Biomedical subjects

V Hoffstein

Publications and source records attributed to V Hoffstein.

133 records · Page 8Linked to original sources

PubMed1981

A simplified breath-holding method for measuring oxygenated mixed venous carbon dioxide pressure.

We have attempted to simplify the breath-holding method for measuring mixed venous PCO2 by the use of a single breath of 100% O2. This method is based on analysis of partial pressures of CO2 in three samples of alveolar gas obtained at 5, 10, and 15 sec of breath-holding after inspiration of 100% oxygen. Assuming exponential build-up of CO2 in alveolar gas, oxygenated mixed venous PCO2 can then be determined. Results in 35 subjects were compared with those of the previously reported breath-holding method for estimating oxygenated mixed venous PCO2 based on inspiring two gas mixtures; correlation coefficient was found to be 0.92. In 17 patients, samples of blood were obtained from the pulmonary artery by percutaneous catheterization; measured values in blood correlated well with the oxygenated non-invasively determined values (r = 0.83).

Blood Gas Analysis↗

PubMed1980

Determination of cardiac output based on breath-holding.

A breath-holding method for determination of cardiac output is described. It is based on the indirect Fick principle applied to carbon dioxide. Mixed venous PCO2 (PvCO2) is measured noninvasively using a CO2 breath-holding technique and PaCO2 is obtained by arterial puncture. Partial pressures are converted into contents using each patient's CO2 dissociation curve, taking into account temperature, hemoglobin, arterial and venous pH. The authors have applied this method to the determination of cardiac output in 20 patients, in whom cardiac output was also measured invasively using either direct Fick or thermodilution method. Mean cardiac output determined using the breath-holding method was 5.48 +/- 2.95 (SD) L/min, compared to 5.54 +/- 2.88 L/min as determined by the direct Fick or thermodilution method. Good correlation was found between the invasive and breath-holding method (r = 0.97, p < 0.001). The authors conclude that cardiac output at rest may be estimated with considerable accuracy from the measurements of PaCO2, CO2 production and the breath-holding mixed venous PCO2 without right-sided cardiac catheterization.

Arteries↗

PubMedDate not supplied

Reduction in snoring with phosphocholinamin, a long-acting tissue-lubricating agent.

The efficacy of a long-acting lubricating and coating agent, phosphocholinamin, in reducing snoring was tested in 12 persons, six of whom received the agent as nose drops and six of whom received a placebo (tap water nose drops). In all subjects, the noise level was measured continuously by using a microphone taped near the cricothyroid notch. In the group treated with phosphocholinamin, the maximum nocturnal decibel level was reduced by a mean +/- SD of 13 +/- 3%, and the snoring index (defined as the number of snores per hour of sleep) was reduced by 25 +/- 12%. In the group treated with placebo, the maximum nocturnal decibel level increased 9 +/- 22% and the snoring index increased 1 +/- 20%. The differences between the two groups were statistically significant (P less than .05). It is concluded that phosphocholinamin can provide a useful medical alternative in the treatment of snoring and that further trials of this agent are indicated.

Administration, Intranasal↗

PubMedDate not supplied

Obstructive sleep apnea and hypertension: from correlative to causative relationship.

Sleep-disordered breathing, manifested by repetitive episodes of partial or complete cessation of breathing during sleep associated with brief arousal and autonomic activation, is estimated to affect as many as 4% of adult men and 2% of adult women. Studies conducted during the 1980s revealed a strong association between sleep-disordered breathing and hypertension. The results of these early studies, which relied on relatively small samples of patients, have been confirmed in recent years by large-scale epidemiologic studies that are controlled for all possible confounding factors. This paper reviews the evidence suggesting a causative relationship between hypertension and disordered breathing in sleep. The authors discuss the possible underlying mechanisms of the two entities and address the clinical implications of this relationship. They conclude by recommending a proactive approach to the diagnosis of breathing disorders in sleep, in order to prevent the cardiovascular sequelae of this syndrome.

Confounding Factors, Epidemiologic↗

PubMedDate not supplied

Comparing pressures required to abolish snoring and sleep apnea.

OBJECTIVE: Snoring and obstructive sleep apnea share similar pathogenesis and similar response to treatment with continuous positive airway pressure (CPAP). The purpose of this study was to compare pressures required to abolish apneas (POSA) with pressures required to abolish snoring (PSNOR). DESIGN: Cross-sectional, nonrandomized cohort study. SETTING: Sleep disorders clinic at St Michael's Hospital - a tertiary referral centre and a teaching hospital of the University of Toronto, Toronto, Ontario. POPULATION STUDIED: Unselected consecutive 441 patients with confirmed sleep apnea who were undergoing a CPAP titration study in the sleep laboratory. INTERVENTIONS: Nocturnal polysomnography using CPAP titration protocol, which required incremental increases in pressure until snoring and apnea were abolished or a maximum pressure of 16 cm H2O was attained. PSNOR and POSA were recorded and compared. RESULTS: Mean (+/- SD) pressures required to abolish snoring and apnea were: PSNOR 8.3+/-2.57 cm H2O and POSA 7.9+/-2.72 cm H2O (P<0.0001). In 75% of patients, the PSNOR was within +/-1 cm H2O of the POSA; in 92%, it was within +/-2 cm H2O; and in 97%, it was within +/-3 cm H2O. CONCLUSIONS: Empirically increasing pressure by 2 cm H2O in patients on CPAP who continue to snore may abolish snoring and apnea without the necessity of another titration study.

Adolescent↗

PubMedDate not supplied

Nitrogen and bolus closing volumes: the effect of beta-agonist bronchodilator aerosol.

Studies of the effect of beta-agonist bronchodilators on closing volume in normal subjects have produced conflicting results. We studied the possibility that these differences might be due to the different methods of measuring closing volume. We measured closing volume by both the nitrogen washout and the bolus techniques in 19 healthy nonsmoking adults before and after inhalation of salbutamol aerosol. Prior to salbutamol, closing volume measured by the nitrogen method (N2 CV) was significantly smaller (p less than 0.02) than the closing volume measured by the bolus method (bolus CV). After salbutamol inhalation, N2 CV increased significantly (p less than 0.05); however, bolus CV did not change, so that following inhalation of salbutamol there was no significant difference between N2 CV and bolus CV. The increase in N2 CV after salbutamol inhalation was associated with an increase in the slope of phase IV (p less than 0.05). We suggest that beta-agonist bronchodilator aerosol has no effect on closing volume in normal individuals and the apparent increase in N2 CV after bronchodilator is probably an artefact.

Adrenergic beta-Agonists↗

PubMedDate not supplied

Pharyngeal and glottic changes following methacholine challenge in normal subjects.

Recent evidence indicates that some normal subjects exhibit glottic narrowing following experimentally induced bronchospasm. Similar findings have been observed during episodes of bronchospasm in asthmatics. The exact mechanism of this effect is unknown but it is thought to occur as part of a generalized reflex response associated with constriction of intrapulmonary airways. We tested the hypothesis that in addition to the glottic changes, coincident with intrapulmonary airway constriction which occurred after inhalation of methacholine, the pharynx would show similar changes. Pharyngeal and glottic cross-sectional areas were measured using the acoustic reflection technique in seven healthy subjects before and after inhalation of metacholine. Before methacholine, pharyngeal and glottic areas (mean +/- SE) were 5.0 +/- 0.2 cm2 and 2.4 +/- 0.3 cm2 respectively. After inhalation of methacholine, these areas were reduced to 4.6 +/- 0.3 cm2 and 1.9 +/- 0.3 cm2 respectively (p less than 0.05). We conclude that inhalation of methacholine induces similar reductions in glottic and pharyngeal areas. The role of local or reflex mechanisms accounting for this reduction remains unclear.

Adult↗