Continuous positive airway pressure versus positive end-expiratory pressure in 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.

Effects of dopamine, ethanol, and mannitol on cardiopulmonary function in patients with adult respiratory distress syndrome.

Dopamine, ethanol, and mannitol were investigated to determine if they could increase pulmonary blood flow and oxygen delivery without significantly increasing intrapulmonary shunt. These drugs were studied in adult patients with respiratory distress following trauma, operation, or sepsis. Intravascular pressure, cardiac output, oxygen consumption and delivery, and limb blood flow and peripheral oxygen delivery were measured in all patients. Hypotensive patients received dopamine in incremental doses of 2 mu g/kg/min until either mean arterial pressure increased 15 mm Hg or heart rate increased by more than 15 beats/min. Ethanol was given as 10% ethanol in 5% dextrose at 2 ml/kg/hr. Mannitol was given as 25 gm of a 25% solution in a single bolus followed by infusion of 8 to 25 gm of 20% solution (mean 10 +/- 2 gm) as a continuous intravenous drip over 1 hour. No drug produced a significant change in intrapulmonary shunt. Ethanol produced significant (p less than 0.05) increases in cardiac index, heart rate, oxygen consumption, and oxygen delivery. Dopamine significantly decreased pulmonary vascular resistance while increasing systemic blood pressure. Visceral blood flow apparently increased while the peripheral vascular response to ischemia remained intact. Mannitol increased oxygen delivery and consumption in both the total body and limb. Thus in patients with adult respiratory distress syndrome (ARDS), increases in pulmonary blood flow can be achieved with several distinct pharmacologic agents without significant increases in intrapulmonary shunt. These increases in flow are generally accompanied by increases in oxygen delivery without increased pulmonary vascular resistance.

Cardiovascular hemodynamics after opsonic alpha-2-surface binding glycoprotein therapy in injured patients.

Depression of reticuloendothelial (RE) phagocytic function has been clearly documented following trauma and operation. This phagocytic failure is mediated in part by depletion of an opsonic glycoprotein. Depletion of this opsonic protein may result in prolonged blood retention of potentially harmful particulates that may interfere with the microcirculation and may possibly result in altered organ function. Isolation and identification of this opsonic protein has led to the finding of the identity between opsonic glycoprotein and cold insoluble globulin (CIg) or so-called plasma fibronectin. Since CIg is concentrated in cryoprecipitate, this blood component was used as a readily available source of opsonic protein for replacement studies. Nine patients were studied following a 1-hour infusion of cryoprecipitate obtained from 10 units of plasma and suspended in a volume of 250 ml. Both the pulmonary shunt fraction and the fraction of dead space ventilation decreased significantly (P = 0.02) after cryoprecipitate administration. Limb blood flow (P = 0.001), limb oxygen consumption (P = 0.001), and reactive hyperemia of the limb (P = 0.05) increased significantly following cryoprecipitate infusion. Cardiac output, total oxygen consumption did not change consistently. The data demonstrate that the infusion of cryoprecipitate resulted in improved pulmonary and microcirculatory function--possibly due to opsonic glycoprotein replacement.

Increased oxygen uptake following phlebotomy and simultaneous fluid replacement in polycythemic patients.

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.

Lung volume and blood oxygenation after intermittent positive pressure breathing.

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.

Cardiac output and pulmonary wedge pressure. Use for evaluation of fluid replacement in trauma patients.

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.

"Blue toe" syndrome. An indication for limb salvage surgery.

We describe 31 patients in whom proximal lesions in the arterial tree were identified as probable sources of emboli causing the "blue toe" syndrome. This syndrome consists of acute digital ischemia caused by microembolization to the digital arteries from a proximal source via a patent arterial tree, as evidenced by an otherwise well-perfused foot. It is closely analogous to the transient ischemic attacks of the brain, and carries the same potential for serious tissue loss because of repeated embolic showers. The prompt delineation and eradication of the embolic source is of prime importance, in addition to restoration of arterial continuity. Along with the other well-known features of chronic severe ischemia, that is, rest pain, gangrene, etc, the "blue toe" syndrome is therefore an indication for limb salvage surgery.

Increased cardiac output and oxygen transport after intraoperative isovolemic hemodilution. A study in patients with peripheral vascular disease.

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.

Spontaneous hemorrhage due to pseudocysts of the pancreas.

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.

Chronic venosus obstruction as a factor in the early failure of bypass grafts in the leg.

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.

Delayed impairment of arterial blood oxygenation in patients with severe head injury: preliminary report.

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.