Fluid restriction and early extubation for successful liver transplantation.
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Biomedical subjects
Publications and source records attributed to K J Falke.
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Pulmonary artery hypertension associated with adult respiratory distress syndrome (ARDS) may increase microvascular filtration pressure by increasing pulmonary capillary pressure (PCP). To evaluate the potential to reverse this consequence of pulmonary artery hypertension, the effects of short-term vasodilator treatment were compared with prostaglandin E1 (PGE1) or nitroglycerin (NTG) on pulmonary hemodynamics and gas exchange. The two vasodilators were infused in ten patients with mild or moderate ARDS at a dosage rate achieving a 20% reduction of the mean arterial pressure. PCP was estimated by graphic analysis of the pulmonary artery occlusion curve, and continuous ventilation-perfusion (VA/Q) distributions were assessed using the multiple inert gas technique. At the given dosages both drugs induced equivalent reductions of the mean pulmonary artery pressure (PAP) from 28.2 +/- 3.6 to 23.7 +/- 3.2 with PGE1 and to 23.4 +/- 3.2 mmHg with NTG. The right atrial and pulmonary artery wedge pressure (PAWP) were also decreased to the same extent associated with the expected decrease in PCP from 17.4 +/- 2.6 to 15.1 +/- 3.3 with PGE1 and to 15.6 +/- 2.7 mmHg with NTG. The estimated PCP values were closely correlated with the values calculated according to Gaar's equation (r = 0.822. n = 23, P less than 0.001) with a regression close to the identity line. The contribution of pulmonary venous resistances to the resistance of the whole pulmonary vascular bed computed as the ratio (PCP- PAWP)/(PAP-PAWP) was 0.28 and remained unchanged during vasodilator infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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The inspiratory work exerted by an electromechanical lung model in drawing a 500 ml breath, was assessed by planimetry of pressure/volume loops for six commercial demand valve CPAP devices (Servo B and C from Siemens, EV-A and UV-2 from Dräger, the Puritan Bennett 7200 and the Engström ERICA) and compared to the loading of a conventional high flow CPAP system. The effect of trigger sensitivity and inspiratory pressure support on inspiratory work was also investigated in some cases. The lung model allowed for calibrated changes in compliance and airway resistance. In the non-assisted CPAP mode, all machines required slightly larger amounts of inspiratory work than the continuous flow CPAP system. Most machines were comparable in performance but the ERICA and the Servo B required up to 22% more work than the continuous flow CPAP system and represented the maximal increase of total work due to any given machine. The greater part of total inspiratory work was due to lung compliance and airway resistance, factors external to the machines. Halving compliance doubled the work and exchanging a 7 for a 9 mm i.d. endotracheal tube in the circuit increased work by about 3% regardless of machine. Decreasing trigger sensitivity from 0 to 2 cm H2O for the Servo B increased work by up to 24%. Using 5 cm H2O of inspiratory pressure support decreased work for all machines up to 36% maximally.(ABSTRACT TRUNCATED AT 250 WORDS)
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Extracorporeal circulation can cause lung damage, which would be especially counterproductive during extracorporeal gas exchange for the treatment of acute respiratory failure. To test the hypothesis that partial venovenous bypass with extracorporeal CO2-removal combined with low-frequency positive pressure ventilation (ECCO2R-LFPPV) can adversely affect lung fluid balance, extravascular thermal lung volume (ETV) and hemodynamics were assessed before, during and after ECCO2R-LFPPV in normal closed chest dogs. In series I dogs (n = 6) subjected to 10 h of ECCO2R-LFPPV, ETV did not change significantly from control (7.1 ml/kg +/- 0.99 SE) during or after bypass. Gravimetric extravascular lung water and lung histology after bypass were found to be normal. In series II dogs (n = 5), subjected to shorter periods of ECCO2R-LFPPV, ETV also remained unchanged. In contrast to previous reports using sheep, pulmonary arterial hypertension during bypass was not observed. Thus, ECCO2R-LFPPV was not associated with increased lung water, pulmonary hypertension or morphological lung changes under the conditions studied and does not seem to cause lung damage in normal lungs.
Understanding the mismatching of ventilation and perfusion (VA/Q) is of special interest in the intensive care setting because - given a stable cardiac output and a given inspiratory oxygen fraction - it allows one to explain certain essential respiratory problems in critically ill patients, namely hypoxemia and hypercarbia. Several different methods are available today for the evaluation VA/Q mismatching. Analysis of the PCO2 and PO2 in arterial and mixed venous blood and mixed expired gas yields information about the quality and the degree of the mismatching present. Calculation of the physiologic dead space (VD/VT) and venous admixture (QVA/QT) from the PCO2 and PO2 data allow the VA/Q mismatching to be quantified according to a three-compartment model of the lung. Determination of the arterial-alveolar nitrogen partial-pressure difference permits a more precise estimation of the true right-to-left shunt as a cause of arterial hypoxemia, but the measurement of the arterial PN2 remains a delicate procedure. The multiple inert gas elimination technique permits virtually continuous ventilation-perfusion distributions to be described over the whole range of VA/Q ratios and has contributed to explaining the pathophysiological mechanisms in various pulmonary diseases. This method, however, is technically very complex and hence will remain a sophisticated investigational tool. Scintigraphic approaches allow the description of regional topographic VA/Q distributions, but their application is still difficult in the intensive care setting.
Extracorporeal CO2-removal (EC-CO2-R) using a membrane lung system was applied for 12 and 20 days respectively in two young men with adult respiratory distress syndrome (ARDS). Neuropathological examination revealed only moderate hypoxic changes of unusual distribution. In the first case nerve cell loss in Sommer's sector of the hippocampus and focal incomplete necroses in both putamina were interpreted as the result of cardiac arrest at the onset of the disease rather than of chronic hypoxia. Findings in the second case were confined to nerve cell necroses of a minor degree in the cerebral cortex. Remarkably, the cerebellum was spared in both cases. Our observations suggest that EC-CO2-R was not associated with neuropathological findings which could be attributed specifically to this procedure.
We have developed and successfully used the first microprocessor-controlled monitors for collection of data on depth, heart rate, and body temperature of one fetal and five adult male freely swimming Weddell seals. Adult seals almost invariably experienced a prompt bradycardia at the start of each dive, and the mean heart rate during diving was significantly lower for dives greater than 20 min (P greater than 0.999). The heart rate was also significantly greater during the ascent portion of dives when compared with the descent portion (P greater than 0.95). The fetal seal experienced a slow onset of bradycardia when its mother dived; during diving the fetal heart rate decreased by an average of 1.1 beats/min for each minute of the dive. The fetal heart rate generally took approximately 10 min to recover to predive levels after its mother resurfaced to breathe. The body temperature of one adult male Weddell seal showed a decrease of greater than 1.5 degrees C from resting levels before dives of greater than 15 min were initiated and a drop of over 2 degrees C before dives of greater than 30 min duration.
Arterial hypoxemia and hence an increased venous admixture (QVA/QT) in the critically ill patient are mainly due to ventilation-perfusion mismatching in low VA/Q lung regions and/or to true intrapulmonary right-to-left shunt (QS/QT). In 16 intensive care patients the low VA/Q component was evaluated by determining the arterio-alveolar nitrogen partial pressure difference (aADN2). Employing a two compartment model of the lung, the fractional blood flow to a perfused and open, gas-filled but non-ventilated compartment (VA/Q = O) which represents all low VA/Q areas was calculated (QO/QT) from the aADN2 data. These results were compared with continuous ventilation-perfusion distributions obtained by using the multiple inert gas elimination technique. There was a close relationship between QO/QT and the perfusion fraction to lung regions with VA/Q ratios less than 0.6 (r = 0.855, p less than 0.001). The difference QVA/QT-QO/QT yielded a close estimation of the QS/QT value computed according to the SF6 retention (r = 0.952, p less than 0.001). We conclude that the measurement of the aADN2 and the calculation of the QO/QT together with the assessment of QVA/QT allow to estimate the contribution of low VA/Q areas and true right-to-left shunt to arterial hypoxemia at maintenance oxygen partial pressures.
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The effects of cardiac denervation on renal function during spontaneous breathing (SB) and controlled mechanical ventilation (CMV) were investigated in six mongrel dogs. Selective and reversible blockade of cardiac afferents was achieved by instillation of procaine 2% into the pericardium. Application of procaine 2% into the pericardium during SB caused a statistically significant depression of urine flow (-55%), of sodium (-64%) and potassium excretion (-42%), and of inulin (-21%) and PAH-clearance (-30%). After institution of CMV with a positive end-expiratory pressure (PEEP) of 10 cm H2O a further, statistically significant decrease in urine flow (-42%) and sodium excretion (-70%) and of the inulin (-15%) and PAH-clearance (-38%) was observed. Global hemodynamics, mean arterial pressure (MAP), central venous pressure (CVP), mean pulmonary artery pressure (MPAP) and cardiac index (CI) did not change significantly after installing procaine 2% into the pericardium during SB. After institution of CMV an increase in CVP and MPAP occurred whereas MAP and CI remained unchanged. During the following periods of spontaneous breathing first with blockade of cardiac afferents and later after washing out the procaine with NaCl 0.9% all parameters of renal function approached control levels as measured in the first period of spontaneous breathing without cardiac denervation.
Arterial blood gas tensions, pH, and hemoglobin concentrations were measured in four free-diving Weddell seals Leptonychotes weddelli. A microprocessor-controlled sampling system enabled us to obtain 24 single and 31 serial aortic blood samples. The arterial O2 tension (PaO2) at rest [78 +/- 13 (SD) Torr] increased with diving compression to a maximum measured value of 232 Torr and then rapidly decreased to 25-35 Torr. The lowest diving PaO2 we measured was 18 Torr just before the seal surfaced from a 27-min dive. A consistent increase of arterial hemoglobin concentrations from 15.1 +/- 1.10 to 22.4 +/- 1.41 g/100 ml (dives less than 17 min) and to 25.4 +/- 0.79 g/100 ml (dives greater than 17 min) occurred during each dive. We suggest that an extension of the sympathetic outflow of the diving reflex possibly caused profound contraction of the Weddell seal's very large spleen (0.89% of body wt at autopsy), although we have no direct evidence. This contraction may have injected large quantities of red blood cells (2/3 of the total) into the seal's central circulation during diving and allowed arterial O2 content to remain constant for the first 15-18 min of long dives. The increase of arterial CO2 tensions during the dive and the compression increase of arterial N2 tensions were also moderated by injecting red blood cells sequestered at ambient pressure. After each dive circulating red blood cells are oxygenated and rapidly sequestered, possibly in the spleen during the first 15 min of recovery.
Arterial blood nitrogen tensions of free-diving Weddell seals (Leptonychotes weddelli) were measured by attaching a microprocessor-controlled blood pump and drawing samples at depth to determine how these marine mammals dive to great depths and ascend rapidly without developing decompression sickness. Forty-seven samples of arterial blood were obtained from four Weddell seals during free dives lasting up to 23 minutes to depths of 230 meters beneath the sea ice of McMurdo Sound, Antarctica. Peak arterial blood nitrogen tensions of between 2000 and 2500 millimeters of mercury were recorded at depths of 40 to 80 meters during descent, indicating that the seal's lung collapses by 25 to 50 meters. Then arterial blood nitrogen tensions slowly decreased to about 1500 millimeters of mercury at the surface. In a single dive, alveolar collapse and redistribution of blood nitrogen allow the seal to avoid nitrogen narcosis and decompression sickness.
Tracheal and alveolar gas composition was studied by mass spectrometry in a patient with severe ARDS treated by low frequency positive pressure ventilation/extracorporeal CO2-removal (LFPPV-ECCO2R). Measured alveolar gas concentrations were compared with values derived from standard respiratory equations. As a result we found that during LFPPV-ECCO2R with a constant endotracheal O2-flow, alveolar gas composition cannot be predicted reliably from standard equations. The reasons for this finding are discussed. We conclude that monitoring of alveolar gas composition by mass spectrometry is of great value during LFPPV-ECCO2R if PAO2, P(A-a)O2 and Qva/Qt are to be determined correctly.
Extracorporeal CO2-removal (ECCO2-R) with low-frequency positive-pressure ventilation (LFPPV) may relieve the acutely injured lung from the burden and the risks of excessively high ventilatory minute volumes and airway pressures. It was the purpose of this study to document the evolution of lung function during clinical ECCO2-R with special emphasis on extravascular lung water. ECCO2-R was applied in a 21-year-old female patient suffering from severe post-traumatic infectious adult respiratory distress syndrome. The indication for ECCO2-R was based on the following findings: total static lung compliance 25 cm X cm H2O-1; arterial pO2 50 mm Hg with an inspiratory oxygen concentration of 100%; intrapulmonary right-to-left shunt over 50% of the cardiac output; and extravascular lung water 24 ml X kg-1 (normal 4.5-7 ml X kg-1). ECCO2-R was shown to provide satisfactory conditions for improving the above-mentioned abnormal parameters of pulmonary function. Pressure-limited low-frequency mechanical ventilation allowed successful management of several pneumothoraces with bronchopleural fistulas which occurred during the procedure. It is concluded that these complications of positive airway pressure would have led to the patient's death under the conditions of conventional mechanical ventilation.