Effects Of Prolonged Mechanical Ventilation Research Articles

A novel nomogram for predicting prolonged mechanical ventilation in lung transplantation patients using extracorporeal membrane oxygenation

Prolonged mechanical ventilation (PMV) is commonly associated with increased post-operative complications and mortality. Nevertheless, the predictive factors of PMV after lung transplantation (LTx) using extracorporeal membrane oxygenation (ECMO) as a bridge remain unclear. The present study aimed to develop a novel nomogram for PMV prediction in patients using ECMO as a bridge to LTx. A total of 173 patients who used ECMO as a bridge following LTx from January 2022 to June 2023 were divided into the training (122) and validation sets (52). A mechanical ventilation density plot of patients after LTx was then performed. The training set was divided in two groups, namely PMV (95) and non-prolonged ventilation (NPMV) (27). For the survival analysis, the effect of PMV was assessed using the log-rank test. Univariate and multivariate logistic regression analyses were performed to assess factors associated with PMV. A risk nomogram was established based on the multivariate analysis, and model performance was further assessed in terms of calibration, discrimination, and clinical usefulness. Internal validation was additionally conducted. The difference in survival curves in PMV and NPMV groups was statistically significant (P < 0.001). The multivariate analysis and risk factors in the nomogram revealed four factors to be significantly associated with PMV, namely the body mass index (BMI), operation time, lactic acid at T0 (Lac), and driving pressure (DP) at T0. These four factors were used to develop a nomogram, with an area under the curve (AUC) of 0.852 and good calibration. After internal validation, AUC was 0.789 with good calibration. Furthermore, goodness-of-fit test and decision-curve analysis (DCA) indicated satisfactory performance in the training and internal validation sets. The proposed nomogram can reliably and accurately predict the risk of patients to develop PMV after LTx using ECMO as a bridge. Four modifiable factors including BMI, operation time, Lac, and DP were optimized, which may guide preventative measures and improve prognosis.

The Age of Older Patients Requiring Prolonged Mechanical Ventilation Is Not the Sole Determinant of Their Long-Term Survival.

Background and Objectives: There are few data on the effects of prolonged mechanical ventilation on elderly patients. Our objective is to investigate the effects of prolonged mechanical ventilation on older patients' successful weaning and long-term survival. Methods: We examined how aging affected the course and results of elderly patients on prolonged mechanical ventilation by contrasting five age groups. Age, sex, cause of acute respiratory failure, comorbidities, discharge status, weaning status, and long-term survival outcomes were among the information we gathered. Results: Patients on prolonged mechanical ventilation who had undergone tracheostomy and had been successfully weaned had a greater one-year survival rate. The 1-year survival rate was poorer for older patients with four or more comorbidities. Regarding the 5-year survival rate, the risk of death was 45% lower in the successfully weaned patients than in the unsuccessfully weaned patients. The risk of death was 46% lower in patients undergoing tracheostomy than in those not undergoing tracheostomy. Older prolonged mechanical ventilation (PMV) patients with four or more comorbidities had an increased risk of death. Conclusions: When it comes to elderly patients on prolonged mechanical ventilation, there are other factors in addition to age that influence long-term survival. Long-term survival is likewise linked to successful weaning and undergoing tracheostomy.

The effects of COVID-19 on respiratory muscle performance: making the case for respiratory muscle testing and training.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection results in multiorgan damage primarily mediated by viral infiltration via angiotensin-converting enzyme-2 receptors on the surface of cells. A primary symptom for many patients is exertional dyspnoea which may persist even beyond recovery from the viral infection. Respiratory muscle (RM) performance was hypothesised as a contributing factor to the severity of coronavirus disease 2019 (COVID-19) symptoms, such as dyspnoea, and outcomes. This was attributed to similarities between patient populations at elevated risk for severe COVID-19 symptoms and those with a greater likelihood of baseline RM weakness and the effects of prolonged mechanical ventilation. More recent evidence suggests that SARS-CoV-2 infection itself may cause damage to the RM, and many patients who have recovered report persistent dyspnoea despite having mild cases, normal lung function or undamaged lung parenchyma. These more recent findings suggest that the role of RM in the persistent dyspnoea due to COVID-19 may be more substantial than originally hypothesised. Therefore, screening for RM weakness and providing interventions to improve RM performance appears to be important for patients with COVID-19. This article will review the impact of SARS-CoV-2 infection on RM performance and provide clinical recommendations for screening RM performance and treatment interventions.

Thoracic mediastinal-occupying ratio predicts recovery and prognosis after lung transplantation.

OBJECTIVESEven after transplantation of favourable donor lungs, some recipients require prolonged weaning from mechanical ventilation, indicating a poor prognosis. We investigated the effects of prolonged mechanical ventilation (PMV) for >14 days on the recovery and survival of patients who underwent cadaveric lung transplantation in relation to their physical traits.METHODSWe retrospectively reviewed patients who underwent cadaveric lung transplantation (age ≥15 years) at a single centre between April 2015 and December 2020 and classified them into PMV and non-PMV groups (>14 and ≤14 days of mechanical ventilation postoperatively, respectively). The factors predicting PMV comprised clinical factors (e.g. marginal donor) and physical features, namely flat chest, narrow fourth intercostal space (length, <5 mm), mediastinal shift, thoracic mediastinal-occupying ratio (TMOR) >40% and sarcopenia, according to the logistic regression analysis. The log-rank test was used to examine the association between TMOR >40% and 3-year prognosis.RESULTSThe PMV group comprised 17 (33%) of 51 recipients. Multivariable logistic analysis showed that the TMOR >40% (odds ratio, 7.3; 95% confidence interval, 1.3–40.1; P = 0.023) was an independent preoperative predictive factor for PMV postoperatively. Stepwise analysis revealed intraoperative extracorporeal membrane oxygenation and reoperation as postoperative predictive factors in addition to TMOR >40%. Recipients with TMOR >40% had significantly worse 3-year survival than other recipients (71.2% vs 100.0%, respectively; P = 0.008).CONCLUSIONSRecipients with a TMOR >40% may be long-term ventilator dependent and have a poor prognosis.

Effect of prolonged mechanical ventilation on cough function and TRPV1 expression

Cough is a pivotal airway protective reflex, yet the effects of prolonged mechanical ventilation (PMV) on cough function are unknown. This study compared the cough function in subjects with PMV (≥ 21 days, n = 29) and those with short-term mechanical ventilation (SMV, ≤ 7 days, n = 27). Cough reflex sensitivity was measured by capsaicin provocation concentrations after extubation. The cough strength of respiratory muscles was assessed by involuntary cough peak expiratory flow (iCPEF). The mRNA expression of transient receptor potential vanilloid 1 (TRPV1), a cough sensor activated by capsaicin, in tracheal tissues was determined. We found that cough reflex sensitivity and iCPEF were significantly lower in the PMV group than in the SMV group. The tracheal expression of TRPV1 was similar in both groups, suggesting that changes in TRPV1 expression may not be a contributing factor. Our finding regarding the cough dysfunction after PMV highlights the need to implement effective airway clearance management and rehabilitation in this population.

Bronchopulmonary dysplasia-A historical perspective.

Bronchopulmonary dysplasia (BPD) was first described by Northway et al in 1967. This article describes the evolution of our understanding of the pathophysiology of BPD and the approaches to treatments of this illness developed over the past fifty years. These interventions had their roots in the understanding of the principles of the surface tension present at air-liquid interfaces, which were developed over 150 years before BPD's initial description. Improving outcomes in neonatal care have led to greater survival of preterm and very preterm infants, and to an evolution of the pathogenesis and pathology of BPD, from an illness caused primarily by barotrauma and oxygen toxicity to one of interruption of lung development. While the incidence of BPD has remained about the same in recent decades, this is because survival of infants born at lower gestational ages is increasing. Understanding of molecular, genetic and physiologic mechanisms has led to newer treatments that have mitigated some of the harmful effects of prolonged mechanical ventilation. Recognition of BPD as a chronic multi-system disease has resulted in further improvements in care after discharge from neonatal intensive care. Since many of the origins of chronic obstructive lung disease in adults are based in childhood respiratory illnesses, improving outcomes of BPD in infancy and childhood will undoubtedly lead to improved respiratory outcomes in the adults that these children will become.

Using ultrasound to examine muscle mass in preterm infants at term-equivalent age.

The aim of this study was to compare the skeletal muscle thickness of three different muscles and muscle groups in 44 preterm infants studied at term-equivalent age and 44 full-term controls: the biceps brachii, quadriceps femoris, and anterior tibial. The study was carried out at the Careggi University Hospital, Florence, Italy, from January 2018 to December 2019. We assumed that impaired muscle thickness in premature infants would be correlated with exposure to risk factors in the postnatal period. When the premature babies reached term-equivalent age, they were statistically significantly thinner and shorter and had a lower head circumference and lower body mass index than the full-term controls. The muscle thicknesses in the proximal and distal districts were statistically significantly smaller in prematurely born than term-born infants. The skeletal muscle thickness was related to the revised Clinical Risk Index for Babies score and days of invasive mechanical ventilation.Conclusion: Our data show that at term-equivalent age the premature babies had lower skeletal muscle mass acquisition than the full-term controls. This was particularly due to critical conditions at birth and the subsequent duration of invasive mechanical ventilation. What is Known: • The deleterious effects of prolonged mechanical ventilation on skeletal muscle function have been reported by adult intensive care studies. • Ultrasound imagines of fat and muscle thickness have been used in neonatology, as the method is safe, portable, and noninvasive. What is New: • Premature babies studied at term-equivalent age had lower muscle acquisition, but similar subcutaneous fat thickness, to full-term controls. • A high revised Clinical Risk Index for Babies score at birth, and prolonged invasive mechanical ventilation, was associated with skeletal muscle impairment.

Effects of Home Mechanical Ventilation on Left Ventricular Function in Sarcoglycanopathies (Limb Girdle Muscular Dystrophies)

Cardiac and respiratory function may be impaired in sarcoglycanopathies, a subgroup of muscular dystrophies due to sarcoglycan proteins (α, β, γ, and δ) genes mutations. Management of patients with restrictive respiratory failure mainly relies on home mechanical ventilation (HMV). Little is known about the cardiac effects of prolonged mechanical ventilation in patients with muscular dystrophy and restrictive respiratory insufficiency. We aimed to assess the effects of HMV on cardiac function in sarcoglycanopathies. We retrospectively included 10 genetically proven patients with sarcoglycanopathy followed at the HMV unit of the Raymond Poincare University Hospital (4 patients with α-sarcoglycanopathy and 6 patients with γ-sarcoglycanopathy). We collected cardiorespiratory clinical baseline data and left ventricular ejection fraction (LVEF) at baseline before initiation of HMV and at the end of follow-up. At baseline, median age was 30.5 years (27 to 39) and median pulmonary vital capacity was 27% of the predicted value (21 to 36). Forty percent of the patients had documented sleep apnea. Cardiomyopathy, defined as LVEF <50%, was found in 3 patients with γ-sarcoglycanopathy. After a median follow-up of 3 years (1.0 to 4.5), there was a significant increase in LVEF after initiation of HMV, that is, 62% (48 to 65) versus 53% (45.5 to 56.5) (p = 0.0039). In conclusion, HMV in sarcoglycanopathies is not harmful and may protect left ventricular function by its thoracic physiological effects.

Treinamento muscular respiratório em pacientes em desmame da ventilação mecânica

Introdução: A fraqueza da musculatura respiratória é uma das principais causas da dificuldade e/ou insucesso no desmame. Para minimizar os efeitos da ventilação mecânica (VM) prolongada, os fisioterapeutas utilizam o treinamento muscular respiratório, sendo o Threshold IMT® o método mais utilizado. Objetivo: Avaliar a eficácia do treinamento muscular respiratório com o uso do aparelho Threshold IMT®, sobre parâmetros respiratórios de pacientes em desmame da VM. Métodos: Os pacientes foram distribuídos aleatoriamente em grupo controle e grupo experimental (GI e GII). Foram avaliados no primeiro dia do início do desmame quanto à força muscular respiratória: Pressão inspiratória máxima/Pressão Expiratória Máxima (PImáx/PEmáx), volume corrente (VC), frequência respiratória (FR) e cardíaca (FC). Diariamente, durante sete dias, o GI recebeu três sessões de fisioterapia convencional e o GII realizou, adicionalmente, treinamento muscular respiratório (TMR) com o Threshold IMT®, uma vez ao dia, no período da tarde, conectado à traqueostomia, sendo três séries de dez repetições com carga de 20% da PImáx. Os dados foram tratados estatisticamente, adotando-se o nível de significância α=0,05. Resultados: Observou-se aumento (p=0,02) na FR e redução da PImáx (p=0,04) no GI, demonstrando aumento do trabalho respiratório e perda de força muscular entre o primeiro e sétimo dia de desmame. No GII, as variáveis não sofreram alterações significativas, observando-se a manutenção da função respiratória. Conclusão: Sendo assim, o TMR foi benéfico, garantindo a manutenção dos parâmetros respiratórios, podendo ser um aliado para o desmame.

84 Prolonged Ventilation Causes P27KIP1 Induced Cell Cycle Arrest in Newborn Rat Lung

Background: In vitro studies have demonstrated that mechanical stretch can inhibit lung cell proliferation. This inhibition of cell growth may lead to reduction of alveolar formation and contribute to the development of bronchopulmonary dyplasia. Objective: To determine the effect of prolonged mechanical ventilation on cell-cycle regulation in a newborn rat model. Methods: 7-day old Wistar rats were ventilated with low/moderate tidal volume and room air for 24 h. Following ventilation arterial blood gas analysis was performed and the animal was killed. Lung tissues were processed for histological or molecular/protein analysis to determine (1) number of proliferating cells by BrdU and phospho-Histone H3 staining and (2) gene and protein expression of cell cycle regulatory proteins by real-time PCR and Western blotting. Results: After 24 h of ventilation arterial blood gas values were within normal range but alveolar formation was reduced. The number of proliferating cells was decreased (BrdU incorporation decreased from 10 to 3 % and phospho-histone H3 positive cells from 0.8 to 0.1%. Expression of CyclinD1 and E1 mRNA and protein was markedly down-regulated. Instead, protein expression of the CDK inhibitor p27Kip1 was significantly increased while its phosphorylation at site T157, T198 and T187 was decreased. Interestingly, CDK inhibitor p16Ink4a levels were decreased by ventilation. Conclusions: Prolonged mechanical ventilation causes cycle arrest of lung cells in newborn rats by increased transcription and nuclear localization of the CDK inhibitor p27Kip1. These data may in part explain the arrest in alveolarization by mechanical ventilation of the neonatal lung.

Effect of prolonged mechanical ventilation on diaphragm muscle mitochondria in piglets

Respiratory muscle weakness is a common problem in the intensive care unit and could be involved in difficulties in weaning from the ventilator after prolonged mechanical ventilation. Animal models have shown that mechanical ventilation itself impairs diaphragm muscle function. In this study we investigated whether diaphragm contractile impairment caused by mechanical ventilation and immobilization in piglets is associated with a derangement in diaphragm mitochondria. Seven piglets received controlled mechanical ventilation during 5 days. A control group of eight piglets were anaesthetized and surgically manipulated in the same way, but were mechanically ventilated for 4-6 h. After mechanical ventilation, diaphragm muscle biopsies were taken for measurements of mitochondria content, mitochondrial respiratory enzymes and markers of oxidative stress. Diaphragm mitochondrial content, as assessed by citrate synthase activities and volume density, was not different between the control and ventilated piglets. Activity of complex IV of the mitochondrial respiratory chain decreased by 21% (P=0.02) when expressed per muscle weight and by 11% (P=0.03) when expressed per citrate synthase activity. There were no changes in the markers of oxidative stress between the two groups. Five days of mechanical ventilation and immobilization decreased the activity of complex IV of the mitochondrial respiratory chain in the diaphragm muscle of the piglets.

Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury.

Mechanical ventilation deteriorates previously injured lung, but little is known about its effect on healthy human lung. This work was designed to assess the effect of prolonged mechanical ventilation on bronchoalveolar lavage (BAL) fluid composition of patients without acute lung injury. Twenty-two ventilated patients (tidal volume 8-10 mL x kg(-1), positive end-expiratory pressure 3-5 cmH2O) without lung injury, who did not develop any complication from the respiratory system during the 2-week study period, were studied. They were subjected to three consecutive BALs, the first during 36 h from intubation, the second at the end of the first week of mechanical ventilation and the third at the end of the second week of mechanical ventilation. Total BAL protein increased during mechanical ventilation (148 +/- 62, 381 +/- 288, 353 +/- 215 microg x mL(-1) BAL for the first, second and third BAL, respectively). In contrast, BAL phospholipids decreased (2.7 +/- 1.1, 1.4 +/- 0.6, 1.2 +/- 0.7 microg x mL(-1) BAL, respectively). Large surfactant aggregates were reduced and inflammatory markers, such as platelet activating factor (PAF), PAF-acetylhydrolase and neutrophils, significantly increased after 1 week, but partially remitted after 2 weeks of mechanical ventilation. In summary, this study demonstrates that prolonged mechanical ventilation even of patients without acute lung injury is associated with the presence of inflammatory markers and surfactant alterations.

COMBINED RESPIRATORY EFFECTS OF COLD AIR WITH SO2 OR NO2 IN SINGLE 1-HOUR EXPOSURES OF HYPERVENTILATING GUINEA PIGS

The present study is a continuation of our previous experiments on repeated 10-min exposures of anesthetized, mechanically ventilated guinea pigs to clean cold dry air (Hälinen et al., 2000a), and to cold air plus gaseous air pollutants (Hälinen et al., 2000b). This time we made continuous 60-min exposures to clean cold dry air, cold air + SO2 at 1 ppm, cold air + NO2 at 1 ppm, and warm humid air + NO2 at 1 ppm, and focused on responses at 10-60 min. Clean cold dry air and cold air + pollutants (n = 8-9 in each group) produced similar cooling in the guinea pig lower respiratory tract. The decreases in intratracheal temperature (Ttr) reached a plateau at 20 min with mean maximal decreases of 9.7-11.3°C from the pre-exposure control values of 36.0-37.3°C. In contrast, there were progressive decreases in esophageal temperature (Toe) during the exposures, indicating constant conductive and evaporative heat losses from the tracheobronchial tissues. The mean maximal decreases in Toe were 1.2-1.4°C from the preexposure control values of 37.8-38.0°C. Clean cold dry air induced 4.5-10.8% mean decreases in peak expiratory flow (PEF) at 10-60 min of exposure, which were statistically nonsignificant due to a relatively large variation between animals. Cold air + SO2 at 1 ppm induced a mean decrease of 11.4% in PEF at 10 min (p < .05), which was spontaneously abolished during the next 10 min of exposure. Cold air + NO2 at 1 ppm caused no decrease, but in fact small, nonsignificant increases in PEF at 30-60 min of exposure. Cold air + NO2 at 1 ppm, and to some extent also cold air + SO2 at 1 ppm, attenuated significantly the mechanical ventilation induced gradual decrease in tidal volume (VT), when compared to clean cold dry air exposure. Cold air + NO2 at 1 ppm, but not warm humid air + NO2 at 1 ppm, increased significantly the proportion of macrophages in the differential count of bronchoalveolar lavage fluid (BALF) white cells when compared to both clean warm humid air and cold dry air. None of the exposure conditions caused morphological or inflammatory changes in the respiratory tissues. In conclusion, continuous 60-min exposures to clean cold dry air, cold air + SO2, and cold air + NO2 produced weaker functional effects on the lower respiratory tract of guinea pigs than our previous consecutive 10-min exposures to these air conditions. After the first 10 min, there was a strong attenuation of the bronchoconstrictor responses, especially to cold air + NO2 at 1 ppm. The small airway effects of prolonged mechanical ventilation were significantly modified by NO2 at 1 ppm in both cold dry and warm humid breathing air. Finally, cold air + NO2 at 1 ppm increased the proportion of macrophages in BALF white cells.

Hemodynamic Responses to Mechanical Ventilation with PEEP

The hemodynamic effects of prolonged mechanical ventilation with positive end-expiratory pressure (PEEP), with and without blood volume augmentation, were studied in 18 beagles anesthetized with halothane (0.7 per cent end-tidal). Addition of 12 cm H2O PEEP during mechanical ventilation in normavolemic dogs was associated with reductions of transmural cardiac filling pressures, cardiac index and stroke index to 50 per cent of control values. Circulatory adaptation did not occur. Filling pressures and flow remained unchanged during the ensuing 8 hours when PEEP was maintained. They returned to control levels when PEEP was discontinued, except for the transmural right ventricular end-diastolic pressure, which remained elevated above control levels. Systemic vascular resistance was unchanged, but pulmonary vascular resistance doubled upon addition of PEEP. Following autologous whole blood transfusion (25 ml/kg) during mechanical ventilation with PEEP, cardiac index returned to, and remained at, control levels. After PEEP was discontinued, cardiac index increased acutely and remained elevated for the remainder of the study period (as long as 7 hours). Comparable transfusion during mechanical ventilation without PEEP elevated cardiac index only transiently. Right atrial, pulmonary capillary wedge, and right and left ventricular end-diastolic pressures showed marked increases relative to atmospheric with PEEP and after transfusion. Calculated transmural pressures demonstrated clear reductions with application of PEEP, followed by increases to control levels with transfusion and further increases to above control when PEEP was discontinued. Study of ventricular function curves revealed that changes in filling pressures and not to changes in ventricular contractility. Transmural pulmonary arterial diastolic pressure rose throughout the 12 hours of study, despite return of pulmonary vascular resistance to control level with removal of PEEP. Thus, acute decreases in cardiac filling pressure, cardiac index, and stroke index persist consequent to application of PEEP, and circulatory adaptation does not occur. The apparent hemodynamic deterioration may be reversed by blood volume augmentation, but when PEEP is discontinued, hypervolemia with consequent increases in filling pressures and a move along a ventricular function curve will occur. Changes in cardiac index will depend upon the overall state of right and left ventricular contractility.

Study on the Effect of Total Intravenous Anesthesia (TIVA) on the Post-operative Respiratory Performance Regarding Early Extubation after Coronary Artery Bypass Graft (CABG) Surgery

The outcome of anaesthesia in coronary artery surgery depends partly on the duration of invasive manipulations including endotracheal intubation. It is ideal to avoid prolonged mechanical ventilation and attempt early extubation. Depressant effect of some anaesthetic agents and narcotics makes it a common practice to ventilate the patients of coronary artery bypass graft (CABG) surgery overnight resulting in unsatisfactory respiratory and haemodynamic performance. This study was aimed at overcoming the effects of prolonged mechanical ventilation after CABG surgery by using Total Intravenous Anaesthesia (TIVA) and by extubating the patient early to achieve a better postoperative respiratory cardiovascular performance. The study was conducted prospectively on 40 patients between 40 to 60 years, divided into two groups of 20 patients each. Gr.-A received infusions of Propofol 2-6 mg/kg/hr, Fentanyl 0.5-1.25 mg/kg/hr and Pancuronium bromide 0.01mg/kg. Postoperatively Propofol was continued in infusion for one hour while Inj. Diclofenac sodium was used as an analgesic. Patients in group B received a typical conventional anaesthesia and were ventilated electively till next morning. The study showed that in CABG surgery, TIVA produces non-significant depression of post-operative respiratory performance which helps in early extubation compared to those receiving conventional anaesthesia and electively ventilated overnight. Key words: TIVA; CABG; Early extubation DOI: 10.3329/jbsp.v29i1.7164J Bangladesh Coll Phys Surg 2011; 29:3-9

Changes in pulmonary vascular resistance following closure of ventricular septal defects.

In five patients with pulmonary arterial hypertension (PAH) associated with ventricular septal or endocardial cushion defects, measurements of pulmonary vascular resistance (PVR) were made up to seven days after surgical closure. Before operation, the ratio of mean pulmonary arterial pressure [See Equation in PDF File] to mean systemic arterial pressure [See Equation in PDF File] averaged 0.77 . Catheters placed at operation were used to measure pressure in the pulmonary artery, a systemic artery, and right and left atria. Cardiac output was determined by dye dilution. Controlled mechanical ventilation maintained a normal alveolar ventilation and arterial PO 2 . Postoperative [See Equation in PDF File], [See Equation in PDF File], and PVR were initially elevated, averaging 42 mm Hg, 0.57, and 1,132 dyne sec cm -5 , respectively. These values decreased to 29, 0.38, and 459 in three to seven days in the four survivors, but rose in the single death. With unassisted ventilation and 100% 0 2 , or with acidosis (pH 7.21), [See Equation in PDF File] and PVR increased as much as +177% and 570%, respectively. These studies show the relative pulmonary vasoconstricting effect of systemic acidosis and of spontaneous unassisted breathing with 100% O 2 . In patients with markedly elevated, but reversible, hyperkinetic pulmonary vascular resistance, the beneficial effects of prolonged mechanical ventilation enabled the pulmonary circulation to return toward normal.