Prospective evaluation of combined high-frequency ventilation in post-traumatic patients with adult respiratory distress syndrome refractory to optimized conventional ventilatory management

This study explores the value of combined high-frequency ventilation (CHFV) in a prospective clinical trial of 35 patients suffering from severe post-traumatic and/or septic adult respiratory distress syndrome (ARDS) who were refractory to conventional controlled mechanical ventilatory (CMV) support. The severity of ARDS was quantified by lung mechanics and gas exchange variables and the patients were classified on clinical grounds as well as on the basis of their respiratory index/pulmonary shunt relationship [RI/(Qsp/Qt)]. During the same time period as the CHFV study, data from these patients were compared to those from 88 ARDS patients who had quantitatively similar degrees of respiratory insufficiency, but who were treated only with controlled mechanical ventilation (CMV). The use of CHFV in the 35 CMV refractory patients resulted in an increase in expired tidal volume (VTE) by reducing the CMV inspired tidal volume (VTI) while increasing the volume component derived from high-frequency ventilation (HFV). This procedure appeared to reveal potentially salvageable ARDS patients who were refractory to CMV. In these patients, CHFV significantly reduced pulmonary mean airway pressure (Paw). The RI also decreased significantly and it was possible to reduce significantly the FIO2. In surviving ARDS patients treated with CHFV, an improvement in blood gases at reduced FIO2, without decreased cardiac output, was produced. The CHFV technique was used for less than or equal to 25 days and resulted in 23% survival of patients who were clinically and physiologically indistinguishable from the patients in the ARDS nonsurvivor group who were treated by CMV only. In surviving CHFV patients the decrease in Paw permitted a sustained, or increased, cardiac output with a rise in the oxygen delivery/oxygen consumption ratio, thus allowing for a higher PaO2 for any given level of pulmonary shunt.     

Ketanserin in the treatment of pulmonary hypertension after valvular surgery: a comparison with sodium nitroprusside

In a prospective randomized trial in patients with a history of preoperative pulmonary hypertension who were undergoing surgery for valvular replacement or annuloplasty, the effects of ketanserin (KET) (12 patients) and sodium nitroprusside (SNP) (14 patients) on the systemic and pulmonary circulation and pulmonary shunt fraction (Qsp/Qt) were studied in the immediate postoperative period. The agents were administered at the moment that pulmonary arterial pressure (PAP) tended to rise and cardiac output started to decrease. After administration, systemic arterial BP, PAP, systemic and pulmonary (PVR) vascular resistance, and right ventricular stroke work (RVSW) decreased significantly in both groups. The decrease in mean pulmonary arterial pressure (p less than .01), PVR (p less than .01), and RVSW (p less than .05) was significantly more pronounced in the KET than in the SNP group. Qsp/Qt significantly (p less than .001) increased in the SNP group, but significantly (p less than .05) decreased in the KET group; the response was significantly different between the two groups (p less than .001). In six patients, SNP converted pacemaker-dependent heart rate into a spontaneous rhythm, whereas this occurred in only one patient in the KET group. We concluded that KET, as opposed to SNP, reduces PVR without increasing Qsp/Qt in the lung, which is particularly advantageous in patients after valvular surgery.     

Arterial blood gas derived variables as estimates of intrapulmonary shunt in critically ill children

Oxygen transport data, prospectively collected from 52 critically ill children, were analyzed to determine whether any derived variable accurately estimated intrapulmonary shunt (Qsp/Qt). Arterial hemoglobin saturation was more closely correlated with Qsp/Qt than was PaO2, alveolar-arterial oxygen gradient, arterial mixed venous oxygen difference (C[a-v]O2), arterial/alveolar oxygen ratio, and the ratio of PaO2 to inspired oxygen (FIO2) (r = 0.8, p less than .0001). When C(a-v)O2 was normal, hemoglobin saturation became a very accurate (r = 0.96) assessment of Qsp/Qt. We conclude that various arterial blood gas derived variables do not accurately reflect Qsp/Qt in critically ill children. In these patients, a pulmonary artery catheter is needed to accurately assess intrapulmonary shunt.     

Unreliability of oxygen tension-based indices in reflecting intrapulmonary shunting in critically ill patients

Measurement of intrapulmonary shunting (Qsp/Qt), a widely used method for monitoring disturbances of pulmonary oxygen transfer in critically ill patients, involves calculation of arterial and mixed venous oxygen contents. In circumstances where mixed venous blood samples are not readily available, oxygen tension-based indices such as the alveolar to arterial oxygen tension differences (P[A-a]O2), arterial oxygen tension to alveolar oxygen tension ratio (PaO2/PAO2), PaO2 to FIO2 ratio (PaO2/FIO2) and respiratory index (RI) are widely utilized to reflect Qsp/Qt. Oxygen content-based indices such as the estimated shunt are not as widely utilized as the oxygen tension indices. In 75 critically ill patients in whom a pulmonary artery catheter was being utilized to augment clinical care, comparisons were made between Qsp/Qt and P(A-a)O2, PaO2/PAO2, PaO2/FIO2, RI, and estimated shunt to determine which index best reflected Qsp/Qt. Correlations between Qsp/Qt and estimated shunt were good (r = .94) and poor for the P(A-a)O2 (r = .62), PaO2/PAO2 (r = .72), PaO2/FIO2 (r = .71), and RI (r = .74). We conclude that there are no real substitutes for venous oxygen contents in critically ill patients. When pulmonary artery blood is not available for analysis, oxygen tension-based indices are unreliable reflectors of Qsp/Qt while the estimated shunt, an oxygen content-based index, provides a more reliable reflection of Qsp/Qt.     

Effect of hydralazine on intrapulmonary shunt

We compared the acute effects of bilateral arteriovenous may be related to levels of PvO2. The hydralazine-associated (p less than .05) decrease in resistance. Mixed venous oxygen fistulas to those of hydralazine infusion on hemodynamics and pulmonary gas exchange in dogs with pulmonary edema induced by administration of oleic acid. Oleic acid significantly (p less than .01) increased intrapulmonary shunt (Qsp/Qt) and pulmonary and systemic vascular resistance, and reduced cardiac output. Once the lesion stabilized, both opening the fistula and infusing hydralazine produced a similar and significant (p less than .01) increase in cardiac output, and a significant (p less than .05) decrease in resistance. Mixed venous oxygen tension (PvO2) closely followed the changes in cardiac output; however, PaO2 did not change. Qsp/Qt significantly (p less than .01) increased with the fistulas open and with hydralazine infusion. Closure of the fistulas or bleeding the animal at the end of the experiment reversed the changes in cardiac output and Qsp/Qt. The comparable increases in cardiac output and Qsp/Qt produced by opening the fistulas or infusing hydralazine may be related to levels of PvO2. The hydralazine-associated PvO2 increase indicates that this drug increased oxygen transport to the tissues even as Qsp/Qt became larger.     

Oxygen tensions and oxyhemoglobin saturations in the assessment of pulmonary gas exchange

We studied the theoretical basis for continuous monitoring of pulmonary gas exchange using arterial and mixed venous oximetry by examining the mathematical relationships between the calculated venous admixture (Qsp/Qt) and the ventilation-perfusion index, which is derived from oxyhemoglobin saturations. We compared this relationship with that between Qsp/Qt and its commonly used estimates: inspired oxygen concentration to arterial blood oxygen tension ratio, arterial to alveolar oxygen tension ratio, and alveolar-arterial oxygen tension difference. The relationship between Qsp/Qt and the oxygen tension-based indices is nonlinear and substantially influenced by changes in inspired oxygen concentration and arteriovenous oxygen content difference. Therefore, it is inaccurate within the clinically acceptable range of arterial blood oxygenation. In contrast, calculation of ventilation-perfusion index from arterial and mixed venous blood oxyhemoglobin saturations provides a linear estimate of Qsp/Qt that is minimally affected by alterations in inspired oxygen concentration or oxygen uptake and, therefore, will allow accurate continuous assessment of pulmonary gas exchange.     

Cardiovascular adjustments and gas exchange during extreme hemodilution in humans

OBJECTIVE: To examine the cardiovascular adjustments and pattern of gas exchange that occur during hemodilution. DESIGN: Nonrandomized prospective study. SETTING: Operating room in a university hospital. PATIENTS: Seven patients undergoing elective aortocoronary artery bypass surgery. INTERVENTIONS: Before initiating cardiopulmonary bypass, the patients' hematocrit levels were decreased to approximately 15%. This hemodilution was done by removing a sufficient amount of autologous blood from the aortic cannula and replacing it with a sufficient amount of crystalloid solution. After the discontinuation of cardiopulmonary bypass, measurements were made at a hematocrit of approximately 15%. Then, after autologous blood infusion, measurements were made at a hematocrit of 20%, followed by more blood infusion to approximately 25% with repeat measurements. MEASUREMENTS AND MAIN RESULTS: The following measurements were made before hemodilution and then at all three levels of hemodilution: heart rate, mean arterial pressure (MAP), right atrial pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. From these measurements, the following derived variables were calculated: cardiac index, systemic vascular resistance, and pulmonary vascular resistance. From measurements of arterial oxygen content, mixed venous oxygen content, and cardiac output, intrapulmonary shunt (Qsp/Qt), oxygen uptake (VO2), oxygen extraction ratio, and oxygen delivery (DO2) were derived. The MAP was lowest (57 +/- 3 [SD] vs. 92 +/- 3 mm Hg) at the lowest hematocrit. The cardiac index was highest (4.0 +/- 0.3 vs. 2.3 +/- 0.6 L/min.m2) at the lowest hematocrit. DO2 was lowest at the lowest hematocrit but VO2 remained constant at all levels of hematocrit. The oxygen extraction ratio increased as hematocrit decreased. With progressive increases in hematocrit, DO2 increased and Qsp/Qt decreased. CONCLUSIONS: The data suggest that, during hemodilution, tissue autoregulation of VO2 and utilization are not impaired, but gas exchange function (Qsp/Qt) is impaired.     

Reduced venous admixture in hemorrhagic hypovolemia: maintenance of arterial oxygenation by selective pulmonary vascular collapse

In nine anesthetized and ventilated swine, a microcomputer calculated cardiac output, venous admixture (Qsp/Qt) and physiologic deadspace (VD/VT) every 20 sec, utilizing dual oximetry and a gas exchange analyzer. After lung injury with ethchlorvynol (ECV), animals were bled 40% blood volume over 40 min. Mean cardiac output decreased 7.0 to 2.2 L/min (p less than .05) accompanied by a decrease in mean Qsp/Qt from 0.28 to 0.14 (p less than .05) and an increase in mean VD/VT from 0.39 to 0.54 (p less than .05). Arterial Hgb saturation (Sao2) increased from 88 +/- 7% to 90 +/- 6%. On regression of all data points for each variable, Qsp/Qt had a positive correlation with cardiac output (r = .90), mean arterial pressure (MAP, r = .87), mean pulmonary artery pressure (MPAP, r = .86), and mixed venous Hgb saturation (Svo2, r = .89, p less than .001). VD/VT had an inverse correlation with cardiac output (r = -.90), MAP (r = -.82), Qsp/Qt (r = -.83), MPAP (r = -.77), and Svo2 (r = -.92, p less than .001). The decreasing Qsp/Qt and increasing VD/VT, with decreasing pulmonary perfusion pressures, were attributed to selective loss of perfusion to alveoli with low ventilation/perfusion ratios.     

Assessing pulmonary function in acute respiratory insufficiency: a clinical charting sheet

A sheet to chart the clinical respiratory variables relevant to acute respiratory insufficiency (ARI) therapy is presented. The chart permits plotting shunt fraction (Qsp/Qt) and efficiency (E or 1--Qsp/Qt) vs. load (L). L is the volume of oxygen (combined and dissolved) that would be exchanged in the lung per minute, if venous blood became fully equilibrated with alveolar gas. L relates cardiac output (Qt), hemoglobin concentration, alveolar oxygen tension, venous oxygen saturation and tension, and the oxygen-hemoglobin combining and oxygen solubility constants. Oxygen consumption (VO2) isopleths are added to the sheet (VO2 = L X E). Qt, VO2, and hence L are indexed per m2 (body surface area), and the approximate normal VO2 range is indicated. Using this sheet hopefully simplifies the correlation of complex pulmonary oxygen exchange data and enhances information recognition and analysis. It provides special help in determining the optimal PEEP in difficult ARI cases. To illustrate its use, a case is detailed.     

Continuous, in vivo pulmonary venous admixture from fiberoptically measured hemoglobin saturations

In six anesthetized swine, pulmonary venous admixture (Qsp/Qt) was calculated by four methods: a) Qsp/Qt 1, fiberoptically measured arterial and mixed venous Hgb saturation (SaO2 and SvO2), PaO2 and PvO2 derived from saturations; b) Qsp/Qt 2, fiberoptically measured SaO2 and SvO2, PaO2 and PvO2 measured by blood gas analysis; c) Qsp/Qt 3, PaO2 and PvO2 measured by blood gas analysis, SaO2 and SvO2 derived from tensions; d) Qsp/Qt 4, SaO2 and SvO2 measured by bench oximetry, PaO2 and PvO2 derived from saturations. Input from the fiberoptic catheters was fed into a computer programmed to calculate Qsp/Qt 1 every 20 sec. Fifty-eight of these values were compared with simultaneously calculated Qsp/Qt 2, 3, and 4. There was no difference between fiberoptic and derived SaO2 or fiberoptic and cooximetric SvO2. Correlations and slopes for Qsp/Qt 1 with Qsp/Qt 2, 3, and 4 were significant (p less than .05). Comparing mean differences, Qsp/Qt 1 was significantly different only from Qsp/Qt 3 (p less than .01). We conclude that dual oximetry reliably tracks Qsp/Qt.     

Hemodynamic profile in severe ARDS: results of the European Collaborative ARDS Study

Objective: Although the acute respiratory distress syndrome (ARDS) was identified as long as 30 years ago, potential therapeutic objectives have been defined from small series rather than large trials. Moreover, relationships between ARDS and hemodynamics are unclear. The European Collaborative ARDS Study was designed to identify factors influencing the pathogenesis, severity, and prognosis of ARDS. Analysis of the hemodynamic profiles collected during this study and of their contribution to the above-mentioned facets of ARDS is the focus of the present report. Design: Prospective clinical study. Setting: 38 European intensive care units (ICUs). Patients and methods: We collected 2758 sets of data from 586 patients, including baseline data, data on proven or suspected causes of ARDS differentiating direct and nondirect lung injury, and data on baseline status including multiple organ dysfunction (MOD) with differentiation of primary ARDS from ARDS secondary to severe systemic disorders. Events during follow-up were also recorded, including whether the acute respiratory failure did or did not improve after 24 h (groups A and B, respectively). When available, hemodynamic data were recorded at enrollment (day 0), on days 1–3, 7, 14, and 21, and at discharge or at the time of death in the ICU. Results: Although the rate of preexisting disease and the nature and rate of complications varied widely among etiologic categories, differences in the hemodynamic profile occurred only between primary and secondary ARDS. Both at inclusion and during the course of the illness, variables that were used to investigate Va/Q mismatch [arterial oxygen tension (PaO₂, arterial oxygen saturation, right-to-left shunt, and the PaO₂/fractional inspired oxygen (FIO₂) ratio] predicted survival. High pulmonary artery pressure (PAP) and low systemic artery pressure (SAP) were also related to the prognosis. In the logistic regression model including hemodynamic and oxygen-related variables, however, the only independent predictors of survival were the ratio of right over left ventricular stroke work (RVSW/LVSW) and the PaO₂/FIO₂ ratio at admission. On day 2, the best prognostic model included: age [odds ratio (OR) = 1.04, p = 0.0004], opportunistic pneumonia as the cause of ARDS (OR = 3.2, p = 0.03), existence of MOD (OR = 1.9, p = 0.03), PaO₂/FIO₂ (OR = 0.96, p = 0.005), and RVSW/LVSW (OR = 25, p = 0.02). A high RVSW/LVSW ratio, high systolic PAP, low diastolic SAP, and low PaO₂/FIO₂, and increased right atrial pressure were negative prognostic indicators during follow-up. Conclusion: In addition to the cause of ARDS and the early time-course of lung function, a high systolic PAP and a low diastolic SAP were strong independent indicators of survival. Received: 6 November 1997 Accepted: 8 July 1998     

高频振动通气在急性呼吸窘迫综合征治疗中的作用

目的　评估高频振动通气 (high frequencypercussiveventilation ,HFPV)在成人ARDS治疗中的有效性和安全性 ,探索ARDS治疗的新途径。方法　临床观察 93例ICU条件下使用HFPV的ARDS病人 ,对常规通气 (conventionalventilation ,CV)和HFPV下的PaO2 /FiO2 、PaCO2 、DO2 、VO2 、Qs/Qt、PEEP/CPAP、PAWP等氧代谢、血流动力学指标和呼吸参数的变化进行统计分析。结果　 93例病人中 ,存活 6 6例 ,死亡2 7例 ,死亡率为 2 9 0 % (除外 7例未死于ICU者 ,实际死亡率为 2 1 5 % )。使用HFPV前后PaO2 /FiO2 、PaC O2 、DO2 、VO2 、Qs/Qt的变化为 (77 6± 2 0 0 )和 (2 0 8 7± 70 8)、 (471 2± 114 7)和 (6 0 1 3± 14 0 9)、(10 7 6± 34 3)和 (14 6 4± 2 3 3)、 (35 7± 2 0 5 )和 (2 4 5± 6 5 ) (P <0 0 5 )。X ray胸片双肺阴影减轻或消失 ,同时可看到病人鼻腔口腔有不等量的混浊液体从呼吸道溢出。结论　HFPV在ARDS治疗中是有效和安全的。临床应用HFPV能明显改善氧代谢 ,提高PaO2 /FIO2 。早期应用和合理化管理能明显降低ARDS的病死率     

Sequential cardiorespiratory patterns in septic shock

Sequential hemodynamic and oxygen transport monitoring was performed in 33 patients with septic shock to define the temporal pattern of physiologic events. Measurements taken over a 24-h period before the hypotensive crisis, defined as the lowest initial mean arterial pressure (MAP), were compared to those taken during the 48 h thereafter. In the 24-h period before the hypotensive crisis, there were increases in cardiac index (CI), central venous pressure (CVP), pulmonary capillary wedge pressure (WP), pulmonary vascular resistance index (PVRI), and pulmonary shunt (Qsp/Qt), but decreases in MAP, systemic vascular resistance index (SVRI) and oxygen delivery (Do2). When sequential cardiorespiratory patterns were examined, oxygen consumption (VO2) fell transiently to significantly low values 12 h before as well as at the time of the hypotensive crisis. SVRI fell and CI rose to values significantly different from normal in the 4 h before the low MAP. During the subsequent 48 h after the hypotensive crisis, CI, CVP, WP, PVRI and Qsp/Qt remained elevated. Values for MAP, SVRI, DO2, and VO2 were significantly reduced. These results demonstrate the existence of antecedent cardiorespiratory alterations that precede the hypotensive episode in septic shock and suggest that flow maldistribution in the systemic circulation is an early event with possible pathogenic significance.     

Sequential cardiopulmonary changes after oleic-acid injury in dogs

Oleic acid (OA) administered to experimental animals increases pulmonary vascular permeability and produces a condition that pathophysiologically resembles adult respiratory distress syndrome (ARDS) in humans. The present study examined the sequence of cardiorespiratory changes after OA infusion and their similarity to ARDS. After a baseline period, mechanically ventilated and anesthetized dogs were administered 0.18 ml/kg body weight OA into the pulmonary artery while hemodynamic and respiratory changes were monitored. After OA infusion, cardiac output fell by 39%, paralleling a 26% decrease in heart rate. Pulmonary vascular resistance (PVR) increased over 200% without a change in pulmonary capillary wedge pressure and initially without an increase in pulmonary artery pressure (PAP). Within 30 min after OA infusion, dynamic pulmonary compliance (Cdyn) was reduced 32% from baseline values, with a coincident increase in the alveolar-arterial PO2 gradient (P[A-a]O2) but without a significant change in the pulmonary shunt fraction (Qsp/Qt). This was followed in 30 min by a further 27% decrease in Cdyn, with a Qsp/Qt in excess of 50%. Both the hematocrit and hemoglobin concentration increased progressively after OA infusion, without a change in plasma protein concentration. The results suggest that the sequence of cardiopulmonary changes after OA injury are initially marked by a decrease in Cdyn and an increase in PVR and P(A-a)O2. This is followed by an increase in Qsp/Qt, PAP, hemoglobin concentration and PCO2. The changes appear related to progressive flooding of the alveolar air space with edema fluid. These findings parallel the sequential cardiorespiratory changes reported to occur in ARDS.     

Effect of increasing inspired oxygen concentration on hemodynamics and regional blood flows

Previous reports suggest that in response to increasing FIO2, peripheral resistance increases, cardiac output falls, and regional blood flow decreases. This study examined the influence of varying FIO2 on pulmonary and systemic vascular resistances (PVR, SVR), cardiac output, ventricular work, and regional blood flows in ten anesthetized Yorkshire white pigs. Each animal served as its own control, and was exposed to varying FIO2 in random order. PCO2 was maintained at 40 +/- 5 torr and body temperature at 38.5 degrees C. Heart rate, systemic arterial pressure, pulmonary artery pressure (PAP), pulmonary capillary wedge pressure, thermodilution cardiac output, and blood flows in the femoral, carotid, renal and superior mesenteric arteries were measured at each FIO2. SVR, PVR, left and right ventricular stroke work (LVSW, RVSW) were calculated. One-way analysis of variance-randomized block design (F-test) showed significant decreases in PAP, PVR, and RVSW with increased FIO2. No change was noted in regional flows, cardiac output, SVR, or LVSW. We conclude that in this animal model administration of oxygen up to an FIO2 of 1.0 had no adverse effect on hemodynamic performance.     

Oxygen delivery-dependent oxygen consumption in acute respiratory failure

OBJECTIVE: To investigate whether oxygen consumption (VO2) is dependent on oxygen delivery (DO2) in adult respiratory distress syndrome (ARDS) and non-ARDS acute respiratory failure. DESIGN: Intervention study of a consecutive sample of patients admitted to the ICU with the diagnosis of acute respiratory failure. SETTING: Tertiary care center. PATIENTS: Thirteen consecutive patients with a diagnosis of ARDS and 11 with a diagnosis of respiratory failure not due to ARDS. Patients were monitored with an oximetric pulmonary artery catheter and mechanically ventilated. INTERVENTIONS: DO2 was decreased by the application of positive end-expiratory pressure (PEEP) (20 cm H2O), and subsequently increased by an iv infusion of dobutamine (10 micrograms/kg.min). RESULTS: After the application of PEEP, DO2 decreased significantly in both groups. However, VO2 decreased significantly (p less than .01) only in the ARDS group. When dobutamine was infused, DO2 increased significantly (p less than .01) in both groups, but VO2 increased only in ARDS patients. DO2 correlated significantly with VO2 both in ARDS (r2 = .81, p less than .01) and in non-ARDS (r2 = .38, p less than .05) patients. The correlation coefficient was significantly higher for ARDS than for non-ARDS patients. Comparing the slopes of the regression lines, a stronger dependency of VO2 on DO2 was found in ARDS than in non-ARDS respiratory failure (p less than .001). The oxygen extraction ratio correlated with DO2 in non-ARDS patients (r2 = .49, p less than .05), but not in ARDS patients. CONCLUSIONS: VO2 is dependent on DO2 over a wide range of DO2 values in acute respiratory failure. This dependency phenomenon is much stronger in ARDS than in respiratory failure due to other causes. Due to the abnormal dependency of VO2 on DO2, changes in the oxygenation status may not be reflected by changes in mixed venous oxygen saturation in ARDS.     

Stable and reproducible porcine model of acute lung injury induced by oleic acid

BACKGROUND AND METHODS: Previous studies on acute lung injury induced with oleic acid did not attempt to limit the influence of secondary changes on pulmonary circulation, and cardiopulmonary variable data were only collected and processed intermittently. Our study was designed to continuously monitor the following variables in five swine: systemic and pulmonary pressure; mixed venous oxygen saturation (SVO2) and arterial oxygen saturation (SaO2); minute oxygen consumption and CO2 production before, during, and for 4 hr after the infusion of oleic acid. A personal computer was programmed to produce 20-sec updates of deadspace ratio (VD/VT), venous admixture (Qsp/Qt), pulmonary (PVR) and systemic vascular resistance (SVR), and cardiac output (Qt) from these data. RESULTS: During the oleic acid infusion, there were increases in PVR, SVR, heart rate (HR), mean pulmonary arterial pressure (MPAP), Qsp/Qt, and VD/VT, and a decrease in Qt, SaO2, and SVO2. Thirty minutes after the oleic acid infusion, there was a further increase in HR, Qsp/Qt, and VD/VT, while MPAP, PVR, and SVR gradually decreased to pre-oleic acid infusion levels. No further decrease in SaO2, SVO2, and Qt was observed during that time. After the 30-min period, there was no further change in the cardiopulmonary variables. CONCLUSION: Our method of continuous monitoring was able to demonstrate in swine both the dynamic changes during, and stability after, the oleic acid infusion.     

Oxygen transport in adult respiratory distress syndrome and other acute circulatory problems: relationship of oxygen delivery and oxygen consumption

OBJECTIVE: To evaluate the evidence that oxygen consumption (VO2) is pathologically dependent on oxygen delivery (DO2). DATA SOURCES: Studies published since 1972 with their relevant bibliographies and computerized search of MEDLINE. STUDY SELECTION: All clinical papers reporting the relationship of: VO2 to DO2 in the adult respiratory distress syndrome (ARDS), sepsis, other critically ill patients, and normal individuals; cardiac output determined by measured VO2 to calculated VO2 from the arterial-mixed venous oxygen difference; blood lactate to DO2; and selected basic science studies. DATA EXTRACTION: Study quality was assessed and all pertinent data were summarized. RESULTS OF DATA EXTRACTION: Normal individuals display physiologic dependence of VO2 at very low levels of DO2 (330 mL/min.m2). Pathologic dependence of VO2 on DO2 entails two concepts: a) VO2 varies directly with DO2 over a wide range of DO2 and b) of particular import, tissue oxygen extraction is compromised. This pathologic supply dependence was initially identified in patients with ARDS; subsequently, it has been demonstrated in patients with sepsis and in a variety of other critically ill individuals. There are substantial, but not uniform, data documenting this dependence of VO2 on DO2 in ARDS. In some studies, this relationship correlates best with increased lactate concentrations. However, increased blood lactate concentrations do not accurately track other evidence of tissue hypoxia. Some researchers have attributed the finding of this supply dependency to artifact, when VO2 is determined by the arterial-mixed venous oxygen difference. However, when these methods are compared, the correlation is excellent. Others have raised the concern that appreciable changes in VO2, even over short periods of time, may result in physiologic increases in DO2. However, when "control" groups have been contemporaneously compared with patients with ARDS using the same methodology, they have not shown supply dependency. Interwoven throughout the studies reviewed is overwhelming and uniform evidence that both mixed venous oxygen tension (PVO2) and mixed venous oxygen content (CVO2) correlate poorly with cardiac output, DO2, or VO2. The inconsistencies in identifying pathologic DO2 dependency may well reflect the unknown variables that exist in patients with ARDS, perhaps better labeled, multiple organ system failure. CONCLUSIONS: Pathologic dependence of VO2 on DO2, especially the inability to increase tissue oxygen extraction, is present in most patients with ARDS and many other critically ill individuals. PVO2 and CVO2 are both unreliable indicators of cardiac output, DO2, or VO2.     

Effect of high-frequency ventilation on histamine-induced lung injury in dogs

We compared the effects of high-frequency oscillation (HFO) and conventional mechanical ventilation (CMV) on dynamic lung compliance (Cdyn), venous admixture (Qsp/Qt), cardiac output, and total lung resistance (RL) in seven mongrel dogs with histamine-induced lung injury. Baseline measurements during CMV were followed by iv infusion of histamine at 100 micrograms/min. Cdyn, Qsp/Qt, cardiac output, and RL were measured in triplicate during CMV and then during HFO. Subsequently, at least one complete set of measurements was recorded again on CMV. During HFO, animals were ventilated at 15 Hz with a tidal volume of 70 to 80 ml. CMV was delivered at 15 to 18 breath/min with a tidal volume of 15 ml/kg. Histamine infusion produced a marked fall in Cdyn, a variable rise in RL, an inconsistent but usually progressive rise in Qsp/Qt, and hypotension. A period of ventilation with HFO made no difference in the Cdyn, Qsp/Qt, or cardiac output changes produced by histamine infusion.     

Pulmonary extravascular water in patients with acute respiratory failure

The purpose of the investigation was to study pulmonary extravascular water levels and pulmonary vascular permeability (PVP) in the pathogenesis of acute respiratory failure (ARF)/acute respiratory distress syndrome (ARDS). Twenty-nine patients with ARF/ARDS and 10 healthy volunteers were examined. Central hemodynamics and oxygen transport were explored, by using a Swan-Ganz catheter. Intrathoracic volemic parameters were studied by the transpulmonary thermodilution technique. PVP was assessed by the pulmonary 67Ga-labelled transferrin leakage index. Plasma colloid osmotic pressure (COP) was measured on an osmometer. In most patients with ARF/ARDS, the pulmonary extravascular water index (PEVWI) was found to be higher (mean 16.9 +/- 1.5 ml/kg). At the same time its value was not greater than 10 ml/kg in 7 (24%) of 29 patients. There were no correlations between PEVWI and PaO2/FiO2 and between pulmonary extravascular water and AaDO2. The PVP index (PVPI) measured by transpulmonary thermodilution was 3.2 +/- 0.2, it being normal in 13 (45%) out of 29 patients. The pulmonary 67Ga-transferrin leakage index was higher in all the patients than in healthy individuals (23.2 +/- 2.9 x 10(-3) vs 5.7 +/- 9.9 x 10(-3)) and correlated with PaO2/FiO2 (r = 0.71; p = 0.01). In patients with ARF/ARDS, COP was lower (19.9 +/- 0.7 mm Hg). There were correlations between COP and PEVWI (r = -0.34; p = 0.01), COP and PVPI (r = -0.40; p = 0.044), COP and PaO2/FiO2 (r = 0.35; p = 0.02). PEVWI correlated with the COP-pulmonary wedge pressure gradient (r = -0.45; p = 0.0024). Hypoxemia correlated with intrapulmonary shunt (Qs/Qt). There was no relationship between Qs/Qt and PEVWI in the group as a whole. According to the ratio of Qs/Qt to PEVWI, the patients were divided into 2 groups. Group 1 comprised 11 patients with the ratio < or = 2; Group 2 included 18 patients with the ratio > or = 2, i.e. with an unproportional shunt enlargement as to the severity of pulmonary edema. A correlation between Qs/Qt and PEVWI was found in both groups: r = 0.82; p = 0.001 with the ratio < or = 2 and r = 0.48; p = 0.04 with the ratio > or = 2. Diverse causes of shunt formation were histologically detected. Thus, pulmonary edema was not identified in 24% of patients with ARF/ARDS. Arterial hypoxemia is associated with the increase in the shunt, but, in a portion of patients, the shunt was caused with atelectasis unassociated with pulmonary edema. Increased pulmonary permeability for transferrin is detectable in ARF/ARDS irrespective the severity of pulmonary edema. The pathogenetic features of lung lesions should be taken into account while choosing a treatment for ARF/ARDS.