Nurs 2200 Asthma Case Study
A case study on asthma presented in Nursing 2200 Nursing Pathophysiology course at Chicago State University
Content
NURS 2200
April 28, 2015
Asthma Case Study
R. Abed, B. Calhoun, D. Coles, J. Fordjour, B. Hall, F. Kassim, T. Mann, J. Medrano, I. Meraz,
A. Ogunsanya & B. Stanton
Patient Name: Kenya
Sex: Female
Age:16
Occupation: Student
Subjective Patient Complaints: Shortness of breath, recurrent asthma attacks from running and
exposure to dog hair, chest tightness.
Objective Data: Wheezing heard on auscultation
Laboratory values:
arterial pH: 7.42
P802:81
PaCO2:34
HCO3:26
Initial FEV1: 52%
Final FEV1: 75%
Initial Vital Capacity: 3510 mL Final Vital Capacity: 3605 mL
Treatment: Inhaled salbutamol solution with the aid of a nebulizer. Patient given a subcutaneous
injection of epinephrine after her breathing didn’t improve. Salbutamol is a short acting beta 2
agonist, a bronchodilator that widens airways. The inhaler primarily works by opening air
passages to allow air to flow in the lungs more freely, thereby relieving symptoms of asthma
such as coughing, wheezing, and shortness of breath.
1. What is the name of the white blood cell responsible for triggering an asthma attack?
Name two chemicals that this cell secretes that leads to constriction of smooth muscle.
The white blood cell that triggers an asthma attack is called a mast cell. These mast cells
come from the bone marrow and are considered the master cells of the immune response. They
are scattered around the connective tissues of the body, including throughout the lungs, bronchi
and bronchioles. When an antigen invades the body, IgE antibodies attach themselves to the
antigen then attach to the mast cells. The mast cells then cause a type I immediate
hypersensitivity reaction. Mast cells release chemotactic mediators that send signals to other
white blood cells to come to the area, such as eosinophils, where the allergic response is
occurring. They also release histamine, a vasodilator, that causes a cascade of allergic reactions
2
such as hives, sneezing, swelling, and in asthma, smooth muscle and mucosa layer swelling. The
constriction of the smooth muscle and mucosa layers of the bronchi prevents air from flowing
into the lungs efficiently, which is why asthma attacks consist of wheezing and coughing.
Porth, C., (2015). Disorders of the Immune Response. In Essentials of pathophysiology:
Concepts of altered health states (4th ed.). Philadelphia: Lippincott Williams & Wilkins.
2. What lung volume(s) is/are commonly measured to ascertain the severity of an asthma attack or
to ascertain the recovery from an attack?
To determine the severity or recovery from an asthma attack, pulmonary function tests
are performed using a spirometer. The spirometer commonly measures the lung vital capacity
(VC) and forced expiratory volume (FEV). Lung vital capacity represents the maximum volume
of air that can be forcibly exhaled from the point of maximal inspiration. The forced expiratory
volume is the expiratory volume achieved in a given time period. For example, FEV1.0
represents the forced expiratory volume that can be exhaled in 1 second. FEV measurements are
usually represented as the percentage of the VC (Porth, 2015).
During an asthmatic reaction the lung vital capacity will not be affected because vital
capacity is not a timed measurement, as seen as in Kenya’s lung volumes. Her vital capacity
when she was having the asthma attack was 3510 mL and once her breathing improved it did not
change dramatically, it read 3605 mL. The forced expiratory volume on the other hand will
decrease due to the narrowing of the airways caused by the constriction of the bronchioles, as
seen in Kenya’s measurements with 52% while having the asthma attack to 75% while stable and
breathing normally.
Porth, C. M. (2015). Essentials of pathophysiology: Concepts of altered health states.
Philadelphia, PA: Wolters Kluwer.
3. How are arterial PO2, PCO2, HCO3, and pH affected during a moderately severe asthma attack
in which hyperventilation occurs?
The arterial partial pressure of oxygen, carbon dioxide, bicarbonate and pH levels all deal
with the amount that is dissolved in the blood. In Kenya’s case, she started hyperventilating
because there’s too much pCO2 in her lungs which caused the asthmatic attack. The pCO2
diffuses quickly in the lungs, which leads to respiratory alkalosis. Therefore, the pCO2 level
needs to be exchanged with pO2 by exhaling it out. Moderate amount of pO2 is needed in order
for Kenya to breathe properly. However, hyperventilation occurs because no sufficient oxygen is
allowed to diffuse into the blood during that period. Also, by reducing the pCO2 level, it allows
3
the blood pH level to increase. But, if the blood pH is too elevated, it can cause hyperventilation
and if ample time has passed without been controlled, it leads to rise in pHCO3.
4. List two types of beta receptors. Which type is found in the lung? In the heart?
Two types of beta receptor cells are termed beta-1 and beta-2. Beta-1 receptor cells
increase cardiac output by raising heart rate, impulse conduction, and contraction, thereby
increasing the left ventricular ejection fraction; increase juxtaglomerular renin secretion; and
increase gastric secretion of ghrelin (the hunger hormone). Beta-2 receptor prompt smooth
muscle relaxation resulting in bronchodilation; reduced GI motility; relaxation of detrusor
muscle of bladder; glycogenolysis and gluconeogenesis; and increased renin secretion (Medical
Dictionary, 2012). Beta-1 receptors are found in the heart, and beta-2 receptors are found in the
lungs.
Beta receptors. (2012). In Segen’s Medical Dictionary Online. Retrieved from http://medicaldictionary.thefreedictionary.com/beta+receptor.
5. Will increasing cellular cAMP help or worsen an asthma attack?
Yes, increasing cellular cAMP (Cyclic adenosine monophosphate) will help an asthma
attack by inhibiting mast cell release of histamine and SRS-A ( Slow-releasing anaphylaxis
substance) and triggers smooth muscle cell relaxation. The goal then is to increase the cAMP
concentrations in mast cells and smooth muscle cells to prevent the release of histamine and
SRS-A, and to prevent smooth muscle cell constriction of airways. This can be accomplished by
several means, the cell enzyme that degrades cAMP, cAMP phosphodiesterase, can be inhibited
by a molecule known as theophylline. Theophylline is a common aerosol inhalant taken by
asthmatics: it is also available in pill form. Theophylline, found in many teas, is an example of a
class of molecules known as methylxanthines. Caffeine is another example of a commonly
occurring methylxanthine. Stimulation of beta receptors on the surface of mast cells and smooth
4
muscle cells leads to an increase in their cellular cAMP, thereby inhibiting release of histamine
and SRS-A.
6. How does stimulation of beta receptors help lesson an asthma attack?
During an asthma attack the mast cell secrete histamine and SRS-A. These two chemicals
trigger the smooth muscle surrounding the lung airway to contract, leading to
bronchoconstriction, . The body response is a fright or flight causing adrenaline or epinephrine,
which are hormones that are secreted by the adrenal medulla to stimulate smooth muscles beta
receptors. Upon stimulation, these receptors cause a relaxation of the smooth muscles of the
bronchi.
7. What is the anatomical basis for wheezing heard during an asthma attack?
Wheezing may result from localized or diffuse airway narrowing or obstruction from the
level of the larynx to the small bronchi. According to the case background the individual has a
difficult time filling their lungs with air. The airway narrowing may be caused by
bronchoconstriction, mucosal edema, external compression, or partial obstruction by a tumor,
foreign body, or tenacious secretions. Wheezes are believed to be generated by oscillations or
vibrations of nearly closed airway walls. Hyperventilation occurs because of the passage of
carbon dioxide occurs 20 times faster than oxygen. If the attack is severe the airway is
significantly narrowed, therefore CO2 is retained raising the PaCo2 lowering the blood PH in
other words, air passing through a narrowed portion of an airway at high velocity produces
decreased gas pressure and flow in the constricted region. The internal airway pressure
ultimately begins to increase and barely reopens the airway lumen. The alternation of the airway
between nearly closed and nearly open produces a "fluttering" of the airway walls and a musical,
"continuous" sound. The flow rate and mechanical properties of the adjacent tissues that are set
into oscillation determine the intensity, pitch, composition, the duration, and timing. Wheezes are
heard more commonly during expiration because normally the airways narrow during this phase
of respiration. If wheezing occurs during expiration alone it is generally indicative of a milder
obstruction than if present during both inspiration and expiration, this suggests that there is more
of a severe airway narrowing. However, most asthmatic patients are unable accurately to
correlate their wheezing (or other respiratory symptoms) to the severity of airway obstruction as
measured objectively by pulmonary function tests.
8. A certain person has a vital capacity of 4000 ml. If he can forcefully expire 3000 cc of the vital
capacity in 1 second, calculate his FEV 1.0.
VC= Vital Capacity
FEV= Volume forcefully expired in 1 second, after maximal inhalation (patient blows air out)
5
Vital capacity is basically proportional to the number of lung alveoli possessed by an
individual. The FEV measurements represent the percent of the vital capacity that can be expired
forcefully and rapidly in a given period of time, such as 1 second for the FEV1.0.
The formula to calculate the FEV 1.0. (1 second forced expiratory volume)
FEV1.0=[(Volume forcefully expired in 1 second, after maximal inhalation) / (VC)] x 100
FEV1.0=[(3000 cc)/4000 ml)] x 100
FEV1.0= 0.75 x 100
FEV1.0= 75%
The patient’s FEV1.0 is 75%
9. What effect will beta-1 receptor stimulation have on someone having an asthma attack? beta-2
receptor stimulation? generalized beta receptor stimulation?
Beta-1 receptor stimulation in someone having an asthma attack will produce cardiac
symptoms such as increased heart rate via the SA node, increased atrial and ventricular cardiac
muscle contractility and overall increased cardiac output.
Beta-2 receptor stimulation in someone having an asthma attack will produce pulmonary
symptoms such as relaxation of the muscles surrounding the bronchi and bronchioles, resulting
in bronchodilation.
Generalized beta-receptor stimulation will produce both bronchodilation and increased
cardiac output in someone having an asthma attack.
Beta-Receptor stimulant. (2002). In The Royal Society of medicine: Medicines. London, United
Kingdom:
Bloomsbury.
Retrieved
from
http://bluestem.csu.edu:2048/login?
url=http://search.credoreference.com.bluestem.csu.edu:2048/content/entry/rsmmeds/beta_recept
or_stimulant/0
10. Can you think of a special precaution that is needed when treating a heart patient with beta
blockade medication, if the heart patient also suffers from asthma? Explain your answer.
Yes, there is a special precaution one must take when treating a heart patient taking beta
blockade medication that also has asthma. Beta blockade medications are known to treat heart
disease, high blood pressure, decrease blood flow to heart muscles, and an irregular heartbeat.
These medications work by blocking the sites of binding of catecholamines like epinephrine and
norepinephrine. (Salpeter, 2003) As a result, this medication would reduce blood pressure.
However, the problem occurs when the site of epinephrine and norepinephrine are blocked.
These two hormones are commonly used to treat “hives, asthma, and other conditions requiring
bronchodilation…” (Beta Blockers) The function of these hormones allow for “vasodilation of
blood vessels of the skeletal muscles and relaxation of bronchiolar smooth muscles.” (Beta
6
Blockers) Ultimately, Beta Blockers may interfere with the passage of air into the lungs and
cause heart rate and blood pressure to be reduced too much. Furthermore, the proper medication
that should be used to treat a patient with this specific situation is to use a Beta 2 agonist. These
medications allow for bronchodilation and protection against Broncho-constrictive stimuli.
(Beta-2 Adrenergic Agonists) Also, studies have shown to be beneficial for individuals with
asthma as well as individuals with COPD.
Beta -2 Adrenergic Agonists. (n.d.) In National Library of Medicine. Retrieved from
www.livertox.nih.gov/Beta2AdrenergicAgonists.htm
Beta Blockers. (n.d.) In Medical Dictionary
Medicaldictionary.thefreedictionary.com/Beta+blockers
Online.
Retrieved
from
www.
Salpeter, S. (2003). Cardioselective Beta Blocker Use in Patients With Asthma and Chronic
Obstructive Pulmonary Disease: An Evidence-Based Approach to Standards of Care. Medscape.
Retrieved from www.medscape.com/viewarticle/464040_4
April 28, 2015
Asthma Case Study
R. Abed, B. Calhoun, D. Coles, J. Fordjour, B. Hall, F. Kassim, T. Mann, J. Medrano, I. Meraz,
A. Ogunsanya & B. Stanton
Patient Name: Kenya
Sex: Female
Age:16
Occupation: Student
Subjective Patient Complaints: Shortness of breath, recurrent asthma attacks from running and
exposure to dog hair, chest tightness.
Objective Data: Wheezing heard on auscultation
Laboratory values:
arterial pH: 7.42
P802:81
PaCO2:34
HCO3:26
Initial FEV1: 52%
Final FEV1: 75%
Initial Vital Capacity: 3510 mL Final Vital Capacity: 3605 mL
Treatment: Inhaled salbutamol solution with the aid of a nebulizer. Patient given a subcutaneous
injection of epinephrine after her breathing didn’t improve. Salbutamol is a short acting beta 2
agonist, a bronchodilator that widens airways. The inhaler primarily works by opening air
passages to allow air to flow in the lungs more freely, thereby relieving symptoms of asthma
such as coughing, wheezing, and shortness of breath.
1. What is the name of the white blood cell responsible for triggering an asthma attack?
Name two chemicals that this cell secretes that leads to constriction of smooth muscle.
The white blood cell that triggers an asthma attack is called a mast cell. These mast cells
come from the bone marrow and are considered the master cells of the immune response. They
are scattered around the connective tissues of the body, including throughout the lungs, bronchi
and bronchioles. When an antigen invades the body, IgE antibodies attach themselves to the
antigen then attach to the mast cells. The mast cells then cause a type I immediate
hypersensitivity reaction. Mast cells release chemotactic mediators that send signals to other
white blood cells to come to the area, such as eosinophils, where the allergic response is
occurring. They also release histamine, a vasodilator, that causes a cascade of allergic reactions
2
such as hives, sneezing, swelling, and in asthma, smooth muscle and mucosa layer swelling. The
constriction of the smooth muscle and mucosa layers of the bronchi prevents air from flowing
into the lungs efficiently, which is why asthma attacks consist of wheezing and coughing.
Porth, C., (2015). Disorders of the Immune Response. In Essentials of pathophysiology:
Concepts of altered health states (4th ed.). Philadelphia: Lippincott Williams & Wilkins.
2. What lung volume(s) is/are commonly measured to ascertain the severity of an asthma attack or
to ascertain the recovery from an attack?
To determine the severity or recovery from an asthma attack, pulmonary function tests
are performed using a spirometer. The spirometer commonly measures the lung vital capacity
(VC) and forced expiratory volume (FEV). Lung vital capacity represents the maximum volume
of air that can be forcibly exhaled from the point of maximal inspiration. The forced expiratory
volume is the expiratory volume achieved in a given time period. For example, FEV1.0
represents the forced expiratory volume that can be exhaled in 1 second. FEV measurements are
usually represented as the percentage of the VC (Porth, 2015).
During an asthmatic reaction the lung vital capacity will not be affected because vital
capacity is not a timed measurement, as seen as in Kenya’s lung volumes. Her vital capacity
when she was having the asthma attack was 3510 mL and once her breathing improved it did not
change dramatically, it read 3605 mL. The forced expiratory volume on the other hand will
decrease due to the narrowing of the airways caused by the constriction of the bronchioles, as
seen in Kenya’s measurements with 52% while having the asthma attack to 75% while stable and
breathing normally.
Porth, C. M. (2015). Essentials of pathophysiology: Concepts of altered health states.
Philadelphia, PA: Wolters Kluwer.
3. How are arterial PO2, PCO2, HCO3, and pH affected during a moderately severe asthma attack
in which hyperventilation occurs?
The arterial partial pressure of oxygen, carbon dioxide, bicarbonate and pH levels all deal
with the amount that is dissolved in the blood. In Kenya’s case, she started hyperventilating
because there’s too much pCO2 in her lungs which caused the asthmatic attack. The pCO2
diffuses quickly in the lungs, which leads to respiratory alkalosis. Therefore, the pCO2 level
needs to be exchanged with pO2 by exhaling it out. Moderate amount of pO2 is needed in order
for Kenya to breathe properly. However, hyperventilation occurs because no sufficient oxygen is
allowed to diffuse into the blood during that period. Also, by reducing the pCO2 level, it allows
3
the blood pH level to increase. But, if the blood pH is too elevated, it can cause hyperventilation
and if ample time has passed without been controlled, it leads to rise in pHCO3.
4. List two types of beta receptors. Which type is found in the lung? In the heart?
Two types of beta receptor cells are termed beta-1 and beta-2. Beta-1 receptor cells
increase cardiac output by raising heart rate, impulse conduction, and contraction, thereby
increasing the left ventricular ejection fraction; increase juxtaglomerular renin secretion; and
increase gastric secretion of ghrelin (the hunger hormone). Beta-2 receptor prompt smooth
muscle relaxation resulting in bronchodilation; reduced GI motility; relaxation of detrusor
muscle of bladder; glycogenolysis and gluconeogenesis; and increased renin secretion (Medical
Dictionary, 2012). Beta-1 receptors are found in the heart, and beta-2 receptors are found in the
lungs.
Beta receptors. (2012). In Segen’s Medical Dictionary Online. Retrieved from http://medicaldictionary.thefreedictionary.com/beta+receptor.
5. Will increasing cellular cAMP help or worsen an asthma attack?
Yes, increasing cellular cAMP (Cyclic adenosine monophosphate) will help an asthma
attack by inhibiting mast cell release of histamine and SRS-A ( Slow-releasing anaphylaxis
substance) and triggers smooth muscle cell relaxation. The goal then is to increase the cAMP
concentrations in mast cells and smooth muscle cells to prevent the release of histamine and
SRS-A, and to prevent smooth muscle cell constriction of airways. This can be accomplished by
several means, the cell enzyme that degrades cAMP, cAMP phosphodiesterase, can be inhibited
by a molecule known as theophylline. Theophylline is a common aerosol inhalant taken by
asthmatics: it is also available in pill form. Theophylline, found in many teas, is an example of a
class of molecules known as methylxanthines. Caffeine is another example of a commonly
occurring methylxanthine. Stimulation of beta receptors on the surface of mast cells and smooth
4
muscle cells leads to an increase in their cellular cAMP, thereby inhibiting release of histamine
and SRS-A.
6. How does stimulation of beta receptors help lesson an asthma attack?
During an asthma attack the mast cell secrete histamine and SRS-A. These two chemicals
trigger the smooth muscle surrounding the lung airway to contract, leading to
bronchoconstriction, . The body response is a fright or flight causing adrenaline or epinephrine,
which are hormones that are secreted by the adrenal medulla to stimulate smooth muscles beta
receptors. Upon stimulation, these receptors cause a relaxation of the smooth muscles of the
bronchi.
7. What is the anatomical basis for wheezing heard during an asthma attack?
Wheezing may result from localized or diffuse airway narrowing or obstruction from the
level of the larynx to the small bronchi. According to the case background the individual has a
difficult time filling their lungs with air. The airway narrowing may be caused by
bronchoconstriction, mucosal edema, external compression, or partial obstruction by a tumor,
foreign body, or tenacious secretions. Wheezes are believed to be generated by oscillations or
vibrations of nearly closed airway walls. Hyperventilation occurs because of the passage of
carbon dioxide occurs 20 times faster than oxygen. If the attack is severe the airway is
significantly narrowed, therefore CO2 is retained raising the PaCo2 lowering the blood PH in
other words, air passing through a narrowed portion of an airway at high velocity produces
decreased gas pressure and flow in the constricted region. The internal airway pressure
ultimately begins to increase and barely reopens the airway lumen. The alternation of the airway
between nearly closed and nearly open produces a "fluttering" of the airway walls and a musical,
"continuous" sound. The flow rate and mechanical properties of the adjacent tissues that are set
into oscillation determine the intensity, pitch, composition, the duration, and timing. Wheezes are
heard more commonly during expiration because normally the airways narrow during this phase
of respiration. If wheezing occurs during expiration alone it is generally indicative of a milder
obstruction than if present during both inspiration and expiration, this suggests that there is more
of a severe airway narrowing. However, most asthmatic patients are unable accurately to
correlate their wheezing (or other respiratory symptoms) to the severity of airway obstruction as
measured objectively by pulmonary function tests.
8. A certain person has a vital capacity of 4000 ml. If he can forcefully expire 3000 cc of the vital
capacity in 1 second, calculate his FEV 1.0.
VC= Vital Capacity
FEV= Volume forcefully expired in 1 second, after maximal inhalation (patient blows air out)
5
Vital capacity is basically proportional to the number of lung alveoli possessed by an
individual. The FEV measurements represent the percent of the vital capacity that can be expired
forcefully and rapidly in a given period of time, such as 1 second for the FEV1.0.
The formula to calculate the FEV 1.0. (1 second forced expiratory volume)
FEV1.0=[(Volume forcefully expired in 1 second, after maximal inhalation) / (VC)] x 100
FEV1.0=[(3000 cc)/4000 ml)] x 100
FEV1.0= 0.75 x 100
FEV1.0= 75%
The patient’s FEV1.0 is 75%
9. What effect will beta-1 receptor stimulation have on someone having an asthma attack? beta-2
receptor stimulation? generalized beta receptor stimulation?
Beta-1 receptor stimulation in someone having an asthma attack will produce cardiac
symptoms such as increased heart rate via the SA node, increased atrial and ventricular cardiac
muscle contractility and overall increased cardiac output.
Beta-2 receptor stimulation in someone having an asthma attack will produce pulmonary
symptoms such as relaxation of the muscles surrounding the bronchi and bronchioles, resulting
in bronchodilation.
Generalized beta-receptor stimulation will produce both bronchodilation and increased
cardiac output in someone having an asthma attack.
Beta-Receptor stimulant. (2002). In The Royal Society of medicine: Medicines. London, United
Kingdom:
Bloomsbury.
Retrieved
from
http://bluestem.csu.edu:2048/login?
url=http://search.credoreference.com.bluestem.csu.edu:2048/content/entry/rsmmeds/beta_recept
or_stimulant/0
10. Can you think of a special precaution that is needed when treating a heart patient with beta
blockade medication, if the heart patient also suffers from asthma? Explain your answer.
Yes, there is a special precaution one must take when treating a heart patient taking beta
blockade medication that also has asthma. Beta blockade medications are known to treat heart
disease, high blood pressure, decrease blood flow to heart muscles, and an irregular heartbeat.
These medications work by blocking the sites of binding of catecholamines like epinephrine and
norepinephrine. (Salpeter, 2003) As a result, this medication would reduce blood pressure.
However, the problem occurs when the site of epinephrine and norepinephrine are blocked.
These two hormones are commonly used to treat “hives, asthma, and other conditions requiring
bronchodilation…” (Beta Blockers) The function of these hormones allow for “vasodilation of
blood vessels of the skeletal muscles and relaxation of bronchiolar smooth muscles.” (Beta
6
Blockers) Ultimately, Beta Blockers may interfere with the passage of air into the lungs and
cause heart rate and blood pressure to be reduced too much. Furthermore, the proper medication
that should be used to treat a patient with this specific situation is to use a Beta 2 agonist. These
medications allow for bronchodilation and protection against Broncho-constrictive stimuli.
(Beta-2 Adrenergic Agonists) Also, studies have shown to be beneficial for individuals with
asthma as well as individuals with COPD.
Beta -2 Adrenergic Agonists. (n.d.) In National Library of Medicine. Retrieved from
www.livertox.nih.gov/Beta2AdrenergicAgonists.htm
Beta Blockers. (n.d.) In Medical Dictionary
Medicaldictionary.thefreedictionary.com/Beta+blockers
Online.
Retrieved
from
www.
Salpeter, S. (2003). Cardioselective Beta Blocker Use in Patients With Asthma and Chronic
Obstructive Pulmonary Disease: An Evidence-Based Approach to Standards of Care. Medscape.
Retrieved from www.medscape.com/viewarticle/464040_4
