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.     

Oxygenation during ventilation by high-frequency oscillation in dogs with acute lung injury

The effect of ventilation by high-frequency oscillation (HFO) on gas exchange in the abnormal lung is not well defined. In this study the efficiency of oxygenation by HFO (stroke volume 2.5 to 3.5 ml/kg, frequency 15 to 30 Hz) and by conventional mechanical ventilation (CMV) (tidal volume 15 to 20 ml/kg, frequency 8 to 15 breath/min) was compared in dogs with acute lung injury. Sixteen normal animals were studied under general anesthesia (halothane) on day 0 (control) and then injected intraperitoneally with 10 mg/kg of paraquat in divided doses over 3 consecutive days. Eight dogs were restudied on day 4 (moderate lung injury) and the other eight dogs on day 8 (more severe lung injury). With acute lung injury there was a progressive decrease in total lung capacity, decrease in lung compliance, and hypoxemia. In the moderate lung injury group, at equal alveolar ventilation, HFO resulted in a significant improvement in oxygenation (PaO2 95 to 104 torr) with a corresponding increase in mean lung volume when compared with CMV. In the severe lung injury animals, there were no significant differences in oxygenation or in mean lung volume between HFO and CMV.     

Frequency and percent inspiratory time for high-frequency jet ventilation

A variety of frequencies and percent inspiratory times (%TI) may be used for high-frequency jet ventilation (HFJV). Five physiologic criteria were used to evaluate various combinations of frequency and %TI: mean airway pressure (Paw), cardiac output, PaCO2, PaO2, and intrapulmonary shunt (Qsp/Qt). At a constant drive pressure, the effects of frequencies of 100, 200, 300, 450, 600, 750, and 900 cycle/min at %TI values of 20%, 30%, and 40% of the respiratory cycle were evaluated and compared with the effects of controlled mechanical ventilation (CMV) at 8 to 12 breath/min. Only at 200 cycle/min and 20% TI, were Paw, cardiac output, PaCO2, PaO2, and Qsp/Qt all the same as the CMV values. At 100 cycle/min and 20% TI, CO2 elimination increased without significantly affecting Paw, cardiac output, PaO2, or Qsp/Qt. These data suggest that HFJV might compromise one or more physiologic variables at certain combinations of frequency and %TI. Therefore, at a fixed drive pressure, there appears to be a narrow range of HFJV ventilator settings that should be considered.     

Eucapnic hyperventilation-induced bronchoconstriction in rabbits.

We examined whether eucapnic hyperventilation with dry air produces the bronchoconstriction in anesthetized, non-sensitized rabbits and in ovalbumin sensitized rabbits. Eucapnic hyperventilation challenge with dry air containing 5% CO2 at room temperature was performed with 4 non-sensitized and 7 sensitized rabbits by mechanical ventilation for 15 min (120 breaths/min, 7 ml tidal volume/kg body weight). Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and 0, 5, 15, and 30 min after hyperventilation. In non-sensitized rabbits, RL and Cdyn did not change significantly. However, in sensitized rabbits, RL increased maximally by 48.9% +/- 9.0% at 5 min, and then decreased to the baseline level at 30 min after challenge. Cdyn decreased maximally by 12.5% +/- 3.5% at 15 min after challenge. These changes were significantly different from the baselines (p < 0.05). Furthermore, to investigate the role of histamine on hyperventilation-induced bronchoconstriction (HIB) in sensitized rabbits, we performed the hyperventilation challenges in 5 sensitized rabbits with the pretreatment of H1-receptor antagonist (chlorpheniramine, 1 mg/kg, i.v.) and found that the maximum increment of RL was suppressed to 24.2% +/- 7.4% of the control, which was significantly lower than the maximal RL in nontreated sensitized rabbits (p < 0.05). We concluded that HIB occurs only in sensitized rabbits and that histamine may play an important role in the development of HIB in sensitized rabbits.     

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.     

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.     

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.     

Systemic cardiac output and distribution during high-frequency oscillation

High-frequency oscillation (HFO) appears to be an alternate, less traumatic mode of ventilating surfactant-deficient patients, because conventional (mechanical) pressure-limited ventilation (CMV) compromises cardiac function at high mean airway pressures. We compared systemic cardiac output and its distribution during HFO and CMV in ten adult rabbits rendered surfactant deficient by repeated pulmonary saline lavage. Cardiac output and organ blood flow were measured using the radionucleotide-labeled microsphere technique during ventilation at a mean airway pressure of 15 cm H2O and an inspired oxygen concentration of 100%. Both cardiac output and organ perfusion were similar during both modes of ventilation.     

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.     

Mechanical ventilation with permissive hypercapnia increases intrapulmonary shunt in septic and nonseptic patients with acute respiratory distress syndrome

OBJECTIVE: To compare the effects of conventional mechanical ventilation with low-volume, pressure-limited ventilation (LVPLV) and permissive hypercapnia on ventilation-perfusion (V/Q) distributions in patients with acute respiratory distress syndrome. We hypothesized that the advantageous cardiopulmonary effects of LVPLV would be greater in patients with sepsis than in those without sepsis. PATIENTS AND INTERVENTIONS: Twenty-two patients with acute respiratory distress syndrome were studied (group 1: 12 patients with hyperdynamic sepsis; group 2: 10 nonseptic patients). Intrapulmonary shunt (Qsp/Qt) (percentage of cardiac output), perfusion of "low" V/Q areas (percentage of cardiac output), ventilation of "high" V/Q areas (percentage of total ventilation [VE]), and deadspace ventilation (percentage of VE) were calculated from the retention/excretion data of six inert gases. Data were obtained during conventional mechanical ventilation and during LVPLV. MEASUREMENTS AND MAIN RESULTS: In group 1, LVPLV increased PaCO(0)rom 38 +/- 6 torr (5.1 +/- 0.8 kPa) to 61 +/- 12 torr (8.1 +/- 1.6 kPa). Qsp/Qt increased from 28 +/- 16% to 36 +/- 17%, whereas Pao2 (84 +/- 15 torr [11.1 +/- 2.0 kPa] vs. 86 +/- 21 torr [11.5 +/- 2.8 kPa]) and Qt (10.6 +/- 2.3 vs. 11.5 +/- 2.5 L x -1) remained unchanged and PVO(2) (40 +/- 4 [5.3 +/- 0.5 kPa] vs. 49 +/- 6 torr [6.5 +/- 0.3]) increased. In group 2, LVPLV increased PaCO(2) from 38 +/- 6 torr (5.1 +/- 0.8 kPa) to 63 +/- 11 torr (8.4 +/- 1.5 kPa). For Qsp/Qt (24 +/- 9% to 34 +/- 16%), the increase was not significant, whereas Qt (7.4 +/- 1.8 vs. 10.2 +/- 2.2 L x -1), PVO(2)(38 +/- 4 torr [5.1 +/- 0.5 kPa] vs. 50 +/- 6 mm Hg [6.7 +/- 0.8 kPa]), and PaO(2) (89 +/- 16 torr [11.9 +/- 2.1 kPa] vs. 98 +/- 19 torr [13.1 +/- 2.5 kPa]) increased. In both groups, the scatter of perfusion distribution (log SDQ) was greater than expected for normal subjects but was not different between the groups or altered by the treatments. CONCLUSIONS: In patients with acute respiratory distress syndrome, LVPLV with permissive hypercapnia, tended to increase Qsp/Qt, without a concomitant decrease of PaO(2). This occurs because, although atelectasis and increased shunt result from the low ventilatory volume, the effects on PaO(2) are offset by increased PVO(2) resulting from the hypercapnic stimulation of cardiac output. This result was independent of the presence or absence of sepsis.     

Partial liquid ventilation combined with kinetic therapy in acute respiratory failure in piglets

OBJECTIVE: To investigate the effect of the combination of kinetic therapy (KT) with partial liquid ventilation (PLV) on gas exchange, lung mechanics and hemodynamics in acute lung injury (ALI). DESIGN: Prospective, randomized, controlled pilot study. SETTING: University research laboratory. SUBJECTS: Eleven piglets weighing 8.3+/-0.9 kg. INTERVENTION: ALI was induced by the infusion of oleic acid (0.08 ml/kg) and repeated lung lavages with 0.9% NaCl (20 ml kg(-1)). Thereafter the animals were randomly assigned either for PLV or a combination of PLV with KT (PLV/KT). The dose of perfluorocarbon administered was 30 ml/kg, evaporative losses were substituted with 5 ml/kg per h. MEASUREMENTS AND MAIN RESULTS: Airway pressures, tidal volumes, dynamic compliance (Cdyn), expiratory airway resistance and arterial blood gases were measured. Hemodynamic monitoring included right atrial, mean pulmonary artery, pulmonary capillary wedge and mean systemic arterial pressures, and continuous flow recording of the pulmonary artery. In both groups the induction of ALI significantly reduced PaO2/FIO2 Cdyn and cardiac output, and significantly increased pulmonary artery pressure. After the initiation of PLV there was a significant increase of PaO2/FIO2, and Cdyn, and a significant decrease of pulmonary artery pressure in both groups. Except the PaCO2, which showed significantly lower values in the PLV/KT group, no variables showed any differences between the two groups. CONCLUSION: The additional use of KT did not show beneficial effects on oxygenation and lung mechanics during PLV. However, at constant minute ventilation PaCO2 levels were significantly lower during PLV/KT, indicating some positive influence on the ventilation/perfusion distribution within the lung. Extreme body positions during PLV/KT did not show any significant hemodynamic side effects.     

Isolated ultrafiltration in cardiogenic pulmonary edema

Twenty patients (ten with mitral and/or aortic valve disease and ten with ischemic heart disease, all in the New York Heart Association class IV, aged between 18 and 74 yr, with cardiogenic pulmonary edema unresponsive to drug treatment) were treated with polysulphone membrane ultrafiltration (UF) in a veno-venous circuit. All patients had dyspnea, pulmonary rales, hypoxemia, tachycardia, hypotension, overhydration, radiologic evidence of engorged pulmonary vasculature, and Kerley-B lines. Systemic and pulmonary arterial pressures, cardiac output (by thermodilution), and intrapulmonary shunt fraction (Qsp/Qt) were determined and chest x-ray was obtained at the beginning and the end of UF. Average duration of the treatment was 150 +/- 28 min; UF volume averaged 3000 +/- 170 ml. UF reduced the Qsp/Qt by 58% from control condition, and did not significantly affect hemodynamic variables. Chest x-rays documented clearing of alveolar edema and venous congestion. These changes were associated with unequivocal clinical improvement and no mechanical ventilation was necessary to improve gas exchange. Short-term fluid subtraction did not result in undesired circulatory alternations. Because the ultrafiltrate composition is similar to plasmatic fluid, no modification in the plasma osmolarity was detected. In conclusion, UF may be considered an effective tool for the treatment of acute pulmonary edema refractory to drug therapy, as an alternative to mechanical ventilation, and as a remedy for excessive extravascular lung water.     

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.     

高频喷射通气辅助单肺通气在Ⅰ型呼吸衰竭患者胸科手术中的应用

【目的】探讨单肺通气（OLV）中非通气侧肺高频喷射通气（HFJV）在I型呼吸衰竭患者中的作用。【方法】选择合并I型呼吸衰竭全麻单肺通气胸科手术患者34例,随机分为两组,每组17例,全麻快速诱导后插入双腔支气管导管,HFJV组（H组）单肺通气后非通气侧肺行HFJV;对照组（C组）行单肺通气。分别于麻醉前（T0）及0LV前（T1）、OLV后10min（T2）、30min（T3）、60min（T4）、术毕恢复双肺通气后10min（T5）行血气分析,计算肺内分流率[肺内分流量／心输出量（Qs／Qt）],同时监测气道压力并计算肺顺应性（Cdyn）。【结果】C组有4例患者由于严重低氧血症退出该研究;与T,时比较,Tz～Ta时两组PaO2均下降,Qs／Qt、气道峰压（Pmax）升高、Cdvn下降（P〈0．05）;与C组比较,H组Tz～Tt时Paoz显著增高、Qs／Qt显著降低,其差异均有统计学意义（P〈0．05）,Pmax、Cm无显著性差异（P〉0．05）。【结论】高频喷射通气辅助单肺通气可降低I型呼吸衰竭患者肺内分流,维持较好的PaO2。     

High-frequency oscillation during simulated altitude exposure

Ventilatory requirements using high-frequency oscillation (HFO) during simulated altitude exposure were investigated in control dogs and animals with oleic acid-induced lung injury. FIO2 values of 0.21 and 1.0 were supplied by bias flow to the normal and injured dogs, respectively. After a control period, animals were exposed to a simulated altitude of 8,000 ft (barometric pressure 564 torr), followed by a second control period at ground level. Both experimental groups had similar values of PaCO2 at ground level and during exposure to reduced barometric pressure. The tidal volume necessary to maintain eucapnia was higher in oleic acid-injured animals compared with the control group; cardiac output and functional residual capacity were lower. The alveolar-arterial oxygen difference was substantially larger in the oleic acid group. Adequate gas exchange can be maintained with HFO during exposure to altitude provided that ventilation and inspired PO2 are not reduced below normobaric levels.     

Cardiopulmonary effects of Intralipid infusion in critically ill patients

Cardiopulmonary effects of 500 ml of 20% iv fat emulsion (Intralipid) infusion in two groups of patients who required mechanical ventilation were evaluated in our Critical Care Center. Group 1 included ten patients void of signs or symptoms of sepsis. Group 2 consisted of ten patients exhibiting clinical and laboratory signs and symptoms of sepsis. Data were measured before and immediately after Intralipid infusion and when serum lipemia cleared. Intralipid infusion precipitated a significant increase in venous admixture (Qsp/Qt) from 13.7 +/- 3.6 (SEM) to 18.0 +/- 6.5% and from 22.0 +/- 4.8 to 25.8 +/- 7.0% in groups 1 and 2, respectively. Mean pulmonary artery pressure (MPAP) increased from 22.7 +/- 4.2 to 29.2 +/- 8.1 mm Hg and 26.4 +/- 6.8 to 28.0 +/- 4.0 mm Hg in groups 1 and 2, respectively. When serum lipemia cleared, Qsp/Qt and MPAP returned to preinfusion levels. We conclude that Intralipid infusion increases pulmonary artery pressure and venous admixture in critically ill patients. These changes are temporary and coincidental with serum lipemia rather than presence or absence of sepsis. Adequate levels of oxygenation should be confirmed during Intralipid infusion in patients with borderline oxygenation.     

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.     

Sodium nitroprusside and positive end-expiratory pressure are not detrimental in canine asymmetric pulmonary edema

The effects of PEEP and subsequent augmentation of cardiac output by sodium nitroprusside (SNP) were examined in a canine model of asymmetric oleic acid injury to the right lung. PEEP (9.2 +/- 0.5 cm H2O) was added to six animals to decrease venous admixture (Qsp/Qt) from 50.6 +/- 4.4% to 16.0 +/- 1.3% (p less than .05). With PEEP, intrapulmonary blood flow distribution (assessed by radioactive microspheres) decreased significantly to nondependent lung regions while increasing to dependent regions. In six other animals, zero end-expiratory pressure (ZEEP) did not alter intrapulmonary blood flow distribution. SNP was then administered to increase cardiac output by 40% (to 2.60 +/- 0.21 L/min in the ZEEP group and to 1.75 +/- 0.27 L/min in the PEEP group). SNP produced no adverse effects on Qsp/Qt or intrapulmonary blood flow distribution. Specifically, SNP did not preferentially dilate pulmonary vessels injured by oleic acid with or without end-expiratory pressure. Thus, administration of a vasodilator drug in asymmetric pulmonary edema appears well tolerated.     

Gas transport during different modes of high-frequency ventilation

Gas transport during high-frequency oscillation (HFO) and high-frequency jet ventilation (HFJV) was compared in a simple lung model of human conducting airways. The delivery of gas to distal airways was assessed by measuring the dilution of 5% CO2, introduced separately into the model. Increasing frequency from 1.0 to only 1.7 Hz redistributed gas into straighter airway paths during HFO. Gas flow rates during HFO were sinusoidal, and CO2 dilution at the most distal airway sampling site was a function of both mean and peak flow rates. CO2 dilution increased as frequency increased, even though tidal volume (VT) was constant. Peak flow increased as either VT or frequency was increased (range 132 to 2167 ml/sec). During HFJV, flow approximated a square-wave function. Peak flows during HFJV were lower than during HFO, except at mean flows less than 167 ml/sec. Although CO2 dilution at the most distal airway sampling site increased as VT increased during HFJV, CO2 dilution actually decreased as frequency was increased at any given VT. Thus, in this model, gas transport in large airways differed during HFO or HFJV, and was related to peak as well as mean flows. Also, the distribution of gas within the airways changed as frequency increased.     

Respiratory index/pulmonary shunt relationship: quantification of severity and prognosis in the post-traumatic adult respiratory distress syndrome

The relationship between the respiratory index (RI = alveolar-arterial oxygen gradient [P(A-a)O2] normalized by PaO2) and the pulmonary shunt (Qsp/Qt) has been examined in 929 studies from 240 critically ill post-traumatic patients. Of these, 88 patients (443 studies) were individuals who developed post-traumatic adult respiratory distress syndrome (ARDS) and 152 were patients (486 studies) who did not develop ARDS. This study demonstrates that the RI to Qsp/Qt [RI/(Qsp/Qt)] relationship was significantly (p less than .0001) increased in patients who developed fatal ARDS compared with those who did not develop ARDS, or with those whose ARDS resolved. Because of the increased oxygen consumption (VO2) in ARDS patients in association with their severe limitations in gas exchange (RI) and increased Qsp/Qt, surviving ARDS patients had a significant increase in the cardiac index which resulted in a higher oxygen delivery to VO2 ratio. ARDS patients showed significant (p less than .0001) evidence of increased pulmonary vascular tone, correlated with the increase in the RI/(Qsp/Qt) relationship. In addition, those patients with high RI/(Qsp/Qt) also had increased right ventricular (RVSW) to left ventricular work (LVSW) ratios which were shown to be a direct function of the rise in RI. This increase in both RVSW/LVSW and RI/(Qsp/Qt) ratios was significantly (p less than .0001) correlated with an increased mortality. Thus, the RI/(Qsp/Qt) relationship, which can be obtained from arterial and mixed venous blood gases and saturations only, can be used to predict the severity of the ARDS process as well as important pulmonary vascular and right ventricular overload consequences.