PubMed Health⌕ Search

Biomedical subjects

S M Scharf

Publications and source records attributed to S M Scharf.

104 records · Page 6Linked to original sources
PubMed1979

Cardiac effects of increased lung volume and decreased pleural pressure in man.

The cardiac effects of increased lung volume and/or decreased intrathoracic pressure were assessed by radionuclide angiography in normal male subjects. Increased lung volume alone produced no change in left ventricular (LV) or right ventricular (RV) end-diastolic size. Decreasing intrathoracic pressure to -30 Torr with a Mueller maneuver led to increases in LV end-diastolic and end-systolic volumes, and to increases in RV diastolic area. LV ejection fraction did not change significantly but RV ejection fraction decreased with the Mueller maneuver. Increases in transmural central venous pressure were also noted with the Mueller maneuver. The effects of combining increased lung volume with the Mueller maneuver were similar to those with the Mueller maneuver alone. These effects are consistent with the hypothesis that producing large negative pleural pressures acts to impede left ventricular outflow (i.e., afterloading) and raises the possibility of similar changes during acute attacks of bronchospasm.

Adolescent↗
PubMed1979

Effects of normal and loaded spontaneous inspiration on cardiovascular function.

To assess the hemodynamic effects of spontaneous inspiration, we studied 12 anesthetized mongrel dogs during normal and loaded inspiration, before and after bilateral cervical vagotomy. Peak aortic flow fell (15--20%) whereas peak pulmonary artery flow rose (15--20%) under all conditions. When aortic flow fell, left ventricular diastolic size decreased whereas aortic and left atrial transmural pressures increased slightly. Right ventricular diastolic size and right atrial transmural pressure increased. During inspiratory loading transmural pressures rose more, but the fall in aortic flow remained the same. After vagotomy, inspiration was prolonged, allowing aortic flow to return to preinspiratory levels. At this time left ventricular diastolic size was increased compared to preinspiratory levels and there were further increases in left atrial and aortic transmural pressures. We have concluded that at least two factors affect aortic flow during inspiration: 1) a decrease in left ventricular preload that is associated with decreased left ventricular compliance, and 2) increased impedance to left ventricular emptying as reflected by the increase in aortic transmural pressure. This may play a greater role during inspiratory loading and when inspiration is prolonged.

Animals↗
PubMed1978

Vocal cord closure. A cause of upper airway obstruction during controlled ventilation.

Studies of vocal cord function were undertaken in a quadriplegic patient requiring ventilatory assistance, and in 2 normal subjects during controlled ventilation in a tank-type respirator. When the patient and the normal subjects relaxed and made no conscious effort to assist the respirator, the vocal cords were observed to close during inspiration and a large pressure gradient (12 to 19 cm H2O) developed across the cords. When the subjects made a slight inspiratory effort ("assist" mode), the cords opened widely during inspiration. There were large increases in flow and tidal volume in the "assist" mode compared with passive ventilation. Measurements of transdiaphragmatic pressure and esophageal pressure showed that these variables did not increase with the slight assist. Thus, increase in ventilation during the "assist" mode appeared to be due to alleviation of inspiratory obstruction at the level of the vocal cords. The same phenomenon was observed in the patient during phrenic nerve pacing. A pacemaker was designed to be triggered by the electromyographic impulse from an accessory muscle of respiration. In this manner, vocal cord opening could be coordinated with the mechanical assist given by the phrenic nerve pacer.

Adult↗
PubMed1978

Restrictive ventilatory defect in a patient with primary pulmonary hypertension.

A patient with the classic features of primary pulmonary hypertension developed a severe restrictive ventilatory defect that worsened during the clinical course. Histologic examination of the lung showed vascular changes consistent with primary pulmonary hypertension and no evidence of pulmonary parenchymal fibrosis. We suggest that severe progressive pulmonary hypertension caused a restrictive ventilatory defect in this patient.

Adult↗
PubMed1977

Cardiovascular effects of increasing airway pressure in the dog.

In paralyzed anesthetized dogs the cardiovascular effects of increasing positive end-expiratory pressure (PEEP) were explored under two conditions: a) end-expiratory lung volume increasing, b) end-expiratory lung volume kept nearly constant by matching pleural pressure rise to end-expiratory airway pressure rise. Two series of experiments were done: I) xenous return was allowed to fall, II) venous return was kept constant by infusion of volume. Right atrial pressure, pulmonary arterial pressure, and left atrial pressure increased under all conditions when measured relative to atmospheric pressure, but increased relative to pleural pressure only under condition a. The rise in left atrial relative to pleural pressure may indicate a degree of left ventricular dysfunction associated with increasing end-expiratory lung volume. Furthermore, when end-expiratory lung volume increased, inequality of the rise in pulmonary artery wedge pressure exceeded the rise in left atrial pressure in series I. From plots of cardiac output as a function of right atrial pressure it was possible to conclude that the decrease in venous return is partially offset by an increase in mean circulatory pressure.

Airway Resistance↗
PubMed1977

Effects of decreasing lung compliance with oleic acid on the cardiovascular response to PEEP.

In 12 anesthetized mongrel dogs on a constant volume ventilator, the response of the cardiovascular system to increasing positive end-expiratory pressure (PEEP) was examined before and after inducing acute lung injury with oleic acid. As PEEP was raised to approximately 16 mmHg, lung volume increased by approximately 900 ml before oleic acid and only 350 ml after. Pleural pressure increased by the same amount, indicating that both lung and chest wall compliance decreased with oleic acid. Right atrial pressure, the back pressure to venous return, also increased by the same amount. Although cardiac output at PEEP = 0 was lower after oleic acid, the relative decrements produced by increasing PEEP were the same as before oleic acid.

Animals↗
PubMed1977

Influence of abdominal pressure and sympathetic vasoconstriction on the cardiovascular response to positive end-expiratory pressure.

The role of changes in abdominal pressure and sympathetically mediated vasoconstriction in the cardiovascular response to positive end-expiratory pressure was evaluated in 9 mongrel dogs. When the abdomen was widely opened, the decrease in cardiac output caused by positive end-expiratory pressure was the same as that found during control studies. When the abdomen was tightly bound, cardiac output was higher at any positive end-expiratory pressure than in control state (P less than 0.01), but the percent decrease produced by increasing positive end-expiratory pressure was the same. alpha-Adrenergic blockade with phenoxybenzamine produced a significantly greater decrease in cardiac output at any given positive end-expiratory pressure and thus appeared to inhibit the previously operative peripheral vascular adjustments to positive end-expiratory pressure. The major compensatory mechanism in the cardiovascular response to positive end-expiratory pressure thus appears to be mediated via alpha-adrenergic sympathetic factors.

Abdomen↗
PubMed1975

Effects of hypoxic and CO hypoxia on isolated hearts.

Isolated perfused dog hearts were made hypoxic by respiring the support dog with low oxygen (hypoxic hypoxia) or with carbon monoxide (CO hypoxia). Each heart was exposed to both types of hypoxia, separately. Effects on coronary flow (Qt), coronary vascular resistance, cardiac oxygen consumption (Vo2), and contractility (%deltadP/dt) were studied. Two series of experiments were done. Series I: At constant perfusion pressure. As oxygen content (Cao2) was lowered from 20 to 5 vol%, Qt doubled with hypoxic hypoxia and almost tripled with CO hypoxia (P less than 0.01). Vo2 and contractility increased with both types of hypoxia. Beta-adrenergic blockade eliminated the increase in VO2 and contractility but not the difference in Qt increase between hypoxic and CO hypoxia. Series II: At constant Qt (with beta-blockade), vascular resistance decreased more with CO than hypoxic hypoxia. Finally, alpha-blockade eliminated the difference in vascular resistance and thus with complete (alpha and beta) blockade, the two types of hypoxia have the same effect and are indistinguishable.

Animals↗
PubMedDate not supplied

Mechanisms of circulatory depression during simulated central apneas in the anesthetized dog.

We recently reported that during simulated central apneas (SCA) heart frequency was more severely depressed than during obstructive apneas. In the present study, we examined factors influencing this response including hypoxia, hypercapnia, mechanoreceptor input and the role of the vagus nerve. In 11 paralyzed and mechanically ventilated animals, SCA was produced by turning the ventilator off for 1 min and on for 1 min. This was done with and without hypoxia, before and after bilateral cervical vagotomy. We also compared the effects of SCA with matched intermittent hypoxia. Under all conditions during room air breathing arterial pO2 fell and pCO2 rose to approximately the same values: 49 and 57 torr, respectively. Compared with baseline, during SCA following room air breathing blood pressure and cardiac output did not change significantly, and heart frequency decreased by 47% (p<0.001). Following 100% O2 breathing, during SCA mean blood pressure did not change, cardiac output decreased by 20% (p<0.05) and heart frequency decreased by 27% (p<0.02), a decrease which was significantly less than that following room air breathing (p<0.02). Immediately upon resuming ventilation, on room air, heart frequency increased by 15 bpm (p<0.02); heart frequency did not increase post-apnea an 100% O2. After vagotomy, following room air breathing, blood pressure increased during apnea by 32% (p<0.001) and heart frequency decreased by only 10% (p<0.05). Oxygen breathing prevented the increase in blood pressure during apnea but heart frequency was still reduced by 16% (p<0.05). During intermittent hypoxia matched for periodicity and pO2 to SCA, there were no changes in heart frequency. We conclude that the cardiovascular response to apnea is more than just that to intermittent hypoxia, and is critically dependent on loss of respiratory mechanoreceptor afferent input, hypercapnia, and an intact vagus nerve. Blood pressure responses are also dependent on the vagus nerve.

Animals↗