Venovenous ECMO for Acute Chronic Heart Failure after Bilateral Lung Transplantation.

ABSTRACT: Venovenous (VV) ECMO is rarely used during decompensated circulatory states. Although VA ECMO is the routine option, VV ECMO may be an option in selected patients. We present a case of pulmonary edema due to acute heart failure in a patient 4- and 12-year post-lung transplantation who received VV ECMO. Using a thoughtful cannulation strategy, VV ECMO, and aggressive ultrafiltration, the patient was successfully decannulated, extubated, and discharged from the hospital. In cardiogenic pulmonary edema, VV ECMO represents an additional, and likely under-utilized tool, especially in patients who are at high risk for ventilator-associated lung injury. Cannula location and size should be given additional consideration to potentially transition to V-AV ECMO configuration if necessary.

Superoxide dismutase 1-modified dental pulp stem cells alleviate high-altitude pulmonary edema by inhibiting oxidative stress through the Nrf2/HO-1 pathway.

High-altitude pulmonary edema (HAPE) is a deadly form of altitude sickness, and there is no effective treatment for HAPE. Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cell isolated from dental pulp tissues and possess various functions, such as anti-inflammatory and anti-oxidative stress. DPSCs have been used to treat a variety of diseases, but there are no studies on treating HAPE. In this study, Sprague-Dawley rats were exposed to acute low-pressure hypoxia to establish the HAPE model, and SOD1-modified DPSCs (DPSCsHiSOD1) were administered through the tail vein. Pulmonary arterial pressure, lung water content (LWC), total lung protein content of bronchoalveolar lavage fluid (BALF) and lung homogenates, oxidative stress, and inflammatory indicators were detected to evaluate the effects of DPSCsHiSOD1 on HAPE. Rat type II alveolar epithelial cells (RLE-6TN) were used to investigate the effects and mechanism of DPSCsHiSOD1 on hypoxia injury. We found that DPSCs could treat HAPE, and the effect was better than that of dexamethasone treatment. SOD1 modification could enhance the function of DPSCs in improving the structure of lung tissue, decreasing pulmonary arterial pressure and LWC, and reducing the total lung protein content of BALF and lung homogenates, through anti-oxidative stress and anti-inflammatory effects. Furthermore, we found that DPSCsHiSOD1 could protect RLE-6TN from hypoxic injury by reducing the accumulation of reactive oxygen species (ROS) and activating the Nrf2/HO-1 pathway. Our findings confirm that SOD1 modification could enhance the anti-oxidative stress ability of DPSCs through the Nrf2/HO-1 signalling pathway. DPSCs, especially DPSCsHiSOD1, could be a potential treatment for HAPE. Schematic diagram of the antioxidant stress mechanism of DPSCs in the treatment of high-altitude pulmonary edema. DPSCs can alleviate oxidative stress by releasing superoxide dismutase 1, thereby reducing ROS production and activating the Nrf2/HO-1 signalling pathway to ameliorate lung cell injury in HAPE.

Swimming-Induced Pulmonary Edema: Evaluation, Diagnosis, and Treatment.

ABSTRACT: Swimming-induced pulmonary edema (SIPE) is a rare but life-threatening acute illness that can occur in otherwise healthy athletes and individuals. Also known as immersion pulmonary edema, SIPE presents in swimmers, snorkelers, and SCUBA divers. It occurs in persons under heavy exertion in cold water temperatures, leading to coughing, shortness of breath, and sometimes blood-tinged sputum. Under these conditions, there is increased pulmonary vascular pressure, which may ultimately lead to pulmonary edema. This article synthesizes the latest data on the prevalence, pathophysiology, etiology, risks, short- and long-term complications, and the efficacy of supportive medical treatment interventions.

Evaluation and Management of the Individual with Recurrent High Altitude Pulmonary Edema.

Luks AM, Grissom CK. Evaluation and Management of the Individual with Recurrent HAPE. High Alt Med Biol. 25:238-246, 2024. Individuals with a history of acute altitude illness often seek recommendations from medical providers on how to prevent such problems on future ascents to high elevation. Although many of these cases can be managed with pharmacologic prophylaxis and counseling about the appropriate rate of ascent alone, there are some situations in which further diagnostic evaluation may also be warranted. One such situation is the individual with recurrent episodes of high altitude pulmonary edema (HAPE), as one of several predisposing factors may be present that warrants additional interventions beyond pharmacologic prophylaxis and slow ascent and may even preclude future travel to high altitude. This review considers this situation in greater detail. Structured around the case of an otherwise healthy 27-year-old individual with recurrent episodes of HAPE who would like to climb Denali (6,190 m), the review examines the known risk factors for disease and then provides guidance regarding when and how to evaluate such individuals and appropriate steps to prevent HAPE on further ascents to high elevation. Except in rare circumstances, a history of recurrent HAPE does not preclude further ascent to high elevation, as a multipronged approach including pharmacologic prophylaxis, careful planning about the rate of ascent, and the degree of physical effort and other strategies, such as preacclimatization, staged ascent, and use of hypoxic tents, can be employed to reduce the risk of recurrence with future travel.

Successful management of pulmonary edema secondary to accidental electrocution in a young dog.

BACKGROUND: Human records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes. CASE PRESENTATION: A 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide ≤ 40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H2O) and positive end-expiratory pressure (3 to 10 cm H2O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation ≥ 96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits. CONCLUSIONS: We present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine.

Managing Patients With Sympathetic Crashing Acute Pulmonary Edema (SCAPE) Using the SCAPE Treatment Protocol: A Case Series.

Pulmonary edema refers to the accumulation of excessive fluid in the alveolar walls and alveolar spaces of the lungs. It is a life-threatening condition with a high mortality rate and requires immediate assessment and management. Use of intravenous nitroglycerin has been advocated for such cases. The authors present a case series of 3 patients who presented to the emergency department with sympathetic crashing acute pulmonary edema (SCAPE) and were managed with high-dose intravenous nitroglycerin and bilevel positive airway pressure support using the SCAPE treatment protocol, leading to early correction of blood pressure, avoidance of endotracheal intubation, and no episodes of hypotension or rebound hypertension. The authors recommend emergency physicians utilize the SCAPE treatment protocol while managing patients with SCAPE.

Safety of hyperbaric oxygen therapy in patients with heart failure: A retrospective cohort study.

BACKGROUND: Hyperbaric oxygen therapy (HBOT) has several hemodynamic effects including increases in afterload (due to vasoconstriction) and decreases in cardiac output. This, along with rare reports of pulmonary edema during emergency treatment, has led providers to consider HBOT relatively contraindicated in patients with reduced left ventricular ejection fraction (LVEF). However, there is limited evidence regarding the safety of elective HBOT in patients with heart failure (HF), and no existing reports of complications among patients with HF and preserved LVEF. We aimed to retrospectively review patients with preexisting diagnoses of HF who underwent elective HBOT, to analyze HBOT-related acute HF complications. METHODS: Research Ethics Board approvals were received to retrospectively review patient charts. Patients with a history of HF with either preserved ejection fraction (HFpEF), mid-range ejection fraction (HFmEF), or reduced ejection fraction (HFrEF) who underwent elective HBOT at two Hyperbaric Centers (Toronto General Hospital, Rouge Valley Hyperbaric Medical Centre) between June 2018 and December 2020 were reviewed. RESULTS: Twenty-three patients with a history of HF underwent HBOT, completing an average of 39 (range 6-62) consecutive sessions at 2.0 atmospheres absolute (ATA) (n = 11) or at 2.4 ATA (n = 12); only two patients received fewer than 10 sessions. Thirteen patients had HFpEF (mean LVEF 55 ± 7%), and seven patients had HFrEF (mean LVEF 35 ± 8%) as well as concomitantly decreased right ventricle function (n = 5), moderate/severe tricuspid regurgitation (n = 3), or pulmonary hypertension (n = 5). The remaining three patients had HFmEF (mean LVEF 44 ± 4%). All but one patient was receiving fluid balance therapy either with loop diuretics or dialysis. Twenty-one patients completed HBOT without complications. We observed symptoms consistent with HBOT-related HF exacerbation in two patients. One patient with HFrEF (LVEF 24%) developed dyspnea attributed to pulmonary edema after the fourth treatment, and later admitted to voluntarily holding his diuretics before the session. He was managed with increased oral diuretics as an outpatient, and ultimately completed a course of 33 HBOT sessions uneventfully. Another patient with HFpEF (LVEF 64%) developed dyspnea and desaturation after six sessions, requiring hospital admission. Acute coronary ischemia and pulmonary embolism were ruled out, and an elevated BNP and normal LVEF on echocardiogram confirmed a diagnosis of pulmonary edema in the context of HFpEF. Symptoms subsided after diuretic treatment and the patient was discharged home in stable condition, but elected not to resume HBOT. CONCLUSIONS: Patients with HF, including HFpEF, may develop HF symptoms during HBOT and warrant ongoing surveillance. However, these patients can receive HBOT safely after optimization of HF therapy and fluid restriction.

Guyton perspective in managing peripartum cardiomyopathy patient with pulmonary edema: a case report.

BACKGROUND: Peripartum cardiomyopathy (PPCM) is a potentially life-threatening pregnancy-related condition characterized by left ventricular dysfunction and heart failure, typically occurring in the peripartum period. Individuals with a history of preeclampsia and hypertension are particularly prone to developing PPCM. Recent research suggests that the condition may be triggered by vascular dysfunction influenced by maternal hormones in the late stages of gestation. The onset of left heart failure results in decreased cardiac output, leading to insufficient perfusion, which in turn, contributes to pulmonary edema and exacerbates tissue hypoxia. This cardiovascular response activates the neurohumoral system, causing peripheral vasoconstriction and elevating both mean capillary filling pressure (MCFP) and central venous pressure (CVP). Early administration of furosemide reduces volume overload due to negative cumulative fluid balance gaining and vasodilation, which increases the velocity of intravascular refilling and causes interstitial edema to resolve. This will decrease interstitial fluid pressure, resulting in decreased mechanical compression to systemic capillary and systemic vein pressure, thus decreasing MCFP and CVP subsequently. Reduced CVP also contributes to increased venous return by decreasing the gradient pressure between MCFP and CVP, resulting in increased cardiac output (CO) and improved tissue oxygenation. CASE: A 33-year-old Asian woman, para 3 at full term pregnancy, admitted to the intensive care unit (ICU) after c-section and tubectomy due to shortness of breath and palpitation. Based on history taking, physical examination and echocardiography the patient fulfilled the criteria of PPCM which was also complicated by pulmonary edema. Despite impending respiratory failure, the patient rejected intubation and continuous positive airway pressure (CPAP), and was given oxygen supplementation through nasal cannula. Furosemide was given rapidly continued by maintenance dose and CVP was monitored. Antihypertensive drug, anticoagulants, and bromocriptine were also administered. After achieving negative cumulative fluid balance the patient's symptoms resolved and was discharged one week later. CONCLUSION: There is a correlation between negative cumulative fluid balance and reduced central venous pressure after early furosemide therapy. Suspicion for PPCM should not be lowered in the presence of preeclampsia, it could delay appropriate treatment and increase the mortality.

High-flow nasal cannula oxygen versus noninvasive ventilation for the management of acute cardiogenic pulmonary edema: a randomized controlled pilot study.

BACKGROUND: Whether high-flow nasal oxygen can improve clinical signs of acute respiratory failure in acute heart failure (AHF) is uncertain. OBJECTIVE: To compare the effect of high-flow oxygen with noninvasive ventilation (NIV) on respiratory rate in patients admitted to an emergency department (ED) for AHF-related acute respiratory failure. DESIGN, SETTINGS AND PARTICIPANTS: Multicenter, randomized pilot study in three French EDs. Adult patients with acute respiratory failure due to suspected AHF were included. Key exclusion criteria were urgent need for intubation, Glasgow Coma Scale <13 points or hemodynamic instability. INTERVENTION: Patients were randomly assigned to receive high-flow oxygen (minimum 50 l/min) or noninvasive bilevel positive pressure ventilation. OUTCOMES MEASURE: The primary outcome was change in respiratory rate within the first hour of treatment and was analyzed with a linear mixed model. Secondary outcomes included changes in pulse oximetry, heart rate, blood pressure, blood gas samples, comfort, treatment failure and mortality. MAIN RESULTS: Among the 145 eligible patients in the three participating centers, 60 patients were included in the analysis [median age 86 (interquartile range (IQR), 90; 92) years]. There was a median respiratory rate of 30.5 (IQR, 28; 33) and 29.5 (IQR, 27; 35) breaths/min in the high-flow oxygen and NIV groups respectively, with a median change of -10 (IQR, -12; -8) with high-flow nasal oxygen and -7 (IQR, -11; -5) breaths/min with NIV [estimated difference -2.6 breaths/min (95% confidence interval (CI), -0.5-5.7), P  = 0.052] at 60 min. There was a median SpO 2 of 95 (IQR, 92; 97) and 96 (IQR, 93; 97) in the high-flow oxygen and NIV groups respectively, with a median change at 60 min of 2 (IQR, 0; 5) with high-flow nasal oxygen and 2 (IQR, -1; 5) % with NIV [estimated difference 0.8% (95% CI, -1.1-2.8), P  = 0.60]. PaO 2 , PaCO 2 and pH did not differ at 1 h between groups, nor did treatment failure, intubation and mortality rates. CONCLUSION: In this pilot study, we did not observe a statistically significant difference in changes in respiratory rate among patients with acute respiratory failure due to AHF and managed with high-flow oxygen or NIV. However, the point estimate and its large confidence interval may suggest a benefit of high-flow oxygen. TRIAL REGISTRATION: NCT04971213 ( https://clinicaltrials.gov ).

Evaluation of HACOR scale as a predictor of non-invasive ventilation failure in acute cardiogenic pulmonary oedema patients: A prospective observational study.

BACKGROUND AND IMPORTANCE: Acute cardiogenic pulmonary oedema (ACPO) is a common indication for non-invasive ventilation (NIV) in the emergency department (ED). HACOR score of >5 is used to predict NIV failure. The predictive ability of HACOR may be affected by altered physiological parameters in ACPO patients due to medications or comorbidities. OBJECTIVES: To validate the HACOR scale in predicting NIV failure among acute cardiogenic pulmonary oedema (ACPO) patients. DESIGN, SETTINGS AND PARTICIPANTS: This is a prospective, observational study of consecutive ACPO patients requiring NIV admitted to the ED. OUTCOME MEASURE AND ANALYSIS: Primary outcome was the ability of the HACOR score to predict NIV failure. Clinical, physiological, and HACOR score at baseline and at 1 h, 12 h and 24 h were analysed. Other potential predictors were assessed as secondary outcomes. MAIN RESULTS: A total of 221 patients were included in the analysis. Fifty-four (24.4%) had NIV failure. Optimal HACOR score was >5 at 1 h after NIV initiation in predicting NIV failure (AUC 0.73, sensitivity 53.7%, specificity 83.2%). As part of the HACOR score, respiratory rate and heart rate were not found to be significant predictors. Other significant predictors of NIV failure in ACPO patients were acute coronary syndrome, acute kidney injury, presence of congestive heart failure as a comorbid, and the ROX index. CONCLUSIONS: The HACOR scale measured at 1 h after NIV initiation predicts NIV failure among ACPO patients with acceptable accuracy. The cut-off level > 5 could be a useful clinical decision support tool in ACPO patient. However, clinicians should consider other factors such as the acute coronary and acute kidney diagnosis at presentation, presence of underlying congestive heart failure and the ROX index when clinically deciding on timely invasive mechanical ventilation.

Continuous Positive Airway Pressure in the Treatment of Pediatric High Altitude Pulmonary Edema: A Case Study.

Treatment of high altitude pulmonary edema (HAPE) can be challenging and is further complicated in the pediatric patient in the prehospital environment. The following case presents a decompensating pediatric patient with HAPE in the prehospital aeromedical environment. It illustrates the potential benefit of continuous positive airway pressure (CPAP) as a treatment modality in the treatment of HAPE.

Guideline adherence in the management of acute pulmonary oedema: Study protocol for a French survey involving cardiologists, emergency physicians and intensivists.

BACKGROUND: Because of their high morbidity and mortality, patients with acute pulmonary oedema (APE) require early recognition of symptoms, identification of precipitating factors and admission to specialized care units (cardiac critical care or intensive care). APE is at the crossroads of different specialties (cardiology, emergency medicine and intensive care medicine). Although multidisciplinary expertise and management may be a strength, it can also be a source of confusion, with unexpected heterogeneity in patient care. We hypothesized that the management of severe APE may be heterogeneous between specialties and, in some situations, may differ from international recommendations. AIM: We designed a survey to compare management of different APE phenotypes according to the physicians' medical specialty, and to compare the results with what experts would do and European guidelines. METHODS: Four clinical cases of typical APE with questions pertaining to the latest guidelines were designed by a Scientific Committee designated by the French Scientific Societies for Cardiology, Emergency Medicine and Intensive Care Medicine. We focused on oxygenation and ventilation strategies, management of precipitating factors, including timing of coronary revascularization, use of diuretics and management of diuretic resistance, and discharge coverage. From 20 June 2022 until 09 September 2022, the four cases of APE (two during hypertensive crises, two during acute coronary syndromes) were proposed to French physicians involved in APE care, and to experts, using an open online survey. To avoid any diagnostic ambiguity, the diagnosis of APE was given at the beginning of each clinical case. RESULTS: The intention is to present the results at national and international conferences and publish them in a peer-reviewed journal. CONCLUSIONS: The results of this survey are intended to pave the way for the generation of novel hypotheses for future clinical trials in case of equipoise between subsets of therapeutic procedures in APE.

Reexpansion pulmonary edema after treatment of primary spontaneous pneumothorax.

A 24-year-old male patient, without further symptoms or comorbidities presented to the emergency room with acute dyspnea after heavy lifting two days before. On auscultation an attenuated vesicular breath was noticed on the right lung. In the initial chest radiograph a right-sided primary spontaneous pneumothorax with minor mediastinal shift was diagnosed. After insertion of a 12-French chest tube the patient's clinical condition deteriorated. The following chest radiograph and computed tomography of the thorax showed a reexpansion pulmonary edema in the right lung. The patient was admitted to the ICU and supportive treatment was initiated. Pulmonary reexpansion edema after drainage of a pneumothorax is a very rare complication with mortality rates reaching up to 20%. The exact pathophysiology remains unknown. Typical Symptoms include dyspnea, hypotension, and tachycardia. To minimize the risk of a pulmonary reexpansion edema, not more than 1200-1800 ml of air should be drained at once and the drainage should be stopped when the patient starts coughing.

Syndromes of Concurrent Hypertension, Diastolic Dysfunction, and Pulmonary or Peripheral Edema in Cardio-Oncology: Case Studies, Literature Review, and New Classification System.

OPINION STATEMENT: Individuals who have ever been diagnosed with cancer are at increased risk for cardiovascular conditions during and after cancer treatment. Especially during cancer treatment, cardiovascular conditions can manifest in many ways, including peripheral or pulmonary edema. Edema can indicate volume overload affecting the heart even without other unequivocal evidence of apparent diastolic or systolic left ventricular dysfunction, particularly at rest. We propose a novel algorithm to streamline the diagnostic evaluation and cardiovascular classification for cancer patients with edema. We initially advise prompt evaluation with a chest X-ray and echocardiogram. We then suggest classification into one of five categories based on the timing of presentation of edema relative to cancer treatment, as well as echocardiography results and the presence or absence of hypertension or lymphatic causes of edema. This classification tool can then be utilized to guide further cardiovascular management suggestions. These concurrent syndromes presenting as edema may indicate the development or aggravation of undiagnosed diastolic dysfunction with or without hypertension, even if transiently present only while on cancer treatment.

Successful treatment of acute respiratory failure following hypertensive crisis in a dog with presumed pheochromocytoma or paraganglioma.

Background: Acute respiratory failure has been reported as one of the manifestations of hypertensive crisis in pheochromocytoma in human medicine. In dogs, no reports have been described as acute respiratory failure following hypertensive crisis. Here, we report the clinical presentation, course, and treatment of acute respiratory failure following the hypertensive crisis in a dog with presumed pheochromocytoma or paraganglioma. Case Description: A 12-year-old neutered male toy poodle was referred for the diagnostic evaluation of a right adrenal gland mass. The dog suddenly exhibited severe dyspnea with abnormal hypertension (systolic blood pressure >200 mmHg) 15 minutes after recovery from the anesthesia for the computed tomography (CT) examination. Pulmonary CT and ultrasonography findings suggested acute onset of severe pulmonary edema. Pulmonary edema was treated with mechanical ventilation (pressure-support ventilation with continuous positive airway pressure) and negative fluid balance after the administration of furosemide. Weaning from mechanical ventilation was successful 24 hours after the onset of respiratory failure. Finally, the dog was discharged 3 days after weaning from ventilation without complications. Conclusion: This report outlines a case of acute respiratory failure following a hypertensive crisis requiring mechanical ventilatory management in a dog. The onset and progression of pulmonary edema were extremely rapid. However, improvement in pulmonary edema was also rapid. Hemodynamic stability, in addition to prompt diagnosis and aggressive therapeutic intervention, including mechanical ventilation, may have contributed to the good prognosis of pulmonary edema following hypertensive crisis in a dog, which we attribute to a catecholamine storm.

Pulmonary edema ex vacuo after drainage of pyo-pneumothorax.

This case presents a rare occurrence of re-expansion pulmonary edema following a drainage of pyo-pneumothorax in a 33-year-old patient. The diagnosis was established through a thoracic radiography, and the treatment consisted of symptomatic management, showing positive progress. Later on, the patient was diagnosed with pleural tuberculosis via GeneXpert testing and subsequently initiated on anti-bacterial therapy.This case report aims to shed light on the infrequent pulmonary edema ex vacuo as a complication of pleural drainage. It explores its causes, risk factors, diagnostic approaches, and treatment options. this study highlights the necessity of effective prevention and management strategies.