Black Hawk, please come down: reflections on a hospital's struggle to survive in the wake of Hurricane Katrina.
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Biomedical subjects
Publications and source records attributed to Bennett P deBoisblanc.
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It is not clear if low end-expiratory pressures contribute to ventilator-induced lung injury in large animals. We sought to determine whether ventilation with a low level of positive end-expiratory pressure (PEEP) worsens preexisting permeability lung injury in dogs. Lung injury was initiated in 20 mongrel dogs by ventilating with nebulized 3N hydrochloric acid until a lower inflection point (LIP) appeared on the respiratory system pressure-volume loop. One group of 10 dogs was then ventilated for 4 hours with PEEP set below the LIP (low PEEP), whereas the remaining group of dogs was ventilated for the same time period with similar tidal volumes but with PEEP set above the LIP (high PEEP). We found histologic evidence of reduced alveolar volumes in the low-PEEP animals. However, there were no differences in neutrophil infiltration, lung lobe weights, pulmonary capillary hemorrhage or congestion, or arterial endothelin-1 concentration between the 2 protocol groups. In conclusion, we were unable to demonstrate that ventilation with PEEP set below the LIP exacerbates hydrochloric acid-induced lung injury in dogs.
In summary, PDT is a bedside procedure that can be performed with very low morbidity by skilled practitioners. Established methods are undergoing constant evolution and we hope that technical adjuncts are improving patient safety. Evaluation of procedural modifications will require evaluation in randomized clinical trials.
Hemodynamic monitoring of critically ill patients, especially those who have ALI or ARDS, is a widely practiced compilation of techniques that largely have not been demonstrated to improve patient outcomes. Indeed, some techniques, such as use of the PAC, may actually be harmful. It seems unlikely that monitoring devices themselves are unreasonably risky to use. Rather it seems more likely that operator errors in gathering and interpreting hemodynamic data and in selecting the appropriate treatment strategies are the culprits. There is promise that ongoing clinical trials and better provider education will soon result in evidence-based recommendations for monitoring the circulation in this patient population.
OBJECTIVE: We hypothesized that an artificial neural network, interconnected computer elements capable of adaptation and learning, could accurately estimate pulmonary artery occlusion pressure from the pulsatile pulmonary artery waveform. SETTING: University medical center. SUBJECTS: Nineteen closed-chest dogs. INTERVENTIONS: Pulmonary artery waveforms were digitally sampled before conventional measurements of pulmonary artery occlusion pressure under control conditions, during infusions of serotonin or histamine, or during volume loading. Individual beats were parsed or separated out. Pulmonary artery pressure, its first time derivative, and the beat duration were used as neural inputs. The neural network was trained by using 80% of all samples and tested on the remaining 20%. For comparison, the regression between pulmonary artery diastolic pressure and pulmonary artery occlusion pressure was developed and tested using the same data sets. As a final test of generalizability, the neural network was trained on data obtained from 18 dogs and tested on data from the remaining dog in a round-robin fashion. MEASUREMENTS AND MAIN RESULTS: The correlation coefficient between the pulmonary artery diastolic pressure estimate of pulmonary artery occlusion pressure and measured pulmonary artery occlusion pressure was.75, whereas that for the neural network estimate of pulmonary artery occlusion pressure was.97 (p <.01 for difference between pulmonary artery diastolic pressure and pulmonary artery occlusion pressure estimates). The pulmonary artery diastolic pressure estimate of pulmonary artery occlusion pressure showed a bias of 0.097 mm Hg (limits of agreement -7.57 to 7.767 mm Hg), whereas the neural network estimate of pulmonary artery occlusion pressure showed a bias of -0.002 mm Hg (-2.592 to 2.588 mm Hg). There was no significant change in the bias of the neural network estimate over the range of values tested. In contrast, the bias for the pulmonary artery diastolic pressure estimate significantly increased with the increasing magnitude of the pulmonary artery occlusion pressure. During round-robin testing, the neural network estimate of pulmonary artery occlusion pressure showed suboptimal performance (correlation coefficient between estimated and measured pulmonary artery occlusion pressure.59). CONCLUSIONS: A neural network can accurately estimate pulmonary artery occlusion pressure over a wide range of pulmonary artery occlusion pressure under conditions that alter pulmonary hemodynamics. We speculate that artificial neural networks could provide accurate, real-time estimates of pulmonary artery occlusion pressure in critically ill patients.
Pulmonary arterial hypertension is common in patients with SSc. Fig. 1 shows the diagnostic and therapeutic approach to PAH in SSc. Doppler echocardiography may suggest the diagnosis, but RHC is necessary to confirm PAH and to measure vasoreactivity. Therapy is directed at the underlying connective tissue disease. Vasoreactive patients often benefit from therapy with high-dose calcium-channel [figure: see text] blockers, but most patients are not vasoreactive. Intravenous epoprostenol and oral endothelin-1 receptor antagonists improve hemodynamic measurements and symptoms in SSc-associated PAH. The therapy of right ventricular failure is focused on vasodilators, inotropes, and diuretics with careful attention to avoiding systemic hypotension. The scleroderma pulmonary-renal syndrome and the scleroderma renal crisis are distinct syndromes with different clinical presentations, histopathologic manifestations, treatments, and outcomes. The scleroderma pulmonary renal syndrome is an autoimmune vasculitis of kidney and lung associated with normal blood pressure. Treatment is supportive, and prognosis is dismal. In contrast, scleroderma renal crisis is associated with systemic hypertension, onion skinning of afferent arterioles, and response to ACE inhibition and renal replacement therapy. Pericardial effusions are common but only occasionally lead to tamponade. Esophageal dysmotility is often associated with aspiration, leading to pulmonary fibrosis, pneumonia, or ARDS. Diffuse bowel involvement may result in pseudo-obstruction, bacterial overgrowth, or malabsorption. Prokinetic agents, antibiotics, and parenteral nutrition may be required.
OBJECTIVES: To measure pulmonary capillary pressure and pulmonary artery occlusion pressures both during control conditions and during acute lung injury and to evaluate the effects of inotropic therapy and volume loading on these measurements after lung injury. DESIGN: Prospective, randomized, controlled laboratory trial. SETTING: University research laboratory. SUBJECTS: Eighteen heartworm-free mongrel dogs. INTERVENTIONS: Dogs were anesthetized (sodium pentobarbital, 30 mg/kg intravenously), intubated, and mechanically ventilated. A femoral artery and vein and the right external jugular vein were cannulated. After a median sternotomy, two pulmonary artery catheters were inserted via the jugular vein into the left and right lower lobar pulmonary arteries. Oleic acid (0.03 mL/kg) was administered to all dogs via the left pulmonary artery catheter, whereas the right lower lobe served as control. A baseline group of dogs received no further interventions, whereas two additional groups were given dobutamine (30-60 microg x kg(-1) x min(-1)intravenously) or saline boluses (1-2 L) before measurements were obtained after oleic acid lung injury. MEASUREMENTS AND MAIN RESULTS: Capillary pressure was estimated in both lower lung lobes by using the pulmonary artery occlusion method. Pulmonary capillary and pulmonary artery occlusion pressures were measured before and 2 hrs after oleic acid administration. Left lower lobar capillary pressure increased in all three groups, as did the difference between capillary pressure and pulmonary artery occlusion pressure. Capillary pressure in the control right lower lobe increased significantly only in the saline-loaded dogs, whereas the difference between the right-sided capillary and occlusion pressures increased only in the dogs given dobutamine. CONCLUSIONS: Oleic acid lung injury increases pulmonary capillary pressure independent of pulmonary artery occlusion pressure. The gradient between the two pressures was not significantly affected by volume loading or dobutamine infusion.