Ventilation-perfusion Imbalance Research Articles

The use of furosemide during Intravenous Immunoglobulin therapy should not always be considered contraindicated

AimsEndothelial damage in acute respiratory distress syndrome (ARDS) increases capillary permeability, resulting in an increase in free lung fluid, interstitial pulmonary edema, and ventilation-perfusion imbalance. Due to their high osmolarity, Intravenous Immunoglobulin (IVIG) treatment may deepen hypoxemia by increasing lung fluid leakage. Adding furosemide to IVIG treatment in ARDS secondary to COVID-19 (CARDS) cases may increase treatment tolerance and success. Materials and methodsIn our study, we aimed to measure the effectiveness of this treatment combination in CARDS cases and to report the observed complications. Patients who were followed up in the 34-bed adult COVID intensive care unit between March 2020/2021 and who received IVIG, high-dose corticosteroid, and furosemide combination therapy were included in the study. Patients' age, gender, comorbidities, Acute Physiology, and Chronic Health Assessment II (APACHE-II), and Sequential Organ Failure Assessment (SOFA) scores were recorded. The day IVIG duration of treatment, additional medical treatments, respiratory support treatments, laboratory examinations, the percentage of involvement of lung lesions (Covid Visual Assessment Scale), clinical outcomes, and treatment complications were recorded. ResultsCombination therapy with found to improve respiratory failure in 50 % of patients. Troponin elevation was found in two patients, femoral artery embolism in one patient, and thrombosis in the femoral vein in one patient. In addition to IVIG treatment, the administration of two doses of immune plasma increased the chance of discharge (P = 0.037) ConclusionIn severe viral ARDS refractory to standard therapy, using furosemide in addition to IVIG therapy has an acceptable side-effect profile and may increase treatment success. Furosemide given during IVIG therapy should not be considered a contraindication in every patient.

Postpneumonectomy Syndrome Leading to Severe Hypoxemia Due to a Sudden Ventilation-perfusion Imbalance.

Postpneumonectomy Syndrome Leading to Severe Hypoxemia Due to a Sudden Ventilation-perfusion Imbalance.

Case Study on Nurse Care for Covid-19 Patients with MDRO (Multiple Drug Resistent Organism) in Isolation Intensive Care Unit, Bali Mandara Hospital

Covid-19 pandemic has made major changes in human civilization. Nurse care becomes more complex for Covid-19 patients who also confirmed with MDRO. MDROs are bacteria resistant to three or more antimicrobials from different classes. This study aims is to know nurse care of patients with Covid-19 and MDRO.The design of this study is qualitative method (case study). The subjects were two patients with Covid-19 and MDRO in Isolation Intensive Care Unit. Data collection techniques were physical and supporting examination, medical record review. Data from the analysis were written descriptively. Priority nursing diagnoses was impaired gas exchange related to ventilation-perfusion imbalance characterized by dyspnea, decreased consciousness. The patient is attached to a VC SIMV mode ventilator. After being treated in Isolation intensive care unit for approximately 14 days, the patient was able to breathe spontaneously with an O2 nasal cannula. The conclusion is nurse care for COVID-19 patients with MDRO is carried out based on isolation precautions (droplet and contact transmission). Nurses are expected to provide professional nurse care to Covid-19 patients with MDRO so the quality of care remains up to standard even during pandemic.

Hepatopulmonary Disorders: Gas Exchange and Vascular Manifestations in Chronic Liver Disease.

This review concentrates on the determinants of gas exchange abnormalities in liver-induced pulmonary vascular disorders, more specifically in the hepatopulmonary syndrome. Increased alveolar-arterial O2 difference, with or without different levels of arterial hypoxemia, and reduced diffusing capacity represent the most characteristic gas exchange disturbances in the absence of cardiac and pulmonary comorbidities. Pulmonary gas exchange abnormalities in the hepatopulmonary syndrome are unique encompassing all three pulmonary factors determining arterial PO2 , that is, ventilation-perfusion imbalance, increased intrapulmonary shunt and oxygen diffusion limitation that, combined, interplay with two relevant nonpulmonary determinants, that is, increased total ventilation and high cardiac output. Behind the complexity of this lung-liver association there is an abnormal pulmonary vascular tone that combines inhibition of hypoxic pulmonary vasoconstriction with a reduced (or blunted) hypoxic vascular response. The pathology and pathobiology include the presence of intrapulmonary vascular dilatations with or without pulmonary vascular remodeling, i.e. angiogenesis. Liver transplantation, the only effective therapeutic approach to successfully improve and resolve the vast majority of complications induced by the hepatopulmonary syndrome, along with a large list of frustrating pharmacologic interventions, are also reviewed. Another liver-induced pulmonary vascular disorder with less gas exchange involvement, such as portopulmonary hypertension, is also considered. © 2018 American Physiological Society. Compr Physiol 8:711-729, 2018.

Wave intensity as a useful modality for assessing ventilation-perfusion imbalance in subclinical patients with hypertension.

Wave intensity (WI) is a novel noninvasive index of circulatory dynamics that reflects ventriculo-arterial coupling. It is calculated as the product of the first derivative of blood pressure and that of flow velocity measured by carotid echocardiography. This study aimed to clarify the clinical implications of WI and its relation with carbon dioxide production (VE/VCO2 slope). Twenty-one healthy volunteers (control group) and 21 patients with hypertension (HT group) underwent cardiopulmonary exercise testing (CPX) and exercise stress echocardiography. WI was assessed in the right carotid artery using an ultrasound system. The first peak of WI (W1) during the early ejection phase was measured at baseline and mitral annular velocity was assessed by tissue Doppler imaging. Ventilatory kinetics during exercise was assessed using the relation of minute ventilation to VE/VCO2 slope. VE/VCO2 slope, W1, and E/E' were greater in the HT group than in the control group. PeakVO2 and VO2 at the anaerobic threshold were lower in the HT group than in the control group. VE/VCO2 slope was significantly correlated with W1 (r=0.58, p<0.01) and E/E' (r=0.44, p<0.01). Stepwise multivariate analysis revealed that W1 was an independent determinant of VE/VCO2 slope (β=0.43, p<0.01). In conclusion, W1 might be able to predict the severity of heart failure without the need for CPX. Moreover, WI may be a useful modality in assessing heart failure pathophysiology based on ventriculo-arterial coupling.

The Clinical Significance of Collateral Ventilation.

Oxygen delivery and carbon dioxide removal being critical to cell survival, mammals have developed collateral vascular and ventilation systems to ensure tissue viability. Collateral ventilation, defined as ventilation of alveoli via pathways that bypass normal airways, is present in humans and many other species. The presence of collateral ventilation can be beneficial in certain disease states, whereas its relative absence can predispose to other diseases. These well defined anatomical pathways contribute little to ventilation in normal humans, but modulate ventilation perfusion imbalance in a variety of diseases, including obstructive diseases, such as asthma and emphysema. These pathways can be affected by pharmaceuticals and inhaled gas compositions. The middle lobe and lingula, constrained by their isolated, segmental anatomy, have reduced collateral ventilation, which predisposes them to disease. Recently, attempts to improve the quality of life of patients with emphysema, by performing nonsurgical lung volume reduction via use of endobronchial valves, have led to mixed results, because the role of collateral ventilation in the success or failure of the procedure was not initially appreciated. This review describes the anatomical pathways of collateral ventilation, their physiology and relationship to disease states, their modulatory effects on gas exchange, treatment considerations, and their effect on diagnostic procedures.

換気障害と肝酵素の異常高値を呈した鈍的外傷性右横隔膜破裂の1例(Ventilation failures and high liver enzymes following blunt trauma are signs of right diaphragm ruptures: a case report)

要旨外傷性右横隔膜損傷は稀であり，確定診断が困難とされている。今回，右肺の換気障害，肝酵素の異常高値および心外閉塞性ショックを呈し，絞扼性肝ヘルニアを伴う外傷性右横隔膜破裂を経験した。症例は28歳男性，交通事故を契機にショック状態となり当院へ搬入された。胸部X線写真（臥位）で右血胸および右横隔膜挙上を認めた。胸部超音波検査で右横隔膜と肝臓が右胸腔方向へ挙上していた。CT画像では，右横隔膜・肝臓の挙上に加え，右横隔膜の不連続性や右横隔膜破裂を疑う所見を認めた。右胸腔ドレーン挿入するも，AaDO2の開大を伴う低酸素血症が遷延し，血液生化学検査所見でCT所見では説明のつかない著しい肝酵素の上昇を認めた。これらの所見より外傷性右横隔膜破裂・絞扼性肝ヘルニアと診断し，緊急で右横隔膜破裂修復術を施行した。術後は経過良好であり，術後2日後のCTで右横隔膜に嵌頓していた肝臓に三日月状の造影不良域を認めた。外傷性右横隔膜損傷の診断は困難であるが，本症例では特徴的な画像所見だけでなく，換気障害やCT所見からは説明がつかない著しい肝酵素の上昇，循環血液量を補正しても残存する心外閉塞性ショックという右横隔膜破裂に関連する病態を捉え，術前に診断することが可能であった。

(988) - An Analysis of Mechanism of Hypoxia in Chronic Thromboembolic Pulmonary Hypertension

In chronic thromboembolic pulmonary hypertension (CTEPH), residual hypoxia remains to be a limitation of physical activity, despite hemodynamic status improved. However, the precise mechanism of hypoxia and the medical contribution to the hypoxia have not been fully clarified. The purpose of our study was to clarify the determinants of hypoxia in CTEPH. We retrospectively analyzed patients with CTEPH who had measured hemodynamic status, respiratory function, and dead space ratio. Patients, who received medical intervention, were measured these parameters before and after treatment. We excluded chronic lung disease. In overall twenty-eight patients (19 female, 64±12 years), arterial oxygen saturation (SaO2) was 91.2±3.6% and dead space ratio (DSR) was 0.63±0.05. As far SaO2, %functional residual capacity (%FRC), mean pulmonary arterial pressure (mPAP) and DSR were significantly correlated (r= 0.53, 0.62, 0.44, p<0.05, respectively). Fifteen in 28 received medical intervention (7 patients were treated by balloon pulmonary angioplasty only, 2 by riociguat only, and 6 by combination of the two treatments). By improvement of mPAP (38.6±9.4 vs 25.2±2.8 mmHg, p<0.05), SaO2 and DSR were significantly improved (90.5±3.6 vs 93.9±1.9%, 0.64±0.5 vs 0.58±0.5, p<0.05, respectively). However %FRC was not improved. Furthermore, abnormality of SaO2 and DSR were persisting despite adequate hemodynamic improvement. Current therapy can improve hypoxia in CTEPH. It also improves DSR by correcting ventilation-perfusion imbalance. However, it is not enough to restore normal blood oxygenation level. It is possible that correcting %FRC is one of clue of the normalization of hypoxia in CTEPH.

Nonpulmonary influences on gas exchange.

There are several determinants governing arterial and mixed venous blood PO2 and PCO2. Ventilation-perfusion imbalance, increased intrapulmonary shunt, and diffusion limitation to oxygen encompass the pulmonary factors. Alternatively, inspired oxygen concentration, overall ventilation, cardiac output, and oxygen consumption (uptake) are contemplated as the four most influential nonpulmonary determinants. All three pulmonary factors plus oxygen uptake cannot be directly modulated, but all the other remaining nonpulmonary determinants are. Inspired oxygen concentration, the amount and pattern of total ventilation, and cardiac output may be, at least in part, relatively well clinically controlled. Arterial PO2 (PaO2) may fall if inspired PO2, overall ventilation, and/or cardiac output decrease, and/or oxygen consumption increases, even though the pulmonary factors remain unchanged. Conversely, if inspired oxygen fraction, ventilation, and/or cardiac output increase, and/or oxygen consumption decreases, PaO2 may improve regardless of the changes operated at the level of the pulmonary determinants. Several pathophysiologic features deserve to be underlined. First, the importance of understanding the role played by mixed venous PO2 as a vital nonpulmonary determinant governing PaO2. Second, the response to 100% oxygen breathing repeatedly exhibits a consistent amount of agreement in the main findings. Third, there is always an interactive interplay between pulmonary and nonpulmonary determinants of PaO2 and arterial PCO2 (PaCO2) in any respiratory disease state following the use of pharmacologic or nonpharmacologic approaches. All in all both PaO2 and PaCO2 become the end-point outcomes of the complex interaction of pulmonary and nonpulmonary factors modulating pulmonary gas exchange. This needs to be unraveled to improve the understanding and management of most acute and chronic respiratory disease states.

Pulmonary vascular abnormalities in chronic obstructive pulmonary disease undergoing lung transplant

Little is known about the structure and function relationships of pulmonary vessels in the most severe chronic obstructive pulmonary disease (COPD) spectrum. We investigated morphometric, cellular, and physiologic characteristics of pulmonary arteries from COPD patients undergoing bilateral lung transplant. Seventeen patients with very severe COPD (forced expiratory volume in 1 second, 24% ± 7%) were assessed using inert gas exchange and pulmonary hemodynamics while breathing ambient air and 100% oxygen. Morphometry, in vitro reactivity to hypoxia, and inflammatory cell counts of pulmonary arteries were measured in explanted lungs. Patients had moderate ventilation-perfusion imbalance along with mild release of hypoxic pulmonary vasoconstriction. Mild pulmonary hypertension was observed in 7 patients. Explanted lungs had predominant emphysema with mild small airway involvement. In vitro reactivity was modestly altered, with relatively preserved endothelium-dependent relaxation, and vascular remodelling was discrete, with intense CD8+ T lymphocytes infiltrate. In vitro reactivity correlated with pulmonary vascular resistance (on ambient air) and oxygen-induced pulmonary artery pressure changes. Patients with pulmonary hypertension had more severe morphologic and physiologic emphysema. In end-stage COPD patients undergoing lung transplant, pulmonary vascular involvement is unexpectedly modest, with low-grade endothelial dysfunction. In this sub-set of COPD patients, pulmonary emphysema may constitute the major determinant of the presence of pulmonary hypertension.

Assessment of cross-sectional lung ventilation–perfusion imbalance in primary and passive pulmonary hypertension with automated V/Q SPECT

Cross-sectional lung ventilation (V)-perfusion (Q) imbalance in primary pulmonary arterial hypertension (PAH) and passive pulmonary hypertension (PH) was characterized by automated V/Q single-photon emission computed tomography (SPECT). Technegas/macro-aggregated albumin SPECT-derived V/Q SPECT and V/Q profile were automatically built to characterize cross-sectional lung V-Q imbalance in 12 patients with primary (idiopathic or familial) PAH and 15 patients with passive PH associated with left ventricular dysfunction or failure. The abnormality of V/Q distribution in these patients was correlated with PaO2 and pulmonary arterial pressure and with lung morphologic changes on computed tomography (CT). Markedly low V/Q ratios (reverse V-Q mismatch) in the background lungs with heterogeneous V/Q distribution was seen in 12 of the 12 (100%) patients with primary PAH and in 10 of the 15 (66%) patients with passive PH, which were predominantly seen in the upper lung zone. Including these regions with reverse V-Q mismatch, the V/Q profile frequently showed flattened peaks with asymmetric and broadened V/Q distribution in all patients, with significant correlation between the standard deviation of V/Q ratios in the entire lungs and PaO2 and mean pulmonary arterial pressure (both; P<0.01). At the regions of the lungs with reverse V-Q mismatch, bronchial lumens compressed by dilated pulmonary arteries and heterogeneous lung attenuations were frequently seen on CT. Patients with primary PAH and passive PH seem to characteristically have a high prevalence of reverse V-Q mismatch indicative of an inadequate hypoxic vasoconstriction reflex on V/Q SPECT, frequently accompanied with heterogeneous lung attenuations and compressed airways on CT.

Lung ventilation–perfusion imbalance in pulmonary emphysema: assessment with automated V/Q quotient SPECT

Tc-99m-Technegas-MAA single photon emission computed tomography (SPECT)-derived ventilation (V)/perfusion (Q) quotient SPECT was used to assess lung V-Q imbalance in patients with pulmonary emphysema. V/Q quotient SPECT and V/Q profile were automatically built in 38 patients with pulmonary emphysema and 12 controls, and V/Q distribution and V/Q profile parameters were compared. V/Q distribution on V/Q quotient SPECT was correlated with low attenuation areas (LAA) on density-mask computed tomography (CT). Parameters of V/Q profile such as the median, standard deviation (SD), kurtosis and skewness were proposed to objectively evaluate the severity of lung V-Q imbalance. In contrast to uniform V/Q distribution on V/Q quotient SPECT and a sharp peak with symmetrical V/Q distribution on V/Q profile in controls, lung areas showing heterogeneously high or low V/Q and flattened peaks with broadened V/Q distribution were frequently seen in patients with emphysema, including lung areas with only slight LAA. V/Q distribution was also often asymmetric regardless of symmetric LAA. All the proposed parameters of V/Q profile in entire lungs of patients with emphysema showed large variations compared with controls; SD and kurtosis were significantly different from controls (P < 0.0001 and P < 0.001, respectively), and a significant correlation was found between SD and A-aDO2 (P < 0.0001). V/Q quotient SPECT appears to be more sensitive to detect emphysematous lungs compared with morphologic CT in patients with emphysema. SD and kurtosis of V/Q profile can be adequate parameters to assess the severity of lung V-Q imbalance causing gas-exchange impairment in patients with emphysema.

Ventilation-perfusion imbalance and chronic obstructive pulmonary disease staging severity

Chronic obstructive pulmonary disease (COPD) is characterized by a decline in forced expiratory volume in 1 s (FEV(1)) and, in many advanced patients, by arterial hypoxemia with or without hypercapnia. Spirometric and gas exchange abnormalities have not been found to relate closely, but this may reflect a narrow range of severity in patients studied. Therefore, we assessed the relationship between pulmonary gas exchange and airflow limitation in patients with COPD across the severity spectrum. Ventilation-perfusion (V(A)/Q) mismatch was measured using the multiple inert gas elimination technique in 150 patients from previous studies. The distribution of patients according to the GOLD stage of COPD was: 15 with stage 1; 40 with stage 2; 32 with stage 3; and 63 with stage 4. In GOLD stage 1, AaPo(2) and V(A)/Q mismatch were clearly abnormal; thereafter, hypoxemia, AaPo(2), and V(A)/Q imbalance increased, but the changes from GOLD stages 1-4 were modest. Postbronchodilator FEV(1) was related to Pa(O(2)) (r = 0.62) and Pa(CO(2)) (r = -0.59) and to overall V(A)/Q heterogeneity (r = -0.48) (P < 0.001 each). Pulmonary gas exchange abnormalities in COPD are related to FEV(1) across the spectrum of severity. V(A)/Q imbalance, predominantly perfusion heterogeneity, is disproportionately greater than airflow limitation in GOLD stage 1, suggesting that COPD initially involves the smallest airways, parenchyma, and pulmonary vessels with minimal spirometric disturbances. That progression of V(A)/Q inequality with spirometric severity is modest may reflect pathogenic processes that reduce both local ventilation and blood flow in the same regions through airway and alveolar disease and capillary involvement.

VISUAL EVOKED POTENTIAL CHANGES IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Aim: The normal visual evoked potential (VEP) reflects the functional integrity of the visual pathways from retinal to occipital striate area. Visual reseptors are sensitive to hypoxemia. Chronic obstructive pulmonary disease (COPD) is a progressive disease, in which hypoxemia occurs due to ventilation-perfusion imbalance. We aimed to evaluate the effects of COPD on VEPs. Methods: Thirty eight COPD patients and 17 healthy control subjects were accepted to the study. Pulmonary function tests were performed to all the participants. VEP of all participants were recorded. Results: P1 (P100) values of both right and left eyes (p=0.008 and p=0.010, respectively) and N2 value of right eye (p=0.030) were significantly higher in COPD patients than the control group. As there was just 1 female COPD patient, the measurements were re-evaluated for just male subjects. P1 values of both right and left eyes were significantly higher in male COPD patients than male control subjects (p=0.031 and p=0.023, respectively). Conclusion: VEPs, particularly P1 value, alters in COPD patients. This change in VEPs was thought to be due to hypoxemia caused by ventilation-perfusion imbalance in COPD.

Efficient clinical application of percutaneous cardiopulmonary support for perioperative management of a huge anterior mediastinal tumor

Efficient clinical application of percutaneous cardiopulmonary support for perioperative management of a huge anterior mediastinal tumor

The impact of bronchiolitis obliterans on late morbidity and mortality after single and bilateral lung transplantation for pulmonary hypertension

Primary pulmonary hypertension (PPH) is a rare cardiovascular disease with a variable course; however, in general, its prognosis is poor. Among the various treatment options available, transplantation (initially heart-lung transplantation, and later isolated single or bilateral lung transplantation) has become an accepted modality. Heart-lung transplantation is necessary only in a minority of patients because right ventricular recovery has been gratifying after isolated lung transplantation. Furthermore, the scarcity of suitable donor organs mandates the achievement of the maximal number of heart and lung transplants from the limited donor pool. Available published data show that both single and bilateral lung transplantation are suitable alternatives for the majority of patients with pulmonary hypertension. Bronchiolitis obliterans syndrome (BOS), the main cause of late mortality and morbidity in lung transplant recipients, affects pulmonary hypertensive patients as it does other recipient subgroups. The available data regarding the impact of BOS on single versus bilateral lung recipients with pulmonary hypertension are somewhat scanty. Although some have suggested that BOS is more prevalent among PPH recipients, this is not uniformly supported through the literature. Other reports have documented severe ventilation-perfusion imbalance associated with graft dysfunction secondary to BOS in single lung transplant recipients with PPH. Despite this, there are no available data to document a significant survival benefit for PPH patients receiving bilateral versus single lung transplantation. Our own transplantation experience at Washington University in St. Louis with pulmonary hypertension shows a trend toward better survival in bilateral lung recipients, although this difference is not significant. Ultimately, both single and bilateral lung replacement seem to be satisfactory transplant options in PPH. Both recipient groups are affected by BOS, and longer follow-up of larger numbers of patients may document superior survival and functional outcome with bilateral lung replacement.

The impact of bronchiolitis obliterans on late morbidity and mortality after single and bilateral lung transplantation for pulmonary hypertension.

Primary pulmonary hypertension (PPH) is a rare cardiovascular disease with a variable course; however, in general, its prognosis is poor. Among the various treatment options available, transplantation (initially heart-lung transplantation, and later isolated single or bilateral lung transplantation) has become an accepted modality. Heart-lung transplantation is necessary only in a minority of patients because right ventricular recovery has been gratifying after isolated lung transplantation. Furthermore, the scarcity of suitable donor organs mandates the achievement of the maximal number of heart and lung transplants from the limited donor pool. Available published data show that both single and bilateral lung transplantation are suitable alternatives for the majority of patients with pulmonary hypertension. Bronchiolitis obliterans syndrome (BOS), the main cause of late mortality and morbidity in lung transplant recipients, affects pulmonary hypertensive patients as it does other recipient subgroups. The available data regarding the impact of BOS on single versus bilateral lung recipients with pulmonary hypertension are somewhat scanty. Although some have suggested that BOS is more prevalent among PPH recipients, this is not uniformly supported through the literature. Other reports have documented severe ventilation-perfusion imbalance associated with graft dysfunction secondary to BOS in single lung transplant recipients with PPH. Despite this, there are no available data to document a significant survival benefit for PPH patients receiving bilateral versus single lung transplantation. Our own transplantation experience at Washington University in St. Louis with pulmonary hypertension shows a trend toward better survival in bilateral lung recipients, although this difference is not significant. Ultimately, both single and bilateral lung replacement seem to be satisfactory transplant options in PPH. Both recipient groups are affected by BOS, and longer follow-up of larger numbers of patients may document superior survival and functional outcome with bilateral lung replacement.

Current status of inhaled nitric oxide therapy in the perinatal period.

The recent discovery of nitric oxide (NO) and the elucidation of its biological roles has been accompanied by significant advances in our understanding of several physiological and pathological processes. Impaired NO synthesis and/or release may underlie the pathophysiology of several cardiopulmonary disorders characterised by hypoxemia and pulmonary hypertension. Inhaled NO produces selective pulmonary vasodilation and appears to be an effective new therapy for infants with pulmonary vasospasm or hypoxemia associated with ventilation-perfusion imbalance. Although formal reports from current randomised and controlled clinical trials of inhaled NO therapy are awaited, preliminary results suggest an improved outcome. NO is, however, still an investigational drug. The limitations of this therapy and its toxicology are reviewed.

Long-term Aspirin Therapy for Hepatopulmonary Syndrome

It is well known that arterial hypoxia can occur with chronic liver disease in adults as well as children.1-3 The clinical syndrome of hypoxia in association with liver disease has been called hepatopulmonary syndrome (HPS) or intrapulmonary vasodilative disease.3,4 In its classic form, HPS is a triad of abnormal arterial oxygenation, hepatic dysfunction, and pulmonary vascular dilation. The primary underlying disease of the hepatobiliary system is mainly liver cirrhosis or other chronic liver disease.4,5 The hypoxia is caused by either right-to-left shunting through arteriovenous connections within the lungs or a ventilation-perfusion imbalance caused by diffuse vasodilation of pulmonary arteries at the precapillary and capillary levels.1-3

Inhaled Nitric Oxide Therapy

To review the basic science, physiology, toxicity, and delivery of inhaled nitric oxide (NO). A literature review of inhaled NO is presented, and a brief discussion of current clinical applications is included. Inhaled NO is a new investigational drug used for selective vasodilation of the pulmonary vasculature. It mimics the effects of endogenously produced endothelium-derived relaxing factor. In addition to selective pulmonary vasodilation, inhaled NO can improve hypoxemia by improving ventilation-perfusion relationships within the lung. The doses of inhaled NO that produce improvements in oxygenation are lower than those needed to produce maximal vasodilation. Inhaled NO is being used in the intensive-care unit to treat critically ill patients with pulmonary hypertension or hypoxemia associated with ventilation-perfusion imbalance. It is also being used in the cardiac catheterization laboratory as a diagnostic tool. Few adverse effects have been associated with the use of inhaled NO. Despite a lack of randomized, controlled studies that show improved outcome in comparison with traditional treatments, inhaled NO seems to be an effective new therapy for patients with pulmonary vasospasm or hypoxemia associated with ventilation-perfusion imbalance. It may also prove to be a valuable diagnostic tool in the cardiac catheterization laboratory.