When Breathing Goes Bad (Asthma)

[Sasha]

When Breathing Goes Bad
Full Article: http://www.ems1.com/columnists/robert-waddell/articles/436913-When-Breathing-Goes-Bad

If you’ve been an EMS provider for more than a month, you have probably cared for a child with asthma. If you haven’t, just wait; currently, more than 9 million children suffer from asthma,2 making it the nation’s third most common cause of hospitalization (0 - 15 years of age). It is also the cause of 14 million lost school days,3 and approximately $10.7 billion in direct health care costs per year. In 2004, 186 children between the ages of 0 and 17 died from fatal asthma,1 a 200 percent increase since 1992.

With statistics like these, it is no wonder that nearly everyone in the United States knows someone with asthma or is asthmatic themselves. It has been shown that children from the inner cities and economically depressed areas are at greater risk for developing asthma than their more affluent suburban and rural peers. Asthma in general has increased in prevalence from 3.6 percent to 6.2 percent within the pediatric population. The Center for Disease Control and Prevention also cites a higher prevalence in children of African and Puerto Rican descent.

Despite asthma being a common malady, many EMS providers don’t have a good working knowledge of the disease or its implications. I can distinctly remember being taught that any asthmatic who can speak in full sentences is compensating and not in crisis. It wasn’t until many years later that I had my first asthma attack, as an adult, and was still able to lecture at a conference and carry on a full conversation, even though my pulse oximetry reading was 63 percent! Without treatment, hypoxic brain damage was inevitable — maybe it was present before the episode (with me, who can tell?). It’s one thing to allow an old paramedic to go without treatment for a few hours, but it’s unacceptable to allow this to occur when a child’s future is at stake.

When I was a kid I had a lot of problems with asthma (haven't had a problem for years except for an occasional fake attack to get out of gym in high school.) and know very little about it, however I found this article educational and figured i'd share.

But question, in the article 'with spacer' is mentioned a couple of times. I know what it is, but why is it so important? They aren't carried here on trucks with services I've ridden with, does anyone carry them on their trucks?

 

[medic417]

What else do you fake?

Actually this is another good reminder for all EMS. We tend to focus on what many call the glamor jobs and forget these non glamorous jobs where we actually can do some good or a lot of harm.

 

[Sasha]

What else do you fake?

Vitals. Definitely vitals

 

[VentMedic]

But question, in the article 'with spacer' is mentioned a couple of times. I know what it is, but why is it so important? They aren't carried here on trucks with services I've ridden with, does anyone carry them on their trucks?

EMS rarely carries MDIs.

The spacer or holding chamber:

Help with correct inspiratory flow rate

Maximize drug delivery to the lungs

Reduces side effects such as thrush and hoarseness

Help eliminate the bad taste by restricting large particles

Easier for patient with limited strengthen or mobility of hands/fingers to use both hands and have up to 5 seconds to inhale.

Highly recommended for MDIs with the HFA propellant since the particles are lighter and it is no longer advised to do the 2 finger from open mouth technique.

 

[mycrofft]

Asthma is just anoher medical condition for us.

Age as a factor because of "what's at stake" is irrelevant. Nice line for an author to try to spice an article up.

Eval and treat. Remember how quickly it can get bad, but also how quickly it can get better...like between when they called and when you arrive. Treat what you see, but be aware you may be catching them on the upswing.

Spacers...the albuteral MDI's we use have an airspace around the tincan, the pt just purses ther lips around the mouthpiece and inhales/pushes the can all the way down and holds it without an airspace between lips and mouthpiece.

A spacer acts like a carbuerator, mixes aerosol better with air to try to get it past the oropharynx and into the bronchial tree. We used to cut short sections of blue inhlation therapy tubing (cost 50 cents each from a long roll) and got very good results versus the twenty dollar spacers our supplier offered and few people could puzzle through the Tranformers-like maneuvers to unfold them.

 

[VentMedic]

A spacer acts like a carbuerator, mixes aerosol better with air to try to get it past the oropharynx and into the bronchial tree. We used to cut short sections of blue inhlation therapy tubing (cost 50 cents each from a long roll) and got very good results versus the twenty dollar spacers our supplier offered and few people could puzzle through the Tranformers-like maneuvers to unfold them.

The carbuerator effect is to achieve a flow of about 30 L/min which is optimal for delivery of the particles to give MDIs.

Most commercial holdering chambers can also be broken down to wash thoroughly.

In the lab, the plastic tubing method decreased deposition because the the static attraction for the particles and turbulent flow. The holding chamber has does not have the same potential for static to mess with particles nor do they adhere to the sides.

Toilet paper rolls and rolled up newspaper or magazines are also not advised since the dust from these devices can do more harm than good.

Holding chambers are also recommended for small children and infants with a mask and are also used for animals.

 

[mycrofft]

Yeah, results from the tubing were mixed, no pun intended.

Don't fake it when a real product is available and works.

The annular turbulence generated by the corrugated walls of the blue tubes theoretically kept the medicine off the walls. Very often there was little or no detectable deposition on the walls (being blue, they show the power nicely) but once in a while one would be a real collector. (The "collectors" also seemed to be issued to people who tried to "hog down" seven or eight hits instead of two by pumping the cannister or could not for the life of them time the spray during their inhalation, not after or before). We had terriffic deposition problems with some of the folding spacers, but it was due to user error and, again, bad technique. Now our MDI mouthpieces do the job nicely, a good developement and better than cutting and using seven inch "blue tubes".

 

[VentMedic]

The new HFAs have changed all the rules. I have to keep a reference card to remember how and when to prime each cannister and we use about 18 different MDIs. I do like the counter feature on some of the MDIs which helps us gauge abuse or misuse.

The HFAs would also be useless with a 7" tubing.

Holding chambers aren't new and have been around for at least 25 - 30 years. In other countries the chamber is included with the meds by the same manufacturers that supply MDIs to the U.S.

 

[VentMedic]

Here's just a little extra tidbit since I know some in EMS love mnemonics and acronyms.

Diseases that have an obstructive component: C-BABE

C - Cystic Fibrosis
B - Bronchitis
A - Asthma
B - Bronchiectasis
E - Emphysema

Restrictive: PAINT

Pleural (fibrosis, effusions, pneumothorax, empyema)
Alveolar (edema, hemorrhage, pus)
Interstitial lung disease (inflammatory- sarcoid or idiopathic)
Neuromuscular (myasthenia)
Thoracic wall (kyphoscoliosis, obesity, ascites, ankylosing spondylitis)

 

[VentMedic]

This is a good paragraph from the article:

Regardless of the criticality of the child or the intensity of your treatment plan, do not delay transport. In the same respect, do not put unjustified pressure on your partner to “get us to the hospital NOW!” An unsafe transport could prove to be more fatal than the asthma. Calm, consistent, controlled care is what will provide the best care possible for the child and prevent them from going into respiratory arrest and becoming one of the 186 children who die each year from asthma.

 

[ResTech]

Bronchiolitis is another cause of difficulty breathing that present's very similar to asthma. Usually, the only difference in presentation is a fever from the viral infection. It is prominent in the pediatric group of less than 2 years of age (usually). RSV is the most likely culprit however, other viruses similar to RSV can cause it as well.

I had a six year old the other day that presented with asthma from an Urgent Care Center. He was a classic presentation of....

- Symptoms began two days earlier with runny nose and non-productive cough that got worse at night.

- Dx with bilateral ear infection at Urgent Care. Mom has history of extrinsic asthma (allergen induced).

- Child was tachypneic at 40-44min, abd muscle usage, initial ambient SpO2 of 89%, diffuse expiratory wheezing and rhonchi, tachycardic at 176. He did not exhibit a cough during care. Despite his difficulty breathing, this little guy was calm and excited to get to ride in the ambulance. He was compensating very well and did fine. One thing I did note while feeling the radial pulse was a very noticeable difference in pulse strength with respirations which almost made the pulse feel irregular... but was pulsus paradoxus from the hyperinflation and increased intrathoracic pressure. I have never felt that before so was cool to get to experience that first hand.

He was given albuterol and ipratropium prior to EMS along with prednisone PO and continued with albuterol enroute. His saturation increased to 98% and maintained. Pt. remained tachycardic around 170 however, abd muscle usage did decrease as a result of improved ventilation. I wanted to use capnography to see the degree of bronchoconstriction and improvement to treatment by my preceptor did not want to put the nasal filter on the child. My guess would have been the ETCO2 would have been normal to slightly less than 35mmHg. I am baffled why so many providers do not utilize capnography on a regular basis with non-intubated patients.

Mom say's child gets wheezy and has some difficulty breathing with colds. Allergy testing has been performed and no specific allergies were detected. PCP also has not dx with asthma.

I'm not sure of the hospital diagnosis since I didnt have a chance to follow-up. But this was a great case to have as a student.

 

[VentMedic]

- Child was tachypneic at 40-44min, abd muscle usage, initial ambient SpO2 of 89%,
++++++++++++++++++++++++++++
He was given albuterol and ipratropium prior to EMS along with prednisone PO and continued with albuterol enroute. His saturation increased to 98% and maintained. Pt. remained tachycardic around 170 however, abd muscle usage did decrease as a result of improved ventilation. I wanted to use capnography to see the degree of bronchoconstriction and
++++++++++++
which almost made the pulse feel irregular... but was pulsus paradoxus from the hyperinflation

Was the increase in SpO2 because you were giving the albuterol with oxygen? I always love hearing that one in the ED. "We put him on a med neb mask and his "sat" went up."

Bronchiolitis is more inflammation, edema, mucus and cellualar debris than bronchoconstriction. Some fail to realize that and give large amounts of albuterol to a child to where the albuterol causes more problems than helps. That is not to say you can't do an albuterol neb to see if there is a bronchoconstriction component that can be relied. Just don't panic or get disappointed if it doesn't help. Often it is the extra O2 that may them few better since 89& is on the cliff side for dropping on the Oxyhemoglobin Dissociation Curve for PaO2.

Pulsus paradoxus is an exaggerated decline in blood pressure during inspiration. Normally, systolic pressure falls less than 10 mm Hg during inspiration. In pulsus paradoxus, it falls more than 10 mm Hg.

You can detect pulsus paradoxus by palpating the radial pulse over several cycles of slow inspiration and expiration. Marked pulse diminution during inspiration can indicate pulsus paradoxus. However, when you check for pulsus paradoxus, remember that irregular heart rhythms and tachycardia cause variations in pulse amplitude and must be ruled out before true pulsus paradoxus can be identified.

 

[vquintessence]

Since bronchiolitis was brought up:

O2 and hydration is perhaps the answer for EMS treatment. Obviously each situation ultimately dictates, but still. How many of you guys carry racemic epi? What are your experiences? Read lots of Racemic Epi holding little effect in the long run... but what about the response you guys see?

Vent already alluded to this, but my $0.02 has been read in various journals over the years have brought to light the huge inadaquecies (sp?) of bronchodilators (little to no improved outcome). Even steroids were cited as inadequate.

Vent/others: I've read/seen saline drops given IN. Is that just to help clear the nose out... or is there more to it than that?

 

[VentMedic]

As you can see we have numerous articles on the subject.

Just type in "bronchiolitis" under "Search for an article" on the left.
http://www.rcjournal.com/


We do take it as a case by case bases. If the infant is a "well-baby" that is other wise healthy, minimal intervention is usually required. It the child was a preemie with BPD underlying, then the approach is different and the SABA and/or LABA may be needed to treat some of the symptoms influenced by the BPD. The same for a child dx'd with cystic fibrosis. Children who are immunosuppresssed also present a problem as do those that have a PNA.

Lab tests wills also be done and that might even include a bronchoscopy for bronchial washings for good specimens and to see the airways.

As for NS in the nose, it is good only if you can retrieve it and it doesn't go much past the nares or you can induce a spastic cough that can compound the situation. We have soft bulb tip yankeurs and olive tips that can gently suction the nose. If we get too aggressive with inserting suction catheters, irritation will occur which will just make the baby and us more miserable and frustrated.

Racemic Epi also has a place and some infants respond to it. We do have a protocol for a continuous epi neb if the infant responds well if it will prevent intubation. The new CPAP devices also give the infant some relief with work of breathing as does HeliOx.

However, there may be only limited things that can be done in the field and few will know if it is PNA, RAD, Bronchiolitis, RSV, RDS, Asthma, BPD or whatever in the field.

This is a good overview of RSV, management and controversies.

Systematic Review of the Biology and Medical Management
of Respiratory Syncytial Virus Infection​

http://www.rcjournal.com/contents/03.03/03.03.0209.pdf

For more in depth information about Asthma, I refer you to the EPR-3. There is a systematic approach to the diagnosis and management.

http://www.nhlbi.nih.gov/guidelines/asthma/index.htm

As well, if the infant's SpO2 does not increase with O2, you may want to consider cardiac or a serious V/Q mismatch. It is possible for a virus or bacterial infection to create a cardiac problem or aggravate a pre-existing one that had not be diagnosed at birth. I also will palpate the liver of an infant during my asssessment.

 

[ResTech]

I always love hearing that one in the ED. "We put him on a med neb mask and his "sat" went up."

What do you mean? Is it not typical for resp patient to show improvement in their SpO2 after neb tx and an important response to report? Just curious abt the sarcasm.

 

[VentMedic]

What do you mean? Is it not typical for resp patient to show improvement in their SpO2 after neb tx and an important response to report? Just curious abt the sarcasm.

If you give oxygen, it is expected the SpO2 will increase. If not you may need to do a challenge to determine cardiac as a possible cause. However, as EMT I would not recommend this unless you have ability to get you and the baby out of a bad situation. And, as an EMT, or even a Paramedic, you will probably not be able to do that.

 

[ResTech]

I'm still not seeing your point. With O2 it is expected to see an increase in SpO2 if diffusion can occur through all the mucous, secretions, and overcome the increased airway resistance, correct?. Isn't the goal of giving albuterol and ipratropium through a nebulizer to decrease airway resistance and promote diffusion of the oxygen being administered? Which ultimately leads to the increase in SpO2?

What do mean by "do a challenge"?

 

[ResTech]

vquintessence... we are allowed to give racemic epi (2.5mL of 1:1000) for croup. Its not in the protocols for anything other than.

 

[VentMedic]

I'm still not seeing your point. With O2 it is expected to see an increase in SpO2 if diffusion can occur through all the mucous, secretions, and overcome the increased airway resistance, correct?. Isn't the goal of giving albuterol and ipratropium through a nebulizer to decrease airway resistance and promote diffusion of the oxygen being administered? Which ultimately leads to the increase in SpO2?

What do mean by "do a challenge"?

But as in you initial post you put SpO2 increased to 98% after the Albuterol/Atrovent neb. The neb was given with O2 in the truck since few run Air unless Specialty. Even with air, on might see an increase in SpO2 with the extra flow and "auto-PEEPing".

The auto-PEEPing part is what also can produce a profound desaturation initially in asthmatics. Once the airways open the "PEEP" is gone which holds the SpO2 slightly higher. One it opens you may also have a change in deadspace ventilation (also thought of once as the "hypoxic drive"). Anything can happen during that period. They will either decompensate or "miraculously" improve. This is a rough few minutes which can even give experienced RRTs a little scare.

So, is it the O2 or is it the meds? That is the question... As I previously stated since 89% hangs on a steep cliff on the Oxyhemoglobin Dissociation Curve for PaO2, an increase in SpO2 can bring up the PaO2 to where the body can sigh with relief and decrease work of breathing. 89% might not seem like much of a drop from 92% but if you look at it on the curve, you will see the significance.

Challenge is when we'll put the infant on 100% O2 to see if there is a change in SpO2. If there is shunting due to a cardiac anomally, there probably won't be. However, before we do that we have a line and meds ready incase we inadvertently close the ductus in a ductal dependent lesion such as seen in cyanotic heart disease.

Read the article Sasha put up yesterday about neonates and O2.

 

[ResTech]

At this point in the game I am interested in the principles of respiratory care and having a firm understanding of the pathophysiology and assessment and treatment of breathing disorders as a Paramedic, not an RRT. A lot of what your talking about takes years of experience and additional education to grasp.

Maybe a patient will improve with just oxygen or maybe it is the meds.... in the field that's not our job to determine though. Our job is to alleviate the degree of distress to give the patient relief and open the airways and improve oxygenation and ventilation which is accomplished with O2 and beta agonists and anticholinergics together. Like I stated in a previous post, O2 alone is not gonna increase an SpO2 in many of the patients EMS encounters when they are so bronchoconstricted and full of mucous and secretions that the O2 can't get to where it needs to be and the airway resistance is so high they can hardly get any air into the lungs.

I been a sole BLS provider for many years so I have had a chance to see how patients respond with just O2 and than how they respond when ALS arrived with neb treatments. Once ALS arrived, the SpO2 increased more with neb treatments than with just the O2 alone and the patient stated greater amount of relief. Granted that is anecdotal observation, but with hundreds of patients its prob safe to assume its right on.

A Paramedic's job in the 20mins or so they have a patient is to stabilize them, give them relief, and get them to the hospital in better shape than they found them. Its up to the physicians to dx and the RN's and RRT's to do 3/4 of what you say we should be considering.