Effect of furosemide on hemodynamics and lung water in acute pulmonary edema secondary to myocardial infarction

Biddle, Theodore L.; Yu, Paul N.

doi:10.1016/0002-9149(79)90049-3

Cited by 84 publications

(21 citation statements)

References 11 publications

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“…Although furosemide and bumetanide do not differentiate between the two different NKCC channels, only NKCC1 is expressed in alveolar epithelial cells (22), whereas NKCC2 expression is confined to the kidney (23). The identification of a critical relevance for NKCC1 in alveolar fluid secretion and cardiogenic edema formation provides an intriguing explanation for the consistent (pre)clinical observation that the initial improvement of respiratory function by the unspecific NKCC blocker and loop diuretic furosemide in lung edema precedes the onset of diuresis and thus, cannot be explained by its renal effects (24,25). Unexpectedly, inhibition of NKCCs by either furosemide or bumetanide also attenuated, in part, absorptive alveolar fluid transport at baseline pressures.…”

Section: Discussionmentioning

confidence: 99%

Chloride transport-driven alveolar fluid secretion is a major contributor to cardiogenic lung edema

Solymosi

Kaestle-Gembardt

Vadász

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Alveolar fluid clearance driven by active epithelial Na + and secondary Cl − absorption counteracts edema formation in the intact lung. Recently, we showed that impairment of alveolar fluid clearance because of inhibition of epithelial Na + channels (ENaCs) promotes cardiogenic lung edema. Concomitantly, we observed a reversal of alveolar fluid clearance, suggesting that reversed transepithelial ion transport may promote lung edema by driving active alveolar fluid secretion. We, therefore, hypothesized that alveolar ion and fluid secretion may constitute a pathomechanism in lung edema and aimed to identify underlying molecular pathways. In isolated perfused lungs, alveolar fluid clearance and secretion were determined by a double-indicator dilution technique. Transepithelial Cl − secretion and alveolar Cl − influx were quantified by radionuclide tracing and alveolar Cl − imaging, respectively. Elevated hydrostatic pressure induced ouabain-sensitive alveolar fluid secretion that coincided with transepithelial Cl − secretion and alveolar Cl − influx. Inhibition of either cystic fibrosis transmembrane conductance regulator (CFTR) or Na + -K + -Cl − cotransporters (NKCC) blocked alveolar fluid secretion, and lungs of CFTR −/− mice were protected from hydrostatic edema. Inhibition of ENaC by amiloride reproduced alveolar fluid and Cl − secretion that were again CFTR-, NKCC-, and Na + -K + -ATPase-dependent. Our findings show a reversal of transepithelial Cl − and fluid flux from absorptive to secretory mode at hydrostatic stress. Alveolar Cl − and fluid secretion are triggered by ENaC inhibition and mediated by NKCC and CFTR. Our results characterize an innovative mechanism of cardiogenic edema formation and identify NKCC1 as a unique therapeutic target in cardiogenic lung edema.epithelial Cl − transport | pulmonary edema T raditionally, the formation of cardiogenic pulmonary edema has been attributed to passive fluid filtration across an intact alveolocapillary barrier along an increased hydrostatic pressure gradient. However, recent studies show that cardiogenic edema is critically regulated by active signaling processes. Activation of mechanosensitive endothelial ion channels increases lung vascular permeability (1), whereas alveolar epithelial cells lose their physiological ability to clear the distal airspaces from excess fluid by their capacity to actively transport ions across the epithelial barrier (2-4).In the intact lung, the predominant force driving alveolar fluid clearance is an active transepithelial Na + transport from the alveolar into the interstitial space. A major portion of the apical Na + entry is mediated by the amiloride-inhibitable epithelial Na + channel (ENaC), with basolateral Na + extrusion through the Na + -K + -ATPase (5). Cl − and water are considered to follow paracellularly for electroneutrality and osmotic balance. In cardiogenic lung edema, the physiological protection against alveolar flooding provided by an intact alveolar fluid clearance is largely attenuated (3, 4). Previously, ...

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Section: Discussionmentioning

confidence: 99%

Chloride transport-driven alveolar fluid secretion is a major contributor to cardiogenic lung edema

Solymosi

Kaestle-Gembardt

Vadász

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…The relative homogeneity of the hae modynamic response to bumetanide at rest was similar to the described profile for other 120 Silke Haemodynamics of Diuretic Therapy in Chronic Heart Failure Echocardiographie shortening in patients with normal ventricular function or severe con gestive heart failure. Redrawn with permission from Dalla Volta et al [40], agents at rest [11,12,[18][19][20][21][28][29][30][31][32][33]. Contrast ing with the resting data of normal distribution type, the exercise results suggested a less ho mogeneous response ( fig.…”

Section: Clinical Findings and Haemodynamic Responsementioning

confidence: 99%

Haemodynamic Impact of Diuretic Therapy in Chronic Heart Failure

Silke

1994

Cardiology

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An immediate improvement in haemodynamic variables and cardiac performance is achieved in chronic heart failure following diuretic therapy, primarily due to reductions in plasma and extracellular fluid volumes. Humoral markers of these alterations are increased plasma renin, angiotensin and aldosterone levels; these increase maximally over the ñrst week of treatment but attenuate during sustained therapy. There are reciprocal alterations in plasma α-atrial natriuretic peptide levels. These findings suggest that the initial volume contraction is maintained, though somewhat attenuated, during chronic therapy. The neurohumoral consequences of diuretic therapy are of particular interest in heart failure, as they may contribute to diuretic resistance. Activation of the renin-angiotensin system favours the proximal tubular reabsorption of sodium and water, which may result in dilutional hyponatraemia. Diuretics have both direct vascular and non-vascular (volume-dependent) haemodynamic actions. Together these substantially reduce the left heart filling pressure (-29%) with a consequent fall in cardiac output ( 10%). Systemic vascular resistance initially increases but subsequently normalizes, allowing cardiac output to return towards control values. Haemodynamic tolerance to diuretics does not usually occur during sustained oral therapy; additionally, echocardiographic contractility indices and exercise capacity may increase. The vasodilator activity of the diuretics is due to prostaglandin release; the initial pressor action is due to activation of the renin-angiotensin system. Direct pulmonary vasodilatation with improved pulmonary compliance remains an interesting possibility. Over the longer term, substantial reductions in left heart filling pressure during exercise occur at unaltered cardiac output. The impact of diuretic therapy on the underlying myocardial disease process is unknown. There is little direct evidence of ventricular remodelling or of improved intrinsic cardiac performance (as distinct from that due to altered loading conditions). In the absence of such information, it would appear reasonable to combine diuretic therapy with a vasodilator or angiotensin converting enzyme inhibitor, even in patients symptomatically well controlled on diuretic alone.

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“…5,24 Loop diuretics have a strong direct vascular action characterized by a prompt (as soon as 5 minutes after IV administration) and sometimes abrupt fall in mean pulmonary pressure, left atrial pressure, cardiac output, and arterial blood pressure irrespective of their diuretic effects, which may take up to 60 minutes to generate a clinically significant diuresis; [28][29][30] unrelated to their diuretic effect is the reduction in lung water content which takes several hours to be of clinical relevance. 31 These observations indicate that the rapid symptomatic improvement, observed within minutes after the intravenous administration of loop diuretics in acute cardiogenic pulmonary edema, is not related to the diuretics, but rather to their vasodilator properties. [28][29][30][31] In NPE, the pharmacological effects of this class of medications are additive to the effects of other cardiovascular agents used in its treatment (ie, beta and alpha blockers), increasing the risk of hypotension without addressing the root of this condition, which is the transient non-cardiogenic stress failure of the blood-gas barrier.…”

Section: Discussionmentioning

confidence: 89%

“…31 These observations indicate that the rapid symptomatic improvement, observed within minutes after the intravenous administration of loop diuretics in acute cardiogenic pulmonary edema, is not related to the diuretics, but rather to their vasodilator properties. [28][29][30][31] In NPE, the pharmacological effects of this class of medications are additive to the effects of other cardiovascular agents used in its treatment (ie, beta and alpha blockers), increasing the risk of hypotension without addressing the root of this condition, which is the transient non-cardiogenic stress failure of the blood-gas barrier. 5,6,8,24 In the treatment of presumed NPE, the loop diuretics are not indicated as first line agents and should be used exclusively to minimize a demonstrable cardiac component complicating the clinical picture, using the lowest possible effective dose and only if the systemic blood pressure, the circulating blood volume, and cerebral perfusion pressure can be maintained.…”

Section: Discussionmentioning

confidence: 89%

Non-Cardiogenic Pulmonary Edema Complicating Electroconvulsive Therapy: Short Review of the Pathophysiology and Diagnostic Approach

Manne¹,

Kasirye²,

Epperla³

et al. 2011

Clinical Medicine & Research

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Two types of pulmonary edema occur in clinical medicine: cardiogenic pulmonary edema (or hydrostatic pulmonary edema) and noncardiogenic pulmonary edema, better known as acute lung injury or acute respiratory distress syndrome (ARDS). Their clinical manifestations are very similar, so the differentiation between them, based only on clinical grounds, may be very difficult, and knowing the precise etiology of the episode of acute pulmonary edema has major implications in the treatment plan. Cardiogenic pulmonary edema is usually due to systolic and/or diastolic left ventricular dysfunction and is typically treated with diuretics, nitrates, and afterload reduction medications such as angiotensin converting enzyme inhibitors, although some cases also require coronary revascularization. Noncardiogenic pulmonary edema is usually secondary to a more systemic severe medical or surgical pathology that triggers the event, and the treatment should be directed to treat that pathology. Oxygen supplementation in the form of mechanical ventilation (invasive or non-invasive) is always required. A rapid diagnosis of the cause of the episode of acute pulmonary edema facilitates a timely and appropriate therapeutic intervention.Electroconvulsive therapy (ECT) is recognized as a well-established, highlyeffective, safe psychiatric treatment. It is estimated that 100,000 patients per year receive a course of ECT across the United States, with an average of 8 to 10 treatments per course of therapy. Severe complications are very infrequent and generally reported as transitory cardiac arrhythmias and severe transitory Acute pulmonary edema complicating electroconvulsive therapy is an extremely uncommon event that has rarely been described in the literature. Different theories, including one suggesting a cardiogenic component, have been proposed to explain its genesis. The present report describes a classic presentation of this condition with review of its potential mechanisms and diagnostic approach. After successful completion of a session of electroconvulsive therapy, a 42-year-old woman with major depressive disorder developed acute systemic high blood pressure, shortness of breath, and hemoptysis. A chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. Initially cardiogenic pulmonary edema was presumed, but an extensive diagnostic work-up demonstrated normal systolic and diastolic left ventricular function, and with only supportive measures, a complete clinical and radiographic recovery was achieved within 48 hours. The present case does not support any cardiogenic mechanism in the genesis of this condition.

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Effect of furosemide on hemodynamics and lung water in acute pulmonary edema secondary to myocardial infarction

Cited by 84 publications

References 11 publications

Chloride transport-driven alveolar fluid secretion is a major contributor to cardiogenic lung edema

Chloride transport-driven alveolar fluid secretion is a major contributor to cardiogenic lung edema

Haemodynamic Impact of Diuretic Therapy in Chronic Heart Failure

Non-Cardiogenic Pulmonary Edema Complicating Electroconvulsive Therapy: Short Review of the Pathophysiology and Diagnostic Approach

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