Development Of Acute Pulmonary Edema Research Articles

Periprocedural acute haemodynamic decompensation during substrate-based ablation of scar-related ventricular tachycardia: a rare and unpredictable event.

Patients with structural heart disease (SHD) undergoing catheter ablation (CA) for ventricular tachycardia (VT) are at considerable risk of periprocedural complications, including acute haemodynamic decompensation (AHD). The PAINESD score was proposed to predict the risk of AHD. The goal of this study was to validate the PAINESD score using the retrospective analysis of data from a large-volume heart centre. Patients who had their first radiofrequency CA for SHD-related VT between August 2006 and December 2020 were included in the study. Procedures were mainly performed under conscious sedation. Substrate mapping/ablation was performed primarily during spontaneous rhythm or right ventricular pacing. A purposely established institutional registry for complications of invasive procedures was used to collect all periprocedural complications that were subsequently adjudicated using the source medical records. Acute haemodynamic decompensation triggered by CA procedure was defined as intraprocedural or early post-procedural (<12 h) development of acute pulmonary oedema or refractory hypotension requiring urgent intervention. The study cohort consisted of 1124 patients (age, 63 ± 13 years; males, 87%; ischaemic cardiomyopathy, 67%; electrical storm, 25%; New York Heart Association Class, 2.0 ± 1.0; left ventricular ejection fraction, 34 ± 12%; diabetes mellitus, 31%; chronic obstructive pulmonary disease, 12%). Their PAINESD score was 11.4 ± 6.6 (median, 12; interquartile range, 6-17). Acute haemodynamic decompensation complicated the CA procedure in 13/1124 = 1.2% patients and was not predicted by PAINESD score with AHD rates of 0.3, 1.8, and 1.1% in subgroups by previously published PAINESD terciles (<9, 9-14, and >14). However, the PAINESD score strongly predicted mortality during the follow-up. Primarily substrate-based CA of SHD-related VT performed under conscious sedation is associated with a substantially lower rate of AHD than previously reported. The PAINESD score did not predict these events. The application of the PAINESD score to the selection of patients for pre-emptive mechanical circulatory support should be reconsidered.

Periprocedural acute hemodynamic decompensation associated with substrate-based ablation of ventricular tachycardia in patients with structural heart disease - rare and nonpredictable event

Abstract Funding Acknowledgements Type of funding sources: None. Background Radiofrequency (RF) catheter ablation is an established treatment method in patients with structural heart disease (SHD) and recurrent ventricular tachycardia (VT). Due to underlying SHD, concomitant heart failure and a high burden of comorbidities, these patients are at considerable risk of periprocedural complications including acute hemodynamic decompensation (AHD) with a reported rate of up to 11%. The PAINESD score [sum of 5, 3, 6, 6, 3, 5, and 3 points for chronic obstructive pulmonary disease (COPD), age &amp;gt;60 years, ischemic cardiomyopathy (ICM), NYHA Class &amp;gt;2, LV ejection fraction (LVEF) &amp;lt;25%, electrical storm (ES), and diabetes mellitus (DM), respectively] was proposed to predict the risk of AHD, and identify the patients who may benefit from pre-emptive use of percutaneous left ventricular assist device (pVAD). Purpose The single-centre, retrospective study investigated the incidence of AHD in large-volume, tertiary referral EP centre and the predictive power of the PAINESD score. Methods We included patients who had their first ablation for SHD-related VT between August 2006 and December 2020. The procedure was performed under conscious sedation except for patients who were on mechanical ventilation because of hemodynamical or electrical instability before the ablation. Substrate mapping/ablation was performed primarily during spontaneous rhythm or right-ventricular pacing. Induced VTs were terminated by overdrive pacing or cardioverted. Activation and entrainment mapping were used rarely – only in well-tolerated VTs. The goal of ablation was to abolish all inducible VTs. A purposely established institutional registry for complications of invasive procedures was used to collect all periprocedural complications that were subsequently adjudicated using the source medical records. AHD triggered by ablation procedure was defined as intraprocedural or early post-procedural (&amp;lt;12 h) development of acute pulmonary oedema or refractory hypotension, requiring urgent intervention including (but not limited to) inotropic agents and/or artificial ventilation and/or pVAD implant. Results The study cohort consisted of 1143 patients (age: 63±13 years, males: 87%, ICM: 67%, ES: 25%, NYHA Class: 2.1±1.0, LVEF: 34±13%, DM: 32%, COPD: 12%). Their PAINESD score was 11.4±6.6 (median: 12, interquartile range: 6–17). The ablation procedure (total duration 187±78 min, RF time: 23±15 min) was complicated by AHD in 13/1143 = 1.1% patients and these adverse events were not predicted by PAINESD score (Figure). Conclusions We observed a substantially lower rate (1.1%) of AHD than previously reported (up to 11%). These events did not accumulate in patients with upper-tertile PAINESD score in whom the highest AHD risk was reported (up to 24%). This observation may be explained by careful substrate-based ablation under conscious sedation that prevents prolonged low-output state related to repeated VT induction and mapping in general anaesthesia.

PO-05-039 PERIPROCEDURAL ACUTE HEMODYNAMIC DECOMPENSATION ASSOCIATED WITH SUBSTRATE-BASED ABLATION OF VENTRICULAR TACHYCARDIA IN PATIENTS WITH STRUCTURAL HEART DISEASE – RARE AND NONPREDICTABLE EVENT

Patients with structural heart disease (SHD) and recurrent ventricular tachycardia (VT) are at considerable risk of periprocedural complications of radiofrequency (RF) catheter ablation including acute hemodynamic decompensation (AHD). The PAINESD score [sum of 5, 3, 6, 6, 3, 5, and 3 points for chronic obstructive pulmonary disease (COPD), age >60 years, ischemic cardiomyopathy (ICM), NYHA Class >2, LV ejection fraction (LVEF) <25%, electrical storm (ES), and diabetes mellitus (DM), respectively] was proposed to predict the risk of AHD, and identify the patients who may benefit from pre-emptive use of percutaneous left ventricular assist device (pVAD). The single-center, retrospective study investigated the incidence of AHD in large-volume, tertiary referral EP center and the predictive power of the PAINESD score. We included patients who had their first ablation for SHD-related VT between August 2006 and December 2020. The procedure was performed under conscious sedation except for patients who were on mechanical ventilation because of hemodynamical or electrical instability before the ablation. Substrate mapping/ablation was performed primarily during spontaneous rhythm or right-ventricular pacing. Activation and entrainment mapping were used rarely, only in well-tolerated VTs. The goal of ablation was to abolish all inducible VTs. AHD triggered by ablation procedure was defined as intra- or early post-procedural (<12 h) development of acute pulmonary oedema or refractory hypotension, requiring urgent intervention like inotropic agents and/or artificial ventilation and/or pVAD implant. The study cohort consisted of 1143 patients (age: 63±13 years, males: 87%, ICM: 67%, ES: 25%, NYHA Class: 2.1±1.0, LVEF: 34±13%, DM: 32%, COPD: 12%). Their PAINESD score was 11.4 ± 6.6 (median: 12, interquartile range: 6–17). The ablation procedure (total duration 187±78 min, RF time: 23±15 min) was complicated by AHD in 13/1143 = 1.1% patients and these adverse events were not predicted by PAINESD score (Figure). We observed a substantially lower rate (1.1%) of AHD than previously reported (up to 11%). These events did not accumulate in patients with upper-tercile PAINESD score in whom the highest AHD risk was reported (up to 24%). This observation may be explained by careful substrate-based ablation under conscious sedation that prevents prolonged low-output state related to repeated VT induction and mapping in general anesthesia.

37 Prognostic role of the lung ultrasound in the acute coronary syndrome

Abstract Aim Acute coronary syndromes (ACS) represent one of the major causes of mortality in our country. Lung ultrasound is an important diagnostic tool in the assessment of lung and pleural diseases; it is easy to perform and provides low-cost analysis and it is also easily learned with a few hours of training. To evaluate the usefulness of lung ultrasound in the early diagnosis of pulmonary congestion in patients admitted to ICU for ACS and to evaluate its possible prognostic role in the short and long term. Methods Forty-three patients with ACS admitted in the ICU of Foggia were enrolled in the study between April 2020 and July 2020 (mean age 64.7 ± 12.7 years, male: 67.4%). Medical history, physical examination, ECG, blood analysis, chest X-ray, lung ultrasound and echocardiography were collected at the admission in ICU, after 24 h and at the dismission. All patients were re-evaluated, through a telephone follow-up 3 months after discharge. The primary endpoints were re-hospitalization at 30 days and the following MACEs: development of acute pulmonary oedema during hospitalization, cardiogenic shock, death and the need for oxygen therapy or the use of non-invasive ventilation. The secondary endpoints were out-of-hospital death from cardiac causes and re-hospitalization after 3 months. Results The analysis of the ROC curves showed that pulmonary ultrasound performed on admission in the ICU predicted more than the thoracic physical examination [AUC 0.536 (0.367–0.699); P = 0.111], chest radiograph (AUC 0.561 (0.391–0.721); P = 0.109] and LVEF [AUC 0.525 (0.357–0.689); P = 0.119], the risk of adverse cardiovascular events hospital, although not reaching the cut-off for statistical significance [AUC 0.661 (0.489–0.806); P = 0.0895]. Among all in-hospital events, pulmonary ultrasound predicted higher sensitivity and specificity [AUC 0.665 (0.493–0.809); P = 0.0927] than chest radiography [AUC 0.588 (0.417–0.745); P = 0.113], clinical examination [AUC 0.550 (0.380–0.711); P = 0.116] and LVEF [AUC 0.515 (0.348–0.680); P = 0.125], the use of oxygen therapy and NIV during hospitalization stay. Conclusions In patients with ACS, on admission lung ultrasound predicts the risk of in-hospital events, particularly the use of oxygen therapy or non-invasive mechanical ventilation more than physical examination, chest X-ray and LVEF estimated by echocardiography. It can be considered a complementary method to echocardiography in the evaluation of cardiac function, allowing to estimate the amount of extra-vascular lung water.

Dynamics in the content of the cytokines in the bronchoalveolar lavage fluid in rats after acute inhalation intoxication by clorine and pyrolysis products, containing hydrogen chloride

It is known that inhalation exposure to chlorine and hydrogen chloride leads to damage to the respiratory system up to the development of acute pulmonary edema in victims. No data on the mechanisms of development of pulmonary edema upon exposure to hydrogen chloride have been found in the available literature. The study was carried out on white outbred male rats, which were divided into 3 groups: Group I control; Group II animals were intoxicated with chlorine at a dose of 1.5 median lethal concentration (30 min); Group III animals were intoxicated with hydrogen chloride at a dose of 1.5 median lethal concentration (30 min). Immediately after exposure to the studied toxicants, as well as after 1, 3 and 6 h, the lung coefficient and the content of cytokines (interleukins-1, 6, 10 and interferon-) in the bronchoalveolar lavage fluid were determined in animals. It was revealed that an increase in the lung coefficient (p 0.05) in animals in groups II and III was accompanied by a significant increase (1.5 times) in the content of the studied cytokines in the bronchial-alveolar lavage fluid compared with animals in group I. III an increase (p 0.05) in the content of cytokines is recorded later only 3 hours after exposure, while it is significantly lower than in animals of group II at all studied periods. Thus, intoxication with hydrogen chloride leads to a slower development of pulmonary edema and an increase in the content of both pro (interleukins-1, 6) and anti-inflammatory cytokines (interleukin-10, interferon-) in the bronchial-alveolar lavage fluid compared to animals, exposed to chlorine intoxication.

Prognostic Significance of Baseline Serum Calcium Levels in Patients with Acute Coronary Syndrome- An Observational Study

Introduction: The risk stratification is very important for the management of patients with Acute Coronary Syndrome (ACS). Extraskeletal calcium plays a critical role in a range of biological processes. There is an urgent need to accurately identify, the additional factors which are important in the clinical course and outcome of patients of ACS. Aim: To evaluate impact of baseline serum calcium levels in patients with ACS and to determine prognostic significance of baseline serum calcium levels in patients with ACS. Materials and Methods: The present observational study was conducted on 100 patients of ACS, over a period of one year from December 2018 to December 2019 at Acharya Shri Chander College of Medical Sciences, Sidhra, Jammu and Kashmir, India. They were divided into three tertile ranges as: hypocalcaemic (&lt;8.1), normocalcaemic (8.1-10.4), hypercalcaemic (&gt;10.4). The clinical outcome was measured in terms of Left Ventricular Ejection Fraction (LVEF) development of acute pulmonary oedema, rates of emergency revascularisation, development of arrhythmias, recurrence of chest pain, mortality within 7 days of admission, readmission rates with reinfarction or any other cardiovascular complication and finally, mortality within 90 days of follow-up. Quantitative variables were compared using ANOVA/Kruskal Wallis Test between the three groups. Results: The mean age of the study population was 73.29±8.11 years. Baseline calcium on admission was found to be &lt;8.1 mg/dL in ACS patients and more common in males, older age group, patients with higher Body Mass Index (BMI) and was associated with worse prognosis as compared to those with normal serum calcium levels. Mortality within 90 days of follow-up occurred in 42.86%, 20% and 6.25% in unstable angina and 39.29% 11.76% and 13.33% in AMI in hypocalcaemic, normocalcaemic and hypercalcaemic groups, respectively. It is inferred that 64% of the patients in hypocalcaemia tertile (n=14) were males in unstable angina and overwhelming 78.57% in AMI. Conclusion: Hypocalcaemia (corrected calcium &lt;8.1 mg/dL) is common in patients of ACS and a predictor of adverse outcomes.

O26-5 - Possible Contribution of Right and Left Ventricular Stroke Volume Mismatch for the Development of Acute Pulmonary Edema

O26-5 - Possible Contribution of Right and Left Ventricular Stroke Volume Mismatch for the Development of Acute Pulmonary Edema

Guideline on the management of acute chest syndrome in sickle cell disease.

1. Department of Haematology, Guy’s and St Thomas’ NHS Foundation Trust 2. Lane Fox Respiratory Unit, St Thomas’ Hospital, Guy’s and St Thomas’ NHS Foundation Trust 3. Department of Haematology, North Middlesex Hospital 4. Department of Paediatric Haematology, Bristol Royal Hospital for Children 5. Department of Haematological Medicine, King’s College Hospital 6. Department of Haematology, Whittington Hospital

Successful transcatheter aortic valve implantation in a Hodgkin lymphoma patient with severe aortic stenosis

Transcatheter aortic valve implantation (TAVI) has emerged as an acceptable treatment modality for patients with severe aortic stenosis (AS) who are deemed unsuitable for conventional surgical aortic valve replacement. TAVI not only provides the treatment of AS, but also makes some other diseases treatable by relieving hemodynamic distress resulting from AS. In this case report, we presented a 74-year-old patient with Hodgkin's lymphoma (HL) that had been left untreated due to the development of acute pulmonary edema caused by severe degenerative AS during chemotherapy. This is the first report of the use of TAVI in a patient with HL.

Severe hypertension and pulmonary edema associated with systemic absorption of topical phenylephrine in a child during retinal surgery

Topical phenylephrine solutions are widely used in eye procedures to promote pupil dilation without cycloplegia. We report a case of intraoperative severe hypertension and acute pulmonary edema occurring in a child during retinal surgery after possible systemic absorption of topical phenylephrine eyedrops. Our objective is to discuss the proper treatment and preventive strategies for such a complication. A 4-year-old, male patient, 18.4 kg in weight, physical status ASA I was admitted for right retinal detachment surgery. Anesthesia was induced with sevoflurane in oxygen, followed by glycopyrrolate (5.0 μg/kg), propofol 25 mg, fentanyl 50 μg and cisatracurium 0.15 mg/kg given intravenously. Anesthesia was maintained with sevoflurane 2-2.5% in a mixture of nitrous oxide and oxygen (60%:40%). After incision, two drops of 10% aqueous phenylephrine were administered topically by the surgeon to the right eye for further pupil dilation. Few minutes later, the noninvasive blood pressure rose to 220/120 mmHg and the heart rate increased to 140 beats/min. Oxygen saturation (SpO2) dropped from 99% (with an inspired oxygen concentration (FiO2) of 0.4) to 82%. Auscultation revealed crepitations throughout the chest and a blood-stained frothy fluid was aspirated from the trachea with possible development of acute pulmonary edema. Hydralazine (5 mg) and furosemide (10 mg) were administered intravenously. Seven minutes later, the blood pressure returned to normal and the SpO2 increased to 92% on FiO2 of 1.0, with decreased intratracheal secretions. After approximately 20 minutes, the SpO2 had improved to 99%, with a FiO2 of 1.0 and the blood pressure was 109/63 mmHg and heart rate was 121 beats/min. The FiO2 gradually reduced back to 0.4 over 30 min with no further desaturation. The patient was discharged from the post anesthesia care unit 5 h after surgery with adequate spontaneous breathing, SpO2 99% on room air, normal blood pressure and pulmonary auscultation. Anesthesiologists and ophthalmologists should be aware of the possible cardiovascular side-effects of topical phenylephrine, and it should be used cautiously with appropriate intraoperative monitoring of hemodynamic variables. Moreover, preventive strategies to minimize systemic absorption of the drug should be taken.

Pulmonary oedema after therapeutic ascitic paracentesis: a case report and literature review of the cardiac complications of cirrhosis

In this study, we describe the development of acute pulmonary oedema and cardiac arrest after therapeutic ascitic paracentesis, in a gentleman with decompensated liver cirrhosis. There was no previous history of cardiorespiratory symptoms or disease. Postmortem examination revealed oedematous and congested lungs with bilateral pleural effusions; in addition, the right heart was dilated and congested. Micronodular cirrhosis was present with histological features of alpha1 antitrypsin deficiency. This is the first study of acute cardiac decompensation after large volume paracentesis. Owing to the postmortem findings, underlying asymptomatic cardiorespiratory disease may have been present. Cirrhosis is associated with cardiovascular complications including cirrhotic cardiomyopathy, portopulmonary hypertension and hepatopulmonary syndrome which may manifest or worsen under situations of haemodynamic stress. This report thus raises the question whether routine screening for cardiovascular abnormalities is warranted in patients with decompensated cirrhosis, particularly before the procedures such as paracentesis that impose significant haemodynamic strain.

Point: Pulmonary edema does occur in human athletes performing heavy sea-level exercise

Point: Pulmonary edema does occur in human athletes performing heavy sea-level exercise

Acute Pulmonary Oedema as a Complication of Hypertension During Pregnancy

Objective. To determine rates of and potential causative factors for acute pulmonary oedema (APO) in hypertensive women. Methods. Statistical analysis, including logistic regression, was applied to the individual patient data (IPD) of all hypertensive women who delivered in 2005 at two comparable units. Results. Of 880 cases analysed, there were no women with APO in unit one and 19 women in unit two. The women with APO received larger quantities of intravenous fluids, delivered at earlier gestations, via Caesarean section, following failed induction of labour and had a longer hospital stay. Conclusion. The development of APO in women with hypertension during pregnancy is associated with high levels of intravenous fluid administration.

Pulmonary Complications After Acute Kidney Injury

The development of respiratory failure in patients with AKI is a particularly devastating consequence that greatly increases patient mortality. When respiratory failure and AKI occur together, the mortality is greater than 80%. A clear understanding of the mechanisms leading to respiratory failure is of great clinical relevance to patients with AKI in order to prevent and treat this life-threatening complication. Pulmonary edema leading to respiratory failure has been a recognized complication of kidney failure since 1901. Remarkably, the pathogenesis of this complication remains elusive, despite over 100 years of clinical and experimental debate in the literature. A review of this literature suggests that there are 4 causes of pulmonary edema leading to respiratory failure in patients with AKI: (1) volume overload (cardiogenic edema), (2) left ventricular dysfunction (cardiogenic edema), (3) increased lung capillary permeability (noncardiogenic edema), and (4) acute lung injury (noncardiogenic edema with inflammation). In this review, these mechanisms are presented in historical context including the original descriptions of pathology and pathophysiology, recent epidemiologic data, and experimental studies in animals. Although volume overload is a well-accepted mechanism of pulmonary edema in patients with AKI, the purpose of this review was to highlight the evidence showing that noncardiogenic edema and acute lung injury also occur. By recognizing that the pulmonary complications of AKI are not simply from volume overload, specific treatment strategies may be discovered and used to improve outcomes in patients with the ominous and life threatening combination of AKI and respiratory failure.

Acute pulmonary oedema during cardiac resynchronization therapy device implantation: management with the activation of intra-aortic balloon pump

In this report, we present the case of two patients who experienced the development of acute pulmonary oedema during biventricular pacemaker implantation for cardiac resynchronization therapy. In both the cases, the activation of an intra-aortic balloon pump improved the clinical condition and the operation could be completed, which would otherwise have to be postponed.

Scanning sports medicine

An Ultracyclist with Pulmonary Edema During the Bicycle Race Across America A recently published case report in the January 2007 issue of Medicine & Science in Sports & Exercise, the official journal of the ACSM, highlights the pitfalls of overly aggressive sodium intake during an endurance race at altitude. It is well known that multiday ultra-endurance athletic events tax the body’s ability to maintain sodium and water homeostasis. Much focus has been placed on the danger associated with excessive water intake without sodium repletion, namely hyponatremia. This case study presents the risk associated with aggressive sodium intake coupled with heavy exertion at a high altitude. The subject presented is an extremely fit 38-year-old male participant in the Bicycle Race Across America who developed severe pulmonary edema while cycling at an altitude of 2380 meters on the fourth day of his race. His daily sodium intake over the course of the race averaged between 1000 and 1100 mEq and his weight on the day of hospitalization was 2.7 kg greater than his prerace weight. The athlete responded appropriately to standard support for pulmonary edema while in the hospital and he made a full recovery. Later, he underwent testing for cardiopulmonary disease or susceptibility to high-altitude pulmonary edema. The results of the entire work-up were negative. The authors hypothesize that the excessive sodium intake led to an expanded extracellular volume, increased hydrostatic pressure, and decreased oncotic pressure. Racing at high altitudes, where a hypoxia-induced rise in pulmonary artery pressures already exists, may have exaggerated the effects of the changes in hydrostatic and oncotic pressures seen with extracellular volume expansion. This, coupled with ambient hypoxia, elevated cardiac output, and reduced renal perfusion associated with sustained highlevel exercise seems to lead to the development of acute pulmonary edema.

An Ultracyclist with Pulmonary Edema during the Bicycle Race Across America

Ultraendurance athletic events tax the limits of physiological homeostasis. Maintenance of sodium and water balance is a particularly difficult challenge in such events. We present the case of a 38-yr-old participant in the Bicycle Race Across America who developed severe pulmonary edema while cycling at an altitude of 2380 m on the fourth day of the race. With hospitalization and standard support for pulmonary edema, he made a quick, full recovery. A post-race work-up revealed no evidence of underlying cardiopulmonary disease or susceptibility to high-altitude pulmonary edema. His weight on the day of hospitalization was 2.7 kg greater than his pre-race weight. We hypothesize that his excessive daily sodium intake (23-25 g, or 1000-1100 mEq) during the course of the race likely led to an expanded extracellular volume, increased hydrostatic pressure, and decreased oncotic pressure. These factors, in combination with ambient hypoxia, elevated cardiac output, and reduced renal perfusion expected with sustained, high-level exercise, may have led to the development of acute pulmonary edema. This case highlights the pitfalls of overly aggressive sodium intake in endurance races, particularly when such races are conducted at high altitude, where the hypoxia-induced rise in pulmonary artery pressures may amplify the effects of changes in hydrostatic and oncotic pressure that occur with extracellular volume expansion.

Levosimendan: A Novel Agent in Heart Failure

Heart failure is characterised by decreased cardiac output, which results in the development of both peripheral hypoperfusion and pulmonary congestion and can lead to the development of acute pulmonary edema. The primary objective in treating a patient with decompensated heart failure is hemodynamic stabilization, which is usually achieved by inotropic support. Classic inotropic agents provide short-term hemodynamic improvement, but their use has been correlated with poor prognosis. Levosimendan, a new calcium sensitizer, offers hemodynamic and symptomatic improvement without increasing cAMP and intracellular calcium concentrations. This agent improves contractility without increasing the risk of cardiac events such as arrhythmias. By combining a positive inotropic action mediated via calcium sensitization and a vasodilatory effect via ATP-dependent potassium channels, it appears to be superior than classic positive inotropic agents. Furthermore, it seems to have prolonged benefit in heart failure patients, and it also has anti-inflammatory and antiapoptotic properties. In conclusion, levosimendan seems to be a particularly promising agent for the treatment of decompensated heart failure, as in addition to improving cardiac output, it has a more favorable side-effect profile than classic inotropic agents, and it affects multiple pathways with key role in the pathophysiology of heart failure.

Cardiac tamponade masking clinical presentation and hemodynamic effects of papillary muscle rupture after acute myocardial infarction

A 67-year-old woman sustained an acute lateral-wall myocardial infarction and was treated with thrombolytic therapy. Postinfarction hypotension developed 3 days later. Clinical findings at that time were consistent with cardiac tamponade, and an echocardiographic study revealed a moderate-sized pericardial effusion. She underwent urgent pericardiocentesis with transient improvement in hemodynamics, followed by deterioration associated with the development of acute pulmonary edema. Follow-up transesophageal echocardiographic imaging revealed papillary muscle rupture with severe mitral regurgitation. The patient underwent urgent surgical intervention consisting of coronary artery bypass grafting and mitral valve replacement. The presence of cardiac tamponade in this patient masked the clinical manifestations of papillary muscle rupture through the hemodynamic effect of tamponade physiology on mitral regurgitation. (J Am Soc Echocardiogr 2002;15:1000-3.)

Assessment of acute pulmonary edema in dogs by electrical impedance imaging.

Acute pulmonary edema was assessed quantitatively in 12 experiments on six anesthetized dogs. Thirty-two copper foil electrodes were placed around each animal's thorax at the level of the third intercostal space. A real-time electrical impedance tomograph was used to form images of the electrical admittivity of the thorax in and near the plane of these electrodes. The lungs were identified by studying the change in admittivity associated with inspiration. Mean admittivity in these lung regions was assessed at 40-min intervals for the next 3-6 hours. In six control experiments, each having a duration of 200 min, the initial admittivity of the lung regions was 102 +/- 16(SD) mS/m. Lung admittivity usually increased during the first 80 min, and then remained within 2 mS/m of its value at 80 min for the remaining 120 min. In six experiments with pulmonary edema, an initial period of change followed by stability was observed. When stability had been attained, 0.07 ml/kg of oleic acid was injected slowly into a central venous site. Five animals received oleic acid, the sixth received a sham injection of saline. In the five receiving oleic acid, lung admittivity rose steadily for the remainder of the experiment. The increase in lung admittivity in these five animals was between 4 and 16 mS/m. In the sham injected experiment, the lung admittivity changed by 1 mS/m. We conclude that impedance imaging can provide semiquantitative assessment of the development of acute pulmonary edema.