Pulmonary Capillary Hydrostatic Pressure Research Articles

NEGATIVE PRESSURE PULMONARY EDEMA AFTER GENERAL ANESTHESIA

Abstract Negative pressure pulmonary oedema is a type of non-cardiogenic pulmonary oedema caused by strong inspiratory effort to overcome obstruction in the upper airways. The main mechanisms responsible for the pathophysiology are the increase in pulmonary capillary hydrostatic pressure and the increase in capillary membrane permeability that develops after the negative intrathoracic pressure increases with inspiratory effort. Although all causes that may lead to upper airway obstruction may play a role in the etiology, the most common factor is laryngospasm that develops during awakening from anaesthesia. Young male smokers under general anaesthesia are more at risk. Onset may vary from a few minutes to several hours after extubation or relief of laryngospasm. It leads to an acute respiratory failure that is potentially life-threatening and usually requires follow-up and treatment in the intensive care unit. The first step in treatment is to relieve airway obstruction and provide oxygen support. Positive pressure ventilation and use of diuretics are beneficial and usually tend to improve within 24-48 hours. The mortality rate is reported to be around 5% in case analysis reports of recent years. Since it is observed more frequently in anaesthetised patients, early diagnosis and treatment in the postoperative period is important. The aim of this review is to present a current perspective on negative pressure pulmonary oedema in the light of the literature.

Targeting pulmonary capillary permeability to reduce lung congestion in heart failure: a randomized, controlled pilot trial.

Lung congestion in patients with heart failure (HF) has traditionally been treated using interventions that reduce pulmonary capillary hydrostatic pressure. The transient receptor potential vanilloid 4 (TRPV4) channel regulates fluid transit across the pulmonary capillary-interface, and represents a novel target to reduce lung water, independent of pulmonary capillary hypertension. This pilot study examined the safety and potential efficacy of TRPV4 blockade as a novel treatment for HF. In this randomized, double-blind, placebo-controlled crossover pilot trial, 11 subjects with chronic, compensated HF were treated with a novel TRPV4 antagonist (GSK2798745) or placebo. The primary endpoint was lung diffusing capacity for carbon monoxide (DLCO ) after 7 days of treatment with GSK2798745 as compared to placebo. Secondary endpoints included additional diffusion parameters, spirometry and safety assessments. Compared to placebo, treatment with GSK2798745 resulted in a trend to improvement in DLCO (placebo: -0.336 mL/mmHg/min; GSK2798745: +0.458 mL/mmHg/min; treatment difference: +0.793 mL/mmHg/min; 95% confidence interval: -0.925 to 2.512) that was not statistically significant. GSK2798745 was well-tolerated with no serious adverse events. In this pilot trial, GSK2798745 was found to be safe and well-tolerated, with a trend toward improved gas transfer. Further investigation is warranted in larger studies to determine whether treatment with TRPV4 antagonists or alternative treatments targeting capillary permeability might be effective to improve lung congestion, pulmonary gas transfer and clinical status in patients with acute or chronic HF.

The haemodynamic basis of lung congestion during exercise in heart failure with preserved ejection fraction

Increases in extravascular lung water (EVLW) during exercise contribute to symptoms, morbidity, and mortality in patients with heart failure and preserved ejection fraction (HFpEF), but the mechanisms leading to pulmonary congestion during exercise are not well-understood. Compensated, ambulatory patients with HFpEF (n = 61) underwent invasive haemodynamic exercise testing using high-fidelity micromanometers with simultaneous lung ultrasound, echocardiography, and expired gas analysis at rest and during submaximal exercise. The presence or absence of EVLW was determined by lung ultrasound to evaluate for sonographic B-line artefacts. An increase in EVLW during exercise was observed in 33 patients (HFpEFLW+, 54%), while 28 (46%) did not develop EVLW (HFpEFLW-). Resting left ventricular function was similar in the groups, but right ventricular (RV) dysfunction was two-fold more common in HFpEFLW+ (64 vs. 31%), with lower RV systolic velocity and RV fractional area change. As compared to HFpEFLW-, the HFpEFLW+ group displayed higher pulmonary capillary wedge pressure (PCWP), higher pulmonary artery (PA) pressures, worse RV-PA coupling, and higher right atrial (RA) pressures during exercise, with increased haemoconcentration indicating greater loss of water from the vascular space. The development of lung congestion during exercise was significantly associated with elevations in PCWP and RA pressure as well as impairments in RV-PA coupling (area under the curve values 0.76-0.84). Over half of stable outpatients with HFpEF develop increases in interstitial lung water, even during submaximal exercise. The acute development of lung congestion is correlated with increases in pulmonary capillary hydrostatic pressure that favours fluid filtration, and systemic venous hypertension due to altered RV-PA coupling, which may interfere with fluid clearance. NCT02885636.

Prolonged respiratory failure due to pulmonary embolism in a young woman: a case report

BackgroundThe pathophysiology of pulmonary edema is generally considered to result from elevated pulmonary capillary hydrostatic pressure due to increased left atrial pressure in consequence of a failing left ventricle.Case presentationWe present a case of pulmonary edema secondary to severe hypalbuminemia under excessive respiratory drive in a 29-year-old Caucasian woman in respiratory distress with detected bilateral central pulmonary embolism.ConclusionIn conjunction with severe hypalbuminemia, even the negative intrathoracic pressure swings of respiratory distress may cause pulmonary edema. Detrimental consequences of non-invasive ventilation due to uncontrolled tidal volume and pressure swings need to be considered when treating patients in hypoxemic respiratory failure with low serum albumin.

The β-Adrenergic Agonist Albuterol Improves Pulmonary Vascular Reserve in Heart Failure With Preserved Ejection Fraction.

Pulmonary vascular resistance fails to decrease appropriately during exercise in patients with heart failure with preserved ejection fraction (HFpEF). Interventions that enhance pulmonary vasodilation might be beneficial in this cohort but could also worsen left atrial hypertension, exacerbating lung congestion. Intravenous β-agonists reduce pulmonary vascular resistance but are not suitable for chronic use. We hypothesized that the inhaled β-adrenergic agonist albuterol would improve pulmonary vasodilation during exercise in patients with HFpEF, without increasing left heart filling pressures. We performed a randomized, double-blind, placebo-controlled trial testing the effects of inhaled albuterol on resting and exercise hemodynamics in subjects with HFpEF using high-fidelity micromanometer catheters and expired gas analysis. The primary end point was pulmonary vascular resistance during exercise. Subjects with HFpEF (n=30) underwent resting and exercise hemodynamic assessment and were then randomized 1:1 to inhaled, nebulized albuterol or placebo. Rest and exercise hemodynamic testing was then repeated. Albuterol improved the primary end point of exercise pulmonary vascular resistance as compared with placebo (-0.6±0.5 versus +0.1±0.7 WU; P=0.003). Albuterol enhanced cardiac output reserve and right ventricular pulmonary artery coupling, reduced right atrial and pulmonary artery pressures, improved pulmonary artery compliance, and enhanced left ventricular transmural distending pressure (all P <0.01), with no increase in pulmonary capillary hydrostatic pressures. Albuterol improves pulmonary vascular reserve in patients with HFpEF without worsening left heart congestion. Further study is warranted to evaluate the chronic efficacy of β-agonists in HFpEF and other forms of pulmonary hypertension. URL: http://www.clinicaltrials.gov . Unique identifier: NCT02885636.

Neurogenic Pulmonary Edema

Neurogenic Pulmonary Edema (NPE) is defined as the acute onset of dyspnea or a decrease in PaO2/FiO2 ratio, following an acute central nervous system (CNS) insult, in the absence of other obvious causes of lung injury. The most important cause of NPE is subarachnoid hemorrhage (SAH), followed by cerebraltrauma and epilepsy. The incidence of NPE after SAH in the literature may vary from 4 to 23% in greater studies, with SAH accounting for 43-73% of cases of NPE. It is postulated that an excessive adrenergic discharge would lead to pulmonary vasoconstriction and a rapid increase in pulmonary capillaryhydrostatic pressure, thus promoting fluid leakage to the alveolar space. NPE is generally treated in a supportive and conservative fashion, and patient management should be focused in the primary insult.

Extravascular lung water measurement in critically ill patients

In intensive care patients, due to increase in hydrostatic pressure and hyperpermeability state, pulmonary edema occurs. In this review, we discussed about definition and amount of extravascular lung water index (EVLWI) which relates to an increasing pulmonary capillary hydrostatic pressure or increasing capillary permeability. EVLWI-to-intrathoracic blood volume ratio is useful in determining the cause of pulmonary edema. EVLWI can be helpful in approximation of the amount of fluid overload and capillary leak in acute inflammatory injury. This is identified as a prognostic marker that is related to respiratory function and mortality in patients with acute respiratory distress syndrome and sepsis. Usage of EVLWI for determining of pulmonary edema in children would be beneficial.

Human Physiology in an Aquatic Environment.

Water covers over 70% of the earth, has varying depths and temperatures and contains much of the earth's resources. Head-out water immersion (HOWI) or submersion at various depths (diving) in water of thermoneutral (TN) temperature elicits profound cardiorespiratory, endocrine, and renal responses. The translocation of blood into the thorax and elevation of plasma volume by autotransfusion of fluid from cells to the vascular compartment lead to increased cardiac stroke volume and output and there is a hyperperfusion of some tissues. Pulmonary artery and capillary hydrostatic pressures increase causing a decline in vital capacity with the potential for pulmonary edema. Atrial stretch and increased arterial pressure cause reflex autonomic responses which result in endocrine changes that return plasma volume and arterial pressure to preimmersion levels. Plasma volume is regulated via a reflex diuresis and natriuresis. Hydrostatic pressure also leads to elastic loading of the chest, increasing work of breathing, energy cost, and thus blood flow to respiratory muscles. Decreases in water temperature in HOWI do not affect the cardiac output compared to TN; however, they influence heart rate and the distribution of muscle and fat blood flow. The reduced muscle blood flow results in a reduced maximal oxygen consumption. The properties of water determine the mechanical load and the physiological responses during exercise in water (e.g. swimming and water based activities). Increased hydrostatic pressure caused by submersion does not affect stroke volume; however, progressive bradycardia decreases cardiac output. During submersion, compressed gas must be breathed which introduces the potential for oxygen toxicity, narcosis due to nitrogen, and tissue and vascular gas bubbles during decompression and after may cause pain in joints and the nervous system.

Understanding negative pressure pulmonary edema.

Understanding negative pressure pulmonary edema.

Albumine sérique et insuffisance cardiaque : données récentes sur un nouveau paradigme

Hypoalbuminemia is a common condition in patients with heart failure and is mainly related to the malnutrition-inflammation complex syndrome. Other causal factors can be involved, which include hemodilution, liver dysfunction, increased transcapillary escape rate, renal and enteral loss. Evidence is growing that hypoalbuminemia independently predicts incident heart failure in patients with end-stage renal disease and elderly patients, as well as mortality in patients with heart failure regardless of left ventricular ejection fraction and clinical presentation. Hypoalbuminemia induces a low plasma oncotic pressure, which facilitates pulmonary edema in patients without critical increase in pulmonary capillary hydrostatic pressures. Hypoalbuminemia may also contribute to the progression of heart failure by favoring myocardial edema, volume overload, diuretic resistance and exacerbation of oxidative stress and inflammation. If relevant, removal of subclinical excess of fluid and renutrition may be indicated in patients with heart failure and hypoalbuminemia. Additional research is warranted to determine the specific role of serum albumin in the pathophysiologic process of heart failure and the potential benefits of targeted therapeutic interventions.

Case Scenario: Acute Postoperative Negative Pressure Pulmonary Edema

A 25-yr-old man (weight, 68 kg; height, 183 cm) presentedto the surgery center for excision of back and thigh schwan-nomas on the same day. The patient’s medical history wassignificant only for his history of multiple schwannoma re-sections and a history of smoking one pack of cigarettes perweek for the past 5 yr. He denied previous problems withgeneral anesthesia, and his baseline peripheral oxygen satu-ration was 99% on ambient air.Thepatientwaspremedicatedwith2mgmidazolam,andanesthesia was induced with 250 mg fentanyl, 500 mg thio-pental, and 8 mg vecuronium given for facilitation of tra-cheal intubation. He was atraumatically intubated with a7-mm ID endotracheal tube using a no. 3 Macintosh laryn-goscope (Teleflex Medical, Research Triangle Park, NC) onthe first attempt with direct visualization of the vocal cords.The patient was turned prone, bilateral breath sounds werereconfirmed, and schwannoma excisions were performed ontheleftthighandtheleftflank.Atotalof0.5mghydromor-phone was administered for analgesia. The intraoperativecoursewasunremarkable.Thepatientwashemodynamicallystable with minimal blood loss and was easily ventilated andoxygenated. A total of 500 ml lactated Ringer’s solution wasadministeredduringthe65-minsurgicalprocedure.Thepa-

Pulmonary/renal interaction

Acute kidney injury contributes to the development of acute lung injury and vice-versa. Volume overload that may occur during renal impairment increases pulmonary capillary hydrostatic pressure. However, experimental evidence clearly shows that lung damage occurs even in the absence of positive fluid balance. However, acute lung injury with its attendant hypoxemia, hypercapnia and mechanical ventilation worsens renal hemodynamics and function. An increasing body of evidence suggests that kidney and lung interact (crosstalk) during severe insults, such as shock, trauma, and sepsis, due to a loss of the normal balance of immune, inflammatory and soluble mediators. Kidney-lung crosstalk in the critically ill constitutes a possibility to analyze mechanisms of multiple organ failure in which the kidney and the lung can play an important role. Consequently, on the clinical side, specific therapeutic options can be hypothesized for kidney/lung dysfunction. Fluid management optimization and prevention of inflammation and lung stretching are currently recommended for the treatment of acute lung and renal injury. Extracorporeal CO2 removal and renal replacement associated with extracorporeal membrane oxygenation might be interesting options for a future approach to pulmonary/renal syndrome.

Brain Natriuretic Peptide Level In Six Basic Underwater Demolitions/SEAL Recruits Presenting With Swimming Induced Pulmonary Edema (SIPE)

Swimming induced pulmonary edema (SIPE) is associated with both SCUBA diving and strenuous surface swimming; however, the majority of reported cases and clinically observed cases tend to occur during or after aggressive surface swimming. Capillary stress failure appears to be central to the pathophysiology of this disorder. Regional pulmonary capillaries are exposed to relatively high pressures secondary to increased vascular volume, elevation of pulmonary vascular resistance, and regional differences in perfusion secondary to forces of gravity and high cardiac output. Acute pulmonary edema can be classified as either cardiogenic or noncardiogenic or both. Cardiogenic pulmonary edema occurs when the pulmonary capillary hydrostatic pressure exceeds plasma oncotic pressure. Noncardiogenic pulmonary edema occurs when pulmonary capillary permeability is increased. Given the pathophysiology noted above, SIPE can be described as a cardiogenic pulmonary edema, at least in part, since an increased transalveolar pressure gradient has been implicated in the pathogenesis of SIPE. Brain natriuretic peptide (BNP) is used in the clinical setting to differentiate cardiac from pulmonary sources of dyspnea, specifically to diagnose cardiogenic pulmonary edema. During clinical management, BNP levels were drawn on six BUD/S recruits simultaneously presenting with pulmonary complaints consistent with SIPE, after an extended surface bay swim. This paper analyzes that data after de-identification and reviews the pathophysiology and clinical management of SIPE.

Tissue Doppler echocardiography for the diagnosis of new-onset heart failure with normal ejection fraction: Influence of serum protein concentration on clinical interpretation in elderly patients

According to Starling's law, low serum colloid osmotic pressure related to hypoproteinaemia is likely to modulate the pulmonary capillary hydrostatic pressure threshold of pulmonary oedema formation. We therefore examined the clinical relevance of bedside tissue Doppler echocardiography in the emergency diagnosis of new-onset heart failure with normal ejection fraction (HFnlEF) according to serum protein concentration. A total of 105 consecutive elderly patients presenting with acute severe dyspnoea were prospectively enrolled. B-type natriuretic peptide (BNP) concentration and spectral tissue Doppler-derived septal E/E' ratio were obtained at presentation. Serum protein concentration was measured immediately after clinical stabilization, with a value of less than 6g/dL defining hypoproteinaemia. The diagnostic performance of E/E' was excellent in normoproteinaemic patients (n=71; area under the receiver-operating characteristic [ROC] curve 0.97; p<0.001) and reasonable in hypoproteinaemic patients (n=34; area under ROC curve 0.83; p<0.001). By multivariable logistic regression analysis, E/E' provided independent and incremental diagnostic information over the Boston score and BNP concentration in patients with a normal serum protein concentration (p<0.01). Critical elevation of pulmonary capillary pressure, defined as E/E'>15, was present in 93% of patients with HFnlEF and normoproteinaemia versus 55% of patients with HFnlEF and hypoproteinaemia (p=0.0017). Septal E/E'>15 is clinically relevant for the emergency diagnosis of new-onset HFnlEF among elderly patients with normal serum protein concentration. Lower abnormal values less than 15 should be considered predictive of this condition in the setting of hypoproteinaemia.

Propofol attenuates oxidant-induced acute lung injury in an isolated perfused rabbit-lung model

Reactive oxygen species have been strongly implicated in the pathogenesis of acute lung injury (ALI). Some animal studies suggest that free radical scavengers inhibit the onset of oxidant-induced ALI. Propofol (2,6-diisopropylphenol) is chemically similar to phenol-based free radical scavengers such as the endogenous antioxidant vitamin E. Both in vivo and in vitro studies have suggested that propofol has antioxidant potential. We hypothesized that propofol may attenuate ALI by acting as a free-radical scavenger. We investigated the effects of propofol on oxidant-induced ALI induced by purine and xanthine oxidase (XO), in isolated perfused rabbit lung, in two series of experiments. In series 1, we examined the relationship between the severity of ALI and the presence of hydrogen peroxide (H2O2). In series 2, we evaluated the effects of propofol on attenuating ALI and the dose dependence of these effects. The lungs were perfused for 90 min, and we evaluated the effects on the severity of ALI by monitoring the pulmonary capillary filtration coefficient (Kfc), pulmonary arterial pressure (Ppa), and the pulmonary capillary hydrostatic pressure (Ppc). In series 1, treatment with catalase (an H2O2 scavenger) prior to the addition of purine and XO resulted in complete prevention of ALI, suggesting that H2O2 may be involved closely in the pathogenesis of ALI. In series 2, pretreatment with propofol at concentrations in excess of 0.5 mM significantly inhibited the increases in the Kfc values, and that in excess of 0.75 mM significantly inhibited the increase in the Ppa values. Propofol attenuates oxidant-induced ALI in an isolated perfused rabbit lung model, probably due to its antioxidant action.

Pulmonary capillary pressure.

Pulmonary capillary pressure is a primary determinant of fluid flux across the pulmonary capillary wall [1]. Increasing pulmonary capillary pressure increases fluid flux out of the capillaries into the interstitium and in the extreme induces pulmonary edema. Pulmonary capillary pressure is itself determined by the mean pulmonary artery pressure, pulmonary vascular resistance, and total blood flow. The distribution of the pulmonary vascular resistance from precapillary arterial to postcapillary venous compartments varies. Accordingly, at any given blood flow rate the hydrostatic pressure in the pulmonary capillaries depends on the magnitude of the resistance to blood flow across the pulmonary circulation and its distribution between precapillary and postcapillary vessels. Since pulmonary capillary pressure cannot be directly measured, the presence and relevance of increased pulmonary capillary hydrostatic pressures to values in excess of pulmonary artery occlusion pressure are often overlooked.

Cardiopulmonary manifestations of fulminant enterovirus 71 infection.

The pathogenesis of acute pulmonary edema and cardiac collapse after enterovirus 71 (EV71) infection are not completely understood. To determine the hemodynamic features and the mechanism of pulmonary edema (PE) after EV71 infection by direct intracardiac monitoring. Prospective clinical and laboratory study at a tertiary medical center. Five consecutive infants, ages 2 to 13 months, with EV71 infection-proved by viral isolation in 4 and antibody in 1-with PE were enrolled. The clinical characteristics were systemically assessed. Hemodynamic profiles were determined every 4 hours by simultaneously implanted pulmonary arterial and central venous catheters during the acute stage. Magnetic resonance imaging revealed that all 5 infants had brainstem lesions. All patients had tachycardia and hyperthermia. Transient systolic hypertension was noted in 1 patient, and 1 presented with hypotension. Pulmonary artery pressure in all 5 infants was normal or mildly elevated (26-31 mm Hg), and central venous pressure ranged from 10 to 22 mm Hg. Pulmonary artery occlusion pressures were normal or slightly elevated (13-16 mm Hg). Systemic and pulmonary vascular resistances were transiently increased in only 1 patient. The stroke volume index decreased to 15.3 to 35.7 mL/M2 (normal: 30-60 mL/M2), but because of the elevated heart rate, the cardiac index did not decrease. All hemodynamics normalized within days. Fulminant EV71 infection may lead to severe neurologic complications and acute PE. The acute PE and cardiopulmonary decompensation in EV71 infection are not directly caused by viral myocarditis. The mechanism of PE may be related to increased pulmonary vascular permeability caused by brainstem lesions and/or systemic inflammatory response instead of increased pulmonary capillary hydrostatic pressure.

Inflammation Doesn't Cause High-Altitude Pulmonary Edema

The role of increased pulmonary artery and pulmonary capillary hydrostatic pressures in the pathogenesis of high-altitude pulmonary edema (HAPE) has been established. However, the issue of whether inflammation is part of the pathophysiologic process is unresolved. These investigators conducted a prospective case study of 16 experienced mountaineers who were susceptible to HAPE (10 had …

Hypertonic-hyperoncotic solution increases canine lymph flows.

Hypertonic-hyperoncotic solutions (HHS) have attracted a lot of interest in the treatment of various forms of hypovolaemic conditions during the last decade. It has been speculated that HHS might even be of therapeutic value in normo- and hypervolaemic conditions by mobilising extravascular fluid. We studied thoracic and abdominal lymphatic flows and circulatory response following the administration of a single bolus injection of hypertonic-hyperoncotic solution, 10% dextran 60 in 7.2% saline (HHS), in a nonhypovolaemic canine model. A modified surgical procedure for collecting thoracic lymph is also presented. Both thoracic and abdominal lymph flow increased significantly by approximately 50% after administration of HHS. Cardiac output and calculated pulmonary capillary hydrostatic pressure increased. Hypertonic-hyperoncotic solution given intravenously as a single injection increased both thoracic and abdominal lymph flows in the initially normovolaemic animal.

Tumor necrosis factor mediates experimental pulmonary edema by ICAM-1 and CD18-dependent mechanisms.

(TNF alpha)-induced sequestration of neutrophils (PMN) in lungs and of the resultant PMN-dependent pulmonary edema. Guinea pig lungs perfused with Ringers-albumin were challenged with TNF alpha (1,000 U/ml) for 90 min, followed by addition of fresh perfusate containing 2 x 10(7) human PMN. TNF alpha challenge caused sequestration of PMN in the pulmonary vascular bed as indicated by a threefold increase in lung tissue myeloperoxidase activity (MPO). The activation of the sequestered PMN with phorbol 12-myristate 13-acetate (PMA; 5 x 10(-9) M) produced threefold increases in pulmonary artery (Ppa) and pulmonary capillary hydrostatic (Pcap) pressures, and twofold increases in lung wet-to-dry weight (W/D) ratio and capillary filtration coefficient (Kf,c) over baseline. TNF alpha prestimulation was required for these responses since activation of PMN with PMA in control lungs produced smaller increases in Ppa and Pcap (P less than 0.01) and did not change the W/D and Kf,c. TNF alpha prestimulation also induced the expression of intercellular adhesion molecule (ICAM-1) on pulmonary vascular endothelial cells. Monoclonal antibodies (mAbs) to the neutrophil CD18 integrin (beta-chain of CD11/CD18 complex) (mAb IB4) and to its endothelial cell ligand ICAM-1 (mAb RR1/1) were used to examine the role of PMN adhesion in the TNF alpha-induced responses. Pretreatment of PMN with mAb IB4 prevented PMN uptake and increases in Ppa, Pcap, Kf,c, and W/D ratio. Addition of mAb RR1/1 to the perfusate reduced PMN uptake by 58%, and prevented the increases in Ppa, Pcap, Kf,c, and W/D ratio, as with mAb IB4. The findings indicate that TNF alpha prestimulation of lungs mediates PMN uptake and that this requires the expression of ICAM-1 and its interaction with CD18 integrin on PMN. The activation of PMN sequestered by ICAM-1-dependent mechanism contributes to the development of pulmonary vascular injury and edema.