671–7.[Abstract]

21 Mikhail G, Gibbs J, Richardson M, et al. An evaluation of nebulized prostacyclin in patients with primary and secondary pulmonary hypertension. Eur Heart J 1997; 18: 1499–504.[Abstract/Free Full Text]

22 Haraldsson A, Kieler-Jensen N, Nathorst-Westfelt U, Bergh CH, Ricksten SE. Comparison of inhaled nitric oxide and inhaled aerosolized prostacyclin in the evaluation of heart transplant candidates with elevated pulmonary vascular resistance. Chest 1998; 114: 780–6.[Abstract/Free Full Text]

23 van Heerden PV, Gibbs NM, Michalopoulos N. Effect of low concentrations of prostacyclin on platelet function in vitro. Anaesth Intensive Care 1997; 25: 343–6.[Medline]

24 Thomas SH, O'Doherty MJ, Fidler HM, Page CJ, Treacher DF, Nunan TO. Pulmonary deposition of a nebulised aerosol during mechanical ventilation. Thorax 1993; 48: 154–9.[Abstract]

25 MacIntyre NR, Silver RM, Miller CW, Schuler F, Coleman RE. Aerosol delivery in intubated, mechanically ventilated patients. Crit Care Med 1985; 13: 81–4.[Medline]




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