[The first wave of COVID-19 in Intensive care]. / La première vague de la COVID-19 aux Soins intensifs, mars-mai 2020.

In December 2019, in Wuhan, a new human infectious pathology was born, COVID-19, consisting above all in pneumoniae, induced by the coronavirus named SARS-CoV-2 because of the respiratory distress it caused (SARS for severe acute respiratory syndrome, and CoV for Coronavirus). A real health and planetary crisis has appeared, much more substantial than that linked to SARS-CoV-1 in 2002-2004 and to MERS-CoV (Middle East Respiratory Syndrome Coronavirus) in 2012. In addition to respiratory damage that can be dramatic, this pathology is complicated by the frequency of cardiovascular, renal and coagulation diseases. Health care systems have had to adapt urgently, in the absence of hindsight from the pathology, and without effective therapeutic weapons. Through this review of the literature, we detail our local practices for the overall management of patients hospitalized in Intensive care.

En décembre 2019, à Wuhan, une nouvelle pathologie infectieuse humaine est née, le COVID-19, consistant avant tout en une pneumonie, induite par le coronavirus nommé SARS-CoV-2 en lien avec l'intensité de la détresse respiratoire qu'il entraîne (SARS pour syndrome respiratoire aigu sévère, et CoV pour coronavirus). Une véritable crise sanitaire et planétaire est apparue, bien plus conséquente que celle liée au SARS-CoV-1 en 2002-2004 et au MERS-CoV (Middle East Respiratory Syndrome Coronavirus) en 2012. Outre une atteinte respiratoire pouvant être dramatique, cette pathologie est complexifiée par la fréquence des atteintes cardiovasculaires, rénales et de la coagulation. Les systèmes de soins de santé ont dû s'adapter urgemment, en l'absence de recul face à la pathologie, et sans armes thérapeutiques efficaces. Au travers de cette revue de la littérature, nous détaillons nos pratiques locales pour la prise en charge globale des patients hospitalisés aux Soins intensifs.

[Acute respiratory distress syndrome]. / Le syndrome de détresse respiratoire aiguë.

Since its first description in 1967, a lot of progress has been made in understanding the pathophysiology, diagnosis and management of acute respiratory distress syndrome (ARDS). This nosological entity is based on the appearance of a diffuse alveolar damage associating pulmonary epithelial barrier disruption with an alveolar filling, both responsible of profound hypoxemia and important morbi-mortality. Nowadays, ARDS remains a frequent syndrome, associated with various etiologies. Diagnosis is based on the occurrence of acute hypoxic respiratory failure not explained by cardiac insufficiency or volume overload, within 7 days after a recognized risk factor, and in the presence of bilateral pulmonary opacities not fully explained by effusions, atelectasis or nodules on the chest radiography. Survivors present an increased risk of developing cognitive decline, depression, post-traumatic stress, and typical ICU related side-effects such as polyneuropathy and sarcopenia. In this context and not withstanding significant recent progress in the field of mechanical ventilation and extra-corporeal respiratory assistance, early diagnosis remains essential to identify patients with ARDS in order to offer them the most appropriate therapy.

Depuis sa première description en 1967, des progrès majeurs ont été réalisés dans la compréhension de la physiopathologie, le diagnostic et la prise en charge du syndrome de détresse respiratoire aiguë (SDRA). Cette entité nosologique repose sur l'apparition d'un dommage alvéolaire diffus associant une rupture de la barrière épithéliale pulmonaire avec un comblement alvéolaire à l'origine d'une hypoxémie profonde. De nos jours, le SDRA reste un syndrome fréquent, grevé d'une mortalité élevée, et prenant source dans de multiples situations pathologiques. Le diagnostic du SDRA repose sur l'apparition d'une insuffisance respiratoire aiguë hypoxique non expliquée par une insuffisance cardiaque ou une surcharge volémique, dans un délai de 7 jours suivant l'apparition d'un facteur de risque reconnu, en présence d'opacités pulmonaires bilatérales non complètement expliquées par des épanchements, des atélectasies ou des nodules. Les survivants sont à haut risque de développer un déclin cognitif, une dépression, ou un stress post-traumatique en plus des effets secondaires classiques d'une longue hospitalisation en unité de soins intensifs que sont la polyneuropathie ou la sarcopénie. Dans ce contexte, et en dépit de progrès importants dans le domaine de la ventilation mécanique et de l'assistance respiratoire par circulation extra-corporelle, il reste primordial d'identifier précocement les patients souffrant de SDRA afin de leur proposer la thérapeutique la plus appropriée dès les premiers signes cliniques.

[How I treat severe beta-blocker poisoning : pharmacological approaches and ECMO]. / Comment je traite... l'intoxication massive aux bêta-bloquants : approches pharmacologiques et place de l'ECMO.

We report the case of a woman with severe beta-blocker poisoning who, after failure of pharmacological therapy, was supported with an ECMO (ExtraCorporeal Membrane Oxygenation) device. We discuss conventional pharmacological treatments and other approaches that have emerged over the past decade such as high dose insulin therapy and lipid emulsions. Major advance has been achieved in the field of ECMO devices and their management. ECMO is now the first line device for refractory acute cardiac and/or pulmonary failure. Finally, we review the role of veno-arterial ECMO in cardiodepressive drug poisoning.

Nous rapportons un cas d'intoxication sévère aux bêta-bloquants. Après l'échec des traitements pharmacologiques, la patiente a bénéficié d'une assistance circulatoire externe de type ECMO (ExtraCorporeal Membrane Oxygenation ou oxygénation par membrane extracorporelle). Nous discutons des traitements pharmacologiques conventionnels et des traitements qui ont émergé durant cette dernière décennie, comme l'insulinothérapie à haute dose et les émulsions lipidiques. L'ECMO a fait des progrès importants ces dernières années et est devenue, à l'heure actuelle, la méthode d'assistance circulatoire externe de première ligne en cas de défaillance cardiaque et/ou respiratoire. Nous verrons sa place dans la prise en charge de l'intoxication massive aux drogues cardiodépressives.

A comparison between four techniques to measure cardiac output.

Cardiac output is an important variable when monitoring hemodynamic status. In particular, changes in cardiac output represent the goal of several circulatory management therapies. Unfortunately, cardiac output is very difficult to estimate, either in experimental or clinical settings. The goal of this work is to compare four techniques to measure cardiac output: pressure-volume catheter, aortic flow probe, thermodilution, and the PiCCO monitor. These four techniques were simultaneously used during experiments of fluid and endotoxin administration on 7 pigs. Findings show that, first, each individual technique is precise, with a relative coefficient of repeatability lower than 7 %. Second, 1 cardiac output estimate provided by any technique relates poorly to the estimates from the other 3, even if there is only small bias between the techniques. Third, changes in cardiac output detected by one technique are only detected by the others in 62 to 100 % of cases. This study confirms the difficulty of obtaining a reliable clinical cardiac output measurement. Therefore, several measurements using different techniques should be performed, if possible, and all such should be treated with caution.

Veno-venous extracorporeal CO2 removal improves pulmonary hemodynamics in a porcine ARDS model.

BACKGROUND: Protective lung ventilation is recommended in patients with acute respiratory distress syndrome (ARDS) to minimize additional injuries to the lung. However, hypercapnic acidosis resulting from ventilation at lower tidal volume enhances pulmonary hypertension and might induce right ventricular (RV) failure. We investigated if extracorporeal veno-venous CO2 removal therapy could have beneficial effects on pulmonary circulation and RV function. METHODS: This study was performed on an experimental model of ARDS obtained in eight anaesthetized pigs connected to a volume-cycled ventilator. A micromanometer-tipped catheter was inserted into the main pulmonary artery and an admittance micromanometer-tipped catheter was inserted into the right ventricle. RV-arterial coupling was derived from RV pressure-volume loops. ARDS was obtained by repeated bronchoalveolar lavage. Protective ventilation was then achieved, and the pigs were connected to a pump-driven extracorporeal membrane oxygenator (PALP, Maquet, Germany) in order to achieve CO2 removal. RESULTS: ARDS induced severe hypercapnic acidosis. Systolic pulmonary artery pressure significantly increased from 29.6±1.8 to 43.9±2.0 mmHg (P<0.001). After the PALP was started, acidosis was corrected and normocarbia was maintained despite protective ventilation. Pulmonary artery pressure significantly decreased to 31.6±3.2 mmHg (P<0.001) and RV-arterial coupling significantly improved (RV-arterial coupling index=1.03±0.33 vs. 0.55±0.41, P<0.05). CONCLUSION: Veno-venous CO2 removal therapy enabled protective ventilation while maintaining normocarbia during ARDS. CO2 removal decreased pulmonary hypertension and improved RV function. This technique may be an effective lung- and RV-protective adjunct to mechanical ventilation.

End of life care in the operating room for non-heart-beating donors: organization at the University Hospital of Liège.

Non-heart-beating (NHB) organ donation has become an alternative source to increase organ supply for transplantation. A NHB donation program was implemented in our institution in 2002. As in many institutions the end of life care of the NHB donor (NHBD) is terminated in the operating room (OR) to reduce warm ischemia time. Herein we have described the organization of end of life care for these patients in our institution, including the problems addressed, the solution proposed, and the remaining issues. Emphasis is given to our protocol elaborated with the different contributors of the chain of the NHB donation program. This protocol specifies the information mandatory in the medical records, the end of life care procedure, the determination of death, and the issue of organ preservation measures before NHBD death. The persisting malaise associated with NHB donation reported by OR nurses is finally documented using an anonymous questionnaire.

[Extracorporeal membrane oxygenation (ECMO) in ICU patients suffering from cardiogenic shock, refractory hypoxemia or cardiac arrest]. / L'ECMO (extracorporeal membrane oxygenation) aux soins intensifs: intérêt chez le patient en choc cardiogénique réfractaire, en hypoxémie réfractaire ou en arrêt cardiaque.

ExtraCorporeal Membrane Oxygenation (ECMO) is a cardiopulmonary assistance device able to support patients in cardiac arrest, refractory cardiogenic shock or refractory hypoxemia otherwise sentenced to death. Recent technical progresses, early indication decision, bedside multidisciplinary implant, specific complications screening and echocardiographic weaning testing are crucial points to allow success of this exceptional technique.

[Prophylaxis of infective endocarditis: improved dental care and oral health rather than systematic antibiotic prophylaxis?]. / Comment je préviens...l'endocardite infectieuse: une meilleure hygiène bucco-dentaire plutôt qu'une antibioprophylaxie systématique?

Prophylaxis for infective endocarditis has been recommended on the basis of the supposed pathophysiology of the disease, although no randomised clinical trial has confirmed its efficacy. Bacteraemia resulting from daily activities is much more likely to cause infective endocarditis than bacteraemia associated with invasive medical procedures. As a result, recommendations for antibiotic prophylaxis tend now to be severely restricted.

Effect of hemodiafiltration on pulmonary hemodynamics in endotoxic shock.

Hemofiltration can improve pulmonary hemodynamics during septic shock. The main objective of the study was to determine whether hemodiafiltration (HDF) would also have beneficial effects on pulmonary hemodynamics during septic shock. In the Endo group, six anesthetized pigs received a 0.5 mg/kg endotoxin infusion over 30 min. In the HDF group (n = 6), HDF was started 30 min after the end of the endotoxin infusion, while in the Control group (n = 4) they received HDF but no endotoxin infusion. Pulmonary hemodynamics were analyzed in detail with a four-element windkessel model. Although in the Control group, HDF did not alter pulmonary hemodynamic parameters, in the HDF group, it was responsible for an amplification of the deleterious pulmonary vascular response to endotoxin insult. Our results show that HDF must be used cautiously in septic shock since it can precipitate right heart failure by increasing pulmonary vascular resistance.

Alteration of left ventriculo-arterial coupling and mechanical efficiency during acute myocardial ischemia.

AIM: Myocardial revascularisation being frequently performed during acute myocardial ischemia, in a hostile hemodynamic environment, we evaluated left ventriculo-arterial (VA) coupling, left ventricular (LV) mechanical efficiency, and the mechanical properties of the systemic vasculature during acute myocardial ischemia. METHODS: In 6 pigs, vascular properties [characteristic impedance (R(1)), peripheral resistance (R(2)), compliance (C), inductance (L), arterial elastance (E(a))] were estimated with a windkessel model. LV function was assessed by the slope (E(es)) of end-systolic pressure-volume relationship (ESPVR), and stroke work (SW) - end-diastolic volume (EDV) relation. Pressure-volume area (PVA) was referred to as myocardial oxygen consumption. VA coupling was defined as E(es)/E(a), and mechanical efficiency as SW/PVA. After baseline recordings, the left anterior descending coronary artery was ligated and hemodynamic measures obtained every 30 minutes for 3 hours. Data are expressed as mean (SEM). RESULTS: Coronary occlusion induced an ESPVR rightward shift, and decreased E(es) from 3.67 (0.33) to 1.92 (0.20) mmHg/ml and the slope of the SW - EDV relationship from 72.3 (3.4) to 40.4 (4.5) mmHg (p<0.001), while E(a) increased from 3.33 (0.56) to 4.65 (0.29) mmHg/ml (p<0.005). This was responsible for a dramatic alteration of VA coupling from 1.22 (0.11) to 0.44 (0.07), (p<0.001). While R2 increased from 1.72 (0.30) to 2.38 (0.16) mmHg x s x ml(-1) (p<0.05) and C decreased from 0.78 (0.16) to 0.46 (0.08) ml/mmHg (p<0.05), R(1) and L were unchanged. Coronary occlusion decreased SW from 4056 (223) to 2580 (122) mmHg.ml (p<0.001), while PVA and SW/PVA decreased from 5575 (514) to 4813 (317) mmHg x ml (NS), and from 0.76 (0.04) to 0.57 (0.03) (p<0.001), respectively. CONCLUSION: Acute myocardial ischemia severely altered left ventriculo-arterial coupling and LV mechanical efficiency. Impaired left VA coupling was due to a combination of augmented arterial elastance, secondary to early vasoconstriction later associated with decreased arterial compliance, and decreased LV contractility.

Effects of U-46619 on pulmonary hemodynamics before and after administration of BM-573, a novel thromboxane A2 inhibitor.

We studied the effects on pulmonary hemodynamics of U-46619, a thromboxane A2 (TXA2) agonist, before and after administration of a novel TXA2 receptor antagonist and synthase inhibitor (BM-573). Six anesthetized pigs (Ago group) received 6 consecutive injections of U-46619 at 30-min interval and were compared with six anesthetized pigs (Anta group) which received an increasing dosage regimen of BM-573 10 min before each U-46619 injection. Consecutive changes in pulmonary hemodynamics, including characteristic resistance, vascular compliance, and peripheral vascular resistance, were continuously assessed during the experimental protocol using a four-element Windkessel model. At 2 mg/kg, BM-573 completely blocked pulmonary hypertensive effects of U-46619 but pulmonary vascular compliance still decreased. This residual effect can probably be explained by a persistent increase in the tonus of the pulmonary vascular wall smooth muscles sufficient to decrease vascular compliance but not vessel lumen diameter. Such molecule could be a promising therapeutic approach in TXA2 mediated pulmonary hypertension as it is the case in pulmonary embolism, hyperacute lung rejection and endotoxinic shock.

Effects of BM-573, a novel thromboxane A2 inhibitor, on pulmonary hemodynamics in endotoxic shock.

Thromboxane A2 is considered to be partially responsible for the increase in pulmonary vascular resistance observed after endotoxin administration and to participate in proinflammatory reactions. The effects of a novel dual TXA2 synthase inhibitor and TXA2 receptor antagonist (BM-573) on pulmonary hemodynamics were investigated in endotoxic shock. 30 mins before the start of a 0.5 mg/kg endotoxin infusion, 6 pigs (Endo group) received a placebo infusion and 6 other pigs (Anta group) received a BM-573 infusion. In Endo group, pulmonary artery pressure increased from 25 +/- 1.8 (T0) to 42 +/- 2.3 mmHg (T60) (p < 0.05) after endotoxin infusion while, in Anta group, it increased from 23 +/- 1.6 (T0) to 25 +/- 1.5 mmHg (T60). This difference is due to a reduction in pulmonary vascular resistance in Anta group while pulmonary arterial compliance changes in Endo group remained comparable with the evolution in Anta group. In Endo group, PaO2 decreased from 131 +/- 21 (T0) to 74 +/- 12 mmHg (T300) (p < 0.05), while in Anta group, PaO2 was 241 +/- 31 mmHg at the end of the experimental period (T300). These results demonstrate that TXA2 plays a major role in pulmonary vascular changes during endotoxin insult. Concomitant inhibition of TXA2 synthesis and of TXA2 receptors by BM-573 inhibited the pulmonary vasopressive response during the early phase of endotoxin shock as well as the deterioration in arterial oxygenation.