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Ventilatory function of the lungs has been studied in 13 post-trauma patients using a two compartment analysis. The analysis is based upon a model of the lung which describes a nitrogen washout curve in terms of fast and slowly ventilated compartments. Data output from a digital computer provides values that compare the fractions of the alveolar ventilation and volume of the two compartments. All patients on initial investigation had large identifiable slow spaces. Subsequent evaluation at a time of clinical improvement showed that the ventilation of the slow space had increased significantly (P less than .003), whereas no change was evident in the volume fraction. The ventilation to volume ratio of the slow space, measured on these two separate occasions increased in twelve of the patients studied. An increase in this ratio correlated with improvement in the patient's clinical condition.

It is suggested that the early failure of bypass grafts in patients with clinical evidence of venous hypertension is a result of increased resistance caused by venous obstruction. The importance of using autogenous vein grafts in such cases is emphasized. One should accept the possibility that arterial reconstruction may result in a less successful outcome in patients with chronic venous disease.

Plasma fibronectin deficiency and opsonic dysfunction exist in critically ill septic surgical, trauma, and burn patients with multiple organ failure. Fibronectin deficiency can be reversed by infusion of fresh plasma cryoprecipitate. The influence of therapy with human cryoprecipitate on lung vascular permeability in septic sheep with plasma fibronectin deficiency following surgery was evaluated. Additionally, selected studies on pulmonary function in septic surgical and trauma patients after infusion of plasma cryoprecipitate were completed. In patients, ventilation-perfusion balance appeared to improve as measured by the multiple inert gas elimination technique. With the lung lymph fistula preparation in fibronectin deficient sheep, infusion of human plasma cryoprecipitate (10 units; 250 ml) delayed the onset and minimized the increase in lung vascular permeability during postoperative Pseudomonas sepsis (5 X 10(9) bacteria, I.V.; 5 X 10(10) bacteria, I.P.). For example, in a first group of sheep, the transvascular protein clearance (TPC) at 2 hrs in septic sheep (n = 4) treated with only saline (volume control) was 20.1 +/- 3.1 ml/hr, compared to 11.23 +/- 0.83 ml/hr in the sheep (n =a 4) treated with fibronectin-rich cryoprecipitate (p less than 0.05). In a second group of sheep, cryoprecipitate depleted of fibronectin by affinity chromatography was used as the control solution. It also did not manifest this protective effect with respect to lung vascular permeability. Thus, at 2 hrs the lymph flow (Qlym) was 30.2 ml/hr and the transvascular protein clearance (TPC) was 18.0 ml/hr in septic sheep given fibronectin-deficient cryoprecipitate. In contrast, in the fibronectin-rich cryoprecipitate treated sheep, the Qlym was 14.8 ml/hr and the TPC was 8.12 ml/hr. It is suggested that fibronectin may influence lung vascular integrity during sepsis following surgery and trauma.

This study evaluates the effects of 30 mg/kg methylprednisolone (MP) administered to eight trauma patient over a 30-minute period during initial resuscitation. Vascular pressures, cardiac index (CI), left ventricular stroke work index (LVSWI), systemic (SVR) and pulmonary (PVR) vascular resistance, oxygen delivery (OD), oxygen consumption (VO2), physiological shunt (shunt), limb blood flow (LBF), limb-oxygen delivery (LOD), and limb oxygen consumption (VLO2) were calculated at control and 1, 2, 4 and 6 hours following MP administration. At 1 hour there was an increase in CI from 2.9 +/- 0.3 to 3.5 +/- 0.3 liters/min/m2 (P less than 0.01), in OD from 961 +/- 172 to 11067 +/- 148 ml/min (P less than 0.05), in VO2 from 178 +/- 16 to 220 +/- 16 ml/min (P less than 0.01), in shunt from 25 +/- 3% to 33 +/- 3% (P less than 0.05), and a decrease in SVR from 1187 +/- 98 to 1945 +/- 87, and in PVR form 222 +/- 22 to 178 +/- 18 dyne sec/cm5 (P less than 0.05). These values returned to control by 4 hours. In spite of a pulmonary wedge pressure (PWP) that did not increase form a control of 5 +/- 2 mm Hg, and a mean arterial blood pressure (MABP) that did not decrease from a control of 86 +/- 5 mm Hg, LVSWI increased significantly at 1 hour (P less than 0.01). LBF, LOD, and VLO2 decreased at 1 hour (P less than 0.05). Since increased cardiac output was associated with increased stroke volume and left ventricular stroke work index, but without an increase in preload (PWP) or a decrease in afterload (MABP), methylprednisolone(MP), in pharmacologic dosage appears to have a positive inotropic effect on the myocardium of trauma patients during resuscitation.

Impaired peripheral oxygen utilization coinciding with an elevated cardiac index, venous oxygen tension, and serum lactate with the loss of reactive hyperemic response have been observed in a large series of resuscitated trauma patients. We tested the hypothesis that these clinical findings were due to an alteration of the microcirculation caused by embolization of intravascular particulate matter. To test this hypothesis, we used the bilateral pump-perfused, isolated canine gracilis muscle preparation which we subjected to microembolization with 15 micrometers polystyrene spheres. Prior to microembolization, oxygen consumption was flow-limited up to 6 ml min-1 (r = .928) and at higher flows, oxygen consumption was independent of flow. Following microembolization, the relationship of oxygen consumption and blood flow remained correlated (r = .893), but there was less oxygen consumption at any given flow rate (P less than .05). Imidazole, 30 mg kg-1, IP administered to prevent platelet aggregation, resulted in the return of oxygen utilization to the preembolization value. PVO2 of the microembolized muscle was significantly higher than in the contralateral muscle, which was abolished after imidazole administration. These data suggest that microembolization leads to an oxygen utilization defect similar to that observed in the resuscitated trauma patient. Since this defect was reversed by imidazole administration, a humoral mechanism in the microcirculatory bed may act to restrict oxygen utilization following microembolization and trauma.

A pronounced depletion of an opsonic protein for hepatic reticuloendothelial (RE) phagocytosis has been demonstrated in critically ill trauma patients. This opsonic alpha(2) surface binding (SB) glycoprotein has immunologic identity and a similar amino acid composition to cold insoluble globulin (CIg). Since CIg can be concentrated in cryoprecipitate, it was utilized as a readily available source of opsonic alpha(2)SB glycoprotein for replacement therapy after injury with documented hypoopsonemia. Six septic patients (2 multiple trauma, 2 thermal burn, and 2 intra-abdominal abscess) were studied to test whether cryoprecipitate infusion would restore this humoral component. Pre- and posttherapy opsonin levels were determined by bioassay and electroimmunoassay. In all patients, severe opsonin depletion was reversed following cryoprecipitate infusion. All patients had a rapid improvement in febrile state, normalization of leukocyte levels, and improvement in pulmonary function as evidenced by decreasing requirements for end expiratory pressure at lowered levels of inspired oxygen. One patient was studied more extensively and demonstrated an increase in cardiac output, limb blood flow, total body and limb oxygen delivery, total body and limb oxygen consumption and a progressive decrease in pulmonary shunt fraction. Thus, opsonic alpha(2)SB glycoprotein deficiency can be reversed by cryoprecipitate infusion in critically ill septic injured patients. Replacement of this humoral factor may be an important therapeutic modality in prevention of multiple organ failure, but it should be administered only after documentation of hypoopsonemia in traumatized patients.

The surgical management of 75 consecutive blunt liver injuries seen at the Albany Medical Center between 1969 and 1973 is reviewed and analyzed. The most common associated injury was right lower rib fractures which were found in one out of three patients. The spleen was the intra-abdominal organ most commonly injured (one out of four patients). The symptoms and signs of blunt liver injury may be misleading, since in one out of five cases there was no clinical evidence of intra-abdominal injury. The findings of fractured ribs on the right side associated with hypotension and a positive peritoneal tap demand immediate abdominal exploration. In patients with large amounts of disrupted hepatic tissue, a wedge resection was preferred over either simple debridement or hepatic lobectomy. A simple technique for limited hepatic resection provided fast, safe control of massive hemorrhage. The overall mortality was 33.3%. In six patients death was ascribed directly to the liver injury. The results of the present study suggest that death from liver injury per se can generally be prevented by prompt adequate surgical control of hemorrhage. When mortality occurs in these patients it is a result of injury to other organ systems.

A drop in the arterial PO2 occurring 24 hours after head injury was identified in eight patients. Traditional modes of therapy include administration of supplemental oxygen and provision of an unobstructed airway. The latter proved to be inadequate to continually maintain the PaO2 at a level consistent with the O2 content of the inspired air. Initially, determination of the PaO2, after institution of supplemental oxygen, may demonstrate adequate oxygenation, but blood gas monitoring should be continued since a delayed fall in arterial oxygen tension may occur 24 hours after head injury. This period of potentially deficient blood oxygenation, if severe enough, may further aggravate preexisting brain damage and profoundly affect the ultimate outcome of the patient. The delayed fall in PaO2 is the result of intrapulmonary shunting principally due to a ventilation/perfusion mismatch. The precise mechanism of the ventilation/perfusion inequality in the brain-injured patient awaits further elucidation, but may differ from the alteration in pulmonary function seen in the Respiratory Distress Syndrome.

The hemodynamic and respiratory effects of spontaneous ventilation with continuous positive airway pressure (CPAP) and mechanical ventilation with positive end-expiratory pressure (PEEP) were compared in nine patients who had adult respiratory distress syndrome. These patients were capable of maintaining spontaneous ventilation (tidal volume above 300 ml. and PaCO2 below 45 torr). Arterial and mixed venous blood gases, cardiac output, oxygen delivery and consumption, pulmonary artery pressure, and pulmonary wedge pressure were measured in 11 instances, with each patient on 5 or 10 cm. H2O CPAP or PEEP, and in nine instances, with each patient on the ventilator but without PEEP (O PEEP). During CPAP, when compared to PEEP at the same level of end-expiratory pressure, mean PaO2 increased significantly (p less than 0.05) and mean physiological shunt decreased (p less than 0.05). In nine of 11 instances, cardiac output was higher on CPAP than on a corresponding level of PEEP. Thus CPAP was more effective than the same amount of PEEP in improving arterial oxygenation by the lung without adversely affecting cardiac output.

Spontaneous hemorrhage caused by erosion of major arteries by a pseudocyst of the pancreas is a rare condition. We have encountered three cases, one involving the abdominal aorta and two the superior pancreaticoduodenal artery. It is important to keep in mind that pseudocyst of the pancreas may cause massive gastrointestinal or intraabdominal bleeding. Operative treatment offers a better chance of survival than more conservative management.

Pharmacologic doses of methylprednisolone sodium succinate were administered to 10 critically ill patients when the steroid was the only variable. Measurements of respiratory and circulatory physiologic parameters were obtained in all patients prior to injection and at 30 and 90 minutes following injection of methylprednisolone sodium succinate. A significant increase in Cardiac Index was seen (P less than .01) which appeared to be in association with a decrease in pulmonary vascular resistance (P less than .01) at a time when physiologic shunting of blood through the lungs increased (P less than .01). These changes imply improved perfusion of non- or poorly ventilated portions of the lungs. Four of ten patients demonstrated removal of lactate by the lung during the control period. Following methylprednisolone sodium succinate injection, 9 of 10 patients demonstrated production or a washout of lactate from the lungs.

The effects of isovolemic hemodilution on cardiac output and oxygen transport in 11 patients during elective vascular surgery were evaluated. Mean hemoglobin level was decreased from 12.5 +/- 0.6 to 10.2 +/- 0.5 g/dL by withdrawing blood and replacing it with an equal volume of colloid. Hemodilution increased cardiac output from 4.8 +/- 0.3 to 6.4 +/- 0.4 L/min, increased oxygen delivery from 830 +/- 75 to 900 +/- 95 mL/min and increased oxygen consumption from 190 +/- 20 to 240 +/- 40 mL/min. Systemic vascular resistance and mean arterial blood pressure decreased significantly, but cardiac filling pressure, pulmonary vascular resistance, heart rate, and intrapulmonary shunt did not change. In four of these patients who did not require all their blood during surgery, 1 unit of their withdrawn blood was reinfused after completion of surgery. In all four patients, cardiac output, oxygen delivery, and oxygen consumption decreased from the pretransfusion values. We conclude that, since intraoperative isovolemic hemodilution increased blood flow and systemic oxygen transport, it may be useful in the intraoperative management of patients with atherosclerotic vascular disease.

Patients recovering from acute respiratory insufficiency are usually not extubated until they can ventilate adequately while breathing spontaneously at ambient end-expiratory pressure (T-tube). It is hypothesized that this period of T-tube breathing might be detrimental to gas exchange since the endotracheal tube abolishes the expiratory retard produced by the glottis and thereby inhibits the patient's ability to maintain adequate functional residual capacity (FRC). To test this hypothesis, pulmonary function of 17 patients was compared during T-tube breathing and Continuous Positive Airway Pressure (CPAP) and after extubation. Intrapulmonary shunt was higher (p less than 0.05) and arterial PO2 and FRC were lower (p less than 0.05) during T-tube breathing than during CPAP or after extubation. In contrast, shunt, PaO2 and FRC were similar during CPAP and after extubation. Furthermore, after extubation there was an increase (p less than 0.05) in mean expiratory airway pressure as compared to T-tube breathing. A comparison of patients extubated from T-tube with patients extubated from CPAP showed no difference in postextubation shunt, PaO2 or FRC. These data suggest that endotracheal intubation should be accompanied by low levels of CPAP and that patients should be extubated directly from CPAP. The practice of placing patients in T-tube prior to extubation should be abandoned as unnecessary and potentially harmful.

To study the effect of interstitial edema on tissue oxygen transport, we infused buffered isotonic saline solution at a rate of 200 ml/kg/hr into mongrel dogs for two hours, measuring oxygen delivery and consumption in a skinned, innervated hindlimb. Hematocrit dropped gradually to 10.8 +/- 3.9%. Muscle water content increased 13% (P less than 0.05). However, oxygen consumption did not change significantly from control of 0.228 +/- 0.029 ml/min/100 gm. Femoral venous oxygen tension fell from control of 62.6 +/- 2.6 mm Hg to 31.4 +/- 2.3 mm Hg. Mean arterial flow increased to nearly twice the control level of 12.5 +/- 1.1 ml/min/100 gm and fell gradually, with the sustained 50% drop in vascular resistance largely explained by expected decreases in blood viscosity. We conclude that interstitial edema did not cause a significant defect in canine skeletal muscle oxygen utilization.

To study the isolated effects of decreased hemoglobin concentration without volume loss, eight patients with the diagnosis of polycythemia were studied following acute phlebotomy and simultaneous volume replacement. These patients had been treated previously by repeated phlebotomy, without volume replacement, to a hemoglobin level of 14.8 +/- 0.5 gm%. Following hemodilution by additional phlebotomy and volume replacement, which further lowered the mean hemoglobin level to 11.4 +/- 0.4 gm%, cardiac index increased significantly from 2.8 +/- 0.3 to 3.5 +/- 0. 3 liter/min/m(2) (P<0.05), oxygen delivery did not change, but total body oxygen consumption increased significantly from 140 +/- 16 to 180 +/- 15 ml/min/m(2) (P<0.05). Mixed venous PO2, systemic and pulmonary vascular resistance decreased significantly (P<0.05). Vascular pressure, heart rate, intrapulmonary shunt, arterial pH and bicarbonate, limb blood flow, limb oxygen delivery and limb oxygen consumption did not change. Thus, with phlebotomy and fluid replacement, a reduction of hemoglobin concentration to a subnormal level increased oxygen consumption without lowering oxygen delivery.

Increased pulmonary artery pressure, an increase in pulmonary vascular resistance and an increase in physiologic dead space are consistent findings in patients with post-traumatic respiratory distress. Since mannitol has been shown to decrease renal vascular resistance following trauma, the effect of a bolus injection of 100 ml of 25% solution of this drug on pulmonary hemodynamics and physiologic dead space was investigated in 11 patients who had suffered multiple trauma. Five minutes after the injection, pulmonary vascular resistance fell (p less than .01), cardiac index increased (p less than .001) and physiologic dead space decreased (p less than .05). In contrast, the administration of 40 mg of furosemide produced no significant change in any of these parameters. Mannitol rapidly equilibrates in the extracellular space and exerts an osmotic effect across cell membranes. We postulate that the beneficial response to mannitol on the pulmonary vascular resistance and the improved perfusion of ventilated regions of the lung is due to a reduction in cell swelling and is not explainable by its diuretic effect. Improvement in the distribution of perfusion of pulmonary blood flow by mannitol may be a useful aid in the treatment of the post-traumatic form of the respiratory distress syndrome.

Functional residual capacity (FRC) was measured in 12 postoperative patients and in one preoperative patient before and after they received intermittent positive pressure breathing (IPPB) with room air for ten minutes at a peak delivered pressure of 15 cm H2O. Ten patients had a normal or low pretreatment FRC. After cessation of IPPB, the mean FRC decreased further. Arterial oxygen tensions, measured in 11 of the 13 patients, decreased in all 11 from a pretreatment mean of 67.8 +/- 4.3 mm Hg to an immediate posttreatment mean of 57.7 +/- 4.2 mm Hg. In five patients repeated arterial blood gases were measured. At 30 minutes, their arterial oxygen tensions had returned to the pre-IPPB values. This study demonstrates that the routine use of IPPB in postoperative patients accentuates preexisting hypoxia and, therefore, must be used with caution.

High-frequency electrocardiograms (HF-ECG) were recorded from rabbits before and after delivery of blunt, nonpenetrating thoracic trauma. The conventional electrocardiographic record showed transient changes following the blow; the HF-ECG showed distinct notching and slurring in the QRS complex in most cases, which persisted throughout the course of the experiment. At autopsy, a contusive lesion of the right ventricle was always found.

Cardiac output and pulmonary wedge pressure (PWP) were used to evaluate the end point of fluid resuscitation in 20 patients suffering from multiple trauma and shock. Eleven patients received crystalloid resuscitation and nine patients received colloid resuscitation. Fifteen of 20 patients had an adequate cardiac output at the termination of resuscitation, but but only six of these patients had a PWP above 10 mm Hg. There was no significant correlation between left ventricular stroke work index and PWP in these patients, either at the completion of resuscitation or during the following three days. Five patients did not achieve adequate cardiac output and four of these patients died, suggesting that cardiac output was the most important criterion for adequate resuscitation. If the goal of fluid resuscitation is to achieve an adequate cardiac output, then PWP was not a reliable guide. Furthermore, using both cardiac output and PWP as a guide to fluid resuscitation of our patients, we found that the type of fluid (crystalloid or colloid) for resuscitation did not influence the course of respiratory distress in these patients up to three days following resuscitation.