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Biomedical subjects

V M Ranieri

Publications and source records attributed to V M Ranieri.

At least 19 recordsLinked to original sources

The accuracy of transcranial Doppler to detect vasospasm in patients with aneurysmal subarachnoid hemorrhage.

OBJECTIVES: To examine the accuracy of transcranial Doppler to detect cerebral vasospasm in a patient population with aneurysmal subarachnoid hemorrhage. DESIGN: Prospective blind comparison of transcranial Doppler with cerebral angiography. Diagnostic accuracy of transcranial Doppler was assessed using receiver operating characteristic (ROC) analysis and likelihood ratios. Sensitivity and specificity were calculated using directly measured middle cerebral artery diameter as reference standard. SETTING: Intensive Care Unit of a large university teaching hospital. PATIENTS AND PARTICIPANTS: Twenty-two patients with subarachnoid hemorrhage were included. Patients underwent angiography on admission and after 8 days to diagnose vasospasm and were defined as having clinical vasospasm, angiographic vasospasm, or no vasospasm. MEASUREMENTS AND RESULTS: Sensitivity and specificity were 1.00 and 0.75 for angiographic vasospasm and both equal to 1.00 for clinical vasospasm diagnosis. A transcranial Doppler mean velocity threshold value of 100 cm/s for angiographic vasospasm and 160 cm/s for clinical vasospasm detection were chosen by ROC analysis. CONCLUSIONS: A Transcranial Doppler mean velocity threshold of 160 cm/s, calculated by the ROC analysis, accurately detects clinical vasospasm. A daily transcranial Doppler examination performed by a trained operator should be routinely used to provide early identification of patients at high risk and to orient therapeutic decisions.

Adult↗

Epidemiology and outcome of acute respiratory failure in intensive care unit patients.

OBJECTIVES: To summarize the prevalence of various forms of acute respiratory failure in acutely ill patients and review the major factors involved in the outcome of these patients. DATA SOURCES AND SELECTION: MEDLINE search for published studies reporting the prevalence or outcome for patients with acute respiratory failure and cited reference studies and abstracts from a recent international meeting in the intensive care medicine field. DATA SYNTHESIS AND EXTRACTION: From the selected articles, information was obtained regarding the prevalence of acute respiratory failure, including acute respiratory distress syndrome and acute lung injury as defined by the North American-European Consensus Conference, the outcome, and the factors influencing mortality rates in this population of patients. CONCLUSIONS: The prevalence of acute respiratory failure varies according to the definition used and the population studied. Nonsurvivors of acute respiratory distress syndrome die predominantly of respiratory failure in <20% of cases. The relatively high mortality rates of acute lung injury/acute respiratory distress syndrome are primarily related to the underlying disease, the severity of the acute illness, and the degree of organ dysfunction.

Humans↗

How respiratory system mechanics may help in minimising ventilator-induced lung injury in ARDS patients.

The main supportive therapy in acute respiratory distress syndrome patients is mechanical ventilation. As with any therapy, mechanical ventilation has side-effects, and may induce lung injury (ventilator-induced lung injury (VILI)/ventilator-associated lung injury). The mechanical factors responsible for VILI are thought to be related to tidal recruitment/derecruitment of previously collapsed alveoli and/or pulmonary overdistension. The volume/pressure (V/P) curve of the respiratory system in patients as well as in animal models of acute lung injury (ALI) has a characteristic sigmoid shape, with a lower inflection point (LIP) corresponding to the pressure/end-expiratory volume required to initiate recruitment of collapsed alveoli, and an upper inflection point (UIP) corresponding to the pressure/end inspiratory volume at which alveolar overdistension occurs. "Protective" ventilatory approaches have therefore set out to minimise mechanical injury by using the V/P curve to individualise positive end-expiratory pressure (PEEP) (PEEP above the LIP) and tidal volume (by setting end-inspiratory V/P below the UIP) since a large number of experimental studies correlate P/V curves to histological and biological manifestations of VILI and two randomised trials showed that protective ventilatory strategy individually tailored to the P/V curve minimised pulmonary and systemic inflammation and decreased mortality in patients with ALI. However, despite the fact that several studies have: 1) proposed new techniques to perform pressure/volume curves at the bedside, 2) confirmed that the lower inflection point and upper inflection point correspond to computed tomography scan evidence of atelectasis and overdistension, and 3) demonstrated the ability of the pressure/volume curve to estimate alveolar recruitment with positive end-expiratory pressure, no large studies have assessed whether such measurement can be performed in all intensive care units as a monitoring tool to orient ventilator therapy. Preliminary experimental and clinical studies show that the shape of the dynamic inspiratory pressure/time profile during constant flow inflation (stress index), allows prediction of a ventilatory strategy that minimises the occurrence of ventilator-induced lung injury.

Humans↗

Proportional assist ventilation.

Partial ventilatory support techniques are intended for patients who are unable to maintain a normal alveolar ventilation, despite normal central control for respiration. Proportional assist ventilation (PAV) is a novel mode of partial ventilatory support in which the ventilator generates an instantaneous inspiratory pressure in proportion to the instantaneous effort of the patient. In theory, PAV should normalize the neuro-ventilatory coupling by making the ventilator an extension of patient's respiratory muscles, while leaving to the patient the entire control of all aspects of breathing. PAV, however, shares a common problem with the conventional partial ventilatory support modes. In mechanically ventilated patients, the respiratory system impedance may change over time. These changes may impair the good matching between ventilator output and patient's ventilatory demand and lead to patient-ventilator asynchrony. To take full advantage of PAV, the authors believe that PAV should continuously and automatically adapt to the respiratory system passive mechanics, assessed by continuous noninvasive measurement of total elastance and resistance.

Algorithms↗

Temporal relationship between endothelin-1 concentrations and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Endothelin 1 (ET-1) is a potent vasoconstrictor that may play a role in cerebral vasospasm following subarachnoid hemorrhage (SAH). However, data regarding its pathogenic role in the development of vasospasm are controversial. We planned a prospective, observational clinical study to investigate the temporal relationship between increased ET-1 production and cerebral vasospasm or other neurological sequelae after SAH. METHODS: ET-1 levels in cerebrospinal fluid (CSF) were measured in 20 SAH patients from admission (within 24 hours from the bleeding) until day 7. Patients received a daily transcranial Doppler study and a neurological evaluation. On day 7, angiography was performed to verify the degree and extent of vasospasm. Patients were then classified as having (1) clinical vasospasm, (2) angiographic vasospasm, (3) no vasospasm, or (4) poor neurological condition without significant vasospasm (low Glasgow Coma Scale score [GCS]). RESULTS: On admission, ET-1 levels were increased in the low-GCS group compared with the other groups (P=0.04). On day 4 ET-1 levels were not significantly different among groups, whereas on day 7 ET-1 levels were significantly increased in both the clinical vasospasm and low-GCS groups compared with the angiographic vasospasm and no vasospasm groups (P<0.005). Moreover, when the low-GCS group was excluded, there was a significant relationship between vasospasm grade and CSF ET-1 levels (R(2)=0.73). CONCLUSIONS: CSF ET-1 levels were markedly elevated in patients with clinical manifestations of vasospasm (day 7) and with a poor neurological condition not related to vasospasm. However, ET-1 levels were low in clinical vasospasm patients before clinical symptoms were evident (day 4) and remained low in angiographic vasospasm patients throughout the study period. Thus, our data suggest that CSF ET-1 levels are increased in conditions of severe neuronal damage regardless whether this was due to vasospasm or to the primary hemorrhagic event. In addition, CSF ET-1 levels paralleled the neurological deterioration but were not predictive of vasospasm.

Cerebral Angiography↗

Mechanical ventilation: lessons from the ARDSNet trial.

The acute respiratory distress syndrome (ARDS) is an inflammatory disease of the lungs characterized clinically by bilateral pulmonary infiltrates, decreased pulmonary compliance and hypoxemia. Although supportive care for ARDS seems to have improved over the past few decades, few studies have shown that any treatment can decrease mortality for this deadly syndrome. In the 4 May 2000 issue of New England Journal of Medicine, the results of an NIH-sponsored trial were presented; they demonstrated that the use of a ventilatory strategy that minimizes ventilator-induced lung injury leads to a 22% decrease in mortality. The implications of this study with respect to clinical practice, further ARDS studies and clinical research in the critical care setting are discussed.

Humans↗

Continuous positive airway pressure facilitates spontaneous breathing in weaning chronic obstructive pulmonary disease patients by improving breathing pattern and gas exchange.

OBJECTIVE: To elucidate the effects of continuous positive airway pressure (CPAP) on breathing pattern, gas exchange and the ability to sustain spontaneous breathing (SB) in chronic obstructive pulmonary disease (COPD) patients with dynamic hyperinflation. DESIGN: Prospective study with two randomised trials of SB without and with CPAP in each patient. SETTING: Medical intensive care units (ICUs) in two university hospitals. PATIENTS: Nine dynamically hyperinflated, intubated COPD patients recuperating from acute exacerbation. INTERVENTIONS: One SB trial with CPAP (5-7.5 cmH2O), one without (control) in each patient. MEASUREMENTS: airway opening pressure, gas flow and thus breathing pattern, oxygen uptake, carbon dioxide excretion, arterial blood gases, dyspnoea and respiratory drive (P100). RESULTS: With CPAP, intrinsic positive end-expiratory pressure (PEEPi) fell from 11.4 to 6.3 cm H2O (p < 0.05). Eight patients sustained SB with CPAP for the maximum time planned (30 min), one failed after 18 min. In contrast, only four patients successfully completed the control trial, the others failing after 5-18 min (p < 0.05). Dyspnoea-gauged on a visual analogue scale by five patients--was less severe or occurred later with CPAP. Breathing with CPAP tended to be slower (18.9 vs 22.2 min(-1), p < 0.05) and deeper (tidal volume 370 vs 323 ml). At the end of the control run, PaCO2 was higher (60 vs 55 mmHg, p < 0.05) and still rising while being stable at the end of the CPAP trial. CONCLUSION: CPAP helps severely ill COPD patients sustain SB. Apparently it does so by promoting slower, deeper breathing and thus facilitating carbon dioxide elimination.

Acute Disease↗

Pressure-time curve predicts minimally injurious ventilatory strategy in an isolated rat lung model.

BACKGROUND: We tested the hypothesis that the pressure-time (P-t) curve during constant flow ventilation can be used to set a noninjurious ventilatory strategy. METHODS: In an isolated, nonperfused, lavaged model of acute lung injury, tidal volume and positive end-expiratory pressure were set to obtain: (1) a straight P-t curve (constant compliance, minimal stress); (2) a downward concavity in the P-t curve (increasing compliance, low volume stress); and (3) an upward concavity in the P-t curve (decreasing compliance, high volume stress). The P-t curve was fitted to: P = a. tb +c, where b describes the shape of the curve, b = 1 describes a straight P-t curve, b < 1 describes a downward concavity, and b > 1 describes an upward concavity. After 3 h, lungs were analyzed for histologic evidence of pulmonary damage and lavage concentration of inflammatory mediators. Ventilator-induced lung injury occurred when injury score and cytokine concentrations in the ventilated lungs were higher than those in 10 isolated lavaged rats kept statically inflated for 3 h with an airway pressure of 4 cm H2O. RESULTS: The threshold value for coefficient b that discriminated best between lungs with and without histologic and inflammatory evidence of ventilator-induced lung injury (receiver-operating characteristic curve) ranged between 0.90-1.10. For such threshold values, the sensitivity of coefficient b to identify noninjurious ventilatory strategy was 1.00. A significant relation (P < 0.001) between values of coefficient b and injury score, interleukin-6, and macrophage inflammatory protein-2 was found. CONCLUSIONS: The predictive power of coefficient b to predict noninjurious ventilatory strategy in a model of acute lung injury is high.

Animals↗

Compensation for increase in respiratory workload during mechanical ventilation. Pressure-support versus proportional-assist ventilation.

Variation in respiratory impedance may occur in mechanically ventilated patients. During pressure-targeted ventilatory support, this may lead to patient-ventilator asynchrony. We assessed the hypothesis that during pressure-support ventilation (PSV), preservation of minute ventilation (V E) consequent to added mechanical loads would result in an increase in respiratory rate (RR) due to the large reduction in tidal volume (VT). WITH proportional-assist ventilation (PAV), preservation of V E would occur through the preservation of VT, with a smaller effect on RR. We anticipated that this compensatory strategy would result in greater patient comfort and a reduce work of breathing. An increase in respiratory impedance was obtained by chest and abdominal binding in 10 patients during weaning from mechanical ventilation. V E remained constant in both ventilatory modes after chest and abdominal compression. During PSV, this maintenance of VE was obtained through a 58 +/- 3% increase in RR that compensated for a 29 +/- 2% reduction in VT. The magnitudes of the reduction in VT (10 +/- 3%) and of the increase in RR (14 +/- 2%) were smaller (p < 0. 001) during PAV. During both PSV and PAV, chest and abdominal compression caused increases in both the pressure-time product (PTP) of the diaphragm per minute (142.9 +/- 26.9 cm H(2)O. s/min, PSV, and 117.6 +/- 16.4 cm H(2)O. s/min, PAV) and per liter (13.4 +/- 2.5 cm H(2)O. s/L, PSV, and 9.6 +/- 0.7 cm H(2)O. s/L, PAV). These increments were greater (p < 0.001) during PSV than during PAV. The capability of keeping VT and V E constant through increases in inspiratory effort after increases in mechanical loads is relatively preserved only during PAV. The ventilatory response to an added respiratory load during PSV required greater muscle effort than during PAV.

Adult↗

[Traditional artificial ventilation. General principles].

Mechanical ventilation is generally applied on patients affected by acute respiratory failure (ARF) on the basis of hemogasanalysis, hemodynamics and X-ray features. The modification of ventilatory pattern is based on problem the modification of data concerning mechanical variation. In this study the most important mechanical measures and their consequences on ventilatory strategy are discussed.

Humans↗

Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.

CONTEXT: Studies have shown that an inflammatory response may be elicited by mechanical ventilation used for recruitment or derecruitment of collapsed lung units or to overdistend alveolar regions, and that a lung-protective strategy may reduce this response. OBJECTIVE: To test the hypothesis that mechanical ventilation induces a pulmonary and systemic cytokine response that can be minimized by limiting recruitment or derecruitment and overdistention. DESIGN AND SETTING: Randomized controlled trial in the intensive care units of 2 European hospitals from November 1995 to February 1998, with a 28-day follow-up. PATIENTS: Forty-four patients (mean [SD] age, 50 [18] years) with acute respiratory distress syndrome were enrolled, 7 of whom were withdrawn due to adverse events. INTERVENTIONS: After admission, volume-pressure curves were measured and bronchoalveolar lavage and blood samples were obtained. Patients were randomized to either the control group (n = 19): tidal volume to obtain normal values of arterial carbon dioxide tension (35-40 mm Hg) and positive end-expiratory pressure (PEEP) producing the greatest improvement in arterial oxygen saturation without worsening hemodynamics; or the lung-protective strategy group (n = 18): tidal volume and PEEP based on the volume-pressure curve. Measurements were repeated 24 to 30 and 36 to 40 hours after randomization. MAIN OUTCOME MEASURES: Pulmonary and systemic concentrations of inflammatory mediators approximately 36 hours after randomization. RESULTS: Physiological characteristics and cytokine concentrations were similar in both groups at randomization. There were significant differences (mean [SD]) between the control and lung-protective strategy groups in tidal volume (11.1 [1.3] vs 7.6 [1.1] mL/kg), end-inspiratory plateau pressures (31.0 [4.5] vs 24.6 [2.4] cm H2O), and PEEP (6.5 [1.7] vs 14.8 [2.7] cm H2O) (P<.001). Patients in the control group had an increase in bronchoalveolar lavage concentrations of interleukin (IL) 1beta, IL-6, and IL-1 receptor agonist and in both bronchoalveolar lavage and plasma concentrations of tumor necrosis factor (TNF) alpha, IL-6, and TNF-alpha, receptors over 36 hours (P<.05 for all). Patients in the lung-protective strategy group had a reduction in bronchoalveolar lavage concentrations of polymorphonuclear cells, TNF-alpha, IL-1beta, soluble TNF-alpha receptor 55, and IL-8, and in plasma and bronchoalveolar lavage concentrations of IL-6, soluble TNF-alpha receptor 75, and IL-1 receptor antagonist (P<.05). The concentration of the inflammatory mediators 36 hours after randomization was significantly lower in the lung-protective strategy group than in the control group (P<.05). CONCLUSIONS: Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung. Whether these physiological improvements are associated with improvements in clinical end points should be determined in future studies.

Cytokines↗

Time-course of impairment of respiratory mechanics after cardiac surgery and cardiopulmonary bypass.

OBJECTIVE: Cardiopulmonary bypass (CPB) is associated with abnormalities of lung function characterized by an increase in static elastance of the respiratory system. We examined the following: a) the effects of CPB on the total inspiratory volume-pressure (V-P) relationship of the respiratory system; b) the relative contribution of the chest wall and lung to the impairment of respiratory system mechanics; and c) the time-course of such impairment. DESIGN: Prospective, interventional study. SETTING: Surgical and medical intensive care units in a teaching hospital. PATIENTS: Eight adult patients scheduled for elective open heart surgery to correct valvular dysfunction. INTERVENTIONS: V-P curves (interrupter technique) of the respiratory system were partitioned between the chest wall and lung by measurements of esophageal pressure. Measurements were obtained before sternotomy (control), immediately after, 4 hrs after, and 7 hrs after separation from CPB. MEASUREMENTS AND MAIN RESULTS: Control V-P relationships of the respiratory system and lung showed lower inflection points (Pflex) at pressure values of 5.9+/-2.3 and 4.3+/-2.5 cm H2O, respectively. Immediately after and 4 hrs after separation from CPB, both curves had sigmoid shapes because of lower Pflex and formation of upper inflection (UIP) points. The pressures corresponding to the Pflex increased significantly (p < .001) by 56%+/-3% and 78%+/-4%, whereas the UIP corresponded to a pressure value of 42.34+/-8.5 and 35.6+/-7.8 cm H2O in the respiratory system and lung, respectively. A linear V-P relationship of the chest wall was observed during the control condition and after separation from CPB. Four hours later, no further increases in the pressure values corresponding to Pflex were observed on the inspiratory V-P curves of the respiratory system and lung, whereas the UIP occurred at a pressure of 35.6+/-9.1 and 29.7+/-8.4 cm H2O, respectively. A UIP was present on the V-P curve of the chest wall at a volume of 0.77+/-0.02 L. Seven hours after separation from CPB, the inspiratory V-P curves of the respiratory system, chest wall, and lung returned to normal. CONCLUSIONS: Sternotomy and CPB produced immediate changes in lung mechanics. Chest wall mechanics were affected only 4 hrs after sternotomy. Seven hours after disconnection from CPB, all mechanics had returned to normal.

Adult↗

Ventilatory support in the acute respiratory distress syndrome.

Ventilatory support in the acute respiratory distress syndrome (ARDS) has undergone considerable transformation in the 1990s. Current approaches include lung protective techniques which, while attempting to recruit and maintain lung volume, limit the shear stresses associated with ventilation by avoiding both alveolar overdistension and cyclical end-expiratory collapse. In addition, gas exchange targets have been liberalized and ventilatory conduct is much more tailored to individual pulmonary mechanics. Assessment of the inspiratory volume-pressure (V-P) curve provides information which can direct ventilator settings. Recent information from clinical trials has provided new insights into appropriate ventilatory modification and set the foundation for future clinical investigations.

Humans↗

Liver inflammation and acute respiratory distress syndrome in a patient receiving hepatitis B vaccine: a possible relationship?

We describe a patient in whom clinical evidence of liver and lung dysfunction developed after he received the second dose of recombinant hepatitis B vaccine, despite no serologic evidence of viral hepatitis. However, liver biopsy specimens demonstrated both surface antigens and core antigens, possibly indicating silent hepatitis B virus infection. A search for an infective etiology for the patient's subsequent clinical deterioration in lung function did not yield pathogens: postmortem examination revealed evidence of immune complex-mediated organ injury in the liver, lungs, and kidneys.

Antigen-Antibody Complex↗