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F Erice

Publications and source records attributed to F Erice.

7 recordsLinked to original sources
PubMed2001

The use of respiratory variations in right atrial pressure to predict the cardiac output response to PEEP.

PURPOSE: The purpose of this study was to determine whether the pattern of respiratory variation in right atrial pressure (Pra) predicts the cardiac output response to positive end-expiratory pressure (PEEP). MATERIALS AND METHODS: We studied 18 patients with a variety of cardiac and pulmonary disorders requiring ventilatory support. A pulmonary artery flotation catheter was in place as part of their routine management. Changes in PEEP were made from 0 to 14 cm H2O to determine the level of PEEP, which increased PO(2) without decreasing cardiac output (ie, assessment of best PEEP). Static lung compliance and auto-PEEP were obtained from the pressure signal on the ventilator. The change in Pra with a spontaneous inspiratory effort (ie, triggered breath) was used to determine whether patients had a restrictive (ie, operating on the flat part of the Starling curve), or nonrestrictive pattern (acting on the ascending part of the Starling curve) as previously described. RESULTS: Cardiac output decreased 0.7 +/- 0.8 L/min (change from baseline P <.05) in the group with an inspiratory decrease in Pra and -0.04 +/- 1.50 L/min (P = NS) in the group without an inspiratory decrease in Pra. The groups were not significantly different. However, the variance in cardiac output was large and, in contrast to our hypothesis, two patients in the group with an inspiratory decrease in Pra did not have a decrease in cardiac output. Pra and pulmonary artery occlusion pressure after the PEEP trial were greater than before, indicating that reflex circulatory adjustments occurred in response to the PEEP. CONCLUSIONS: The inspiratory pattern in Pra does not predict the response to cardiac output to PEEP in individual patients. This is most likely because of reflex adaptations in the circuit that occur with the application of PEEP. The response of a patient to PEEP is affected by the patient's volume reserves, filling status of the right atrium, and neurosympathetic activity.

Adult↗
PubMed1995

Effect of baroreceptor activation and systemic hypotension on plasma endothelin 1 and neuropeptide Y.

To determine whether endothelin (ET-1) and neuropeptide Y (NPY) release are controlled by the carotid sinus (CS) baroreceptor or local endothelial mechanisms, we isolated and pump perfused the CS in eight chloralose-anesthetized dogs and controlled systemic arterial pressure (SAP) with an elevated reservoir connected to both femoral arteries. This allowed the SAP to be kept constant while CS pressure was varied from 55.8 +/- 2.0 (low CS) to 192 +/- 1.9 (high CS) mmHg (1 mmHg = 133.3 Pa) or CS pressure to be kept constant while SAP was lowered to 53.9 +/- 1.8 mmHg (low SAP). There was no significant change in ET-1 when CS pressure was varied (control, 2.08 +/- 0.50; low CS, 2.18 +/- 0.51; high CS, 2.11 +/- 0.38 pg/mL), but ET-1 was significantly higher during low SAP (2.93 +/- 0.49 pg/mL, p < 0.05). This increase was not observed with vagi and CS intact in six dogs or with vagi intact and CS constant in four dogs. In contrast, plasma NPY was significantly higher in the low CS condition (619.13 +/- 66.87 pg/mL) versus high CS condition (528.88 +/- 45.19 pg/mL, p < 0.05) and did not change during hypotension. In conclusion, NPY, but not ET-1, is affected by CS baroreceptor manipulation, and plasma ET-1 increases in response to hemorrhagic hypotension when modulating reflexes are abolished.

Animals↗
PubMed1994

Systemic and diaphragmatic oxygen delivery-consumption relationships during hemorrhage.

When tissue O2 delivery falls below a critical threshold, tissue O2 uptake (VO2) becomes limited. We compared critical O2 delivery and critical and maximum O2 extraction ratios of the resting and contracting left hemidiaphragm with those of nondiaphragmatic tissues in seven dogs. The left hemidiaphragm was perfused through the left inferior phrenic artery with blood from the left femoral artery. Phrenic venous blood was sampled through a catheter in the inferior phrenic vein. Systemic O2 delivery was reduced in stages by controlled hemorrhage. Left diaphragmatic VO2 during rest and during 3 min of continuous stimulation (3 Hz) of the left phrenic nerve and VO2 of the remaining nonleft hemidiaphragmatic tissues were measured at each stage. Critical diaphragmatic O2 delivery for the resting diaphragm averaged 0.8 +/- 0.16 ml.min-1.100 g-1 with a critical O2 extraction ratio of 65.5 +/- 6%. In the contracting diaphragm, they averaged 5.1 +/- 0.9 ml.min-1.100 g-1 and 81 +/- 5%, respectively. Whole body O2 delivery at which resting diaphragmatic VO2 became supply limited was similar to that for nondiaphragmatic tissues. By comparison, supply limitation of VO2 occurred at a higher systemic O2 delivery in the contracting diaphragm than in the rest of the body despite the increase in critical diaphragmatic extraction ratio. Thus, oxygenation of the isolated diaphragm does not appear to be preferentially preserved during generalized reductions in O2 delivery. These results suggest that, in diseases associated with increased work of breathing and decreased O2 delivery, the diaphragm may become metabolically impaired before limitation of VO2 is observed systemically.

Animals↗
PubMed1993

Diaphragmatic function before and after laparoscopic cholecystectomy.

BACKGROUND: Diaphragm dysfunction is a primary cause of ventilatory impairment after upper abdominal surgery. Laparoscopic procedures may result in less dysfunction. To test this, diaphragmatic function was studied in ten healthy adult patients undergoing elective laparoscopic cholecystectomy and in five undergoing laparoscopic hernia repair. METHODS: Respiratory gas exchange, ventilation, and breathing pattern were measured before and 3 h after surgery. Respiratory drive was evaluated from the relationship of P0.1 to end-tidal carbon dioxide (PETCO2) during tidal breathing. Diaphragm contractile function was assessed from maximal transdiaphragmatic pressure (Pdimax), and Pdi during a maximal sniff maneuver (Pdisniff). RESULTS: Oxygen consumption and carbon dioxide production did not change after surgery. Pdimax decreased by more than 50% in the laparoscopic cholecystectomy group, but Pdisniff did not change. Tidal volume and the ratio of inspiratory time over total cycle time decreased by 30% and 13%, respectively, PETCO2 increased by 9%, and minute ventilation did not change. In contrast, there was no variation in ventilatory function in patients undergoing laparoscopic hernia repair. In both groups, P0.1 did not change, which excludes depressed respiratory drive as an explanation for the decreased Pdimax in laparoscopic cholecystectomy. Contractile failure of the diaphragm was discounted as well, because Pdisniff did not change, even in the laparoscopic cholecystectomy group. CONCLUSIONS: Although laparoscopic cholecystectomy does not increase metabolic demands in the early postoperative period, it impairs diaphragm function. The internal site of surgical intervention appears to be the critical variable determining diaphragmatic inhibition after laparoscopic abdominal surgery.

Adult↗