The effect of acute pulmonary edema on pulmonary vascular resistance: significance for the interpretation of dilated upper lobe vessels on chest radiographs

Dilation of upper lobe pulmonary vessels is an important radiographic sign of acute, left heart failure. A prominent theory is that perivascular edema causes increased resistance at the lung bases and inverts the normal perfusion gradient such that upper lobe blood flow exceeds lower lobe flow. This theoretical increase in flow is thought to cause dilatation of upper lobe vessels. Previous experimental studies determined indirectly changes in resistance from changes in the perfusion gradient: Results were contradictory. We measured directly the effect of edema on resistance in isolated canine lungs. Resistance increased linearly with edema. The magnitude of increase was small, however, and insufficient to cause inversion of the perfusion gradient. Our data indicate that interstitial pulmonary edema does not cause significant redistribution of blood flow. We suggest that dilated upper lobe vessels are veins acting as pulmonary venous manometers, reflecting elevated left atrial pressure, not increased blood flow.     

Clinical value of lung uptake of iodine-123 metaiodobenzylguanidine (MIBG), a myocardial sympathetic nerve imaging agent, in patients with chronic heart failure

This study investigated the clinical value of I-123 MIBG pulmonary accumulation and washout in patients with chronic heart failure (CHF). Nineteen patients with CHF and 15 normal volunteers (NL) were included. The uptake ratio of heart to mediastinum (H/M), that of lung fields to mediastinum (L/M), and washout rate (WR) of the heart and lung fields were calculated in anterior planar images and compared with results of echocardiography and cardiac catheterization. In the CHF group, the lung uptake in delayed images increased and lung WR was decreased, suggesting pulmonary endothelial lesions. Furthermore, there was a negative correlation between right and left lung WR and pulmonary arterial diastolic pressure (PA(D)) and pulmonary arterial systolic pressure (PA(s)) in the CHF group. Since the WR of MIBG reflected PA, it may be used as an index of severity of cardiac dysfunction.     

Cardiopulmonary effects of volume expansion in man: radiographic manifestations

Cardiovascular and humoral responses to extremes of sodium intake (10-1500 mEq/day) were studied. Chest radiographs of eight normal men were obtained to measure changes in heart volume and central vascular structures. Echocardiographic measurements of cardiac chamber dimensions were also obtained. Sodium loading resulted in a 16-mm-Hg increase in mean arterial pressure and increases in cardiac output, stroke volume, left ventricular end-diastolic volume, and all radiographically determined cardiac dimensions. There was direct correlation between the radiographic cardiac dimensions and left ventricular end-diastolic volume. There was no echocardiographic evidence of pericardial fluid. After sodium loading, there was enlargement of the superior vena cava, innominate veins, azygos vein, pulmonary vessels, and the aortic knob. Small pleural effusions were commonly seen. Volume expansion may cause radiographic changes that may mimic those associated with congestive heart failure. This may particularly be the case in patients with renal failure, those receiving dialysis treatment, or patients receiving large volumes of intravenous fluids.     

Quantitative determination of regional extravascular lung water and regional blood volume in congestive heart failure

Regional extravascular lung water (rELW) and blood volume (rBV) in five controls and 14 patients with congestive heart failure (CHF) were measured by constant infusion of H215O and inhalation of 11CO using positron emission tomography (PET). The analysis of 18 regions per patient revealed a relatively homogeneous level of rELW in the controls (mean = 0.11 +/- 0.02 g/cc; range, 0.08-0.21), whereas this increase in patients with CHF (0.17 +/- 0.02 g/cc; range, 0.10-0.51). The rBV was 0.21 +/- 0.02 g/cc in the controls and 0.17 +/- 0.02 g/cc in patients with CHF. A good correlation was found between the severity of chronic heart failure (according to the grading of the New York Heart Association) and mean extravascular lung water (ELW) (r = 0.69), as well as between CHF and the ratio rELW/rBV (r = 0.87); however, the correlation to hemodynamic data was less satisfactory (cardiac index, r = 0.45; pulmonary capillary wedge pressure, r = 0.47; ejection fraction, r = 0.60). In supine controls, a progressive decrease in regional blood volume from the basal to the apical regions was observed, whereas the differences in ELW were only small. In patients with chronic heart failure, ELW in the basal parts was markedly increased, whereas in the apical regions, only minor deviations from the controls were observed. In the basal regions of these patients, the blood volume was reduced by about 30%. Instead of the normal basoapical gradient of blood volume, these patients showed a rather flat distribution. Radiographic findings of pulmonary edema generally appeared together with an ELW level of greater than 0.14 g/cc.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary edema and respiratory insufficiency in acute pancreatitis.

Pulmonary edema, cardiac enlargement, and respiratory insufficiency may occur in patients with acute pancreatitis. The mechanisms are complex and incompletely understood, but probable etiologic factors include fluid overload, left ventricular failure, impaired respiratory excursion and microatelectasis, and a nonspecific response of the lung to various types of pulmonary injury including hypotension, intravenous crystalloids, and the effects of circulating pancreatic enzymes. Recognition of the association of pulmonary edema and respiratory insufficiency with pancreatitis is importance because early treatment with positive pressure breathing, careful fluid management and diuretics, and corticosteroids may prevent the development of irreversible respiratory failure.     

Effectiveness of chest radiography,lung ultrasound and thoracic computed tomography in the diagnosis of congestive heart failure

Hydrostatic pulmonary edema is as an abnormal increase in extravascular water secondary to elevated pressure in the pulmonary circulation, due to congestive heart failure or intravascular volume overload. Diagnosis of hydrostatic pulmonary edema is usually based on clinical signs associated to conventional radiography findings. Interpretation of radiologic signs of cardiogenic pulmonary edema are often questionable and subject. For a bedside prompt evaluation, lung ultrasound (LUS) may assess pulmonary congestion through the evaluation of vertical reverberation artifacts, known as B-lines. These artifacts are related to multiple minimal acoustic interfaces between small water-rich structures and alveolar air, as it happens in case of thickened interlobular septa due to increase of extravascular lung water. The number, diffusion and intensity of B lines correlates with both the radiologic and invasive estimate of extravascular lung water. The integration of conventional chest radiograph with LUS can be very helpful to obtain the correct diagnosis. Computed tomography (CT) is of limited use in the work up of cardiogenic pulmonary edema, due to its high cost, little use in the emergencies and radiation exposure. However, a deep knowledge of CT signs of pulmonary edema is crucial when other similar pulmonary conditions may occasionally be in the differential diagnosis.     

Exercise in heart failure: should aqua therapy and swimming be allowed?

PURPOSE: Although exercise training is established as an integrated part of treatment regimes in both patients with transmural myocardial infarction (MI) and chronic congestive heart failure (CHF), there is no consensus yet on the appropriateness of water exercises and swimming. One reason is the lack of information concerning both central hemodynamic volume and pressure responses during immersion in these patients. METHODS: This paper presents explorative studies on changes in cardiac dimensions and central hemodynamics during graded immersion and swimming in patients with moderate and/or severe MI and in patients with moderate and/or compensated severe CHF. For comparison purposes, healthy subjects were assessed. Measurements were performed by using Swan-Ganz right heart catheterization, subxiphoidal echocardiography, and Doppler-echocardiography. RESULTS: The major findings were: 1) Indicators of an increase in preload were seen in patients with moderate and severe MI. In both patient groups, upright immersion to the neck and supine body position at rest in the water resulted in abnormal mean pulmonary artery pressure (PAm) and mean pulmonary capillary pressures (PCPm), respectively. During low-speed swimming (20-25 m.min(-1)), the PAm and/or PCPm were higher than during supine cycle ergometry at a load of 100 W. 2) Left ventricular overload and decrease and/or no change in stroke volume occurred in patients with severe CHF who were immersed up to the neck. 3) Patient's well-being was maintained despite hemodynamic deterioration. CONCLUSION: The acute responses during immersion and swimming suggest the need for additional studies on long-term changes in cardiac dimensions and central hemodynamic in both patients with severe MI and severe CHF who undergo a swimming program, compared with nonswimming patients with MI and CHF of similar etiology and severity of disease.     

Anomalous pulmonary venous connection of entire left lung with intact atrial septum.

Three cases of total unilateral pulmonary venous connection of the left lung with intact atrial septum are described. All patients were acyanotic and had findings of volume overload of the right side of the heart. An anomalous vertical vein in the superior mediastinum and large pulmonary arteries were visible on the plain chest radiograph, similar to what is seen in cases of total anomalous pulmonary venous connection. Selective pulmonary angiography delineated the anomalous connection of the left pulmonary veins and documented the absence of an atrial septal defect.     

The measurement of extravascular lung density with SPECT imaging and its relationship with ventilatory abnormalities in patients with congestive heart failure

BACKGROUND: Patients with congestive heart failure (CHF) have increased ventilatory equivalent for carbon dioxide (Ve/VCO(2)), which may contribute to the symptom of exercise-induced hyperpnea. We have developed a technique in which simultaneous blood volume single photon emission computed tomography imaging and transmission tomography are used to measure extravascular lung density (ELD). We investigated the correlation between Ve/VCO(2) and ELD in patients with CHF. METHODS AND RESULTS: Thirteen patients with stable CHF and eleven control subjects were studied. Attenuation-corrected blood volume emission tomography was acquired with simultaneous transmission tomography to measure pulmonary blood volume and total lung density, respectively. Seven CHF patients underwent maximal exercise treadmill testing with online respiratory gas analysis. ELD was calculated as total lung density minus pulmonary blood volume. SPECT and transmission tomography were repeated immediately after exercise. CHF patients had significantly higher total lung density and ELD compared with normal subjects. No differences in pulmonary blood volume were observed. There was a significant inverse correlation between ELD and left ventricular ejection fraction at rest in CHF patients (r = -0.77, P <.001). A strong correlation was also found between post-exercise ELD and Ve/VCO(2) at peak exercise (r = 0.74, P =.008) and at anaerobic threshold (r = 0.67, P =.024). CONCLUSION: Patients with chronic CHF have increased ELD. The correlation between ELD and Ve/VCO(2) suggests that increased lung water may contribute to the ventilatory abnormalities seen in patients with CHF.     

R?ntgen appearances of pulmonary edema and their clinical and physiologic correlates (author's transl)]

With the rapid increase in the number of intensive care units in surgical and medical departments knowledge of early radiologic signs of pulmonary edema gains in importance. On the basis of investigations by American authors typical changes in the distribution of pulmonary blood supply can be shown, in good correlation with pressure changes in the pulmonary vein in left heart failure. When pressure rises in the pulmonary vein the well-know changes of interstitial or alveolar (acinary) pulmonary edema arise. Differential diagnosis between pulmonary edema due to left heart failure and edema from other causes is aided on the one hand by the presence of interstitial pulmonary edema and redistribution of blood, on the other hand by the abnormaly large heart and configuration. Neither R?ntgen appearances nor type of distribution of pulmonary edema are specific for any given cause. In all cases of pulmonary edema, the primary-peripheral excepted, clinical signs either occur later than X ray findings or will be absent altogether. Respiratory physiology permits, according to the severity of the edema, proof of hypoxemia with pronounced differences in the regional ventilation-perfusion quotient up to marked reduction of compliance and increase of resistance.     

Morphologic consideration of heart failure (author's transl)]

The left ventricle in left heart failure can be elliptical, spherical or funnel shaped. There is no firm correlation between the different shapes and the hemodynamics. Left ventricular failure results in dilatation, deformation and loss of funnel function of the left atrium. In more advanced stages of left ventricular failure the pulmonary veins become coiled, dilated and narrow stepwise instead of the normal harmonic narrowing to the periphery. The pulmonary parenchyma exhibits fibrosis and septal siderosis at that stage. Heart failure cells can be observed frequently. In later stages, when pulmonary arteries and the right ventricle is involved, secondary global heart failure develops. Right ventricular failure may lead to necrosis of liver cells with jaundice and elevated levels of liver specific enzyms. Primary global failure has no hemodynamic consequences on the pulmonary circulation, as long as left and right ventricular failure are of equal severity. If one form prevails, the clinical picture will be that of left or right ventricular failure respectively.     

Quantitative determination of regional extravascular lung water and regional blood volume in congestive heart failure

Regional extravascular lung water (rELW) and blood volume (rBV) in five controls and 14 patients with congestive heart failure (CHF) were measured by constant infusion of H₂ ¹⁵O and inhalation of ¹¹CO using positron emission tomography (PET). The analysis of 18 regions per patient revealed a relatively homogenous level of rELW in the controls (x=0.11±0.02 g/cc; range, 0.08–0.21), whereas this increased in patients with CHF (0.17±0.02 g/cc; range, 0.10–0.51). The rBV was 0.21±0.02 g/cc in the controls and 0.17±0.02 g/cc in patients with CHF. A good correlation was found between the severity of chronic heart failure (according to the grading of the New York Heart Association) and mean extravascular lung water (ELW) (r=0.69), as well as between CHF and the ratio rELW/rBV (r=0.87); however, the correlation to hemodynamic data was less satisfactory (cardiac index, r=0.45; pulmonary capillary wedge pressure, r=0.47; ejection fraction, r=0.60). In supine controls, a progressive decrease in regional blood volume from the basal to the apical regions was observed, whereas the differences in ELW were only small. In patients with chronic heart failure, ELW in the basal parts was markedly increased, whereas in the apical regions, only minor deviations from the controls were observed. In the basal regions of these patients, the blood volume was reduced by about 30%. Instead of the normal basoapical gradient of blood volume, these patients showed a rather flat distribution. Radiographic findings of pulmonary edema generally appeared together with an ELW level of greater than 0.14 g/cc. We conclude that the amount and distribution of fluid in pulmonary congestion can be noninvasively assessed by PET.Dedicated to Prof. Dr. Hans-Stephan Stender on his 65th birthday     

Circulatory response to acute hypobaric hypoxia in conscious dogs.

Hemodynamics were studied in seven conscious dogs during acute hypobaric stress at 14,000 ft simulated altitude. Silastic catheters were chronically implanted in the pulmonary artery, left atrium, and aorta. Pulmonary and central aortic pressures, cardiac output, and pulmonary blood volume were determined under conditions of normoxia and acute hypoxia in a hypobaric chamber maintained at 446 mm Hg pressure (14,000 ft). Altitude resulted in significant increases in heart rate, cardiac output, pulmonary blood volume, and pulmonary artery pressure. Left atrial pressure and calculated systemic vascular resistance decreased during hypobaric hypoxia while stroke volume, stroke work index, arterial pressure and pulmonary vascular resistance remained unchanged. Arterial blood PO2 decreased markedly at altitude, and all animals hyperventilated with resultant systemic hypocarbic alkalosis. The combination of elevated pulmonary arterial pressure and increased pulmonary blood volume may by an etiologic factor in the development of high-altitude pulmonary edema.     

慢性心力衰竭的CT表现

目的:探讨慢性心力衰竭的CT表现。材料和方法:回顾性分析28例慢性心力衰竭的CT表现。结果:左心室增大16例、右心室增大8例、左心房增大6例、右心房增大4例,左、右心房增大3例,肺水肿24例、胸腔积液25例、肺动脉扩张3例、升主动脉扩张5例和冠状动脉钙化7例。左心衰CT示肺水肿、左心室扩大和胸腔积液。右心衰CT示右心室扩大、主肺动脉扩张和胸腔积液。全心衰竭CT示左右心室扩大,肺水肿和双侧胸腔积液。结论:CT可显示心脏各房室扩大、大动脉扩张、肺水肿、胸腔和心包积液以及冠状动脉钙化,为诊断原发心脏疾病及慢性心力衰竭提供重要依据。     

Analysis of left ventricular diastolic function using magnetic resonance imaging

Heart failure is not always due to an alteration in systolic function, and a diastolic dysfunction could explain many cases of heart failure with a normal systolic function. Diastolic function depends on the left ventricular filling capacity to ensure a normal stroke volume. It is routinely measured with transthoracic echocardiography, as it is an easily accessible non-invasive test. The MRI, using flow sequences, shows good agreement with the echocardiography, analysing the diastolic function in a practical way, by the flow into the mitral valve and pulmonary veins. In this sense, the analysis of diastolic function should be added as part of a routine cardiac MR examination.     

Bilateral basal Xe-133 retention and ventilation/perfusion patterns in mild and subclinical congestive heart failure

The Xe-133 ventilation pattern in congestive heart failure (CHF) was assessed using 24 inpatient ventilation/perfusion studies performed to rule out pulmonary embolism. Patients with histories of CHF, myocardial infarction (MI), and cardiomyopathy were included in the study. Frank pulmonary edema, pulmonary embolism, and other known lung diseases such as chronic obstructive lung disease, tumor, and pneumonia were excluded. Fifteen of the 24 patients had abnormal ventilation scans. Twelve of the 15 showed bilateral basal Xe-133 retention on washout; the remaining 3 showed diffuse, posterior regional retention. On perfusion scans, 14 of the 15 abnormal ventilation patients showed evidence of CHF such as inverted perfusion gradient, enlarged cardiac silhouette, or patchy perfusion, and all of them had a history of CHF or cardiac disease. Nine of the 24 patients had normal ventilation scans, including normal washout patterns. Seven of the nine had normal perfusion (p less than 0.01). Four of the nine normal ventilation patients had a history of cardiac disease or CHF but no recent acute MI. Bilateral basal regional Xe-133 retention, coupled with perfusion scan evidence of CHF such as inverted perfusion gradient, enlarged cardiac silhouette, and patchy perfusion pattern, appears to be a sensitive and characteristic ventilation/perfusion finding in mild or subclinical CHF.     

Radiographic diagnosis of cardiogenic pulmonary edema]

Development of pulmonary edema (increased extravascular lung water) is a common and sometimes life-threatening clinical problem in critical-care unit patients. There are three principal causes: cardiac failure, overhydration, and increased pulmonary capillary permeability. Among these, cardiogenic edema consists of left heart failure and overhydration. Determining the specific cause of any given case of pulmonary edema is important and leads to more rapid and definitive treatment. A plain chest film can often explicate the cause of edema with a high degree of accuracy if careful attention is given to certain radiographic features. The principal features useful for correctly determining the cause of edema in a high percentage of cases are the distribution of pulmonary blood flow, distribution of pulmonary edema, and vascular pedicle width. Ancillary features are pulmonary blood volume, bronchial cuffing, septal lines, pleural effusion, and air bronchograms. Cardiac size and shape as well as specific intracardiac calcifications could also help distinguish cardiogenic from noncardiogenic pulmonary edema.     

X-ray changes in the thoracic organs in acute heart infarct

Chest X-rays were used to evaluate the hemodynamic status of 86 patients with acute myocardial infarction. The chest films, divided into three groups depending on the degree of pulmonary venous hypertension revealed: grade 1, pulmonary-venous congestion; grade 2, interstitial pulmonary edema; grade 3, diffuse alveolar edema. On clinical examination, four grades of congestive heart failure were distinguished in acute myocardial infarction. In 69% of our patients radiological and clinical grading of left ventricular failure led to precisely the same conclusions. Pulmonary capillary wedge pressure was measured in 31 patients with acute infarction. Radiological criteria of the degree of pulmonary vascular congestion, when related to pulmonary capillary wedge measurements, provide a basis for consistent therapy of left ventricular failure secondary to acute myocardial infarction.     

Right and left ventricular function and incidence of major complications in acute inferior myocardial infarct. Study by equilibrium-gated radioisotope angiography

By means of equilibrium gated radionuclide angiography (EGRA) 67 patients were studied with first inferior acute myocardial infarction (AMI) within 4 days of the onset of symptoms and 12 normal volunteers. Ejection fraction (EF) of the left ventricle (LV) and right ventricle (RV) was computed. The regional wall motion (RWM) was evaluated by parametric images of amplitude and phase (Fourier analysis). The following major in-hospital complications were diagnosed in 41 patients (61%): postinfarction angina, congestive heart failure (CHF), high-degree atrioventricular (AV) block, ventricular tachycardia or ventricular fibrillation, shock, extension of infarction, pericarditis, pulmonary embolism and acute pulmonary edema. A significant correlation between RVEF and the extent of RVRWM abnormalities and the incidence of major complications was found. In particular, the incidence of shock and CHF was significantly correlated with that of the RV disfunction, while the LVEF was generally in the normal range despite a high incidence of LVRWM abnormalities. In the patients developing high-degree AV block this correlation did not reach statistical significance; in this group, 10 of 12 patients developed other major complications. Also in 10 of 13 cases with CHF, other complications arose during the period of hospitalization. In conclusion the disfunction of the RV can identify the subgroup of patients with inferior AMI who are at high risk for developing major complications, especially shock and CHF. AV block and CHF have a severe prognostic meaning, because they occur usually in association with other major complications.     

腺相关病毒介导心肌肌浆网钙离子ATP酶2a基因转导对慢性心力衰竭大鼠的短期治疗作用

目的 研究腺相关病毒为载体的心肌肌浆网钙离子ATP酶2a(SERCA2a)基因转导对慢性心力衰竭(CHF)大鼠的短期治疗作用.方法 将大鼠分为4个组:对照组,CHF组,CHF eGFP组和CHF SERCA2a组.采用腹主动脉缩窄术建立慢性心力衰竭大鼠模型,应用经腹心包腔内注射术分别将生理盐水、携带eGFP基因的重组腺相关病毒和携带SERCA2a基因的重组腺相关病毒导入CHF组、CHF eGFP组和CHF SERCA2a组大鼠心脏.于导入后10天检测各组大鼠的心脏收缩和舒张功能、SERCA2a蛋白表达水平和活性.结果 慢性心力衰竭大鼠心脏内转导入SERCA2a基因10天后,CHF eGFP组SERCA2a蛋白表达水平和活性较CHF组大鼠明显增加(SERCA2a蛋白表达增加80.7%,活性增加89.9%),但低于对照组大鼠蛋白表达水平(约为对照组的67.6%)和活性水平(约为对照组的77.7%);大鼠的心脏功能随着SERCA2a功能的增强而改善,左室收缩压峰值和左室内压最大下降速率已达到对照组水平,左室舒张末压力和左室内压最大上升速率虽未达到对照组水平,但较CHF组明显改善.结论 CHF大鼠心脏SERCA2a蛋白表达水平及活性较对照大鼠明显下降;SERCA2a基因转导对慢性心力衰竭具有良好的短期治疗作用.