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8 -> [Music]
18.599 -> persistent pulmonary hypertension of the
21.189 -> newborn pathophysiology by dr. Andrea
24.16 -> Moscatelli hello my name is Umberto
28.029 -> Moscatelli and I'm director of the
30.189 -> neonatal and pediatric intensive care
31.839 -> unit at Casa de Children's Hospital in
35.5 -> this video we will address the
37.39 -> pathophysiology and the treatment of
39.46 -> persistent pulmonary hypertension of the
41.62 -> newborn or PPHN we will start with a
46.239 -> brief review of the pathophysiology of
49.29 -> transition circulation and PPHN because
53.32 -> it is extremely important to plan the
56.29 -> treatment of a baby with pulmonary
58.15 -> hypertension during fetal life pulmonary
61.689 -> vascular resistance is high and most of
64.839 -> the oxygenated blood coming from the
68.409 -> placenta to the right atrium is diverted
71.14 -> towards the foramen ovale and the ductus
74.5 -> arteriosus into the systemic circulation
78.03 -> the features as a low content of oxygen
82.84 -> in blood with a saturation which is
86.08 -> about 60 and the pao2 of 20 nevertheless
90.43 -> it is he's able to maintain a good
95.409 -> delivery of oxygen to tissues because
98.95 -> both the ventricle are working in
101.38 -> parallel towards the systemic
103.24 -> circulation during fetal life pulmonary
107.29 -> vascular resistance is I because the
110.26 -> lines are not ventilated but also
112.479 -> because there is a relative excess of
115.92 -> vasoconstricting agents like in the
118.869 -> tailing and Ron works in respect to the
121.93 -> vacillating agents the main was the
125.229 -> leading agents are nitric oxide and
128.399 -> prostacyclin nitric oxide increases the
132.67 -> levels of cGMP while the process icons
139 -> increase the levels of CA MP into the
143.26 -> smooth muscle cells GMP is metabolized
146.889 -> by the phosphodiesterases type v while
149.709 -> CA NP is
151.48 -> metabolized by phosphodiesterases type 3
154.3 -> and with increase in cgmp and CA NP
159.75 -> nitric oxide and prostitute a pulmonary
166.42 -> vasculature during the transition at
170.56 -> birth there is a rapid fall in pulmonary
174.069 -> vascular resistance with an increased
176.579 -> inflow of ten folds this is due to the
180.549 -> fact that her lungs become distended but
184.66 -> also because the written respiration the
187.45 -> increased oxidant
188.769 -> tension in blood and the increase of
191.349 -> flow to the lungs with the increasing
194.95 -> fuel stress would stimulate the
197.14 -> production of nitric oxide and
199.42 -> prostaglandins and they also activate
203.19 -> potassium channels would have a direct
207.69 -> vasodilatory effect on the pulmonary
210.22 -> vessels during a normal transition we
214.54 -> have an increase in flow to the lungs
217.239 -> and because the increase in systemic
221.65 -> pressures after the separation from the
224.56 -> placenta we have the closure of the
226.989 -> foramen ovale and the increase in oxygen
231.01 -> content in blood would lead to the
233.739 -> constriction of - to certain users so
237.4 -> now the delivery of oxygen to the
241.47 -> peripheral tissues in is mainly
244.09 -> dependent on the oxygen content of blood
248.41 -> respect to the cardiac output because
250.66 -> the right and the left ventricle are now
253.959 -> working in series and there is a slight
256.599 -> decrease in the cardiac output of the
260.38 -> newborn the last step in this adaptive
265.479 -> process is vascular remodeling which
269.05 -> takes place in the first week of life
271.26 -> with a reduction in the thickness of the
275.65 -> muscular layer of the pulmonary vessels
278.11 -> with a third decrease in pulmonary
281.05 -> vascular resistance in the PPHN
285.4 -> we have the persistence of I pulmonary
288.37 -> vascular resistance with a right left
292.24 -> front towards the foramen ovale and the
296.71 -> ductus arteriosus so the baby enters
301.06 -> this fascist cycle of hypoxia where I
304.12 -> parked the ITER cacnea acidosis and cold
306.76 -> are triggering pulmonary
308.44 -> vasoconstriction with increase in the
310.96 -> pulmonary vascular resistance and right
313.57 -> to left front auto maintaining hypoxia
318.03 -> PPHN is affecting two of 1,000 live born
322.9 -> to an infant's and it is complicating
325.69 -> ten percent of neonatal respiratory
328.33 -> failures of term with a five to ten
331.21 -> percent mortality despite adequate
333.88 -> therapy and 25% of newborns with
337.39 -> moderate to severe impaired neo logical
341.26 -> development the main cause of PPHN is
345.52 -> meconium aspiration syndrome followed by
349.03 -> primary PPHN RDS and pneumonia sepsis
353.68 -> and lung iPod leisure so we might have
357.64 -> an abnormal constriction of normally
360.25 -> developed vessels like in parenchymal
362.68 -> diseases but we can also have a normal
366.19 -> parenchyma with a normal muscular
368.68 -> ization of the pulmonary vessels which
370.81 -> happens to be the case of ideal Patek
374.83 -> PPHN which has been associated with the
379.39 -> closure in neutral of the Duke disorder
381.94 -> users or to the mother with the material
385.3 -> therapy with a serotonin reuptake
388.68 -> inhibitors the last cause of pulmonary
393.31 -> hypertension could be lung hyperplasia
396.43 -> and CDH where we have reduction in the
401.02 -> closer cross sectional area of the
403.33 -> pulmonary vessels all these conditions
406.6 -> share a certain amount of vascular
409.84 -> remodeling with an increase in thickness
412.72 -> of the middle layer of the pulmonary
415.15 -> vessels and Annis tension
418.18 -> of the muscular ization in to adalah at
422.199 -> the in Fastenal interest in our level
425.789 -> this is the case of idea Patek PPHN
431.009 -> where the substrate of pulmonary
433.99 -> hypertension is related to vascular
437.259 -> anomalies and it is also being it has
441.52 -> also been described in congenital
443.83 -> diaphragmatic hernia
445.24 -> while in parenchymal diseases the
447.94 -> substrate for pulmonary hypertension
450.19 -> is mainly functional and there is a less
453.46 -> extent of pathological remodeling and
458.11 -> muscular ization we can have an increase
462.13 -> in the pulmonary pressure just because
465.729 -> there is an increase of flow through the
468.46 -> lungs even if the resistance the
473.259 -> vascular resistance of the pulmonary
474.699 -> vessels is normal this can happen in
478 -> case of in cases of pulmonary overflow
481.72 -> which we might see in patients with VSD
486.34 -> large ventricular septal defects or in
489.58 -> babies with a large pattern ductus
492.43 -> arteriosus another cause of increase in
497.38 -> the pulmonary pressure is related to the
501.34 -> increase of the pressures in the left
503.56 -> atrium which is usually associated to an
507.789 -> obstruction to the inflow of the left
510.699 -> ventricle like in mitral stenosis or can
514.12 -> be associated with a dysfunction of the
517.75 -> left ventricle in this case the only way
520.779 -> to reduce the pulmonary pressure is to
524.56 -> fix the mitral stenosis or to sustain
528.6 -> the contractile function of the left
531.76 -> ventricle done does in improving its its
536.29 -> function a condition that should be
539.339 -> always excluded in a baby with PPHN is
544.12 -> an obstructed total anomalous pulmonary
547.27 -> venous return
549.41 -> point of clarification total anomalous
552.709 -> pulmonary venous return T a PVR refers
556.19 -> to heart defects in which none of the
558.199 -> pulmonary veins are connected to the
560.149 -> left atrium instead connecting to other
562.91 -> systemic veins or chambers of the heart
564.98 -> an obstructive T a PVR
567.56 -> pulmonary venous drainage is also
569.93 -> obstructed or narrowed making it
572.209 -> difficult for blood to return from the
574.1 -> lungs to the heart such babies
577.22 -> they present at birth in fraught with
580.899 -> pulmonary edema with a right-to-left
586.1 -> front towards the ductus arteriosus and
590.42 -> a severe pulmonary hypertension and an
594.62 -> abstract T a PVR can be excluded if we
598.31 -> can demonstrate with cardiac echo the
601.579 -> presence of the of at least three of the
604.67 -> venous returns to the left atrium so if
609.949 -> we put everything into practice we can
614.18 -> go through the K through a real case we
617.839 -> have a 41 weeks gestational age baby who
621.769 -> was delivered by caesarian section
624.019 -> because of acute fetal distress during
626.779 -> labor the amniotic fluid was stained
629.959 -> with meconium and the baby has been
632.029 -> resuscitated at birth on ICU admission
636.47 -> she was extremely disoriented with
642.189 -> hypertension a capillary refill of more
646.759 -> than seven seconds and a severe
649.279 -> respiratory and metabolic acidosis
655.809 -> thinking into account of the history and
661.24 -> looking at the chest x-ray the admission