CASE

STUDIES ON
MAJOR
CONCEPTS
OXYGENATION
 ASTHMA
By: ALCE

Case Scenario – Mrs. Ty is a 38-year-old woman brought to a walk-in health care center by her neighbor. Mrs. Ty is in
obvious respiratory distress. She is having difficulty breathing with audible high-pitched wheezing and is having difficulty
speaking. Pausing after every few words to catch her breath, she tells the nurse, “I am having a really bad asthma attack.
My chest feels very tight and I cannot catch my breath. I took my albuterol and Vanceril, but they are not helping.” Mrs. Ty
hands her neighbor her cell phone and asks the neighbor to dial a telephone number. “That number is my husband’s boss.
My husband just started working for an asbestos removal company about a month ago. He is usually on the road
somewhere. Can you ask his boss to get a message to him that I am here?”
History of Present Illness – While auscultating Mrs. Ty’s lung sounds, the nurse hears expiratory wheezes and scattered
rhonchi throughout. Mrs. Ty is afebrile. Her vital signs are blood pressure 142/96, pulse 88, and respiratory rate 34. Her
oxygen saturation on room air is 86%. Arterial blood gases (ABGs) are drawn. Mrs. Ty is placed on 2 liters of humidified
oxygen via nasal cannula. She is started on intravenous (IV) fluids and receives an albuterol nebulizer treatment.
Pathophysiology

Inflammation has a central role in the pathophysiology of asthma. As noted in the definition of asthma, airway inflammation
involves an interaction of many cell types and multiple mediators with the airways that eventually results in the characteristic
pathophysiological features of the disease: bronchial inflammation and airflow limitation that result in recurrent episodes of
cough, wheeze, and shortness of breath. The processes by which these interactive events occur and lead to clinical asthma
are still under investigation. Moreover, although distinct phenotypes of asthma exist (e.g., intermittent, persistent, exercise-
associated, aspirin-sensitive, or severe asthma), airway inflammation remains a consistent pattern. The pattern of airway
inflammation in asthma, however, does not necessarily vary depending upon disease severity, persistence, and duration of
disease. The cellular profile and the response of the structural cells in asthma are quite consistent.
Concept Map

Causes
•• Overuse
Overuse ofof aspirin
aspirin
•• Stress
Stress
•• Cold
Cold airs
airs
•• Food
Food Allergies
Allergies
•• Upper
Upper RTI
Risk Factors RTI Signs and
•• CHF
CHF Symptoms
•• Genetics
Genetics •• Bronchospasm
Bronchospasm
•• Allergies
Allergies •• Edeme
Edeme of
of bronchial
bronchial
•• Ages
Ages 2-17
2-17 mucosa
mucosa
•• Pulmonary
Pulmonary Embolism
Embolism •• Accumulation
Accumulation of
of mucus
mucus

Asthma
 BRONCHITIS
By: ADUNA

A 22-year-old woman with asthma and active tobacco use presented to an emergency room with a 1-day history of dyspnea, cough, and
left shoulder pain.
Chief complain: dyspnea, cough, and left shoulder pain
Past history: Her father and mother both have hypertension. Her only brother died from pneumonia 2 years ago. She was diagnosed to
have an asthma when she was 16 years old. She was given salbutamol for her asthma. She is non alcoholic but smokes 3 sticks per
day.
Present: She is walking home from the supermarket where she works as a cashier when suddenly she felt shortness of breath. At first
she thought it was just normal as she is walking but the next day became worse. Her dyspnea worsen and now she got cough and
shoulder pain on the left shoulder.
Labs: Her initial physical examination was notable for a blood pressure of 138/56, heart rate of 105 beats per minute, temperature of
39.6°C, respiratory rate of 23 breaths per minute, and an oxygen saturation of 97% while breathing ambient air.
Pathophysiology

Factors like cigarette smoking, respiratory infection or environmental polluntants can lead into inflammation of the
bronchial walls and this could lead into muscosal thickening, epithelial cell desquamation and denudation of the
membrance. At times, an upper respiratory infection can progress to infection of the lower respiratory tract resulting
into bronchitis. (Reference: Diagnosis and management of Acute Bronchitis, Doug Knutson MD)
Concept Map
 EMPHYSEMA
By: BAYAUA

Case Scenario: A 38 year old female amateur astronomer, all the while knowing better, has smoked since she was 18 years old. She has
been having trouble for years with the smoke and the light of the cigarette impairing her ability to see the more distant galaxies through her
telescope, but she has not been willing to quit yet. Additionally, she has noticed a mild, occasionally productive cough for the past 3-4 months.

She finally decides to visit her family physician who, after making appropriate patient-centered inquiries as to how her astrophotography hobby
is going, finds that she has been smoking about one pack per day for the past 20 years. Her only other past medical history includes
hypertension for which she is using lisinopril, metoprolol, and hydrochlorothiazide.

History Of Present Illness: The cough has been present for almost a year. She has had no fever or chills. She does admit to more shortness
of breath when she exercises over the past six months.

The cough is worse whenever she spends the night out in the country taking astrophotos where she is exposed to the smoke of the nearby
wildfires.

Family History: Family history of COPD

Pathophysiology

Permanent enlargement of airspaces distal to the terminal

bronchioles, emphysema creates an environment leading to a
dramatic decline in the alveolar surface area available for gas
exchange. Loss of individual alveoli with septal wall destruction
leads to airflow limitation via two mechanisms
Concept Map

Family history of
COPD

has smoked
since she was noticed a mild,
18 years old occasionally
productive cough
for the past 3-4
EMPHYSEMA
months.
The cough has
been present for
almost a year.
She has had no past medical
he has been history includes
fever or chills.
smoking about hypertension for
  one pack per day which she is using
She does admit to
for the past 20 lisinopril,
more shortness of
years metoprolol, and
breath when she
exercises over the hydrochlorothiazide
past six months .
 SLEEP APNEA
By: BERNABEO

Case Scenario: A 36-year-old man who worked as a dimensional control surveyor caused a vehicle accident while he
was driving at the work site. Although he experienced loss of consciousness at the time of the accident, he had no other
symptoms.  His brain computed tomography and laboratory test did not show any specific findings. Medical tests were
conducted to evaluate his fitness for work. Decreased sleep latency was observed on the electroencephalography
image, which is suggestive of a sleep disorder. He frequently experienced daytime sleepiness and his Epworth
sleepiness score was 13. The polysomnography showed a markedly increased apnea-hypopnea index of 84.3.

History of Present Illness:

loss of consciousness while driving

Pathophysiology

Sleep apnea is a potentially serious sleep disorder in which breathing repeatedly stops and
starts. If you snore loudly and feel tired even after a full night's sleep, you might have sleep
apnea.
Concept Map:

SIGNS & SYMPTOMS RISK FACTORS

Awakening with dry

Irritability Excessive Weight Older Adults
mouth
     
 

Gasping for air

Smoking
Morning headache during sleep Medical conditions
 
 

Difficulty staying Family History Nasal Congestion

asleep (insomnia) Loud snoring
   
 
Use of alcohol,
Episodes in which sedatives, or
Excessive daytime Neck Circumference
you stop breathing tranquilizers
sleepiness
(hypersomnia) during sleep  
 
 
   
 
 
 FLAIL CHEST
By: COCUSA

A 36 Years old male brought to Emergency hospital department due to injured in bicycle accident because he was hit and
car by a car. His vital sign BP: 70/90 RR: 12 Pulse rate: 70 Temp: 34.5. His assessment He had flail ribs in both the front
and back of his chest under the shoulder blade. The nursing intervention The ribs were repaired in a staged approach first
the left side where the pain was greater and then the right side. He need immediate surgery operation because his front and
back ribs severely injured.
 Pathophysiology

The movement of air in and out of the lungs is dependent on changes in intrathoracic pressure. Inspiration relies on the
coordinated function of respiratory muscle groups including the diaphragm, external intercostal, parasternal internal intercostal and
accessory muscles. The descent of the diaphragmatic dome increases in the vertical dimension of the chest cavity and creates
negative pressure. The diaphragm alone can maintain adequate ventilation at rest. The intercostals play an increasingly important
role to inspiration during exercise and in pathologic states. Exhalation is usually passive due to the elastic recoil of the lung, but
the abdominal muscles and the intercostals may participate. With a flail chest, the continuity of the chest wall is disrupted, and the
physiologic action of the ribs is altered. The motion of the flail segment is paradoxical to the rest of the chest. It is paradoxical
because the flail segment moves inward while the rest of the chest wall moves outward. The severity of this paradoxical motion
and the physiological effect is determined by three factors; pleural pressure, the extent of the flail, and the activation of intercostals
muscles during inspiration.

A flail segment of the chest wall will negatively affect respiration in three ways: ineffective ventilation, pulmonary contusion, and
hypoventilation with atelectasis. There is ineffective ventilation because of increased dead space, decreased intrathoracic pressure
and increased oxygen demand from injured tissue. Pulmonary contusion in adjacent lung tissue is almost universal with flail chest.
Pulmonary contusion leads to edema, hemorrhage and may eventually have some element of necrosis. Pulmonary contusion impairs
gas exchange and decreases compliance. Hypoventilation and atelectasis result from the pain of the injury. The pain causes
splinting which decreases the tidal volume and predisposes to the formation of atelectasis.
 Complications
Symptoms:
 Severe pain
 extreme pain in your chest
 Chest wall deformity
 tenderness in the area of your chest where the bone has
come away  Dyspnea

 significant difficulty in breathing  Loss of exercise endurance

 bruising and inflammation Diagnosis

 uneven rising or falling of your chest when breathing  computed tomography (CT) scan

 X-ray
 ANEMIA
By: DELA CRUZ

Case Scenario: A 10-year-old child with past medical history of recurrent illnesses was admitted in this hospital 1 and a half month back
through OPD with the following complains of
Fever& headache
Fatigue & dizziness
Shortness of breath on exertion
Weight loss with loss of appetite
Loss of Taste sensation.
Tingling and numbness.
History of Past Illness: He experienced generalized fits 3 years back, for 2-3 minutes, followed by unconsciousness, associated with urinary
incontinence & frothing. For which he got admitted in civil hospital where he received injections for 15 days & blood transfusion.
History of Present Illness: According to his mother he has suffered different illnesses in the last 3 months for which different diagnosis were
made and treated.
• He once suffered from an episode of bleeding for which hemophilia was considered by the doctor but not proven.
• He was also diagnosed as nephrotic syndrome by one doctor, because of puffiness of the face.
• 2 months ago, he presented with the symptoms of fever, motion, vomiting. Which was eventually subsided in hospital by palliative
treatment.
• 1.5 month back he got admitted in this hospital and on the very vague history and varying diagnosis a detailed physical examination &
laboratory investigation were done to rule out nephrotic syndrome and hemophilia.
Pathophysiology

Megaloblastosis describes a heterogeneous group of disorders that share common morphologic characteristics: large cells
with an arrest in nuclear maturation. Nuclear maturation is immature relative to cytoplasmic maturity. Hence, these cells,
which can be seen in bone marrow aspirates and in peripheral smears, have been called megaloblasts. These abnormalities
are due to impaired DNA synthesis and, to a lesser extent, RNA and protein synthesis. Megaloblastic changes are most
apparent in rapidly dividing cells such as blood cells and gastrointestinal cells. In addition to large nucleated red blood cells,
hypersegmented neutrophils can be seen on peripheral smears, and giant bands occur in bone marrow. The common
feature in megaloblastosis is a defect in DNA synthesis in rapidly dividing cells. To a lesser extent, RNA and protein
synthesis are impaired. Unbalanced cell growth and impaired cell division occur since nuclear maturation is arrested. More
mature RBC precursors are destroyed in the bone marrow prior to entering the blood stream
Concept Map Signs and Symptoms Risk Factors

Gender, Genetics,
Fatigue
Lifestyle

Pallor Vegetarian Diet

Shortness of Breath
Pregnancy

Lightheadedness
Alcoholism

Dizziness
ANEMIA Cancer
Treatment
Fast/Irregular Heartbeat

Low Intake of
Tingling/Numbness Fruits/Vegetables
in Hands or Feet Low Intake of
Fruits/Vegetables

Balance or Gait
Hemodialysis 
Problems

Vision Loss
 PLEURAL EFFUISON
By: MUNGCAL

Case Scenario: A 47-year-old man with a medical history of hypertension, diabetes, hyperlipidemia, and OSA
presented with a 7- to 10-day history of progressively worsening dyspnea on exertion, with a walking distance of 60
feet. He had bilateral lower extremity swelling and was prescribed furosemide without clinical improvement. At
baseline, he used three pillows for sleeping. The patient was noncompliant with his CPAP treatment. He had no
smoking history and was retired from working in technology sales. On review of systems, he denied cough, chest
pain, hemoptysis, fevers, chills, or weight loss.
History of Present Illness: Apparently all right 2 weeks ago high-grade fever (remittent)- 14 days pain in the right-side
chest – 14 days (sharp, deep, stabbing, intensified by deep/respiration/cough)
Cough-14 days sputum- white purulent, (blood tinged sputum episode- 10 days back)
Loose stool and right lumbar pain- 10 days
Pathophysiology
 Increase hydrostatic pressure
 Decrease oncotic pressure
 Unable to remain the fluid within the intravascular space
 Fluid shift interstitial space
 Effusion
 Concept Map

SIGNS AND RISK

SYMPTOMS FACTORS
 
DEFINITION Heart failure
  Shortness of breath. Bacterial pneumonia
An abnormal collection of fluid between the thin layers Dry cough. lung cancer and other
tumours with lung
of tissue (pleura) lining the lung and the wall of the Pain metastases
Pulmonary embolism
chest cavity.

Feeling of chest heaviness or

Nephrotic syndrome
tightness.
Hypothyroidism
Inability to lie flat.
Ovarian tumours
Inability to exercise.
Tuberculosis
Generally feeling unwell.
 COPD
By: OMLANG
The patient is a 60-year-old white female presenting to the emergency department with acute onset shortness of breath. 
Symptoms began approximately 2 days before and had progressively worsened with no associated, aggravating, or
relieving factors noted. She had similar symptoms approximately 1 year ago with an acute, chronic obstructive pulmonary
disease (COPD) exacerbation requiring hospitalization. She uses BiPAP ventilatory support at night when sleeping and has
requested to use this in the emergency department due to shortness of breath and wanting to sleep.
She denies fever, chills, cough, wheezing, sputum production, chest pain, palpitations, pressure, abdominal pain,
abdominal distension, nausea, vomiting, and diarrhea.

She does report difficulty breathing at rest, forgetfulness, mild fatigue, feeling chilled requiring blankets, increased urinary
frequency, incontinence, and swelling in her bilateral lower extremities that is new onset and worsening. Subsequently, she
has not ambulated from bed for several days except to use the restroom due to feeling weak, fatigued, and short of breath.
Family History: There are no known ill contacts at home. Her family history includes significant heart disease and prostate
malignancy in her father. Social history is positive for smoking tobacco use at 30 pack years. She quit smoking 2 years ago
due to increasing shortness of breath. She denies all alcohol and illegal drug use. There are no known foods, drugs, or
environmental allergies.
Pathophysiology

COPD results from the combined processes of peripheral airway inflammation and narrowing of the
airways. This leads to airflow limitation and the destruction and loss of alveoli, terminal bronchioles
and surrounding capillary vessels and tissues, which adds to airflow limitation and leads to
decreased gas transfer capacity. The extent of airflow limitation is determined by the severity of
inflammation, development of fibrosis within the airway and presence of secretions or exudates.
Reduced airflow on exhalation leads to air trapping, resulting in reduced inspiratory capacity, which
may cause breathlessness (also known as dyspnea) on exertion and reduced exercise capacity.
Concept Map
 ACUTE RESPIRATORY FAILURE
By: ONIA

Case Scenario: Patient is a 75-year-old, female, Filipino, from Bulacan, a known case of hypertension and rheumatoid arthritis who came in due to
difficulty of breathing of few minutes.

History of Present Illness: The patient was apparently well until.

Six days prior to admission, patient experienced fever with associated cough, consulted an outside institution and was given unknown dose of Cefixime,
Paracetamol 500mg/tab, and Salbutamol nebulization. 
 
2 hours prior to admission, patient experienced sudden onset of difficulty of breathing with shortness of breath and upon arrival at ER, patient was in
respiratory distress with increased BP, tachycardia, tachypnea and desaturations.
 
Vital Signs: BP 170/110mmHg     HR 145bpm     RR 30 cpm    T 36.7°C      O2sat 80%

Family History: HPN and DM2 Maternal

Pathophysiology

Indirect or direct lung injury> Immune response is triggered> damaged

alveolar cells> release of chemical mediators such as histamine,
bradykinin> bronchoconstriction> impairment in gas exchange> ARF
 ACUTE RESPIRATORY FAILURE
Concept Map:
SIGNS AND SYMPTOMS:
 HYPERCAPNIC
- Dyspnea
- Headache
- Papilledema
- Tachycardia, Hypertension
- Drowsiness, Coma
- Systemic vasodilation, heart failure
- Respiratory Acidosis
 HYPOXEMIC
- Dyspnea, tachypnea
- Cyanosis
- Neurologic: restlessness,
apprehension, confusion, motor
impairment, impaired judgement
- Tachycardia and Hypertension as
cardiac output increases in effort to
increase oxygen to tissues
- As hypoxemia progresses,
dysrhythmias, hypotension and
decreased cardiac output develops
- Metabolic Acidosis
TREATED WITH:
 Drugs depending on underlying cause
of respiratory failure- bronchodilators,
antibiotics for underlying infections,
analgesics and sedatives for pain and
anxiety.
 Oxygen therapy
 CPAP therapy
 Airway Management
RISK FACTORS
 Age
 Pulmonary Infection
 Cigarette Smoking
 Chronic Lung Disease
 Upper or lower Obstruction
 Congenital Heart Problem
 Opiate and sedative medications
(benzodiazepine)
 Muscle System abnormalities
 CNS disorders
 Pneumothorax
 Hypercoagulable State
 ARDS (Acute Respiratory Distress Syndrome)
By: PANOPIO
A 42-year-old male with no significant past medical history presented to the emergency department (ED) with severe abdominal pain. Work-up revealed acute
pancreatitis due to alcohol consumption. He disclosed being a binge drinker. Gallbladder disease, the most common cause of acute pancreatitis, was ruled out with
imaging and laboratory studies. The patient was admitted to the hospital and treated according to the standard of care for management of acute pancreatitis which
included aggressive fluid resuscitation and pain management. On hospital day 3, he developed mild shortness of breath. Although the etiology of his respiratory
symptoms was initially unclear, upon further inquiry, he recalled several episodes of vomiting prior to arrival in the ED. Your suspicion for aspiration and possible
aspiration pneumonia are raised. The patient is placed on supplemental oxygen via nasal cannula with no improvement. High flow nasal cannula (HFNC) is ordered and
initiated with significant improvement in respiratory symptoms. He has a mild non-productive cough and low-grade fever. A chest x-ray revealed mild vascular congestion
and a possible right middle lobe opacity. He is pan-cultured and started empirically on antibiotics to cover aspiration pneumonia, he is also given diuretics for suspected
volume overload. Overnight, he became tachypneic with respiratory rate in the 40s and increased work of breathing. Peripheral oxygen saturation (SpO2) was 82%
despite titration of fraction of inspired oxygen (FiO2) to 100% on HFNC. He was intubated, placed on mechanical ventilation and transferred to the ICU for management. A
chest x-ray following intubation revealed diffuse bilateral infiltrates. He was initially placed on standard ventilatory settings with brief improvement but, over the next
several hours, it became increasingly difficult to oxygenate him despite titration of FiO2 to 85% on the ventilator. He was given an additional dose of intravenous (IV)
diuretic with no improvement. An arterial blood gas (ABG) revealed arterial oxygen of 70mmHg and a repeat CXR revealed progression of diffuse bilateral infiltrates.
Acute respiratory distress syndrome (ARDS) was suspected and ARDS specific ventilatory strategies were initiated.
You are a nurse caring for your newest admission, a 68-year-old retired teacher
who has a 50 pack-year history of smoking, which resulted in emphysema. She
attends exercise classes at her local gym seeking to maximize her oxygenation.
Recently, the patient has begun to contemplate the use of portable oxygen to
decrease her workload to breathe.
History of Present Illness: Work-up revealed acute pancreatitis due to alcohol consumption. The patient was admitted to the hospital and treated according to the
standard of care for management of acute pancreatitis which included aggressive fluid resuscitation and pain management.
On day 3 at the hospital the patient developed mild shortness of breath. Overnight the patient became tachypneic. The patient was intubated and was placed on
mechanical ventilator. Acute respiratory distress syndrome (ARDS) was suspected.
Family history: None
History of Past Illness: A 42-year-old male with no significant past medical history presented to the emergency department (ED).
 A
By: PERENA
 WHOOPING COUGH (PERTUSSIS
By: SANTOS

Case Scenario: A mother had a child 5 years old female, had an active coughing and she noticed that her child
is tired because of coughing and she noticed also that her child coughing has sounds like wheezing her
child skin is cold. She immediately take her baby to the center.
History of Present Illness: Diagnosed with Asthma since first check up when her baby’s 1 year old.
Family History: The mother of the patient also have an Asthma & Hypertension.
 Pathophysiology

Humans are the sole reservoir for B pertussis and B parapertussis. B pertussis, a

gram-negative pleomorphic bacillus, is the main causative organism for pertussis. (B
parapertussis is less common than B pertussis and produces a clinical illness that is
similar to, but milder than, that produced by B pertussis.) B pertussis spreads via
aerosolized droplets produced by the cough of infected individuals, attaching to and
damaging ciliated respiratory epithelium. B pertussis also multiplies on the respiratory
epithelium, starting in the nasopharynx and ending primarily in the bronchi and
bronchioles.
Pertussis is highly contagious, developing in approximately 80-90% of susceptible
individuals who are exposed to it. Most cases occur in the late summer and early fall.
A mucopurulent sanguineous exudate forms in the respiratory tract. This exudate
compromises the small airways (especially those of infants) and predisposes the
affected individual to atelectasis, cough, cyanosis, and pneumonia. The lung
parenchyma and bloodstream are not invaded; therefore, blood culture results are
negative.
Transmission of pertussis can occur through direct face-to-face contact, through
sharing of a confined space, or through contact with oral, nasal, or respiratory
secretions from an infected source.
Concept Map

Sign & symptoms

Early symptoms
Runny nose
Low-grade fever (generally
minimal throughout the course of
the disease)
Mild, occasional cough
Apnea – a pause in breathing (in
babies)
  Later stage symptoms

Paroxysms (fits) of many, rapid

coughs followed by a high-pitched
“whoop” sound

Vomiting (throwing up) during or

after coughing fits

Exhaustion (very tired) after

coughing fits