Biomedical subjects

P J Feustel

Publications and source records attributed to P J Feustel.

At least 19 recordsLinked to original sources

PubMed1995

Orbital fractures in children.

OBJECTIVE: To determine if the pattern of orbital fractures may be influenced by the changing craniofacial ratio of the growing child, as the orbit is the boundary between the face and the cranium. DESIGN: Retrospective case series of 40 patients between the ages of 1 year and 16 years with orbital fractures. SETTING: The Albany (NY) Medical Center Hospital, a tertiary level 1 trauma center. OUTCOME MEASURES: The sex, age, site, and mechanism of injury, associated injury, and treatment methods for children admitted to the Albany Medical Center Hospital with orbital fractures between July 1986 and June 1992. RESULTS: Fourteen children had fractures of the orbital roof, 10 children had fractures of the orbital floor, 14 children had mixed fractures, and two children had fractures of the medial wall. The mean age (4.8 +/- 3.3 years) of the 14 patients with roof fractures was significantly less than the mean age (12.0 +/- 4.2 years) of the 26 children with other orbital fractures. Logistic regression demonstrated that the age at which the probability of lower orbital fractures exceeds the probability of orbital roof fractures is 7.1 +/- 1.0 years. Orbital roof fractures had a significantly greater likelihood of associated neurocranial injuries. The need for surgical repair was significantly lower among children with roof fractures as well as among children 7 years of age and younger. CONCLUSIONS: Orbital roof fractures are a type of skull fracture that occur primarily in younger children as a consequence of the proportionally larger cranium and the lack of frontal sinus pneumatization. Lower orbital fractures are a type of facial fracture that occur primarily in older children as a consequence of the increased vulnerability of the face due to growth and the pneumatization of the paranasal sinuses.

Adolescent↗

PubMed1995

Effect of hemorrhagic shock and reperfusion on the respiratory quotient in swine.

OBJECTIVES: Respiratory quotient, the ratio of CO2 production to oxygen consumption (VO2), is principally affected by the fuel source used for aerobic metabolism. Since the respiratory quotient, VO2, and CO2 production cannot be directly measured easily, indirect calorimetry is commonly used to determine the value of these variables at the airway level (i.e., airway respiratory quotient, airway VO2, and airway CO2 production). However, under nonsteady-state conditions, a variety of phenomena can alter the relationship between true metabolic activity and measurements determined by indirect calorimetry. During exercise, for example, airway respiratory quotient increases as anaerobic threshold is reached because of the disproportionate increase in airway CO2 production that results from the CO2 liberated through the buffering of excess hydrogen ions by bicarbonate. We hypothesized that hemorrhage and reinfusion might change airway respiratory quotient in a consistent manner as shock is produced and reversed. DESIGN: Prospective laboratory study. SETTING: University animal laboratory. SUBJECTS: Eight pigs (25 +/- 2 [SD] kg), anesthetized with fentanyl and relaxed with pancuronium bromide, and mechanically ventilated on room air. INTERVENTIONS: The animals were sequentially hemorrhaged and then autotransfused while metabolic and hemodynamic measurements were obtained, using continuous indirect calorimetry and continuous applications of the Fick principle. Hemoglobin, arterial lactate concentration, and blood gases for calibration were measured serially. Analysis of variance was used to compare various periods in time. MEASUREMENTS AND MAIN RESULTS: Between baseline and peak hemorrhage, and between peak hemorrhage and postreinfusion, all of the following variables changed significantly (p < .05): airway VO2 (baseline 6.4 +/- 0.9 mL/min/kg, peak hemorrhage 3.9 +/- 0.6 mL/min/kg, postreinfusion 7.0 +/- 1.4 mL/min/kg); airway CO2 production (baseline 5.5 +/- 0.9 mL/min/kg, peak hemorrhage 4.5 +/- 0.9 mL/min/kg, postreinfusion 6.0 +/- 1.4 mL/min/kg); airway respiratory quotient (baseline 0.87 +/- 0.07, peak hemorrhage 1.16 +/- 0.07, postreinfusion 0.87 +/- 0.05); lactate concentration (baseline 2.4 +/- 1.2 mmol/L, peak hemorrhage 6.7 +/- 1.9 mmol/L, postreinfusion 5.1 +/- 2.0 mmol/L); and delta PCO2 (venous PCO2-PaCO2) (baseline 4.5 +/- 3.6 torr [0.6 +/- 0.5 kPa], peak hemorrhage 12.1 +/- 5.3 torr [1.6 +/- 0.7 kPa], postreinfusion 2.7 +/- 2.7 torr [0.4 +/- 0.4 kPa]). CONCLUSIONS: Airway respiratory quotient increases in hemorrhagic shock and decreases again as shock is reversed during reinfusion. This phenomenon appears related to the buffering of excess of hydrogen ion during hemorrhagic shock.

Animals↗

PubMed1995

Cerebral blood flow and blood volume in response to O2 and CO2 changes in normal humans.

Changes in cerebral blood volume (CBV) after head injury may be an important determinant of intracranial pressure (ICP). To determine the normal response of CBV to hypoxemia, hypercapnia, and hypocapnia, eight normal subjects (5 males and 3 females; ages 25 to 43) were studied under these conditions. Cerebral blood volume was measured using an external collimated gamma detector to determine 99m-Tc-labeled red blood cell (RBC) activity in the intracranial vascular pool, and cerebral blood flow (CBF) was determined by internal carotid artery duplex scanning. Hypocapnia (Paco2 = 26.0 +/- 1.7 mm Hg, mean +/- SE) was achieved by hyperventilation, hypercapnia (Paco2 = 47.8 +/- 1.5 mm Hg) was achieved by inhalation of 6% CO2, and hypoxemia (Pao2 = 38.1 +/- 1.1 mm Hg, O2 saturation = 76.7 +/- 2.0%) was achieved by inhalation of 10% O2. Changes in CBF and CBV were determined by comparing the values in each condition to the immediately preceding period of normoxia and normocapnia. For conditions of hypocapnia, hypercapnia, and hypoxemia, the percentage of change in CBV was: -7.2 +/- 0.01, 12.8 +/- 0.01, and 5.2 +/- 0.03, respectively. The simultaneous percentage of change in CBF for the same conditions was -30.7 +/- 4.0, 29.5 +/- 9.2, and 18.4 +/- 6.9, respectively. For all conditions, changes in CBF were greater than changes in CBV; however, this was most pronounced during hypocapnia induced by hyperventilation. Because the change in CBV reflects the potential change in ICP in response to treatment, therapeutic hyperventilation may impair CBF to a greater degree than it reduces ICP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Effect of hyperventilation, mannitol, and ventriculostomy drainage on cerebral blood flow after head injury.

Therapies to lower intracranial pressure (ICP) after traumatic brain injury (TBI) include hyperventilation (HV), intravenous mannitol (IM), and cerebrospinal fluid drainage from a ventriculostomy (DV). To determine the effects of these therapies on cerebral blood flow (CBF), fiberoptic oximetry was used to measure jugular venous O2 saturation (SjvO2) as an index of the CBF to cerebral metabolic rate for O2 (CMRO2) ratio after IM (25 g IV for more than 5 min), DV (3 min), or HV (increase respiratory rate by 4) therapy for elevated ICP. Assuming CMRO2 is constant, changes in SjvO2 reflect changes in CBF. Continuous measurements of SjvO2, ICP, blood pressure, arterial O2 saturation, and end-tidal CO2 were obtained in 22 patients with a Glasgow Coma Scale score of 5.3 +/- 0.4 (mean +/- SD) in the first 5 days after TBI. Therapy was initiated a total of 196 times when ICP was > 15 mm Hg for > 5 minutes, and measurements made at 20 minutes after treatment were compared with those made just before. After DV, ICP fell in 90% of the observations by 8.6 +/- 0.7 mm Hg (mean +/- SEM, n = 119); after IM, ICP fell in 90% of the observations by 7.4 +/- 0.7 mm Hg (n = 43); and after HV, ICP fell in 88% of the observations by 6.3 +/- 1.2 mm Hg (n = 14). In patients where ICP fell, SjvO2 increased by 2.49 +/- 0.7% saturation (from 68.0 +/- 1.3%) with IM, but only by 0.39 +/- 0.4% saturation (from 67.2 +/- 0.9%) with DV.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1995

Effects of ethanol on respiratory function in traumatic brain injury.

It has been observed that traumatic brain injury (TBI) increases the susceptibility of the brain to subsequent hypoxia, and prolonged apnea occurs in ethanol (EtOH)-treated animals following brain injury. This investigation tests the hypothesis that EtOH suppresses ventilation and hypercapnic respiratory drive following TBI. Immature pigs were anesthetized with halothane and received a 2 to 3 atm fluid-percussion brain injury. Respiratory parameters, including tidal volume, frequency, ventilation (VE), and arterial blood gases were measured on 100% O2 and on 5% to 6% inspired CO2 in O2 prior to and at 10, 60, 120, and 180 minutes after TBI. Hypercapnic response sensitivity (S) was measured as the change in VE per mm Hg increase in PaCO2. Intracranial pressure, mean arterial blood pressure, heart rate, brain temperature, glucose, and EtOH levels were also monitored. Three groups were studied: the first group of six received EtOH (3.5 gm/kg, intragastrically) without brain injury; the second group of six received TBI without EtOH; the third group of eight received EtOH and TBI. Ethanol levels were 121 +/- 13 (standard error of the mean) mg/dl in the EtOH/TBI group (136 +/- 25 in the EtOH group) at the time of injury, and 175 +/- 12 mg/dl in the EtOH/TBI group (200 +/- 20 mg/dl in the EtOH group) at 120 minutes after injury. The EtOH/TBI animals had significantly lower VE and S, and higher PaCO2 following brain injury (p < 0.05, repeated-measures analysis of variance). No significant differences were identified between groups for pH, PaCO2, intracranial pressure, heart rate, brain temperature, or glucose levels. Ethanol intoxication leads to significant impairment of respiratory control following traumatic brain injury and may contribute to brain injury in intoxicated trauma victims.

Alcoholic Intoxication↗

PubMed1994

Feasibility of continuous oxygen delivery and cardiac output measurement by application of the Fick principle.

Continuous mixed venous oxygen saturation (SVO2) measurements from fiberoptic pulmonary artery catheters, arterial oxygen saturation (SaO2) measurements from pulse oximetry, and minute-by-minute oxygen consumption (VO2) measurements from indirect calorimetry can be used for near-continuous estimation of cardiac output (Qt) and oxygen delivery (DO2) by application of the Fick Principle. Assumptions required for calculation of blood oxygen contents include constant hemoglobin concentration (Hgb) and constant or negligible physically dissolved oxygen. First, the influence of these assumptions on continuous Qt and DO2 determinations was tested. Unmeasured changes in Hgb resulted in substantial error in calculated Qt, whereas calculated DO2 was minimally affected. Both Qt and DO2 were little altered by errors in PaO2 or PVO2. Second, the effects of SVO2, SaO2, and VO2 measurement errors on Qt and DO2 calculations under normal and extreme conditions were quantified. Relative errors in SVO2 were increased by a factor of 4.2 in Qt estimations and by a factor of 3.2 in DO2 measurements under normal conditions. These factors increased with increasing SVO2, and thus, Qt and DO2 became increasingly unreliable as oxygen extraction fell. Third, we compared continuous measurements of Qt and DO2 with intermittent measurements made by thermodilution cardiac output and blood sampling, and found correlation coefficients of 0.85 for Qt and 0.89 for DO2. Fourth, common measurement errors in VO2 and DO2 calculated in this way were found to bias regressions between VO2 and DO2, and this bias could be minimized only if the DO2 range were high and SVO2 were low.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗

PubMed1994

Continuous measurement of jugular venous oxygen saturation in response to transient elevations of blood pressure in head-injured patients.

Following traumatic brain injury, continuous jugular venous oxygen saturation (SjvO2) measurements have been made and used to assess cerebral oxygenation. Transients of SjvO2 may reflect cerebral blood flow (CBF) changes if measurements are made over a short period of time during which cerebral metabolic rate for oxygen is assumed unchanged. In response to alterations in perfusion pressure, transients of SjvO2 may indicate the extent to which autoregulation has been preserved after injury. The effect of arterial pressure changes on SjvO2 was measured in 14 severely head-injured patients (Glasgow Coma Scale score < 8) within 36 hours of injury. Mean arterial blood pressure (MABP), arterial oxygen saturation, and intracranial pressure (ICP) data were also continuously recorded by a computer at the patients' bedside. The reliability of the SjvO2 oximetry measurements varied among patients, and an average 38% of SjvO2 measurements were off by more than 6% saturation, necessitating recalibration. During periods of satisfactory catheter performance, 120 instances were found in which MABP was elevated more than 8 torr (mean +/- standard deviation: 32 +/- 13 torr) due to endotracheal suctioning. In 94 of these measurements, there was an associated increase in the ICP of 5 torr or more, averaging 16.6 +/- 10.2 torr. The SjvO2 was 0.62 +/- 0.10 before the increase in MABP and rose to a peak of 0.77 +/- 0.10 during the maximum MABP elevation, suggesting increased CBF during the transient hypertension. In 34 of 37 instances of persistent blood pressure elevations lasting for more than 10 minutes (mean 16.0 +/- 8.0 minutes), the SjvO2 elevation persisted (average duration 15.0 +/- 12.4 minutes), suggesting impaired or lost autoregulatory vasoconstriction. The presence or absence of hyperemia was unrelated to the extent of the autoregulation response. Results indicate that SjvO2 rises with increasing perfusion pressure during and after endotracheal suctioning, suggesting a feeble or absent autoregulatory response following traumatic brain injury.

Adolescent↗

PubMed1993

Effects of ethanol in traumatic brain injury.

The effects of ethanol intoxication on brain injury and cerebral blood flow (CBF) were investigated in a porcine fluid-percussion model of traumatic brain injury (TBI). Immature swine, under halothane anesthesia (1%), had a TBI delivered with a fluid-percussion device. The experimental group (n = 10) received ethanol (3.5 gm/kg) via gastric tube followed in 1 h by TBI. Two groups of control animals received normal saline and TBI (n = 10) or ethanol and no TBI (n = 5). Mean arterial blood pressure (MAP), intracranial pressure (ICP), arterial blood gases, and serum lactate were monitored for 3 h after the injury. CBF was measured with radiolabelled 15-micron diameter microspheres. Neuropathologic changes were evaluated and graded after formalin perfusion and brain removal at 3 h postinjury. The ethanol level 60 min post-head injury was 198 +/- 70 (SD) mg/dL in the ethanol+TBI group. At 90 min postinjury and thereafter, ethanol+TBI animals compared with TBI only animals had significantly lower MAP (63 +/- 26 mmHg vs 91 +/- 15 mmHg) and lower cerebral perfusion pressure (50 +/- 25 mmHg vs 78 +/- 15), and at 180 min postinjury, lower CBF (87 +/- 37% vs 62 +/- 79% of preinjury levels). Ethanol+TBI animals had higher blood lactates (28 +/- 11 mg/dL vs 13 +/- 6 mg/dL) than TBI only animals. Ethanol+TBI animals also had significantly longer postinjury apneas (11 +/- 8 min vs 0.6 +/- 0.4 min), with three of ten ethanol-treated animals never recovering spontaneous respiration. Ethanol intoxication produced hemodynamic and respiratory changes, which may have a deleterious effect on outcome and mortality after brain injury.

Alcoholic Intoxication↗

PubMed1993

Vascular clearance and organ uptake of G- and F-actin in the rat.

This study comparatively evaluated the kinetics of removal and organ distribution of circulating G- and F-actin. Both F- and G-actin were cleared in two phases (fast component with a t1/2 of 3-5 min and a slow component with a t1/2 of hours). There was no effect of dose on either the fast- or slow-compartment clearance kinetics at the doses tested (5-100 micrograms/100 g body wt). However, at the same challenging dose of F- and G-actin, more F-actin was removed during the rapid phase. Although the time constants (Tfast) for F- and G-actin removal from the vasculature during the initial rapid phase were the same, during the slow phase the time constants (Tslow) for removal of F-actin were less (P < 0.001) than that of G-actin. The fraction of F-actin removed during the rapid phase ranged from 33 to 63% and was significantly greater (P < 0.01) than the fraction of G-actin removed during this phase (10-33%). The liver was the main organ of localization, and autoradiographic studies of liver tissue demonstrated that G-actin monomers were removed by Kupffer cells, whereas F-actin was predominantly removed by hepatic sinusoidal endothelial cells. In vivo endotoxin activation of Kupffer cells enhanced the rate of G-actin removal and increased liver localization of G-actin but had no effect on F-actin removal. This further supports a role for Kupffer cells in the clearance of G-actin. These studies therefore demonstrate that F- and G-actin clearance mechanisms are different. G-actin removal, presumably mediated by its binding to vitamin D binding protein, is accomplished by Kupffer cells, whereas F-actin removal at the same doses is due mainly to hepatic endothelial cell uptake.

Actins↗

PubMed1993

Lung function in workers refining phosphorus rock to obtain elementary phosphorus.

Elevated levels of phosphoric acid, phosphorus pentoxide, fluorides and coal tar pitch volatiles were present in workplace air of a two-oven industrial refinery. One hundred thirty-one workers prospectively underwent annual pulmonary function testing (forced vital capacity, forced expiratory volume in 1 second, and forced expiratory flow). Regression of these spirometric data, analyzed longitudinally over 3 to 7 years and also cross-sectionally reveals no residual significant effect of industrial exposure after adjusting for the effect of age and smoking. This industrial exposure contributes only weakly and inconsistently to the well-documented reduction of spirometric lung function that occurs from smoking alone. No significant reductions of spirometry occurred in exposed nonsmokers or former smokers.

Adult↗

PubMed1993

Optimal outcome after tibial arterial bypass.

To evaluate factors for the optimal outcome after tibial arterial bypass for lower extremity ischemia, we analyzed our experience with 1,359 such bypasses during the last ten years. There were 869 males and 490 females, of whom 739 patients (54 percent) had diabetes. The average age was 68 years. One thousand and twenty-four bypasses were performed using the atraumatic valve incision in situ technique, 281 bypasses using free vein grafts and 54 bypasses with synthetic materials. These bypasses were taken to the anterior tibial (312 patients), posterior tibial (341 patients), peroneal (520 patients) and dorsalis pedis arteries (125 patients). Inflow arteries included external iliac (two patients), common (435 patients), superficial (472 patients) and profunda femoris arteries (259 patients). In certain instances, popliteal and tibial arteries were used for inflow (short bypasses). Limb salvage was the significant indication (95 percent). The overall cumulative primary patency rate at five years was 68 percent and secondary patency was 76 percent. In situ bypasses had the best secondary patency rate of 80 percent at five years followed by free vein grafts of 70 percent and synthetic bypasses of 33 percent. The choice of inflow or outflow arteries did not influence the patency rate in any category. The overall limb salvage rate was 94 percent at five years. Short bypasses using free vein grafts had a similar patency to long free vein graft but lower patency than long in situ bypasses. These data demonstrate that bypasses to tibial arteries, using autogenous vein for ischemia of the lower extremity and limb salvage, have long term durability. In situ bypass with a complete saphenous vein is the best conduit for such reconstructions. We suggest that tibial arterial bypass should be strongly considered in all instances for limb salvage when autogenous vein is available before resorting to primary amputation.

Aged↗

PubMed1992

A pediatric trauma center without a pediatric surgeon: a four-year outcome analysis.

Approximately 25% of all injury victims are in the pediatric age group, and one in four injured children will require a pediatric trauma center. According to the American College of Surgeons as well as many state guidelines, a level I pediatric trauma team should be directed by a pediatric surgeon. In 1986, the pediatric surgeon left our pediatric trauma center, but the center remained open under a cooperative effort by the adult trauma surgeons and pediatric intensivists. We have retrospectively reviewed the charts of all pediatric trauma patients (age less than or equal to 15 years) for the subsequent 4 years to determine the outcome of treatment without a pediatric surgeon. During this period, we treated 303 pediatric patients with multiple or serious single-system injuries. The mean age was 6.9 +/- 0.3 (SEM) years and 66% were boys. Falls were the cause of injury in 31% of the patients, with pedestrian/bicycle, motor vehicle crashes, and penetrating injuries resulting in 26%, 19%, and 3% of the injuries, respectively. The mean ISS was 15.6 +/- 0.8, and 73% of the patients had at least one AIS greater than or equal to 3. Surgical procedures were required in 48% of the patients. There were 27 deaths in this group, most commonly related to head injury (89%). The mean Pediatric Trauma Score of the patients who died was 1.6 +/- 0.8 and no patient with a Pediatric Trauma Score greater than 7 died.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1992

Fick-derived hemodynamics. Oxygen consumption measured directly vs oxygen consumption calculated from CO2 production under steady state and dynamic conditions.

Indirect calorimetry is being used increasingly as a tool for hemodynamic monitoring via the Fick equation. This investigation was undertaken to examine the use of carbon dioxide elimination (VCO2A) and related respiratory quotient (RQA) to calculate oxygen uptake (VO2A) and estimate oxygen consumption (VO2) during steady-state and dynamic hemodynamic conditions. Nine patients undergoing abdominal aortic surgery were studied intraoperatively and Fick-derived hemodynamic measurements were made using a monitoring system employing indirect calorimetry, pulse oximetry, and pulmonary artery oximetry. Comparisons were made between measured VO2A and calculated VO2A derived from the VCO2A and the initial RQA (RQi), which is assumed not to change. Prior to aortic crossclamping (steady state), there were no significant differences between the measured and calculated methods with respect to oxygen consumption (184 +/- 24 ml/min vs 185 +/- 17 ml/min), oxygen delivery (753 +/- 141 ml/min vs 769 +/- 178 ml/min), and cardiac output (4.7 +/- 0.6 L/min vs 4.7 +/- 0.7 L/min). However, immediately following aortic unclamping (dynamic state), the RQA changed precipitously from the baseline RQi. Consequently, significant differences between the measured and calculated methods were noted in oxygen uptake (213 +/- 41 ml/min vs 193 +/- 25 ml/min, p < 0.001), oxygen delivery (780 +/- 297 ml/min vs 716 +/- 296 ml/min, p < 0.001), and cardiac output (5.8 +/- 2.2 L/min vs 5.3 +/- 1.8 L/min, p < 0.001). Additionally, following unclamping, the peak VO2A was 242 +/- 49 compared with a cVO2A of only 198 +/- 22 (p < 0.01). We conclude that the use of VCO2A to calculate VO2A may lead to erroneous measurements under dynamic conditions, such as unclamping of the abdominal aorta.

Aorta, Abdominal↗

PubMed1992

Human cerebrovascular response to oxygen and carbon dioxide as determined by internal carotid artery duplex scanning.

Alterations in arterial oxygen and carbon dioxide influence cerebrovascular resistance and therefore cerebral blood flow (CBF), but the magnitude of these CBF responses have not been well defined in normal humans. Duplex scanning (B-mode imaging and pulsed Doppler shift analysis) was used to measure internal carotid blood flow (ICBF) as an indicator of CBF in 20 normal subjects during alterations of arterial O2 and CO2. End-tidal PCO2 (PETCO2) was measured by mass spectrometry, arterial oxygen saturation by pulse oximetry, and unilateral (right) ICBF by duplex scanning. A variety of gas mixtures were administered to achieve hypoxemia (FIO2 = 0.075-0.10) and hypercapnia (FICO2 = 0.05) or the subject was asked to hyperventilate to PETCO2 = 16-24 mm Hg. The ICBF was determined five times in each of six conditions: (1) normoxia/normocapnia; (2) normoxia/hypercapnia; (3) normoxia/hypocapnia; (4) hypoxia/normocapnia; (5) hypoxia/hypercapnia; and (6) hypoxia/hypocapnia. During normoxia and normocapnia, the mean ICBF was 330 +/- 19 (SEM) mL/min. Specific CO2 reactivity was 7.4 +/- 0.7 mL/min/mmHg, which is equivalent to 2.3% +/- 0.1% of normocapnic blood flow per mm Hg change in CO2. During normocapnia, ICBF increased by 2.9 +/- 0.9 mL/min for each percentage decrease in oxygen saturation. Using an ANOVA with repeated measures to fit the responses, the following statistically significant relationship was found: ICBF (mL/min) = 333 + 6.3.(PETCO2 - 40) + 2.7 DSO2 +/- 81 where DSO2 is arterial desaturation (100 - arterial saturation). An additional "between subject" variation had a mean of 0 and a standard deviation of 82 mL/min. There was no statistically significant evidence of an interaction between O2 and CO2 response. Our data suggest that hypoxia and carbon dioxide changes will alter CBF simultaneously and additively. Duplex scanning of the internal carotid artery, which can be performed at the bedside, is sufficiently sensitive to detect changes in ICBF and internal carotid artery oxygen delivery.

Adult↗

PubMed1990

Oxygen delivery and consumption in head-injured and multiple trauma patients.

Critically ill patients often demonstrate that whole body oxygen consumption (VO2) is dependent on oxygen delivery (DO2). In this retrospective study, the relationship of VO2 to DO2 in patients with isolated head injury (HI, n = 18) was compared to that in patients with multiple trauma (MT, n = 60) without serious head injury. Mean pulmonary capillary wedge pressure, central venous pressure, arterial PCO2, cardiac index, and oxygen delivery were significantly lower in HI, but oxygen consumption was not different in the groups. In both groups, changes in DO2 (delta DO2) within each patient were significantly correlated with changes in VO2 (delta VO2) in that same patient. This relationship was not different between the HI patients, (delta VO2 = (0.20 +/- 0.02) delta DO2), and the MT patients (delta VO2 = (0.17 +/- 0.01) delta DO2). When these groups were further divided into those with high hematocrit (greater than 32%) and low hematocrit (less than 32%), HI patients with a low hematocrit demonstrated a steeper regression slope, with 26 +/- 3% of the DO2 change being reflected in the VO2 change. This was significantly greater than the slope in HI patients with high hematocrit (13 +/- 3%) and the MT patients at high (19 +/- 2%) or low (16 +/- 2%) hematocrits. These data show a correlation between changes in oxygen delivery and consumption that is similar in both head-injury patients and multiple trauma patients without serious head injury. This relationship was greatest in head-injured patients at low hematocrit. This relationship of VO2 and DO2 in both groups suggests an influence of neurohumoral factors rather than local tissue phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Immediate preoperative phlebotomy with autologous blood donation for aortic replacement.

The preferential use of autologous blood provided by phlebotomy can reduce the need for homologous blood transfusion in patients undergoing extensive elective operations. This blood is usually provided either by intraoperative isovolemic hemodilution or phlebotomy one to two weeks preoperatively. To minimize the intraoperative time delay or preoperative period between phlebotomy and operation required in these patients, we performed preoperative isovolemic hemodilution in 69 patients one to two days prior to elective aortic replacement for infrarenal aneurysmal disease. Patients underwent phlebotomy a mean of 0.57 +/- 0.01 liter of whole blood; volume was replaced with lactated Ringer's solution. Hematocrit levels decreased from a mean value of 42.9 +/- 0.4 per cent to 33.7 +/- 0.3 per cent. Mean intraoperative blood loss was 1.2 +/- 0.05 liters. Hemodynamic parameters (blood pressure, cardiac output, pulmonary capillary wedge pressure, central venous pressure, oxygen delivery and systemic vascular resistance) remained stable throughout the perioperative and intraoperative time periods. In addition, we evaluated the technical modification of exclusion aneurysmorrhaphy (n = 50) versus open aneurysmorraphy (n = 19) on reduction of intraoperative homologous blood transfusion in these patients. Seventy-two per cent (36 of 50) of patients whose aneurysms were excluded received no homologous blood intraoperatively. Blood loss was decreased in the excluded versus open aneurysmorraphy group, 920 +/- 90 milliliters versus 2,030 +/- 250 milliliters, as were homologous blood transfusion requirements, 175 +/- 35 milliliters versus 570 +/- 119 milliliters. Two patients died (2.9 per cent mortality rate), and there was no increase in morbidity. Surgical treatment of large aortic aneurysms is frequently performed on an urgent basis; thus, provision of autologous blood for this operation in a short period of time may be beneficial. Isovolemic hemodilution performed during the immediate preoperative period can reduce homologous blood requirements and be safely performed without adverse effects on mortality, morbidity and myocardial performance. Exclusion aneurysmorrhaphy may further reduce dependence on homologous blood.

Aorta, Abdominal↗

PubMed1990

Remote distal arteriovenous fistula to improve infrapopliteal bypass patency.

The results of the use of prosthetic materials for femorocrural bypass surgery have been less than optimal. The creation of a distal anastomotic arteriovenous fistula to augment blood flow and velocity through the graft is well known. However, it may create turbulence at the anastomosis and steal blood flow away from the distal artery. A canine model was developed to evaluate the effect of fistula size on graft/arterial hemodynamics. In 16 patients we have constructed a distal arteriovenous fistula, which is remote from the distal anastomosis, and we studied the effect of such fistulas on bypass patency and distal arterial hemodynamics. Patients selected for this procedure had multiple previously failed reconstructions and limb-threatening ischemia and did not have usable autogenous vein. Femorotibial bypass graft reconstructions were performed with polytetrafluoroethylene followed by the creation of a side-to-side arteriovenous fistula 5 to 15 cm below the distal anastomosis in the same artery and accompanying veins. We have achieved a 1-year patency of 67% with a 75% limb salvage rate. We also serially measured blood flow and velocity within the bypass, the arteriovenous fistula, and the distal outflow vessel using duplex scanning after surgery. Mean estimated blood flow through the bypass during the immediate postoperative period was 264 ml/min, the arteriovenous fistula was 157 ml/min, and the distal artery was 19 ml/min. Unlike an arteriovenous fistula created at the distal anastomosis, a remote distal arteriovenous fistula not only increases graft blood flow but also augments native arterial blood flow between the distal anastomosis and fistula and thus may improve distal limb perfusion.

Animals↗

PubMed1989

Plasma fibronectin synthesis in normal and injured humans as determined by stable isotope incorporation.

In humans, plasma fibronectin decreases early after operative injury, burn, or trauma, followed by a rapid restoration with a secondary decline typically observed if such patients become septic. We determined the rate of plasma fibronectin and plasma fibrinogen synthesis in normal subjects and injured patients using a stable isotope incorporation technique with [15N]glycine. During a constant 14-h infusion of [15N]glycine, the enrichment of [15N]glycine in both the free plasma glycine precursor pool as well as the urinary hippurate pool was determined; the latter used as an estimate of intracellular hepatic precursor enrichment. [15N]Glycine enrichment in both plasma fibronectin and fibrinogen was also quantified. The synthesis rate (Js/V) expressed in micrograms per milliliter of plasma per hour and the fractional synthesis rate (FSR) expressed as percentage of the plasma pool produced per day were determined. In normal subjects, the FSR for plasma fibronectin using 15N enrichment into urinary hippurate was 35.35 +/- 1.46%/d, whereas the Js/V was 4.45 +/- 0.19 micrograms/ml plasma per h. In normal subjects, the FSR for plasma fibronectin using 15N enrichment into free plasma glycine was 14.73 +/- 0.63%/d, whereas the Js/V was 1.98 +/- 0.09 micrograms/ml plasma per h. Early (2-3 d) after burn injury, fibronectin synthesis was increased (Js/V = 5.74 +/- 0.36; P less than 0.05), whereas later after injury, fibronectin synthesis began to decline (Js/V = 3.52 +/- 0.24; P less than 0.05) based on 15N enrichment of urinary hippurate. In contrast, the Js/V and FSR of plasma fibrinogen, a well-documented acute-phase plasma protein, revealed a sustained elevation (P less than 0.05) after injury in both the trauma and burn patients. Thus, plasma fibronectin synthesis is elevated early postinjury, which may contribute to the rapid restoration of its blood level. However, once fibronectin levels have normalized, the synthesis of plasma fibronectin appears to decline.

Adult↗