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PPHN
LISA CARRUTHERS
JANUARY 24TH 2019
MANAGEMENT OF PERSISTANT PULMONARY
HYPTERTENTION OF THE NEWBORN
THE CASE Term baby boy born with small amount of meconium no PPROM APGARS OF 445 requiring a few minutes of PPV HR always gt100 No significant antental HX Second trimester US = normal serologies negative baby brought to NICU as still experiencing respiratory distress and cyanosis
On Exam
bull Low temperature (356)
bull AE decreased on right side
bull Persistent Cyanosis
bull Scaphoid Abdomen
bull Saturation of 84
bull Worsening saturation when agitated
INTERVENTIONS
BOTH groups of nurses were on it
Oxygen placed in an attempt to increase saturations (very little improvement )
Attention brought to the fact the baby was cold and heat increased
IV placed for fluidsGlucose
BPs taken (all equal and systolics in 50rsquos)
Post saturation suggested = (by this time baby decompensated a little as was agitated and pre sat was 82 post sat was 70)
Grunting was audible and retractions worsened Peep applied but only made the baby increasingly agitated and saturations worsened
On auscultation AE significantly decreased on right side STAT CXR and gas orderedhellip
CXR
SURPRISE
Unexpected Congenital diaphragmatic hernia
The groups brainstormed and realized the baby needed to be intubated STAT (as bagging the baby increases air in the abdomen and further compresses the lungs making ventilation and oxygenation increasingly difficult )
The importance of placing a repogle to LWS to further decompress the stomach was also mentioned and done
Recognized lined would need to be placed
There remained a significant difference in the prepost saturations which is when we discussed the likelihood of the baby of having PPHN requiring further interventionshellip
hellipand the point of this presentation
WHAT IS PPHN
Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition after birth It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia secondary to right-to-left shunting of blood at the foramen ovale and ductus arteriosus
While in the womb the fetus receives oxygen through the umbilical cord so the lungs need little blood supply There is high blood pressure in the lungs so blood in the pulmonary artery is sent away from the lungs through the PDA
Normally when a babys born and begins breathing the blood pressure in the lungs falls and blood flow to the lungs increases However sometimes the normal process of vessel relaxation is altered the lung blood vessels fail to dilate properly and remain vasoconstricted
Right-to-left shunting at the ductus arteriosus (Deoxygenated blood enters the arterial circulation and results in hypoxemia)
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
THE CASE Term baby boy born with small amount of meconium no PPROM APGARS OF 445 requiring a few minutes of PPV HR always gt100 No significant antental HX Second trimester US = normal serologies negative baby brought to NICU as still experiencing respiratory distress and cyanosis
On Exam
bull Low temperature (356)
bull AE decreased on right side
bull Persistent Cyanosis
bull Scaphoid Abdomen
bull Saturation of 84
bull Worsening saturation when agitated
INTERVENTIONS
BOTH groups of nurses were on it
Oxygen placed in an attempt to increase saturations (very little improvement )
Attention brought to the fact the baby was cold and heat increased
IV placed for fluidsGlucose
BPs taken (all equal and systolics in 50rsquos)
Post saturation suggested = (by this time baby decompensated a little as was agitated and pre sat was 82 post sat was 70)
Grunting was audible and retractions worsened Peep applied but only made the baby increasingly agitated and saturations worsened
On auscultation AE significantly decreased on right side STAT CXR and gas orderedhellip
CXR
SURPRISE
Unexpected Congenital diaphragmatic hernia
The groups brainstormed and realized the baby needed to be intubated STAT (as bagging the baby increases air in the abdomen and further compresses the lungs making ventilation and oxygenation increasingly difficult )
The importance of placing a repogle to LWS to further decompress the stomach was also mentioned and done
Recognized lined would need to be placed
There remained a significant difference in the prepost saturations which is when we discussed the likelihood of the baby of having PPHN requiring further interventionshellip
hellipand the point of this presentation
WHAT IS PPHN
Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition after birth It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia secondary to right-to-left shunting of blood at the foramen ovale and ductus arteriosus
While in the womb the fetus receives oxygen through the umbilical cord so the lungs need little blood supply There is high blood pressure in the lungs so blood in the pulmonary artery is sent away from the lungs through the PDA
Normally when a babys born and begins breathing the blood pressure in the lungs falls and blood flow to the lungs increases However sometimes the normal process of vessel relaxation is altered the lung blood vessels fail to dilate properly and remain vasoconstricted
Right-to-left shunting at the ductus arteriosus (Deoxygenated blood enters the arterial circulation and results in hypoxemia)
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
INTERVENTIONS
BOTH groups of nurses were on it
Oxygen placed in an attempt to increase saturations (very little improvement )
Attention brought to the fact the baby was cold and heat increased
IV placed for fluidsGlucose
BPs taken (all equal and systolics in 50rsquos)
Post saturation suggested = (by this time baby decompensated a little as was agitated and pre sat was 82 post sat was 70)
Grunting was audible and retractions worsened Peep applied but only made the baby increasingly agitated and saturations worsened
On auscultation AE significantly decreased on right side STAT CXR and gas orderedhellip
CXR
SURPRISE
Unexpected Congenital diaphragmatic hernia
The groups brainstormed and realized the baby needed to be intubated STAT (as bagging the baby increases air in the abdomen and further compresses the lungs making ventilation and oxygenation increasingly difficult )
The importance of placing a repogle to LWS to further decompress the stomach was also mentioned and done
Recognized lined would need to be placed
There remained a significant difference in the prepost saturations which is when we discussed the likelihood of the baby of having PPHN requiring further interventionshellip
hellipand the point of this presentation
WHAT IS PPHN
Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition after birth It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia secondary to right-to-left shunting of blood at the foramen ovale and ductus arteriosus
While in the womb the fetus receives oxygen through the umbilical cord so the lungs need little blood supply There is high blood pressure in the lungs so blood in the pulmonary artery is sent away from the lungs through the PDA
Normally when a babys born and begins breathing the blood pressure in the lungs falls and blood flow to the lungs increases However sometimes the normal process of vessel relaxation is altered the lung blood vessels fail to dilate properly and remain vasoconstricted
Right-to-left shunting at the ductus arteriosus (Deoxygenated blood enters the arterial circulation and results in hypoxemia)
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
CXR
SURPRISE
Unexpected Congenital diaphragmatic hernia
The groups brainstormed and realized the baby needed to be intubated STAT (as bagging the baby increases air in the abdomen and further compresses the lungs making ventilation and oxygenation increasingly difficult )
The importance of placing a repogle to LWS to further decompress the stomach was also mentioned and done
Recognized lined would need to be placed
There remained a significant difference in the prepost saturations which is when we discussed the likelihood of the baby of having PPHN requiring further interventionshellip
hellipand the point of this presentation
WHAT IS PPHN
Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition after birth It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia secondary to right-to-left shunting of blood at the foramen ovale and ductus arteriosus
While in the womb the fetus receives oxygen through the umbilical cord so the lungs need little blood supply There is high blood pressure in the lungs so blood in the pulmonary artery is sent away from the lungs through the PDA
Normally when a babys born and begins breathing the blood pressure in the lungs falls and blood flow to the lungs increases However sometimes the normal process of vessel relaxation is altered the lung blood vessels fail to dilate properly and remain vasoconstricted
Right-to-left shunting at the ductus arteriosus (Deoxygenated blood enters the arterial circulation and results in hypoxemia)
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
SURPRISE
Unexpected Congenital diaphragmatic hernia
The groups brainstormed and realized the baby needed to be intubated STAT (as bagging the baby increases air in the abdomen and further compresses the lungs making ventilation and oxygenation increasingly difficult )
The importance of placing a repogle to LWS to further decompress the stomach was also mentioned and done
Recognized lined would need to be placed
There remained a significant difference in the prepost saturations which is when we discussed the likelihood of the baby of having PPHN requiring further interventionshellip
hellipand the point of this presentation
WHAT IS PPHN
Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition after birth It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia secondary to right-to-left shunting of blood at the foramen ovale and ductus arteriosus
While in the womb the fetus receives oxygen through the umbilical cord so the lungs need little blood supply There is high blood pressure in the lungs so blood in the pulmonary artery is sent away from the lungs through the PDA
Normally when a babys born and begins breathing the blood pressure in the lungs falls and blood flow to the lungs increases However sometimes the normal process of vessel relaxation is altered the lung blood vessels fail to dilate properly and remain vasoconstricted
Right-to-left shunting at the ductus arteriosus (Deoxygenated blood enters the arterial circulation and results in hypoxemia)
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
WHAT IS PPHN
Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition after birth It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia secondary to right-to-left shunting of blood at the foramen ovale and ductus arteriosus
While in the womb the fetus receives oxygen through the umbilical cord so the lungs need little blood supply There is high blood pressure in the lungs so blood in the pulmonary artery is sent away from the lungs through the PDA
Normally when a babys born and begins breathing the blood pressure in the lungs falls and blood flow to the lungs increases However sometimes the normal process of vessel relaxation is altered the lung blood vessels fail to dilate properly and remain vasoconstricted
Right-to-left shunting at the ductus arteriosus (Deoxygenated blood enters the arterial circulation and results in hypoxemia)
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
Right-to-left shunting at the ductus arteriosus (Deoxygenated blood enters the arterial circulation and results in hypoxemia)
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
PREPOST SATURATIONS
When checking for a prepost differential we place the sat probe on the RIGHT HAND Pre ductal relates to part of the aortic opening nearest the ductus arteriosus
and measures the level of oxygen in the blood after blood leaves the heart but BEFORE it reaches the ductus arteriosus where it gets sent to the upper extremities (like the brain)
The left hand as a pre-saturation detector is not used it has been unclear if the ductus arteriosus influences left-hand arterial perfusion So right hand = gold standard
A difference between the pre and post saturations as little as 5 can indicate PPHN
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
Howeverhellip Right-to-left shunting at the ductus arteriosus and foreman ovale means blood ejected into the aorta will have low oxygen content because of the mixing at the atrial level In this setting there would be little if any difference between the pre and post-ductal saturation values =low sats but similar Still has PPHN
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
CAUSES
Presence of increased muscularization of the pulmonary arterioles which is usually present at birth The presence of muscle where there shouldnrsquot be = decreased diameter of the pulmonary arterioles = resistance to blood flow into the lungs and encourages right-to-left shunting away from the lungs
Pulmonary vasospasm Hypoxemia (ex Our birth asphyxias)
Acidosis
Hypothermia (Causes metabolic acidosis)
Sepsis
Polycythemia (hyperviscosity increases PVR)
Decreased lung size pulmonary hypoplasia
congenital diaphragmatic hernia (like our case)
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
SIGNS amp SYMPTOMS
Cyanosis (decreased blood flow to lungs because of shunting due to increased PVR = purpleblue blood)
Usually seen in term or post-term infants (increasingly being dx in prems
such as those with ++ hypoplastic lungs hx of oligohydramnios )
Tachypnea
May or may not have murmur
Hypoxemia
Prepost differential possible
Diagnosis is confirmed with an echocardiogram These babies could also be a cardiac malformation
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
TREATMENT
REDUCE STIMULATION
Noise control SHHHHHHHHHHHHHHHHHHHHHHHHHH
Dim ambient lightscover eyes
MINIMAL STIMULATION
Agitation usually aggravates PPHN with initial transient increase of oxygenation followed by precipitous drop of oxygenation
Sedation (Fentanyl morphine and depending on BPs Midazolam may be
necessary if baby sensitive and shunting ++) Sedation may be necessary before manipulationsprocedures Discuss this with MD
WE TRY TO AVOID PARALYSIS UNLESS ABSOLUTELY NECESSARY (some studies suggest it may increases mortality )
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
TREATMENT CONTINUED
Antibiotics if risk of infection
Avoid hypoglycemia amp hypocalcemia
Hypoglycemia may lead to reduced ATP formation (energy needed for cells)
Inotropes
Vasopressors may be needed to keep the systemic pressure above pulmonary pressure = decrease right-to-left shunting
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
WHY DO WE WANT DECENT BPrsquoS
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
TREATMENT CONTINUED
Mechanical ventilation Conventional mechanical ventilation pressure limited or volume-controlled
High frequency ventilator
ldquoGentlerdquo ventilation strategies with optimal PEEP relatively low PIP and some permissive hypercapnia are now being recommended to ensure adequate lung expansion without causing barotrauma
Vasorelaxant Inhaled NO
Prostaglandin PGE1 or PGI2 (prostacyclin)
Others Trial of sildenafil milrinone surfactant
Extracorporeal membrane oxygenation (ECMO)
supportive measure that essentially gives time for the neonatal heart and lung to recover from the underlying pathology)
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
OXYGEN THERAPY in PPHN
High oxygen concentration and low PaCO2 are commonly used for PPHN as it relaxes the pulmonary arteries
However it is recommended that PaCO2 levels should not be lower than 35 since also CO2 controls cerebral perfusion
Oxygen is a potent vasodilator
Supplemental oxygen should be provided to achieve PaO2 between 50 and 80 mmHg
Hyperoxia (PaO2 gt 100 mmHg) does not enhance pulmonary vasodilation and increases the formation of oxygen free radicals that increases pulmonary arterial contractility and impairs vasodilator response to iNO
SO WATCH YOUR PAO2 LEVELS AND SATURATIONS
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
INO
Inhaled Nitric Oxide (iNO) is a pulmonary vasodilator for
infants with PPHN Nitric oxide is produced by the endothelial cells and causes pulmonary
vasodilation
Inhaled NO is inactivated by
hemoglobin in the circulation and hence has minimal systemic vasodilator effect Inhaled NO causes vasodilation of pulmonary blood vessels that are adjacent to well-ventilated alveoli and decreases intrapulmonary right-to-left shunting
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
iNO CONTINUED
Do not wean FiO2 on ventilator below 30 when an infant is on NO
Nitric oxide has been found to have an affinity for hemoglobin
Nitric oxide binds to create methemeglobin a toxic byproduct that can potentially interfere with tissue oxygen delivery and result in hypoxia
We monitor the methemeglobin (MetHb) on our gases to make sure the level stays in the safe range
INO is usually started at 20ppm (studies show more = no increased
efficacy and causes increased adverse effects in our population )
When decision is made to discontinue iNO it is weaned GRADUALLY (as per RT protocol) to avoid rebound PPHN
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
iNO Protocol
Babies on NO are to be bagged with NO as they can decompensate rapidly should the gas
be removed from the pulmonary system
ONLY an RT can do this Nitric Oxide like oxygen is a gas that is considered a medication It is an inhaled gas with special indications side effects and administration protocols in which Respiratory Therapists are specially trained Nitric oxide is therefore specialized to RTrsquos and not nurses
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
SUDDEN DETERIORATION
If the baby is deteriorating rapidly - call the RT STAT
As a nurse you MAY bag with 100 FiO2 until the RT is at bedside if the baby is significantly decompensating
(Be aware with the sudden removal of NO from the baby they may not improve significantly bagging with oxygen alone)
The RT will then bag the baby with the appropriate amount and pressure of Nitric Oxide
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
GOOD JOB TEAM
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
THANK YOU
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
REFERENCES (no they are not APA format)
Impact of pulse oximetry screening on the detection of duct dependent congenital heart disease a Swedish prospective screening study in 39thinsp821 newborns BMJ 2009 338 doi httpsdoiorg101136bmja3037 (Published 09 January 2009)
Neonatal Pulmonary Hypertension Pediatr Crit Care Med 2010 Mar 11(2 Suppl) S79ndashS84 doi 101097PCC0b013e3181c76cdc
UPDATE ON PPHN MECHANISMS AND TREATMENT Jayasree Nair MBBS MD Semin Perinatol 2014 Mar 38(2) 78ndash91 doi 101053jsemperi201311004
Steinhorn H and Farrow K (2007) Pulmonary Hypertension in the Neonate NeoReviews 8 (1) e14 - e21 doi101542neo8-1-e14
The management of neonatal pulmonary hypertension Rami Dhillon httpdxdoiorg101136adc2009180091
NO in the NICU protocol (MCH weebly) httpmuhcnicuweeblycomrespiratory-systemhtml
HYPERLINK Persistent Pulmonary Hypertension (PPHN) (MCH weebly) httpmuhcnicuweeblycomadministration-of-ino-in-the-nicuhtml
