Biomedical subjects

Paolo Taccone

Publications and source records attributed to Paolo Taccone.

6 recordsLinked to original sources

PubMed2004

Continuous positive airway pressure delivered with a "helmet": effects on carbon dioxide rebreathing.

OBJECTIVE: The "helmet" has been used as a novel interface to deliver noninvasive ventilation without applying direct pressure on the face. However, due to its large volume, the helmet may predispose to CO2 rebreathing. We hypothesized that breathing with the helmet is similar to breathing in a semiclosed environment, and therefore the PCO2 inside the helmet is primarily a function of the subject's CO2 production and the flow of fresh gas through the helmet. DESIGN: Human volunteer study. SETTING: Laboratory in a university teaching hospital. SUBJECTS: Eight healthy volunteers. INTERVENTIONS: We delivered continuous positive airway pressure (CPAP) with the helmet under a variety of ventilatory conditions in a lung model and in volunteers. MEASUREMENTS AND MAIN RESULTS: Gas flow and CO2 concentration at the airway were measured continuously. End-tidal PCO2, CO2 production, and ventilatory variables were subsequently computed. We found that a) when CPAP was delivered with a ventilator, the inspired CO2 of the volunteers was high (12.4 +/- 3.2 torr [1.7 +/- 0.4 kPa]); b) when CPAP was delivered with a continuous high flow system, inspired CO2 of the volunteers was low (2.5 +/- 1.2 torr [0.3 +/- 0.2 kPa]); and c) the inspired CO2 calculated mathematically for a semiclosed system model of CO2 rebreathing was highly correlated with the values measured in a lung model (r = .97, slope = 0.92, intercept = -1.17, p < .001) and in the volunteers (r = .94, slope = 0.96, intercept = 0.90, p < .001). CONCLUSIONS: a) The helmet predisposes to CO2 rebreathing and should not be used to deliver CPAP with a ventilator; b) continuous high flow minimizes CO2 rebreathing during CPAP with the helmet; and c) minute ventilation and Pco2 should be monitored during CPAP with the helmet.

Adult↗

PubMed2003

An increase of abdominal pressure increases pulmonary edema in oleic acid-induced lung injury.

Increased abdominal pressure is common in intensive care unit patients. To investigate its impact on respiration and hemodynamics we applied intraabdominal pressure (aIAP) of 0 and 20 cm H(2)O (pneumoperitoneum) in seven pigs. The whole-lung computed tomography scan and a complete set of respiratory and hemodynamics variables were recorded both in healthy lung and after oleic acid (OA) injury. In healthy lung, aIAP 20 cm H(2)O significantly lowered the gas content, leaving the tissue content unchanged. In OA-injured lung at aIAP 0 cm H(2)O, the gas content significantly decreased compared with healthy lung. The excess tissue mass (edema) amounted to 30 +/- 24% of the original tissue weight (455 +/- 80 g). The edema was primarily distributed in the base regions and was not gravity dependent. Heart volume, central venous, pulmonary artery, wedge, and systemic arterial pressures significantly increased. At aIAP 20 cm H(2)O in OA-injured lung, the central venous and pulmonary artery pressures further increased. The gas content further decreased, and the excess tissue mass rose up to 103 +/- 37% (tissue weight 905 +/- 134 g), with homogeneous distribution along the cephalocaudal and sternovertebral axis. We conclude that in OA-injured lung, the increase of IAP increases the amount of edema.

Abdomen↗

PubMed2003

Physiologic rationale for ventilator setting in acute lung injury/acute respiratory distress syndrome patients.

OBJECTIVES: To review the physiologic approach to setting mechanical ventilation in acute lung injury/acute respiratory distress syndrome. DATA SOURCES: MEDLINE search from 1979 to the present. DATA SELECTION: Personal selection of some articles we believe relevant for understanding acute lung injury/acute respiratory distress syndrome physiopathology and its physiologic management. DATA SUMMARY: Knowing the underlying pathology is key to estimating the potential for recruitment. The potential for recruitment is rather low when the consolidation of pulmonary units exceeds collapse, as in diffuse pneumonia. In contrast, when pulmonary unit collapse exceeds consolidation, as in acute lung injury/acute respiratory distress syndrome from extrapulmonary origin, the potential for recruitment may be high. To exploit the potential for recruitment, a transpulmonary pressure greater than the opening pressure must be applied to the lung. To do so, chest wall elastance must be measured or estimated. To avoid collapse after recruitment, a positive end-expiratory pressure greater than the compressive forces operating on the lung and an alveolar ventilation sufficient to prevent absorption atelectasis must be provided. Indeed, avoidance of stretch (low airway plateau pressure) and prevention of cyclic collapse and reopening (adequate positive end-expiratory pressure and alveolar ventilation) are the physiologic cornerstones of mechanical ventilation in acute lung injury/acute respiratory distress syndrome. When considering all the randomized clinical trials reported so far, it is tempting to speculate that transpulmonary pressure and stresses, rather than tidal volume per se, are the key factors that may have an impact on mortality. CONCLUSIONS: The majority of physiologic, experimental, and clinical trial data converge on one simple concept: treat the lung gently.

Humans↗

PubMed2003

Resuscitation from hemorrhagic shock: experimental model comparing normal saline, dextran, and hypertonic saline solutions.

OBJECTIVE: To compare the effectiveness of normal saline, dextran, hypertonic, and hypertonic-hyperoncotic solutions in hemorrhagic shock. DESIGN: Laboratory investigation. SETTING: University hospital, Emergency Surgery and Intensive Care staff. SUBJECTS: Thirty-two large white female pigs. INTERVENTIONS: Routine care included: anesthesia and sedation (ketamine 10 mg/kg, droperidol 0.25 mg/kg, diazepam 0.7 mg/kg, fentanyl 0.006 mg/kg, 2% enflurane, 20% nitrous oxide, pancuronium bromide 0.13 mg/kg); volume-controlled ventilation (Paco(2) 35-40 torr; 4.7-5.4 kPa); cannulation of right carotid artery and pulmonary artery. Three flow probes (subdiaphragmatic aorta, superior mesenteric artery, right renal artery) and regional venous catheters (superior mesenteric vein, right renal vein) were positioned. Animals were bled to 45 mm Hg for 1 hr and resuscitated with four different fluids and blood to normal aortic blood flow and hemoglobin. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure and blood flow through abdominal aorta ([OV0312](aor)), mesenteric artery ([OV0312](mes)), and renal artery ([OV0312](ren)) were continuously monitored. Cardiac output, systemic and regional oxygen delivery ([U1E0A]o(2), [U1E0A]o(2mes), [U1E0A]o(2ren)), and consumption ([OV0312]o(2), [OV0312]o(2mes), [OV0312]o(2ren)) were recorded every 30 mins. Baseline [OV0312](aor) was restored with different amounts of fluids in the four groups: normal saline (91.35 +/- 22.18 mL/kg); dextran (16.24 +/- 4.42 mL/kg); hypertonic (13.70 +/- 1.44 mL/kg); and hypertonic-hyperoncotic (9.11 +/- 1.20 mL/kg). The amount of sodium load was less using dextran and hypertonic-hyperoncotic and sodium levels were only transiently increased after hypertonic infusion. Mean arterial pressure and cardiac output were normalized in all groups. Animals resuscitated with normal saline and dextran showed increased pulmonary artery pressures. [U1E0A]o(2) was significantly higher after hypertonic-hyperoncotic infusion, because of reduced hemodilution. Hypertonic and hypertonic-hyperoncotic normalized [OV0312](mes), [U1E0A]o(2mes), [OV0312]o(2mes), [OV0312](ren), and [U1E0A]o(2ren), whereas normal saline and dextran did not achieve this result. At the end of the experiment, hypertonic-hyperoncotic maintained mean arterial pressure, cardiac output, and [U1E0A]o(2) until the end of observation in contrast to normal saline, dextran, and hypertonic. CONCLUSIONS: Resuscitation with a small volume of hypertonic-hyperoncotic solution allows systemic and splanchnic hemodynamic and oxygen transport recovery, without an increase in pulmonary artery pressure. It only transiently increased sodium concentration.

Animals↗

PubMed2003

Effect of different inspiratory rise time and cycling off criteria during pressure support ventilation in patients recovering from acute lung injury.

OBJECTIVE: With many mechanical ventilators, it is possible to modify the time to reach the selected airway pressure and the criteria for cycling off the inflation during pressure support ventilation. This study evaluated the effect of different inspiratory rise time and cycling off criteria on breathing pattern and work of breathing. DESIGN: Clinical study. SETTING: University laboratory. PATIENTS: Ten intubated patients recovering from acute lung injury (PaO2/FiO2 245 +/- 26 torr, positive end-expiratory pressure 9 +/- 3 cm H2O). INTERVENTIONS: We studied two inspiratory rise time criteria (shortest and longest, 0% and 40% of the breath cycle time) and two cycling off criteria (lowest and highest, 5% and 40% of the peak inspiratory flow) at 5 and 15 cm H2O of pressure support. Respiratory rate, tidal volume, and inspiratory and expiratory work of breathing (WOBI and WOBE) were measured. MEASUREMENTS AND MAIN RESULTS: At both levels of pressure support ventilation, the shortest inspiratory rise time significantly reduced the WOBI from 0.77 +/- 0.32 to 0.56 +/- 0.23 J/L and from 0.24 +/- 0.28 to 0.08 +/- 0.09 J/L without affecting respiratory rate or tidal volume. At 15 cm H2O of pressure support ventilation, the lowest cycling off criteria significantly reduced respiratory rate from 24.9 +/- 12.1 to 21.5 +/- 12.7 beats/min and increased tidal volume from 0.51 +/- 0.17 to 0.60 +/- 0.26 L. At both levels of pressure support ventilation, the modification of cycling off criteria did not influence WOBI and WOBE. CONCLUSIONS: Our results suggest that in patients recovering from acute lung injury during pressure support ventilation, a) the shortest inspiratory rise time reduces the WOBI; and b) at 15 cm H2O of pressure support ventilation, the lowest cycling off criteria reduces the respiratory rate and increases the tidal volume without modifying the WOBI and WOBE. Modifications of inspiratory rise time and cycling off criteria must be carefully adjusted during pressure support ventilation.

Adult↗

PubMed2003

Decrease in PaCO2 with prone position is predictive of improved outcome in acute respiratory distress syndrome.

OBJECTIVE: To determine whether gas exchange improvement in response to the prone position is associated with an improved outcome in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). DESIGN: Retrospective analysis of patients in the pronation arm of a controlled randomized trial on prone positioning and patients enrolled in a previous pilot study of the prone position. SETTING: Twenty-eight Italian and two Swiss intensive care units. PATIENTS: We studied 225 patients meeting the criteria for ALI or ARDS. INTERVENTIONS: Patients were in prone position for 10 days for 6 hrs/day if they met ALI/ARDS criteria when assessed each morning. Respiratory variables were recorded before and after 6 hrs of pronation with unchanged ventilatory settings. MEASUREMENTS AND MAIN RESULTS: We measured arterial blood gas alterations to the first pronation and the 28-day mortality rate. The independent risk factors for death in the general population were the Pao2/Fio2 ratio (odds ratio, 0.992; confidence interval, 0.986-0.998), the minute ventilation/Paco2 ratio (odds ratio, 1.003; confidence interval, 1.000-1.006), and the concentration of plasma creatinine (odds ratio, 1.385; confidence interval, 1.116-1.720). Pao2 responders (defined as the patients who increased their Pao2/Fio2 by > or =20 mm Hg, 150 patients, mean increase of 100.6 +/- 61.6 mm Hg [13.4 +/- 8.2 kPa]) had an outcome similar to the nonresponders (59 patients, mean decrease -6.3 +/- 23.7 mm Hg [-0.8 +/- 3.2 kPa]; mortality rate 44% and 46%, respectively; relative risk, 1.04; confidence interval, 0.74-1.45, p =.65). The Paco2 responders (defined as patients whose Paco2 decreased by > or =1 mm Hg, 94 patients, mean decrease -6.0 +/- 6 mm Hg [-0.8 +/- 0.8 kPa]) had an improved survival when compared with nonresponders (115 patients, mean increase 6 +/- 6 mm Hg [0.8 +/- 0.8 kPa]; mortality rate 35.1% and 52.2%, respectively; relative risk, 1.48; confidence interval, 1.07-2.05, p =.01). CONCLUSION: ALI/ARDS patients who respond to prone positioning with reduction of their Paco2 show an increased survival at 28 days. Improved efficiency of alveolar ventilation (decreased physiologic deadspace ratio) is an important marker of patients who will survive acute respiratory failure.

Aged↗