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Biomedical subjects

L M Bigatello

Publications and source records attributed to L M Bigatello.

At least 19 recordsLinked to original sources

Acute lung injury after pulmonary resection.

Primary Acute Lung Injury (ALI) after lung resection (or "post-pneumonectomy pulmonary edema") is a rare form of acute respiratory failure characterized by dyspnea, hypoxemia, diffuse infiltrates on chest radiogram, and rapid evolution often unresponsive to therapy. ALI occurs almost exclusively following pneumonectomy, within 3 days from surgery and without a preceding cause. Factors implicated in its pathogenesis may include excessive fluid administration, alveolar injury during one-lung ventilation, pulmonary hypertension, and impaired lymph drainage. There is no specific therapy. Suggested measures in the perioperative care include the meticulous maintenance of physiological stability, judicious fluid restriction, and the limitation of ventilatory volumes and pressures.

Humans↗

Pathophysiology and management of the flail chest.

Flail chest occurs when a series of adjacent ribs are fractured in at least 2 places, anteriorly and posteriorly. This section of the chest wall becomes unstable and it moves inwards during spontaneous inspiration. The physiological impact of a flail chest depends on multiple factors, including the size of the flail segment, the intrathoracic pressure generated during spontaneous ventilation, and the associated damage to the lung and chest wall. Treatment varies with the severity of the physiologic impairment attributable to the flail segment itself. Immediate surgical fixation may decrease morbidity, but conservative treatment with positive pressure ventilation is preferred when multiple injuries to the intrathoracic organs are present.

Contusions↗

Different modes of assisted ventilation in patients with acute respiratory failure.

The aim of the present study was to verify that the patient/ventilator interaction is similar, regardless of the mode of assisted mechanical ventilation (i.e. pressure- or volume-limited) used, if tidal volume (VT) and peak inspiratory flow (PIF) are matched. Therefore, the authors compared the effects of three different modes of assisted ventilation on the work of breathing (WOB) and gas exchange in patients with acute respiratory failure. For Protocol 1, in seven patients, the authors compared pressure support, assist pressure control and assist control (with square and decelerating wave inspiratory flow pattern) set to deliver the same VT and PIF. For Protocol 2, in another 10 patients, the authors compared pressure support and assist control with high (0.8 L x s(-1)) and low (0.6 L x s(-1)) PIFs set to deliver the same VT. In Protocol 1, there was no difference in WOB and gas exchange between the three modes of assisted ventilation tested. In Protocol 2, the decrease of PIFs during assist control significantly increased WOB. In conclusion, different modes of assisted ventilation similarly reduce work of breathing and provide adequate gas exchange at fixed tidal volume and peak inspiratory flow only. During assist control, tidal volume and peak inspiratory flow (set by the physician) are the main determinants of the patient/ventilator interaction.

Acute Disease↗

Hemodynamic monitoring.

The goal of hemodynamic monitoring is to maintain adequate tissue perfusion. Classical hemodynamic monitoring is based on the invasive measurement of systemic, pulmonary arterial and venous pressures, and of cardiac output. Since organ blood flow cannot be directly measured in clinical practice, arterial blood pressure is used, despite limitations, as estimate of adequacy of tissue perfusion. A mean arterial pressure (MAP) of 70 mm Hg may be considered a reasonable target, associated with sign of adequate organ perfusion, in most patients. In the approach to hypotension, which is the most common cause of hemodynamic instability in critical ill patients, increasing levels of monitoring may be used. Assuming that central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP) are adequate estimates of the volume of the systemic and pulmonary circulation respectively, the following decision tree is suggested: 1) make a working diagnosis based on the relationship between pressure (CVP and PAOP) and cardiac output or stroke volume (CO or SV); 2) consider conditions that may alter reliability of CVP and PAOP in estimate adequately circulating volumes such as abnormal pressure/volume relationship (compliance) of the RV or LV, increased intrathoracic pressure (PEEP, autoPEEP, intra-abdominal pressure), valvular heart disease (mitral stenosis); 3) look at the history; 4) separating RV and LV by reciprocal variations of CVP, PAOP and SV. CVP is often used as sole parameter to monitor hemodynamic. However CVP alone may not differentiate between changes in volume (different venous return curve) or changes in contractility (different starling curve). Finally, other techniques such as echocardiography, transesophageal Doppler and volume-based monitoring system are now available.

Blood Pressure↗

Permissive hypercapnia.

The term permissive hypercapnia defines a ventilatory strategy for acute respiratory failure in which the lungs are ventilated with a low inspiratory volume and pressure. The aim of permissive hypercapnia is to minimize lung damage during mechanical ventilation; its limitation is the resulting hypoventilation and carbon dioxide (CO2) retention. In this article we discuss the rationale, physiologic implications, and implementation of permissive hypercapnia. We then review recent clinical studies that tested the effect of various approaches to permissive hypercapnia on the outcome of patients with acute respiratory failure.

Adult↗

The effects of pressurization rate on breathing pattern, work of breathing, gas exchange and patient comfort in pressure support ventilation.

The aim of this study was to investigate the effects of different pressurization rates during pressure support ventilation on breathing pattern, work of breathing, gas exchange and patient comfort in patients with acute lung injury. The pressurization rate modifies the initial pressure ramp by changing the initial peak flow rate: the increase in pressurization rate is associated with a decrease in the time to reach the level of pressure support ventilation by increasing the peak flow rate. Ten intubated patients (age 64+/-17 yrs, body mass index 24+/-17 Kg x m(-2), arterial oxygen tension/inspired oxygen fraction 214+/-59) were studied in random order varying the pressurization rate at 5 and 15 cmH2O of pressure support ventilation. Breathing comfort was evaluated by a visual analogue scale. Increasing the pressurization rate caused an increase of peak flow rate from 473+/-141 mL x s(-1) to 758+/-302 mL x s(-1) at pressure support ventilation 5 (p<0.05) and from 481+/-126 mL x s(-1) to 1,121+/-175 mL x s(-1) at pressure support ventilation 15 (p<0.05). At the lowest pressurization rate the tidal volume was the lowest, the respiratory rate and the work of breathing were the highest (p<0.05) compared with other pressurization rates. Excluding the lowest pressurization rate, in all the other pressurization rates tested the breathing pattern and the work of breathing did not change. The lowest and the highest pressurization rates caused the worst patient comfort (p<0.05). The gas exchange was stable throughout the study. The presented results suggest: 1) the lowest pressurization rate caused the lowest tidal volume, highest respiratory rate and highest work of breathing; 2) at the other pressurization rates no differences in breathing pattern and work of breathing were observed; and 3) the patient's comfort was worse at the lowest and highest pressurization rates.

Adult↗

Comparison of the effects of nitric oxide, nitroprusside, and nifedipine on hemodynamics and right ventricular contractility in patients with chronic pulmonary hypertension.

STUDY OBJECTIVES: The effects of inhaled nitric oxide (NO) on hemodynamics and right ventricular (RV) contractility were compared with those of nitroprusside and nifedipine in 14 patients with severe chronic pulmonary hypertension. STUDY DESIGN: Micromanometer and balloon-tipped right heart catheterization were performed. Inhaled NO, IV nitroprusside, and sublingual nifedipine were administered sequentially while patients breathed > 90% oxygen. SETTING: Cardiac catheterization laboratory in a tertiary care teaching hospital. PATIENTS: Fourteen patients with severe pulmonary hypertension unrelated to left ventricular dysfunction. MEASUREMENTS AND RESULTS: During NO inhalation, mean systemic arterial pressure (MAP) was unchanged, but pulmonary artery (PA) pressure ([mean +/- SEM] 49 +/- 2 mm Hg vs 44 +/- 2 mm Hg; p < 0.01), pulmonary vascular resistance (PVR; 829 +/- 68 vs 669 +/- 64 dyne x s x cm(-5); p < 0.01) and RV end-diastolic pressure (RVEDP; 12 +/- 1 vs 10 +/- 1 mm Hg; p < 0.01) decreased. Stroke volume index (SVI; 31 +/- 2 vs 35 +/- 3 mL/m(2); p < 0.05) increased, and the first derivative of RV pressure at 15 mm Hg developed pressure (RV +dP/dt at DP15) was unchanged. During nitroprusside administration, MAP decreased (105 +/- 5 vs 76 +/- 5 mm Hg; p < 0.01), PA was unchanged (48 +/- 2 vs 45 +/- 3 mm Hg; p = not significant), and PVR decreased (791 +/- 53 vs 665 +/- 53 dyne x s x cm(-5); p < 0.01). RV +dP/dt at DP15 increased (425 +/- 22 vs 465 +/- 29 mm Hg/s; p < 0.05), but SVI was unchanged. Nifedipine decreased MAP (103 +/- 5 vs 94 +/- 5 mm Hg; p < 0.01), PA and PVR were unchanged, RVEDP increased (12 +/- 1 vs 14 +/- 2 mm Hg; p < 0.01), and RV +dP/dt at DP15 decreased (432 +/- 90 vs 389 +/- 21 mm Hg/s; p < 0.05). CONCLUSIONS: Inhaled NO is a selective pulmonary vasodilator in patients with chronic pulmonary hypertension that improves cardiac performance without altering RV contractility. Nitroprusside caused a similar degree of pulmonary vasodilation. In contrast to inhaled NO, nitroprusside caused systemic hypotension associated with an increase in RV contractility. Acute administration of nifedipine did not cause pulmonary vasodilation, but RVEDP increased and RV contractility decreased.

Administration, Inhalation↗

Intraoperative monitoring of myocardial ischemia.

Cardiovascular complications are commonly observed in surgical patients, and myocardial ischemia is the most important determinant of perioperative morbidity. The clinical criteria defining a patient population at increased risk for cardiovascular events are presented. The authors review the principles of monitoring and diagnosing myocardial ischemia, focusing on eletrocardiography and TransEsophageal Echocardiography. These patients must be closely followed long after the end of surgery, since the risk for cardiac morbidity is high for several hours postoperatively.

Echocardiography, Transesophageal↗

Inhaled nitric oxide delivery by anesthesia machines.

UNLABELLED: Inhaled nitric oxide (NO) is a selective pulmonary vasodilator used to treat intraoperative pulmonary hypertension and hypoxemia. In contrast to NO delivered by critical care ventilators, NO delivered by anesthesia machines can be complicated by rebreathing. We evaluated two methods of administering NO intraoperatively: via the nitrous oxide (N(2)O) flowmeter and via the INOvent (Datex-Ohmeda, Madison, WI). We hypothesized that both systems would deliver NO accurately when the fresh gas flow (FGF) rate was higher than the minute ventilation (VE). Each system was set to deliver NO to a lung model. Rebreathing of NO was obtained by decreasing FGF and by simulating partial NO uptake by the lung. At FGF > or = VE (6 L/min), both systems delivered an inspired NO concentration ([NO]) within approximately 10% of the [NO] set. At FGF < VE and complete NO uptake, the N(2)O flowmeter delivered a lower [NO] (70 and 40% of the [NO] set at 4 and 2 L/min, respectively) and the INOvent delivered a higher [NO] (10 and 23% higher than the [NO] set at 4 and 2 L/min, respectively). Decreasing the NO uptake increased the inspired [NO] similarly with both systems. At 4 L/min FGF, [NO] increased by 10%-20% with 60% uptake and by 18%-23% with 30% uptake. At 2 L/min, [NO] increased by 30%-33% with 60% uptake and by 60%-69% with 30% uptake. We conclude that intraoperative NO inhalation is accurate when administered either by the N(2)O flowmeter of an anesthesia machine or by the INOvent when FGF > or = VE. IMPLICATIONS: Inhaled nitric oxide (NO) is a selective pulmonary vasodilator. In a lung model, we demonstrated that NO can be delivered accurately by a N(2)O flowmeter or by a commercial device. We provide guidelines for intraoperative NO delivery.

Administration, Inhalation↗

Nitric oxide: modulation of the pulmonary circulation.

Nitric oxide (NO) is synthetized throughout the body by the enzyme NO synthase (NOS), cyclic GMP transduction pathway causes pulmonary vasodilatation anti-platelets aggregation and inhibition of leukocyte adhesion. Inducible NOS is expressed in leukocytes in response to a variety of inflammatory stimuli and can be inhibited by corticosteroids. Inhaled NO is a selective pulmonary vasodilator. In USA inhaled NO was approved by FDA for hypoxemic respiratory failure in infants and children. In adults it may be useful in various clinical therapy: pulmonary hypertension, lung transplantation, ARDS but new clinical investigations are necessary.

Administration, Inhalation↗

Assessment of errors when expiratory condensate PCO2 is used as a proxy for mixed expired PCO2 during mechanical ventilation.

OBJECTIVES: We designed a series of experiments to determine whether expiratory water condensate (PconCO2) can be used as a proxy for mixed expired gas collection. METHODS: In 18 adult mechanically ventilated patients with ARDS (40 samples), simultaneous collections of arterial blood, expiratory water trap condensate, mixed expired gas, and minute ventilation were used to calculate VCO2 and VD/VT. To assess the effect of temperature, a constant gas flow (PCO2 10-30 mm Hg) was bubbled through water at temperatures of 19.5-37 degrees C. Gas and water samples were collected, immediately analyzed for PCO2, and a temperature correction factor was calculated. A lung model was constructed using a 5 L anesthesia bag connected to a mechanical ventilator with a heated humidifier. Temperature at the Y-piece was set to approximately 37 degrees C and CO2 was injected into the bag to establish an end-tidal PCO2 of 20-70 mm Hg. After equilibration, condensate was collected, PCO2 was measured, and the temperature-corrected PCO2 was compared to PECO2. The capnogram at points along the expiratory limb circuit was used to evaluate gas mixing. RESULTS: There was an over-estimation of PECO2 by PconCO2 (p < 0.001) for the patient data, resulting in an underestimation of VD/VT (p < 0.001) and an overestimation of VCO2 (p < 0.001). The temperature correction factor for PCO2 in water was -0.010 (about half of the factor used for whole blood). The bias between temperature-corrected PconCO2 and PECO2 was 0.3 +/- 3.2 mm Hg in the lung model. Mixing in the expiratory limb was poor, as evaluated by the capnogram. CONCLUSIONS: Even with temperature correction, we failed to precisely predict PECO2 from PconCO2. For measurement of VD/VT and VCO2, we do not recommend methods that use PconCO2.

Adult↗

Inaccuracies of nitric oxide delivery systems during adult mechanical ventilation.

BACKGROUND: Various systems to administer inhaled nitric oxide (NO) have been used in patients and experimental animals. We used a lung model to evaluate five NO delivery systems during mechanical ventilation with various ventilatory patterns. METHODS: An adult mechanical ventilator was attached to a test lung configured to separate inspired and expired gases. Four injection systems were evaluated with NO injected either into the inspiratory circuit 90 cm proximal to the Y piece or directly at the Y piece and delivered either continuously or only during the inspiratory phase. Alternatively, NO was mixed with air using a blender and delivered to the high-pressure air inlet of the ventilator. Nitric oxide concentration was measured from the inspiratory limb of the ventilator circuit and the tracheal level using rapid- and slow-response chemiluminescence analyzers. The ventilator was set for constant-flow volume control ventilation, pressure control ventilation, pressure support ventilation, or synchronized intermittent mandatory ventilation. Tidal volumes of 0.5 l and 1 l were evaluated with inspiratory times of 1 s and 2 s. RESULTS: The system that premixed NO proximal to the ventilator was the only one that maintained constant NO delivery regardless of ventilatory pattern. The other systems delivered variable NO concentration during pressure control ventilation and spontaneous breathing modes. Systems that injected a continuous flow of NO delivered peak NO concentrations greater than the calculated dose. These variations were not apparent when a slow-response chemiluminescence analyzer was used. CONCLUSIONS: NO delivery systems that inject NO at a constant rate, either continuously or during inspiration only, into the inspiratory limb of the ventilator circuit produce highly variable and unpredictable NO delivery when inspiratory flow is not constant. Such systems may deliver a very high NO concentration to the lungs, which is not accurately reflected by measurements performed with slow-response analyzers.

Adult↗