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Biomedical subjects

N A Bergman

Publications and source records attributed to N A Bergman.

At least 37 records · Page 2Linked to original sources
PubMed1984

Fourier analysis of effects of varying pressure waveforms in electrical lung analogs.

Six voltage waveforms were devised to simulate pressure curves of varying configuration for use in artificial ventilation. These waveforms were subjected to Fourier analysis and terms of the resulting series applied to a simple two-branch resistive-capacitive circuit intended to represent a lung analog using computer simulation. Current (analogous to flow) and charge (analogous to volume) in each branch could be graphically displayed. Differences among the waveforms in such attributes as efficiency, inspiratory work, volume introduced per unit of mean pressure applied, and relative volume distribution between the two branches could be demonstrated. All waveforms were capable of delivering a predetermined volume to the circuit with adjustment of their peak pressure (voltage). It was not possible to designate any of the waveforms as "superior" since advantage in one attribute, such as efficiency, was accompanied by deficiencies in other characteristics such as uneven volume distribution. Despite obvious severe limitations on physiological interpretations of such data, Fourier analysis of respiratory waveforms appears to be a useful teaching, illustrative, and exploratory method.

Computers↗
PubMed1983

Contribution of the closure of pulmonary units to impaired oxygenation during anesthesia.

Associations between airway closure, alveolar-arterial oxygen tension difference (A-aDO2), and positive end-expiratory pressure (PEEP) were investigated in anesthetized, paralyzed, artifically ventilated patients. The difference between closing capacity (CC) and functional residual capacity (FRC) was measured with a modified standard technique using a bolus of N2 to detect airway closure in denitrogenated patients. At FIO2 = 0.4 during anesthesia before application of PEEP, A-aDO2 was larger than expected in comparable conscious subjects and increased at about 1 mmHg/yr of age. CC was below FRC in young subjects but above FRC in older subjects, the two coinciding at about age 43 yr. Thus, during anesthesia both A-aDO2 and CC-FRC increased with age. The proximity and point of coincidence of CC and FRC suggested that CC is reduced during anesthesia. In patients whose CC exceeded FRC, imposition of PEEP estimated to be sufficient to elevate FRC above CC decreased A-aDO2 to a level comparable to that in patients exhibiting airway closure below FRC without PEEP. Patients in whom CC was initially below FRC failed to improve oxygenation with PEEP. At least half of the decrease in A-aDO2 associated with application of PEEP persisted for 20-30 min after the withdrawal of PEEP, although the withdrawal resulted in an immediate recurrence of airway closure above FRC. The authors conclude that closure of pulmonary units operates in some circumstances to contribute to pulmonary dysfunction in anesthetized patients but is neither the only nor necessarily the most important such mechanism.

Anesthesia, General↗
PubMed1982

Reduction in resting end-expiratory position of the respiratory system with induction of anesthesia and neuromuscular paralysis.

Resting end-expiratory position (REEP) of the respiratory system was monitored continuously using spirometric recording in eleven patients during transition from consciousness to thiopental hypnosis and following subsequent administration of succinylcholine. REEP decreased following thiopental and was little affected by subsequent relaxant in most patients. A fall in REEP was observed within 30 s after thiopental, and a lower, stable level of REEP was attained within approximately 15-45 s. Mean volume of gas expelled from the lungs was 189 (SE 32) ml BTPS. It is concluded that the previously extensively documented decrease in functional residual capacity associated with anesthesia occurs immediately on induction and requires a short, but finite, time for apparent stabilization.

Adolescent↗
PubMed1981

The Basenji-Greyhound dog: antigen-induced changes in lung volumes.

Subdivisions of lung volume, closing volume (CV), pulmonary resistance (RL) and dynamic pulmonary compliance (Cdyn) were measured before and after bronchial challenge with Ascaris suum in seven ascaris-sensitive Basenji-Greyhound (BG) crossbreed dogs. RL increased from a control value of 1.41 +/- 0.43 (mean +/- SE) cm H2O/L/sec to 21.4 +/- 5.15 (P Less Than 0.01) and Cdyn decreased from 163 +/- 32 ml/cm H2O to 43 +/- 11 (P Less Than 0.01) in the first 15 min following ascaris-antigen aerosol (AAA) challenge. Vital capacity (VC) decreased from 1581 +/- 147 ml to 944 +/- 86 (P Less Than 0.005) ml and residual volume (RV) increased from 381 +/- 63 to 577 +/- 68 ml (P Less Than 0.005) following AAA challenge. We conclude that the pulmonary mechanical changes in the BG dog following antigen challenge more closely resemble the changes observed in acute human asthma than do changes occurring in the mongrel dog.

Aerosols↗
PubMed1979

Ketamine block of bronchospasm in experimental canine asthma.

Experimental asthma was induced in dogs previously sensitized to ascaris antigen by ventilation with ascaris antigen, in an aerosol, for 10 min. Before the administration of antigen, there was no significant difference in pulmonary airways resistance (RL) during thiopentone and ketamine anaesthesia. In dogs anaesthetized with thiopentone, RL increased significantly from a pre-antigen control of 0.36 +/- 0.13 (mean +/- SEM) kPa litre-1 s to 1.56 +/- 0.38 at 5 min after administration of antigen. In dogs anaesthetized with ketamine, RL before (0.30 +/- 0.10) and 5 min after antigen (0.47 +/- 0.18) was not significantly different. Beta adrenergic blockade with propranolol abolished the protective effect of ketamine so that there was no significant difference in the maximal increase (5 min after antigen) in RL in dogs anaesthetized with ketamine (2.92 +/- 0.74) or thiopentone (3.28 +/- 1.16). Beta adrenergic blockade also increased pre-antigen RL in both groups (ketamine 0.87 +/- 0.24; thiopentone 0.77 +/- 0.32).

Airway Resistance↗
PubMed1976

Lidocaine and increased respiratory resistance produced by ultrasonic aerosols.

Respiratory resistance significantly increased from 5.0 to 8.0 cm H2O/1/sec in anesthetized patients who were given ultrasonically nebulized water for 20 minutes via an endotracheal tube. Intravenous administration of lidocaine failed to reverse the provoked increase in resistance. In another group, respiratory resistance significantly increased from 5.8 to 7.5 cm H2O/1/sec in response to nebulized water despite prior and con-current intravenous administration of lidocaine. In a third group, initial respiratory resistance was 5.6 cm H2O/1/sec and did not increase during a 20-minute challenge with intratracheally administrered ultrasonically nebulized 2 per cent lidocaine. In a final group, resistance was increased from 5.0 to 6.9 cm H2O/1/sec with nebulized water. When challenge was continued with nebulized 2 per cent lidocaine, resistance remained elevated for about 10-12 minutes. It then decreased and returned to its initial control value at about 17 minutes, despite continuing lidocaine aerosol administration. Lidocaine, when administered intratracheally as an aerosol, both prevented and reversed provoked increases in respiratory resistance. Intravenously administered lidocaine was ineffective. Intratracheal administration of ultrasonically nebulized lidocaine might be another useful technique for management of bronchoconstriction in anesthetized patients.

Aerosols↗