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Biomedical subjects

H E Fessler

Publications and source records attributed to H E Fessler.

11 recordsLinked to original sources
PubMed1995

Polystyrene microspheres decrease bronchial artery resistance in anesthetized sheep.

The use of microspheres to measure tissue blood flow requires that the microspheres themselves do not alter regional arterial tone. To determine whether microspheres affected bronchial artery resistance, we cannulated and perfused the bronchial artery in anesthetized sheep. In seven sheep, the change in bronchial artery pressure at constant flow was recorded during infusion of 5 doses (1 x 10(5), 2 x 10(5), 5 x 10(5), 1 x 10(6), and 1.5 x 10(6)) of 15-microns microspheres. Microspheres produced a dose-dependent, self-limited decrease in bronchial artery pressure (1.5 x 10(6) microspheres decreased bronchial artery pressure by 36% for 31 min). This was a decrease in bronchial artery resistance, as evidenced by a shift in the slope, but not the intercept, of a pressure-flow curve (n = 4 sheep). Left atrial injection of 1 x 10(7) microspheres decreased bronchial artery resistance by 17% in six sheep with intact bronchial arteries in which flow was measured by ultrasound probe. The adenosine-receptor antagonist 8-phenyltheophylline attenuated the fall in resistance by 79% (n = 4 sheep). Cyclooxygenase inhibition by indomethacin attenuated the response by 37% (n = 4 sheep). These results suggest that microspheres caused the release of adenosine and a vasodilator prostaglandin. Repetitive measurements of bronchial blood flow by microspheres could overestimate true bronchial blood flow if the interval between measurements is < 30 min.

Animals↗
PubMed1995

CPAP reduces inspiratory work more than dyspnea during hyperinflation with intrinsic PEEP.

Hyperinflation with intrinsic positive end-expiratory pressure (PEEPi) loads the respiratory muscles and causes dyspnea in obstructive lung disease. Continuous positive airway pressure (CPAP) has shown some efficacy in reducing inspiratory work and dyspnea. However, in obstructive lung disease, inspiratory work and dyspnea may be increased by additional factors that may not be affected by CPAP. Therefore, to study the effects of hyperinflation with intrinsic PEEP and CPAP in isolation, we used a mechanical analog of airway closure to increase end-expiratory lung volume in normal subjects. In five subjects in whom inspiratory work was measured, increasing end-expiratory lung volume by 1 and 2 L increased inspiratory work per breath from 0.42 +/- 0.04 J to 1.17 +/- 0.15 J (p < 0.05 compared with baseline) and 1.58 +/- 0.22 J (p < 0.05 compared with baseline and to the lesser level of hyperinflation). Although CPAP reduced work per breath and per minute to levels not significantly different from baseline, it had little effect on dyspnea. In ten subjects hyperinflated to 2.4 +/- 0.12 L above FRC, breathing could be sustained 19.5 +/- 4.5 min before quitting the load. This was increased to 26.7 +/- 5.2 min by 10 cm H2O CPAP (p = 0.052). Inspiratory dyspnea was modestly reduced by CPAP during these endurance trials. We conclude that CPAP can substantially ameliorate the respiratory work load induced by hyperinflation with intrinsic PEEP. However, the effects of CPAP on dyspnea and endurance are more limited. This suggests that the limits to breathing at high lung volumes are related to factors in addition to respiratory muscle work, and that CPAP may be of more value in reducing the work than in relieving the distress of obstructive lung disease.

Adult↗
PubMed1994

Effects of hyperinflation and CPAP on work of breathing and respiratory failure in dogs.

Increased end-expiratory lung volume (EELV) and airway resistance are both characteristic features of obstructive lung disease. Increased EELV alone loads the respiratory muscles and may cause respiratory failure, changes that could be reversed by continuous positive airway pressure (CPAP). To study the effects of elevated EELV on respiration without increased airway resistance, we used a mechanical analogue of airway closure to increase EELV in six spontaneously breathing anesthetized dogs. Hyperinflation of 0.84 +/- 0.11 liter for 30 min decreased minute ventilation from 4.8 +/- 0.37 to 3.5 +/- 0.21 l/min and increased arterial PCO2 from 40.3 +/- 1.5 to 73.2 +/- 8.1 Torr (both P < 0.01). Inspiratory work per breath increased 3-fold, work per liter increased 3.7-fold, and work per minute increased 2.8-fold (all P < 0.01). CPAP at 15 cmH2O restored minute ventilation to 4.3 +/- 0.3 l/min and reduced arterial PCO2 to 54 +/- 6.6 Torr (NS vs. baseline). All measurements of inspiratory work were also restored to baseline, but cardiac output was reduced (baseline 3.09 +/- 0.36, hyperinflation 2.71 +/- 0.36, hyperinflation + CPAP 1.94 +/- 0.29 l/min; P < 0.05, baseline vs. hyperinflation + CPAP). We conclude that increases in EELV mimic important features of airway obstruction, increase inspiratory work, and can cause respiratory failure independent of increased airway resistance. This respiratory failure is reversed by CPAP at the potential expense of hemodynamic compromise.

Animals↗
PubMed1994

Hyperinflation with intrinsic PEEP and respiratory muscle blood flow.

Increased end-expiratory lung volume and intrinsic positive end-expiratory pressure (PEEP) are common in obstructive lung disease, especially during exacerbations or exercise. This loads the respiratory muscles and may also stress the circulatory system, causing a reduction or redistribution of cardiac output. We measured the blood flow to respiratory muscles and systemic organs using colored microspheres in 10 spontaneously breathing anesthetized tracheotomized dogs. Flows during baseline breathing (BL) were compared with those during hyperinflation (HI) induced by a mechanical analogue of airway closure and with those during an inspiratory resistive load (IR) that produced an equivalent increase in inspiratory work and time-integrated transdiaphragmatic pressure. Cardiac output was unchanged during IR (3.19 +/- 0.27 l/min at BL, 3.09 +/- 0.34 l/min during IR) but was reduced during HI (2.14 +/- 0.29 l/min; P < 0.01). Among the organs studied, flow was unaltered by IR but decreased to the liver and pancreas and increased to the brain during HI. For the respiratory muscles, flow to the diaphragm increased during IR. However, despite a 1.9-fold increase in inspiratory work per minute and a 2.5-fold increase in integrated transdiaphragmatic pressure during HI, blood flow to the diaphragm was unchanged and flow to the scalenes and sternomastoid fell. The only respiratory muscle to which flow increased during HI was the transversus abdominis, an expiratory muscle. We conclude that the circulatory effects of hyperinflation in this model impair inspiratory muscle perfusion and speculate that this may contribute to respiratory muscle dysfunction in hyperinflated states.

Animals↗
PubMed1993

Effects of positive end-expiratory pressure and body position on pressure in the thoracic great veins.

Positive end-expiratory pressure (PEEP) commonly decreases cardiac output. The major cause of this is believed to be decreased venous return due to increased right atrial pressure. We hypothesized that when the lungs were hyperinflated they could also restrict venous return by directly compressing the thoracic vena cavae. We measured the longitudinal distribution of pressure in the thoracic vena cavae of 10 dogs on and off 10 mm Hg PEEP, in the supine (S), prone (P), right lateral (RL), and left lateral decubitus (LL) positions. In the superior vena cava (SVC) both on and off PEEP, and in the inferior vena cava (IVC) off PEEP, pressure fell uniformly from the thoracic inlet to the right atrium. However, in the IVC on PEEP, intravascular pressure fell abruptly by up to 5 mm Hg. This pressure drop occurred in a discrete (1 to 2-cm) segment of the IVC, suggesting a localized increased in extravascular surface pressure. When this pressure inflection was present, changes in right atrial pressure had no effect on pressure in the IVC upstream of the inflection, consistent with a "vascular waterfall." These observations were most prominent in the LL, least common in the RL, and variably present in the P and S positions. Occlusion of the right bronchus intermedius prior to PEEP (preventing right lower, middle, and accessory lobe inflation) prevented the appearance of the pressure inflection during PEEP in the LL but not in the S or P positions. We conclude that PEEP impedes venous return partly by direct compression of the IVC, predominantly in positions in which the IVC is non-dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of systolic and diastolic positive pleural pressure pulses with altered cardiac contractility.

Positive pleural pressure (Ppl) decreases left ventricular afterload and preload. The resulting change in cardiac output (CO) in response to these altered loading conditions varies with the baseline level of cardiac contractility. In an isolated canine heart-lung preparation, we studied the effects of positive Ppl applied phasically during systole or diastole on CO and on the cardiac function curve (the relationship between CO and left atrial transmural pressure). When baseline cardiac contractility was enhanced by epinephrine infusion, systolic and diastolic positive Ppl decreased CO equally (1,931 +/- 131 to 1,419 +/- 124 and 1,970 +/- 139 to 1,468 +/- 139 ml/min, P less than 0.01) and decreased the pressure gradient driving venous return. However, neither shifted the position of the cardiac function curve, suggesting that the predominant effect of positive Ppl was decreased preload. When baseline cardiac contractility was depressed by severe respiratory acidosis, diastolic positive Ppl pulses caused no significant change in CO (418 +/- 66 to 386 +/- 52 ml/min), the cardiac function curve, or the pressure gradient for venous return. However, systolic positive Ppl pulses increased CO from 415 +/- 70 to 483 +/- 65 ml/min (P less than 0.01) and significantly shifted the cardiac function curve to the left. Thus the effect of Ppl pulsations on CO works through different mechanisms, depending on the state of cardiac contractility.

Animals↗
PubMed1992

Effects of positive end-expiratory pressure on the canine venous return curve.

To study the mechanism whereby positive end-expiratory pressure (PEEP) decreases venous return, we used a closed-chest canine venous bypass preparation to study the effects of 10 mm Hg PEEP on the systemic venous pressure-flow curves from the superior and inferior vena cava (SVC and IVC). These curves were characterized by three variables: the critical downstream pressure below which venous return was maximal (PCRIT), the conductance to venous return (GVR), and the effective upstream pressure driving venous return. PEEP reduced venous return by decreasing the maximal venous return even when the pressures at the outflow of the IVC and SVC were maintained below zero. PEEP increased PCRIT in the SVC and IVC (SVC: -0.31 +/- 0.53 to 3.21 +/- 0.84; IVC: -0.41 +/- 0.64 to 5.23 +/- 1.02 (SE) mm Hg; p less than 0.005). GVR in the SVC was reduced (52.5 +/- 26 to 37.8 +/- 5.3 (SE) ml/min/mm Hg; p less than 0.005), but changes in the IVC did not reach statistical significance. These changes were partially offset by increases in the upstream pressure driving venous return (SVC: 9.44 +/- 0.54 to 12.25 +/- 0.71; IVC: 9.42 +/- 0.69 to 12.51 +/- 1.02 (SE) mm Hg; p less than 0.01). Analysis of these findings suggests that PEEP may alter venous return through effects on the peripheral circulation, independent of its effects on the heart.

Animals↗
PubMed1991

Effects of positive end-expiratory pressure on the gradient for venous return.

The major mechanism whereby positive end-expiratory pressure (PEEP) decreases cardiac output is believed to be a decrease in the pressure gradient for venous return. However, although PEEP increases right atrial pressure (PRA), It may also elevate mean systemic pressure (PMS), the static circulatory filling pressure that is the upstream pressure for venous return. In an intact canine preparation, we studied the effects of 15 cm H2O PEEP on cardiac output, PRA, and PMS (the equilibrium PRA during ventricular fibrillation). To examine the role of neurovascular reflexes, PEEP was applied before and after either carotid sinus and vagal denervation (CSV) or total spinal anesthesia with arterial pressure restored by epinephrine infusion (SAE). To examine the effects of PEEP-induced elevations of abdominal pressure, the abdomen was bound or widely opened and the abdominal contents exteriorized. With reflexes intact, neither binding nor opening the abdomen altered the rise in PMS during PEEP. CSV attenuated the rise in Pms by 17% (Control, 4.89 +/- 0.3 SE; CSV, 4.04 +/- 0.22 mmHg; p less than 0.01), and SAE attenuated it by 49% (Control, 4.21 +/- 0.27; SAE, 2.14 +/- 0.31 mmHg; p less than 0.00005). After either CSV or SAE, the rise in Pms was not affected by binding. PEEP decreased (Pms-PRA) only when the abdomen was bound because of a greater rise in PRA, or during SAE because of a lesser rise in Pms. Under control conditions, PEEP increased Pms and PRA equally [(PRA-Pms) = 3.89 +/- 0.26 without PEEP versus 4.13 +/- 0.29 mm Hg with PEEP]. We conclude that PEEP increases Pms by both reflex and mechanical means independent of increased abdominal pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1990

Positive pleural pressure decreases coronary perfusion.

Pressure surrounding the heart (PSH) rises with maneuvers that increase pleural pressure. This may decrease left ventricular (LV) oxygen demand by reducing LV afterload. However, positive PSH may also directly impede coronary flow. To study the effects of positive PSH on coronary perfusion, PSH was increased in 10-mmHg increments from 0 to 60 mmHg in an isolated canine heart-lung preparation with constant venous return, arterial pressure, and lung volume. Increased PSH caused a rapid significant (P less than 0.001) fall in left atrial transmural pressure (PLATM) of up to 1.28 +/- 0.31 mmHg. With constant venous return and lung volume, this was interpreted to reflect decreased LV afterload. However, at levels of PSH greater than 30 mmHg, initial decreases in PLATM were followed by sustained increases, suggesting that there was a deterioration in cardiac function despite the lower level of afterload. Increased PSH was also associated with decreases in circumflex coronary artery flow [flow (ml/min) = 52.4 - 0.4PSH, P less than 0.01]. Moreover, when the circumflex coronary artery was maximally dilated with adenosine, the effects of PSH were amplified [flow (ml/min) = 137.9 - 1.78PSH, P less than 0.001], indicating that positive PSH mechanically impeded coronary flow. When PSH was raised to 60 mmHg for 90 s, the aortic-coronary sinus lactate concentration difference fell from 0.71 +/- 0.09 to 0.10 +/- 0.21 mM (mean +/- SE, P less than 0.001, n = 8), suggesting myocardial ischemia. We conclude that positive PSH directly decreases myocardial perfusion. This may lead to ischemic cardiac dysfunction, especially in patients with low arterial pressure or coronary artery disease.

Animals↗
PubMed1988

Mechanism of reduced LV afterload by systolic and diastolic positive pleural pressure.

To investigate the mechanism by which increased pleural pressure (Ppl) assists left ventricular (LV) ejection, we compared the effects of phasic systolic or diastolic increases in Ppl (40-60 mmHg) with use of an isolated canine heart-lung preparation with constant venous return. Positive Ppl during systole (S) caused left atrial transmural pressure (Platm = Pla - Ppl) to decrease by 1.25 +/- 0.46 (SE) mmHg (P less than 0.025). Central blood volume (CBV), the volume of blood in the heart, lungs, and thoracic great vessels, decreased by 29 +/- 4.0 (SE) ml (P less than 0.001). When Ppl was raised for an equal duration during diastole (D), the decrease in Platm was not significant, but there was a significant decrease in CBV (10.5 +/- 4.1 ml, P less than 0.05). With constant venous return, these changes suggested that phasic elevations in Ppl in either S or D assisted LV ejection by decreasing LV afterload. To test the hypothesis that positive Ppl during D reduced afterload by emptying the thoracic aorta, we compared the effects of diastolic positive Ppl with a rigid aorta vs. a compliant aorta. Although there was no statistical difference in the effects of diastolic positive Ppl on Platm, the decrease in CBV was significantly greater when the aorta was compliant than when it was rigid (23 +/- 2.2 vs. 17 +/- 2.7 ml, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗