# Nebulised Saline



## enjoynz (Oct 27, 2007)

Hi All!
I was wondering if you could give me an answer about nebulised Saline
for pt's suffering from smoke inhalation.
We use to have protocol to give it here years ago, but it is not taught any more.
Do you have it as part of your training still and if not can someone tell
me what the reason is for not giving it anymore. 
I was talking to my ambulance partner  (EMT-I ) about it yesterday and he wasn't sure why it was stopped either. :unsure:

Cheers Enjoynz


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## Ridryder911 (Oct 27, 2007)

Why? Humidified oxygen would do about as much good... I guess, in some cases it would not hurt however; I can remember exactly which one, but humidified oxygen is contraindicated. 

R/r 911


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## Grady_emt (Oct 28, 2007)

Neb Saline = poor mans Humidified O2


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## enjoynz (Oct 28, 2007)

Humidified O2 is a new one to me, sorry. 
We only have straight O2 here.
It sounds interesting, can you tell me how it works, please?

Cheers Enjoynz


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## MMiz (Oct 28, 2007)

enjoynz said:


> Humidified O2 is a new one to me, sorry.
> We only have straight O2 here.
> It sounds interesting, can you tell me how it works, please?
> 
> Cheers Enjoynz


It comes in a little clear bottle that attaches to an O2 regulator/tubing.  You can get more info here.


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## enjoynz (Oct 28, 2007)

Ridryder911 said:


> Why? Humidified oxygen would do about as much good... I guess, in some cases it would not hurt however; I can remember exactly which one, but humidified oxygen is contraindicated.
> 
> R/r 911



So what are the contraindications for using humidified O2, please?
Can it be used for smoke inhalation?

Cheers Enjoynz


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## enjoynz (Oct 28, 2007)

MMiz said:


> It comes in a little clear bottle that attaches to an O2 regulator/tubing.  You can get more info here.



Thanks for that!
Cheers Enjoynz


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## VentMedic (Oct 28, 2007)

Nebulized saline as humidity? Sterile preservative free water is used for humidity in most respiratory humidity systems.  If giving a NS neb, one might as well toss in some albuterol to at least be therapeutic.

The sterile water humidification bottle pictured in the link is for comfort and not therapy. It is used for patients that might be wearing a nasal cannula more than 24 hours. 

No absolute contraindications for humidity with a relative contraindication for bronchospastic patients or those that suffer from cold induced asthma.  

For smoke inhalation a high FiO2 may be required if the CO levels (carboxyhemoglobin) are high.  These patients may also require a high flow humidity system and be able to maintain the high FiO2.  Many large bore tubing humidity systems will decrease flow as FiO2 is increased due to decreased air entrainment (Venturi principle of operation).  Due to facial burns the patient may not tolerate a standard aerosol mask and a face tent may need to be used but this system is high flow with a lower FiO2 delivery.  

Hospitals will also have the ability to deliver high humidity, high flow (up to 40 liters) via their specially designed nasal cannula systems.  This may be better tolerated provided the nares are not inflamed. 

All of these systems I just mentioned can deliver high flow humidity and are capable of being titrated to an FiO2 of .21 - .28 to get the patient off the oxygen clock.

For prehospital smoke inhalation, a NRBM may still be the best bet for a higher FiO2 until the CO levels are known.


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## emt/ff71185 (Oct 29, 2007)

We don't have a humidifying system but I hear that just filling a neb with water instead of albuteral will do the job.  Is this true?


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## Rattletrap (Oct 29, 2007)

Ridryder911 said:


> Why? Humidified oxygen would do about as much good... I guess, in some cases it would not hurt however; I can remember exactly which one, but humidified oxygen is contraindicated.
> 
> R/r 911



Paraquat poisoning?

Vent and/or rid chime in on this one. I remember something about paraquat poisoning and not using Oxygen on a NREMT EMT-I85 knowledge exam about 4 years ago.


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## Ridryder911 (Oct 29, 2007)

Rattletrap said:


> Paraquat poisoning?
> 
> Vent and/or rid chime in on this one. I remember something about paraquat poisoning and not using Oxygen on a NREMT EMT-I85 knowledge exam about 4 years ago.



I believe you are right. I could not recall if it was paraquat or mustard gas poisoning? I do remember something that the more humidified oxygen, the potential for chemical burns?... Too many bridges have been crossed since then....

R/r 911


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## VentMedic (Oct 29, 2007)

emt/ff71185 said:


> We don't have a humidifying system but I hear that just filling a neb with water instead of albuteral will do the job.  Is this true?



The water would also have to be preservative free. NEVER use tap water. You would also have to have the ability to bronchodiate in case of bronchospasm since a neb is designed to break down the particles into a very small size, much smaller then a humidifier designer specifically for humidification of the upper airways.  So, you would have to switch to NS/Albuterol.  All of this can cause time to be wasted when there are other assessment and treatment priorities before humidifying oxygen. 

Prehospital, humidification rarely if ever necessary.  Even for patients with trachs, a short time off their humidifier and on an oxygen mask or trach collar with a venturi adapter will be okay. 

For smoke inhalation, giving oxygen at a high FiO is priority for the CO. You do not want to be messing around with a 40% neb and water.  If necessary, the person will be traveling to the HBO system with a NRBM until they are in place for the dive.  Surviving the Carbon Monoxide is the priority. For burn patients, exposing them to unnecessary cold water vapor may also accelerate their heat loss.   

*Rattletrap and Rid,*
Okay, I have to look the chemicals up. I remember having some of this back in FF school many, many years ago.  However, I don't remember seeing it on the HazMat recert CEUs. 

I know we keep mineral oil around for potassium or magnesium exposure as well a few other chemicals where water is not advised.


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## Emtgirl21 (Oct 30, 2007)

I'm sorry but, I you hand me a NS neb when I can't breath. I may just take the oxygen tubing and choke you with it. Hello! Give me something that will help me to breath!


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## Ridryder911 (Oct 30, 2007)

Here is a trivia question. There is a medical condition (common in pediatrics, until surgical repair) that one can actually cause more harm by giving oxygen to them, than withholding it. (I know Vent already knows this..) 

R/r 911


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## jrm818 (Oct 30, 2007)

Oxygen is indeed contraindicated in paraquat poisining - paraquat is reduced to radical form in the lungs, a form which oxygen will then oxidize the cation form of paraquat and superoxide.  Superoxide is really really good at destroying pretty much everything in the nieghborhood, and the enzyme in the body responsible for processing it isn't quick enough.  The cycle can then repeat itself, as paraquat acts much like a catalyst.  The consequence is that paraquat inhalation is extremetly toxic, much moreso than by other routes.  Plus, if you live, it can cause all kinds of other problems, particularly neurologic problems, due to a couple of different, but similar, chemical reactions.

Rid's trivia:

I'm going to take an easier out - I'm sure this is not the answer you were looking for, but apparenlty "being a newborn in need of recussitation" is a condidtion in high Fi02 can be harmful.

My guess is that its a vascular congenital defect, which is exacerbated by the vasoconstricting influence of o2 though?


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## VentMedic (Oct 30, 2007)

Thanks for the update on paraquat poisining .



Ridryder911 said:


> Here is a trivia question. There is a medical condition (common in pediatrics, until surgical repair) that one can actually cause more harm by giving oxygen to them, than withholding it. (I know Vent already knows this..)
> 
> R/r 911



Rid's question is a good one because you will be seeing more of this population as adults that have been surgically repaired as infants and peds.  Oxygen will no longer be a detriment to them but don't expect an SpO2 of 99% either.



			
				jrm818 said:
			
		

> I'm going to take an easier out - I'm sure this is not the answer you were looking for, but apparenlty "being a newborn in need of recussitation" is a condidtion in high Fi02 can be harmful.



NRP has re-examined its use of O2 in the delivery room.
http://www.hopkinscme.edu/ofp/eneonatalreview/Newsletters/1206.html#article2



			
				jrm818 said:
			
		

> vasoconstricting influence of o2 though?



Oxygen is actually a potent vasodilator.  In utero the baby's pulmonary vasular resisitance (PVR) is high when the lungs are not active in respiration. When the baby takes its first breath at even room air (21%) after birth, PVR decreases, and pulmonary blood flow increases dramatically as the lungs assume the function of gas exchange.


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## sabbymedic (Oct 30, 2007)

We use nebulized saline to add to our Ventolin especially for pediatric administration. The equipment list put out by the MOH reqiures a bottle for humidified O2 and all it is is a bottle that you put sterile water in and the O2 travels through it to make it less dry. Saline does the same but you are using a neb mask for nothing really.


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## jrm818 (Oct 30, 2007)

VentMedic said:


> Oxygen is actually a potent vasodilator.  In utero the baby's pulmonary vasular resisitance (PVR) is high when the lungs are not active in respiration. When the baby takes its first breath at even room air (21%) after birth, PVR decreases, and pulmonary blood flow increases dramatically as the lungs assume the function of gas exchange.



i was thinking of systemic arterioles, not pulmonary, which are the opposite. in hindsight, not only did I not make that clear, but it also doesn't make very much sense - it's unlikely that a systemic problem would as direcly influenced by high Fi02 as would a pulmonary problem.  Besides, if the mystery condition were systemic normal room air should also elicit the problem (excpt in cases of respiratory compromise), since high 02 saturation is the norm. :blush:

Also, since you acutaly konw the answer to the trivia question, and focused your post on pulmonary reactions to higher O2 concentrations, I think it would be a good guess that the answer lies in the lungs somewhere...


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## VentMedic (Oct 30, 2007)

jrm818 said:


> Besides, if the mystery condition were systemic normal room air should also elicit the problem (excpt in cases of respiratory compromise), since high 02 saturation is the norm. :blush:



Very true and often the baby is placed on subambient oxygen as low as 16% if necessary by adding more nitrogen.

If Rid doesn't jump in sooner, I'll post some good links later or try to add to his post.


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## Ridryder911 (Oct 30, 2007)

Go ahead Vent.... I was reviewing some literature in teaching PALS, ped.'s refresher portion, etc. and was reviewing T o F. Surprising how much I had forgotten. 

Not trying to hijack the thread, but it appears the initial post/question has been answered. 

R/r 911


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## enjoynz (Oct 30, 2007)

You guys and gals go for it. I'm just going along for the ride!

Cheers Enjoynz


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## VentMedic (Oct 30, 2007)

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.


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## jrm818 (Oct 30, 2007)

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?


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## VentMedic (Oct 31, 2007)

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:


> No evidence is available to support a recommendation for using a specific oxygen concentration between 21% and 100% at present. If an oxygen concentration <100% is used to initiate resuscitation, crossover to 100% oxygen is recommended if there is no improvement in 90 seconds.



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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## jrm818 (Oct 31, 2007)

VentMedic said:


> 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.
> 
> .



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?


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## VentMedic (Nov 1, 2007)

*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.


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