Background: In patients with chronic heart failure, physical evaluation and clinical judgment may be inadequate for prognostic stratification. Hypothesis: Information obtained with simple bedside tests would be helpful in patient management. Methods: We report on 142 outpatients with systolic heart failure seen at our heart failure unit from 2007 to 2010 (ages 69.4 ± 8.9 years; ejection fraction [EF] 30.6 ± 6.1%; 43% with implanted defibrillators and/or resynchronization devices). At their first visit, we assessed levels of brain natriuretic peptide (BNP) (pg/mL), evaluated transthoracic conductance (TFC) (1/k ) by transthoracic bioimpedance, and performed echocardiography. Results: Four-year mortality was 21.2%. At multivariate analysis, surviving and deceased subjects did not differ regarding New York Heart Association, age, gender, heart failure etiology, or EF at index visit. Patients who died had higher BNP and TFC (BNP = 884 ± 119 pg/mL vs 334 ± 110 pg/mL; TFC = 50 ± 8/k vs 37 ± 7/k , both P < 0.001]. Patients with BNP < 450 pg/mL and TFC < 40/k had a 2.1% 4-year mortality, compared to 46.5% mortality of patients having BNP ≥ 450 pg/mL and TFC ≥ 40/k . BNP ≥ 450 pg/mL and TFC ≥ 40/k showed high sensitivity (91%) and specificity (88%)in identifying patients who died at follow-up. Conclusions: The combined use of BNP and impedance cardiography during the first assessment of a patient in a heart failure unit identified those carrying a worse medium-term prognosis. This approach could help the subsequent management of patients, allowing better clinical and therapeutic strategies.

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Introduction Large pleural and pericardial effusion is a common finding in lung cancer patients. However, a chronic large pleural effusion and the “lung entrapment” fenomenon, due to the neoplastic lung infiltration, could precipitate the re–expansion pulmonary edema (REPO) after the thoracentesis procedure. REPO is a rare and potentially life–threatening complication after large volume thoracentesis. It is characterized by alveolar infiltration in the reexpanded lung.Indeed, in the presence of “lung entrapment”, REPO development could be due not only to and excessive fluid removal, but also to the development of an excessively negative intrapleural pressure (&lt; – 20 mmHg). As the REPO is often associated to an hemodynamic impairment, in patients with concomitant severe pericardial effusion, this condition could cause cardiac tamponade and the optimal therapeutic approach could be challenging.In this perspective, the decision on the effusion to be drained first, in this population, is not always straightforward.Case report In a 62 years –old woman with severe respiratory failure, a chest CT scan showed a massive left –sided pleural effusion with a complete collapse of the left lung, a severe pericardial effusion (35 mm) and the presence of malignant mediastinal nodes. (Figure 1).In the ICU a left thoracentesis was performed, with an early drainage of 1400 ml, the drain was then clamped. 30 minutes later, the patient developed a severe acute respiratory failure. An urgent chest x ray revealed an ipsilateral pulmonary oedema (Figure2). The patient was then treated with respiratory support with cPAP and intravenous diuretic therapy. Afterward, a rapid hemodynamic derangement occurred, with cardiac tamponade. An emergency echoguided pericardiocentesis was then performed followed by an immediate recovery. A repeated thorax CT scan revealed an advanced pulmonary tumor (Figure 3). Discussion In this case all the risk factors for REPO were coexistent: chronic pleural effusion and lung cancer. In addition, the large pericardial effusion represented a complicating factor in this situation as both the cPAP and the REPO’s hypovolemia may have brought to a clinical tamponade. In this context, where a neoplastic severe pleural and pericardial effusions are coexistent, it is essential to know which possible complications may occur after a large volume thoracentesis in order to prevent a high risk urgent pericardial drainage in patient with severe respiratory distress.

A 55–years–old patient presents to emergency room with extensive anterior STEMI, complicated by acute pulmonary edema. The ECG showed sinusal tachycardia, Q waves in V1–V3, ST elevation &gt;2mm V2–V6. The echocardiogram showed akinesia of the apex and anterolateral wall with severe reduction of contractile function (LVEF 30%). The patient was treated with CPAP, dual antiplatelet therapy and diuretics; the urgent coronary angiography showed three–vessel disease with occlusion of the proximal LAD, treated with PCI and two drug–eluting stents implantation. 48 after admission to ICU, the patient developed "combined" shock (IC↓ RVS↓ WP↑), sustained by both severe cardiac dysfunction and a septic complication, requiring inotropes and targeted antibiotic therapy (noradrenaline 0.02 gamma/Kg/min and piperacillin/tazobactam i.v). At 96 hours there was a recovery of contractile function and haemodynamics (CI from 1.8 to 2.7). Weaned from inotropes, he began therapy with low doses of ACE inhibitor, beta blocker, antialdosteronic. On the 7th day of hospitalization, without ischemic and/or electrolyte "triggers", the patient developed "arrhythmic storm" with incessant sustained ventricular tachycardias. Arrhythmias persisted despite antiarrhythmics (magnesium sulfate, amiodarone, lidocaine), IOT, sedation, mechanical ventilation. The temporary pacemaker for overdrive pacing was placed in. After placement of IABP, the patient underwent revascularization of residual coronary artery stenosis. Despite 1 hour of assistance (ABLS), incessant ventricular tachycardia persisted; a third–level center for VA–ECMO inside support was called. After positioning VA–ECMO there was progressive clinical stabilization and –concomitantly– a progressive reduction of ventricular tachycardias. ECMO support was needed for over 7 days due to persistence of arrhythmic storm; it was slowly weaned with stabilization of the patient; an AICD was implanted. Residual function of the left ventricle was mild reduced (LVEF40%) despite protracted CPR. There wasn’t residual cognitive impairment. Implementation of multidisciplinary teams in the spoke centers would improve protocols and early treatments in patients with cardiogenic shock; spoke centers would provide early access to life–saving therapies and safe transfer to hub centers.

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