Michigan EMS Expo 2004

Bob Page, AAS, NREMT-P, CCEMT-P, I/C

Asthma: Pathophysiology

Asthma is increased sensitivity of the trachea and bronchi and bronchioloes to

various stimuli. The condition is a widespread REVERSIBLE narrowing of the
smaller airways. May also be accompanied by increased mucous production.

Incidence: 50% of all cases develop before age 10

33% develop after age 30
“Asthma in the older patient may be another OPD”

Two main types of asthma: Extrinsic and Intrinsic.

Extrinsic: Allergic reaction to inhaled irritants that the patient has an

allergy to. A family history of allergies such as hayfever is a predisposing
factor. Onset is usually in childhood or early adolescent.

Intrinsic: Stimuli other than allergies initiate the attack. Respiratory

infections, exposure to cold air, exertion and exercise can also trigger the
attack. Drugs such as aspirin have also been linked to this form of asthma.
Stress and cigarette smoke are also included in this group.

Pathophysiology
1. Extrinsic or intrinsic factors
trigger an airway reaction
2. Patient develops bronchospasm
and bronchoconstriction.
3. Patient develops bronchial
edema/inflammation.
4. Increased mucous production
forms a plug in the smaller
airways.
5. Difficulty exhaling – air trapping
6. Poor gas exchange. Hypoxia,
hypercarbia.
7. Increased respiratory water loss
– dehydration.
8. ABG’s or capnometry shows
PaCO2 is low (if patient is still
wheezing. High PaCO2 / ETCO2
respiratory / ventilatory failure.
Asthma: Assessment Findings

1. Dyspnea during exhalation.

2. Anxiety – hypoxia – can’t breathe.
3. Tachypnea.
4. Non-productive cough.
5. Retractions
6. Expiratory wheezes.
7. Accessory muscle use. Abdominal
muscle use to aid in exhalation.
8. Pulsus paradoxus, secondary to air
trapping.
• Absence of wheezing = ventilatory
failure
• Lethargy, confusion = respiratory
failure

50
40
30
20
10
0
Time

Asthma: Acute Management

1. Control the Airway – position of comfort.

2. Oxygen: humidified, high flow, high concentration.
3. Encourage the patient to cough up secretions.
4. Assist ventilations if needed – consider the need to intubate.
5. Start an IV of NS. (Assess the need to rehydrate).
6. Attach a cardiac monitor. Run a four lead baseline. 12 lead ECG may be
necessary if the patient has a cardiac history or if this attack is unexplained.
7. Attach Pulse Oximetry and Capnography
8. Consider albuterol 2.5mg via SVN.
9. Consider Xopenex (levalbuterol) 1.25 mg via SVN
10. Consider or ipratroprium (Atrovent) 500mcg via SVN with albuterol.
11. Consider terbutaline 0.25mg SC.
12. Consider epinephrine 1:1000 (1mg/ml) 0.3 – 0.5mg SC
13. Consider steroid preparation methylprednisolone (Solu-medrol) 125 mg IV
especially on long transports.
14. Consider Magnesium sulfate

Use the beta drugs with caution on patients that are over 55 y.o., excessively
tachycardic (>130), history of hypertension or cardiac problems.

Asthmatics should not receive sedatives, antihistamines, or aspirin.

Status Asthmaticus: asthma attack refractory to conventional bronchodilators /

epinephrine. Consider aminophylline 5-7mg/kg over 30 minutes.

CEU Article # 7
“Asthma Attack!”
By Bob Page, AAS, NREMT-P, CCEMT-P, I/C
Director of Emergency Care Education
St. John’s Regional Health Center
Springfield, Missouri

Case Presentation

On a cool, crisp autumn night, you are called to a residence for a person
who is having trouble breathing. On arrival you locate the patient, a 28
year old man who appears to be in acute respiratory distress. You discover
that his name is Bill Miller and that he has a history of asthma. He states
this latest attack started about 25 minutes ago and he has used his
“inhaler” twice without relief. He tells you he believes that his puffer is
empty.

He is speaking in short, but complete sentences. His skin is pink, warm,

and dry. Initial vital signs are BP 138/84, pulse is 100 and regular,
respiration’s are 26 and slightly labored. As you auscultate the chest, you
hear pronounced wheezes bilateral, primarily on exhalation. Bill is denying
any other pain or discomforts. He compares this attack similar to others he
has had in the past that has been reversed with his inhaler. He claims he
has allergies to several pollens and molds, and to penicillin.

Room air pulse oxymetry (SpO2) shows 92% and a pulse rate of 98. You
apply humidified O2 via non rebreather mask at 15 lpm. Within 3 minutes,
the pulse ox reads 94% yet Bill is still not breathing any easier. An IV is
established of Normal Saline running at 125cc/hr. Cardiac monitor is
applied and shows a sinus rhythm rate of 98 with normal axis and narrow
complexes. You prepare to administer albuterol via small volume
nebulizer. The patient is familiar with the device and immediately picks it
up and begins using it. After about 5 minutes, he nods his head to
acknowledge that the medication is helping him breathe easier.

Transport time is about 20 minutes from the closest facility. Medical

Control is contacted and advised you to repeat the albuterol treatment
continuously enroute to the hospital. The doctor also orders you to
administer methyprednisolone (Solu-medrol) 125 mg IVP. After two
albuterol treatments, Bill is feeling much better and his work of breathing
has decreased and his SpO2 is at 98%. He still has some wheezing
bilateral, though much less than the original findings. Bill’s pulse rate has
dropped to about 88 and he is having a mild productive cough. He thanks
you for your help as you turn over care to the emergency department.
Background

Asthma is a common inflammatory disease that involves periodic episodes

of severe but reversible bronchial obstruction. Frequent repeated attacks
may lead to irreversible damage in the lungs and the development of
chronic asthma. Asthma effects nearly 10 million Americans and is
responsible for about 4000 - 5000 deaths per year. Asthma is more
common is children and young adults, yet can occur anytime in life.

There are two basic types of asthma. The first one is called extrinsic
asthma and involves acute episodes triggered by an allergic reaction to an
inhaled irritant. Frequently there is a family history of allergies like
hayfever. The onset usually occurs during childhood or in young adults.
About 50% of the time it occurs before age 10. Childhood asthma usually
improves with age. The second type of asthma is intrinsic asthma. In this
disease, other types of stimuli initiate the acute attack. These stimuli
include respiratory infection, exposure to cold air, exercise and exertion,
drugs such as aspirin, stress, and inhalation of irritants like cigarette
smoke. Intrinsic asthma usually has an adult onset after age 30 in 33%.
Many patients have a combination of the two types.

Pathophysiology

The bronchi and bronchioles are very responsive to irritants, leading to

contraction of the smooth muscle (bronchoconstriction), inflammation with
edema (swelling), and increased secretion of thick mucous. These
changes can block the airways, totally or partially, and interfere with the air
flow and oxygen supply. In extrinsic asthma, the allergic reaction causes
release of chemical mediators like histamine that causes the
bronchospasms, edema and increased mucous secretion. This reaction
also stimulates the vagus nerve, causing a reflex bronchoconstriction. The
second stage of the allergic reaction occurs a few hours later. During this
stage, the increased leukocytes (white blood cells) release additional
chemical mediators that cause tissue damage. Left untreated, frequented
and prolonged attacks can lead to chronic asthma later in life. The
mechanisms behind intrinsic attacks are not fully understood.

Partial obstruction of the smaller airways results in air trapping with

hyperinflation of the lungs. Air passes into the areas distal to the
obstruction (alveoli), but are only partially exhaled. Since exhalation is a
passive process, less force is available to move air out, and forced
expiration often collapses the bronchial wall, creating a further barrier to
exhalation. The residual volume (air left in the lungs after exhalation)
increases and as a result. It becomes harder to inhale fresh air or to cough
to effectively remove the mucous. To better understand this air trapping,
try this experiment. Take several breaths and exhale only partially before
inhaling again. After a few breaths you will see how hard it is to inhale, or
to cough. This is what an asthma attack feels like.

Total obstruction of the airway results when mucous plugs completely

block the airflow in an already narrowed passage. This leads to atelectasis
(collapse of the alveoli). The air left in the alveoli diffuses out and is not
replaced. This could lead to collapse of the lung. Both a partial and total
obstruction will lead to hypoxia. Oxygen levels are further depleted by the
increased demand by the muscles of respiration and by the stress of the
individual fighting for air. Hypoxemia causes vasoconstriction if the
pulmonary blood vessels, slowing blood flow and increasing the workload
on the right side of the heart.

With repeated acute asthma attacks, irreversible damage occurs in the

lungs. The bronchial walls become thickened, and fibrous tissue resulting
from the frequent infections that follow attacks develops in atelectic areas.
Because it is impossible to remove all of the tiny mucous plugs in the small
airways, complications are common following frequent episodes of asthma.

Assessment Findings

The assessment can begin enroute by simply knowing what time it is.
Because our circadian rhythm (internal clock), naturally occurring anti-
inflammatory hormones are at high levels in the morning and low at night.
For this reason, asthma conditions often get worse at night. On initial
assessment you will usually find the patient sitting upright, leaning forward
with hands on knees. This is referred to as the “tripod position”. They are
frequently and obviously using accessory muscles to breathe. Retractions
may also be noted. Less obvious is accessory muscles of the abdomen
that are used for exhalation. Sometimes you may need to place your hand
on their abdomen as they breathe to feel for accessory muscle use. The
patient may also have a productive cough of thick, tenacious mucous. This
is encouraged!

Respiratory distress is obvious. You will probably often experience audible

wheezes, even heard without a stethescope. Still, listen carefully with the
stethescope in all lung fields, anterior and posterior. Not all that wheezes
is asthma! Asthma usually has diffuse wheezing, that is, heard bilateral in
all lung fields on expiration. Localized wheezing, say in just one area of
the lung, usually indicates foreign body obstruction or other localized
pathology irritation. Rhonchi, a sound heard in larger upper airways on
inhalation is frequently called “inspiratory wheezes.” Also, beware of the
person who goes from wheezes to no sounds. Absence of wheezing
generally points to ventilatory failure.

The heart rate will be increased, tachycardia is common as a response to

hypoxia and also stress response of not being able to breathe. Another
possible finding in severe cases is pulsus paradoxus. This condition
refers to the loss or diminishing of the strength of radial pulses on
inhalation. Pulsus paradoxus occurs as increased air trapping cause
increase in the pressure inside of the chest. Upon inhalation, the pressure
rises. The increase in pressure presses on the vena cava filling the heart
and reduces the blood flow going to the heart. As blood going in is
reduced, so is the blood going out, therefore a drop in pulse strength and
even in severe cases, blood pressure. Pulsus paradoxus can also be
observed by measuring the blood pressure during an asthma attack. The
first systolic sound is heard on exhalation and there is a gap of 10m/hg or
more before the sounds are heard on both exhalation and inspiration.

Acid Base Changes

Initially, hyperventilation occurs causing increased CO2 elimination. This

will lead to a decrease in hydrogen ions and increased pH. This produces
a state known as respiratory alkalosis. If you have a capnometry unit, it
would show decreased CO2 (less than 35mm/hg). In time however, all the
work of breathing will tire the patient and decreased respiratory effort and
weaker coughs occur. Severe respiratory distress is apparent.
Hypoventilation leads to hypoxemia.

Respiratory failure is indicated by a diminished level of consciousness, and

possibly cyanosis. Blood gas measurements that show a PaO2 (not pulse
ox) level of less than 50mm/hg or a PaCO2 of more than 50 mm/hg. A
capnometry unit will show ETCO2 of more than 50 mm/hg. So you don’t
have a blood gas or capnometry machine? If the attack is so severe that
the patient cannot talk at all, the PO2 level is probably less than 50 mm/hg.

History and Management

Knowing the history and medications of these patients is very important to

the management of the patient with an asthma attack. Fortunately, most
patients who have asthma are aware of thier condition and are good at self
management and of indicating the severity of the attack. They may also
know more about the drug you are giving them than you do. (I’ve had 7
year olds set up their own breathing treatments faster than I could!) My son
is 10 and he is a skillful user of his inhalers!

The best way to avoid an attack is to avoid the asthma causing irritants or
drugs like aspirin. Good ventilation in the home and workplace are
recommended. When an attack occurs, controlled breathing techniques
and a reduction in anxiety often lesson the severity and the extent of the
attack because a feeling of panic often aggravates the condition. Regular
swimming sessions are of great benefit, particularly to children, to
strengthen chest muscles and improve cardiovascular fitness.

Patients with a history of asthma are usually on a regimen on meds to

control various stages of asthma and asthma attacks. Many asthmatics
carry inhalers such as albuterol U.S.P., also recognized by the trade
names of Proventil  or Ventolin. Other acute inhalers include
terbutaline (Brethine ), metaproterenol (Alupent), and isoetharine
(Bronkosol). Albuterol is frequently given to small children as a syrup.
Terbutaline, albuterol, metaproterenol, and isoetharine are all beta 2
specific drugs that are bronchodilators used for acute asthma attacks.
Epinephrine and isoproterenol for years were used for asthma. The new
beta 2 drugs are just as effective, but have minimal heart rate effects.
Another inhaler that may be seen is Atrovent (ipratroprium). This drug has
the combined effects of ventolin and atropine in one.

As a long term anti-inflammatory, some patients may be on steroid

glucocorticoid inhaler such as beclomethasone (Beclovent). These drugs
work to minimize the second stage allergic reaction in the airways.
Beclomethasone has no use in the acute attack. Cromolyn sodium (Intal)
is a prophylactic medication that is administered by inhalation on a daily
basis. This drug inhibits the release of the chemical mediators from the
epithelial cells, thus minimizing the allergic response of the tissues.
Cromolyn sodium is used by athletes as a preventative measure, but has
no use in the acute asthma attack.

Out of Hospital Management

BLS care should begin immediately. O2 should be humidified (if at all

possible) and administered high flow via NRB mask. The humidification is
especially important in small children. The humidified O2 will help loosen
the mucous and make it easier to cough up. Remember, the mucous
finishes of the obstruction! On the other hand, giving dry O2 can actually
dry the mucous, causing plugs.

Try to calm and reassure the patient. Coach their breathing efforts. Allow
the patient to assume the most comfortable position for breathing. If the
patient has their own inhaler and knows how to use it, allow them to do so.
In some jurisdictions, EMT-B’s are allowed to assist in the delivery of an
albuterol inhaler after first contacting Medical Control. Contact your
Medical Director to find out what your service allows.

ALS Care

Paramedics should take an active, aggressive role in the management of

the patient with an acute asthma attack. Your approach should be one of
understanding the problem, then basing your treatment on this. Look
carefully at the medicines that the patient is on, sometimes they include
clues as to what works on this patient. Remember, asthma is a lower
airway obstruction (bronchoconstriction) so traditional upper airway
procedures such as intubation, do NOT relieve the problem!

IV access should be established with an isotonic crystalloid solution such

as normal saline or lactated ringers. Since the drugs you may give later will
have some effect on the cardiovascular system, it is a good idea to
establish the IV prior to any medication administration. At times this may
not be possible, however. Consult with your local protocol or medical
director for what is accepted in your area. IV rate should be adjusted to
about 125cc/hr. A person who has endured an asthma attack for several
minutes can start to dehydrate. This is especially true in children. The
average adult, breathing normally will exhale 400ml of water in a day. In
acute asthma with increased respiratory rate, a “day’s worth of breathing”
may occur in just several minutes.

Since the problem is bronchoconstriction, your first medication should be a

bronchodilator. Perhaps the most widely used and safest drug used today
is albuterol (Ventolin, Proventil). The common adult dose is 2.5mg (0.5ml
of a 0.5% solution mixed with 2.5 cc of normal saline in an updraft small
volume nebulizer. Children would receive 0.03ml/kg of the 0.5% solution in
a nebulizer. Pre-filled, pre-measured dosage containers are available
(0.083% 3 ml) where no mixing is required, just pop the cap and add to
the nebulizer. The drug is nebulized with O2 running at least 6 lpm. Start at
6 lpm; it may take more to nebulize the drug. Caution should be taken with
running nebulizer in line with a humidifier. I have seen the O2 tubing pop
off due to increased back pressure caused by the nebulizer. Some
paramedics have even used a separate O2 line not connected into a
humidifier for the nebulizer. While at the same time, they continue to
administer humidified O2 via nasal cannula at 6 lpm. This way, the patient
gets extra O2 while using the inhaler, in between puffs. Albuterol may be
repeated if the first dose was ineffective or if more is needed to maintain
the effect. Some services advocate continuous treatment for the duration
of the transport. Check your local protocol.

Although albuterol and other beta 2 drugs are designed to have minimal
cardiac effect, it has been reported to increase heart rate or some ectopy.
Therefore, a cardiac monitor should be utilized when a patient is using
these drugs. A few cases of reflex bronchoconstriction have been reported
after albuterol administration so be aware of this fact.

Some patients may not respond immediately to a beta 2 drug. These

cases of bronchoconstriction may be caused by parasympathetic
(cholinergic) or vagal stimuli. In this case, atropine may be added to the
inhaler with the second dose of albuterol. The dose in this case is 1mg
mixed in with the albuterol. Atropine, a drug used primarily to increase
heart rate, also blocks the cholinergic response that causes
bronchoconstriction. It comes packaged in 1mg in 1ml vials for this
purpose. Simply draw this amount out and add it to the 3ml of albuterol
and let them inhale it. Reflex bradycardias are not seen here partly due to
the local absorption and use of the drug and the fact that there is not a
parasympathetic crisis at the heart (bradycardia) at this time. The
combination of atropine and albuterol has properties that will prevent
bronchoconstriction while at the same time, cause bronchodilation! Which
patients may this treatment be useful? Look at their meds! Earlier we
mentioned the drug Atrovent (ipratropium.) If the patient is on this
medication, then consider starting with an albuterol, atropine mixture. The
drug (Atrovent) is also available so if you have it, it should be used after or
with albuterol administration.

In the event the patient is not moving air well enough or is unconscious
and can not hold a nebulizer, you could try terbutaline (Brethine ) 0.25
mg via subcutaneous injection. Terbutaline is another beta 2 specific drug
that has worked very well in acute asthma. Again, as with any beta drug,
monitor heart rate and rhythm carefully as terbutaline can cause
tachycardias.

In cases that are refractory to the above drugs, the old standby,
epinephrine may be used in subcutaneous injection. The dose is 0.3 to 0.5
mg of 1:1000. Pediatric dose is 0.01mg/kg (of 1:1000) Watch carefully for
tachycardias. Use epinephrine with extreme caution, if at all in patients
with known cardiovascular disease or those over age 55. Today’s beta 2
drugs are as effective as epinephrine and should be used before as to
minimize possible cardiovascular effects.

Status Asthmaticus

Status asthmaticus is a prolonged or repeated asthma attack that cannot

be broken with bronchodilators or epinephrine. It may occur as a sudden
onset or may be more insidious. It is frequently precipitated by a viral
respiratory infection. These patients need rapid transport to the hospital
and aggressive ventilatory support. Some texts have suggested an
administration of aminophylline to bronchodilate. Aminophylline (5-7mg/kg)
is a xanthine bronchodilator that must be mixed with 50-100ml of D5W and
administered as a drip over 20-30 minutes.

Paramedics should consider intubation a last resort in these cases. Even

after intubation, the problem of bronchconstriction still remains. Intubation
makes it easier for you to provide aggressively ventilatory support.
Experience has shown that if the patient has had to be intubated before to
help him breathe during an asthma attack, then I am prepared to do the
same. Always allow your drugs a chance to work. In children, every effort
should be made to avoid intubation unless absolutely necessary. Children
are harder to wein off a ventilator in the long run because of the restrictive
and obstructive pathology.

If the bronchoconstriction is broken by the beta 2 drugs, you may receive

orders to administer a steroid anti-inflammatory agent such as
methylprednisolone (Solu-Medrol). The common dose is 125mg IVP.
Although the drug generally takes about 3 hours to start working, it is will
be of benefit to prevent recurrence of the attack.

Summary

Asthma is a common disease that is reversible with prompt recognition and

aggressive management. Left untreated, asthma can and does kill. About
4000 - 5000 die annually from the preventable reversible condition. The
key is patient education and chronic management of their condition and
emergency provider's knowledge of the pathophysiology and drug options
in the management of acute bronchoconstriction.

Selected References

Bledsoe, B., Paramedic Emergency Care 3rd. Edition Brady 1997

Sanders, M. Mosby’s Paramedic Textbook Mosby 1996

Gould, B. Pathophysiology for Health Related Professions. Saunders 1997

Fremgen, B. Medical Terminology: An Anatomy and Physiology Systems

Approach Brady Prentice Hall 1997

Cason, D. Paramedic Field Care. Mosby, ACEP 1997

Bledsoe, B Prehospital Emergency Pharmacology 4th Edition Brady 1996

DeLorenzo, R. Sneezes, Wheezes and Breezes: Listening to the Chest

JEMS 1995:20:10

Critical Care Paramedic Program: University of Maryland Baltimore County

1997

Cohen, S Pediatric Emergencies 1982 Lippencott

Thibodeau, G Anthony’s Textbook of Anatomy and Physiology Times

Mirror 1990

Gonsoulin, S Prehospital Drug Therapy Mosby 1994

Quiz for CEU Article # 7 Asthma Attack! 1 hr Cat-IB Winter 1998

Name:

Address
City/state/Zip

Multiple Choice: Circle the correct answer

1. Asthma accounts for about _______ deaths per year.

A. 10 million B. 1000
C. 4000 - 5000 D. 6000 - 7000
2. The two basic types of asthma are
A. intrinsic and extrinsic B. alpha and beta
C. allergy and toxic D. stable and unstable
3. Asthma is more common in children and young adults than adults.
A. True B. False
4. Prolonged or repeated asthma attacks that are not responsive to bronchodilators is..

A. Status epilepticus B. Status asthmaticus

C. Status bronchoconstriction D. C.O.P.D.

5. Allergic reactions cause release of the chemical mediator known as _________.

A. Histamine B. Albuterol

C. Atropine D. Prothrombin

6. Which of the following conditions is NOT a presentation of an asthma attack?

A. Bronchodilation B. Mucous production

C. Edema D. Bronchdilation

7. BLS management of an acute asthma attack includes

A. High flow, humidified O2 B. Position of comfort

C. Encourage coughing D. All of the above

8. Wheezing always means bronchoconstriction and asthma

A. True B. False

9. A patient suffering an asthma attack loses his/her radial pulses upon inhalation. This
condition is called..

A. Pulse defect B. Pulsus paradoxus

C. Pulse deficit D. Pulse pressure

10. Which of the following medications prescribed to a patient would indicate a possible
history of bronchoconstriction or asthma?

A. Nitroglycerin B. Insulin
 C. Digitalis D. Ventolin

EMT’s STOP HERE: Paramedics must complete questions 11-15 for category IB credit.

11. Which of the following drugs is not a beta 2 agent?

A. Albuterol B. Methylprednisolone

C. Terbutaline D. Metaproterenol

12. Beta 2 drugs primarily are used to cause...

A. Vasodilation B. Bronchoconstriction

C. Bronchodilation D. Diuresis

13. IV fluids are frequently needed in an acute asthma attack because....

A. The patient may become dehydrated

B. The patient usually has a low blood pressure

C. The patient may become overhydrated

D. The patient may need fluids for tachycardia

14. What is the action of atropine in an acute asthma attack?

A. Increases heart rate B. Decreases heart rate

C. Prevents bronchodilation D. Blocks cholinergic bronchoconstriction

15. Which of the following drugs is generally NOT effective in the acute asthma attack?

A. Ventolin B. Cromolyn sodium

C. Alupent D. Atrovent

Return Quiz and Self-addressed stamped envelope to St. John’s EMS Education Programs

Attn CEU Articles

1235 E. Cherokee

Spriingfield, MO 65804