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Biomedical subjects

P R Freund

Publications and source records attributed to P R Freund.

At least 19 recordsLinked to original sources
PubMed1991

A prospective study of intraoperative pulse oximetry failure.

Since pulse oximetry is now an ASA standard for intraoperative monitoring, we sought to determine the intraoperative failure rate for this device. We prospectively evaluated the intraoperative failure rate of our pulse oximeters at the four University of Washington Hospitals (University of Washington Medical Center, Veterans Affairs Medical Center [VAMC], Children's Hospital and Medical Center, and Harborview Medical Center [HMC]) recorded from April 1989 to August 1989. We defined failure as the inability to obtain any oximetry reading for a cumulative period of more than 30 minutes during any anesthetic procedure after all equipment malfunctions had been eliminated. Our puse oximeters failed in 124 of 11,046 cases studied; this is a failure rate of 1.12%, which ranged from 0.56% at HMC to 4.24% at VAMC. The failure rate at VAMC (4.24%) was significantly higher than the other hospitals (p less than 0.001). Those cases associated with the pulse oximeter failure had the following characteristics: (1) an ASA status of 3 or higher, (2) lengthy operations, and (3) elderly patients. When the device did fail in a patient, it did not function for 32% of the mean anesthesia time. We conclude that the intraoperative use of the pulse oximetry can provide information about blood oxygen saturation in most patients. However, in approximately 1% of the patients we studied in the operating room, mechanically functioning pulse oximeters failed to provide readings of blood oxygen saturations during routine operative use.

Equipment Failure↗
PubMed1990

Microcomputer-based data acquisition system for clinical research.

We have described a computerized data acquisition system for clinical investigation that can record over fifty physiologic variables from up to twenty-four electronic monitors. The information is acquired by a personal computer using RS-232C serial communications and analog-to-digital conversion. In its present configuration the system records information from a Spacelabs 500 series physiologic monitor, Hewlett-Packard physiologic monitor with the Careport computer interface, SARA mass spectrometer, Nellcor pulse oximeter, Neurotrac processed EEG, Lawrence cardiac output monitor, Hewlett-Packard capnometer, and Bourns spirometer. The software can be easily modified to accommodate other physiologic monitors. The system records parameter or waveform information and writes the data into a file that can be accessed by commercially available graphical and statistical packages. The data acquisition system is easy to use, transportable, and inexpensive.

Humans↗
PubMed1990

Placement of esophageal stethoscope by acoustic criteria does not consistently yield an optimal location for the monitoring of core temperature.

The esophageal stethoscope has evolved into a device for both acoustic and core temperature monitoring. To test whether routine placement according to acoustic criteria results in placement of the core temperature sensor in the region of contiguity between the esophagus and the heart, we determined the depth of placement electrocardiographically. All patients were undergoing nonthoracic elective operations requiring general anesthesia and tracheal intubation. First, we established that different observers selected the same esophageal depth within +/- 1 cm electrocardiographically, using the criterion of a symmetric biphasic P wave of maximal amplitude (7 patients). Then, in 30 more patients, we compared routine acoustic placements with the depths of the maximal-amplitude biphasic P wave. Stethoscopes placed according to acoustic criteria were within +/- 3 cm of P-wave depths in 15 of 30 patients. In the remaining patients, measured discrepancies ranged up to 13.5 cm. We conclude that the prevailing stethoscope design, with a thermistor at the tip, below the acoustic window, does not ensure placement of the thermistor within the optimal region for monitoring of core temperature. A modification in design that would take advantage of the reliability of electrocardiographic positioning is suggested.

Acoustics↗
PubMed1990

Cystic fibrosis, vasoactive intestinal polypeptide, and active cutaneous vasodilation.

The transmitter substance for the active cutaneous vasodilation that accompanies sweating during hyperthermia in humans is unknown. Hökfelt et al. (Nature Lond. 284: 515-521, 180) hypothesized that it is vasoactive intestinal polypeptide (VIP) that is cotransmitted with acetylcholine. Heinz-Erian et al. (Science Wash. DC 229: 1407-1408, 1985) reported that VIP innervation is sparse in the skin of persons with cystic fibrosis (CF). A corresponding attenuation of active vasodilation in these subjects would be evidence that VIP is involved in this effector mechanism of human thermor-regulation. Immunocytochemical analysis of skin biopsies from four men with CF confirmed that VIP innervation was sparse. We also analyzed immunoreactivity for calcitonin gene-related peptide (CGRP; normal), substance P (normal), and neuropeptide Y (low). VIP-immunoreactive Merkel cells were abnormal. Despite sparse VIP-immunoreactive innervation, our CF subjects' cutaneous vascular responses to hyperthermia were normal. Because VIP was not completely absent, this evidence is insufficient to rule out VIP as the vasodilator transmitter. However, the CGRP and substance P innervation we observed could mean that release of one or both of these peptides was the mechanism of the fully developed active cutaneous vasodilation.

Adult↗
PubMed1989

Does acute hypoxemia blunt sympathetic activity in hyperthermia?

Sympathetic alpha-adrenergic function is depressed by hypoxemia per se; does addition of another sympathoexcitatory stimulus elicit normal responses in other sympathetic effector pathways? We activated by hyperthermia four sympathetic pathways: alpha-adrenergic [norepinephrine (NE) release], beta-adrenergic [plasma renin activity (PRA)], cholinergic (sweating), and peptidergic (active vasodilation). In the first test, five normothermic men were exposed to hypoxemia for 10 min (control), then hypoxemia plus heat for 30 min, and then heat with normoxia for 8-10 min over a continuous 48- to 50-min period. Heating was controlled with a water-perfused suit. Time courses and magnitudes of heat-induced increments in body temperature, forearm blood flow, and sweat rate were normal during hypoxemia and unaffected by switching to normoxia. Hypoxemia exaggerated increases in plasma NE, epinephrine, PRA, and heart rate but had no additional effects on blood pressure. In a second 50-min test (2 men) with normoxic control (10 min), heating plus normoxia (20 min), and heating plus hypoxemia (20 min), effects of hypoxemia on all variables were as in the first test. Thus, acute moderate hypoxemia did not blunt active cutaneous vasodilation or sweating and exaggerated increases in catecholamines and heart rate, indicating maintained peripheral autonomic function.

Acute Disease↗
PubMed1987

Transesophageal Doppler scanning versus thermodilution during general anesthesia. An initial comparison of cardiac output techniques.

Measurement of cardiac output has become an essential feature of anesthetic management of patients with cardiac disease requiring operation. Thermodilution by way of a Swan-Ganz catheter is the current popular technique for cardiac output determination. Unfortunately, this method is costly and has an associated irreducible morbidity rate and has, in rare instances, resulted in death. The suprasternal ultrasonographic Doppler technique has shown promise for measuring cardiac output noninvasively; however, it is too cumbersome for continuous intraoperative use. In an effort to overcome this limitation, the esophageal stethoscope was modified to accept a Doppler probe. Herein, we have reported an initial comparison of transesophageal Doppler scanning and thermodilution in 23 adult men during general anesthesia. The average difference between thermodilution and descending cardiac output was 0.16 +/- 0.81 liters/min. The correlation between thermodilution and descending cardiac output increased with operator experience. In the last 13 patients, there was an average correlation of 0.85. After the equipment was mastered and improvements in design were made, descending cardiac output had a high correlation with thermodilution and appeared to track the dynamic changes during general anesthesia.

Aged↗
PubMed1987

Propranolol reduces bupivacaine clearance.

Propranolol reduces the clearance of lidocaine by both reducing hepatic blood flow and inhibiting lidocaine metabolism. The authors investigated the possibility that propranolol reduces the clearance of bupivacaine as well. Bupivacaine, 30-50 mg, was administered intravenously to six normal human volunteers, over 10-15 min on two occasions, at least 2 weeks apart. Propranolol, 40 mg orally every 6 h, was used on one occasion, beginning 24 h prior to the bupivacaine administration. The sequence of the sessions was randomized. Twenty-two venous blood samples were obtained over 36 h in order to determine bupivacaine clearance, terminal elimination rate constant, and volume of distribution. All subjects experienced mild CNS toxicity, consisting of tinnitus, facial tingling, or subtle visual disturbances, associated with peak venous plasma concentrations of 0.81 to 2.7 micrograms/ml. Mean bupivacaine clearance was 0.33 +/- 0.12 l/min for the control session and 0.21 +/- 0.12 l/min during propranolol use, a significant 35% reduction (P less than 0.01). The terminal elimination rate constant (beta) was 0.27 +/- 0.16 h-1 for the control session and 0.14 +/- 0.069 h-1 with propranolol (P less than 0.05); terminal elimination half-lives were 2.6 and 4.9 h, respectively. Volume of distribution was unchanged. Because bupivacaine clearance should be relatively insensitive to hepatic perfusion, it appeared that propranolol caused a substantial inhibition of bupivacaine metabolism at the level of the hepatocyte. These data suggest that concomitant use of propranolol could result in the accumulation of a toxic concentration of bupivacaine.

Adult↗
PubMed1987

Unaltered norepinephrine-heart rate relationship in exercise with exogenous heat.

We measured plasma norepinephrine (NE) concentration, an index of sympathetic nervous activity, and epinephrine (E), an index of adrenal medulla activity, in six normal young men during mild to severe exercise, with and without superimposed heat stress. The primary objective was to observe whether the normally close relationship between heart rate and log NE concentration in upset when heart rate at a given work load is increased by heat stress. Exercise, beginning at 50 W, was graded in 50-W increments lasting 10 min each up to 200 W, which lasted 5-10 min. Each subject went through the protocol twice, once with skin temperature kept low by a water-perfused suit and then with skin temperature raised to 38 degrees C. Exogenous heart stress raised log circulating NE concentration in proportion to the rise in heart rate at a given work load so that the usual relationship between these variables, previously observed during other stresses, was preserved. In contrast to some other stresses, heat stress had no added effect on E concentration, indicating that this stress during exercise raises sympathetic neural activity (as reflected in the rise in NE) without stimulating additional adrenal release of E.

Adult↗
PubMed1987

Effect of spontaneous sighs on arterial oxygenation during isoflurane anesthesia in humans.

The presence, frequency, and volume of spontaneous sighs was evaluated in 21 (ASA 1-2) supine patients aged 44 +/- 15.2 (SD) yr, during isoflurane-nitrous oxide anesthesia. Before induction the inspiratory capacity of each patient was determined. After induction of anesthesia and tracheal intubation patients breathed spontaneously except for three manual inflations to each patient's predetermined inspiratory capacity at the beginning and end of surgery. Arterial blood gas tensions were measured before and 5 min after each set of mechanical deep breaths and each hour during surgery, the mean duration of which was 2 +/- 0.09 hr. Spontaneous sighs occurred in 13 of 21 patients. The average frequency was 6 +/- 4 sighs/hr. At FIO2 = 0.5, nonsighing patients had an initial PaO2 of 229 +/- 59 mm Hg and sighers had an initial PaO2 of 162 +/- 57 mm Hg (P less than 0.05). Arterial oxygen did not change in sighing patients during the course of surgery, while in nonsighing patients the PaO2 decreased from the initial value of 229 +/- 60 mm Hg to 170 +/- 63 mm Hg (P less than 0.05). Mechanical deep breaths administered at the end of surgery produced no improvement in oxygenation in either sighers or nonsighers. The presence or absence of sighs did not correlate with PaO2 or PACO2. Though the results suggest that spontaneous sighs in some patients may function to help maintain arterial oxygenation, all patients maintained their PaO2 while breathing spontaneously under general anesthesia in the supine position.

Adult↗
PubMed1987

Respiratory effects of nalbuphine and butorphanol in anesthetized patients.

A double-blind, randomized study was conducted in 16 patients who were anesthetized with 50% nitrous oxide in oxygen and given either 0.17 mg/kg butorphanol or 0.86 mg/kg nalbuphine, and whose respiratory depression was assessed by the response of minute ventilation to increasing carbon dioxide concentrations. The slopes of the carbon dioxide ventilatory response curves [delta VE/delta PCO2(L.min-1 X %CO2(-1)] were 7.45 +/- 1.17 with nalbuphine and 2.42 +/- 0.56 with butorphanol. Butorphanol caused significantly (P less than 0.025) greater respiratory depression than nalbuphine. The results of this study caution against the indiscriminate use of butorphanol in the perianesthetic setting.

Anesthesia, General↗
PubMed1985

Sweat rate vs. forearm blood flow during lower body negative pressure.

Skin blood flow is inhibited when hyperthermia and added hypovolemic stresses are superimposed. We tested the hypothesis that part of this inhibition is a reduced drive for cutaneous active vasodilatation (AVD) with sweat rate (SR) taken as an indirect measure of the efferent drive for cutaneous AVD. We also inquired whether SR itself changes with redistribution of blood volume. Six healthy supine men were subjected to lower body negative pressure (LBNP) after heating in water-perfused suits increased esophageal temperatures (Tes) to a mean of 37.2 degrees C and at least doubled SR and forearm vascular conductance (FVC). Heating continued throughout LBNP and recovery. Sweat rate did not decrease with LBNP onset, although SR-Tes slopes during LBNP were reduced 28% from control. In four subjects the SR-Tes slope did not recover when LBNP was discontinued. These observations suggest that SR is not an effector of the low-pressure baroreflex. In contrast to SR, FVC abruptly fell 22% at the onset of LBNP. Thereafter, FVC-Tes slopes near zero or less occurred. The major effector for FVC inhibition with LBNP appears to be the neural vasoconstrictor system. A minor component due to reduced drive for cutaneous AVD probably occurs as well.

Adult↗
PubMed1985

Plasma renin activity and forearm blood flow in paraplegic humans.

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28-47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.

Adult↗
PubMed1979

Blockade of the pressor response to muscle ischemia by sensory nerve block in man.

Differential nerve block from peridural anesthesia was used to determine a) if the pressor response to muscle ischemia in man is caused by stimulation of small sensory nerve fibers and b) if these fibers contribute to cardiovascular-respiratory responses during dynamic exercise. Four men exercised at 50-100 W for 5 min. Muscle ischemia and a sustained pressor response were produced by total circulatory occlusion of both legs beginning 30 s before the end of exercise and continuing for 3 min postexercise. During regression of full motor and sensory block, motor strength recovered while sensory block continued; the pressor response was blocked as long as sensory anesthesia persisted (two subjects). During blockade of the pressor response, cardiovascular-respiratory responses to exercise gradually returned from augmented to normal (preblock) levels. Sensory blockade was incomplete in two subjects and the pressor response was not fully blocked. We conclude that stimulation of small sensory fibers during ischemia elicits the pressor response, but that these fibers appear not to contribute to cardiovascular-respiratory responses during mild dynamic exercise with adequate blood flow.

Adult↗