Olfa Hamzaoui

Effects of changes in vascular tone on the agreement between pulse contour and transpulmonary thermodilution cardiac output measurements within an up to 6-hour calibration-free period*

Objectives: To examine whether the agreement between pulse contour and transpulmonary thermodilution cardiac index (CI) measurements is altered by changes in vascular tone within an up to 6-hr calibration-free period. Design: Observational study. Setting: Medical intensive care unit of a university hospital. Patients: Fifty-nine critically ill patients. Interventions: None. Measurements and Main Results: Data from 59 critically ill patients equipped with a PiCCO device were retrospectively analyzed. The database contained the transpulmonary thermodilution CI (CIT) value obtained at each time point the device was calibrated and the pulse contour CI (CIPC) value recorded immediately before this time point. Seven subsets of CI pairs were defined according to intervals of time elapsed from the previous calibration (within the first 30 mins, between 30 mins and 1 hr, and every hour up to 6 hrs). In the whole set of 400 CI pairs, CIPC correlated with CIT (r2 = .68, p < .001). The bias ± sd was 0.12 ± 0.61 L/min/m2, and the percentage error was 35%. Among the seven time-interval subsets, the percentage error was <30% only in the two first ones (27% and 26%, respectively). When changes in systemic vascular resistance by >15% occurred (129 times), CIPC correlated with CIT (r2 = .64), the bias ± sd was 0.12 ± 0.62 L/min/m2, and the percentage error was 36%. In the subset of CI pairs recorded within the 1-hr calibration-free period while vascular resistance changed by >15% (n = 32), the bias ± sd was 0.04 ± 0.47 L/min/m2 and the percentage error was 29%. Conclusions: Our study in critically ill patients suggests that the agreement between pulse contour cardiac output and transpulmonary thermodilution cardiac output was not significantly influenced by changes in vascular tone. However, after a 1-hr calibration-free period, recalibration may be encouraged. Such a procedure provides helpful information drawn from other thermodilution-derived variables.

Critical care management and outcome of severe Pneumocystis pneumonia in patients with and without HIV infection

BackgroundLittle is known about the most severe forms of Pneumocystis jiroveci pneumonia (PCP) in HIV-negative as compared with HIV-positive patients. Improved knowledge about the differential characteristics and management modalities could guide treatment based on HIV status.MethodsWe retrospectively compared 72 patients (73 cases, 46 HIV-positive) admitted for PCP from 1993 to 2006 in the intensive care unit (ICU) of a university hospital.ResultsThe yearly incidence of ICU admissions for PCP in HIV-negative patients increased from 1993 (0%) to 2006 (6.5%). At admission, all but one non-HIV patient were receiving corticosteroids. Twenty-three (85%) HIV-negative patients were receiving an additional immunosuppressive treatment. At admission, HIV-negative patients were significantly older than HIV-positive patients (64 [18 to 82] versus 37 [28 to 56] years old) and had a significantly higher Simplified Acute Physiology Score (SAPS) II (38 [13 to 90] versus 27 [11 to 112]) but had a similar PaO2/FiO2 (arterial partial pressure of oxygen/fraction of inspired oxygen) ratio (160 [61 to 322] versus 183 [38 to 380] mm Hg). Ventilatory support was required in a similar proportion of HIV-negative and HIV-positive cases (78% versus 61%), with a similar proportion of first-line non-invasive ventilation (NIV) (67% versus 54%). NIV failed in 71% of HIV-negative and in 13% of HIV-positive patients (p < 0.01). Mortality was significantly higher in HIV-negative than HIV-positive cases (48% versus 17%). The HIV-negative status (odds ratio 3.73, 95% confidence interval 1.10 to 12.60) and SAPS II (odds ratio 1.07, 95% confidence interval 1.02 to 1.12) were independently associated with mortality at multivariate analysis.ConclusionThe yearly incidence of ICU admissions for PCP in HIV-negative patients in our unit increased from 1993 to 2006. The course of the disease and the outcome were worse in HIV-negative patients. NIV often failed in HIV-negative cases, suggesting that NIV must be watched closely in this population.

Early administration of norepinephrine increases cardiac preload and cardiac output in septic patients with life-threatening hypotension

IntroductionWe sought to examine the cardiac consequences of early administration of norepinephrine in severely hypotensive sepsis patients hospitalized in a medical intensive care unit of a university hospital.MethodsWe included 105 septic-shock patients who already had received volume resuscitation. All received norepinephrine early because of life-threatening hypotension and the need to achieve a sufficient perfusion pressure rapidly and to maintain adequate flow. We analyzed the changes in transpulmonary thermodilution variables associated with the increase in mean arterial pressure (MAP) induced by norepinephrine when the achieved MAP was ≥65 mm Hg.ResultsNorepinephrine significantly increased MAP from 54 ± 8 to 76 ± 9 mm Hg, cardiac index (CI) from 3.2 ± 1.0 to 3.6 ± 1.1 L/min/m2, stroke volume index (SVI) from 34 ± 12 to 39 ± 13 ml/m2, global end-diastolic volume index (GEDVI) from 694 ± 148 to 742 ± 168 ml/m2, and cardiac function index (CFI) from 4.7 ± 1.5 to 5.0 ± 1.6 per min. Beneficial hemodynamic effects on CI, SVI, GEDVI, and CFI were observed in the group of 71 patients with a baseline echocardiographic left ventricular ejection fraction (LVEF) >45%, as well as in the group of 34 patients with a baseline LVEF ≤45%. No change in CI, SVI, GEDVI, or CFI was observed in the 17 patients with baseline LVEF ≤45% for whom values of MAP ≥75 mm Hg were achieved with norepinephrine.ConclusionsEarly administration of norepinephrine aimed at rapidly achieving a sufficient perfusion pressure in severely hypotensive septic-shock patients is able to increase cardiac output through an increase in cardiac preload and cardiac contractility. This effect remained in patients with poor cardiac contractility except when values of MAP ≥75 mm Hg were achieved.

Arterial pressure allows monitoring the changes in cardiac output induced by volume expansion but not by norepinephrine.

Objective: To evaluate to which extent the systemic arterial pulse pressure could be used as a surrogate of cardiac output for assessing the effects of a fluid challenge and of norepinephrine. Design: Observational study. Setting: Medical intensive care unit. Patients: Patients with an acute circulatory failure who received a fluid challenge (228 patients, group 1) or in whom norepinephrine was introduced or increased (145 patients, group 2). Interventions: We measured the systolic, diastolic, and mean arterial pressure, pulse pressure, and the transpulmonary thermodilution cardiac output before and after the therapeutic interventions. Main Results: In group 1, the fluid challenge significantly increased cardiac output by 24% ± 25%. It significantly increased cardiac output by ≥15% (+35% ± 27%) in 142 patients (“responders”). The fluid-induced changes in cardiac output were correlated with the changes in pulse pressure (r = .56, p < .0001), systolic arterial pressure (r = .55, p < .0001), diastolic arterial pressure (r = .37, p < .0001), and mean arterial pressure (r = .52, p < .0001). At multivariate analysis, changes in pulse pressure were significantly related to changes in stroke volume (multiple r = .52) and to age (r = .12). A fluid-induced increase in pulse pressure of ≥17% allowed detecting a fluid-induced increase in cardiac output of ≥15% with a sensitivity of 65[56–72]% and a specificity of 85[76–92]%. The area under the receiver operating characteristic curves for the fluid-induced changes in mean arterial pressure and in diastolic arterial pressure was significantly lower than for pulse pressure. In group 2, the introduction/increase of norepinephrine significantly increased cardiac output by 14% ± 18%. The changes in cardiac output induced by the introduction/increase in the dose of norepinephrine were correlated with the changes in pulse pressure and systolic arterial pressure (r = .21 and .29, respectively, p = .001) but to a significantly lesser extent than in group 1. Conclusions: Pulse pressure and systolic arterial pressure could be used for detecting the fluid-induced changes in cardiac output, in spite of a significant proportion of false-negative cases. By contrast, the changes in pulse pressure and systolic arterial pressure were unable to detect the changes in cardiac output induced by norepinephrine.

SvO2 to monitor resuscitation of septic patients: let's just understand the basic physiology

Real-time monitoring of mixed venous oxygen blood saturation (SvO2) or of central venous oxygen blood saturation is often used during resuscitation of septic shock. However, the meaning of these parameters is far from straightforward. In the present commentary, we emphasize that SvO2 - a global marker of tissue oxygen balance - can never be simplistically used as a marker of preload responsiveness, which is an intrinsic marker of cardiac performance. In some septic shock patients, because of profound hypovolemia or myocardial dysfunction, SvO2 can be low but obviously cannot alone indicate whether a fluid challenge would increase cardiac output. In other patients, because of a profound impairment of oxygen extraction capacities, SvO2 can be abnormally high even in patients who are still able to respond positively to fluid infusion. In any case, other reliable dynamic parameters can help to address the important question of fluid responsiveness/unresponsiveness. However, whether fluid administration in fluid responders and high SvO2 would be efficacious to reduce tissue dysoxia in the most injured tissues is still uncertain.

Pneumopathie à mycoplasme : une cause rare de syndrome de détresse respiratoire aiguë (SDRA) et de résistance potentielle aux antibiotiques

INTRODUCTION Acute respiratory distress syndrome caused by Mycoplasma pneumoniae infection has rarely been described. OBSERVATION We report a case of community-acquired pneumonia occurring in a patient with Downs syndrome. Persisting hypoxemia raised the questions of nosocomial pneumonia, of the occurrence of a fibrosing alveolitis or of the resistance of the strain to macrolides. After a long period of very severe respiratory impairment, the evolution was progressively favourable and the patient was discharged from ICU with full respiratory recovery 43 days after admission. CONCLUSION Acute respiratory distress syndrome caused by M. pneumoniae infection is rare but must be considered when the appropriate clinical and radiological pattern occurs. The question of the susceptibility of the strain to macrolides has to be raised in some circumstances.

Handgrip Strength Predicts Difficult Weaning But Not Extubation Failure in Mechanically Ventilated Subjects

BACKGROUND: Muscle weakness, defined by the Medical Research Council scale, has been associated with delay in mechanical ventilation weaning. In this study, we evaluated handgrip strength as a prediction tool in weaning outcome. METHODS: This was a 1-y prospective study in 2 ICUs in 2 university hospitals. Adult patients who were on mechanical ventilation for at least 48 h and eligible for mechanical ventilation weaning were screened for inclusion. Handgrip strength was evaluated using a handheld dynamometer before each spontaneous breathing trial (SBT). Attending physicians were unaware of handgrip strength and decided on extubation according to guidelines. RESULTS: Eighty-four subjects were included (median age 66 [53–79] y, with a median Simplified Acute Physiology Score II of 49 [37–63]). At the first evaluation, median handgrip strength was significantly associated with weaning outcome as defined by international guidelines: simple (20 [12–26] kg), difficult (12 [6–21] kg), or prolonged (6 [3–11] kg) weaning (P = .008). Time to liberation from mechanical ventilation and ICU stay were significantly longer for subjects classified as having muscle weakness according to the handgrip strength-derived definition (P = .02 and P = .03, respectively). In multivariate analysis, known history of COPD (odds ratio [OR] 5.48, 95% CI 1.44–20.86, P = .01), sex (OR 6.16, 95% CI 1.64–23.16, P = .007), and handgrip strength at the first SBT (OR 0.89, 95% CI 0.85–0.97, P = .004) were significantly associated with difficult or prolonged weaning. Extubation failure, as defined by re-intubation or unscheduled noninvasive ventilation within 48 h after extubation, occurred 14 times after 92 attempts, leading to an extubation failure rate of 15%. No association was found between handgrip strength and extubation outcome. CONCLUSIONS: Muscle weakness, assessed by handgrip strength, is associated with difficult or prolonged mechanical ventilation weaning and ICU stay, but not with extubation outcome.

Cas cliniquePneumopathie à mycoplasme : une cause rare de syndrome de détresse respiratoire aiguë (SDRA) et de résistance potentielle aux antibiotiquesMycoplasma-related pneumonia: A rare cause of acute respiratory distress syndrome (ARDS) and of potential antibiotic resistance

INTRODUCTION Acute respiratory distress syndrome caused by Mycoplasma pneumoniae infection has rarely been described. OBSERVATION We report a case of community-acquired pneumonia occurring in a patient with Downs syndrome. Persisting hypoxemia raised the questions of nosocomial pneumonia, of the occurrence of a fibrosing alveolitis or of the resistance of the strain to macrolides. After a long period of very severe respiratory impairment, the evolution was progressively favourable and the patient was discharged from ICU with full respiratory recovery 43 days after admission. CONCLUSION Acute respiratory distress syndrome caused by M. pneumoniae infection is rare but must be considered when the appropriate clinical and radiological pattern occurs. The question of the susceptibility of the strain to macrolides has to be raised in some circumstances.

Evolving concepts of hemodynamic monitoring for critically ill patients

The last decades have been characterized by a continuous evolution of hemodynamic monitoring techniques from intermittent toward continuous and real-time measurements and from an invasive towards a less invasive approach. The latter approach uses ultrasounds and pulse contour analysis techniques that have been developed over the last 15 years. During the same period, the concept of prediction of fluid responsiveness has also been developed and dynamic indices such as pulse pressure variation, stroke volume variation, and the real-time response of cardiac output to passive leg raising or to end-expiration occlusion, can be easily obtained and displayed with the minimally invasive techniques. In this article, we review the main hemodynamic monitoring devices currently available with their respective advantages and drawbacks. We also present the current viewpoint on how to choose a hemodynamic monitoring device in the most severely ill patients and especially in patients with circulatory shock.

Norepinephrine in septic shock: when and how much?

Purpose of review Norepinephrine is the first-line agent recommended during resuscitation of septic shock to correct hypotension due to depressed vascular tone. Important clinical issues are the best timing to start norepinephrine, the optimal blood pressure target, and the best therapeutic options to face refractory hypotension when high doses of norepinephrine are required to reach the target. Recent findings Recent literature has reported benefits of early administration of norepinephrine because of the following reasons: profound and durable hypotension is an independent factor of increased mortality, early administration of norepinephrine increases cardiac output, improves microcirculation and avoids fluid overload. Recent data are in favor of targeting a mean arterial pressure of at least 65 mmHg and higher values in case of chronic hypertension. When hypotension is refractory to norepinephrine, it is recommended adding vasopressin, which is relatively deficient during sepsis and acts on other vascular receptors than &agr;1-adernergic receptors. However, increasing the dose of norepinephrine further cannot be discouraged. Summary Early administration of norepinephrine is beneficial for septic shock patients to restore organ perfusion. The mean arterial pressure target should be individualized. Adding vasopressin is recommended in case of shock refractory to norepinephrine.