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enjoynz
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Nebulised Saline
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Cyanotic Congenital Heart Defects
great website with good video.
http://www.pediatricheartsurgery.com/
Philadelphia Adult Congenital Heart Center
http://philachd.org/health_info/cyanotic.html
Good Cardiac info
http://www.rjmatthewsmd.com/
http://www.rjmatthewsmd.com/Definitions/congenital_heart_disease.htm
Hypoplastic Left Heart Syndrome
Pulmonary Atresia
Tetralogy of Fallot
Transposition of the Great Arteries
Tricuspid Atresia
Truncus Arteriosus
Total Anomalous Pulmonary Venous (P-V) Connection
Children with cyanotic heart disease have a right-to-left shunt and therefore demonstrate systemic arterial desaturation. Infants with cyanotic heart disease may be divided into two physiologically distinct groups, those with decreased pulmonary blood flow and those with increased pulmonary blood flow.
Ductal Dependent Pulmonary Blood Flow (Decreased Pulmonary Blood Flow)
These children have decreased systemic venous blood entering the pulmonary circulation. Children in this group may have obstruction to flow from the pulmonary ventricle either at the outlet ( Tetralogy of Fallot, Pulmonary Atresia) or inlet (Tricuspid Atresia). Children whose pulmonary blood flow is dependent on a patent ductus arteriosus (PDA) may present with severe hypoxemia and acidosis as the ductus closes. These children will have a higher Hb level to increase O2 content and oxgen delivery.
Ductal Dependent Systemic Blood Flow (Increased Pulmonary Blood Flow)
Children with ductal dependent systemic blood flow have increased pulmonary blood flow but decreased systemic blood flow due to obstruction of systemic output which can occur at a variety of locations. These infants may have acceptable arterial saturation but develop decreased oxygen delivery as a result of decreased systemic output ( hypoplastic left heart syndrome, interrupted aortic arch, co-arctation.) These children may present with profound shock due to dramatic reduction in systemic perfusion and oxygen delivery if the ductal flow is inadequate. Systemic blood flow in patients with severe left ventricular outflow obstruction is dependent on flow through a patent ductus arteriosus into the aorta distal to the obstruction.
For cyanotic heart defects with reduced pulmonary blood flow, the most rapid and effective first-line therapy is IV administration of prostaglandin E1 (PGE1). PGE1 serves to reopen the ductus arteriosus or prevent it from closing. This allows partially desaturated systemic arterial blood to enter the pulmonary artery and be oxygenated.
Oxyen is a potent vasodilator. It decreases the pulmonary vascular resistance in the lungs which then closes the ductus arteriosus. By keeping oxygen at 21% or less, the PVR will remain high thus keeping the ductus arteriosus open until surgical intervention.
Many of the older congenital heart defect adults are on waiting lists for heart transplants. I have met several recently who are approaching the age of 50 and have had rather full lives after their repairs even with a steady diet of cardiac meds and lasix.
Now if you want to know how this ties into nebulized saline...
Many years ago in the nursery we were not allowed to put cardiac babies into humidified hoods in fear that they would "soak up" the humidity and increase the chance for CHF. We have since debunked that theory. Bronchodilators were also ordered by minutes (1 - 2 minutes) and not a standard dosage.
great website with good video.
http://www.pediatricheartsurgery.com/
Philadelphia Adult Congenital Heart Center
http://philachd.org/health_info/cyanotic.html
Good Cardiac info
http://www.rjmatthewsmd.com/
http://www.rjmatthewsmd.com/Definitions/congenital_heart_disease.htm
Hypoplastic Left Heart Syndrome
Pulmonary Atresia
Tetralogy of Fallot
Transposition of the Great Arteries
Tricuspid Atresia
Truncus Arteriosus
Total Anomalous Pulmonary Venous (P-V) Connection
Children with cyanotic heart disease have a right-to-left shunt and therefore demonstrate systemic arterial desaturation. Infants with cyanotic heart disease may be divided into two physiologically distinct groups, those with decreased pulmonary blood flow and those with increased pulmonary blood flow.
Ductal Dependent Pulmonary Blood Flow (Decreased Pulmonary Blood Flow)
These children have decreased systemic venous blood entering the pulmonary circulation. Children in this group may have obstruction to flow from the pulmonary ventricle either at the outlet ( Tetralogy of Fallot, Pulmonary Atresia) or inlet (Tricuspid Atresia). Children whose pulmonary blood flow is dependent on a patent ductus arteriosus (PDA) may present with severe hypoxemia and acidosis as the ductus closes. These children will have a higher Hb level to increase O2 content and oxgen delivery.
Ductal Dependent Systemic Blood Flow (Increased Pulmonary Blood Flow)
Children with ductal dependent systemic blood flow have increased pulmonary blood flow but decreased systemic blood flow due to obstruction of systemic output which can occur at a variety of locations. These infants may have acceptable arterial saturation but develop decreased oxygen delivery as a result of decreased systemic output ( hypoplastic left heart syndrome, interrupted aortic arch, co-arctation.) These children may present with profound shock due to dramatic reduction in systemic perfusion and oxygen delivery if the ductal flow is inadequate. Systemic blood flow in patients with severe left ventricular outflow obstruction is dependent on flow through a patent ductus arteriosus into the aorta distal to the obstruction.
For cyanotic heart defects with reduced pulmonary blood flow, the most rapid and effective first-line therapy is IV administration of prostaglandin E1 (PGE1). PGE1 serves to reopen the ductus arteriosus or prevent it from closing. This allows partially desaturated systemic arterial blood to enter the pulmonary artery and be oxygenated.
Oxyen is a potent vasodilator. It decreases the pulmonary vascular resistance in the lungs which then closes the ductus arteriosus. By keeping oxygen at 21% or less, the PVR will remain high thus keeping the ductus arteriosus open until surgical intervention.
Many of the older congenital heart defect adults are on waiting lists for heart transplants. I have met several recently who are approaching the age of 50 and have had rather full lives after their repairs even with a steady diet of cardiac meds and lasix.
Now if you want to know how this ties into nebulized saline...
Many years ago in the nursery we were not allowed to put cardiac babies into humidified hoods in fear that they would "soak up" the humidity and increase the chance for CHF. We have since debunked that theory. Bronchodilators were also ordered by minutes (1 - 2 minutes) and not a standard dosage.
Vent:
Thanks for the info.
If I am understanding this correctly, oxygen would only be detrimental to the ductal dependent systemic population correct? I would think that in the first case, where pulmonary circulation was dependent on keeping the ductus arteriosis, high FiO2 would decrease vascular resistance in the pulmonary arterioles, thus increasing flow to the lungs and keeping the ductus open.
However, it sounded like Rid was thinking specifically of the tetralogy of Fallot when he said oxygen could be detrimental, which is one of the defects in the first catagory (decreased pulmonary flow). I would think that oxygen would acutally be beneficial in such a patient, as an increase in PVR would surve to exacerbate a right-to-left shunt and both decrease pulmonary circulation and increase the amount of deoxygenated blood entering systemic circulation (via the septal defect). Oxygen would decrease PVR, increasing the flow of blood from the RA into the pulmonary arteries, and decreasing right-left shunting.
Rid/Vent: Am i leading myself astray?
Also, It would seem that a pre-hospital diagnoisis of any of these problems is pretty much impossible. Is there any symptomology that would cause you to withold O2 to a cyanotic newborn?
Thirdly: anyone have thoughts on why high-flow O2 is still being taught for newborn resuscitation for all us pre-hospital types, if it's losing favor in-hospital. Is this just another case of "it's always been done that way, and oxygen is always good for the patient" ? Anyone have protocols which advise witholding O2?
Thanks for the info.
If I am understanding this correctly, oxygen would only be detrimental to the ductal dependent systemic population correct? I would think that in the first case, where pulmonary circulation was dependent on keeping the ductus arteriosis, high FiO2 would decrease vascular resistance in the pulmonary arterioles, thus increasing flow to the lungs and keeping the ductus open.
However, it sounded like Rid was thinking specifically of the tetralogy of Fallot when he said oxygen could be detrimental, which is one of the defects in the first catagory (decreased pulmonary flow). I would think that oxygen would acutally be beneficial in such a patient, as an increase in PVR would surve to exacerbate a right-to-left shunt and both decrease pulmonary circulation and increase the amount of deoxygenated blood entering systemic circulation (via the septal defect). Oxygen would decrease PVR, increasing the flow of blood from the RA into the pulmonary arteries, and decreasing right-left shunting.
Rid/Vent: Am i leading myself astray?
Also, It would seem that a pre-hospital diagnoisis of any of these problems is pretty much impossible. Is there any symptomology that would cause you to withold O2 to a cyanotic newborn?
Thirdly: anyone have thoughts on why high-flow O2 is still being taught for newborn resuscitation for all us pre-hospital types, if it's losing favor in-hospital. Is this just another case of "it's always been done that way, and oxygen is always good for the patient" ? Anyone have protocols which advise witholding O2?
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Both categories are ductal dependent including the T of F.
Occasionally oxygenation even at the low SpO2 range of 70 is difficult to maintain so PGE1 will be relied on to keep the ductus arteriosus open. The FiO2 may be brought up to .21 or a little higher. If the SpO2 starts to climb to abruptly, it may be back to subambient FiO2.
My favorite defect is HLHS (Hypoplastic Left Heart Syndrome) which is a rather common defect in the congenital category.
http://fn.bmj.com/cgi/content/full/90/2/F97
This article has some good info but it mentions going as low as 14% on the subambient O2. The lowest I've used is 15%. Buffering these babies for acidosis is also a challenge. If NaHCO3 is used, beware of sodium tox. If THAM is used, you're chasing glucose levels.
As far as pre-hospital, cardiac lesions are now detected in utero, hopefully. Occasionally a defect goes undetected for a few days while the PDA is present. If the baby is blue and limp, the ductus is probably almost closed creating severe hypoxemia and acidosis. At this point a prehospital team may have to ventilate by BVM or intubate, try fluids and hope there is a Children's Hospital that does cardiac babies close by. An emergent septoplasty may be done in the cath lab. If the etiology is unknown you will still have to follow your protocols for infant resuscitation.
Neonatal transport teams (RN, RT) utilize heart sounds, CXR (heart shape and pulmonary vasculature markings), O2 shunt equations, O2 challenge test and other lab results to give them a clue if the pediatrician at the sending hospital is not sure due to lack of other diagnostics. Usually if a baby fails to oxygenate or the oxygenation remains the same regardless of FiO2, without any obvious pulmonary problem, cardiac is suspected.
3)As far as resuscitating an infant with .21 in the field; what is the cause of delivery in the field. If the infant was distressed in utero, mec or cord, it is going to be at risk for developing PPHN (Persistent Pulmonary Hypertension). This baby will need high FiO2 in attempts to reduce the PVR. The body senses it still needs to rely on the fetal mechanisms of survival. The .21 resuscitation is all that may be needed to reduce the PVR in a baby that is "slow to start" in L&D.
quote from the article in my previous post eNeonatal Review:
Now for those wondering what's with all of this posting about something that appears to have little to do with EMS. As I mentioned before, you will start to hear a lot about the cyanotic heart defects in the adult population as they come of age. Many of these patients are followed by pediatric cardiologists well into their adult life. A very well known actress discovered she had an ASD in her adult life. It was surgically closed at a Children's Hospital.
And, there is so much to learn in medicine and to discover how the body makes the best of a bad situation until surgical intervention.
Occasionally oxygenation even at the low SpO2 range of 70 is difficult to maintain so PGE1 will be relied on to keep the ductus arteriosus open. The FiO2 may be brought up to .21 or a little higher. If the SpO2 starts to climb to abruptly, it may be back to subambient FiO2.
My favorite defect is HLHS (Hypoplastic Left Heart Syndrome) which is a rather common defect in the congenital category.
http://fn.bmj.com/cgi/content/full/90/2/F97
This article has some good info but it mentions going as low as 14% on the subambient O2. The lowest I've used is 15%. Buffering these babies for acidosis is also a challenge. If NaHCO3 is used, beware of sodium tox. If THAM is used, you're chasing glucose levels.
As far as pre-hospital, cardiac lesions are now detected in utero, hopefully. Occasionally a defect goes undetected for a few days while the PDA is present. If the baby is blue and limp, the ductus is probably almost closed creating severe hypoxemia and acidosis. At this point a prehospital team may have to ventilate by BVM or intubate, try fluids and hope there is a Children's Hospital that does cardiac babies close by. An emergent septoplasty may be done in the cath lab. If the etiology is unknown you will still have to follow your protocols for infant resuscitation.
Neonatal transport teams (RN, RT) utilize heart sounds, CXR (heart shape and pulmonary vasculature markings), O2 shunt equations, O2 challenge test and other lab results to give them a clue if the pediatrician at the sending hospital is not sure due to lack of other diagnostics. Usually if a baby fails to oxygenate or the oxygenation remains the same regardless of FiO2, without any obvious pulmonary problem, cardiac is suspected.
3)As far as resuscitating an infant with .21 in the field; what is the cause of delivery in the field. If the infant was distressed in utero, mec or cord, it is going to be at risk for developing PPHN (Persistent Pulmonary Hypertension). This baby will need high FiO2 in attempts to reduce the PVR. The body senses it still needs to rely on the fetal mechanisms of survival. The .21 resuscitation is all that may be needed to reduce the PVR in a baby that is "slow to start" in L&D.
quote from the article in my previous post eNeonatal Review:
Now for those wondering what's with all of this posting about something that appears to have little to do with EMS. As I mentioned before, you will start to hear a lot about the cyanotic heart defects in the adult population as they come of age. Many of these patients are followed by pediatric cardiologists well into their adult life. A very well known actress discovered she had an ASD in her adult life. It was surgically closed at a Children's Hospital.
And, there is so much to learn in medicine and to discover how the body makes the best of a bad situation until surgical intervention.
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Vent I'm sorry to keep asking questions, but I still feel like I'm missing something. I realized that T of F was ductal dependent, but I thought that there were two differnt catagories of ductal dependent malformations, with opposide directions of flow through the ductus (one pulmonary to systemic, the other the inverse, depending on which vascular system has insufficent flow).
My impression was that in T of F, there is insuffiecnt pulmonary blood flow due to right-left shunting, which diverts too much blood to the systemic ciruclation. In this case, lowering PVD (eg. by administring high FiO2) would increase pulmonary blood flow, and partially ameliorate the problem. The result would be increased flow through the ductus from the ascending aorta to the pulmonary arteries.
No?
T of F: severity is dependent on the degree of pulmonary stenosis.
Moderate or severe pulmonary stenosis (often the case): more systemic venous blood will be shunted from the right ventricle through the VSD and into the aorta.
Mild pulmonary stenosis: resistance to pulmonary outflow will be less than or equal to SVR, there will be little shunting through the VSD; even as the PVR decreases, cyanosis may not present in this simple form of T of F.
Flow, both liquid and gas, will seek the path of least resistance.
Moderate or severe pulmonary stenosis (often the case): more systemic venous blood will be shunted from the right ventricle through the VSD and into the aorta.
Mild pulmonary stenosis: resistance to pulmonary outflow will be less than or equal to SVR, there will be little shunting through the VSD; even as the PVR decreases, cyanosis may not present in this simple form of T of F.
Flow, both liquid and gas, will seek the path of least resistance.
Last edited by a moderator: