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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in electrocardiograms, blood pressure, pH, and partial pressure of gases (Po2 and Pco2) in arterial blood were studied in goats poisoned by urea or ammonium compounds under spontaneous and artificial respiration and in nonconvulsive state. Abnormal electrocardiogram patterns, such as ventricular flutter, ventricular premature beat, atrioventricular dissociation, depression of ST-segment and sinus tachycardia, were all observed after the occurrence of tetanic convulsion. The electrocardiogram pattern seen at the respiratory arrest showed sinus or supraventricular tachycardia; respiratory arrest preceded cardiac arrest in all the goats, but one. Blood pressure was markedly elevated, accompanied with tetanic convulsion. Po2 decreased gradually and the level was below 30 mm Hg (37.0 degrees C) at respiratory arrest and the final opisthotonus. Artificial respiration starting at the final opisthotonus could delay the cardiac arrest. Under nonconvulsive urea-poisoning with gallamine triethiodide and with artificial respiration of air or a mixture of air and oxygen to elevate the Po2 level, changes of electrocardiogram, blood pressure, and Po2 were similar to those seen under convulsive urea-poisoning. The main cause of death was discussed and presumed to be respiratory and cardiovascular failure.
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PMID:Electrocardiographic observation on goats with urea-ammonia poisoning and a consideration on the main cause of death. 60 86

To investigate the antagonistic effect of naloxone on fentanyl-induced respiratory depression, 55 patients (randomly divided into various study and control groups were studied during nitrous-oxide-oxygen-halothane anaesthesia. Respiratory depression after 0.1 mg of fentanyl was totally reversed by 10 microgram/kg of naloxone, measured as 100% restoration of spontaneous respiration, normal minute volume and end-tidal CO2, while 15 microgram/kg of naloxone was needed to antagonize 0.2 mg of fentanyl. The respective control groups remained apnoeic. If no fentanyl had previously been administered, there was no difference in the respiratory behaviour of naloxone-treated and control patients, which indicates that no unspecific analeptic effect of naloxone could be demonstrated. The circulatory changes after fentanyl were nearly reversed by naloxone, as has been found earlier with other narcotics. Recovery from anaesthesia was scored from 0 to 10 (using a modification of Apgar scores for newborns), and somewhat higher mean scores were obtained with the naloxone-treated patients than with their controls. However, higher postoperative pain scores were recorded in these patients as well as a higher incidence of nausea and vomiting. The study demonstrates the dose-relationships of fetanyl and naloxone for estimation of total antagonism; however, the use of naloxone for partial antagonism at the termination of anaesthesia cannot be based on these findings.
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PMID:Antagonism of fentanyl with naloxone during N2O+O2+ halothane anaesthesia. 60 61

Inhalation of the equimolecular mixture N2O - O2 rapidly achieves good analgesia in cases of coronary occlusion. This mixture was used with 51 patients (37 to 85 years old) with beneficial results on pain in 4 cases out of 5. This effect can be improved by giving a small amount of pethidine with the inhalation. In this way the respiratory depression of the full dose of narcotic analgesics is avoided. In halation of the mixture does not produce undesirable cardio-circulatory or respiratory changes. The oxygen content of the mixture increases patients' PaO2 without the risk of hyperoxia.
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PMID:[Nitrous oxide analgesia in myocardial infarction (author's transl)]. 60 76

The cardiovascular effects of intravenous droperiodol 5 mg were measured in 20 patients during steady state enflurane-nitrous oxide-oxygen or enflurane-oxygen anaesthesia, droperiodol produced significant decreases in SVR and BP and increases in HR and Qt which were maximal after five minutes, somewhat less five minutes, somewhat less five minutes later, and back to control values 15 minutes after administration. SV was not significantly altered by droperiodol during enflurane-nitrous oxide-oxygen at any time after administration. During enflurane-oxygen anaesthesia droperidol reduced SVR and BP after five and ten minutes but did not significantly alter any other variable. All variables had returned to control levels 15 minutes after droperiodol during enfluarne-oxygen anaesthesia. These data demonstrate that droperidol produces a significant though transiet reduction of BP and SVR during enfluane anaesthesia which is associated with no change or an increase in Qt. Our findings suggest that droperidol causes minimal or no myocardial depression when used during potent inhalation anaesthesia and may have a place as an amnesic supplement and/or "afterload" reducer during light enflurance anaesthesia.
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PMID:Cardiovascular effects of droperiodol during enflurane and enfluarne-nitrous oxide anaethesia in man. 62 3

Anesthetic indices for methoxyflurane, enflurane, and isoflurane in oxygen and halothane in nitrous oxide and oxygen (50:50), were determined in rats using measurements of heart and brain concentrations of the volatile agents at the endpoints of anesthesia, respiratory arrest and cardiac failure. The indices related respiratory arrest to anesthesia (respiratory index-A1r), cardiac failure to anesthesia (cardiac index-AIc) and respiratory arrest to cardiac failure (cardiorespiratory index-AIcr). Isoflurane had a significantly higher AIr (3.1) and AIc (5.7) than enflurane (AIr 1.8, AIc 3.3), methoxyflurane (AIr 2.2, AIc 3.7) and halothane in nitrous oxide and oxygen (AIr 2.4, AIc 3.7). These indices were also higher than those previously determined for halothane (AIr 2.3, AIc 3.0). Isoflurane had a higher AIcr (1.9) than halothane (1.6). Enflurane had a significantly lower AIr (1.8) than any of the other agents studied. These findings suggested a greater margin of safety for isoflurane, especially with respect to the heart, and a greater potential for respiratory depression for enflurane than for the other agents. Nitrous oxide decreased the amount of halothane necessary to produce anesthesia, but also that needed to produce respiratory arrest or cardiac failure. The addition of nitrous oxide, therefore, did not significantly enhance the overall safety of halothane anesthesia with respect to potential respiratory or cardiac depression.
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PMID:Anesthetic indices--further data. 62 24

In 12 patients with coronary artery disease and typical exercise-induced angina pectoris hemodynamic and ECG studies were performed at rest and during ergometer load in supine position. During the attacks of angina there was a significant ST-depression in all cases accompanied by elevated pulmonary capillary wedge pressures (PCP) and pulmonary artery mean pressures (PAM). Intravenous administration of 40 mg furosemide showed consistent hemodynamic changes. Cardiac output (CO) dropped significantly by 15.9 per cent at rest (p is less than 0.001) and by 6.9 per cent during exercise (p is less than 0.005). The PCP during exercise following furosemide decreased from 32.9 mmHg to 11.8 mm Hg (p is less than 0.001) and was paralleled by a significant decrease of PAM, indicating reduction of ischemia-related hemodynamic impairment. Furthermore, there was a striking improvement of Ecg findings during ergometer load in 9 of 12 patients as well as a relief of anginal pain in 11 of 12 patients. The present demonstration of antianginal properties of furosemide may be explained by the reduction of ventricular volumes and pressures, resulting in a decrease of myocardial wall stress. These effects are suggested to be related to the peripheral venodilator capacity of furosemide in conjunction with its diuretic properties. Thus, in patients with left ventricular dysfunction secondary to ischemia, intravenous furosemide may have salutary effects on myocardial oxygen requirements resembling the action of nitroglycerin, but without its oxygen-wasting effects on tachycardia.
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PMID:[Effects of furosemide on hemodynamic, electrocardiographic, and symptomatic responses to exercise in patients with angina pectoris (author's transl)]. 63 18

Maximum exercise testing using treadmill walking and cycle ergometry was compared in 40 male patients who had suffered a myocardial infarction in the preceeding twelve months. Maximum oxygen uptake was on average 17% greater in the treadmill than the cycle test and maximum heart rate was also higher, but the rate pressure product (RPP) was a similar due to a higher blood pressure in the cycle ergometer test. Eleven subjects showe ST-segment depression greater than 1 min and eight subjects showed ST-segment elevation greater than 1 mm. There was a close relationship (r2 = 0.96) between the magnitude of ST-segment changes in the two tests. Four subjects showing ST depression of 1 mm in the treadmill test showed depression during the cycle ergometer test which was less than this conventionally "positive" value. In these subjects RPP was lower during cycling than in treadmill walking. With both tests maximum ST-segment changes were measured immediately on stopping exercise: resolution of ST depression was more rapid than ST elevation. The two exercise testing modes are closely comparable in their ability to reveal changes of myocardial ischemia.
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PMID:Comparison of the electrocardiographic changes induced by maximam exercise testing with treadmill and cycle ergometer. 63 26

Elective cesarean section was performed in a consecutive series of 30 patients with full-term pregnancies who were not in labor. Epidural (lidocaine, 1.5 per cent, with epinephrine, 1:200,000) and general anesthesia (thiopental, nitrous oxide-oxygen, succinylcholine infusion) was used alternately. Neonatal acid-base values and Apgar scores showed no significant difference between the two anesthetic groups, and most infants were vigorous at birth. The neurologic recoveries of the infants showed no significant difference between the two groups. In the group receiving epidural anesthesia, there was a significant correlation between maternal hypotension and weak rooting and sucking reflexes of the infants during the first two days. All infants of high-risk obstetric patients in the series, independent of anesthetic technique used, had abnormal neurologic activity, as evidenced by either depression of muscle tone and the reflexes or all the tested variables. Neurologic assessment as followed in this series is a sensitive indicator of the effects of fetal stress factors acting during cesarean section.
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PMID:Neurologic activity of infants following anesthesia for cesarean section. 64 54

Pulmonary artery catheterization was performed in thirty-nine critically burned patients. Hemodynamic changes, induced by thermal injury and its therapy, were measured. Pulmonary wedge pressure was found to be a more reliable indicator of circulating volume, whereas central venous pressure was often misleading. Measurements of both pulmonary hemodynamics and cardiac output were necessary to manage patients requiring high levels of pulmonary end-expiratory pressure (PEEP). These measurements enable one to define optimum PEEP levels which provide maximum oxygen delivery to the tissues. Depressed myocardial function was seen in the early phase of the injury. In this period dopamine administration increased left ventricular stroke work index with minimal changes in filling pressures. The usefulness of dopamine in treating this early myocardial depression deserves further study. Catheter-related complications were minimal when the catheters were used for periods of three days or less.
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PMID:Pulmonary artery catheterization and thermodilution cardiac output determination in the management of critically burned patients. 66 8

The postoperative respiratory depressant effect of fentanyl in combination with flunitrazepam (Rohypnol) was assessed in awake and in unconscious patients. In awake patients respiratory function was measured with blood-gas analyses. For measurements in unconscious patients the administration of nitrous oxide/oxygen was continued postoperatively and the respiratory depression was judged from the increase in respiratory minute volume after the i.v. administration of 0.05 mg naloxone (Narcan). In the group of awake patients blood-gasvalues were within the normal range after anaesthesia with flunitrazepam (1 mg) and fentanyl (0.80 mcg/kg body weight/10 min anaesthesia; last fentanyl given 40 min before the end of the operation), and the administration of naloxone was without any effect. If, however, naloxone was given while the patients were kept under light nitrous oxide/oxygen anaesthesia, the effect was different. The respiratory minute volume was considerably less than its predicted value in all groups of patients having received fentanyl, and naloxone caused a marked increase in respiratory minute volume and in respiratory rate. In a group of patients which have received no opiate but enflurane, naloxone showed no effect. After premedication with pethidine as compared with flunitrazepam the effect of naloxone on ventilation was more pronounced. This marked difference in the postoperative effect of fentanyl on ventilation depending on the state of consciousness has to be attributed to an interaction between a residual respiratory depressant effect of fentanyl and the effect of unconsciousness. Since after the combined use of flunitrazepam and fentanyl deep postoperative sleep occurs quite frequent, a residual effect of fentanyl should always be antagonized with naloxone to protect the patients from a possible hazardous effect of this interaction.
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PMID:[Respiratory depression after fentanyl and antagonism by naloxone (author's transl)]. 67 31


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