Risk Of Pulmonary Edema Research Articles

GW24-e0444 Distinguish PVOD from PAH: Case Report and Review of Literature

ObjectivesPulmonary veno-occlusive disease (PVOD) is a rare type of pulmonary hypertension, with similar clinical presentation to pulmonary arterial hypertension (PAH) but poorer prognosis and higher possibility to develop sever pulmonary...

The risk of development of perioperative myocardial lesions and acute left ventricular insufficiency in the patients presenting with pheochromocytoma

Differential diagnostics of coronary heart disease (CHD) and catecholamine-induced cardiomyopathy was undertaken in 19 of the 106 patients presenting with pheochromocytoma. Group 1 included 13 patients having the history of acute myocardial infarction. Diagnostics of CHD was performed following the adequate preoperative alpha-blockade (supplemented by Β-blockade whenever indicated). Group 2 was comprised of 6 patients suffering pulmonary oedema (normotensive, 10-70 min after removal of the tumour) and showing the elevated levels of biomarkers of myocardial necrosis and/or ischemic-type changes of ECG in the early postoperative period. The clinically significant myocardial ischemia requiring correction was documented only in one of the 19 patients. The two groups were not significantly different in terms of the mean tumour size and duration of surgery, the quality of preoperative compensation, and intraoperative fluctuations of arterial pressure. The mean age of the patients in group 1 (47 years) was much higher than that in group 2 (29 years). All patients in group 2 exhibited the predominantly adrenalin-type secretion whereas 10 patients of group 1 had the noradrenalin-type secretion and two others mixed-type secretion with the predominance of noradrenalin release. It was shown that the patients with the predominantly adrenaline-type secretion by the tumour were at higher risk of pulmonary oedema. The possibility of application of alpha-methylparatyrosine having beneficial effect on contractile activity of myocardium as the main agent for preoperative preparation is discussed.

Fluid and Vasopressor Management for Cesarean Delivery Under Spinal Anesthesia

The purpose of this Continuing Professional Development module is to review the physiology of maternal hypotension induced by spinal anesthesia in pregnant women, and the effects of fluids and vasopressors. Maternal hypotension induced by spinal anesthesia is caused mainly by peripheral vasodilatation and is not usually associated with a decrease in cardiac output. Although the intravenous administration of fluids helps to increase cardiac output, it does not always prevent maternal hypotension. Three strategies of fluid administrations are equivalent for the prevention of maternal hypotension and a reduced need for vasopressors: (1) colloid preload; (2) colloid coload; and (3) crystalloid coload. Crystalloid preload is not as effective as any of those three strategies. Unlike phenylephrine, ephedrine can cause fetal acidosis. Therefore, phenylephrine is recommended as first line treatment of maternal hypotension. A phenylephrine infusion (25-50 μg·min−1) appears to be more effective than phenylephrine boluses to prevent hypotension, and nausea and vomiting. In pre-eclamptic patients, spinal anesthesia produces less hypotension than in normal pregnant women and fluid volumes up to 1,000 mL are usually well tolerated. Therefore mild to moderate intravascular volume loading is recommended, keeping in mind the increased risk for pulmonary edema in this population. In pre-eclamptic patients, hypotension can be treated either with ephedrine or phenylephrine, and phenylephrine infusions are not recommended. A volume loading regimen other than crystalloid preload should be adopted. A phenylephrine infusion during elective Cesarean delivery is beneficial for the mother and safe for the newborn.

Transapical Left Ventricular Vent (TLVV) during Artero-Venous ECMO Support: A Bridge to Solution in Acute Cardiogenic Shock

Purpose One of the main limitations of artero-venous ECMO (AV-ECMO) support is the inappropriate unloading of the left ventricle (LV). The increased risk of pulmonary edema and impairs LV function reduces the possibility of recovery or the feasibility of a permanent LVAD implantation or heart transplantation. The solution proposed is the surgical implantation of a transapical LV vent (TLVV) through a minimally invasive approach. TLVV reduces significantly the pulmonary edema and it gives the chance to convert AV- ECMO circuit to a short-term LVAD as a bridge to solution. Methods and Materials From January 2010 to June 2012, 16 patients supported by pheripheral AV ECMO for cardiogenic shock underwent TLVV implantation. Cannulation was done through a mini-torachotomy with the seldinger technique using an arterial high-flow cannula. TLVV was connected to the venous inflow line of the AV ECMO. The switch from AV ECMO to short term LVAD has been done in two stages: the weaning from the right circulatory support (intermediate stage: A-A ECMO) and the subsequent weaning from the oxygenator. Results In-hospital mortality was 47,5 %. In 12 patients (75,0%) pulmonary function significantly improved. AV ECMO circuit was simplified to a short term LVAD in 10 patients. Ten pts were bridged to a definitive treatment: heart transplantation in 3 patients, permanent LVAD implantation in 2 patients and bridge to recovery in 5 patients. In hospital survival in patients arrived to these solutions was 8/10 (80,0%). Conclusions TLVV improved pulmonary function and it gave the possibility to switch from the A-V ECMO to a short-term LVAD. After clinical stabilization of patients it was possible to access to a definitive treatment. We think that in the setting of an AV ECMO, TLVV implantation is useful in order to identify the best candidate for permanent LVAD, heart transplantation or recovery reducing significantly the risk of unsuccess.

Hypertension pulmonaire et insuffisance cardiaque : le rôle de la vascularisation pulmonaire

Left heart disease is the most common cause of pulmonary hypertension. Increased left-sided filling pressure leads to passive postcapillary venous hypertension. In some patients, pulmonary vasoconstriction and vascular remodeling may lead to a further increase in pulmonary pressure. When precapillary hypertension component is associated to left heart failure, the elevation of pulmonary pressure is out of proportion with left atrial pressure: transpulmonary gradient greater than 12 mmHg (mean pulmonary pressure – mean capillary pressure) and pulmonary vascular resistance greater than three Wood units. Precapillary pulmonary hypertension is common in severe systolic heart failure. Before cardiac transplantation, increased pulmonary vascular resistance greater than 3,5 Wood units are reported in 19 to 35% of patients. In those patients vasoreactivity tests are performed with inotropic and/or systemic and/or pulmonary agents to determine the risk of right heart failure after transplantation. There is no pulmonary vascular resistance level above which transplantation is contraindicated. Cardiac assistance may be used before and after transplantation when pulmonary hypertension is severe and not reversible with conventional treatment and/or pulmonary vasodilators. The contribution of precapillary PH in diastolic heart failure is not known but can be significant and lead to disproportionate PH particularly in elderly. The precapillary component of pulmonary hypertension could be a therapeutic target for specific pulmonary vasodilators. Until now pharmacological trials has been disappointing and those medications can be dangerous because of increasing blood flow to the pulmonary capillaries with a risk of pulmonary edema when left sided pressure are still elevated.

Pulmonale venookklusive Erkrankung – eine seltene Form der pulmonalen Hypertonie

Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary hypertension. So far some 200 cases have been published worldwide. Since the latest classification, agreed at a meeting in Venice in 2003, PVOD is included in the group of pulmonary arterial hypertension (PAH). It has been hypothesized that it represents endothelial dysfunction of unknown cause. Although it has many features in common with idiopathic PAH, it partially differs from it phenotypically. After exclusion of known causes of pulmonary hypertension, such as diseases of pulmonary interstitial tissue, acral clubbing and rales suggest PVOD. The findings typical in the computed tomogram of the chest include prominent septal lines, centro-acinar opacities and mediastinal lymphadenopathy. In addition to arterial lesions PVOD is particularly characterized by lesions in the venous vascular bed. PVOD has a poor prognosis. Treatment with medication approved for PAH may carry the risk of pulmonary edema. Currently the immediate listing for lung- or combined lung-heart-transplantation is recommended, once the diagnosis of PVOD has been established.

Pulmonary edema after competitive breath-hold diving

During an international breath-hold diving competition, 19 of the participating divers volunteered for the present study, aimed at elucidating possible symptoms and signs of pulmonary edema after deep dives. Measurements included dynamic spirometry and pulse oximetry, and chest auscultation was performed on those with the most severe symptoms. After deep dives (25-75 m), 12 of the divers had signs of pulmonary edema. None had any symptoms or signs after shallow pool dives. For the whole group of 19 divers, average reductions in forced vital capacity (FVC) and forced expiratory volume in the first second (FEV(1)) were -9 and -12%, respectively, after deep dives compared with after pool dives. In addition, the average reduction in arterial oxygen saturation (Sa(O(2))) was -4% after the deep dives. In six divers, respiratory symptoms (including dyspnea, cough, fatigue, substernal chest pain or discomfort, and hemoptysis) were associated with aggravated deteriorations in the physiological variables (FVC: -16%; FEV(1): -27%; Sa(O(2)): -11%). This is the first study showing reduced spirometric performance and arterial hypoxemia as consequences of deep breath-hold diving, and we suggest that the observed changes are caused by diving-induced pulmonary edema. From the results of the present study, it must be concluded that the great depths reached by these elite apnea divers are associated with a risk of pulmonary edema.

NALOXONE-INDUCED PULMONARY EDEMA

INTRODUCTION:Naloxone, an opiate antagonist, is used for complete or partial reversal of opioid effects. Significant adverse reactions of the drug include hypertension, ventricular arrhythmias, cardiac arrest, seizures and pulmonary edema. Questions have arisen regarding the risk of pulmonary edema when using naloxone in opiate dependent patients. The presumed cause of the edema is an adrenergic crisis with a large increase in catecholamines.

Occult alveolar haemorrhage in pulmonary veno-occlusive disease

Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary arterial hypertension that affects predominantly post-capillary pulmonary vessels. A major concern with PVOD is the poor response to available therapies and the risk of pulmonary oedema with continuous intravenous epoprostenol. The present authors hypothesised that alveolar haemorrhage may be a characteristic feature of pulmonary veno-occlusive disease, as compared with other forms of pulmonary arterial hypertension that predominantly involve pre-capillary pulmonary arteries. This paper reports a series of 19 patients with either PVOD (n = 8) or idiopathic pulmonary arterial hypertension (IPAH; n = 11) who underwent bronchoalveolar lavage. Cytological analyses were performed and differential counts were made on Perls-stained preparations. The Golde score was used to assess alveolar haemorrhage. As compared with IPAH, PVOD was characterised by a higher percentage of haemosiderin-laden macrophages (40+/-37 versus 3+/-6%), resulting in elevated Golde scores (81+/-88 versus 4+/-10). It was concluded that occult alveolar haemorrhage is a common feature of pulmonary veno-occlusive disease. Detecting occult alveolar haemorrhage may be of interest in the diagnostic approach of pulmonary veno-occlusive disease.

Cardiac Disease in Pregnancy

After completing this article, readers should be able to: 1. Describe how the cardiovascular changes of pregnancy can affect the woman who has cardiac disease. 2. Review the importance of preconception counseling. 3. Discuss the purpose of a multidisciplinary team approach to the management of the woman who has cardiac disease during pregnancy. 4. Review delivery management of women who have cardiac disease. Pregnancy causes considerable physiologic change in women, particularly in their cardiovascular systems. Circulating blood volume increases dramatically, and cardiac output increases up to 50% by the end of pregnancy. Pregnant women who have cardiac disease must be able to accommodate these normal changes to have a successful pregnancy. Inability to do so can result in increased morbidity and mortality. Cardiac disease is an important cause of nonobstetric mortality during pregnancy and can result in significant morbidity. (1)(2) Approximately 10% of all maternal deaths in the United States can be attributed to cardiac disease, a number that has remained consistent for the last half century. (1) In one study of 1,000 pregnant women who had various types of cardiac disease and were followed by the same health-care team over a 10-year period, more than 75% of the women had no complications during pregnancy. (2) Among the remaining 25%, the following complications were seen most often: The overall maternal mortality rate in this group was 2.7%, and the stillbirth and spontaneous abortion rate was 7.7%. Cardiac disease covers a wide range of conditions, including congenital heart disease, acquired disease such as rheumatic valvular disease, and coronary disease. It is estimated that 1% to 3% of women either have cardiac disease entering pregnancy or are diagnosed with cardiac disease while they are pregnant. …

Hydrogen sulphide.

Hydrogen sulphide (H2S) is the primary chemical hazard in natural gas production in 'sour' gas fields. It is also a hazard in sewage treatment and manure-containment operations, construction in wetlands, pelt processing, certain types of pulp and paper production, and any situation in which organic material decays or inorganic sulphides exist under reducing conditions. H2S dissociates into free sulphide in the circulation. Sulphide binds to many macromolecules, among them cytochrome oxidase. Although this is undoubtedly an important mechanism of toxicity due to H2S, there may be others H2S provides little opportunity for escape at high concentrations because of the olfactory paralysis it causes, the steep exposure-response relationships, and the characteristically sudden loss of consciousness it can cause which is colloquially termed 'knockdown.' Other effects may include mucosal irritation, which is associated at lower concentrations with a keratoconjunctivitis called 'gas eye' and at higher concentrations with risk of pulmonary oedema. Chronic central nervous system sequelae may possibly follow repeated knockdowns: this is controversial and the primary effects of H2S may be confounded by anoxia or head trauma. Treatment is currently empirical, with a combination of nitrite and hyperbaric oxygen preferred. The treatment regimen is not ideal and carries some risk.

Pulmonary edema associated with the treatment of preterm labor: what critical care nurses need to know

Knowledge of the physiologic changes, conditions, and therapies of pregnancy that increase the risk of pulmonary edema enables nurses to influence the outcome of their patients who develop medical complications while undergoing tocolytic therapy. Cooperation between perinatal and critical care nurses ensures optimal care of both the mother and the fetus.

Threshold values of colloid-osmotic pressure, serum albumin or protein during perioperative period

The water flux across the capillary membrane is directly related to a gradient of hydrostatic and colloid osmotic forces. The membrane is not an absolute barrier to proteins. Any change in the capillary permeability tends to decrease the plasmatic colloid osmotic pressure. The interstitial space includes a perimicrovascular space and a compliant connective tissue space, where oedema accumulates. The lymphatics may easily drain excess filtration, but cannot clear constituted oedema. Primarily, the risk of pulmonary oedema determines the lower limit of the colloid osmotic pressure. During the perioperative period, any extrapolation of the colloid, osmotic pressure from protidaemia or albuminaemia would be approximate. Two major conclusions can be drawn from the results of Guyton and Lindsey. First, in the absence of left ventricular failure, a 50% decrease in colloid osmotic pressure does not increase extravascular lung water. Second, in the case of left ventricular failure, when the left atrial pressure exceeds 10 mmHg, a 50% decrease in colloid osmotic pressure significantly increases the risk of pulmonary oedema. In these experiments, an impairment in capillary membrane permeability is likely. As a result, the threshold at which extravascular water starts to accumulate cannot be precisely defined. However, in the perioperative period, capillary membrane permeability is frequently altered by the acute phase reaction. Finally, in most perioperative clinical situations, a 50% decrease in colloid osmotic pressure may not require any treatment.

A computer model for analysis of fluid resuscitation

Injuries involving massive blood loss, such as burns, combat wounds, and injuries resulting from car accidents, require fluid resuscitation. The risk involved in fluid therapy is overloading of the circulation, resulting in pulmonary edema which can lead to death. The risk of pulmonary edema may be eliminated by proper determination of maximal infusion volume and rate. Reabsorption of fluid from the extravascular compartment and infusion of fluid following blood loss results in reduction of the hematocrit. This is accompanied by an increase in the heart's preload and afterload. Coronary driving pressure and flow increase due to increased volume. However, because of the reduced hematocrit this increase in coronary flow may not be sufficient to compensate the myocardium, in terms of oxygen supply, for the increase in oxygen consumption. A model of the cardiovascular system, including an extravascular compartment, was designed to analyze the effects of fluid infusion on hemodynamic variables, cardiac oxygen balance, and the redistribution of fluid between intravascular and extravascular compartments. The results indicate that edema is not the only possible adverse effect of overloading the cardiovascular system with fluids. The simulation demonstrated that in certain cases the heart's oxygen balance can become negative. Limiting the rate of infusion can reduce this risk.

Quantitative Hemodynamic Effects of Acute Volume Expansion in Severe Preeclampsia

The role of acute volume expansion in severe preeclampsia remains controversial, with advocates claiming an improvement in maternal hemodynamics and maternal-fetal status whereas opponents fearing severe hypertensive responses and the risk of pulmonary edema.

Effects of angiographic contrast media on colloid oncotic pressure

Angiographic contrast media are known to induce alterations in cardiovascular dynamics which may result in acute pulmonary edema. The risk of pulmonary edema was previously shown to be negatively correlated to the level of colloid oncotic pressure (COP). It was also shown that the gradient between COP and left ventricular end-diastolic pressure (LVEDP) represents a better predictor of pulmonary edema than does LVEDP alone. The present report evaluates the effects of a bolus injection of contrast media on those pressures, as predisposing factors for pulmonary edema. Our data are based on 15 unselected patients admitted for coronary angiography. The plasma volume increased by 16.5% (2,903 to 3,384 ml.) at two minutes after injection of a 50 c.c. bolus of meglumine diatrizoate (Renographin 76%) and had returned towards normal at 30 minutes. In parallel the COP decreased from 23.4 ± 2.4 to 19.6 ± 2.3 mm. Hg (P < 0.001) to return the 22.7 ± 2.6. The COP-LVEDP gradient decreased by 8.7 mm. Hg (8.4 to −0.3, P < 0.001). Such a gradient was well within the danger zone of pulmonary edema. These findings further clarify the mechanisms of pulmonary edema induced by contrast media.

An "oncometer" of clinical measurement of colloid osmotic pressure of plasma.

Measurement of colloid osmotic pressure complements measurements of pulmonary artery wedge pressure for assessing the risks of pulmonary edema and constitutes an increasingly important reference for purposes of guiding selection of colloid or crystalloid fluids in patients with acute cardiac disease. We describe a simple device for its routine clinical measurement. A membrane, selectively impermeable to molecules of relative molecular mass (Mr) greater than 30000, is rigidly mounted between a sample chamber and a reference chamber filled with isotonic saline. A pressure transducer measures the negative pressure developed in the reference chamber and displays it on a digital panel meter. The sensor chamber accommodates samples of 50 to 300 microliter. Equilibration is completed within 2 min. A control solution of human serum albumin (50 g/liter) is measured to confirm the accuracy of calibration of the system, with reproducible readings of 25.9 g/cm2 within one SD (equivalent to 0.4 g/cm2). Technical simplicity of operation and modest costs of disposables have made feasible the routine measurement of colloid osmotic pressure.

Cardiogenic shock: can the prognosis be improved?

The prognosis in cardiogenic shock remains poor despite improvements in treating other complications of acute myocardial infarction. In some situations, left ventricular function can be improved by increasing the vascular volume, but the benefits of increasing the cardiac uutput must be balanced agains the risk of pulmonary edema. Monitoring of volume therapy is best done via the pulmonary route. The goal of drug therapy is to raise arterial blood pressure and make the heart pump more effectively. An aggressive approach will not cure great numbers of extensive myocardial damage remains, but it will identify those who are hypovolemic or who have other correctable contributory factors. Most important, this approach may help to identify therapies currently in use that may actually increase rather than lessen myocardial damage.

Burns, Shock, and Plasma Volume Regulation.

This volume by two professors of surgery is a clear and detailed summary of the outstanding research and clinical treatment of burns and burn shock being carried out at the laboratories and burn unit at Washington University in St. Louis. This organization is recognized as one of the two outstanding burn centers in the world and is the source of origin of one of the two currently prominent methods of treatment. The book presents the views of its authors and does not attempt to reflect the research and opinions of other major centers. Their study is presented in detail; in most cases the text represents an adoption of material previously published. It is an excellent summary of the authors' work which is original and farreaching. One may have a few doubts about some rather authoritarian statements in the text; for instance, "The risk of pulmonary edema is no greater with

Heat effects in British service personnel in Iraq

1. 1. The division of heat effects into heat syncope, heat exhaustion and heat hyperpyrexia is advisable as although borderline cases do occur the clinical picture is as a rule clear-cut and the prognosis and treatment are radically different. 2. 2. Heat Exhaustion. Electrolytic imbalance and dehydration appear to be of primary importance in the genesis of heat exhaustion. The lean, spare type with a low systolic pressure is particularly prone to heat exhaustion and the age group is lower than in the heat hyperpyrexia cases. The quantitative estimation of the urinary chlorides is a simple and reliable test in the differential diagnosis of these cases and in sodium chloride and glucose we possess a safe and effective remedy. If intravenous therapy is indicated this must be controlled by charting the intake and output and estimating the haemoconcentration, otherwise there is a risk of pulmonary oedema. The prognosis in heat exhaustion is excellent provided the condition is recognized in time and adequately treated, otherwise cases may die of circulatory failure or go on to heat hyperpyrexia. 3. 3. Heat Hyperpyrexia. This is always a grave syndrome: the mortality is usually at least 30 per cent. and may be considerably more. Alcohol and age are accessory and adverse factors and the condition is more frequent in the fat and plethoric. The essential factor is the failure of the heat regulating centre with the suppression of sweating, although in the more protracted cases it is probable that an auto-intoxication is responsible for the prolonged pyrexia. Thermantidote measures and the nursing of these cases in artificially cooled wards are the basis of treatment. 4. 4. Prophylaxis. ( a) Ample cool drinking water containing 10 grains of sodium chloride to the pint, together with a total consumption of at least 1 ounce of sodium chloride a day is a paramount necessity in all endemic areas during the hot weather. ( b) The provision of air conditioned or artificially cooled wards in hospitals in endemic areas is as essential as the provision of a well-equipped operating theatre.