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.     

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.     

Continuous positive airway pressure is beneficial in treatment of smoke inhalation

This study demonstrates that continuous positive airway pressure (CPAP) improves pulmonary function after smoke inhalation by dogs. Sixteen dogs were anesthetized with iv sodium pentobarbital. Arterial and mixed venous blood gas tensions; carboxyhemoglobin concentration (COHgb); mean systemic arterial (MAP), mean pulmonary arterial (MPAP), and pulmonary arterial wedge (WP) pressures; heart (HR) and respiratory (f) rates; cardiac output (CO); and airway pressure (Paw) were measured. Intrapulmonary physiologic shunt (Qsp/Qt) and pulmonary (PVR) and systemic (SVR) vascular resistances were calculated. The animals then breathed an aerosol of smoke and were divided randomly into 2 groups. The treatment group breathed spontaneously on 8-torr CPAP whereas the control group continued to breathe spontaneously at ambient pressure. After inhalation of smoke, Qsp/Qt, MPAP, PVR, COHgb, HR, and f rose, whereas PaO2 and MAP fell in untreated animals. When CPAP was applied, PaO2 and Qsp/Qt returned nearly to baseline values. Mean f also was significantly lower in the treated animals. We found that the early institution of CPAP improves oxygen exchange in the lungs after the inhalation of smoke.     

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.     

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.     

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.     

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.     

Effect of leukotriene inhibitor LY-171883 on the pulmonary response to Escherichia coli endotoxemia

The effect of the leukotriene D4 (LTD4) receptor antagonist, LY-171883, on the respiratory and cardiovascular changes in endotoxemia was studied in 20 unanesthetized sheep. In group 1 (n = 2), 4 mg/kg LY-171883 was injected iv. In group 2 (n = 12), Escherichia coli endotoxin (1 micrograms/kg) was infused iv, and in group 3 (n = 6), 4 mg/kg LY-171883 was administered 15 min before and 30 min after the same dose of endotoxin. Infusion of LY-171883 in group 1 did not alter baseline ventilatory and cardiovascular measurements. A two-phase pulmonary response was observed in group 2: an early pulmonary hypertension phase in which pulmonary artery pressure (PAP) increased from 18.7 to 51.2 mm Hg (p less than .001), with a fall in cardiac index (CI) from 171 to 114 ml/min.kg (p less than .01). The ratio of peak inspiratory/expiratory flow rate (PIF/PEF) increased from 1.08 to 1.35 (p less than .01) and the respiratory rate from 50 to 70 breath/min (p less than .005) 30 min postendotoxin. The flow rate measured at midexpiration time (V50) decreased from 81% to 25% of its peak expiration (p less than .001) and the airway resistance increased from 3.8 to 32.7 cm H2O/L.sec (p less than .001). The second permeability phase was characterized by an increase in pulmonary lymph flow (QL) from 8.5 to 35.2 ml/h (p less than .01), a decrease in PaO2 from 76 to 61 torr (p less than .01), and an increase in pulmonary shunt ratio (Qsp/Qt) from 16% to 31% (p less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Hemodynamic profiles of prostaglandin E1, isoproterenol, prostacyclin, and nifedipine in experimental porcine pulmonary hypertension

BACKGROUND AND METHODS: We compared the hemodynamic effects of four vasodilators in experimental embolic pulmonary hypertension in a randomized controlled trial, using nine pigs weighing 16 to 23 kg. After anesthesia induction and cannulation with arterial, central venous, and thermodilution output pulmonary artery catheters, animals were repetitively embolized with glass beads (60 to 160 mu) in order to establish pulmonary hypertension (pulmonary artery pressure [PAP] doubled from baseline). Prostaglandin E1 (PGE1), isoproterenol, prostacyclin (PGI2), and nifedipine were compared at doses producing equivalent reduction in systemic BP. RESULTS: Only PGE1 and PGI2 decreased both PAP and pulmonary vascular resistance (PVR). PGE1 decreased PAP from 39 +/- 1 to 33 +/- 1 mm Hg; prostacyclin decreased PAP from 38 +/- 1 to 31 +/- 1 mm Hg and produced the largest increase in cardiac output (Qt). Isoproterenol did not change PAP, markedly increased heart rate (162 +/- 8 to 216 +/- 11 beats/min), and resulted in significant arrhythmias. Nifedipine increased PVR from 1044 +/- 113 to 1125 +/- 100 dyne.sec.cm-5 and decreased Qt. CONCLUSIONS: Vasodilators demonstrate unique hemodynamic drug profiles. Isoproterenol infusion is characterized by tachycardia and arrhythmias. Both PGE1 and PGI2 effectively decrease PAP and PVR. Nifedipine depressed Qt significantly in this glass-bead embolization model of acute pulmonary hypertension.     

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.     

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.     

High-frequency jet ventilation versus intermittent positive-pressure ventilation

Airway pressures and cardiorespiratory variables were compared for conventional ventilation (CV) and high-frequency jet ventilation (HFJV), at a similar fraction of inspired O2 (FIO2), positive end-expiratory pressure (PEEP) and PaCO2 in 11 ICU patients. For CV and HFJV, respectively, peak (PAP) and mean airway pressures (Paw) were 15.4 and 9.1 mm Hg and 4.4 and 5 mm Hg. Cardiac index (CI) was 2.54 and 2.60 L/min X m2, total systemic vascular resistance index (SVRI) 2846 and 2923 dyne X sec/cm5 X m2, PaO2 207 and 149 torr, and Qsp/Qt 7% and 11%. HFJV decreased significantly PAP and was less likely to produce pulmonary barotrauma. Cardiac indices were not different, indicating that this variable may be affected by Paw. HFJV neither increased nor decreased CI at similar PEEP and PaCO2 as compared to CV. The decrease in PaO2 and increase in Qsp/Qt may be due to small inspired gas volumes potentiating microatelectasis. On the basis of this study, we recommend initiating HFJV at FIO2 of 0.9 and PEEP of 5 cm H2O, and monitoring both PAP and Paw.     

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.     

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.     

Dimethylthiourea ameliorates acute lung injury induced by phorbol myristate acetate in dogs.

BACKGROUND AND METHODS: The protective effects of dimethylthiourea, a potent scavenger of hydroxy radical (.OH) and hydrogen peroxide, in experimental lung injury in large animals remain controversial. The present study was designed to determine whether dimethylthiourea can ameliorate the acute lung injury produced in dogs by phorbol myristate acetate. Six dogs were infused with dimethylthiourea (0.75 g/kg in saline) for 1.5 hrs, beginning 1 hr before an i.v. bolus injection of phorbol myristate acetate (17 micrograms/kg); six dogs received phorbol myristate acetate (17 micrograms/kg) alone; and six dogs were infused with saline alone. Hemodynamic changes, arterial oxygenation, and the development of lung edema were monitored for 4 hrs after phorbol myristate acetate injection to assess the extent of lung damage. RESULTS: As compared with the dogs that received phorbol myristate acetate alone, the edematous lung damage was significantly reduced in those dogs that received dimethylthiourea as well as phorbol myristate acetate. In the dimethylthiourea-treated dogs, the lung wet/dry weight ratios were smaller (p less than .01); protein concentrations in lung lavage fluid were lower (p less than .01); the decrease in PaO2 was significantly reduced (p less than .01); and there were significant reductions in the alveolar-arterial oxygen tension difference (P[A-a]O2) (p less than .01) and shunt (Qsp/Qt) (p less than .05). Also, dimethylthiourea significantly lowered the increased mean pulmonary arterial pressure levels during the second half of the experiment. CONCLUSIONS: These experimental data suggest that dimethylthiourea is capable of reducing the neutrophil-mediated lung injury produced by the release of hydroxy radical and/or hydrogen peroxide in dogs exposed to phorbol myristate acetate.     

Hypoxic pulmonary vasoconstrictor response with asymmetric oleic acid injury in the dog

The hypoxic pulmonary vasoconstrictive (HPV) response is characterized by two components: intrapulmonary blood flow redistribution and pulmonary artery pressure (PAP) augmentation. Whether both remain intact after oleic acid lung injury has not been assessed. In an asymmetric model of right lung oleic acid edema, we examined the relative magnitude of each component on the HPV response to right lung inspired hypoxia. Before oleic acid administration, right lung hypoxia decreased perfusion to the right lung from 1.41 +/- 0.12 to 1.16 +/- 0.15 L/min (p = .07), while PAP increased from 15.8 +/- 0.8 to 18.1 +/- 0.6 mm Hg (p less than .05). Regional hypoxia caused right lung pulmonary vascular resistance (PVR) to increase from 480 +/- 45 to 797 +/- 114 dyne.sec/cm5 (p less than .01). After right lung injury with oleic acid, regional hypoxia decreased perfusion to the right lung from 0.91 +/- 0.11 to 0.71 +/- 0.10 L/min (p less than .05), while PAP increased from 18.8 +/- 0.8 to 21.5 +/- 1.0 mm Hg (p less than .05). With hypoxia, right lung PVR increased from 1232 +/- 260 to 1933 +/- 336 dyne.sec/cm5 (p less than .01). We conclude that the pulmonary vasoconstrictive response to inspired hypoxia persists after oleic acid lung injury, causing significant increases in PVR. Consequently, both the blood flow redistribution and the PAP augmentation components of the HPV response to inspired hypoxia remain unchanged.     

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.     

Elevated pulmonary artery systolic storage volume associated with redistribution of pulmonary perfusion

The possibility that an increased pulmonary arterial systolic storage volume (PASSV) correlates with a significant redistribution of pulmonary perfusion was examined in 30 surgical patients. Right ventricular stroke work index (RVSWI) was used as an index of distribution of pulmonary perfusion. The systolic storage volume was calculated from the pulmonary arterial compliance and mean pulmonary arterial distending pressure. Pulmonary arteriolar pressures were computed by Fourier analysis. Pulmonary arterial compliance was derived from the pulmonary arterial time constant and pulmonary arterial resistance. There was a linear relationship between PASSV and RVSWI (r = .81, p less than .001). Also, a direct correlation was found between RVSWI and pulmonary arterial time constant (r = .45, p less than .01). When the patients were divided into three groups according to the severity of pre-existing disease, linear relationships between PASSV and RVSWI were present in all groups, and the slopes were not different among the three groups. The patients were also divided into two groups based on a storage volume fraction of stroke volume index, to evaluate the effect of other hemodynamic data on the PASSV. Comparison of the two groups revealed that pulmonary arterial pressure and pulmonary arterial compliance were significantly higher in the group with a high storage volume fraction (p = .05 and p = .01, respectively). RVSWI and time constant were also significantly different between the groups (p less than .01 and p less than .01, respectively). We conclude that the pressure work generated by the right ventricle improved the distribution of pulmonary perfusion by increasing PASSV.     

Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.