Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RESPIRATION, ARTIFICIAL”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,207 records · Page 67Linked to original sources
PubMedDate not supplied

[High density respiratory syndrome: II. The mechanics of forced respiration with artificial resistive load under normobaric pressure].

The dynamics of forced inhale (I series) and exhale (II series) parameters with additional external artificial resistive load was studied under normobaric conditions. The artificial resistance to breathing increased stepwise using removable diaphragms with sequential decrease of hole diameter from 25, 17, 13, 9, 7.5, 4.5 to 3 mm. While studying forced inhale the diaphragms were set up at Fleish pipe airflow input. In the case of forced inhale the diaphragms were set up at the pipe output. A phenomenon is revealed which consists in appearance of respiratory flow oscillations on the "flow-volume" curves during forced breathing with an increase of resistive load. Frequency maxima of the oscillations were located within the range of 6-15 Hz. The possible mechanisms for appearance of respiratory muscle tremor and respiratory flow oscillations are under discussion.

Adolescent↗
PubMed1982

Short-term toxicological studies with impromidine (SK&F 92676): a specific histamine H2-receptor agonist.

Impromidine is a specific, potent histamine H2-receptor agonist. The present paper describes the results of acute and short-term repeated-dose toxicity studies with impromidine in rodents and dogs. The intravenous LD50 was 9.6 mg kg-1 in male mice, 12.7 mg kg-1 in female mice and 25.5 mg kg-1 in rats. The minimum lethal dose in dogs after 30 min intravenous infusion was 27.7 mg kg-1 during the infusion and 4 mg kg-1 within 14 days. In 12- or 14-day tests in rats by the intravenous (maximum dose 3.24 mg per kg per day) and subcutaneous (maximum dose 20 mg per kg per day) routes, impromidine had no serious toxicological effects. In 12- or 14-day studies in dogs by the i.v. (maximum dose 0.259 mg per kg per day) and intramuscular (maximum dose 0.5 mg per kg per day) routes, impromidine caused vasodilation, tachycardia and vomiting. In a few dogs, at the highest dose levels, there was erosion and irritation of the gastrointestinal tract and myocardial damage. Other minor pathological changes were seen in the liver, kidneys and pancreas. No changes were seen other than those to be expected from the pharmacological actions of impromidine as an H2-receptor agonist. Studies in anaesthetized rats, either spontaneously respiring or sustained by artificial respiration, indicate that, at acute doses, impromidine causes death by respiratory failure.

Animals↗
PubMed1963

[CARDIAC MASSAGE].

Explore the source record for details and available documents.

Heart Arrest↗
PubMed1993

[Acute respiratory arrest associated with medullary lesion in a case of multiple sclerosis].

We present a case history of a patient with multiple sclerosis who developed an abrupt onset of respiratory arrest associated with medullary lesion. A 27-year-old man developed shallow, totally irregular, ataxic respirations with aggravation of bulbar palsy and quadriplegia in the course of multiple sclerosis. As respiration was almost arrested, artificial respiration was started and continued for five days. Respiration was almost normal after 16 days from the onset of respiratory arrest. MRI showed bilateral, medullary lesions without upper cervical lesions. Pyramidal tracts, medial lemnisci, and paramedian reticular formations in medulla were damaged bilaterally. We supposed that the medullary lesions involved dual respiratory systems: a voluntary system and an automatic system, and caused acute respiratory arrest.

Acute Disease↗
PubMed1976

[Experimental and clinical studies of transvenous electrophrenic respiration (author's transl)].

The transvenous electrophrenic respiration (EPR) is one of the effective and relatively simple method for artificial respiration. Twenty seven mongrel dogs were subjected to the experiment which were subdevided into 4 groups. Stimulation is 44 times in group 1, 22 times in group 2 and 3. Ventilation is carried out by Harverd Respirator in group 4. The normal arterial pressure, the normal minute ventilatory volume and the normal arterial blood gases were unchanged for a 5 hour period of experiment in group 2. However, the frequent stimulation such as 44 times/min. in group 1 yielded the hypotension, the decreased ventilatory volume and brought the congestion of the portal venous area and rendered the subjects to death. The systemic pressure remained in slightly lowered levels in group 2, 3 and 4 at the end of a 24 hour of experiment. The ventilatory volume decreased one third of initial values in group 2 and 3 at the end of a 24 hour of experiment. The pulmonary arterial pressure decreased in group 3 significantly, whereas it increased in positive pressure respiration in group 4. Intermittent clinical application of EPR was performed in three patients. The arterial pressure, minute ventilatory volume, arterial gases and central venous pressure were maintained normal. The following conclusions were obtained: 1) EPR is more physiologic than positive pressure respiration in ventilatory and circulatory aspects. 2) Undesiable conditions of stimulation cause complications such as neural fatigue, portal hypertension, etc. 3) Intermittent clinical application of EPR has been quite successful in supporting the ventilation of the patients.

Adult↗
PubMed1982

[Emergency measures at the site of the accident from the anesthesiologist's viewpoint].

Within the scope of emergency medicine nearly every arrest of respiration and circulation must be treated in its critical phase by clearing the airways, artificial respiration and external cardiac compression. Chances for a successful cardiopulmonary resuscitation can be essentially improved, if the lifesaving emergency-treatment is improved by suitable technical measures. Start of an intravenous infusion, suctioning the airways with techniques, insertion of oropharyngeal airways, intratracheal intubation or in special cases coniotomy and transtracheal insufflation improve the chances of oxygenation. Simultaneously must be treated complicating accident effects as pneumothorax and shock. Additional administration and intravenous or intratracheal application of sympathicomimetic drugs, counteraction of acidosis with sodium bicarbonat often are the only possibility to continue successfully the cardiopulmonary resuscitation. In scope of emergency care the electrical external defibrillation is for treatment of fibrillation the best method to be applied.

Accidents↗
PubMed1980

Retransfusion acidosis and ventilation.

The blood pressure of dogs anaesthetized with 0.1 g/kg of chloralose was reduced to 40 mm Hg by arterial bleeding. Thirty percent of the drawn blood refluxed spontaneously, the rest was retransfused either suddenly arterially or slowly in 15 minutes by the venous route. In other groups a total quantity of 25 ml/kg was drawn from an artery at a rate of 50 ml/kg and after about one minute the entire quantity of blood was rapidly retransfused through the artery. The control group breathed spontaneously, the other groups were given artificial respiration, or the sinus nerves and the vagus were transected separately or simultaneously, or transection was combined with artificial ventilation.

Acidosis↗
PubMed2006

[Prevention of ventilator-associated pneumonia: review of national and international guidelines].

Both in the USA and in Europe the most frequent hospital-acquired infection in intensive care units is the ventilator-associated pneumonia. Particularly, patients with artificial respiration are at risk. Their risk to acquire a nosocomial pneumonia is six to twenty-one times higher than for patients breathing without artificial help. Established risk factors are, amongst others, old age, tracheotomy or reintubation, defective immune functions, already existing pulmonary infections and lifestyle-dependent factors like smoking. Recent scientific results indicate that endogenous infections are the most important reason for the development of a ventilator-associated pneumonia. Infections are initiated by microaspiration of bacteria from the oropharynx. Bacterial colonisation of the mouth is often favoured by an increased gastric pH-value, a secondary effect of the accompanying medicinal therapy. On a national as well as an international level there are evidence-based guidelines for the prevention of ventilator-associated pneumonia available. A comparison of guidelines of the US-American "Centers for Disease Control and Prevention" (CDC) with those of the German "Robert Koch-Institut" reveals deviating recommendations. Differences concern especially the changing of respiratory tubes, the use of filters and of closed humidifying systems. Additionally there are not yet recommendations for every aspect of infection prevention. However, recent studies show that regular surveillance of infections, further training of staff members and critically considering the invasive use of medical devices are able to reduce the rate of nosocomial infections and especially ventilator-associated pneumonia.

Bacterial Infections↗
PubMed1982

[Animal experiment studies on the mechanism of action of flunitrazepam (Rohypnol) on the circulation and respiration].

In 29 experiments performed on relaxed cats with artificial respiration, the effects of 0.015; 0.03; 0.06 mg flunitrazepam per kg body weight i.v. with N2O basal anaesthesia and of 0.06 mg flunitrazepam per kg without basal anaesthesia were examined in respect to mean arterial blood pressure, heart rate and the efferent action potentials of the N. sympathicus and the N. phrenicus. In all experiments, a mild and short-term reduction in blood pressure, a slight tachycardia and a very brief inhibition of the sympathetic nerve were observed. Definite actions exercised by flunitrazepam consisted of an inhibition of the respiratory centre which was due to a reduction of the extent and intensity of the inspiratory discharges of the phrenic nerve, although the breathing rate was increased. A comparison of the tests with flunitrazepam alone and in combination with N2O yielded definite differences only in the case of the asphyxia tests. The combination produced a significant inhibition of the vagus centre which was absent when flunitrazepam was used alone.

Adrenergic Fibers↗