A smoking cessation telephone resource: feasibility and preliminary evidence on the effect on health care provider adherence to smoking cessation guidelines.
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Biomedical subjects
Publications and source records attributed to T W Marcy.
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The onset of agitation and distress in a mechanically ventilated patient should initiate a careful assessment that considers whether there has been progression of the underlying disease, a new medical complication, or adverse effects from medical interventions and procedures, including intubation and mechanical ventilation. This article focuses on problems that relate to mechanical ventilation and the interactions of the "patient-ventilator system". The authors suggest an initial approach to the patient who develops respiratory distress, and then review the appropriate indications for sedative and paralytic medications.
Recent evidence that volume-cycled mechanical ventilation may itself produce lung injury has focused clinical attention on the pressure waveform applied to the respiratory system. There has been an increasing use of pressure-controlled ventilation (PCV), because it limits peak cycling pressure and provides a decelerating flow profile that may improve gas exchange. In this mode, however, the relationships are of machine adjustments to ventilation and alveolar pressure are not straightforward. Consequently, setting selection remains largely an empirical process. In previous work, we developed a biexponential model of PCV that provides a conceptual framework for understanding these interactions (J. Appl. Physiol. 67: 1081-1092, 1989). We tested the validity of this mathematical model in a single-compartment analogue of the respiratory system across wide ranges of clinician-set variables (frequency, duty cycle, applied pressure) and impedance conditions (inspiratory and expiratory resistance and system compliance). Our data confirm the quantitative validity of the proposed model when approximately rectilinear waves of pressure are applied and appropriate values for impedance are utilized. Despite a fixed-circuit configuration, however, resistance proved to be a function of each clinician-set variable, requiring remeasurement of system impedance as adjustments in these variables were made. With further modification, this model may provide a practical as well as a conceptual basis for understanding minute ventilation and alveolar pressure fluctuations during PCV in the clinical setting.
A technique that improves the efficiency of alveolar ventilation should decrease the pressure required and reduce the potential for lung injury during mechanical ventilation. Alveolar ventilation may be improved by replacing a portion of the anatomic dead space with fresh gas via an intratracheal catheter. We studied the effect of intratracheal gas insufflation as an adjunct to volume cycled ventilation in eight sedated, paralyzed patients with a variety of lung disorders. Continuous flows of 2, 4, and 6 L/min were delivered through a catheter positioned 1 or 10 cm above the carina. Carbon dioxide production, inspiratory minute ventilation, and peak and mean airway pressures did not change over the range of flows tested. PaCO2 and dead space volume/tidal volume decreased significantly as joint functions of catheter flow and position (p < 0.001). The highest catheter flow (6 L/min) and most distal catheter position (1 cm above the carina) were the most effective combination tested, averaging a 15% reduction in PaCO2 (range 9 to 23%). Certain characteristics of the expiratory capnogram were helpful in predicting the observed reduction in PaCO2. Tracheal gas insufflation may eventually prove a useful adjunct to a pressure-targeted strategy of ventilatory management (in either volume-cycled or pressure controlled modes), particularly when the total dead space is heavily influenced by its anatomic component.
Tracheal gas insufflation (TGI) improves the efficiency of CO2 elimination accomplished by conventional mechanical ventilation, primarily by reducing the anatomic (series) dead space volume. Dead space proximal to the catheter tip can be reduced by two methods. Fresh gas introduced at the carinal level during inspiration may effectively "bypass" the upper airway. Alternatively, proximal dead space can be "washed out" with fresh gas during expiration to reduce CO2 rebreathing. We examined these two modes of TGI-aided dead space reduction in nine paralyzed normal dogs receiving conventional mechanical ventilation and compared these results to those obtained with a catheter that delivered fresh gas continuously at the same flow rate, thereby accomplishing both bypass and washout. Total inspired tidal volume and cycling frequency were held constant. Differences in CO2 elimination efficiency among the TGI modes were flow dependent. Continuous catheter flow at 5 or 10 L/min reduced PaCO2 and physiologic dead space fraction (VD/VT) more than either proximal bypass or end-expiratory washout (p < 0.001). At the same catheter flow settings expiratory washout tended to improve VD/VT more than did inspiratory bypass. Under the conditions tested, constant tracheal insufflation of fresh gas improves alveolar ventilation by mechanisms that include, but are not limited to, a functional reduction in the dead space proximal to the catheter tip.
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Increased awareness of pressure-related injury to the alveolar-capillary interface has renewed interest in modes of ventilation that limit alveolar distention such as pressure-controlled ventilation (PCV). We examined respiratory system mechanics and gas exchange during PCV in six dogs. Our data conformed to the predictions of our single-compartment mathematical model of respiratory dynamics during PCV (J Appl Physiol 1989; 67:1081-92). For a fixed pressure (Pset) and inspiratory time fraction (Tl/Ttot) (15 cm H2O and 0.3, respectively), minute ventilation (VE) reached a well-defined plateau as frequency (f) increased from 10 to 50 breaths/min and tidal volume (VT) fell progressively. Concomitantly, the physiologic dead-space fraction (VD/VT) increased from 0.50 +/- 0.04 to 0.85 +/- 0.04, and arterial PCO2 (PaCO2) rose from 39 +/- 4 to 76 +/- 12 mm Hg. At a fixed combination of frequency, applied pressure, and Tl/Ttot (40 breaths/min, 15 cm H2O, and 0.3), VE did not change when we introduced fresh gas continuously from an intratracheal catheter. However, PaCO2 and VD/VT fell progressively as catheter flow increased from zero to 14 L/min (60 +/- 12 to 40 +/- 12 mm Hg and 0.83 +/- 0.03 to 0.25 +/- 0.14 mm Hg, respectively). We conclude that during PCV at a fixed Pset and Tl/Ttot increasing frequency caused VT to fall and VE to reach a plateau. Declining VT was associated with a rise in PaCO2 because of a subsequent fall in alveolar ventilation. Insufflating fresh gas by an intratracheal catheter increased alveolar ventilation and improved CO2 elimination by washing out the anatomic dead space.(ABSTRACT TRUNCATED AT 250 WORDS)
In the setting of acute lung injury, ventilatory strategies that adjust minute ventilation (VE) to achieve eucapnia often lead to alveolar rupture or damage. Tracheal gas insufflation (TGI) reduces the VE requirements of conventional mechanical ventilation by decreasing the effective dead-space fraction (VD/VT) of each breath. We studied the effect of catheter flow rate (Vcath) and position as well as catheter tip diameter and configuration on CO2 elimination during TGI-augmented pressure-controlled ventilation (PCV) in normal dogs. We studied three catheter positions (1, 5, and 10 cm above the carina) at Vcath of 2, 5, and 10 L/min (n = 6). When the catheter tip was positioned 1 cm above the carina, PaCO2 decreased significantly from a baseline (PCV alone) of 67 +/- 10 mm Hg to 52 +/- 11, 43 +/- 9, and 32 +/- 7 mm Hg (p < 0.05) at Vcath of 2, 5, and 10 L/min, respectively. For the same Vcath values, positioning the catheter tip 10 cm above the carina increased PaCO2 to 54 +/- 15, 46 +/- 12, and 40 +/- 11 mm Hg. Advancing the catheter tip 2 cm below the carina did not improve PaCO2 significantly (n = 3). At a catheter position of 1 cm above the carina and a Vcath of 10 L/min, changing the luminal inner diameter (1.5 versus 3.0 mm) or tip configuration (open tip versus occluded tip with two side holes) of the catheter did not change PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: To assess complications of bronchoalveolar lavage in the intubated, mechanically ventilated patient. DESIGN: A retrospective, consecutive case series. SETTING: Medical, surgical, and bone marrow transplant critical care units at a university teaching hospital. PATIENTS: Ninety-nine consecutive critically ill, mechanically ventilated patients undergoing bronchoalveolar lavage were included in the study. INTERVENTIONS: All patients underwent bronchoalveolar lavage using a standard method designed to maximize the safety of the procedure. MEASUREMENTS: Each patient's hospital chart was reviewed for immediate and delayed medical complications of the procedure, including cardiac arrhythmias, bleeding, and hemodynamic disturbances. Specific indices of lung mechanics (peak inspiratory airway pressure and static compliance) and oxygenation (alveolar to arterial oxygen tension gradient [P(A-a)O2] and the ratio of FIO2/PaO2) were measured before and 4 hrs after bronchoalveolar lavage to assess durable physiologic consequences of the procedure. RESULTS: No complications occurred that required premature termination of bronchoalveolar lavage. Three patients exhibited adverse effects (hypotension in two and wheezing in one) immediately after the procedure, all of which resolved promptly with treatment. No statistically significant changes were observed in the variables of arterial oxygenation or pulmonary mechanics. Although the sample mean did not change significantly for any of the oxygen variables, 19% of the patients experienced widening of the P(A-a)O2 by greater than 100 torr (greater than 13.3 kPa). A systematic analysis indicated that there was no statistically significant relationship between readily available clinical variables (including duration of mechanical ventilation before bronchoalveolar lavage and prebronchoalveolar lavage P[A-a]O2), and deterioration in oxygenation after the procedure. CONCLUSIONS: We conclude that bronchoalveolar lavage is a well-tolerated procedure in critically ill, mechanically ventilated patients, provided that risk factors for complications are corrected before the procedure and one adheres to procedural guidelines focused on patient safety. Clinically important complications are uncommon. Some patients exhibit deterioration in oxygen after bronchoalveolar lavage; this occurrence cannot be predicted before the procedure.
Conventional ventilatory support of patients with the adult respiratory distress syndrome (ARDS) consists of volume-cycled ventilation with applied positive end-expiratory pressure (PEEP). Unfortunately, recent evidence suggests that this strategy, as currently implemented, may perpetuate lung damage by overinflating and injuring distensible alveolar tissues. An alternative strategy--termed inverse ratio ventilation (IRV)--extends the inspiratory time, and, in concept, maintains or improves gas exchange at lower levels of PEEP and peak distending pressures. There are two methods to administer IRV: (1) volume-cycled ventilation with an end-inspiratory pause, or with a slow or decelerating inspiratory flow rate; or (2) pressure-controlled ventilation applied with a long inspiratory time. There are several real or theoretical problems common to both forms of IRV: excessive gas-trapping; adverse hemodynamic effects; and the need for sedation in most patients. Although there are many anecdotal reports of IRV, there are no controlled studies that compare outcome in ARDS patients treated with IRV as opposed to conventional ventilation. Nonetheless, clinicians are using IRV with increasing frequency. In the absence of well-designed clinical trials, we present interim guidelines for a ventilatory strategy in patients with ARDS based on the literature and our own clinical experience.
A sophisticated system of pulmonary host defense strives to maintain the functional integrity of the lung against the threats of infections, toxins, and malignancy. Congenital and acquired defects in the immune mechanisms of this host defense are associated with a variety of pulmonary disorders that include infections with usual or opportunistic organisms; inflammatory disorders; and malignancies. The age of the patient, associated abnormalities, family history, and the type of pulmonary and systemic diseases that are present provide clues to the specific underlying disorder. Laboratory tests including immunoglobulin levels, lymphocyte subset enumeration, and tests of lymphocyte function can help to confirm the clinical impression. Determination of the specific disorder allows the physician to anticipate possible complications, initiate appropriate prophylactic measures, and, in an increasing number of diseases, offer specific therapy.
A variety of infectious and noninfectious pulmonary disorders can present with pulmonary infiltrates with peripheral eosinophilia. Specific therapies are available for many of the pulmonary eosinophilic syndromes and failure to treat these syndromes can result in the development of irreversible lung disease. Clearly, an infectious etiology needs to be excluded before initiating glucocorticoid therapy for a presumed hypersensitivity reaction. However, the distinction between infectious and noninfectious processes can be difficult to make on clinical grounds alone. For these reasons, the evaluation of a patient presenting with this problem provides an interesting challenge to the physician.
The quantitation of substances in the epithelial lining fluid (ELF) of the lower respiratory tract, as obtained by bronchoalveolar lavage (BAL), is not precise because of the variable dilution of the ELF by the instilled lavage fluid. It has been reported that the absolute concentration of proteins in ELF can be determined by using the ratio of urea concentration in BAL fluid to that in serum as a method to calculate the volume of ELF recovered by BAL. Furthermore, it has been suggested that the error caused by diffusion of urea into the instilled lavage fluid can be minimized by instilling only 100 ml (5 X 20 ml) of saline rather than 300 ml (6 X 50 ml). We tested the validity of this method by collecting and individually analyzing aliquots from 2 different BAL protocols--a 100-ml (5 X 20 ml) BAL and a 300-ml (6 X 50 ml) BAL--performed in 6 healthy, nonsmoking subjects. Total protein, albumin, and urea were measured in each aliquot and in pooled fluid from each BAL procedure, and urea was measured in serum. In the 300-ml BAL, total protein and albumin concentrations tended to decrease progressively from the second to the sixth aliquots. In contrast, the urea concentration increased progressively from the first to the sixth aliquots. The concentration of albumin in ELF, calculated from the concentration of urea and albumin in each BAL aliquot, tended to decrease in each successive aliquot, becoming significant by the fourth aliquot.(ABSTRACT TRUNCATED AT 250 WORDS)
Although not conclusive, several lines of evidence suggest that cigarette smoking alters the respiratory tract's ability to defend itself from infection. Some subjects with chronic bronchitis have colonization of the lower respiratory tract with bacteria. Both patients with chronic respiratory disease and healthy smokers appear to have a higher frequency of respiratory infections and an increased severity of symptoms when infected. Children exposed passively to cigarette smoke have higher rates of respiratory illnesses. Yet the marked variability in the incidence of infection in the smoking population suggests that there are subtle factors that predispose some smokers to more risk of infection than others. Cigarette smoking is associated with alterations in mechanisms of the host defense system, even in asymptomatic individuals (summarized in Table 3). Ciliary function is impaired, mucous volume is increased, humoral response to antigens altered, and quantitative and qualitative changes in cellular components occur. Some of these alterations in host defense mechanisms are dose related; others revert to normal after smoking cessation. Yet, it is unknown if one or all of these alterations cause any significant compromise of host defense or if other factors, as yet unidentified, may be important. Answers to these questions await a more thorough elucidation of normal host defense function.
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A patient with incomplete Fanconi syndrome (no metabolic acidosis) presented with muscle weakness and biochemical and radiographic evidence of osteomalacia. Despite hypophosphatemia and increased PTH levels, circulating concentrations of 1,25-dihydroxyvitamin D were inappropriately low. Treatment with the vitamin D metabolite and hydrochlorothiazide was attended by enhanced calcium and phosphorus balance. Impaired vitamin D metabolism may play a role in the pathogenesis of osteomalacia in the Fanconi syndrome.