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(Chest. 2000;118:39-46.)
© 2000 American College of Chest Physicians

Effects of Nitric Oxide Inhalation After Pulmonary Thromboendarterectomy for Chronic Pulmonary Thromboembolism*

Hideaki Imanaka, MD; Hiroshi Miyano, MD; Muneyuki Takeuchi, MD,; Keiji Kumon, MD, and Motomi Ando, MD

* From the Surgical Intensive Care Unit, National Cardiovascular Center, Osaka, Japan.

Correspondence to: Hideaki Imanaka, MD, Surgical Intensive Care Unit, National Cardiovascular Center, 5–7-1 Fujishiro-dai, Suita, Osaka, Japan 565-8565; e-mail: imanakah{at}hsp.ncvc.go.jp


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: To examine the hypothesis that nitric oxide (NO) inhalation improves hemodynamics and gas exchange in patients with chronic pulmonary thromboembolism after pulmonary thromboendarterectomy.

Design: Prospective crossover clinical study.

Setting: Surgical ICU in a national education and research hospital.

Patients: Seven patients (mean age ± SD, 54 ± 11 years) who underwent elective pulmonary thromboendarterectomy for chronic pulmonary thromboembolism.

Interventions: Patients breathed 20 parts per million of NO gas for 30 min at 12-h intervals until extubation of the trachea.

Measurements and results: Hemodynamics and arterial blood gas levels were analyzed before, during, and after NO inhalation. Waveform of pulmonary artery pressure (PAP) was evaluated using fractional pulse pressure (PPf): (systolic PAP - diastolic PAP)/mean PAP. After surgery, pulmonary vascular resistance decreased, PPf decreased, and cardiac index increased significantly. At the first trial, NO inhalation resulted in a slight improvement in arterial oxygen tension (from 173 ± 33 to 196 ± 44 mm Hg; p < 0.05), while hemodynamics did not change significantly. Twelve hours later, NO inhalation decreased pulmonary vascular resistance index (from 312 ± 98 to 277 ± 93 dyne·s·cm-5/m2; p < 0.01), while the change in oxygenation was not significant.

Conclusions: Immediately after pulmonary thromboendarterectomy for chronic pulmonary thromboembolism, NO inhalation improved oxygenation; at 12 h after surgery, NO inhalation resulted in decreased pulmonary vascular resistance, although both changes were small.

Key Words: chronic pulmonary thromboembolism • fractional pulse pressure • nitric oxide inhalation • pulmonary thromboendarterectomy


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Chronic pulmonary thromboembolism (CPTE) shows poor prognosis due to right ventricular failure induced by severe pulmonary hypertension and progressive hypoxia.1 2 3 4 Pulmonary thromboendarterectomy (PTE) has recently been proposed as surgical correction for CPTE.5 6 After the surgery, several mechanisms, such as reperfusion lung edema,7 remaining emboli, and exacerbation of underlying peripheral vascular disease,8 9 10 may cause pulmonary hypertension. To prevent right ventricular failure due to residual pulmonary hypertension, treatment with prostaglandin I2 analog and prostaglandin E14 11 have been proposed. Owing to their nonselective effect on systemic vasculature, however, resultant systemic hypotension may limit their use in treating pulmonary hypertension after PTE.

Inhaled nitric oxide (NO) is a potent pulmonary vasodilator. NO inhalation can decrease pulmonary vascular resistance (PVR) associated with minimally affecting systemic vascular resistance in ARDS,12 13 postcardiac surgery pulmonary hypertension,14 primary pulmonary hypertension,15 and persistent pulmonary hypertension of the newborn.16 Therefore, NO inhalation might be expected to decrease PVR after PTE, without causing hemodynamic instabilities. In fact, some case reports have suggested that NO inhalation improves postsurgical pulmonary hypertension and hypoxia after PTE.17 18 There have been, however, no systematic studies to determine the effects of NO inhalation on hemodynamics and gas exchange after PTE for CPTE.

To test the hypothesis that NO inhalation improves hemodynamics and gas exchange after PTE for CPTE, we designed a prospective study of patients.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
This study was approved by the institutional ethics committee on human research, and informed consent was obtained from each patient and his or her family. In this study, we enrolled seven consecutive patients with CPTE (mean age ± SD, 54 ± 11 years) who underwent elective surgery of PTE from 1998 to 1999.

Preoperatively, the patients demonstrated hypoxia at rest (PaO2, 38.9 to 69.8 mm Hg), dyspnea, and, with New York Heart Association (NYHA) functional class II in one patient and class III in six patients, restricted activity (Table 1 ). Six patients required oxygen therapy at home. Cardiac catheterization showed marked pulmonary hypertension (systolic pulmonary artery pressure [PAP], 74.0 ± 15.3 mm Hg) and low cardiac index (1.89 ± 0.34 L/min/m2; Table 2 ). Lung perfusion scintigrams revealed, in four patients, multiple defects in both lungs; in three patients, multiple defects were found, mainly in the right lung. Pulmonary arteriograms revealed occlusion and stenosis from the lobar to segmental arteries. Deep vein thrombosis was established in all patients. Three patients showed hyperlipidemia, and another had blood coagulation abnormalities with deficiencies of protein C, protein S, and antithrombin III.


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  		Table 1.. Patient Profile*

 

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  		Table 2.. Preoperative and Postoperative Cardiac Catheterization*

 
Operation and Postoperative Care
A Greenfield filter was inserted in the inferior vena cava of each patient before PTE surgery, and all patients had been receiving anticoagulation therapy. All patients electively underwent PTE surgery by median sternotomy under deep hypothermia (16°C) and intermittent circulatory arrest.5 6 Other relevant surgical data were as follows: duration of anesthesia, 414 ± 35 min; operation, 312 ± 45 min; cardiopulmonary bypass, 186 ± 29 min; aortic clamp, 132 ± 33 min; and total circulatory arrest, 62 ± 30 min. Average bleeding volume was 654 mL, and four patients received allotransfusion (400 to 1,460 mL).

When the patients were admitted to the ICU, they were sedated with IV administration of fentanyl, 0.5 to 1 g/kg/h, at least for 12 h. On admission to the ICU, prostaglandin E1, 26 ± 9 ng/kg/min, was administered in all patients; nitroglycerin, 0.42 ± 0.21 µg/kg/min, in five patients; and dobutamine, 5.3 ± 2.7 µg/kg/min, in six patients. These sedatives and vasodilators were adjusted by attending physicians independently of the study protocol, although their dosages were fixed during each measurement.

The mechanical ventilation settings (model 8400STi; Bird Products; Palm Springs, CA) were as follows: synchronized intermittent mandatory ventilation (SIMV), pressure-controlled ventilation (PCV), respiratory rate of 10 to 15 breaths/min, and pressure support ventilation (PSV) of 10 cm H2O. We adjusted the pressure control level and fraction of inspired oxygen (FIO2) to obtain a tidal volume of 10 mL/kg and PaO2 > 100 mm Hg. The respiratory rate was adjusted to keep mild hypocapnia (PaCO2 of about 35 to 40 mm Hg). In practice, the initial settings were as follows: SIMV rate, 11.6 ± 2.4 breaths/min; PCV, 14.7 ± 2.8 cm H2O; and FIO2, 0.59 ± 0.17. Our ventilatory weaning policy was to decrease the SIMV rate, to decrease FIO2 to < 0.5, and then to evaluate respiratory condition with PSV of 7 to 10 cm H2O; if judged appropriate, endotracheal tubes were removed.19 We chose pressure-limit ventilation modes such as PCV and PSV because the restriction of peak inspiratory pressure was necessary to prevent barotrauma.20

Protocols
After waiting 2 to 3 h for hemodynamics to stabilize after surgery, we started the measurements. After baseline measurements remained stable for 30 min, the first preinhalation data were collected. Then, inhalation of NO was carried out in a crossover fashion. Inhalation of NO at 20 parts per million (ppm) was instituted for 30 min, and data were collected. In addition, 30 min after the termination of NO inhalation, a third set of measurements was taken. This on/off trial of NO inhalation was repeated every 12 h until the patient was extubated.

The NO inhalation delivery system has been described elsewhere.13 21 Briefly, 400 ppm of NO in N2 (Kyoto Medical Gas KK; Kyoto, Japan) was mixed with air using an oxygen/air blender (Bird Products). The blender outlet was connected to the high-pressure air inlet of the ventilator. The blender was adjusted to deliver 20 ppm of NO. The inspired NO concentration was analyzed with an NO analyzer (NOA280; Sievers Instruments; Boulder, CO). Constant FIO2 was maintained during each measurement using a medical gas analyzer (M1025B; Hewlett Packard; Andover, MA). Ventilatory parameters, including FIO2, positive end-expiratory pressure (PEEP), PCV level, and minute ventilation, were maintained constant during each NO trial.

Parameters
BP was measured at the radial artery. A 7.5F Swan-Ganz catheter (Abbott Laboratories; North Chicago, IL) was inserted at the right common jugular vein. Cardiac output was measured with a thermodilution technique by injecting 10 mL of cold saline solution. This procedure was repeated four or five times and averaged. BP, PAP, central venous pressure, and ECG data were digitally stored at a sampling rate of 200 Hz/channel using Windaq data acquisition software (Dataq Instruments; Akron, OH). The pressures were calibrated to 50 mm Hg using a mercury manometer. Systolic, diastolic, and mean PAP data were obtained at end expiration. Five measurements were performed and averaged. To evaluate the pulsatility of the pulmonary artery, we calculated the fractional pulse pressure (PPf) as follows: PPf = (systolic PAP - diastolic PAP)/mean PAP.22 Reports suggest that PPf is a key value in interpreting PAP wave form and in differentiating CPTE from primary pulmonary hypertension.22 23 CPTE involves a relatively proximal section of the pulmonary artery, and we speculate that pathologic changes caused by PTE surgery may cause changes in the PAP waveform and in PPf.

Statistical Analysis
Data are shown as mean ± SD. Analysis of variance was used to compare the means of different conditions. Where applicable, post hoc analysis was performed using a two-tailed paired t test with Bonferroni’s correction. Statistical significance was accepted at a level of p < 0.05.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Extubation was done after 37 ± 26 h (range, 15 to 90 h) in the ICU, and none of the patients needed reintubation. At 24 h and 36 h after surgery, only three subjects were studied, because the NO trial was performed in intubated patients. Length of ICU stay was 4.3 ± 2.3 days (range, 2 to 9 days). Six of the patients were discharged from the hospital. On postoperative day 15, one patient died due to sudden hemoptysis following hypoxia and circulatory deterioration. Compared with preoperative data, PAP and PVR decreased, and cardiac index increased after PTE surgery (Table 2) . New York Heart Association functional class evaluations improved to class I in four patients and to class 2 in two patients. Immediately after PTE, the PPf also significantly decreased, from 1.18 ± 0.14 (Table 2) to 0.82 ± 0.19 (Table 3 Go ; p < 0.01).


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  		Table 3.. Effects of NO Inhalation at Each Measurement*

 

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  		Table 3A.. Continued

 
Throughout the protocol, the institution and termination of NO inhalation was performed safely without any sign of rebound phenomena. The first NO trial was performed after 2 to 3 h stabilization of hemodynamics in the ICU. The first trial of NO inhalation resulted in a slight but statistically significant increase in PaO2 (173 ± 33 to 196 ± 44 mm Hg; p < 0.05), while cardiac index and PAPs did not change significantly (Fig 1 , top, A, and Table 3 ). After the second inhalation of NO, 12 h later, PVRI and systolic PAP decreased significantly without a significant change in PaO2 (Fig 1 , top, A, and Table 3 ). At 24 h and 36 h, statistical significance was diminished due to the decreased number of patients, although we observed changes in gas exchange and in hemodynamics similar to those at 12 h (Fig 1 , bottom, B, and Table 3 ). Throughout the protocol, arterial BP was stable regardless of NO inhalation. There were no consistent reductions in systemic vascular resistance index (SVRI) observed over time during the measurement. After NO inhalation, PaO2 and pulmonary vascular resistance index (PVRI) returned to the baseline values (Fig 2 ).



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  		Figure 1.. Effects of each period of postoperative NO inhalation on variables. Top, A: at 0 h and 12 h in the ICU. Bottom, B: at 24 h and 36 h in the ICU. The effects are shown as percentage change from the baseline. The first trial of NO inhalation was performed after 2 to 3 h stabilization of hemodynamics in the ICU. Measurement was repeated every 12 h until extubation. At 24 h and 36 h after surgery, only three subjects were studied because the NO trial was performed in intubated patients. Evaluated variables are PaO2, cardiac index (CI), systolic and mean PAPs (PAs and PAm), PVRI, mean BP (BPm), and SVRI. *p < 0.05 vs baseline; #p < 0.01 vs baseline.

 


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  		Figure 2.. PaO2, PVRI, and cardiac index before, during, and after postoperative NO inhalation. The first trial of NO inhalation was performed after 2 to 3 h stabilization of hemodynamics in the ICU. Measurement was repeated every 12 h. At 24 h and 36 h after surgery, only three subjects were studied because the NO trial was performed in intubated patients. Data are for before, during, and after NO inhalation. *p < 0.05 vs baseline; #p < 0.01 vs baseline.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The main findings of this study are as follows: (1) After PTE for CPTE, pulmonary hypertension improved, and (2) inhalation of NO immediately after surgery improved oxygenation without significantly changing pulmonary hemodynamics, whereas >= 12 h after surgery it decreased PVR without a significant change in oxygenation.

PTE and Clinical Implication of NO Inhalation
Our findings that hemodynamics and gas exchange improve in CPTE patients after PTE correlate with reports of San Diego group (Table 2) .2 3 4 24 PTE has been widely performed as surgical treatment; however, reperfusion lung edema resulting in hypoxia and the need for prolonged mechanical ventilation is a common postoperative complication.7 Several mechanisms have been suggested to account for pulmonary hypertension that occurs even when thrombi in the proximal pulmonary artery have been successfully removed after PTE. Reperfusion lung edema itself can cause pulmonary hypertension.7 The adverse effects of cardiopulmonary bypass may also result in pulmonary hypertension.14 The remodeling of small distal arteries in nonoccluded areas may be associated with pulmonary hypertension in CPTE, because pulmonary hypertension is more severe in CPTE than in acute pulmonary embolism even with comparable degrees of vascular obstruction.8 Moser and Bloor10 have reported pulmonary hypertensive changes in the small pulmonary arteries downstream from nonthrombosed arteries.

Several strategies, such as vasodilatation and NO inhalation, are indicated for treating postoperative pulmonary hypertension in CPTE.4 Although the use of vasodilators to prevent pulmonary vasoconstriction makes sense, their use is limited by the adverse systemic vasodilatation associated with hypotension and impairment of myocardial perfusion, which may lead to right ventricular failure.18 On the other hand, inhaled NO is a potent pulmonary vasodilator, and its use is not usually accompanied by severe adverse systemic effects. Thus, inhaled NO is suitable for treating persistent pulmonary hypertension and gas exchange impairment after PTE.17 18

In this prospective study, we found that immediately after PTE, the inhalation of NO improved oxygenation significantly, and it decreased PVR and PAPs in the later phase. An improvement of oxygenation during NO, similarly in ARDS,12 13 may result from redistribution of pulmonary blood flow from poorly ventilated lung units toward well-ventilated ones. Gårdebäck et al17 have reported a case in which reperfusion edema and hypoxia following PTE were successfully treated with NO inhalation. Pinelli et al18 have also reported similar successful treatment with NO in a case of PTE that was followed by acute and persistent pulmonary hypertension, gas exchange impairment, and heart dysfunction. However, as Gårdebäck et al17 suggest, response to NO in CPTE patients may be unpredictable, and depends partly on the degree of mechanical obstruction and partly on the nature of secondary hypertensive changes in otherwise unaffected vessels. After PTE, we also have to consider secondary hypertensive changes even when obstructions have been removed. Consequently, serial evaluation of the effects of NO inhalation after PTE is required. To our knowledge, this is the first report to evaluate effects of NO inhalation periodically in postoperative CPTE patients.

Our study does not offer any evidence as to why the effects of NO inhalation at 12 h after surgery were different from the initial administration. We can, however, suggest several possible reasons. First, each patient had received vasodilators such as prostaglandin E1 and nitroglycerin immediately after the surgery. If this medication had effectively dilated pulmonary vessels, NO inhalation may have less potential to enhance pulmonary vasodilatation. Second, after PTE surgery, the response to NO may have changed differently between in oxygenation and in pulmonary vasodilatation. In ARDS, the concentration of NO that improves oxygenation is lower than that required for pulmonary vasodilatation.12 Reperfusion lung edema after PTE is often compared to localized ARDS,17 so we reason that a similar difference may be manifest after PTE. In other words, it is possible that 20 ppm of NO concentration is not enough for pulmonary vasodilatation, but is sufficient for improving oxygenation in the acute phase, when the greatest adverse effects of cardiopulmonary bypass on pulmonary hypertension are likely to occur.14 In the later period, the vasodilatation response to NO may be more sensitive, resulting in pulmonary vasodilatation, whereas high concentrations of NO may dilate shunt-like vessels and worsen oxygenation, as has been reported in ARDS.12 Gårdebäck et al17 also reported a case in which oxygenation improved during postoperative NO inhalation, despite an unpromising preoperative response to NO of slightly reducing PVR and no improvement of oxygenation.17 Further study is needed to corroborate our observations and to evaluate the effect of NO inhalation on morbidity and mortality.

Clinical Implications of PPf
Immediately after PTE, the PPf of PAP decreased from 1.18 ± 0.14 (Table 2) to 0.82 ± 0.19 (Table 3) . In CPTE, thrombi tend to obstruct the proximal pulmonary arteries, while primary pulmonary hypertension involves peripheral vessels. These thrombi attached to the proximal arteries mechanically stiffen the arterial wall and increase proximal resistance without comparably increasing peripheral arterial resistance. This type of pathologic change would increase pulse pressure relative to mean PAP.22 23 Nakayama et al22 have reported that PPf is greater in CPTE than in primary pulmonary hypertension. We still do not know, however, whether the PAP waveform in CPTE changes after PTE surgery, or how NO inhalation affects the waveform after PTE. We speculate that removal of the proximal thrombi in CPTE mainly decreases proximal resistance, resulting in lower PPf. In our study, significant decreases in PPf and mean PAP after PTE suggest that proximal obstruction in CPTE was successfully removed.

This study includes several limitations. First, the changes we found during NO inhalation were small. Because of small sample size, lack of control group, relatively large standard deviations, and small differences during NO, we are reluctant to extrapolate the findings directly into clinical relevance. Second, because we performed the NO trial only in intubated subjects, firm conclusions can be probably drawn from data measured within the first 12 h. Third, sedatives, vasodilators, and catecholamines were adjusted by attending physicians, although the dosage was fixed during each measurement. Further study is needed to evaluate the interactions between such medications and NO inhalation.

In conclusion, NO inhalation improved oxygenation without significant changes in pulmonary hemodynamics immediately after PTE surgery; at 12 h after surgery, it decreased PVR without significantly changing oxygenation.


   Footnotes
 
Abbreviations: CPTE = chronic pulmonary thromboembolism; FIO2 = fraction of inspired oxygen; NO = nitric oxide; NYHA = New York Heart Association; PAP = pulmonary artery pressure; PCV = pressure-controlled ventilation; PEEP = positive end-expiratory pressure; PPf = fractional pulse pressure; ppm = parts per million; PSV = pressure support ventilation; PTE = pulmonary thromboendarterectomy; PVR = pulmonary vascular resistance; PVRI = pulmonary vascular resistance index; SIMV = synchronized intermittent mandatory ventilation; SVRI = systemic vascular resistance index

Received for publication September 7, 1999. Accepted for publication February 8, 2000.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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