Perioperative goal-directed therapy with uncalibrated pulse contour methods: impact on fluid management and postoperative outcome.

Previous meta-analyses suggest that perioperative goal-directed therapy (GDT) is useful to decrease postoperative morbidity. Most GDT studies analysed were done with pulmonary artery catheters, oesophageal Doppler and calibrated pulse contour methods. Uncalibrated pulse contour (uPC) techniques are an appealing alternative but their accuracy has been questioned. The effects of GDT on fluid management (volumes and volume variability) remain unclear. We performed a meta-analysis of randomized controlled trials investigating the effects of GDT with uPC methods on postoperative outcome. The primary endpoint was postoperative morbidity. Fluid volumes and fluid volume variability (standard deviation/mean) over the GDT period were also studied. Nineteen studies met the inclusion criteria (2159 patients). Postoperative morbidity was reduced with GDT (OR 0.46, 95% CI 0.30-0.70, P<0.001). The volume of colloids was higher [weighted mean difference (WMD) +345 ml, 95% CI 148-541 ml, P<0.001] and the volume of crystalloids was lower (WMD -429 ml, 95% CI -634 to -224 ml, P<0.01) in the GDT group than in the control group. However, the total volume of fluid (WMD -220 ml, 95% CI -590 to 150 ml, P=0.25) and the variability of fluid volume (34% vs 33%, P=0.98) were not affected by GDT. The use of GDT with uPC techniques was associated with a decrease in postoperative morbidity. It was not associated with an increase in total fluid volume nor with a decrease in fluid volume variability.

Digital innovations and emerging technologies for enhanced recovery programmes.

Enhanced recovery programmes (ERPs) are increasingly used to improve post-surgical recovery. However, compliance to various components of ERPs-a key determinant of success-remains sub-optimal. Emerging technologies have the potential to help patients and caregivers to improve compliance with ERPs.Preoperative physical condition, a major determinant of postoperative outcome, could be optimized with the use of text messages (SMS) or digital applications (Apps) designed to facilitate smoking cessation, modify physical activity, and better manage hypertension and diabetes. Several non-invasive haemodynamic monitoring techniques and decision support tools are now available to individualize perioperative fluid management, a key component of ERPs. Objective nociceptive assessment may help to rationalize the use of pain medications, including opioids. Wearable sensors designed to monitor cardio-respiratory function may help in the early detection of clinical deterioration during the postoperative recovery and to address 'failure to rescue'. Activity trackers may be useful to monitor early mobilization, another major element of ERPs. Finally, electronic checklists have been developed to ensure that none of the above-mentioned ERP elements is omitted during the surgical journey.By optimizing compliance to the multiple components of ERPs, digital innovations, non-invasive techniques and wearable sensors have the potential to magnify the clinical and economic benefits of ERPs. Among the growing number of technical innovations, studies are needed to clarify which tools and solutions have real clinical value and are cost-effective.

Pulse pressure variation as a tool to detect hypovolaemia during pneumoperitoneum.

BACKGROUND: Pulse pressure variation (DeltaPP) and systolic pressure variation (SPV) induced by mechanical ventilation have been proposed to detect hypovolaemia and guide fluid therapy. During laparoscopic surgery, chest compliance is decreased by pneumoperitoneum. This may affect the value of SPV and DeltaPP as indicators of intravascular volume status. Thereby, we investigated the effects of pneumoperitoneum and hypovolaemia on SPV and DeltaPP. METHODS: We measured DeltaPP, SPV and the inspiratory (Deltaup) and expiratory (Deltadown) components of SPV, at baseline, during pneumoperitoneum, during pneumoperitoneum and hypovolaemia and after the return to baseline conditions, in 11 mechanically ventilated rabbits. Pneumoperitoneum was induced by inflating the abdomen with carbon dioxide, and hypovolaemia was induced by controlled haemorrhage. RESULTS: Pneumoperitoneum induced an increase in SPV from 8.5 +/- 1.6 to 13.3 +/- 2.6 mmHg (+56%, P < 0.05) as a result of an increase in Deltaup from 2.0 +/- 1.0 to 6.7 +/- 2.1 mmHg (+236%, P < 0.05), but no significant change in Deltadown, nor in DeltaPP. Haemorrhage induced a significant (P < 0.05) increase in SPV from 13.3 +/- 2.6 to 19.9 +/- 3.7 mmHg (+50%), in Deltadown from 6.6 +/- 3.3 to 14.0 +/- 4.9 mmHg (+112%) and in DeltaPP from 11.1 +/- 4.8 to 24.9 +/- 9.8% (+124%) but no change in Deltaup. All parameters returned to baseline values after blood re-infusion and abdominal deflation. CONCLUSIONS: SPV is modified by haemorrhage but it is also influenced by pneumoperitoneum. In contrast, DeltaPP is modified by haemorrhage but not by pneumoperitoneum. These findings suggest that DeltaPP should be used preferentially instead of SPV to detect hypovolaemia and guide fluid therapy during laparoscopic surgery.

Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock.

STUDY OBJECTIVE: To investigate whether the respiratory changes in peak velocity (Vpeak) of aortic blood flow could be related to the effects of volume expansion on cardiac index. DESIGN: Prospective clinical study. SETTING: Medical ICUs of a university hospital (20 beds) and of a nonuniversity hospital (15 beds). PATIENTS: Nineteen sedated septic shock patients who were receiving mechanical ventilation and who had preserved left ventricular (LV) systolic function. INTERVENTION: Volume expansion. MEASUREMENTS AND RESULTS: Analysis of aortic blood flow by transesophageal echocardiography allowed beat-to-beat measurement of Vpeak before and after volume expansion. Maximum values of Vpeak (Vpeakmax) and minimum values of Vpeak (Vpeakmin) were determined over one respiratory cycle. The respiratory changes in Vpeak (Delta Vpeak) were calculated as the difference between Vpeakmax and Vpeakmin divided by the mean of the two values and were expressed as a percentage. The indexed LV end-diastolic area (EDAI) and cardiac index were obtained at the end of the expiratory period. The volume expansion-induced increase in cardiac index was > or = 15% in 10 patients (responders) and < 15% in 9 patients (nonresponders). Before volume expansion, Delta Vpeak was higher in responders than in nonresponders (20 +/- 6% vs 10 +/- 3%; p < 0.01), while EDAI was not significantly different between the two groups (9.7 +/- 3.7 vs 9.7 +/- 2.4 cm(2)/m(2)). Before volume expansion, a Delta Vpeak threshold value of 12% allowed discrimination between responders and nonresponders with a sensitivity of 100% and a specificity of 89%. Volume expansion-induced changes in cardiac index closely correlated with the Delta Vpeak before volume expansion (r(2) = 0.83; p < 0.001). CONCLUSION: Analysis of respiratory changes in aortic blood velocity is an accurate method for predicting the hemodynamic effects of volume expansion in septic shock patients receiving mechanical ventilation who have preserved LV systolic function.

Right ventricular response to high-dose almitrine infusion in patients with severe hypoxemia related to acute respiratory distress syndrome.

OBJECTIVE: To evaluate the effects of high-dose almitrine infusion on gas exchange and right ventricular function in patients with severe hypoxemia related to acute respiratory distress syndrome (ARDS). DESIGN: Prospective study. SETTING: Medicosurgical intensive care department (ten beds). PATIENTS: Nine patients with ARDS and severe hypoxemia (PaO2/FIO2 ratio, <150 torr [20 kPa]). INTERVENTION: High-dose almitrine infusion (16 microg/kg/min for 30 mins). MEASUREMENTS AND MAIN RESULTS: Gas exchange and hemodynamic parameters were recorded before and after almitrine infusion. Right ventricular function was evaluated by using a fast response thermistor pulmonary artery catheter that allowed measurement of right ventricular ejection fraction and calculation of right ventricular end-diastolic and end-systolic volumes. Almitrine did not significantly alter arterial oxygenation and intrapulmonary shunt. Almitrine increased mean pulmonary arterial pressure (MPAP) from 31 +/- 4 to 33 +/- 4 mm Hg (p < .05), pulmonary vascular resistance index from 353 +/- 63 to 397 +/- 100 dyne x sec/ cm5 x m2 (p < .05), and right ventricular end-systolic volume index from 71 +/- 22 to 77 +/- 21 mL/m2 (p < .05); almitrine decreased right ventricular ejection fraction from 36% +/- 7% to 34% +/- 8% (p < .05). Stroke volume index and cardiac index did not change. The almitrine-induced changes in right ventricular ejection fraction were closely correlated with the baseline MPAP (r2 = .71, p < .01). CONCLUSION: In patients with severe hypoxemia related to ARDS, high-dose almitrine infusion did not improve arterial oxygenation and impaired the loading conditions of the right ventricle. The decrease in right ventricular ejection fraction induced by almitrine was correlated with the baseline MPAP. Thus, high-dose almitrine infusion may be harmful in ARDS patients with severe hypoxemia and pulmonary hypertension.

Extending inspiratory time in acute respiratory distress syndrome.

OBJECTIVE: To assess the short-term effects of extending inspiratory time by lengthening end-inspiratory pause (EIP) without inducing a clinically significant increase in intrinsic positive end-expiratory pressure (PEEPi) in patients with acute respiratory distress syndrome (ARDS). DESIGN: Controlled, randomized, crossover study. SETTING: Two medical intensive care units of university hospitals. PATIENTS: Sixteen patients with early (< or =48 hrs) ARDS. INTERVENTION: We applied two durations of EIP (0.2 secs and extended) each for 1 hr while keeping all the following ventilatory parameters constant: FIO2, total PEEP (PEEPtot = applied PEEP + PEEPi), tidal volume, inspiratory flow, and respiratory rate. The duration of extended EIP was titrated to avoid an increase of PEEPi of > or =1 cm H2O. MEASUREMENTS AND MAIN RESULTS: Despite an increase in mean airway pressure (20.6 +/- 2.3 vs. 17.6 +/- 2.1 cm H2O, p < .01), extended EIP did not significantly improve PaO2 (93 +/- 21 vs. 86 +/-16 torr [12.40 +/- 2.80 vs. 11.46 +/- 2.13 kPa] with 0.2 secs EIP, NS). However, although the difference in PaO2 between the two EIP durations was <20 torr (<2.66 kPa) in 14 patients, two patients exhibited a >40 torr (>5.33 kPa) increase in PaO2 with extended EIP. Extended EIP decreased PaCO2 (62 +/- 13 vs. 67 +/- 13 torr [8.26 +/- 1.73 vs. 8.93 +/- 1.73 kPa] with 0.2 secs EIP, p < .01), which resulted in a higher pH (7.22 +/- 0.10 vs. 7.19 +/- 0.09 with 0.2 secs EIP, p < .01) and contributed to a slight increase in arterial hemoglobin saturation (94 +/- 3 vs. 93 +/- 3% with 0.2 EIP, p < .01). No significant difference in hemodynamics was observed. CONCLUSION: In patients with ARDS, extending EIP without inducing a clinically significant increase in PEEPi does not consistently improve arterial oxygenation but enhances CO2 elimination.

[Mechanical ventilation-related variability of stroke volume. Clinical evaluation and therapeutic implications]. / Variabilité respiratoire du volume d'éjection sous ventilation mécanique. Evaluation clinique et implications thérapeutiques.

Mechanical ventilation induces cyclic changes in left ventricular stroke volume. These variations are mainly related to the expiratory decrease in left ventricular preload following the inspiratory decrease in right ventricular filling and ejection. Therefore, the magnitude of the respiratory changes in left ventricular stroke volume reflect the sensitivity of the heart to the cyclic changes in preload induced by mechanical insufflation. At the bedside, the respiratory changes in left ventricular stroke volume can be assessed by the analysis of the arterial pressure (arterial catheter) or aortic blood velocity (echocardiography) wave forms. The respiratory changes in arterial pressure and in aortic blood velocity have been shown to be accurate predictors of fluid responsiveness and of the hemodynamic effects of positive end-expiratory pressure.

Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation.

According to the Frank-Starling relationship, a patient is a 'responder' to volume expansion only if both ventricles are preload dependent. Mechanical ventilation induces cyclic changes in left ventricular (LV) stroke volume, which are mainly related to the expiratory decrease in LV preload due to the inspiratory decrease in right ventricular (RV) filling and ejection. In the present review, we detail the mechanisms by which mechanical ventilation should result in greater cyclic changes in LV stroke volume when both ventricles are 'preload dependent'. We also address recent clinical data demonstrating that respiratory changes in arterial pulse (or systolic) pressure and in Doppler aortic velocity (as surrogates of respiratory changes in LV stroke volume) can be used to detect biventricular preload dependence, and hence fluid responsiveness in critically ill patients.

Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure.

In mechanically ventilated patients with acute circulatory failure related to sepsis, we investigated whether the respiratory changes in arterial pressure could be related to the effects of volume expansion (VE) on cardiac index (CI). Forty patients instrumented with indwelling systemic and pulmonary artery catheters were studied before and after VE. Maximal and minimal values of pulse pressure (Pp(max) and Pp(min)) and systolic pressure (Ps(max) and Ps(min)) were determined over one respiratory cycle. The respiratory changes in pulse pressure (DeltaPp) were calculated as the difference between Pp(max) and Pp(min) divided by the mean of the two values and were expressed as a percentage. The respiratory changes in systolic pressure (DeltaPs) were calculated using a similar formula. The VE-induced increase in CI was >/= 15% in 16 patients (responders) and < 15% in 24 patients (nonresponders). Before VE, DeltaPp (24 +/- 9 versus 7 +/- 3%, p < 0.001) and DeltaPs (15 +/- 5 versus 6 +/- 3%, p < 0.001) were higher in responders than in nonresponders. Receiver operating characteristic (ROC) curves analysis showed that DeltaPp was a more accurate indicator of fluid responsiveness than DeltaPs. Before VE, a DeltaPp value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 94% and a specificity of 96%. VE-induced changes in CI closely correlated with DeltaPp before volume expansion (r(2) = 0. 85, p < 0.001). VE decreased DeltaPp from 14 +/- 10 to 7 +/- 5% (p < 0.001) and VE-induced changes in DeltaPp correlated with VE-induced changes in CI (r(2) = 0.72, p < 0.001). It was concluded that in mechanically ventilated patients with acute circulatory failure related to sepsis, analysis of DeltaPp is a simple method for predicting and assessing the hemodynamic effects of VE, and that DeltaPp is a more reliable indicator of fluid responsiveness than DeltaPs.

Cardiorespiratory efficacy of thrombolytic therapy in acute massive pulmonary embolism: identification of predictive factors.

The aim of this study was to evaluate the contribution of clinical, angiographic and haemodynamic findings in predicting the cardiorespiratory efficacy of thrombolytic therapy in acute massive pulmonary embolism. Haemodynamic measurements and pulmonary angiography were performed before (H0) and 12 h after (H12) initiating thrombolytic therapy in 23 patients with acute massive pulmonary embolism (Miller index > or =20/34), and free of prior cardiopulmonary disease. Patients were divided into two groups according to the variation in oxygen delivery (deltaDO2) between H0 and H12: deltaDO2 >20% (responders, n=10) and deltaDO2 < or =20% (nonresponders, n=13). Before thrombolysis, clinical and angiographic findings were similar in both groups. Mean right atrial pressure (RAP) and total pulmonary (vascular) resistance (TPR) were higher, while cardiac index (CI), DO2 and mixed venous oxygen saturation (Sv,O2) were lower in responders. DO2 and Sv,O2 were more closely correlated with deltaDO2 than RAP, TPR and CI. Eight out of the 10 responders and two out of the 13 nonresponders had an Sv,O2 <55%, while nine of the responders and two of the nonresponders had a DO2 <350 mL x min(-1) x m(-2). In conclusion, the initial oxygen delivery and mixed venous oxygen saturation may predict the cardiorespiratory efficacy of thrombolytic therapy in acute massive pulmonary embolism. When pulmonary angiography is performed, measurement of mixed venous oxygen saturation may be a simple method by which to select patients for thrombolytic therapy.

Clinical use of respiratory changes in arterial pulse pressure to monitor the hemodynamic effects of PEEP.

In ventilated patients with acute lung injury (ALI) we investigated whether respiratory changes in arterial pulse pressure (DeltaPP) could be related to the effects of PEEP and fluid loading (FL) on cardiac index (CI). Measurements were performed before and after application of a PEEP (10 cm H2O) in 14 patients. When the PEEP-induced decrease in CI was > 10% (six patients), measurements were also performed after FL. Maximal (PPmax) and minimal (PPmin) values of pulse pressure were determined over one respiratory cycle and DeltaPP was calculated: DeltaPP (%) = 100 x ((PPmax - PPmin)/ ([PPmax + PPmin]/2)). PEEP decreased CI from 4.2 +/- 1.1 to 3.8 +/- 1.3 L/min/m2 (p < 0.01) and increased DeltaPP from 9 +/- 7 to 16 +/- 13% (p < 0.01). The PEEP-induced changes in CI correlated with DeltaPP on ZEEP (r = -0.91, p < 0.001) and with the PEEP-induced increase in DeltaPP (r = -0.79, p < 0.001). FL increased CI from 3.5 +/- 1.1 to 4.2 +/- 0.9 L/min/m2 (p < 0.05) and decreased DeltaPP from 27 +/- 13 to 14 +/- 9% (p < 0.05). The FL-induced changes in CI correlated with DeltaPP before FL (r = 0.97, p < 0.01) and with the FL-induced decrease in DeltaPP (r = -0.85, p < 0.05). In ventilated patients with ALI, DeltaPP may be useful in predicting and assessing the hemodynamic effects of PEEP and FL.

[Probable effect of hemofiltration on hemodynamics and tissue oxygenation in shock secondary to severe malaria]. / Rôle probable de l'hémofiltration sur l'hémodynamique et l'oxygénation tissulaire lors d'un état de choc au décours d'un paludisme grave.

The authors report a case of severe Plasmodium falciparum malaria in a French Guyana endemic area with secondary myocardial dysfunction treated by usual symptomatic therapy and continuous veno-venous haemofiltration (CVVH). Haemodynamic investigations revealed hyperkinetic shock and oxygen supply dependence. Haemodynamic remained critical under conventional therapy and CVVH was introduced. Haemodynamic parameters improved rapidly with reduced oxygen debt. In the absence of associated bacterial, viral and fungal infections, the systemic inflammatory response syndrome with shock and impairment of consciousness seems to be linked to severe Plasmodium falciparum malaria. The benefits and the probable mechanisms of action of CVVH are discussed.

[Voluntary drug poisoning cases admitted to an emergency care unit]. / Intoxications médicamenteuses volontaires reçues dans un service d'accueil des urgences.

OBJECTIVES: The aim of this study was to ascertain the specific nature of voluntary drug intoxications seen in emergency wards receiving adult patients. METHODS: From July 1992 to June 1993, all patients presenting at the emergency room with voluntary drug intoxication were assessed retrospectively. There were 727 patients (482 females and 245 males, mean age 33.3 +/- 12 years, age range 15-92) admitted for 804 episodes of voluntary drug intoxication. RESULTS: A past history of psychiatric problems or drug abuse was found in 42.8 and 9.1% of the patients respectively. The time laps between ingestion and consultation was noted for 43% (5 h 30 +/- 9 h, range 15-4320 min). The drug ingested was identified in 89% of the cases and 1.7 drugs were ingested per episode (range 1-8). Generally, only 1 (52%) or 2 (21%) drugs were ingested. Nonbarbituric psychotropic agents were ingested in 79.7% of the cases. Alcohol had also been consumed in 36.5% of the cases. Treatment was gastric lavage in 34.4%, activated carbon in 16.7%, flumazenil in 16.9%, naloxone and N-acetyl-cysteine in 3.4%. Twelve patients required intubation. Patients were admitted to a medical (n = 156) or psychiatric (n = 67) ward or an intensive care unit (n = 61). Nearly 25% of the patients left hospital either against medical advice or left without notice. CONCLUSION: Voluntary drug intoxications seen in emergency rooms require care by a well coordinated team of clinicians and psychiatrists.

Cardiovascular repercussions of seizures during cyclic antidepressant poisoning.

Cyclic antidepressant overdose involves a risk of generalized seizures and cardiovascular disturbances. We have conducted a retrospective study to test the hypothesis of a relationship between generalized seizures and the onset of arrhythmia, hypotension or cardiac arrest during cyclic antidepressant intoxication. Patients who had seizures after ingestion of toxic amounts of tri- or tetracyclic antidepressants were included. Limb-lead QRS complex duration and systolic blood pressure were recorded before and after seizure. Twenty-four of the 388 patients (6.2%) who were admitted to our ICU over a four-year period had seizures (2.3 +/- 2 seizures/patient). Cardiac repercussions of cyclic-induced seizure were frequent and severe. In the postictal period, broadening of the QRS duration or hypotension occurred or were exacerbated in at least 41% and 29% of cases, respectively. In three patients (12.5%), the seizure-induced cardiovascular state was life-threatening and required massive alkalinization therapy and vasopressors, and two of the three required cardiac massage or cardioversion. Prior to seizure, these three patients had severe intoxications characterized by QRS duration > or = 120 ms and systolic blood pressure < or = 80 mm Hg. The results of this work confirm the potential risk of cardiovascular deterioration after cyclic antidepressant-induced seizure and raise the question of a prophylactic approach especially towards the subgroup with unstable hemodynamic status.