Inhaled nitric oxide for adult respiratory distress syndrome after pulmonary resection

Background. The adult respiratory distress syndrome (ARDS) developing after pulmonary resection is usually a lethal complication. The etiology of this serious complication remains unknown despite many theories. Intubation, aspiration bronchoscopy, antibiotics, and diuresis have been the mainstays of treatment. Mortality rates from ARDS after pneumonectomy have been reported as high as 90% to 100%.

Methods. In 1991, nitric oxide became clinically available. We instituted an aggressive program to treat patients with ARDS after pulmonary resection. Patients were intubated and treated with standard supportive measures plus inhaled nitric oxide at 10 to 20 parts/million. While being ventilated, all patients had postural changes to improve ventilation/perfusion matching and management of secretions. Systemic steroids were given to half of the patients.

Results. Ten consecutive patients after pulmonary resection with severe ARDS (ARDS score = 3.1 ± 0.04) were treated. The mean ratio of partial pressure of arterial oxygen to the fraction of inspired oxygen at initiation of treatment was 95 ± 13 mm Hg (mean ± SEM) and improved immediately to 128 ± 24 mm Hg, a 31% ± 8% improvement (p < 0.05). The ratio improved steadily over the ensuing 96 hours. Chest x-rays improved in all patients and normalized in 8. No adverse reactions to nitric oxide were observed.

Conclusions. We recommend the following treatment regimen for this lethal complication: intubation at the first radiographic sign of ARDS; immediate institution of inhaled nitric oxide (10 to 20 parts per million); aspiration bronchoscopy and postural changes to improve management of secretions and ventilation/perfusion matching; diuresis and antibiotics; and consideration of the addition of intravenous steroid therapy.     

Prevention of Reperfusion Injury by Inhaled Nitric Oxide in Lungs Harvested From Non-Heart-Beating Donors

Background. In lung transplantation using non-heart-beating donors (NHBD), the postmortem period of warm ischemia exacerbates lung ischemia-reperfusion injury. We hypothesized that inhaled nitric oxide (NO) would reduce ischemia-reperfusion injury, and thus ameliorate the viability of the lung graft.

Methods. A blood-perfused, isolated rat lung model was used. Lungs were flushed and harvested from non-heart-beating donors after 30 minutes of in situ warm ischemia. The lung was then stored for 2 hours at 4°C. Inhaled NO at 30 ppm was given either during the period of warm ischemia, during reperfusion, or during both periods. Lung ischemia-reperfusion injury was assessed after 1 hour of reperfusion by measuring pulmonary vascular resistance, coefficient of filtration, wet-to-dry lung weight ratio, and myeloperoxidase activity.

Results. A severe IR injury occurred in lungs undergoing ischemia and reperfusion without NO as evidenced by high values of pulmonary vascular resistance (6.83 ± 0.36 mm Hg · mL⁻¹ · min⁻¹), coefficient of filtration (3.02 ± 0.35 mL · min⁻¹ · cm H₂O⁻¹ · 100 g⁻¹), and wet-to-dry lung weight ratio (8.07 ± 0.45). Lower values (respectively, 3.31 ± 0.44 mm Hg · mL⁻¹ · min⁻¹, 1.49 ± 0.34 mL · min⁻¹ · cm H₂O⁻¹ · 100 g⁻¹, and 7.44 ± 0.43) were observed when lungs were ventilated with NO during ischemia. Lung function was further improved when NO was given during reperfusion only. All measured variables, including myeloperoxidase activity were significantly improved when NO was given during both ischemia and reperfusion. Myeloperoxidase activity was significantly correlated with coefficient of filtration (r = 0.465; p < 0.05).

Conclusions. These data suggest that inhaled NO significantly reduces ischemia-reperfusion injury in lungs harvested from non-heart-beating donors. This effect might be mediated by inhibition of neutrophil sequestration in the reperfused lung.     

Reversibility of Cardiac Dysfunction After Valve Replacement in Elderly Patients With Severe Aortic Stenosis

Background. The role of aortic valve replacement for aortic stenosis has not been fully defined in terms of the postoperative reversibility of cardiac dysfunction and pulmonary hypertension in elderly patients.

Methods. Cardiac function, assessed by radioisotope ventriculography and catheterization data, was evaluated before and after operation, and their results were compared between preoperative and postoperative data in each group of younger patients (<69 years, group I, n = 29) and elderly patients (≥70 years, group II, n = 21).

Results. One month postoperatively the peak ejection rate determined by radioisotope ventriculography improved significantly in comparison with the preoperative value in elderly patients (preoperatively, 228 ± 38 versus postoperatively, 319 ± 116% end-diastolic volume per second, p < 0.05), although their preoperative peak ejection rate was severely depressed. The postoperative peak filling rate of the elderly group was not completely reversible to almost normal value, whereas that of the younger group was completely reversible. Early diastolic peak filling rate (one-third peak filling rate) was not reversible in both two groups. Pulmonary hypertension in the elderly patients was reversible to postoperative almost normal pulmonary artery pressure despite the severity of aortic stenosis (systolic pulmonary artery pressure preoperatively, 37 ± 16 mm Hg versus postoperatively, 25 ± 5 mm Hg, p < 0.02; diastolic pulmonary artery pressure preoperatively, 15 ± 6 mm Hg versus postoperatively, 10 ± 4 mm Hg, p < 0.05).

Conclusions. Both cardiac dysfunction, reflected by reduction of peak ejection rate, and pulmonary hypertension in elderly patients with severe aortic stenosis were reversed, reaching almost normal values 1 month after operation.     

Inhaled Low-Dose Nitric Oxide for Postoperative Care in Patients with Congenital Heart Defects

Abstract: Postoperative pulmonary hypertensive crisis is a major problem that may account for a substantial part of the postoperative mortality and morbidity. We, therefore, evaluated the effect of inhalation of low-dose nitric oxide (NO) on postoperative care in pediatric patients with pulmonary hypertension. We studied 10 infants and children ages 1–108 months (median age, 11 months) with congenital heart disease associated with pulmonary hypertension. The NO and N, gas mixture was then mixed with varied quantities of air and oxygen and delivered into a respirator instead of an inspiratory tube. Patients were treated with inhaled NO for 38.6 ± 19.6 h (range 1–200 h). All patients were eventually weaned from high level sedation and respirator. The NO concentration ranged from 2 to 5 parts per million. During NO inhalation patients demonstrated a statistically significant reduction in systolic pulmonary arterial pressure by approximately 26%; from 55 ± 10 to 41 k 10 mm Hg. inhalation of NO resulted in a significant increase of Pao₂ from 110 ± 16 to 149 ± 20 mm Hg. A-aDo₂ significantly decreased from 284 ± 27 to 247 ± 31 mm Hg. In conclusion, we have shown that a low-dose NO inhalation acted as a pulmonary vasodilator in patients with preexisting pulmonary hypertension.     

Anaphylactic/anaphylactoid reactions during cardiac surgery

Over a 12-month period, 1,743 patients were retrospectively evaluated for anaphylactic/anaphylactoid reactions during cardiac surgery. Reactions to protamine, vancomycin, blood, and metocurine were observed in eight patients (0.46%). Base-line to reaction mean arterial pressures decreased from 81 ± 9 mmHg to 50 ± 7 mmHg (mean ± SD; p < 0.001), cardiac output increased from 4.6 ± 0.6 L/min to 6.5 ± 1.2 L/min (p < 0.005), stroke volume increased from 49 ± 11 to 83 ± 22 ml/beat (p < 0.02), and systemic vascular resistance decreased from 1,294 ± 137 to 563 ± 127 dyne/sec/cm⁻⁵ (p < 0.001). Two patients developed pulmonary artery hypertension, while only one patient developed bronchospasm. Initial hypertnsion during anaphylacticlanaphylactoid reactions is due to decreased systemic vascular resistance, not myocardial depression.     

Valved homograft replacement of aneurysmal pulmonary arteries for severely symptomatic absent pulmonary valve syndrome

Background. Patients with absent pulmonary valve syndrome (APVS) with respiratory distress (RD) have previously had a high mortality. In 1990 we adopted a strategy of primary repair including total replacement of the aneurysmal central pulmonary arteries (PAs) for patients with RD.

Methods. Retrospective review was made of 54 consecutive patients with APVS between 1960 and 1998. Median age and weight were 4 months and 4.8 kg. RD was present in 23 patients (10 neonates, 16 required ventilation). Fifteen patients had repair with homograft replacement of the PAs and VSD closure (group 1). Twenty-seven patients had transannular patch with VSD closure with PA-plasty (group 2, n = 21) or without PA plasty (group 3, n = 6). Twelve had miscellaneous procedures (group 4); in 6 the VSD was left open.

Results. Operative, 1-, 5-, and 10-year survivals were 83%, 80%, 78%, and 78%, respectively. Risk factors for operative mortality in multivariate analysis were RD (p = 0.04), neonates (p = 0.02), weight less than 3 kg (p = 0.02), open VSD (p = 0.02) and surgery before 1990 (p = 0.04). Since 1990 operative mortality has decreased to 11% (p = 0.04). RD was the only time-related predictor of survival in multivariate analysis (p = 0.004). In patients with RD, survival with homograft was 73% versus 41% with other techniques (p = 0.2). Mean follow-up was 72 ± 50 months. There were no significant differences in freedom from reintervention rates among the surgical groups (p = 0.08).

Conclusions. Aggressive homograft replacement of the central pulmonary arteries has been associated with improved survival in patients with APVS especially in neonates with severe RD.     

Inhaled Nitric Oxide During Extracorporeal Membrane Oxygenation for the Treatment of Severe Persistent Pulmonary Hypertension of the Newborn

Abstract: Inhaled nitric oxide (NO) as a complementary treatment was studied in 10 neonates during extracorporeal membrane oxygenation (ECMO) therapy of various persistent pulmonary hypertension of the newborn (PPHN)-associated diseases. At individually different levels of inhaled NO (20–80 ppm), the mean Pao₂ increased by 59.7% in 6 responders, but it remained unchanged in 4 nonresponders. Adverse side effects of the NO inhalation were tolerable. It was associated with a reversible decrease of the mean arterial blood pressure in 1 patient. During prolonged NO inhalation, the methemo-globin (met-Hb) level increased to 0.9-4.6% in 6 patients. Based on these preliminary results, we conclude that inhaled NO during ECMO can improve oxygenation in some PPHN patients. Further studies with control groups are needed to determine whether inhaled NO can shorten ECMO treatment or improve the rate of survival among PPHN patients.     

Inhaled iloprost to control residual pulmonary hypertension following pulmonary endarterectomy

Objective: Pulmonary endarterectomy (PEA) is the standard therapy for patients with chronic thromboembolic pulmonary hypertension (CTEPH). In the immediate postoperative period, persistent pulmonary hypertension increases the risk of acute respiratory or right heart failure. In pulmonary arterial hypertension, prostanoid inhalation has been found to improve pulmonary hemodynamics, right ventricular function, gas exchange, and clinical outcome. We report the results of a double-blinded randomized trial with the aerosolized prostacyclin analogue iloprost in patients with residual pulmonary hypertension after PEA. Methods: Twenty-two patients (age, 55 ± 13 years; 8 females; propofol- and sufentanil-based anesthesia; pressure-controlled mechanical ventilation) were randomized to receive either a single dose of 25 μg aerosolized iloprost (iloprost group; n = 11) or normal saline (placebo group; n = 11) immediately after postoperative ICU admission. Primary endpoints were changes in gas exchange, pulmonary and systemic hemodynamics, and clinical outcome. Results: Iloprost significantly enhanced cardiac index (CI) and reduced mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance [PVR (dyn s cm⁻⁵)] in contrast to placebo. Placebo: pre-inhalation 413 ± 195 versus post-inhalation 404 ± 196 at 30 min (p = 0.051), 415 ± 189 at 90 min (p = 0.929). Iloprost: pre-inhalation 503 ± 238 versus post-inhalation 328 ± 215 at 30 min (p = 0.001), 353 ± 156 at 90 min (p = 0.003). Blood oxygenation remained unchanged. Conclusion: In addition to the effect of PEA, iloprost reduces residual postoperative pulmonary hypertension, decreases right ventricular afterload and may facilitate the early postoperative management after PEA.     

Right ventricular dysfunction and pulmonary valve replacement after correction of tetralogy of Fallot

Background. Correction of tetralogy of Fallot often leads to pulmonary regurgitation, sometimes warranting pulmonary valve replacement, for which indications and timing to achieve optimal results are not yet clear. This retrospective study describes follow-up and reinterventions in our tetralogy of Fallot population.

Methods. Review of all consecutive patients operated on for tetralogy of Fallot between 1977 and 2000 was conducted. Included are date and type of repair, Doppler echocardiography (two-dimensional echocardiography), electrocardiographs, reoperations, and physical condition.

Results. Total repair was performed in 171 patients at a mean age 1.9 ± 2.5 years, follow-up time counted 9.6 ± 7.0 years. Right ventriculotomy was used in 92%, and transatrial ventricular septal defect closure was used in 8%; 74% received a transannular outflow patch. Twenty-year survival was 91%. Last follow-up electrocardiographs showed right bundle branch block in 67% and serious arrhythmias in 11%. Two-dimensional echocardiography demonstrated severe pulmonary insufficiency and dilated right ventricle in 31% and 38%, respectively, increasing with postrepair age (p < 0.001). Poor clinical condition (New York Heart Association class II+) and echocardiographic proof of right atrial dilatation (p = 0.012) and arrhythmias (p = 0.03) were significantly associated. Furthermore, the influence of residual hemodynamic lesions, such as a remaining ventricular septal defect or pulmonary stenosis, or right ventricular dilatation was important (p = 0.04). Reintervention was necessary in 32 patients (19%; 10-year freedom, 83%), including angioplasty for residual stenosis and pulmonary valve replacement. At a mean age of 9.2 years after correction, 14 patients received a homograft, and 2 patients received a heterograft. In 7 patients the right ventricle returned to normal dimensions and symptoms disappeared. The incidence of right ventricular dilatation was considerably higher (p = 0.020) in patients with a transannular patch; the transatrial approach showed the opposite (p = 0.03), and patients presented with lower QRS duration (p = 0.007), although no difference could be found between survival after both surgical techniques. Effects of early timing (correction < 6 months) on right ventricular dysfunction could not be established.

Conclusions. Severe right ventricular dilatation and pulmonary regurgitation secondary to outflow tract repair in tetralogy of Fallot are frequently occurring sequelae developing slowly over time. Indications for pulmonary valve replacement remain controversial because echocardiographic findings or arrhythmias are not always accompanied by deterioration of clinical condition. However, right atrial dilatation and additional hemodynamic lesions demand increased vigilance. Transatrial repair is associated with a favorable outcome.     

Partial left ventriculectomy for idiopathic dilated cardiomyopathy: early results and six-month follow-up

Background. Recent reports show that partial left ventriculectomy improves hemodynamic and functional status in patients with dilated cardiomyopathy. This study sought to determine the effects of partial left ventriculectomy on clinical outcome and left ventricular function during 6-month follow-up.

Methods. Twenty-two patients underwent partial left ventriculectomy. Mitral valve repair was performed whenever possible, otherwise the valve was replaced. Hemodynamic and functional data were obtained at baseline, as well as 2 weeks and 6 months postoperatively.

Results. Overall, 7 of 22 patients died; there were three early and four late deaths. One-year survival was 68% ± 10%. Ejection fraction increased from 23.9% ± 6.8% before the operation to 40.7% ± 12.5% at 2 weeks and to 36.8% ± 7.7% at 6 months (p < 0.001, for both). The cardiac index before the operation, at 2 weeks, and at 6 months was 2.3 ± 0.8, 2.9 ± 0.6, and 3.4 ± 1.0 L/m² per minute, respectively (p = 0.035, and p = 0.009, compared with baseline). The increase in ejection fraction 2 weeks postoperatively was less in patients with left circumflex artery dominance (10.9% ± 3.2% compared with 19.9% ± 10.7%, respectively, p = 0.017). At 6-month follow up, all surviving patients except one improved New York Heart Association functional class when compared with preoperative status (from 3.8 ± 0.4 to 1.4 ± 0.6, p = 0.0002).

Conclusions. Early hemodynamic improvement after partial left ventriculectomy was maintained during midterm follow-up.     

Comparison of outcomes between living donor and cadaveric lung transplantation in children

Background. Long-term survival in lung transplant is limited by bronchiolitis obliterans (BOS). We compared outcomes in pediatric living donor bilateral lobar (LL) vs cadaveric lung transplant (CL).

Methods. Children were studied who had LL or CL with at least 1 year follow-up. Data collected included acute rejection episodes, pulmonary function tests (PFT), BOS, and survival. Mean age was 13.36 ± 3.16 years in LL and 12.00 ± 4.19 years in CL patients (p = 0.37, ns).

Results. There was no difference in rejection (p = 0.41, ns). CL had rejection earlier (2.48 ± 3.84 months) than LL (13.60 ± 10.74 months; p = 0.02). There was no difference in 12 month PFT. But at 24 months, LL had greater forced expiratory volume in 1 second (FEV₁) (p = 0.001) and FEF_25–75% (p = 0.01) than CL. BOS was found in 0/14 LL vs 9/11 (82%) CL after 1 year (p = 0.04). After 2 years, 0/8 LL and 6/7 (86%) CL had BOS (p < 0.05). LL had 85% survival vs 79% for CL at 12 months. At 24 months, LL survival was 77% vs 67% for CL.

Conclusions. Pediatric LL had less BOS and better pulmonary function than CL. As BOS is a determinant of long-term outcome, we believe LL is the preferred lung transplant method for children.     

Repair of anomalous left main coronary artery arising from the pulmonary artery in infants: long-term impact on the mitral valve

Background. Infants presenting with anomalous left coronary artery off the pulmonary artery (ALCAPA) are generally in heart failure and often have significant mitral valve regurgitation (MR). Although establishing a dual coronary circulation is the procedure of choice, there remains controversy as to how the mitral valve is handled.

Methods. We reviewed our experience with this lesion at St. Louis Children’s Hospital. Over the past 15 years, 17 infants under 18 months of age have undergone repair, with all but one being treated with reimplantation of the left coronary artery into the aorta; the other underwent the Takeuchi procedure (intrapulmonary artery baffle) and was excluded from this evaluation. The average age and weight at operation were 0.5 ± 0.3 years and 6.1 ± 1.9 kg, respectively. All presented with varying degrees of heart failure and 9 patients also had either moderate or severe MR.

Results. There was one early and no late deaths after reimplantation of the left coronary artery. The left ventricular function postrepair improved from a preoperative shortening fraction of 0.19 ± 0.09 to 0.34 ± 0.08 (p < 0.01). Moderate or severe MR was present in 2 patients postoperatively, and both developed significant obstruction in the left coronary artery postoperatively as well. Both underwent mitral valve repair and revascularization of the left coronary artery.

Conclusions. Excellent results can be obtained in the treatment of this very high-risk group of patients. Mitral valve repair is not generally necessary at the time of the initial operation. However, should MR recur or persist late, it may herald the presence of a coexistent, significant coronary stenosis. Cardiac catheterization should be performed to assess the patency of the left coronary artery before performing mitral valve surgery.     

吸入一氧化氮对室间隔缺损手术后肺动脉高压的疗效观察

目的　观察吸入一氧化氮(nitricoxide,NO)治疗室间隔缺损 (ventricularseptaldefect,VSD)术后肺动脉高压 (pulmonaryhypertension ,PH)的疗效。 方法　 2 0例VSD术后PH病人分别吸入 2 0×10 -6 、6× 10 -6 NO ,监测吸入前后的血流动力学、氧合指标。结果　吸入 2 0× 10 -6 NO后明显降低肺动脉压、肺循环阻力、肺内分流率、肺泡动脉血氧分压差 ,提高动脉血氧分压、氧供指数 ;以上指标停吸NO后恢复吸入NO前水平 ;再吸入 6× 10 -6 NO后恢复吸入 2 0× 10 -6 NO后水平 ,并维持至停吸NO后。吸入前后体循环压及阻力无变化。结论　吸入NO是治疗VSD手术后PH的一种有效的方法。     

Improved clinical outcomes in patients undergoing coronary artery bypass grafting with coronary endarterectomy

Background. Coronary artery bypass grafting (CABG) with coronary endarterectomy (CE) has been associated with increased morbidity and mortality. We sought to evaluate the impact of recent advances in operative and perioperative management on outcomes after CE.

Methods. One hundred fifty-one consecutive patients undergoing first-time CABG with CE between 1991 and 1997 were compared with a concurrent group of 757 patients undergoing CABG without CE (Control).

Results. Age, gender, left ventricular ejection fraction, percent nonelective were similar in both groups. Compared with control, the CE group had a higher incidence of hypertension (80% versus 71%, p = 0.02), diabetes (42% versus 32%, p = 0.01), prior myocardial infarction (MI) (68% versus 59%, p = 0.05), peripheral vascular disease (36% versus 16%, p < 0.001), renal failure (15% versus 4%, p < 0.001), and three-vessel coronary disease (81% versus 70%, p = 0.007), resulting in higher Society of Thoracic Surgeons database predicted mortality (4.9 ± 5.9% versus 3.9 ± 4.6%, p = 0.05). Despite the higher risk profile of the CE group, hospital mortality (CE 2.0%, Control 1.2%) and the incidence of major complications such as cerebrovascular accident (CVA) (0.7% versus 1.5%), major respiratory complications (8% versus 5%), and postoperative MI (3% versus 1.4%) were similar between the groups (all p = NS). In a multiple logistic regression analysis, prolonged cardiopulmonary bypass time was an independent predictor of postoperative MI (odds ratio 1.2, CI 1.05 to 1.39, p < 0.01) and the use of heparin-bonded cardiopulmonary bypass circuits of reduced MI rate (odds ratio 0.25, CI 0.08 to 0.76, p < 0.01). Mean follow-up for 94% of patients was 30 ± 19 months (range 1 to 83 months). Five-year survival after CE was 70 ± 5%, with 96% of patients in Canadian Cardiovascular Society class I/II.

Conclusions. In a contemporary series of carefully selected patients, mortality and major complications after CE are now similar to CABG without CE. CE itself is not an independent predictor of postoperative MI. Functional class of hospital survivors is excellent.     

Intraaortic Balloon Counterpulsation Improves Right Ventricular Failure Resulting From Pressure Overload

Background. Right ventricular (RV) dysfunction is common after heart transplantation, and myocardial ischemia is considered to be a significant contributor. We studied whether intraaortic balloon counterpulsation would improve cardiac function using a model of acute RV pressure overload.

Methods. In 10 anesthetized sheep, RV failure was induced using a pulmonary artery constrictor. Baseline measurements included mean systemic blood pressure, RV peak systolic pressure, cardiac index, and RV ejection fraction. Myocardial and organ perfusion were measured using radioactive microspheres.

Results. After pulmonary artery constriction, there was an increase in RV peak systolic pressure (32 ± 2 to 60 ± 3 mm Hg; p < 0.01) and a decrease in mean systemic blood pressure (68 ± 4 to 49 ± 2 mm Hg; p < 0.01), RV ejection fraction (0.51 ± 0.04 to 0.16 ± 0.02; p < 0.01), and cardiac index (2.48 ± 0.04 to 1.02 ± 0.11; p < 0.01). Blood flow to the RV did not change significantly, but there was a significant reduction in blood flow to the left ventricle. The initiation of intraaortic balloon counterpulsation (1:1) using a 40-mL intraaortic balloon inserted through the left femoral artery resulted in an increase in mean systemic blood pressure (49 ± 2 to 61 ± 3 mm Hg; p < 0.01), cardiac index (1.02 ± 0.11 to 1.45 ± 0.14; p < 0.05), RV ejection fraction (0.16 ± 0.02 to 0.23 ± 0.02; p < 0.01), and blood flow to the left ventricle.

Conclusions. In a model of right heart failure, the institution of intraaortic balloon counterpulsation caused a significant improvement in cardiac function. Although RV ischemia was not demonstrated, the augmentation of left coronary artery blood flow by intraaortic balloon counterpulsation and subsequent improvement in left ventricular function suggest that left ventricular ischemia contributes to RV dysfunction, presumably through a ventricular interdependence mechanism. Therefore, study of the safety and efficacy of intraaortic balloon counterpulsation in the management of patients with acute right heart dysfunction is warranted.     

Effect of inhaled nitric oxide on venous admixture depends on cardiac output in patients with acute lung injury and acute respiratory distress syndrome

Background: It has been shown that inhaled nitric oxide (NO) reduces intrapulmonary venous admixture (Q_VA/Q_T) and improves oxygenation in patients suffering from acute respiratory distress syndrome (ARDS). The change in Q_VA/Q_T during NO inhalation varies individually. Factors known to influence the respiratory response to NO are the NO conceritration and the level of shunt before NO administration. Other factors that may modify the effect on gas-exchange during NO breathing are unknown.
Methods: We studied the effect of 40 ppm inhaled NO on pulmonary gas-exchange and haemodynamics in 37 patients with acute lung injury (ALI) and ARDS, respectively, and factors that may influence the respiratory response to NO.
Results: Inhalation of 40 ppm NO produced a decrease in mean pulmonary artery pressure (MPAP) from 33.1±7.2 to 30.2±6.8 (mean±SD) mmHg (P<0.0001) while pulmonary artery wedge pressure (PAWP), cardiac output and mean arterial pressure remained constant. Change in Q_VA/Q_T during NO inhalation depended on the preinhalation cardiac output and had no association with mixed venous oxygen tension, MPAP-PAWP, and Q_VA/Q_T before NO delivery. Q_VA/Q_T decreased in 26 patients (group 1) and increased in 11 patients (group 2) during NO inhalation. In group 1, cardiac output was lower than in group 2 (8.6 vs. 12.2 1-min^-1; P<0.0005).
Conclusion: We conclude that the change in venous admixture during inhalation of 40 ppm NO depends on cardiac output. If preinhalation cardiac output is high, 40 ppm NO can adversely affect gas exchange in patients with ALI and ARDS.     

Reperfusion injury significantly impacts clinical outcome after pulmonary transplantation

Background. Reperfusion injury after pulmonary transplantation can contribute significantly to postoperative pulmonary dysfunction. We hypothesized that posttransplantation reperfusion injury would result in an increase in both in-hospital mortality and morbidity. We also hypothesized that the incidence of reperfusion injury would be dependent upon the cause of recipient lung disease and the interval of donor allograft ischemia.

Methods. We performed a retrospective study of all lung transplant recipients at our institution from June 1990 until June 1998. One hundred patients received 120 organs during this time period. We compared two groups of patients in this study: those experiencing a significant reperfusion injury (22%) and those who did not (78%).

Results. In-hospital mortality was significantly greater in patients experiencing reperfusion injury (40.9% versus 11.7%, p < 0.02). Posttransplantation reperfusion injury also resulted in prolonged ventilation (393.5 versus 56.8 hours, p < 0.001) and an increased length of stay in both the intensive care unit (22.2 versus 10.5 days, p < 0.01) and in the hospital (48.8 versus 25.6 days, p < 0.03). The incidence of reperfusion injury could not be attributed to length of donor organ ischemia (221.5 versus 252.9 minutes, p < 0.20). The clinical impact of reperfusion injury was significantly greater in patients undergoing transplantation for preexisting pulmonary hypertension (6/14) than those with chronic obstructive pulmonary disease or emphysema alone (6/54) (42.9% versus 11.1%, p < 0.012).

Conclusions. Clinically significant pulmonary reperfusion injury increased in-hospital mortality and morbidity resulting in prolonged ventilation, length of stay in the intensive care unit, and cost of hospitalization. The incidence of reperfusion injury was not dependent upon the duration of donor organ ischemia but increased with the presence of preoperative pulmonary hypertension. These findings suggest that recipient pathophysiology and donor allograft quality may play important roles in determining the incidence of reperfusion injury.     

Total anomalous pulmonary venous connection: surgical repair with a double-patch technique

A double-patch technique has been used to repair total anomalous pulmonary venous connection in 35 patients (mean age, 4.9 months; mean weight, 4.2 kg). In all patients with supracardiac or subdiaphragmatic type of total anomalous pulmonary venous connection, repair has been accomplished by enlarging the "new" left atrium. There were three early deaths (3 of 35 = 8.6%) and no late deaths in a mean follow-up of 30 months (3 to 71 months). We propose this double-patch technique as an alternative surgical option for total anomalous pulmonary venous connection.     

Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension.

Patients with mitral valve disease can develop pulmonary artery hypertension that persists after mitral valve replacement. In 1987, nitric oxide (NO) was reported to be an important factor accounting for the biologic activity of endothelium-derived relaxing factor. Inhaled NO was subsequently reported to be a selective pulmonary vasodilator in animals and patients. Therefore we investigated the vasodilating effect of inhaled NO in patients with mild pulmonary artery hypertension after mitral valve replacement. Six patients who underwent mitral valve replacement for mitral stenosis presented with a mean pulmonary artery pressure greater than 25 mmHg within 24 h after surgery. During mechanical ventilation at FIO2 0.5, NO (36.8-38.4 ppm) was breathed for 10 min. Hemodynamic data were recorded before NO, after 10 min of NO inhalation, and 30 min after the end of NO inhalation. Statistically significant (P < 0.05) hemodynamic response to inhaled NO included a transient decrease in systolic (-10%), diastolic (-8%), and mean (-10%) pulmonary artery pressures; a decrease in pulmonary vascular resistance (-22%); an increase in mixed venous hemoglobin O2 saturation (+6%); and a decrease in arteriovenous O2 content difference (-7%). During NO inhalation, there was no change in systemic arterial or pulmonary wedge pressures. Methemoglobin levels remained < 1%. Inhalation of this concentration of NO for 10 min causes transient pulmonary artery vasodilation and hemodynamic improvement in patients with mild chronic pulmonary artery hypertension after mitral valve replacement.     

Comparison of clinical results for unilateral and bilateral thoracoscopic lung volume reduction

Background. It is widely believed that bilateral thoracoscopic lung volume reduction (BTLVR) yields superior results when compared with unilateral thoracoscopic lung volume reduction (UTLVR) with regard to spirometry, functional capacity, oxygenation and quality of life results.

Methods. To address these issues, we compared the results of patients undergoing UTLVR (N = 338 patients) and BTLVR (N = 344 patients) from 1993 to 1998 at five institutions. Follow-up data were available on 671 patients (98.4%) between 6 and 12 months after surgery, and a patient self-assessment was obtained at a mean of 24 months.

Results. It was found that BTLVR provides superior improvement in measured postoperative percent change in FEV₁ (L) (UTLVR 23.3% ± 55.3 vs BTLVR 33% ± 41, p = 0.04), FVC(L) (10.5% ± 31.6 vs 20.3% ± 34.3, p = 0.002) and RV(L) (−13% ± −22 vs −22% ± 17.9, p = 0.015). BTLVR also provides a slight improvement over UTLVR in patient’s perception regarding improved quality of life (UTLVR 79% vs BTLVR 88%, p = 0.03) and dyspnea relief (71% vs 61%, p = 0.03). There was no difference in mean changes in Po₂ (mm Hg) (UTLV 4.5 ± 12.3 vs BTLVR 4.9 ± 13.3, p = NS), 6-minute walk (UTLVR 26% ± 66.1 vs BTLVR 31% ± 59.6, p = NS) or decreased oxygen utilization (UTLVR 78% vs BTLVR 74%, p = NS).

Conclusions. These data suggest that both UTLVR and BTLVR yield significant improvement, but the results of BTLVR seem to be superior with regard to spirometry, lung volumes, and quality of life.