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Background In patient requiring vasopressors, the radial artery pressure may underestimate the true central aortic pressure leading to unnecessary interventions. When using a femoral and a radial arterial line, this femoral-to-radial arterial pressure gradient (FR-APG) can be detected. Our main objective was to assess the accuracy of non-invasive blood pressure (NIBP) measures; specifically, measuring the gradient between the NIBP obtained at the brachial artery and the radial artery pressure and calculating the non-invasive brachial-to-radial arterial pressure gradient (NIBR-APG) to detect an FR-APG. The secondary objective was to assess the prevalence of the FR-APG in a targeted sample of critically ill patients. Methods Adult patients in an intensive care unit requiring vasopressors and instrumented with a femoral and a radial artery line were selected. We recorded invasive radial and femoral arterial pressure, and brachial NIBP. Measurements were repeated each hour for 2 h. A significant FR-APG (our reference standard) was defined by either a mean arterial pressure (MAP) difference of more than 10 mmHg or a systolic arterial pressure (SAP) difference of more than 25 mmHg. The diagnostic accuracy of the NIBR-APG (our index test) to detect a significant FR-APG was estimated and the prevalence of an FR-APG was measured and correlated with the NIBR-APG. Results Eighty-one patients aged 68 [IQR 58–75] years and an SAPS2 score of 35 (SD 7) were included from which 228 measurements were obtained. A significant FR-APG occurred in 15 patients with a prevalence of 18.5% [95%CI 10.8–28.7%]. Diabetes was significantly associated with a significant FR-APG. The use of a 11 mmHg difference in MAP between the NIBP at the brachial artery and the MAP of the radial artery led to a specificity of 92% [67; 100], a sensitivity of 100% [95%CI 83; 100] and an AUC ROC of 0.93 [95%CI 0.81–0.99] to detect a significant FR-APG. SAP and MAP FR-APG correlated with SAP (r2 = 0.36; p, Key messages A significant radial-to-femoral pressure gradient occurs in nearly one-fifth of patients in ICU. Repeated non-invasive assessment of the radial-to-brachial pressure gradient was significantly correlated with the invasive radio-femoral arterial pressure gradient.

Acute respiratory distress syndrome (ARDS) was first described about 30 years ago. Modern definitions and statements have recently been proposed to describe ARDS accurately, but none is perfect. Diffuse alveolar damage is the basic pathological pattern most commonly observed in ARDS, and the term includes permeability edema. The alveolar epithelium of the alveolar-capillary barrier is clearly a key component requiring repair, given its multipotent functional activity. Lung inflammation and neutrophil accumulation are essential markers of disease in ARDS, and a wide variety of pro- and anti-inflammatory cytokines have been described in the alveolar fluid and blood of patients. These molecules still have to prove their value as diagnostic or prognostic biomarkers of ARDS.Supportive therapy in ARDS improved in the past decade; mechanical ventilation with lung protective strategies and patient positioning are gaining interest, but the indications for corticosteroids for ARDS are still debated. Nitric oxide may have a place in the treatment of one-third of patients. Novel approaches, such as surfactant replacement and liquid ventilation, may further improve supportive therapy. Innovative interventions may be on the horizon in treatments that help to resolve or modulate common pathways of ARDS, such as inflammation (eg, granulocyte-colony stimulating factor) or epithelial repair (eg, keratinocyte growth factor).

Pulmonary artery occlusion pressure (Ppao) may not reflect left ventricular (LV) filling pressure during mechanical ventilation with positive end-expiratory pressure (PEEP) either because the catheter tip is not in zone III conditions or because pericardial pressure (Ppc) is also elevated. Ppc can be estimated from pleural pressure (Ppl) or, when right ventricular (RV) function is normal, from right atria[ pressure (Pra) (Am Heart J 108:603–605,1984). If the pericardium limits LV diastolic filling or RV diastolic compliance changes, then these estimates of Ppc may be inaccurate. We previously showed that nadir Ppao, immediately after abrupt PEEP removal, reflects on-PEEP LV filling pressure (Am J Physiol 249:H770–H776, 1985). We performed this study to determine if (1) the pericardium limits LV filling pressure during PEEP and (2) on-PEEP LV filling pressure can be estimated by on-PEEP Ppao minus Pra or nadir Ppao. We compared these relations when RV performance was normal (control), after induction of acute ventricular failure (AVF) with propranolol, and after subsequent induction of acute lung injury (AVF-OA) with oleic acid in an acute, anesthetized, closed-chest intact canine model (n = 7). PEEP was increased from 0 to 15 cm H2O in 5-cm H2O increments. Nadir Ppao was measured on termination of 15 cm H2O PEEP. Juxtacardiac Ppl and Ppc increased parallel to increasing PEEP in all conditions except at 0 and 5 cm H2O PEEP in two dogs during AVF, when Ppc exceeded Ppl by as much as 4 mm Hg. Pre and Ppc covaried linearly in all conditions and at all levels of PEEP, although Pre was greater than Ppc (by 5.5 + 1.2 mm Hg [x + SE] in control, 7.1 + 2.1 mm Hg in AVF, and 6.6 + 1.5 in AVF-OA; P

To determine whether mixed venous blood gas sampling obtained by pulmonary artery catheter (PAC) is influenced by the speed of withdrawal.Prospective, observational study.Surgical intensive care unit at a university hospital.Twenty-five patients in the early postoperative period of cardiac surgery.After verification of the adequate position of the PAC, measurements of mixed venous blood gas oxygen saturation, oxygen partial pressure (PO(2)), carbon dioxide partial pressure (PCO(2)), pH and bicarbonates were obtained at two different rates of withdrawal. A slow sampling was taken at a mean speed of 3 ml/min and a fast sampling at 18 ml/min for each patient. The mean difference in venous oxygen saturation between slow and fast samplings was -0.18+/-1.3%, venous PO(2): -0.2+/-1.3 mmHg, venous PCO(2): 0.1+/-0.9 mmHg, venous pH: 0+/-0.03, venous bicarbonates: 0.03+/-0.5 mmol/l.Using the BlandAltman method, we showed a satisfactory agreement between slow and fast mixed venous blood gas sampling techniques when measuring PO(2), oxygen saturation, PCO(2), pH and bicarbonates though a PAC.

Objective: Transesophageal echocardiography is a diagnostic and monitoring modality. The objectives of our study were to compare the diagnoses obtained with continuous transesophageal echocardiography and hemodynamic monitoring in the intensive care unit, to determine interobserver variability of diagnosis obtained with both modalities, and to evaluate its impact. Design: Prospective cohort study. Setting: Surgical intensive care unit. Patients: Consecutive hemodynamically unstable patients after cardiac surgery. Interventions: At admission, unstable patients were monitored during 4 hrs with transesophageal echocardiography and standard hemodynamic monitoring. The critical care physician evaluated the patients based on all information except the transesophageal echocardiography at 0, 2, and 4 hrs and formulated a hypothesis on the most likely cause of hemodynamic instability. Transesophageal echocardiography information was provided after each evaluation. To evaluate interobserver variability, all the hemodynamic and echocardiographic information was gathered, randomized, and evaluated by five clinicians for the hemodynamic data and five echocardiographers for the transesophageal echocardiography data. The evaluators were blinded to all other information. Kappa statistics were used to evaluate agreement. Impact of transesophageal echocardiography was assessed retrospectively by using the Deutsch scale. Results: Twenty patients qualified for the study. The agreement between the hemodynamic and echocardiographic diagnosis showed a kappa at admission, 2 hrs, and 4 hrs of 0.33, 0.47, and 0.28. The interobserver agreement for the initial diagnosis (p = .014) and between all evaluators (p

There is a growing interest in the intraoperative and intensive care use of inhaled epoprostenol (PGI2) for the treatment of pulmonary hypertension (PHT) and hypoxia of cardiac or non-cardiac origin. We report our experience with this form of therapy.A retrospective chart review of all patients who received inhaled PGI2 over a one-year period was undertaken. Demographic, hemodynamic, oxygenation status, mode of administration, side effects, duration of hospital stay, and mortality were noted.Thirty-five patients, of which 33 (92%) were in the intensive care unit, received inhaled PGI2. Of the 27 patients whose pulmonary artery pressure (PAP) was monitored, a significant decrease in mean PAP from 34.8 +/- 11.8 mmHg to 32.1 +/- 11.8 mmHg was observed within one hour after the start of therapy (P=0.0017). Selective pulmonary vasodilatation occurred in 77.8% of the patients. Thirty-three patients had arterial blood gases before and after therapy. There was an improvement in the PaO2/FIO2 ratio in 88% of these with a 175% improvement on average. The ratio of PaO2/FIO2 improved from 108 +/- 8 to 138 +/- 105 (P=0.001). Six patients (17%) presented hypotension, two had subsequent pneumothorax, one had bronchospasm and in one patient PGI2 inhalation was stopped because of increasing peak pulmonary pressures from the secondary flow coming from the nebulizer. Mortality of the cohort was 54%.Inhaled PGI2 can be useful in the treatment of patients with PHT and severe hypoxia. It can however be associated with systemic side effects.

In the anesthetized closed-chest canine model of Gram-negative endotoxemia (n = 10), we tested the hypothesis that the effect of cardiac cycle-specific intrathoracic pressure pulses delivered by a heart rate-(HR) synchronized high-frequency jet ventilator (sync HFJV) on systolic ventricular performance is dependent on the level of preload. To control for HFJV frequency, hemodynamic responses were also measured at fixed frequency within 15% of HR (async HFJV). Biventricular stroke volumes (SV) were measured by electromagnetic flow probes. Measurements were made before (baseline) and 30 min after infusion of 1 mg/kg Escherichia coli endotoxin (serotype 055:B5) and then after 2 mg/kg propranolol at both low (less than 10 mmHg) left ventricular filling pressure (LVFP) and high (greater than 10 mmHg) LVFP. Ventricular function curves, aortic pressure-flow (P-Q) relationships, and venous return (VR) curves were analyzed. We found that endotoxin did not alter VR curves but shifted the aortic P-Q curves to the left with pressure on the x-axis (P less than 0.05). Volume loading increased SV (P less than 0.01) because of a rightward shift of the VR curve. No specific differences occurred with either sync or async HFJV during endotoxin, presumably because of preserved VR and shifted aortic P-Q. The lack of cardiac cycle-specific effects of ITP appears to be due to the selective endotoxin-induced changes in peripheral vasomotor tone that counterbalance any depressed myocardial contractility.

2(respective survival rate of 80 and 100%), and despite the recommendations of the American-European acute respiratory distress syndrome (ARDS) consensus, 3 no study has been appropriately designed to address the clinical outcome of ARDS patients treated with inhaled nitric oxide (NO). This pilot randomised controlled clinical trial of ARDS patients was implemented to study the efficacy of inhaled NO on lung function; the impact of inhaled NO on morbidity and mortality; and the feasibility of conducting a large multicentre trial. 30 established ARDS (with lung injury score 4

A patient with end-stage congestive cardiomyopathy had progressive hemodynamic deterioration while awaiting orthotopic heart transplantation. Attempts to support cardiovascular function by high-dose dobutamine infusions were complicated by life-threatening cardiac arrhythmias. The addition of the noncatecholamine inotropic agent, amrinone, improved ventricular performance, enabling reduction of the dose of dobutamine and resolution of the cardiac arrhythmias. Beta receptor stimulation by dobutamine combined with phosphodiesterase inhibition by amrinone may additively or synergistically augment cardiac function despite severe congestive heart failure and also have an adrenergic "sparing effect."

Approximately one-third of cases of severe sepsis result in death. Endogenous activated protein C (ApC) plays a key role in the regulation of the inflammation, fibrinolysis and coagulation associated with severe sepsis. In a recently published phase III trial, protein C Worldwide Evaluation in Severe Sepsis (pROWESS), intravenous administration of recombinant human ApC (rhApC) 24 µg/kg/h for 96 h to patients with severe sepsis resulted in a 6.1% reduction in absolute mortality and a 19.4% reduction in the relative risk of death from any cause within 28 days (number needed to treat = 16). This dose is now being applied in clinical practice.rhApC is recommended for the treatment of severe sepsis (sepsis associated with acute organ dysfunction) occurring as a result of all types of infection (Gram-negative bacterial, Gram-positive bacterial and fungal). A panel of Canadian clinicians experienced in the treatment of severe sepsis and the management of critical care patients has developed this consensus document to assist clinicians in appropriate patient selection and management of potential challenges associated with rhApC therapy.

This pilot randomized controlled clinical trial of patients with ARDS was implemented to study the impact of inhaled nitric oxide (inhNO) on lung function, morbidity, and mortality. Thirty patients with ARDS were randomly allocated to usual care or usual care plus inhNO. The optimal dose of inhNO was determined to be between 0.5 and 40 parts-per-million daily. All therapeutic interventions were standardized. ARDS resulted mainly from sepsis (25 of the 30). During the first 24 h, the hypoxia score increased greatly in patients treated with inhNO +70.4 mm Hg (+59%) versus +14.2 mm Hg (+9.3%) for the control group (p = 0.02), venous admixture decreased from 25.7 to 15.2% in the inhNO group, and from only 19.4 to 14.9% in the control group (p = 0.05). After the first day of therapy no further beneficial effect of inhNO was detected. Forty percent of the patients treated with inhNO were alive and weaned from mechanical ventilation within 30 d after randomization compared with 33.3% in the control group (p = 0.83). The 30-d mortality rate was similar in the two groups; most deaths (11 of 17) were due to multiple organ dysfunction syndrome. This study shows that inhNO, in this population, may improve gas exchange but does not affect mortality.