Increase In Intrapulmonary Shunt Research Articles

Impact of Positive End-Expiratory Pressure and FiO2 on Lung Mechanics and Intrapulmonary Shunt in Mechanically Ventilated Patients with ARDS Due to COVID-19 Pneumonia.

Purpose: This study aimed to investigate the effects of inspired oxygen fraction (FiO2) and positive end-expiratory pressure (PEEP) on gas exchange in mechanically ventilated patients with COVID-19. Methods: Two FiO2 (100%, 40%) were tested at 3 decreasing levels of PEEP (15, 10, and 5 cmH2O). At each FiO2 and PEEP, gas exchange, respiratory mechanics, hemodynamics, and the distribution of ventilation and perfusion were assessed with electrical impedance tomography. The impact of FiO2 on the intrapulmonary shunt (delta shunt) was analyzed as the difference between the calculated shunt at FiO2 100% (shunt) and venous admixture at FiO2 40% (venous admixture). Results: Fourteen patients were studied. Decreasing PEEP from 15 to 10 cmH2O did not change shunt (24 [21-28] vs 27 [24-29]%) or venous admixture (18 [15-26] vs 23 [18-34]%) while partial pressure of arterial oxygen (FiO2 100%) was higher at PEEP 15 (262 [198-338] vs 256 [147-315] mmHg; P < .05). Instead when PEEP was decreased from 10 to 5 cmH2O, shunt increased to 36 [30-39]% (P < .05) and venous admixture increased to 33 [30-43]% (P < .05) and partial pressure of arterial oxygen (100%) decreased to 109 [76-177] mmHg (P < .05). At PEEP 15, administration of 100% FiO2 resulted in a shunt greater than venous admixture at 40% FiO2, ((24 [21-28] vs 18 [15-26]%, P = .005), delta shunt 5.5% (2.3-8.8)). Compared to PEEP 10, PEEP of 5 and 15 cmH2O resulted in decreased global and pixel-level compliance. Cardiac output at FiO2 100% resulted higher at PEEP 5 (5.4 [4.4-6.5]) compared to PEEP 10 (4.8 [4.1-5.5], P < .05) and PEEP 15 cmH2O (4.7 [4.5-5.4], P < .05). Conclusion: In this study, PEEP of 15 cmH2O, despite resulting in the highest oxygenation, was associated with overdistension. PEEP of 5 cmH2O was associated with increased shunt and alveolar collapse. Administration of 100% FiO2 was associated with an increase in intrapulmonary shunt in the setting of high PEEP. Trial registration: NCT05132933.

Evaluation of Almitrine Infusion During Veno-Venous Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome in Adults.

This single-center case series investigated the effect of almitrine infusion on PaO2/fraction of inspired oxygen (FIO2) in 25 patients on veno-venous extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. A positive trial was defined as an increase of PaO2/FIO2 ratio ≥20%. Thirty-two trials were performed. Twenty (62.5%, 95% confidence interval, 37.5%-75%) trials in 18 patients were positive, with a median PaO2/FIO2 ratio increase of 35% (25%-43%). A focal acute respiratory distress syndrome and inhaled nitric oxide therapy were more frequent in patients with a positive response to almitrine. We observed no complications of almitrine use.

Effect of sedation with detomidine and butorphanol on pulmonary gas exchange in the horse

BackgroundSedation with α2-agonists in the horse is reported to be accompanied by impairment of arterial oxygenation. The present study was undertaken to investigate pulmonary gas exchange using the Multiple Inert Gas Elimination Technique (MIGET), during sedation with the α2-agonist detomidine alone and in combination with the opioid butorphanol.MethodsSeven Standardbred trotter horses aged 3–7 years and weighing 380–520 kg, were studied. The protocol consisted of three consecutive measurements; in the unsedated horse, after intravenous administration of detomidine (0.02 mg/kg) and after subsequent butorphanol administration (0.025 mg/kg). Pulmonary function and haemodynamic effects were investigated. The distribution of ventilation-perfusion ratios (VA/Q) was estimated with MIGET.ResultsDuring detomidine sedation, arterial oxygen tension (PaO2) decreased (12.8 ± 0.7 to 10.8 ± 1.2 kPa) and arterial carbon dioxide tension (PaCO2) increased (5.9 ± 0.3 to 6.1 ± 0.2 kPa) compared to measurements in the unsedated horse. Mismatch between ventilation and perfusion in the lungs was evident, but no increase in intrapulmonary shunt could be detected. Respiratory rate and minute ventilation did not change. Heart rate and cardiac output decreased, while pulmonary and systemic blood pressure and vascular resistance increased. Addition of butorphanol resulted in a significant decrease in ventilation and increase in PaCO2. Alveolar-arterial oxygen content difference P(A-a)O2 remained impaired after butorphanol administration, the VA/Q distribution improved as the decreased ventilation and persistent low blood flow was well matched. Also after subsequent butorphanol no increase in intrapulmonary shunt was evident.ConclusionThe results of the present study suggest that both pulmonary and cardiovascular factors contribute to the impaired pulmonary gas exchange during detomidine and butorphanol sedation in the horse.

La circulation pulmonaire dans le syndrome de détresse respiratoire aiguë

Pulmonary artery pressure increases in almost all patients with the acute respiratory distress syndrome. The elevation is attenuated by the release of endogenous vasodilators which counterbalance the effects of endogenous vasoconstrictors. By inhibiting hypoxic pulmonary vasoconstriction, the endogenous vasodilators contribute to the increase in intrapulmonary shunt. On the other hand, the administration of vasodilators in the airways, such as nitric oxide, reduces pulmonary artery pressure and improves gas exchange by diverting pulmonary blood flow to better-ventilated regions. These beneficial effects have unfortunately not been associated with an increased survival in patients with the acute respiratory distress syndrome. The rise in pulmonary artery pressure increases right ventricular afterload and can lead to acute cor pulmonale. The frequency and mortality of this complication have recently decreased, perhaps in relation with the use of lower tidal volumes during mechanical ventilation, which limit the plateau pressure, the compression of pulmonary vessels by the airways, and the right ventricular afterload.

Endothelin receptor blockade in canine oleic acid-induced lung injury.

To investigate the effects of endogenous endothelins on pulmonary haemodynamics and gas exchange in oleic acid lung injury. Prospective experimental study in dogs. Animal research laboratory in a university teaching hospital. SUBJECTS. Seventeen anaesthetised and ventilated mongrel dogs. Nine pretreated dogs received an infusion of the endothelin A and B receptor antagonist bosentan (10 mg/kg) started before oleic acid. Eight treated dogs received bosentan started 90 min after oleic acid. Cardiac index (CI) was manipulated by inflating an inferior vena caval balloon or by opening a femoral arterio-venous bypass. Pulmonary vascular resistance was defined by measuring the gradient between mean pulmonary artery pressure (MPAP) and occluded PAP (PAOP) at five levels of CI. Intrapulmonary shunt was measured using the inert gas SF(6). Pretreatment with bosentan prevented the oleic acid-induced shift of (MPAP-PAOP)/CI plots to higher pressures, but did not affect the increase in intrapulmonary shunt. Treatment of established oleic acid lung injury with bosentan had no effect. Pretreatment, but not treatment, with bosentan, in the dose used, blunted the oleic acid-induced increase in pulmonary vascular resistance, suggesting that endothelins contribute to the increase in pulmonary vascular tone in the early stages of oleic acid lung injury.

Thoracic epidural anesthesia as an adjunct to general anesthesia for cardiac surgery: Effects on ventilation-perfusion relationships

Postoperative hypoxemia remains a serious and frequent complication after cardiac surgery. Development of atelectasis during anesthesia appears to be a major factor in producing the increase in intrapulmonary shunt and consequently impaired gas exchange after cardiopulmonary bypass. Postoperative hypoxemia can produce significant ill effects, including increase in duration of postoperative ventilation, pulmonary complications, myocardial ischemia, and neurologic impairment. These complications are associated with prolonged intensive care unit (ICU) and hospital length of stay, resulting in significant increase in cost.

Matrix metalloproteinase inhibitor prevents acute lung injury after cardiopulmonary bypass.

Acute lung injury (ALI) after cardiopulmonary bypass (CPB) results from sequential priming and activation of neutrophils. Activated neutrophils release neutral serine, elastase, and matrix metalloproteinases (MMPs) and oxygen radical species, which damage alveolar-capillary basement membranes and the extracellular matrix, resulting in an ALI clinically defined as adult respiratory distress syndrome (ARDS). We hypothesized that treatment with a potent MMP and elastase inhibitor, a chemically modified tetracycline (CMT-3), would prevent ALI in our sequential insult model of ALI after CPB. Anesthetized Yorkshire pigs were randomized to 1 of 5 groups: control (n=3); CPB (n=5), femoral-femoral hypothermic bypass for 1 hour; LPS (n=7), sham bypass followed by infusion of low-dose Escherichia coli lipopolysaccharide (LPS; 1 microgram/kg); CPB+LPS (n=6), both insults; and CPB+LPS+CMT-3 (n=5), both insults plus intravenous CMT-3 dosed to obtain a 25-micromol/L blood concentration. CPB+LPS caused severe lung injury, as demonstrated by a significant fall in PaO(2) and an increase in intrapulmonary shunt compared with all groups (P<0.05). These changes were associated with significant pulmonary infiltration of neutrophils and an increase in elastase and MMP-9 activity. All pathological changes typical of ALI after CPB were prevented by CMT-3. Prevention of lung dysfunction followed an attenuation of both elastase and MMP-2 activity. This study suggests that strategies to combat ARDS should target terminal neutrophil effectors.

Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study.

Respiratory failure secondary to cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors previously found that the increase in intrapulmonary shunt was well correlated with the amount of atelectasis. They tested the hypothesis that post-CPB atelectasis can be prevented by a vital capacity maneuver (VCM) performed before termination of the bypass. Eighteen pigs received standard hypothermic CPB (no ventilation during bypass). The VCM was performed in two groups and consisted of inflating the lungs during 15 s to 40 cmH2O at the end of the bypass. In one group, the inspired oxygen fraction (FIO2) was then increased to 1.0. In the second group, the FIO2 was left at 0.4. In the third group, no VCM was performed (control group). Ventilation-perfusion distribution was measured with the inert gas technique and atelectasis by computed tomographic scanning. Intrapulmonary shunt increased after bypass in the control group (from 4.9 +/- 4% to 20.8 +/- 11.7%; P < 0.05) and was also increased in the vital capacity group ventilated with 100% oxygen (from 2.2 +/- 1.3% to 6.9 +/- 2.9%; P < 0.01) but was unaffected in the vital capacity group ventilated with 40% oxygen. The control pigs showed extensive atelectasis (21.3 +/- 15.8% of total lung area), which was significantly larger (P < 0.01) than the proportion of atelectasis found in the two vital capacity groups (5.7 +/- 5.7% for the vital capacity group ventilated with 100% oxygen and 2.3 +/- 2.1% for the vital capacity group ventilated with 40% oxygen. In this pig model, postcardiopulmonary bypass atelectasis was effectively prevented by a VCM.

Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study.

Respiratory failure after cardiopulmonary bypass (CPB) remains a major complication after cardiac surgery. The authors tested the hypothesis that atelectasis is an important factor responsible for the increase in intrapulmonary shunt after CPB. Six pigs received standard CPB (bypass group). Six other pigs had the same surgery but without CPB (sternotomy group). Another six pigs were anesthetized for the same duration but without any surgery (control group). The ventilation-perfusion distribution was measured with the inert gases technique, extravascular lung water was quantified by the double-indicator distribution technique, and atelectasis was analyzed by computed tomography. Intrapulmonary shunt increased markedly after bypass but was unchanged over time in the control group (17.9 +/- 6.2% vs. 3.5 +/- 1.2%; P < 0.0001). Shunt also increased in the sternotomy group (10 +/- 2.6%; P < 0.01 compared with baseline) but was significantly lower than in the bypass group (P < 0.01). Extravascular lung water was not significantly altered in any group. The pigs in the bypass group showed extensive atelectasis (32.3 +/- 28.7%), which was significantly larger than in the two other groups. The pigs in the sternotomy group showed less atelectasis (4.1 +/- 1.9%) but still more (P < 0.05) than the controls (1.1 +/- 1.6%). There was good correlation between shunt and atelectasis when all data were pooled (R2 = 0.67; P < 0.0001). Atelectasis is produced to a much larger extent after CPB than after anesthesia alone or with sternotomy and it explains most of the marked post-CPB increase in shunt and hypoxemia. Surgery per se contributes to a lesser extent to postoperative atelectasis and gas exchange impairment.

Lazaroid pretreatment preserves gas exchange in endotoxin-treated dogs

Purpose : The lazaroids are a new class of potent free-radical scavengers. We tested whether U-74389G, a lazaroid, could attenuate some of the adverse cardiopulmonary effects of sepsis. Methods : Dogs were randomized to receive either 10 mg/kg U-74389G (n = 10), or a saline control (n = 11). After baseline measurements of hemodynamics and gas exchange, they were then randomized to receive either 0.2 mg/kg endotoxin or a saline infusion. Measurements of hemodynamics and gas exchange were repeated. The study was concluded 70 minutes after endotoxin infusion and the lungs were then removed for histologic evaluation. Results : In endotoxin-treated control animals, P0 2 decreased (278 ± 123 mm Hg to 67 ± 13 mm Hg, P < .05) and intrapulmonary shunt increased (12.9% ± 1.1% to 28.2% ± 11.4%, P < .05) after endotoxin. Pretreatment with U-74389G attenuated the decrease in PO 2 (476 ± 61 mm Hg to 226 ± 143) and the increase in intrapulmonary shunt (12.6% ± 6.1% to 14.3% ± 6.8%) observed after endotoxin. The extent of lung injury and systemic hemodynamics were similar between control or U-74389G-treated dogs. Conclusions : A free-radical-scavenger can attenuate the gas exchange defect commonly associated with endotoxin but it does not improve the derangement of systemic hemodynamics.

Ventilation-perfusion inequality and diffusion impairment in acutely injured lungs

To assess the significant role of diffusion impairment and its unequal distribution in acutely injured lungs with alveolar flooding, oleic acid was intravenously injected into twenty-five mongrel dogs. The animals were divided into two groups, A and B. 0.1% CO in air was delivered, as an inspired gas, to the animals of group A. Simultaneously, saline containing a trace amount of six foreign inert gases was infused through a peripheral vein. While allowing the animals in group B to breathe air, saline containing ethylene, acetylene and freon 22 was infused. After injection of oleic acid, group A revealed increase in intrapulmonary shunt accompanied by a marked broadening of ventilation-perfusion ( V ̇ A Q ̇ ) and diffusing capacity-perfusion ( G Q ̇ ) distributions. A considerable amount of total cardiac output was received by the lung areas with low G Q ̇ ratios where significant diffusion limitation was predicted to occur. Group B showed that excretion of freon 22 (gas with lower diffusivity) in injured lungs was considerably distorted as compared to those of ethylene and acetylene (gases with higher diffusivities), again ascertaining the importance of diffusion limitation in lungs with exudate in alveolar regions.

Effects of Consecutive Protected Specimen Brushing and Bronchoalveolar Lavage on Gas Exchange and Hemodynamics in Ventilated Patients

To assess cardiovascular effects and the oxygenation status of mechanically ventilated patients undergoing protected specimen brushing (PSB) and bronchoalveolar lavage (BAL) under fiberoptic bronchoscopy (FOB). A prospective study. Polyvalent intensive care unit in a university hospital. Twelve consecutive, critically ill, intubated, and mechanically ventilated patients with hemodynamic failure requiring invasive monitoring with an indwelling radial artery catheter and indwelling Swan-Ganz catheter were included in the study. Hemodynamic measurements, arterial and mixed-venous blood gas analyses, and arterial blood lactate analysis were performed before and at the end of a 10-min period of mechanical ventilation with a fractional concentration of oxygen in the inspired gas (FIO2) of 1.0. The same measurements and blood samplings were repeated at the end of the PSB procedure, at the end of the BAL procedure, and 1 h after the end of the BAL. During the study period the ECG, arterial oxygen saturation (SaO2), and mixed-venous oxygen saturation (SvO2) were continuously monitored. A moderate increase in both mean arterial pressure and mean pulmonary arterial pressure was observed during the FOB procedure (p < 0.05). One hour after the end of BAL, the PaO2 decreased when compared with values recorded at the beginning of the procedure with the same FIO2 (p < 0.05). An increase in intrapulmonary shunt was observed at the end of BAL (p < 0.01). A moderate increase in PaCO2 was also observed after PSB (p < 0.05) and after BAL (p < 0.01). Monitoring of SaO2 permitted us to observe a significant and sustained decrease after the end of the FOB procedure from 10 to 60 min. The decrease in SvO2 was less pronounced but reached statistical significance. We conclude that PSB and BAL under FOB are well tolerated in critically ill, mechanically ventilated patients with hemodynamic disturbances requiring inotropic or vasopressor agents (or both); however, a modest impairment in arterial oxygenation was observed after the end of the FOB procedure.

Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor.

In septic shock, hypotension, disseminated intravascular coagulation, and neutrophil activation are related to the activation of the blood coagulation contact system. This study evaluates in dogs the effect of the C1-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associated with endotoxic shock. Two groups were included: controls, which received Escherichia coli endotoxin, and a C1-INH group in which C1-INH was infused before E. coli endotoxin administration. In both groups, endotoxin produced hypodynamic shock; however, the decrease in the systolic index and the ventricular systolic work indexes were greater in controls than the C1-INH group. In controls, the arterial O2 partial pressure decreased by 30% and the alveolo-arterial O2 difference increased by 625%, these parameters remained unchanged in the C1-INH group. Hypoxemia was associated with increased intrapulmonary shunt, decreased blood coagulation contact factors, and decreased C3c. In contrast, C1-INH administration prevented endotoxin-induced hypoxemia, the increase in intrapulmonary shunt, and the decrease in blood coagulation contact factors. This study shows that, in dogs with endotoxic shock, pulmonary dysfunction is associated with an activation of the blood coagulation contact phase system. An inhibition of this system by C1-INH prevented the hypoxemia induced by endotoxic shock.

A Comparison of Labetalol and Nitroprusside for Inducing Hypotension During Major Surgery

The hemodynamic and intrapulmonary shunt effects of intravenous labetalol and nitroprusside were compared during induced hypotension for major spinal surgery. A randomized, double-blind protocol was used in which 20 patients, ASA physical status I or II, received either nitroprusside infusion (n = 10) or labetalol bolus injections of 10 mg every 10 min (n = 10) until mean arterial blood pressure was reduced to 55-60 mm Hg. Pulmonary artery pressures were measured and mixed venous samples obtained via a pulmonary artery catheter. Nitroprusside increased heart rate significantly more than labetalol during the period of hypotension. When compared with prehypotension baseline values, nitroprusside increased heart rate significantly with a concomitant significant decrease in systemic vascular resistance. Cardiac output increased significantly 60 min after hypotension was achieved in patients treated with nitroprusside. Systemic vascular resistance decreased significantly below baseline levels in patients treated with labetalol but without changes in cardiac output, heart rate, or mean pulmonary artery pressure. There was a 122% increase in intrapulmonary shunt with nitroprusside administration, compared with an 11% increase with labetalol. Labetalol was effective for inducing hypotension and was not associated with an increase in heart rate, intrapulmonary shunt, or cardiac output as seen with nitroprusside.

Tumor Necrosis Factor-Induced Neonatal Pulmonary Hypertension: Effects of Dazmegrel Pretreatment

The endogenously produced cytokine, tumor necrosis factor-alpha (TNF-alpha), has been shown in adult animal models to be associated with many of the pathophysiologic effects of sepsis, including systemic hypotension and hemorrhagic necrosis. TNF-alpha can induce the release of various vasoactive arachidonic acid metabolites, suggesting that TNF-alpha may act either directly or via intermediary substances in producing its effects. The pathophysiologic role of TNF-alpha in neonatal sepsis, especially its potential effect on pulmonary vascular tone, is presently unknown. To assess the role of TNF-alpha in neonatal sepsis, 19 piglets (19 +/- 5 d old) were anesthetized, intubated, paralyzed, mechanically ventilated, and catheterized to assess pulmonary and systemic vascular hemodynamics and pulmonary gas exchange. The multiple inert gas elimination technique was used to assess ventilation perfusion matching. A 30-min infusion of human recombinant TNF-alpha (250 micrograms/kg total dose) was administered to animals pretreated with either 10 mg/kg dazmegrel, a thromboxane synthase inhibitor (n = 9) or placebo (n = 10). TNF-alpha alone induced a prompt and sustained rise in pulmonary arterial pressure and pulmonary vascular resistance that continued at least for 2 h after onset of the infusion. In contrast, the animals pretreated with dazmegrel demonstrated no rise in pulmonary vascular resistance until 2 h after the onset of the infusion. Neither group of animals demonstrated a significant decline in arterial PO2 or evidence from inert gas analysis of VA/Q mismatching or increase in intrapulmonary shunt.(ABSTRACT TRUNCATED AT 250 WORDS)

Neonatal group B streptococcal sepsis: effects of late treatment with dazmegrel.

Neonatal group B streptococcal (GBS) sepsis produces pulmonary arterial hypertension and hypoxemia that are preventable by pretreatment with the selective thromboxane A2 synthase inhibitor, dazmegrel. In the present experiment we administered dazmegrel (8 mg/kg) 2 h after the initiation of a 2 1/2 h infusion of 5 X 10(8) GBS/kg/h in ten 2- to 3-wk-old piglets. The multiple inert gas elimination technique was used to measure intrapulmonary shunt and alveolar ventilation to pulmonary perfusion mismatching. Thromboxane B2, the stable metabolite of thromboxane A2, and 6-keto-prostaglandin F1 alpha, the stable metabolite of prostacyclin, were assayed in arterial blood. Pulmonary arterial pressure increased immediately after initiation of the GBS infusion, rising from 12 +/- 2 to 34 +/- 4 torr (p less than 0.02); pulmonary vascular resistance increased by 400% (p less than 0.01). Arterial hypoxemia developed (p less than 0.02) in association with an increase in the low ventilation-perfusion ratio index but without a significant increase in intrapulmonary shunt. Thromboxane B2 levels increased 10-fold. Infusion of the carrier substance for dazmegrel after 2 h of GBS infusion produced no change in any variables. In contrast, infusion of the drug resulted in the return to pre-GBS infusion baseline values for both pulmonary arterial pressure and pulmonary vascular resistance. However, no improvement in arterial pO2 or in the low ventilation-perfusion ratio index occurred. Both pulmonary vascular resistance and pulmonary arterial pressure remained normal for 0.5 h after dazmegrel administration despite continued GBS infusion. Thromboxane B2 levels were decreased 30 min after dazmegrel (p less than 0.02), but remained greater than pre-GBS levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic Management in Clinical Acute Hypoxemic Respiratory Failure: Dopamine vs Dobutamine

We investigated short-term hemodynamic effects of dopamine and dobutamine in eight patients with acute hypoxemic respiratory failure. We tested the hypothesis that for a similar increase in cardiac output, left ventricular filling pressure (pulmonary capillary wedge pressure [PCWP]) would increase with dopamine and decrease with dobutamine. Dopamine increased cardiac output (p less than 0.05), stroke volume (p less than 0.05), and PCWP (p less than 0.01). Cardiac output increased almost 20 percent when PCWP increased 50 percent with dopamine. In contrast, despite a mean 30 percent increase in cardiac output with dobutamine (p less than 0.01), PCWP decreased. In six of these patients, left ventricular end-diastolic volumes and end-systolic volumes were measured using scintigraphic techniques. In all patients, end-diastolic volume increased with dopamine (p less than 0.05); and in four of six, end-systolic volume increased. In contrast, with dobutamine, in five of six patients, end-diastolic volume decreased; and in all six patients, end-systolic volume decreased. There was a small increase in intrapulmonary shunt with both drugs. We conclude that if an inotropic agent is required to increase cardiac output in patients with acute hypoxemic respiratory failure, dobutamine is probably preferred over dopamine.

Relationship between Hypoxemia and Urinary Catecholamines Excretion in Subarachnoid Hemorrhage and Hypertensive Intracerebral Hemorrhage

Relationship between pulmonary insufficiency and urinary catecholamines excretion in 34 patients with hypertensive intracerebral hemorrhage or subarachnoid hemorrhage in the acute stage was evaluated. The hypoxemia was not induced by pulmonary hypoventilation but by an increase in alveolar-arterial oxygen difference. As it was known that administration of catecholamines brought an increase in intrapulmonary shunt, the relationship between alveolar-arterial oxygen difference and urinary catecholamines excretion was investigated. Alveolar-arterial oxygen difference positively correlated with urinary catecholamines excretion. The patients with increased alveolar-arterial oxygen difference had an increased intrapulmonary shunt. Maximum diameter of hematoma in 20 patients with hypertensive intracerebral hemorrhage had a significantly positive correlation with their alveolar-arterial oxygen difference. Administration of phentolamine and propranolol decreased the intrapulmonary shunt followed by a decrease in alveolar-arterial oxygen difference through reducing pulmonary vascular resistance and cardiac output, respectively. Trimethaphan camsilate also decreased these two values without any change in pulmonary vascular resistance or cardiac output. From these facts, it can be speculated that an overactivity of the sympathetic nerves exists in the acute stage of hypertensive intracerebral hemorrhage and subarachnoid hemorrhage, and that elevated catecholamines play an important role in increasing the intrapulmonary shunt followed by hypoxemia through acting on the pulmonary vascular bed, through action on the efferent sympathetic nerves to the pulmonary vascular bed, and/or through increasing cardiac output.

Does increased pulmonary blood flow redistribute towards edematous lung units?

Unilobar pulmonary edema secondary to increased capillary permeability was produced utilizing oleic acid infusion into the left lower lobe pulmonary artery of seven dogs. This model was used to determine whether random changes in cardiac output produced by opening and closing arteriovenous fistulae were associated with changes in fractional perfusion to the edematous lobe (as determined by differentially labeled radiomicrospheres) thus explaining changes in intrapulmonary shunt. With an increase in cardiac output from a mean (+/- SD) of 1.6 +/- 0.5 liters/min to 2.6 +/- 0.8 liters/min (P less than 0.01), mean (+/- SD) injured lobar shunt as measured from O2 contents of lower lobar pulmonary venous blood and mixed venous blood increased from 54.4 +/- 3.0% to 74.4 +/- 22.1% while total intrapulmonary shunt increased from 12.0 +/- 4.0% to 16.0 +/- 3.7% (P less than 0.01). This increase in intrapulmonary shunt was, however, not associated with preferential perfusion of the edematous lobe, the mean (+/- SD) of the perfusion to the edematous lobe expressed as a percentage of the cardiac output being 16.6 +/- 1.6% at the low cardiac output and 16.9 +/- 1.4% at the high cardiac output. It is concluded that redistribution of blood flow towards the edematous lobe does not occur with increases in cardiac output and therefore does not account for the increased intrapulmonary shunt.

Occurrence of pulmonary insufficiency in abdominal trauma.

The alteration of pulmonary function in 35 patients with abdominal trauma admitted to the Trauma ICU of Oska University Hospital were studied. A fall of PaO2 reaching the lowest level on the third post-traumatic day, incomplete recovery even on the seventh posttraumatic day and of longer duration was remarkable in comparison to those seen after elective abdominal surgery. Thirty two patients recovered without need of particular respiratory control but remaining three died with progressive decrease of PaO2 in spite of the intensive respiratory care. The hypoxia seen in the fatal cases was irresponsive to the administration of 100 per cent O2 with mechanical ventilation. Therefore, increase in intrapulmonary shunt was likely to be responsible for their fatal course.