Cardiogenic pulmonary edema (CPE) is characterized by the development of acute respiratory failure associated with the accumulation of fluid in the lung’s alveolar spaces due to an elevated cardiac filling pressure. All cardiac diseases, characterized by an increasing pressure in the left side of the heart, can cause CPE. High capillary pressure for an extended period can also cause barrier disruption, which implies increased permeability and fluid transfer into the alveoli, leading to edema and atelectasis. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of procoagulant processes, cell death, and mechanical stretch. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance. Some studies claim that these patients may have higher levels of surfactant protein B in the bloodstream. The correct approach to patients with CPE should include a detailed medical history and a physical examination to evaluate signs and symptoms of CPE as well as potential causes. Second-level diagnostic tests, such as pulmonary ultrasound, natriuretic peptide level, chest radiograph, and echocardiogram, should occur in the meantime. The identification of the specific CPE phenotype is essential to set the most appropriate therapy for these patients. Non-invasive ventilation (NIV) should be considered early in the treatment of this disease. Diuretics and vasodilators are used for pulmonary congestion. Hypoperfusion requires treatment with inotropes and occasionally vasopressors. Patients with persistent symptoms and diuretic resistance might benefit from additional approaches (i.e., beta-agonists and pentoxifylline). This paper reviews the pathophysiology, clinical presentation, and management of CPE.
1 December 2016 in Journal of Cardiothoracic and Vascular Anesthesia
Both the role and the importance of magnesium in clinical practice have grown considerably in recent years. Emerging evidence suggests an association between loss of magnesium homeostasis and increased mortality in the critical care setting. The underlying mechanism is still unclear, but an increasing number of in vivo and in vitro studies on magnesium’s immunomodulating capabilities may shed some light on the matter. This review aims to discuss the evidence behind magnesium homeostasis in critically ill patients, and its link with intensive care unit mortality via a likely magnesium-induced dysregulation of the immune response. The underlying pathogenetic mechanisms, and their implications for clinical outcomes, are discussed. The available evidence strongly supports the crucial role of magnesium in immune system regulation and inflammatory response. The loss of magnesium homeostasis has been associated with an elevated risk of bacterial infections, exacerbated sepsis progression, and detrimental effects on the cardiac, respiratory, neurological, and renal systems, ultimately leading to increased mortality. However, magnesium supplementation has been shown to be beneficial in these conditions, highlighting the importance of maintaining adequate magnesium levels in the intensive care setting.
There is no consensus on which lung-protective strategies should be used in cardiac surgery patients. Sparse and small randomized clinical and animal trials suggest that maintaining mechanical ventilation during cardiopulmonary bypass is protective on the lungs. Unfortunately, such evidence is weak as it comes from surrogate and minor clinical endpoints mainly limited to elective coronary surgery. According to the available data in the academic literature, an unquestionable standardized strategy of lung protection during cardiopulmonary bypass cannot be recommended. The purpose of the CPBVENT study is to investigate the effectiveness of different strategies of mechanical ventilation during cardiopulmonary bypass on postoperative pulmonary function and complications. The CPBVENT study is a single-blind, multicenter, randomized controlled trial. We are going to enroll 870 patients undergoing elective cardiac surgery with planned use of cardiopulmonary bypass. Patients will be randomized into three groups: (1) no mechanical ventilation during cardiopulmonary bypass, (2) continuous positive airway pressure of 5 cmH2O during cardiopulmonary bypass, (3) respiratory rate of 5 acts/min with a tidal volume of 2–3 ml/Kg of ideal body weight and positive end-expiratory pressure of 3–5 cmH2O during cardiopulmonary bypass. The primary endpoint will be the incidence of a PaO2/FiO2 ratio <200 until the time of discharge from the intensive care unit. The secondary endpoints will be the incidence of postoperative pulmonary complications and 30-day mortality. Patients will be followed-up for 12 months after the date of randomization. The CPBVENT trial will establish whether, and how, different ventilator strategies during cardiopulmonary bypass will have an impact on postoperative pulmonary complications and outcomes of patients undergoing cardiac surgery. ClinicalTrials.gov, ID: NCT02090205 . Registered on 8 March 2014.
Background: Optimal pain control with limited muscle weakness after total hip arthroplasty (THA) is paramount for a swift initiation of physical therapy and ambulation, thus expediting hospital discharge. FICB (Fascia Iliaca Compartment Block) has been recommended because it offers pain control with a low risk of motor block. PENG (Pericapsular Nerve Group) block with LFCN (Lateral Femoral Cutaneous Nerve) has been proposed as an alternative that offers comparable pain control with a lower risk of motor block; however, evidence is limited. We aimed to investigate the degree of muscle weakness and pain control with PENG + LFCN. Methods: Patients undergoing elective THA from November 2022 to October 2023 have been retrospectively analyzed. The degree of quadriceps femoris muscle paresis was assessed with the MRC scale at 6 h postoperatively. Secondary outcomes: NRS score at 6, 12, and 24 h, total opioid consumption, and time to first rescue opioid. Results: In total, 80 patients were included in the study, 57 received PENG + LFCN, and the remaining 23 received FICB. PENG + LCFN resulted in a higher MRC at 6 h (4 [4; 5] vs. 3 [2; 4] p = 0.0001) and better pain control (mean difference [95% CI] at 6 h, 0.93 [0.14; 1.72], at 12 h, 0.47 [−0.49; 1.43], and at 24 h, 0.39 [0.25; 1.2], p = 0.0006). Less PRN opioids were requested in the PENG + LFCN vs. FICB groups (7.5 [0; 15] MME vs. 60 [40; 80], p = 0.001). Conclusions: PENG + LFCN was associated with less muscle weakness, better pain control, and less rescue opioids in patients undergoing elective THA. A larger prospective study is needed to confirm this finding.