Abstract: To investigate the ability of a new stroke volume variation algorithm to predict fluid responsiveness during general anesthesia and mechanical ventilation in animals with multiple extrasystoles.
Abstract: Second-generation FloTrac software has been shown to reliably measure cardiac output (CO) in cardiac surgical patients. However, concerns have been raised regarding its accuracy in vasoplegic states. The aim of the present multicenter study was to investigate the accuracy of the third-generation software in patients with sepsis, particularly when total systemic vascular resistance (TSVR) is low.
Abstract: A new system has been developed to assess global end-diastolic volume (GEDV), a volumetric marker of cardiac preload, and extravascular lung water (EVLW) from a transpulmonary thermodilution curve. Our goal was to compare this new system with the system currently in clinical use.
Abstract: The arterial pulse pressure variation induced by mechanical ventilation (deltaPP) has been shown to be a predictor of fluid responsiveness. Until now, deltaPP has had to be calculated offline (from a computer recording or a paper printing of the arterial pressure curve), or to be derived from specific cardiac output monitors, limiting the widespread use of this parameter. Recently, a method has been developed for the automatic calculation and real-time monitoring of deltaPP using standard bedside monitors. Whether this method is to predict reliable predictor of fluid responsiveness remains to be determined.
Abstract: In anesthetized patients without cardiac arrhythmia the arterial pulse pressure variation (PPV) induced by mechanical ventilation has been shown the most accurate predictor of fluid responsiveness. In this respect, PPV has so far been used mainly in the decision-making process regarding volume expansion in patients with shock. As an indicator of the position on the Frank-Starling curve, PPV may actually be useful in many other clinical situations. In patients with acute lung injury or with acute respiratory distress syndrome, PPV can predict hemodynamic instability induced by positive end-expiratory pressure and recruitment maneuvers. PPV may also be useful to prevent excessive fluid restriction/depletion in patients with pulmonary edema, and to prevent excessive ultrafiltration in critically ill patients undergoing hemodialysis or hemofiltration. In the operating room, a goal-directed fluid therapy based on PPV monitoring has the potential to improve the outcome of patients undergoing high-risk surgery.
Abstract: 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.
Abstract: Several studies have shown that maximizing stroke volume (or increasing it until a plateau is reached) by volume loading during high-risk surgery may improve post-operative outcome. This goal could be achieved simply by minimizing the variation in arterial pulse pressure (deltaPP) induced by mechanical ventilation. We tested this hypothesis in a prospective, randomized, single-centre study. The primary endpoint was the length of postoperative stay in hospital.
Abstract: OBJECTIVES: To review the advantages and limitations of dilution methods to assess extravascular lung water (EVLW) at the bedside and to discuss the clinical value of EVLW measurements. DATA SOURCE: Experimental and clinical studies were searched in PUBMED by using "extravascular lung water" and "dilution method" as keywords and further selected as studies investigating either the reliability or the clinical usefulness of dilution methods to assess EVLW. Related articles and the reference lists of selected studies were scanned for additional relevant references. CONCLUSIONS: Both the double-indicator (thermo-dye) dilution and the single-indicator (cold saline) dilution methods showed close agreement with gravimetric measurement of EVLW (the reference ex vivo method) and have the advantage of being available at the bedside. Most limitations of dilution methods have been described in experimental conditions and lead to an underestimation of EVLW. These limitations include large pulmonary vascular obstruction, focal lung injury, and lung resection. Dilution methods provide an easy and clinically acceptable estimation of EVLW in most critically ill patients, including those with acute respiratory distress syndrome (ARDS). Assessing EVLW may be useful to predict outcome, to diagnose pulmonary edema, to better characterize patients with ARDS, to guide fluid therapy, and to assess the value of new treatments or ventilatory strategies in patients with pulmonary edema.
Abstract: In order to turn a fluid challenge into a significant increase in stroke volume and cardiac output, 2 conditions must be met: 1) fluid infusion has to significantly increase cardiac preload and 2) the increase in cardiac preload has to induce a significant increase in stroke volume. In other words, a patient can be nonresponder to a fluid challenge because preload does not increase during fluid infusion or/and because the heart (more precisely, at least 1 of the ventricles) is operating on the flat portion of the Frank-Starling curve. Volumetric markers of cardiac preload are therefore useful for checking whether cardiac preload effectively increases during fluid infusion. If this is not the case, giving more fluid, using a venoconstricting agent (to avoid venous pooling), or reducing the intrathoracic pressure (to facilitate the increase in intrathoracic blood volume) may be useful for achieving increased cardiac preload. Arterial pulse pressure variation is useful for determining whether stroke volume can/will increase when preload does increase. If this is not the case, only an inotropic drug can improve cardiac output. Therefore, the best option for determining the usefulness of, and monitoring fluid therapy in critically ill patients is the combination of information provided by the static indicators of cardiac preload and arterial pulse pressure variation.
Abstract: OBJECTIVE: The purpose of this study was to compare dP/dt(max) estimated from a femoral artery pressure tracing to left ventricular (LV) dP/dt(max) during various alterations in myocardial loading and contractile function. PARTICIPANTS: Seventy patients scheduled for elective coronary artery bypass surgery. METHODS: All patients were instrumented with a high-fidelity LV catheter, a pulmonary artery catheter, and a femoral arterial catheter. In 40 patients, hemodynamic measurements were performed before and after passive leg raising and before and after calcium administration (5 mg/kg); and in 30 other patients, hemodynamic measurements were performed before and after dobutamine infusion (5 microg/kg/min over 10 minutes). RESULTS: LV and femoral dP/dt(max) were significantly correlated (r = 0.82, p < 0.001), but femoral dP/dt(max) systematically underestimated LV dP/dt(max) (bias = -361 +/- 96 mmHg/s). Passive leg raising induced significant increases in central venous pressure and LV end-diastolic pressure, but femoral dP/dt(max), stroke volume, and LV dP/dt(max) remained unaltered. Calcium administration induced significant and marked increases in LV dP/dt(max) (23% +/- 9%) and femoral dP/dt(max) (37% +/- 14%) associated with a significant increase in stroke volume (9% +/- 2%). Dobutamine infusion also induced significant and marked increases in LV dP/dt(max) (25% +/- 8%) and femoral dP/dt(max) (35% +/- 12%) associated with a significant increase in stroke volume (14% +/- 3%). Overall, a very close linear relationship (r = 0.93) and a good agreement (bias = -5 +/- 17 mmHg/s) were found between changes in LV dP/dt(max) and changes in femoral dP/dt(max). A very close relationship was also observed between changes in LV dP/dt(max) and changes in femoral dP/dt(max) during each intervention (leg raising, calcium administration, and dobutamine infusion). CONCLUSION: Femoral dP/dt(max) underestimated LV dP/dt(max), but changes in femoral dP/dt(max) accurately reflected changes in LV dP/dt(max) during various interventions.
Abstract: OBJECTIVE: To investigate factors that may influence the estimation of extravascular lung water (EVLW) with a single (cold) indicator compared with assessment using two indicators (thermo-dye dilution). DESIGN: Post hoc analysis of an electronic hemodynamic database. SETTING: Surgical intensive care unit of a university hospital. PATIENTS: Forty-eight critically ill patients monitored by the thermo-dye dilution technique in the postoperative period. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The EVLW was simultaneously assessed by the thermo-dye dilution technique (EVLWref) and estimated by transpulmonary thermodilution (EVLWest). EVLWref index ranged between 1 and 40 mL/kg (mean 10 +/- 7 mL/kg) and EVLWest between 2 and 39 mL/kg (mean 9 +/- 6 mL/kg). EVLWref was closely correlated (r = .96) with EVLWest. The mean difference (bias) between EVLWref and EVLWest was -0.5 +/- 1.9 mL/kg. The bias was not influenced by the weight, height, body surface area, body mass index, Pao2, intrathoracic blood volume, cardiac output, or dosage of vasoactive agents. In contrast, the bias was slightly but significantly influenced by EVLWref, Pao2/Fio2 ratio, tidal volume, and level of positive end-expiratory pressure. CONCLUSIONS: In our surgical intensive care unit population, the estimation of EVLW by transpulmonary thermodilution was influenced by the amount of EVLW, the Pao2/Fio2 ratio, the tidal volume, and the level of positive end-expiratory pressure. However, compared with the double indicator method, transpulmonary thermodilution estimation remained clinically acceptable even in patients with severe lung disease.
Abstract: Mechanical ventilation induces cyclic changes in vena cava blood flow, pulmonary artery blood flow, and aortic blood flow. At the bedside, respiratory changes in aortic blood flow are reflected by "swings" in blood pressure whose magnitude is highly dependent on volume status. During the past few years, many studies have demonstrated that arterial pressure variation is neither an indicator of blood volume nor a marker of cardiac preload but a predictor of fluid responsiveness. That is, these studies have demonstrated the value of this physical sign in answering one of the most common clinical questions, Can we use fluid to improve hemodynamics?, while static indicators of cardiac preload (cardiac filling pressures but also cardiac dimensions) are frequently unable to correctly answer this crucial question. The reliable analysis of respiratory changes in arterial pressure is possible in most patients undergoing surgery and in critically ill patients who are sedated and mechanically ventilated with conventional tidal volumes.
Abstract: OBJECTIVE: To investigate whether the respiratory variation in inferior vena cava diameter (DeltaD(IVC)) could be related to fluid responsiveness in mechanically ventilated patients. DESIGN: Prospective clinical study. SETTING: Medical ICU of a non-university hospital. PATIENTS: Mechanically ventilated patients with septic shock (n=39). INTERVENTIONS: Volume loading with 8 mL/kg of 6% hydroxyethylstarch over 20 min. MEASUREMENTS AND RESULTS: Cardiac output and DeltaD(IVC) were assessed by echography before and immediately after the standardized volume load. Volume loading induced an increase in cardiac output from 5.7+/-2.0 to 6.4+/-1.9 L/min (P<0.001) and a decrease in DeltaD(IVC) from 13.8+/-13.6 vs 5.2+/-5.8% (P<0.001). Sixteen patients responded to volume loading by an increase in cardiac output > or =15% (responders). Before volume loading, the DeltaD(IVC) was greater in responders than in non-responders (25+/-15 vs 6+/-4%, P<0.001), closely correlated with the increase in cardiac output (r=0.82, P<0.001), and a 12% DeltaD(IVC) cut-off value allowed identification of responders with positive and negative predictive values of 93% and 92%, respectively. CONCLUSION: Analysis of DeltaD(IVC) is a simple and non-invasive method to detect fluid responsiveness in mechanically ventilated patients with septic shock.
Abstract: STUDY OBJECTIVE: To assess the value of the global end-diastolic volume (GEDV) evaluated by transpulmonary thermodilution as an indicator of cardiac preload. DESIGN: Prospective clinical study. SETTING: Medical ICU of a university hospital (20 beds). PATIENTS: Thirty-six patients with septic shock. INTERVENTIONS: Volume loading and dobutamine infusion. MEASUREMENTS AND RESULTS: Hemodynamic parameters were evaluated in triplicate by the transpulmonary thermodilution technique: (1) before and after 66 fluid challenges in 27 patients, and (2) before and after 28 increases in dobutamine infusion rate in 9 patients. Volume loading induced a significant (p < 0.001) increase in central venous pressure (CVP) from 10 +/- 4 to 13 +/- 4 mm Hg, in GEDV index from 711 +/- 164 to 769 +/- 144 mL/m(2), in stroke volume index (SVI) from 36 +/- 12 to 42 +/- 12 mL/m(2), and in cardiac index (CI) from 3.4 +/- 1.1 to 3.9 +/- 1.2 L/min/m(2) (mean +/- SD). Changes in GEDV index were correlated (r = 0.72, p < 0.001) with changes in SVI, while changes in CVP were not. The increase in SVI was > 15% in 32 of 66 instances (positive response). The preinfusion GEDV index was lower (637 +/- 134 mL/m(2) vs 781 +/- 161 mL/m(2), p < 0.001) in the cases of positive response, and was negatively correlated with the percentage increase in GEDV index (r = - 0.65, p < 0.001) and in SVI (r = - 0.5, p < 0.001). Dobutamine infusion induced an increase in SVI (32 +/- 11 mL/m(2) vs 35 +/- 12 mL/m(2), p < 0.05) and in CI (2.8 +/- 0.6 L/min/m(2) vs 3.2 +/- 0.6 L/min/m(2), p < 0.001) but no significant change in CVP (13 +/- 3 mm Hg vs 13 +/- 3 mm Hg) and in GEDV index (823 +/- 221 mL/m(2) vs 817 +/- 202 mL/m(2)). CONCLUSION: In patients with septic shock, our findings demonstrate that, in contrast to CVP, the transpulmonary thermodilution GEDV index behaves as an indicator of cardiac preload.
Abstract: STUDY OBJECTIVE: To identify and critically review the published peer-reviewed, English-language studies investigating predictive factors of fluid responsiveness in ICU patients. DESIGN: Studies were collected by doing a search in MEDLINE (from 1966) and scanning the reference lists of the articles. Studies were selected according to the following criteria: volume expansion performed in critically ill patients, patients classified in two groups (responders and nonresponders) according to the effects of volume expansion on stroke volume or on cardiac output, and comparison of responder and nonresponder patients' characteristics before volume expansion. RESULTS: Twelve studies were analyzed in which the parameters tested were as follows: (1) static indicators of cardiac preload (right atrial pressure [RAP], pulmonary artery occlusion pressure [PAOP], right ventricular end-diastolic volume [RVEDV], and left ventricular end-diastolic area [LVEDA]); and (2) dynamic parameters (inspiratory decrease in RAP [Delta RAP], expiratory decrease in arterial systolic pressure [Delta down], respiratory changes in pulse pressure [Delta PP], and respiratory changes in aortic blood velocity [Delta Vpeak]). Before fluid infusion, RAP, PAOP, RVEDV, and LVEDA were not significantly lower in responders than in nonresponders in three of five studies, in seven of nine studies, in four of six studies, and in one of three studies, respectively. When a significant difference was found, no threshold value could discriminate responders and nonresponders. Before fluid infusion, Delta RAP, Delta down, Delta PP, and Delta Vpeak were significantly higher in responders, and a threshold value predicted fluid responsiveness with high positive (77 to 95%) and negative (81 to 100%) predictive values. CONCLUSION: Dynamic parameters should be used preferentially to static parameters to predict fluid responsiveness in ICU patients.
Abstract: 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.
Abstract: 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.
Abstract: 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.
Abstract: 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.
Abstract: 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.
Abstract: 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.
Abstract: 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.
Abstract: 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.
Abstract: 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.
Abstract: 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.
