Clinical studies of measuring extravascular lung water by the thermal dye technique in critically ill patients

We measured extravascular lung water (EVLW) by the thermal-dye technique in a broad group of critically ill patients who had either acute cardiac or noncardiac illnesses. A portable AP supine chest roentgenogram, reviewed blindly, was used to classify patients as to the presence or absence of pulmonary edema; by clinical history we categorized patients into either a cardiac or noncardiac (ie, ARDS) group. With a normal chest roentgenogram, the mean EVLW was 5.6 +/- 1.8 ml/kg, and the pulmonary capillary wedge pressure (PCWP) was 11.3 +/- 5.3 mm Hg (mean +/- SD). In contrast, patients with pulmonary edema on a cardiac basis had a mean EVLW of 10.2 +/- 3.1 ml/kg (mean PCWP, 20.5 +/- 8.2 mm Hg), while patients with clinically defined noncardiac pulmonary edema and a normal PCWP (11.6 +/- 5.7 mm Hg) had a mean EVLW of 15.8 +/- 4.6 ml/kg, significantly higher than in the cardiac group (p less than 0.001). On a severity system of 014, the EVLW increased in parallel to the severity of the chest radiologic appearance of edema in both the cardiac (r2 = .44; p less than 0.001) and noncardiac (r2 = .59; p less than 0.001) patients. This study defined a normal range of thermal-dye EVLW in critically ill patients without radiologic evidence of pulmonary edema. We further demonstrated the increased pulmonary microvascular permeability of noncardiac pulmonary edema compared with cardiac edema by the greater EVLW at normal microvascular hydrostatic pressures in the former group.     

Permeability pulmonary edema following lung resection

The etiology of edema associated with pulmonary resection was investigated in five patients during the immediate postoperative period. Three patients received pneumonectomy while two patients had one lobe resected. All patients suffered from severe respiratory distress and had x-ray evidence of diffuse interstitial pulmonary edema within 12 hours of surgery. Hemodynamic data were obtained with radial and pulmonary artery catheters. Edema fluid was obtained along with blood samples for simultaneous determination of protein and albumin content. All patients studied had normal or high cardiac output, normal cardiac filling pressures, and edema fluid protein to serum protein ratio of 0.6 or greater suggestive of permeability changes contributing to edema fluid accumulation. Calculated shunt fraction exceeded 25 percent in all patients. Pulmonary edema has been noted in patients following pulmonary resection in the early postoperative period. In patients reviewed here, two factors appeared to be significant. First is an increase in pulmonary capillary pressure associated with passage of a normal to high cardiac output in a reduced volume pulmonary vascular bed. The second factor, as demonstrated by protein content in the edema fluid, is injury to the alveolar capillary membrane.     

Negative pressure pulmonary edema in the coronary care unit

A 63-year-old woman with no known cardiac history presented with pulmonary edema accompanied by electrocardiographic evidence of ischemia. Echocardiography demonstrated normal cardiac dimensions, normal wall motion and mild diastolic dysfunction. Despite repeat attempts at extubation following aggressive diuresis, the patient required ongoing ventilatory support. Although cardiac catheterization revealed normal coronary arteries, computed tomography revealed a 4 cm 9 cm multinodular goiter extending into the mediastinum and compressing the trachea. A diagnosis of negative pressure pulmonary edema should be considered in the differential diagnosis of any patient presenting with acute heart failure.     

Hypovolemia and hypotension complicating management of acute cardiogenic pulmonary edema

After the acute onset of heart failure and in the absence of acute myocardial infarction, plasma volume may occasionally be depleted to the extent that the patient presents with clinical signs of circulatory shock. In five patients, the acute onset of clinical and radiographic signs of cardiogenic pulmonary edema were associated with reduction in arterial blood pressure and cardiac output. The pulmonary arterial wedge pressure was within normal limits but a reduction in plasma volume was demonstrated, which is best explained by the rapid translocation of plasma water that represented pulmonary (and most likely also peripheral) edema fluid. The infusion of 5 percent albumin solution significantly increased cardiac output, mean arterial pressure and cardiac work, reversed lactic acidosis, enhanced furosemide-induced diuresis and was followed by a decrease in both clinical and radiographic signs of pulmonary edema. These observations confirm that volume expansion may constitute appropriate treatment for some patients with cardiogenic pulmonary edema who may present with hypotension and who are unresponsive to conventional therapy.     

Pulmonary artery wedge pressure and extravascular lung water in patients with acute cardiogenic pulmonary edema requiring mechanical ventilation

This study describe the values of pulmonary artery wedge pressure (PAWP) and the extravascular lung water (EVLW) index in patients with acute cardiogenic pulmonary edema who require mechanical ventilation. Ten consecutive patients with acute cardiogenic pulmonary edema who required mechanical ventilation were studied. Cardiac index was determined with thermodilution. Central venous pressure and PAWP were measured with a pulmonary artery catheter. EVLW index was determined with the thermal dye dilution technique, using a commercially available computer system. Measurements were made at regular preset intervals after the initiation of mechanical ventilation. PAWP was normal at baseline (11.6+/-0.9 mm Hg, range 8 to 17) and did not change. EVLW index was elevated at baseline (13.7+/-1.5 ml/ kg) and decreased to a normal value after 24 hours (8.6+/-1.2 ml/kg, p = 0.02). Concomitantly cardiac index increased from 2.61+/-0.24 to 3.61+/-0.14 L/min/m2 (p = 0.05). There was no correlation between PAWP and EVLW index. Fluid balance was +1,221+/-908 ml after 24 hours and there was a weight gain of 0.88+/-1.06 kg after 24 hours. Thus, patients with acute cardiogenic pulmonary edema requiring mechanical ventilation may have a normal PAWP after mechanical ventilation has been initiated. In a hemodynamic unstable situation, these patients may require fluid challenges to improve cardiac output, despite the presence of pulmonary edema. The pulmonary edema, measured as EVLW index, resolves rapidly when cardiac performance improves, despite positive fluid balances and weight gain in the first 24 hours.     

An autopsy case of neurogenic pulmonary edema due to suicide by hanging]

A 43-year-old man died of pulmonary edema after hanging himself. His cardiac function and renal function were normal. No aspiration, trauma, or overhydration was present, and high doses of catecholamine had not been administered. Autopsy findings revealed hypoxic brain damage, cerebral edema and pyknosis of nerve cells in the medulla oblongata. These findings resulted in a diagnosis of neurogenic pulmonary edema. To our knowledge, there have been no previous reports of neurogenic pulmonary edema due to airway obstruction.     

Uremic pulmonary edema

Pulmonary edema fluid analyses and hemodynamic evaluations were performed in two uremic patients with acute pulmonary edema. The colloid osmotic pressure of the pulmonary edema fluid ranged from 57 per cent to 93 per cent that of the serum. Although cardiac function was normal in both patients, the serum colloid osmotic pressure--pulmonary artery wedge pressure gradients were markedly reduced. Uremic pulmonary edema is the result of alterations of pulmonary intravascular Starling forces and increases in pulmonary capillary membrane permeability, allowing for the efflux of protein-rich fluid from the capillaries into the lung.     

Comparison of angiographic findings and demographic variables in patients with coronary artery disease presenting with acute pulmonary edema versus those presenting with chest pain

One hundred nineteen patients admitted to the coronary care unit with pulmonary edema were retrospectively reviewed to identify the demographic characteristics and underlying cardiac disorders of this population. The patients with pulmonary edema were compared with 119 patients admitted to the coronary care unit with chest pain. Cardiac catheterization in 71 patients with pulmonary edema and 93 with chest pain showed left main and 3-vessel coronary artery diseases to be equally common in both groups, although anginal pain was infrequent in patients with pulmonary edema (n = 28, 24%). Left ventricular function was reduced in the patients with pulmonary edema compared with those with chest pain (mean ejection fraction 42 vs 59%; p < 0.001). More patients with pulmonary edema were black, and had diabetes and preexisting hypertension than those with chest pain. The results of cardiac catheterization were the same for black and white patients with pulmonary edema. In conclusion, patients with pulmonary edema have a high incidence of cardiac disease, and pulmonary edema may be 1 manifestation of silent myocardial ischemia. Important demographic differences exist between patients admitted with pulmonary edema and those who present with chest pain.     

Noncardiogenic pulmonary edema following hydrochlorothiazide ingestion

A 57-year-old woman presented in severe respiratory distress 30 minutes after ingesting hydrochlorothiazide. Pulmonary edema was evident clinically and radiographically. A noncardiogenic etiology was suggested by the lack of jugular venous distention, S3 gallop, or pedal edema, and the presence of a normal cardiac silhouette on chest radiograph. The patient's pulmonary edema remitted with supportive therapy.     

Postobstruction pulmonary edema

Several occurrences of pulmonary edema following relief of acute upper airway obstruction have been reported. The edema is associated with normal cardiac filling pressures and responds promptly to conservative therapy. Its origin may be attributed to the cardiopulmonary effects of the vigorous inspiratory effort that the spontaneously breathing patient generates to overcome respiratory obstruction (the Müller maneuver). A patient with postobstruction pulmonary edema complicated by hypovolemia and myocardial infarction is described. Prompt invasive hemodynamic monitoring in selected high-risk patients is suggested.     

Œdème aigu du poumon secondaire à l’administration intraveineuse de β2 mimétiques pour asthme aigu grave

We report the case of a severe acute pulmonary edema secondary to the administration of salbutamol to a patient admitted for severe asthma. The diagnosis of acute pulmonary edema was suspected on the clinical examination, chest radiography, biological (plasmatic Pro-BNP rate) and echocardiographic findings. Rapid improvement under dobutamine and mechanical ventilation argue in favour of cardiogenic pulmonary edema. The young age of our patient, the absence of history of cardiovascular disease and the chronology of this complication onset regarded to salbutamol infusion could suggest β2 agonist involvement in this event. The improvement of cardiac function on echocardiography and the normal results obtained with myocardial perfusion scintigraphy performed 35 days later show the left ventricular reversible dysfunction.     

Hypertrophic cardiomyopathy: a case of refractory recurrent pulmonary edema

An unusual case of acute pulmonary edema without associated arrhythmias in a 33-year-old woman is reported. The patient suffered recurrent pulmonary edema refractory to medication and eventual cardiac arrest. Successful emergency myectomy following cardiac arrest allowed the patient to resume an active lifestyle despite significant diastolic abnormality. During an 18-month follow-up the patient suffered one brief episode of pulmonary edema.     

Cardiac dysfunction and pulmonary edema following scorpion envenomation

Cardiac dysfunction with pulmonary edema following scorpion envenomation (SE) has been documented only in a few isolated case reports. We conducted a systematic hemodynamic study in five consecutive patients (mean age, 21.6 +/- 8 years) presenting with pulmonary edema occurring a few hours (9.6 +/- 5.2 hours) after SE. All patients had increased pulmonary capillary wedge pressure (mean, 25 +/- 1.8 mm Hg) while the systemic vascular resistance was elevated only in one. The stroke volume index was markedly depressed (21.7 +/- 3.6 ml/sq m) whereas cardiac index was normal or slightly decreased (2.5 +/- 0.4 L/min/sq m). Cerebral infarct and sudden cardiac arrest were the cause of death in two patients. In the three survivors, all the hemodynamic disturbances and respiratory abnormalities disappeared within a few days. We conclude that cardiac dysfunction was found in all five patients and this was reversible in the three surviving the acute episode.     

Cardiovascular management in acute hypoxemic respiratory failure

This paper reviews recent data concerning the interactions among pulmonary edema, intrapulmonary shunt and cardiac output in acute hypoxemic respiratory failure. In canine oleic acid edema, a 5 mm Hg reduction in pulmonary wedge pressure significantly reduces edema, but a corresponding increase in colloid osmotic pressure does not. When pulmonary wedge pressure is lowered, cardiac output can be maintained with infusions of nitroprusside, dopamine or dobutamine. Each vasoactive agent improves ventricular pumping function, and the increase in cardiac output is due in part to peripheral circulatory actions of the drugs. Although pulmonary shunt increases with these vasoactive agents, increased shunt is due not to their pulmonary vasoactivity but to the associated increase in pulmonary blood flow. Positive end-expiratory pressure reduces venous return by raising right atrial pressure, and it does not depress ventricular pumping function. Rather, positive end-expiratory pressure increases ventricular filling pressure at a given end-diastolic volume; it does not reduce and probably increases edema, yet it reduces shunt by redistributing the edema. These interpretations suggest several goals for cardiovascular management in acute hypoxemic respiratory failure: (1) the lowest pulmonary wedge pressure consistent with adequate cardiac output; and (2) the least positive end-expiratory pressure consistent with saturation of adequate circulating hemoglobin on nontoxic inspired oxygen.     

Therapeutic use of nitroglycerin in pulmonary edema and cardiac asthma in myocardial infarct patients

The effect of sublingual medication with nitroglycerin taken in a dose of 0.5-1 mg was studied in 101 patients with myocardial infarction (77 had pulmonary edema and 34 had cardiac asthma). In patients with edema of the lungs nitroglycerin reduced dyspnoea, in some cases of cardiac asthma it arrested the attack. It was found that nitroglycerin reduced central venous pressure, the diastolic-systolic index of the pulmonary rheogram, the systolic, diastolic and mean pressure in the pulmonary artery, and arterial pressure in the greater circulation. With the intake of the drug, cardiac output decreased almost significantly, whereas the peripheral pressure did not change. It is concluded that the use of nitroglycerin in a dose of 0.5 mg in the treatment of cardiac asthma and pulmonary edema in patients with acute myocardial infraction is advisable.     

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Bilateral electrolytic lesions of the anterior hypothalamus in unrestrained rats resulted in the development, within 2 hours, of arterial hypertension, tachycardia, hyperthermia, and increased locomotor activity, often leading to pulmonary edema and death. Similar lesions in paralyzed, artificially ventilated rats produced comparable changes in arterial blood pressure and body temperature with a similar time course. The arterial hypertension was a consequence of an increase in total peripheral resistance to 15% of control with a reduction in cardiac output to 49% of control. Arterial hypertension, elevated peripheral resistance, and diminished cardiac output were reversed toward normal by alpha-receptor blockade with phentolamine (1 mg/kg, iv). Bilateral adrenalectomy, adrenal demedullation, or adrenal denervation performed prior to lesion placement prevented the development of arterial hypertension and pulmonary edema as well as the changes in peripheral resistance, cardiac output, and body temperature. We conclude that arterial hypertension following lesions of the anterior hypothalamus is due to a neurally mediated increase in peripheral resistance initiated by the release of adrenal medullary catecholamines and that pulmonary edema is due to myocardial failure secondary to the ensuing ventricular overload. Structures originating in or passing through the anterior hypothalamus may exert selective control over the adrenal medulla independent of vasomotor neurons.     

超声心动图检测高原肺水肿患者心功能变化

目的 :探讨高原肺水肿患者心脏结构和功能变化。方法 :西藏日喀则地区 （海拔 390 0 m ）肺水肿患者 5 4例 ,治疗前后进行彩色多普勒超声心动图检查。结果 :高原肺水肿期心率加快 ,左室射血分数、短轴缩短率和心排出量均高于治疗后 ,室间隔运动幅度减低 ,左室舒张末期内径减小 ,其右室和肺动脉内径则大于治疗后 ,而治疗前后的肺静脉内径未见显著差异。结论 :高原肺水肿患者左室收缩功能增强 ,右室及肺动脉内径增大、压力升高。     

ARDS due to ingestion of denatured rapeseed oil

Among the different etiologies of noncardiogenic acute pulmonary edema is found the administration or ingestion of various substances. We have studied two patients with ARDS secondary to the ingestion of toxic oil. Both patients presented similar roentgenographic findings characterized by interstitial and alveolar infiltration in "butterfly" distribution, pleural effusion, and a normal cardiac silhouette. The two cases also showed a pulmonary compliance either normal or slightly diminished. With the aid of artificial ventilation, they evolved favorably, gaseous exchange and chest x-ray films returning to normal 16 and 22 days after admission.     

Pheochromocytoma-induced acute pulmonary edema and reversible catecholamine cardiomyopathy mimicking acute myocardial infarction.

Acute noncardiogenic pulmonary edema and catecholamine-induced cardiomyopathy as the first presentations of pheochromocytoma are uncommon events, but usually rapidly fatal. A 36-year-old man presented acute pulmonary edema in a setting of hypertensive emergency after arthroscopy, later developing catecholamine-induced cardiotoxicity mimicking an acute myocardial infarction, with elevation of cardiac damage markers, normal coronary arteries, and with full recovery from electrical abnormalities. Magnetic resonance imaging revealed a right adrenal mass. Elevated levels of catecholamines and metanephrines, and a positive 131I-metaiodobenzylguanidine scan confirmed a pheochromocytoma. Once the patient had been hemodynamically stabilized, he was successfully operated.     

The ICU chest film: cardiac versus pulmonary disease

We have discussed several diseases that diffusely affect the pulmonary parenchyma. The diagnostic problem is to separate cardiac pulmonary edema from noncardiac pulmonary edema, diffuse interstitial fibrosis, and lymphangitic spread of carcinoma. Frequently, this may not be possible by radiographic means alone, and additional historic and physiologic information must be obtained. It is also important to know that cardiac pulmonary edema may present in a focal or regional distribution in patients with chronic obstructive pulmonary disease. Several additional radiographic tests may be used to evaluate abnormal pulmonary parenchymal densities seen on the portable chest radiograph, when the differential diagnosis includes increased extravascular water, pneumonia, and pulmonary fibrosis. The easiest of these tests to perform is the gravitational shift test.