Reduction In Minute Ventilation Research Articles

Breathing pattern and ventilation during oral feeding in term newborn infants

The effect of oral feeding on breathing pattern and ventilation was studied in 19 healthy term neonates in the semiupright supine position. Ventilation was measured with a nasal flowmeter, and sucking pressure via a modified nipple that permitted milk delivery. The feeding pattern in these infants consisted of an initial period of continuous sucking followed by intermittent sucking for the remainder of the feed. A significant reduction in minute ventilation (P less than 0.01) was observed during continuous sucking, and resulted entirely from a reduction in breathing frequency (P less than 0.01). Tidal volume did not change (P greater than 0.05), but prolongation of expiration (P less than 0.01) and shortening of inspiration (P less than 0.05) were also observed. During intermittent sucking, the minute ventilation was similar to that of the control period. However, smaller but significant changes in breathing frequency and in duration of inspiration and expiration persisted during intermittent sucking. Our results document a significant reduction in ventilation during the initial part of oral feeding in term neonates, and subsequent recovery with continued feeding. Depending on the magnitude of this reduction in ventilation, cyanosis and bradycardia may develop in some infants during oral feeding.

1453 APNEA AND BRADYCARDIA DURING ORAL FEEDING IN TERM NEONATES

Recent studies in infants have demonstrated substantial reduction in minute ventilation during oral feeding. The aim of the present study was to determine the incidence of cyanosis and bradycardia during oral feeding as a result of the reduction in minute ventilation or apnea. Heart rate, sucking pressure, respiratory efforts and airflow were monitored continuously during feeding in 50 term neonates (mean birth weight 3.5 kg, gestational age 39.7 weeks) in the first week of life. Bradycardia (≤100/min) occurred in 9 (18%) infants during the continuous sucking phase of oral feeding. Six of these episodes were preceded by apnea and the remaining 3 episodes were associated with hypopnea (marked reduction in minute ventilation). Airway obstruction occurred during most of the apneic episodes (5/6) and two resulted in cyanosis. The apnea and bradycardia resolved spontaneously with continued feeding in all except one infant. The only intervention performed was discontinuation of feeding in this infant. No episodes of isolated bradycardia or aspiration (associated with coughing and/or choking) was seen in any of the infants monitored. Our results suggest that apnea and transient bradycardia occur more frequently than previously recognized in term infants during oral feeding. This presumably reflects the inability of some infants in coordinating the feeding and breathing patterns during the first week of life and should be considered normal unless it persists beyond the neonatal period. Supported by grants by NIH (HL-01156) and March of Dimes (5-426).

JET VENTILATION USING LOW OR HIGH FREQUENCIES, DURING BRONCHOSCOPY

Jet ventilation, through a bronchoscope, was evaluated using a lung model (normal compliance and increased airway resistance). Three I/E ratios (0.25, 0.43, 0.67) and seven rates of ventilation (from 20 to 230 cycles per min (c min-1) were studied with the bronchoscope either unoccluded or partially occluded by a telescope. Increases in I/E ratio induced increases in minute ventilation, peak airway pressure, end-expiratory pressure and lung volume. Increase in the rate of ventilation decreased peak airway pressure, increased end-expiratory pressure and lung volume; minute ventilation increased in parallel with the increase in the rate of ventilation or remained constant when a high I/E ratio was used. The introduction of the telescope reduced minute ventilation, as a result of a decrease in the amount of air entrained, and increased end-expiratory pressure and lung volume. The risk of barotrauma as a result of high peak pressure is reduced during high frequency jet ventilation, but the increase in lung volume, particularly when the telescope is introduced, may be of clinical importance.

Interaction between cold and altitude exposure on pulmonary circulation of cattle.

Hereford calves were exposed in a temperature-controlled hypobaric chamber to environmental temperatures of -2 to 1 degree C (cold) at altitudes of 1,524 m (resident altitude) and 3,048 m 1) to characterize the effects of cold exposure on the pulmonary circulation; 2) to examine the role of cold-induced hypoventilation on the pulmonary circulation; and 3) to examine the interaction between cold and hypoxia on the pulmonary circulation. Cold exposure produced a significant increase in pulmonary arterial pressure (Ppa), pulmonary arterial wedge pressure (Ppaw), and pulmonary vascular resistance (PVR) at both 1,524 and 3,048 m without affecting cardiac output. Concomitantly, cold exposure caused reductions in minute ventilation, respiratory rate, end-tidal O2 tension (PETO2), and arterial O2 tension (PaO2). Tidal volume, end-tidal CO2 tension, and arterial CO2 tension increased. Neither arterial pH nor O2 consumption changed during cold exposure. These results indicated that both pulmonary arterial and venous vasoconstriction were responsible for the pulmonary hypertension associated with cold exposure. Acute exposure to 3,048 m during cold exposure produced increases in Ppa and PVR that were similar to those elicited by cold exposure at 1,524. It was concluded that altitude exposure neither attenuated nor potentiated the effect of cold exposure on the pulmonary circulation; rather, altitude and cold exposure interacted additively. O2 administered during cold exposure to restore PETO2 and PaO2 to control values partially restored Ppa and PVR to control values. This suggested that a portion of the pulmonary hypertension associated with cold exposure was due to hypoxic pulmonary vasoconstriction elicited by the cold-induced alveolar hypoventilation.

Respiratory Depression After Epidural Morphine???An Experimental and Clinical Study

This study was comprised of an experimental part (20 volunteers) and a clinical part (10 surgical patients). In the experimental part, the effects of either 2-, 4-, or 10-mg doses of epidural morphine on ventilatory responses to a standardized CO2 challenge were studied in healthy volunteers. In the clinical part, ventilatory responses to CO2 were evaluated in patients receiving 4 mg of epidural morphine for pain relief after gall bladder surgery. Naloxone infusion was given to five volunteers to determine whether ventilatory changes due to epidural morphine could be prevented. Using a nonrebreathing method, end-tidal PCO2 (PETCO2) and minute ventilation (tidal volume X frequency) were measured before and 1, 5, 8, 13, and 22 hr after epidural morphine injection. Ventilation was stimulated by 4% CO2 in 21% O2 and 75% N2. In the experimental study, a dose-related depression of ventilatory drive was seen after epidural morphine. After 2- and 4-mg doses, increases in PETCO2 were present up to 5 hr after injection with a corresponding reduction in minute ventilation. Ten mg of epidural morphine was followed by a significant reduction in minute ventilation and an increase in PETCO2 that started 1 hr after injection, peaked at 5 hr, and then remained almost unchanged for the next 17 hr. PETCO2 was higher and remained elevated longer in surgical patients than in volunteers given the same amount of epidural morphine (4 mg).(ABSTRACT TRUNCATED AT 250 WORDS)

Supersensitivity to the respiratory stimulatory effect of TRH in 5,7-dihydroxytryptamine-treated rats

Rats treated neonatally with pargyline and 5,7-dihydroxytryptamine (5,7-DHT) have an elevated p aCO 2 and reduced minute ventilation when given 0.7% halothane in oxygen as adults. Serotonin content in the spinal cord of 5,7-DHT treated rats was undetectable and TRH content was reduced by 35%. The 5,7-DHT treated rats were supersensitive to the increase in minute ventilation and CO 2 sensitivity produced by intraventricular TRH. It is possible that the supersensitivity to exogenous TRH after neonatal 5,7-DHT treatment may be secondary to decreased availability of TRH in the CNS.

Respiratory Depression after Epidural Morphine???An Experimental and Clinical Study

This study was comprised of an experimental part (20 volunteers) and a clinical part (10 surgical patients). In the experimental part, the effects of either 2-, 4-, or 10-mg doses of epidural morphine on ventilatory responses to a standardized CO2 challenge were studied in healthy volunteers. In the clinical part, ventilatory responses to CO2 were evaluated in patients receiving 4 mg of epidural morphine for pain relief after gall bladder surgery. Naloxone infusion was given to five volunteers to determine whether ventilatory changes due to epidural morphine could be prevented. Using a nonrebreathing method, end-tidal Pco2 (PETCO2) and minute ventilation (tidal volume × frequency) were measured before and 1, 5, 8, 13, and 22 hr after epidural morphine injection. Ventilation was stimulated by 4% CO2 in 21 % O2 and 75% N2. In the experimental study, a dose-related depression of ventilatory drive was seen after epidural morphine. After 2− and 4-mg doses, increases in PETCO2 were present up to 5 hr after injection with a corresponding reduction in minute ventilation. Ten mg of epidural morphine was followed by a significant reduction in minute ventilation and an increase in PETco2 that started 1 hr after injection, peaked at 5 hr, and then remained almost unchanged for the next 17 hr. PETco2 was higher and remained elevated longer in surgical patients than in volunteers given the same amount of epidural morphine (4 mg). Naloxone infusion (5 μg·kg−1·hr−1), prevented the reduction of minute volume and decreased the elevation of PETco2 due to epidural morphine. After larger doses (10 μg·kg−1·hr−1), minute volume and respiratory frequency were well above control levels, and PETco2 was restored to near control values. Thus infusion of naloxone could prevent the respiratory changes after 4 mg of epidural morphine.

Medullary ventral surface GABA receptors affect respiratory and cardiovascular function

We previously demonstrated that GABA and muscimol administered either into the cisterna magna or the fourth ventricle to chloralose-anesthetized cats cause respiratory depression, hypotension, and bradycardia. Injection of these substances into the lateral and third ventricles had no effect. In order to localize the site of action, muscimol and GABA were applied by Perspex rings to the ventral surface of the medulla. Application of muscimol (0.25–2.6 μg) to Schlaefke's area in 6 cats reduced minute ventilation from 443 ± 38 to 291 ± 52 ml/min by reducing tidal volume from 31.8 ± 2.3 to 17.6 ± 1.4 ml, without changing respiratory rate and duration of inspiration. Hypotension and bradcardia were also observed. Application of GABA (0.14–4.86 mg) produced similar effects on respiratory activity and arterial blood pressure. No significant effects occured high doses of these agents were applied to Loeschcke's and Mitchell's areas. Application of bicuculline (5–25 μg) to Schlaefke's area had the opposite effect of muscimol and GABA on respiratory activity and blood pressure, and reversed the respiratory and cardiovascular depressant effects of both agents. We conclude that GABA receptors are present at Schlaefke's area, and that activation of these receptors results in respiratory depression, hypotension, and bradycardia. Our results suggest that GABA may be an important inhibitory neurotransmitter in the modulation of respiratory and cardiovascular control.

Diaphragmatic breathing exercises. Therapy in chronic obstructive pulmonary disease.

DIAPHRAGMATIC breathing exercises have long been advocated in the therapy of patients with chronic obstructive pulmonary disease (COPD). The control of diaphragmatic excursions is accomplished by (1) consciously contracting the muscles of the anterior abdominal wall to obtain preferential descent of the diaphragm during inspiration, (2) assuming the head-down, supine, or leaning-forward posture to facilitate a diaphragmatic breathing pattern, and (3) placing weights or strapping belts on the abdomen to force the diaphragm craniad. 1-3 Often, dyspnea is relieved by these maneuvers, but it is uncertain what are the mechanisms responsible for the improvement. The following hypotheses have been suggested: (1) reduction of minute ventilation with maintenance of alveolar ventilation, (2) slowing of inspiratory flow rates, (3) improvement of ventilation-perfusion relationships at the bases of the lungs, (4) diminution of the work of breathing, and (5) promotion of a feeling of well-being. Reduction of Dead-Space Ventilation The hypothesis that reduced

Interactions of levallorphan and meperidine.

The respiratory effects of meperidine and levallorphan mixtures were studied in 5 healthy volunteers. The majority of pulmonary function tests and gas uptake studies gave either no evidence of change or only changes typical of opioids in general. Meperidine, 1.65 mg. per kilogram, intramuscularly, increased the end‐tidal CO2 tension by 6 torr with concommitant reduction in minute ventilation. Addition of levallorphan, 0.01, 0.02, or 0.04 mg. per kilogram caused only greater sedation. Even the sensitive test of ventilatory response to carbon dioxide challenge failed to distinguish mixtures of meperidine and levallorphan. During periods of controlled, elevated alveolar CO2 tension (48 ± 1 torr), meperidine, 1.1 mg. per kilogram, intravenously, depressed respiration 8 L. per minute. This depression was not significantly prevented or antagonized by levallorphan (0.014 mg. per kilogram). Levallorphan, 1.0 mg., produced respiratory depression equivalent to that produced by 40 mg. of meperidine. The interaction of the two is compatible with the hypothesis of competitive dualism.

Pre and post operative pulmonary function test -Part 1 Thoraenp1asty

Twenty of thoracoplasty cases were studied pre and post-operatively with spirometry and bronchos-pirometry. Total vital capacity and maximal breathing capacity have reduced in aþout same proportion.and was about 20% reduction in 5-6 rib resection. However. timed vital capacity showed only slight reduction in both 1 second and 3-second value, and no significant difference was seen according to the number of resected rib. Bronchospirometric study showed relatively small reduction in minute ventilation. oxygen consumption and vital capacity of operated side. Except one case of 7 rib resection in 3 stages who showed 30% reduction, there was 10-15% reduction in average. among which the least reðuction was seen in vital capacity.