Duration of Ventricular Ejection during Spontaneous Breathing and Positive Pressure Ventilation in Newborn Infants

Neonatology ◽  
1986 ◽  
Vol 50 (3) ◽  
pp. 130-135 ◽  
Author(s):  
Mark Reller ◽  
Uma R. Kotagal ◽  
Richard A. Meyer ◽  
Samuel Kaplan
PEDIATRICS ◽  
1973 ◽  
Vol 52 (1) ◽  
pp. 128-131
Author(s):  
Eduardo Bancalari ◽  
Tilo Gerhardt ◽  
Ellen Monkus

Increasing experience with the use of continuous transpulmonary pressure, either positive or negative, during the last years has clearly demonstrated the success of this mode of therapy in IRDS.1-3 Forty newborn infants with this disease have been treated with continuous negative pressure (CNP) in the Newborn Intensive Care Unit, Department of Pediatrics, University of Miami School of Medicine, using a modified incubator-respirator.* Twenty-one required only CNP, three of whom died (14%). Among the 19 who needed CNP plus intermittent positive pressure ventilation, nine died (47%). All required more than 70% oxygen to maintain a Pao2 over 50 mm Hg before using CNP.


2013 ◽  
Vol 59 (4) ◽  
pp. 479-484 ◽  
Author(s):  
J. G. Maccari ◽  
C. Teixeira ◽  
A. Savi ◽  
R. P. de Oliveira ◽  
A. S. Machado ◽  
...  

Author(s):  
Ola D Saugstad

ABSTRACT Newborn infants in need of positive pressure ventilation at birth should initially be given 21% O2 from term to gestational age 33 weeks. Gestational ages 29-32 weeks could be given initially FiO2 of 0.21-0.30. For ≤ 28 weeks FiO2 of 0.30 or more should be given initially. FiO2 should then be adjusted according to the oxygen saturation response assessed by pulse oximetry. After delivery room stabilisation oxygen saturation targets of 85-89% increases the risk of mortality and necrotizing enterocolitis. In spite an oxygen target of 90-95% increases the risk of ROP this is presently the recommended range. How to cite this article Saugstad OD. Oxygenation of the Newborn. Donald School J Ultrasound Obstet Gynecol 2016;10(2):170-171.


2018 ◽  
Vol 124 (5) ◽  
pp. 1319-1325 ◽  
Author(s):  
Maria Skytioti ◽  
Signe Søvik ◽  
Maja Elstad

Spontaneous breathing has beneficial effects on the circulation, since negative intrathoracic pressure enhances venous return and increases cardiac stroke volume. We quantified the contribution of the respiratory pump to preserve stroke volume during hypovolemia in awake, young, healthy subjects. Noninvasive stroke volume, cardiac output, heart rate, and mean arterial pressure (Finometer) were recorded in 31 volunteers (19 women), 19–30 yr old, during normovolemia and hypovolemia (approximating 450- to 500-ml reduction in central blood volume) induced by lower-body negative pressure. Control-mode noninvasive positive-pressure ventilation was employed to reduce the effect of the respiratory pump. The ventilator settings were matched to each subject’s spontaneous respiratory pattern. Stroke volume estimates during positive-pressure ventilation and spontaneous breathing were compared with Wilcoxon matched-pairs signed-rank test. Values are overall medians. During normovolemia, positive-pressure ventilation did not affect stroke volume or cardiac output. Hypovolemia resulted in an 18% decrease in stroke volume and a 9% decrease in cardiac output ( P < 0.001). Employing positive-pressure ventilation during hypovolemia decreased stroke volume further by 8% ( P < 0.001). Overall, hypovolemia and positive-pressure ventilation resulted in a reduction of 26% in stroke volume ( P < 0.001) and 13% in cardiac output ( P < 0.001) compared with baseline. Compared with the situation with control-mode positive-pressure ventilation, spontaneous breathing attenuated the reduction in stroke volume induced by moderate hypovolemia by 30% (i.e., −26 vs. −18%). In the patient who is critically ill with hypovolemia or uncontrolled hemorrhage, spontaneous breathing may contribute to hemodynamic stability, whereas controlled positive-pressure ventilation may result in circulatory decompensation. NEW & NOTEWORTHY Maintaining spontaneous respiration has beneficial effects on hemodynamic compensation, which is clinically relevant for patients in intensive care. We have quantified the contribution of the respiratory pump to cardiac stroke volume and cardiac output in healthy volunteers during normovolemia and central hypovolemia. The positive hemodynamic effect of the respiratory pump was abolished by noninvasive, low-level positive-pressure ventilation. Compared with control-mode positive-pressure ventilation, spontaneous negative-pressure ventilation attenuated the fall in stroke volume by 30%.


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