NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses

Ms. Kerstine Iza Benolerao, RN

Bambam2017 Bambam2017
AIRFLOW OF THE HEALTHY LUNGS
OBSTRUCTIVE LUNG DISEASE
Air breathed in will go to the pharynx, then the
trachea, the bronchi, bronchioles, and alveoli
ASTHMA
ALVEOLI – this is where gas exchange happens
- Characterized by chronic airway
inflammation resulting to airway
hyperresponsiveness, mucosal edema and
- OBSTRUCTIVE LUNG DISEASE
increased mucous production.
a. There is lesser gas exchange because of
- It is a reversible obstructive lung disease;
lesser air flow into and out of the alveoli.
however, as pathophysiologic changes
b. There is a blockage that is causing an
increase it may become irreversible.
alteration of the airflow which is present in
the following conditions:
a. Asthma
b. Bronchiectasis
c. Chronic Bronchitis
d. Emphysema
e. Foreign Body Obstruction
- RESTRICTIVE LUNG DISEASE
I. There is lesser airflow since the lungs are Predisposing Factors:
restricted to fill to its full capacity - Atopy
II. This is due to stiffness in the lungs or
- Female Gender
muscles surrounding it.
Causal Factors
a. Pneumonia
• Exposure to indoor and outdoor allergens
b. Pleurisy
• Occupational sensitizers
c. Pleural Effusion
Contributing Factors
d, Pneumothorax
1. Respiratory infections
e. Respiratory depression 2. Air pollution
3. Active/ passive smoking
due to CNS disease/ CNS depressants, Muscular 4. Other ( diet, small size at birth)
weakness, chest wall
Risk Factors for exacerbations:
1. Allergens
Deformities: 2. Respiratory infections
- Acute Respiratory Distress Syndrome 3. Exercise and hyperventilation
(ARDS) 4. Weather changes
- Sudden Infant Death Syndrome (SI) 5. Exposure to sulfur dioxide
6. Exposure to food, additive, medications
Symptoms:

• Wheezing
• Cough

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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017 Bambam2017
• Dyspnea • Allergic reactions accompanied with the
• Chest tightness asthma
• Laboratory Tests
Remember: When there is inflammatory
- Eosinophilia will show in blood tests
response, mast cells release several chemicals
during acute episodes
called MEDIATORS and these will include:
- Elevated serum IgE if it is due to
Histamine, Radicanine, Prostenoids,
allergies
Ctyokines, Leukotrienes and other mediators.
- Arterial blood gas analysis –
This will perpetuate the inflammatory response.
hypocapnia due to rapid
When this happens, there is increased blood flow
respirations resulting to respiratory
in the vessels, vasoconstriction and there is a leak
alkalosis.
of fluid from the vasculature because those
mediators will increase cell permeability or *If a patient will breathe out fast or rapidly, they get
vascular permeability and then it will attract WBCs rid of too much CO2 which cause hypocapnia
to the area which will cause mucous secretion and
bronchoconstriction. *When there is low CO2 that will lead to respiratory
alkalosis
CLINICAL MANIFESTATIONS:
• Pulse oximetry reveal decreased O2
• Symptoms occur progressively over a few saturations
days before acute attacks. In some cases,
it may occur abruptly. MEDICAL MANAGEMENT
• Cough - may occur with or without mucus • Administering O2 when hypoxic
production • Checking of blood gases during severe
• Dyspnea – due to constricted airways attacks (to make sure that the patient is not
• Wheezing – first on expiration then on acidosis)
progressing to wheezing on inspiration • Pulse oximetry monitoring (for patients who
- expiration needs effort and prolonged because are acutely ill or has acute attacks)
the body is having difficulty getting rid of the extra • Treatment of underlying allergic reaction if
air inside the lung due to Bronchoconstriction precipitated by allergens (main precipitants
of asthma attacks)
• Tachycardia • Administration of smooth muscles
• Diaphoresis relaxants and steroids (inhaled or
• Cyanosis – due to hypoxemia (late sign) systemically)
• Status Asthmaticus – life threating • Spirometry (can be done if patient can
condition wherein there is severe tolerate it before giving treatment and also
continuous reaction. after giving treatment to see the
• Respiratory failure if not managed improvement and effectivity of the
immediately treatment

DIAGNOSTICS PHARMACOLOGIC MANAGEMENT

- Medical history and Physical ❑ Short Acting

Assessment
a. Short-acting beta2- adrenergic agonists (SABA)
• Known familial history
- relaxes smooth muscles
• Environmental factors
e.g. albuterol, levalbuterol, pirbuterol

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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
Acute exacerbation: 25 – 5 mg every 20 mins for
3 doses (nebulized)
4 – 6 puffs from MDI (meter dose inhaler) every 20
mins for 3 doses (given via spacer)
b. Anticholinergics – inhibit muscarinic cholinergic
receptors and reduce vagal tone of the airway.
e.g. Ipratropium or tiotropium
Acute exacerbation: 0.5 mg every 20 mins for 3
doses (nebulized) can be given together w/ SABA
8 puffs from MDI every 20 mins for 3 doses (given
via spacer)
TAKE NOTE: acetylcholine binds to muscarinic
receptors and lead to bronchoconstriction, increased
mucus secretion and inflammation. If we give
anticholinergics, they will reduce the vagal tone of
the airway and inhibit muscarinic cholinergic
receptors.
❑ Long- acting Medications
a. Corticosteroids
- most effective and potent anti – inflammatory
- they work by suppressing the inflammatory genes
to reduce inflammation and mucus production
- this can be given via inhalation e.g budesonide,
fluticasone
- systemic preparations for rapid control of
symptoms e.g. methylprednisolone, prednisolone,
prednisone (oral)
b. Mast cell stabilizers – stabilizes mast cells, may
be used for prophylactic treatment; contraindicated
for acute exacerbations
Example: cromolyn Na and nedocromil
TAKE NOTE: One of the mediators of the
inflammatory response are MAST CELLS
c. Long-acting beta agonists (LABA)- long term
prevention of symptoms particularly those occuring
at night time; indicated for exercise induced asthma.
(e.g., salmeterol and formoterol (inhaled) give 12
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hours of bronchodilation; albuterol (oral) can give 8
hours or more of bronchodilation
d. Methylxanthines
1. Theophylline- works by relaxing airway
muscle (bronchodilatory effect) and
supresses response to allergens and irritants
(anti-inflammatory effects)
- given in conjunction with
inhaled corticosteroids to manage nighttime
asthma
e. Leukotriene modifiers
• Leukotriene receptor antagonists- inhibits
receptors of cysteinyl leukotrienes which are
potent inflammatory mediators, e.g.,
montelukast and zafirlukast
• 5-Lipoxygenase inhibitor- inhibits production
of leukotrienes e.g., Zileuton (Zyflo)
f. Immunomodulators
- prevent IgE binding to receptors of basophils and
mast cells e.g., Omilazumab
- mast cells and basophils are part of the
inflammatory process so if you prevent the binding
to the receptors, it will also prevent exacerbation
NURSING MANAGEMENT:
• Assess respiratory status- vital signs, pulse
oximeter, breathe sounds, work of breathing
and chest excursions
• Administer medications immediately
especially in acute exacerbations and
monitor response by checking respiratory
status.
• Spirometry before and after giving
medications- if the patient is very short of
breath and they cannot tolerate spirometry
that is fine, the patient’s needs to be given
medications immediately and then after an
hour spirometry can be done
• Administer fluids to keep the patient hydrated
• Patient education especially on triggers and
signs and symptoms of progressive or early
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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017 Bambam2017
progression of exacerbations, educate on Abnormal bronchodilation, edema, scarring,
the proper use of metered dose inhalers and ulceration
emphasize the importance of adherence to a
↓
medication regimen
Accumulated secretion cause blockage
↓
BRONCHIECTASIS
- a chronic, irreversible dilation of the bronchi and Atelectasis of alveoli distal to the obstruction
bronchioles due to the destruction of the muscles
and elastic connective tissues ↓
- caused by pulmonary infections, cystic fibrosis, TB, Reduced vital capacity
rheumatic disease, and other disorders
- affects mostly of the lobes of the lungs and is ↓
usually localized and it also affects women than men
Decreased ventilation
PATHOPHYSIOLOGY
↓
Pulmonary infection/underlying disease process
Ventilation perfusion mismatch
↓
↓
Inflammatory process
Hypoxemia
↓
CLINICAL MANIFESTATIONS:
Damage to muscular and elastic structure of the
1. Chronic cough
bronchial wall
2. Copious amount of purulent sputum lasting
↓ months to years – some may only produce
sputum during acute upper respiratory tract
Abnormal bronchodilation, edema, scarring, infection
ulceration 3. Hemoptysis- form ulceration in the bronchi
↓ due to acute inflammation
4. Dry bronchiectasis- episodic hemoptysis with
Severely impaired clearance of secretions little or no sputum usually a sequela of TB
↓ 5. Dyspnea with extensive bronchiectasis
6. Wheezing may be manifested due to blocked
Colonization of bacteria develop airways.
7. Fatigue- because if the patient is hypoxic,
↓
they will have reduced oxygenation so it lead
Cycle of inflammation and bronchial damage to fatigue
8. Clubbing of fingers due to respiratory
insufficiency
DIAGNOSTICS:

• Medical history and physical exam

• Sputum analysis
• CT-scan- reveals bronchial dilation
ON THE OTHER HAND

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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
• Chest X-ray- shows pleural changes,
atelectasis, increased pulmonary markings
• CBC- nonspecific finding, but may show
anemia with elevated WBC count
Goals of Treatment:
1. Promoting bronchial drainage
2. Clear excessive secretions from affected
portion of the lungs
3. Prevent of control infection
• Antibiotic therapy and chest physiotherapy
are important modalities of treatment
MEDICAL AND SURGICAL MANAGEMENT:
➢ Chest physiotherapy with percussion and
postural drainage to manage secretions and
lessen infections
➢ Supportive treatment
- IVF or oral hydration to maintain hydration
status
- oxygen supplementation for hypoxic
patients
➢ Bronchoscopy
- for removal of mucopurulent sputum if
needed
- bronchoscopy is a procedure that will look
directly at the airways in the lungs using a
thin lighted tube or the bronchoscope and it
is put in the nose or the mouth and then it
moves down to the throat and the windpipe
then into the airways
➢ Surgical resection
- resection of the bronchioectatic lung in
patients with advanced disease; involve
sites that will be completely resected for
optimal symptom control especially for
those patients who have massive
hemoptysis
PHARMACOLOGIC MANAGEMENT:
1. Antibiotic therapy for exacerbations- empiric
coverage while waiting for the results of the
sputum culture and sensitivity
- pseudomonas aeruginosa- requires more
aggressive oral or IV antibiotic therapy
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2. Bronchodilators- to help with management of
secretions and improve bronchospasm
3. Corticosteroids- may be considered daily in
patients with significant obstructive
physiology
NURSING MANAGEMENT:
1. Assess and monitor respiratory status- vital
signs, pulse oximetry, spirometry
2. Assist with or perform chest physiotherapy
3. Administer medications as indicated
4. Administer supplemental O2 as needed
5. Ensure adequate nutrition and hydration
6. Promote adequate rest
7. Provide patient education in promoting
postural drainage, importance of hydration
on assisting with management of secretions,
lifestyle modifications such as cessation of
smoking, proper nutrition, and immunization
for influenza and pneumococcal pneumonia
vaccine
CHRONIC BRONCHITIS
- long term inflammation of the bronchi; a form of
COPD
- defined with presence of cough and sputum
production for at least 3 months a year in 2
consecutive years
- major cause is smoking followed by exposure to
environmental irritants or a family history of
bronchitis
PATHOPHYSIOLOGY
Smoke/ environmental pollutants (dust, second-
hand smoke, fumes, allergens)
↓
Irritation of airways
↓
Inflammatory process occurs
↓
Constant inflammation
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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017 Bambam2017
↓ Medical Management
Increased mucus secreting glands and goblet cells 1. O2 Supplementation for hypoxia depending
on severity
↓
2. Blood gas studies for patient who have acute
Increased mucus production shortness of breath
3. Pulmonary rehabilitation – program to help
↓ improve the wellbeing of patients with
Mucus plugging chronic respiratory problems
a. Exercise program
↓ b. Disease management training
c. Nutritional counselling
Narrowing of airways
d. Psychological counselling
↓
Pharmacologic Management
Shortness of breath, hypoxia, chest discomfort
• Bronchodilators to relax airways
• Corticosteroids to lessen inflammation in the
airways
• Antibiotics for underlying infection
Nursing Management

• Monitoring respiratory function

• Administering O2 supplements as needed
• Administer medications as prescribed and
educate patient on its importance
• Educate patient on lifestyle changes
Because of the increased mucus glands, it will cause o Smoking cessation, avoidance of
an increased mucus production and inflammation known irritant or wearing of protective
that will lead to constriction of airway gear such as masks when constantly
exposed to fumes
Clinical Manifestation • Educate patient on pursed lip breathing to
open airways when feeling short of breath
1. Frequent coughing with sputum
2. Wheezing
3. Shortness of breath EMPHYSEMA
4. Chest tightness
• Abnormal distention of air spaces distal to
Diagnostics the terminal bronchioles and destruction of
1. Medical history and physical assessment the alveolar walls leading to a decreased
2. Pulmonary function test to check how much surface area for gas exchange
air the lungs can hold • Damage and hyperinflation of the alveolar
3. Chest Xray to rule out other causes of cough walls
4. Ct scan of the chest for a clearer picture of • Form of COPD
the lungs • Risk factors: smoking, air pollutant
5. Sputum tests to check for underlying exposure, genetics (deficiency in alpha-1
infections antitrypsin, an enzyme inhibitor that protects

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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017 Bambam2017
the lung parenchyma) and respiratory Clinical Manifestations
infections
1. Hallmark presentation: limitation of
expiratory flow with intact inspiratory flow
Subtypes based on the lung changes a. Longer exhalation time compared to
inhalation time
1. Panlobular (panacinar) – destruction of the
2. Chronic cough and sputum production that
respiratory bronchiole, alveolar duct and
may be present for several years before
alveolar
onset of dyspnea
a. Dilation of airspaces with little
3. Tachypnea and dyspnea on mild exertion
inflammatory disease
with severe disease
4. Weight loss
a. Due to dyspnea interfering with
eating and causing increased O2
consumption
5. Barrel shaped chest
a. Due to hyperinflation and loss of lung
elasticity
Diagnostics

2. Centrilobular – localized to proximal 1. Medical history and physical examination

respiratory bronchioles with focal destruction 2. Spirometry – done before and after giving
a. Most common type associated with inhaled bronchodilators
smoking 3. Arterial blood gases – to determine
oxygenation status especially in advance
diseases
4. Screening for alpha 1 antitrypsin deficiency
for patients <45 y.o with familial history of
COPD
5. CT scan of the chest to help diagnose and
rule out other causes
MEDICAL MANAGEMENT
1. Managing exacerbation and treatment of
underlying cause
2. Supplemental oxygen as required
Pathophysiology 3. Prescribing medication such as
corticosteroids and bronchodilators
Exposure to smoke, air pollutants, lung infections
4. Referral to a smoking cessation program
release of inflammatory mediators inflammatory
process increased mucus production, and PHARMACOLOGIC MANAGEMENT
destruction of the lung parenchyma (respiratory
bronchioles, alveolar ducts, alveoli) dilation of 1. Bronchodilators
airspace and destruction of their walls increased a. Relaxes smooth muscles and widen
dead space impaired oxygen diffusion hypoxemia airways

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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
b. Can be given as needed or regularly
given daily via pressurized metered-
dose inhaler – ideally via spacer
2. Corticosteroid
a. Short trial may be given to the patient
to see if it improves lung function, but
it is not ideal for long term use
3. Combination therapy of beta 2 agonists
with corticosteroids in inhalation form
a. E.g formoterol/budesonide
(Symbicort), vilanterol/fluticasone
(Breo Ellipta)
4. Mucolytic agents to help manage
secretions
5. Antitussive agents to help manage
coughs
NURSING MANAGEMENT
1. Assess patient including the use of
spirometry before and after administering
bronchodilators if tolerated
2. Monitor respiratory status and signs of
improvement or decline
3. Monitor vital signs including blood gases,
pulse oximetry, mentation status for patients
who are in acute exacerbation
4. Administer O2 when needed and as
appropriate for the patient to maintain O2
saturation of at least 90 % and PaO2 of at
least 60mmHg in the blood gas
5. Monitoring the patient’s mental status and
blood gases will determine if the patient is in
hypercapnia especially in acute exacerbation
6. Educate patient on the importance of
smoking cessation and refer to support
groups
7. Educate patient on the proper use of
metered dose inhalers with spacers
8. Administer medications as prescribed and
educate the patient about its purpose and
effect
Surgical Management of Patients with advanced
COPD
1. Bullectomy
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A. Removal of bullous emphysema. Bullae do
not contribute to ventilation and compress
the lungs.
B. A giant bulla is a complication of
emphysema.
C. In areas of the lung completely damaged by
the disease, air pockets can develop. These
areas threaten the patient’s health not only
because of the underlying emphysema. As
an air pocket, it grows and takes up space in
the chest cavity and can encroach on the
lungs.
D. It is performed with the use of a video
assisted thorascope or limited thoracotomy
incision.
2. Lung Volume Reduction Surgery
- Removal of a portion of the diseased lung
parenchyma to reduce hyperinflation and
allow expansion of functional tissue.
3. Lung transplantation
- Definitive surgical treatment of severe
COPD. However, it is costly and donors are
hard to find.
LARYNGEAL OBSTRUCTION
- Obstruction of the larynx due to edema post
exposure to triggers such as allergens,
exercise, stress, and inflammation.
- Those with history of hereditary angioedema
may have episodic attacks.
- Obstruction can also be caused by foreign
bodies.
PATHOPHYSIOLOGY
Foreign bodies aspirated may block off the air at the
pharynx, larynx, or trachea
OR
Irritants that will cause swelling of the laryngeal
mucous membranes can cause edema
OR
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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
Inflammation at the throat from conditions such as
laryngitis, severe anaphylaxis, or scarlet fever can
cause closing of the vocal cords.
- All conditions above can lead to hypoxia
and suffocation which is life threatening
CLINICAL MANIFESTATIONS:
✓ Low oxygen saturation – because there is
blockage of air flow
✓ Accessory muscle use on breathing –
retractions in the neck or abdomen because
the body is trying to compensate for the lack
of oxygen.
✓ Patients are at risk of collapse due to the lack
of airflow in the airways and may need
mechanical ventilation - If there is no oxygen,
there is less perfusion in the vital organs of
the body which will lead to the patient's
collapse
DIAGNOSTICS
• Obtaining patient history such as history of
airway problems, recent infections, pain,
fever, neck surgeries/trauma and physical
assessment. (All of these will prompt the care
provider that a possible laryngeal obstruction
has taken place). However, if the patient
comes in and is unable to talk who is in
distress, stridoring, and already have these
restrictions, do a very quick ABCD
assessment then do interventions
• Xray can confirm laryngeal obstruction as
long as it does not delay treatment.
Especially for those patients who are on the
brink of collapse.
MEDICAL MANAGEMENT
• When the patient has signs of asphyxia
• Airway maneuvers should be done to open
the airway and check for foreign bodies. This
can be done through Head tilt chin lift or the
jaw thrust maneuvers.
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• Start CPR if no air passage is detected. (If no
air movement from nose or mouth; if patient
is silent). Perform the Advanced Life Support
(ALS) Protocol. Use of bag valve mask
because it is an instrument that will help
induce positive air pressure for the patient’s
airway; or Use an endotracheal intubation
will have to be done to ventilate patient.
Some patients with blocked off throats up or
from the larynx up cannot use an
endotracheal tube. A tracheostomy will have
to be put in place. A tracheal tube will be
placed to be connected to a mechanical
ventilator.
II. RESTRICTIVE LUNG DISEASE
PNEUMONIA
- inflammation of the lung parenchyma due to
bacteria, virus, or fungi
Types of Pneumonia: Community Acquired
Pneumonia; Hospital Acquired Pneumonia;
Ventilator Acquired Pneumonia (VAP)
Community Acquired Pneumonia (CAP)
✓ A disease occurring in the community or
within 48 hours of hospitalization
✓ Staphylococcus pneumoniae is the most
common cause of CAP for less than 60
years old (<60 yo) and those above 60
years old (>60 yo) with comorbidities.
✓ Haemophilus influenzae affects the older
adults with comorbidities frequently
✓ Cytomegalovirus: the most common
cause of CAP for patients who are
immunocompromised.
Hospital Acquired Pneumonia (HAP)
• Occurring more than 48 hours of
hospitalization that did not appear to be
incubating prior to admission.
Ventilator Acquired Pneumonia (VAP)
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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
• Occurs after more than 48 hours of
endotracheal intubation
• Patients who are immunocompromised and
with comorbidities may predispose patients
as well as apiration, supine positioning,
prolonged hospitalization
TAKE NOTE!!!
• Bacteria in the hospital may be transferred to
the patient through numerous procedures.
(Examples: NGT insertions; if patient does
not wash his/her hands)
• Patients who are quite ill and are receiving
CNS depressants will lead to decreased gag
reflex and impaired.
Common Organisms responsible for HAP include:
• The Enterobacter species, Escherichia coli,
H. influenzae, Klebsiella species, Proteus,
Serratia marcescens, Pseudomonas
aeruginosa, methicillin-sensitive or
methicillin-resistant Staphylococcus aureus
(MRSA) and S. pneumoniae.
TAKE NOTE!
• Mortality rate is high especially with
staphylococcal pneumonia.
PATHOPHYSIOLOGY
Entry of organisms into the lower respiratory tract
==> Inflammatory response – migration of WBC to
the alveoli ==> Formation of exudates and mucosal
edema ==> Occlusion of the bronchi or alveoli ==>
Decreased diffusion of Oxygen and carbon dioxide
in the affected parts of the lungs ==> Hypoventilation
==> Ventilation-perfusion (V/Q) mismatch in
affected parts of the lungs ==> Poorly oxygenated
blood enters the left side of the heart ==> Arterial
hypoxemia
SIGNS AND SYMPTOMS:
• Fever, respiratory symptoms, purulent
sputum (decreased if patient is dehydrated)
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and leukocytes due to the inflammatory
process in the lungs.
• Pleuritic chest pain
• Shortness of breath due to hypoxemia
• Orthopnea – due to hypoventilation
• Crackles due to consultation of lung tissue
DIAGNOSTICS:
• Medical history and physical exam
• Blood works (Full blood count for WBC levels
and blood cultures to check which organism
is causing the infection)
• Chest X-ray – to see how bad the lungs are
• Sputum cultures
MEDICAL AND PHARMACOLOGICAL
MANAGEMENT
• Antipyretics for fever
• Antitussive for cough
• Nasal decongestants
• Oxygen supplementation and pulse oximetry
monitoring
• Noninvasive ventilation (NIV) or mechanical
ventilation for respiratory failure
• CAP - antibiotic therapy depending on the
clinical features and as indicated in the
guidelines of antibiotics prescribed for
pneumonia
• HAP - Antibiotic therapy past culture and
sensitivity
• Usually, patients are given broad spectrum
antibiotics while waiting for the results.
These are given IV especially when the
patient is unstable. Monotherapy or
combination of drugs can be used.
Assessment of patient 72 hours post
initiation.
• Viral pneumonia - supportive treatment e.g.
hydration since fever and tachypnea may
cause fluid loss. Warm inhalation,
Antihistamines
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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
NURSING MANAGEMENT
❑ Monitor respiratory status through regular
vital signs and pulse oximetry
❑ Administering antibiotics as prescribed
❑ Promote a position of comfort that will allow
easier breathing
❑ Monitor for signs of deterioration and sepsis
❑ Administer oxygen as needed
❑ Monitoring patient’s blood gases and cardiac
output in cases of severe pneumonia
requiring mechanical ventilation
❑ Educate the patient about NIV
PLEURISY
❑ Inflammation of the layers of the pleura
(parietal and visceral) often associated with
pleural effusion
PATHOPHYSIOLOGY
1. Infections, TB, trauma to the chest, collagen
disease, pulmonary infarction or pulmonary
embolus, primary or metastatic CA
2. Inflammatory process around the lungs
3. Inflammation of tissue - accumulation of fluid in
the pleural space
4.Pain on breathing specially inspiration (sharp,
stabbing pain)
CLINICAL MANINFESTATIONS
❑ Pleuritic pain on breathing exacerbated by
breathing in deeply, coughing or sneezing
which is relieved when the patient holds
one’s breath and occurs usually in one side
DIAGNOSTICS
❑ Medical history and physical exam
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❑ Auscultation - pleural friction rub (rubbing of
inflamed and roughened pleural surfaces)
❑ Chest x-ray
❑ Sputum analysis
❑ Thoracentesis to obtain a sample of the
pleural fluid and determine the cause, and
remove excess fluid accumulation for better
breathing
MEDICAL AND PHARMACOLOGICAL
MANAGEMENT
❑ Goal of management is to identify the cause
and alleviate pain
❑ Treatment of underlying condition will
resolve the inflammation of the pleura
❑ Monitoring for signs and symptoms of pleural
effusion - SOB, decreased chest wall
excursion
❑ Analgesics for pain such as NSAIDS
NURSING MANAGEMENT
❑ Monitoring deterioration of patient
❑ Enhancing comfort through positioning on
bed to ease pain or warm/cold compress
❑ Alleviating pain through regular pain as
prescribed
❑ Educate patients in splinting the chest on
coughing
PLEURAL EFFUSION
❑ A collection of fluid in the pleural space and
is usually secondary to another disease
process such as heart failure, TB,
pneumonia, pulmonary infection, nephrotic
syndrome, connective tissue disease, PE
and neoplastic tumors.
PATHOPHYSIOLOGY
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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
1.Primary disease process (inflammation,
malignancy, PE, trauma)
2.Altered permeability of pleural membranes,
vascular disruption or decreased lymphatic drainage
or complete lymphatic vessel blockage
3.Increased hydrostatic pressure
4.Exudative pleural effusion
1.Primary disease (from nephrotic syndrome or
cirrhosis)
2.Hypoalbuminemia
3. Reduced intravascular oncotic pressure
4.Transudative pleural effusion
1.Primary disease (CHF, superior vena cava
syndrome)
2. Increased capillary hydrostatic pressure (systemic
or pulmonary) circulation
3.Imbalance of hydrostatic pressure
4.Transudative pleural effusion
PATHOPHYSIOLOGY
Primary disease (CHF, superior vena cava
syndrome)
Increased capillary hydrostatic pressure (systemic
or pulmonary circulation
Imbalance of hydrostatic pressure
Transudative pleural effusion
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Discussion: Transudative occurs due to increased
hydrostatic pressure or low plasma oncotic
pressure. Caused by CHF, cirrhosis, nephrotic
syndrome, PE, hypoalbuminemia. Exudative occurs
due to inflammation and increased capillary
permeability. Caused by pneumonia, cancer, TB,
viral infection, PE, autoimmune.
CLINICAL MANIFESTATIONS
• Dyspnea due to the distortion of the
diaphragm and chest wall during respiration
due to presence of fluid in the pleural space.
• Cough-mid and non-productive. Purulent
sputum and severe cough are associated
with pneumonia.
• Chest pain due to the irritation of the pleura.
Usually describe as a sharp, stabbing pain
which is exacerbated by deep breathing and
can radiate to the upper abdomen or
ipsilateral shoulder (on the same side)
• Fever due to underlying infection.
DIAGNOSTICS
• Medical history and physical examination
-asymmetrical chest expansion-delay on the
side of the affected area.
-decreased breath sound to the affected
area.
-dullness of percussion.
• Radiologic
-chest x-ray (presents an effusion)
-CT scan of the chest (can determine the
amount of effusion)
• Invasive
-Thoracentesis- to remove fluid, obtain
specimen testing of the pleural fluid for gram
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stain, culture, AFB stains, cytologic studies,
chemistry studies, and biopsy.
MEDICAL AND PHARMACOLOGICAL
MANAGEMENT
Goal: Identify and treating the underlying cause,
prevent reaccumulation of fluid, relieve respiratory
symptoms and discomfort.
• Chest tube insertion- Placement of a chest
tube into the pleural space to drain excess
fluid connected to a water seal.
• Thoracentesis- remove fluid, obtain
specimen and relieve dyspnea.
-can be done under a guided ultrasound to
drain the excess fluid.
• Chemical Pleurodesis- done in cases of
malignancy wherein frequent reaccumulation
of fluid is anticipated.
• Pleural Catheter- small catheter attached to
a drain bottle and managed as outpatient
-for patients with malignant pleural effusion
with short to intermediate life expectancy.
NURSING MANAGEMENT
a. Assisting in medical and surgical
management
b. Proper documentation of procedure and fluid
during thoracentesis
c. Monitoring and ensuring that the chest tube
drainage is working as well as proper
recording of output from the tube.
d. Alleviating pain by giving regular analgesics
or other medications for breakthrough pain.
e. Educating patient on care of the pleural
catheter.
PNEUMOTHORAX
-occurs when the parietal or visceral pleura is
breached and exposed to positive atmospheric
pressure. Air enters the pleural cavity and
impairs oxygenation.
Pathophysiology according to types:
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• Simple pneumothorax- air enters
the pleural space via a breach in the
pleura through a rupture of an air-
filled bleb or blister on the surface of
the lung or a bronchopleural fistula.
Then air accumulates in the plural
cavity.
• Traumatic pneumothorax- air
enters the pleural space via a
laceration from the lung itself or from
a wound in the chest wall from:
• Blunt trauma penetrating chest trauma or
abdominal trauma and diaphragmatic tears.
• Invasive thoracic procedures such as
thoracentesis, transbronchial lung biopsy,
and insertion of a subclavian line or viral
trauma from mechanical ventilation.
• Open pneumothorax- a type of traumatic
pneumothorax, air freely goes in and out of
the thoracic cavity due to large chest wound.
The lung collapses and mediastinal shifting
occurs to the unaffected side every time the
patient breathes in and shifts to the injured
side on expiration this will lead to serious
circulatory problems.
• Tension pneumothorax- air enter
the pleural space via a laceration in
the lung or chest wall injury. In this
type, the air is trapped inside the
cavity after each inspiration. Thus,
the pressure will increase with every
breath causing the lungs to collapse
and shifting of the heart and blood
vessels to the unaffected side.
Circulatory compromise results as
the intrathoracic pressure increases
leading to decreased cardiac output
and cardiac failure.
CLINCAL MANIFESTATIONS
Manifestations will depend on the severity of the
pneumothorax:
• Pain, sudden and pleuritic in nature.
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• Dyspnea and sudden accessory muscle
use
• Anxiety and air hunger
• Cyanosis from hypoxemia
• Acute respiratory distress-when the
pneumothorax is large this may lead to
collapse of the lungs.
• For tension pneumothorax-air hunger,
agitation, central cyanosis, hypotension,
tachycardia, diaphoresis, jugular venous
distention, respiratory distress.
DIAGNOSTICS
• Medical history and physical examination
-trachea may or may not be at midline
depending on the severity.
-chest expansion may be unequal with
decreased expansion at the affected
side.
-decreased or absent breath sounds
depending on the severity.
-percussion reveals hyperresonance
For tension pneumothorax- diagnose is primarily
through clinical findings on the patient’s presentation
which require immediate intervention:
-trachea is shifted away from the affected side and
chest may be in a hyper expansion state. The
manifestations will be tachycardia, hypotension,
jugular vein distention, and respiratory distress.
• ABG Studies- to measure the degree of acid
base imbalance brought about by the injury.
• Imaging
- chest x-ray
-CT scan
-chest ultrasound
MEDICAL AND SURGICAL MANAGEMENT
Goal: evacuate air or blood from the pleural space
to allow the lung to expand properly. Management
depends on severity of the pneumothorax.
1. Decompression of the pleural cavity
1.A. Chest tube insertion (Thoracostomy)
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- French 28 tube is inserted to the 2nd intercostal
space, thinnest part of the chest wall and reduced
risk of contracting the thoracic nerve.
-French 32 or higher if with hemothorax and it is
inserted at the 4th or 5th intercostal space at the
midaxillary line. Suction may be applied at 20 mmHg
pressure, or it may be connected to a water seal
drainage.
1.B. Thoracentesis
- needle aspiration of air or fluid from the pleural
space.
1.C. Thoracotomy
- a surgical opening of the chest wall if more than
1500 ml of blood is evacuated from thoracentesis
or drained from the chest tube.
- done as an emergency if the patient has
suspected cardiovascular injury post chest trauma
1.D. For patients with tension pneumothorax
- a large bore needle inserted at the 2nd intercostal
space at the midclavicular line. Then insertion of
the chest tube thereafter
2. Sealing the chest wound
- maybe initially done with the use of gauze
impregnated with petrolatum applied with
pressure until surgical intervention is done
3. Administering Oxygen and the use of
pulse oximetry
- patient may become hypoxemic
- high concentration of supplemental O2
may be indicated for severe pneumothorax
4. Blood transfusion
- for excessive blood loss; autotransfusion
may be done if large amount of blood is
drained from the chest tube in a short span
of time.
PHARMACOLOGIC MANAGEMENT:
1. Antibiotic Therapy
- coverage for infection with open chest
wounds or treatment of pneumothorax as a
consequence of bacterial pneumonia
2. Analgesics for pain
- analgesics will be got given regularly and
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also a stronger analgesic will be given for
breakthrough pain
NURSING MANAGEMENT:
1. Assess for breath sounds
2. Monitor for signs of hypoxia and administer
supplemental oxygen
3. Monitor for signs of decreased cardiac output
- lamentation status the blood pressure if the
patient becomes tachycardic then that is a
sign that the body is compensating for the
decreased cardiac output but if later on the
there will be a cardiac failure then the patient
will become bradycardic
4. Promote comfort and reduce pain
5. Assist with chest tube insertion and carefully
monitor the amount of drainage from the
chest tube if with pneumohemothorax
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Alteration of normal functioning of the medulla and
pons due to CNS depressants/ disorders →
decreased response to increasing CO2 levels and
increased O2 levels → ineffective respiratory drive
adjustment → hypoxia and hypercapnia
• Neuromuscular disease/ neuromuscular
blocking agents
Primary problem (neuromuscular disease/
neuromuscular blocking agents → respiratory
muscle weakness → decrease chest wall
compliance → decreased muscular response to the
brain signals for respiration → hypoxia and
hypercapnia
• Chest wall deformities
Primary problem (kyphoscoliosis) → decreased
chest wall compliance → decreased tidal volume →
hypoxia and hypercapnia

RESPIRATORY DEPRESSION
- a condition wherein breathing is slow and CLINICAL MANIFESTATIONS:
ineffective leading to inadequate gas exchange
• Early
- hypoxia
Respiratory depression can be due to: - slow or shallow breathing
• CNS depressants (medications, alcohol, - tiredness
drugs) - daytime drowsiness
• CNS disorders (stroke, tumors, trauma) • Late
• Neuromuscular diseases (myasthenia - Confusion
gravis, ALS, Guillain Barre Syndrome, - drowsiness
muscular dystrophy) - Cyanosis
- apnea
• Sleep apnea
- seizures
• Chest wall deformities (kyphoscoliosis)
• Obesity hypoventilation syndrome- due to
altered chest wall mechanics from morbid
obesity
• Chronic lung disease – leading to blocked DIAGNOSTIC TESTS
airways
• Congenital hypoventilation syndrome (failure 1. Imaging studies- X-ray of the chest to check
of automatic control of breathing) for abnormalities; CT scan or MRI of the
brain to check for tumors
2. Lung function test
PATHOPHYSIOLOGY 3. Blood gas test- to see if the patient is
acidotic
• CNS depressants/ CNS disorders

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4. Pulse oximetry- to check for the patient's 1. Bronchodilators to open the airways
saturation - beta agonists (albuterol, salmeterol,
5. Screening for toxins in the body- that formoterol)
might be causing the respiratory depression 2. Theophylline
6. Sleep studies- to diagnose sleep related - stimulate the respiratory center and
disorders increase diaphragm muscle contractility
- promotes smooth muscle relaxation of the
MEDICAL AND SURGICAL MANAGEMENT:
airways
1. Treatment of the primary cause of 3. Anticholinergics
hypoventilation - tiotropium (long acting), atropine (short
2. Oxygen therapy acting)
- to prevent the sequelae of the long- 4. Medroxyprogesterone
standing hypoxemia - increases the central respiratory drive
- COPD patients may also have O2 - effective in obesity-hypoventilation
supplementation if they meet the criteria for syndrome and central hypoventilation
O2 supplementation syndrome
- patients with neuromuscular problems - it can increase the risk for
should not be given O2 without ventilatory thromboembolism
support because if you just keep giving them 5. Acetazolamide
oxygen and their lungs aren't expanding so it - inhibits carbonic anhydrase increasing
won't do anything they will need the positive bicarbonate excretion and because there is
and expiratory pressure from a machine to increased bicarbonate excretion it will cause
help them breathe in metabolic acidosis and indirectly it will
3. Weight loss for obese patients stimulate ventilation because if the body is in
4. Continuous positive airway pressure acidosis our body will also try to compensate
(CPAP), Bi level Positive Airway pressure by trying to breathe in to get more oxygen
(BiPAP) or intubation for acute into the body
hypoventilation
NURSING MANAGEMENTS
- depending on the severity of hypoxemia or
hypercapnia 1. Assess respirations and pulse oximetry and
5. Nocturnal BiPAP for patients with chronic monitor regularly
respiratory failure related to COPD, 2. Assess for mental status of patient to check
neuromuscular disease, thoracic for confusion.
deformities, and for idiopathic
Rationale: because if the brain is not getting enough
hypoventilation
the oxygen causing changes in mental status and or
6. Surgery for chest wall deformities
alterations
7. Diaphragm pacing
- placement of an electrode on the phrenic 3. Administer oxygen supplement as indicated
nerve connected to a subcutaneous receiver. 4. Educate patient on the use of CPAP or
An electric current passing through the BIPAP
transmitter will cause diaphragmatic
contraction Rationale: because for patient who are first time
users of this machine it can be quite scary because
it gives off so much air or pressure into the mouth
PHARMACOLOGIC MANAGEMENT: and the nose so it's important to know how to deal

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with it that they have to breathe with the machine so
the treatment will be effectives.
5. Take caution on administering opioids or
other CNS depressants
ACUTE RESPIRATORY DISTRESS SYNDROME
→ Majority of the patients develop pulmonary
or non-pulmonary infection
→ The most common cause is pneumonia
followed by severe sepsis. Other causes
can be hemorrhage and shock due to
trauma, severe acute pancreatitis,
transfusion- associated lung injuries and
drug interactions
→ PATHOPHYSIOLOGY:
CLINICAL MANIFESTATION
1. Rapid onset of severe dyspnea 72 hrs. after
the precipitating event
2. Arterial hypoxemia nonresponding to
supplementary O2
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3. Bilateral infiltrates seen at chest x-ray with
quiz progression
4. Decreased pulmonary compliance
DIAGNOSTICS
1. Physical Assessment
a. An increase work of breathing, accessory
muscle use, intercostal retractions
b. Crackles upon auscultation due to
consolidation of alveoli
2. Test for plasma brain natriuretic peptide (BNP)
to distinguish from cardiogenic or pulmonary
edema
- The blood concentration of BNP is significantly
elevated in patients with heart failure (shortness
of breath can be due to cardiogenic or pulmonary
edema
3. ECG to check for heart failure
4. Transthoracic echocardiography if BNP is
inclusive
Medical Managements
1. aggressive supportive care
a. endotracheal intubation and mechanical
ventilation
b. circulatory support by giving vasopressors and
inotropes for the treatment of hypotension -
hypovolemia results from the leakage of fluid into
the interstitial space and decreased cardiac
output is due to high levels of peep which will all
lead to hypotension
c. IVF
d. nutritional support
e. prone positioning to allow better breathing for
the patient
f. sedation so that the patient will be able to rest
for a decreased oxygen consumption and for the
patient to not fight off the machine
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2. Arterial blood gas analysis, pulse oximetry,
pulmonary function tests are regularly monitored
- Results will determine the adjustments for the
O2 concentration and ventilation settings
3. PEEP
- The pressure keeps the alveoli open which
will improve arterial oxygenation and improving
V/Q (Ventilation perfusion) mismatch
- This is adjusted in the ventilator settings
- Goal: O2 saturations >90% with the lowest
possible Fraction of inspired oxygen (FiO2) ad
PaO2 of >60 mmHg
(FiO2 - concentration of Oxygen in the gas
mixture)
Pharmacologic management
- There is no specific Pharmacologic
management for ARDS
- Sedation (Lorazepam, midazolam, Propofol)
or neuromuscular blocking agents (rocuronium,
alcuronium, vecuronium) may be given to
ventilated patients to: a. Reduce physiological
stress from respiratory failure
b. Improve tolerance of invasive life support
This will keep the patient from fighting with the
machine as the ventilator can be very
uncomfortable to the patient
Nursing Management
1. Patents with ARDS are critically ill therefore
frequent monitoring of status is needed to
evaluate effectiveness of treatment.
2. Position the patient to allow better ventilation
3. Turning the patient to improve perfusion and
drainage secretions
4. Provide a calm environment to promote rest
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5. Reduce the patient's anxiety to decrease
oxygen expenditure and provide reassurance in
the event that paralytic agents are given to the
patient
6. Monitor the ventilator and its connections
closely
7. Provide VTE Prophylaxis as ordered and use
of Thrombo-embolus deterrent (TED) stockings
8. Pressure ulcers prevention for ventilated
patients
9. Ensuring comfortable position for the patient
and proper alignment
10. Educating family members
Sudden Infant Death Syndrome (SIDS)
- Deaths in infants younger than 12 months
occurs suddenly, unexpectedly, and cannot be
explained despite a thorough investigation
including a complete autopsy, examination of the
death scene, and review of the clinical and social
history
- Classic presentation: An infant put to bed
after feeding, and are normal during interval
checks but then found dead in the same position
they have been placed on
Clinical Manifestations
1. Some live patients may be seen after a Brief
Resolved Unexplained Event (BRUE) BRUE-
Maybe interrupted SIDS or related to it; or a
whole other phenomena a. cyanosis
b. breathing difficulties
c. Abnormal Limb movement
- Patients with BRUE may have a completely
normal physical exam after the episode (50%),
febrile (25%), and have infection (25%)
Physical findings on patients with SIDS
Serosanguineous watery, frothy mouth, or
mucoid discharge from mouth or nose reddish-
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blue mottling on the face and dependent portion
of the body
marks on pressure points well cared for
appearance with no skin trauma no
environmental contribution to the unexpected
death
Diagnostics
A workup will be done for a patient brought to the
ED after a BRUE
1. Rapid bedside glucose test
2. arterial blood gases for severely ill or have
persistent symptoms
3. blood workup and urine exam including
toxicology screenings
4. 12 lead ECG
5. Complete septic workup which includes
lumbar puncture for patients under 2 months or
if with significant evidence of infection and
include antibiotic administration
6. Upper airway studies
Medical management
1. paramedics who arrived in the scene will
resuscitate an infant in cardiorespiratory arrest
the patient will be brought to the emergency
department
2. admission in the icu for cardiac and
respiratory monitoring including arterial oxygen
saturation for critical or unstable patients
3.infants who are stable but had cyanosis altered
mental state or tone should be admitted
4. stable children will have continuous
cardiorespiratory monitoring to determine apnea
or bradyarrhythmia’s
Nursing Management
1. Patients admitted after a BRUE
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- monitor cardiac and respiratory status
closely
-assist with procedures needed to be taken for
workup
- educate parents on the procedures to be
done and the purpose of cardiorespiratory
monitoring,
2. Procedure after SIDS
- Empathize and be compassionate with
family and inform them in a quiet environment
- Expression of sorrow and sympathy may be
given but avoid statements like
"I know how you feel" because that will just
induce anger
Current recommendations on Sleep Positions
and the infant sleep environment
Place the infant on its back for sleep on a firm,
tight-fitting mattress in a crib that meets current
federal safety standards
Remove pillows, quilts, comforters, sheepskins,
stuffed toys, and other soft items from the crib
Do Not place the infant on a water bed, sofa, soft
mattress, pillow or another soft surface to sleep
Consider using a sleeper or sleep sack as an
alternative to blankets or other covers Make sure
that the infant's head remains uncovered during
sleep place the infant so that its feet’s are
positioned at the foot of the crib
If a thing blanket is used, tuck it around the crib
mattress positioned up only as far as the infant's
chest
Prevention
- Start prenatal care early
- Avoid cigarettes, alcohol or other drugs while
pregnant
- breastfeed if possible
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- burp the baby during and after feedings • Remove extra air.
- place baby on a firm flat mattress in a safety Tension pneumothorax
approved crib, avoid pillows, blankets, foam
pads or waterbeds • → EMERGENCY. Air hunger, cyanosis,
Hypotensive. Increased pulse rate.
- do not restrain the baby while sleeping Jugular vein distention.
- improve the room's ventilation by using a fan Traumatic pneumothorax
- side sleeping and prone positioning is not • Chest tube drainage → Lower than the
advised heart and lungs Oscillation in fluid=
normal.
- bed sharing should be avoided (suffocation
from loose clothing, or a sleeping adult, or to • Alarming= bubbles. Leak in tubing/ chest
overheating) • antibiotic, pain relief for client

LEC NOTES: Read on FOR MIDTERMS PASAAR CUTIE~

Pneumonia CARE OF CLIENTS WITH CHEST TUBE

DRAINAGE
Noninvasive ventilator - tight fitting mask so no
air leak. Only when client is breathing on their Acute respiratory distress syndrome→
own. Breathe in with machine secondary disease

BIPAP – non-invasive form of therapy for patient → rapid onset of dyspnea

suffering from sleep apnea → pulmonary edema- caused by cardiogenic
CPAP -continuous positive airway pressure. and respiratory problems. PNP is taken to check.
Only 1 steady. A bit difficult for client to exhale. If high it is due to cardiac problems
This is usually done in clients who have COPD, (cardiomyopathy etc).
continuous oxygen.
If result is borderline:
GCS8 Intubation:
• → thoracentesis → difference in X-ray →
Sedative medications decreased pulmonary compliance
Neuromuscular blocking agent-given before SIDS→ Asthma → Given right away-->
intubation. IV. After 1 minute it will start to work. ALBUTEROL- dose is 5.25 every 20
mins
• monitor every hour • Breathe 4-6 times through mouth while
• Sputum Analysis → green/ rust colored sealing mouthpiece.
• During acute exacerbations-->albuterol
Pleural Effusion
will lessen constriction of muscle.
Low albumin= lesser pull of fluid, lesser oncotic • 8 puffs every __ for 3 doses
pressure, fluid seeps out/ increased pressure→ • Corticosteroid→ potent anti-
inflammatory. If recovered, don’t need to
TRANSUDATIVE
continue, only to stabilize inflammatory
Pneumothorax- air is introduced in pleural process during acute stage. Long acting-
space. ->fluticasone
• Leukotriene modifiers
Management of Pneumothorax

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• Spirometry→ Chronic bronchitis→
MUCUS PRODUCTION, due to increase
in goblet cells in airway due to
inflammation
• Bronchiectasis-->dilation of bronchi and
bronchioles
• If bronchioles constantly dilated →
difficult to remove secretions, which then
accumulates causing dyspnea and a
source of infection
GOAL:
Prevent infection
Promote bronchial drainage Help client to
PULMONARY REHABILITATION:
• Exercise
• Disease Management
• Oxygen Therapy (as needed)
• Counselling
• Emphysema→ abnormal distention of air
spaces. Expanded. Inflated. Difficult to get
rid of CO2
Additional Notes from links:
Sudden infant death syndrome (SIDS)
Sudden infant death syndrome (SIDS) –
sometimes known as "cot death" – is the sudden,
unexpected and unexplained death of an
apparently healthy baby.
In the UK, more than 200 babies die suddenly
and unexpectedly every year. This statistic
may sound alarming, but SIDS is rare and the
risk of your baby dying from it is low.
Most deaths happen during the first 6 months of
a baby's life. Infants born prematurely or
with a low birthweight are at greater risk. SIDS
also tends to be slightly more common in baby
boys.
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• SIDS usually occurs when a baby is
asleep, although it can occasionally
happen while they're awake.
• Parents can reduce the risk of SIDS by
not smoking while pregnant or after the
baby is born, and always placing the
baby on their back when they sleep (see
below).
What causes SIDS?
The exact cause of SIDS is unknown, but it's
thought to be down to a combination of factors.
Experts believe SIDS occurs at a particular stage
in a baby's development and that it affects
babies vulnerable to certain environmental
stresses.
This vulnerability may be caused by being born
prematurely or having a low birthweight, or
because of other reasons that have not been
identified yet.
Environmental stresses could include tobacco
smoke, getting tangled in bedding, a minor
illness or a breathing obstruction. There's also an
association between co-sleeping (sleeping with
your baby on a bed, sofa or chair) and SIDS.
Babies who die of SIDS are thought to have
problems in the way they respond to these
stresses and how they regulate their heart rate,
breathing and temperature.
Although the cause of SIDS is not fully
understood, there are a number of things you
can do to reduce the risk.
What can I do to help prevent SIDS?
Below is a list of things you can do to help
prevent SIDS.
Do:
● always place your baby on their back to sleep
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● place your baby in the "feet to foot" position
– with their feet touching the end of the cot,
Moses’ basket, or pram
● keep your baby's head uncovered – their
blanket should be tucked in no higher than their
shoulders
● let your baby sleep in a cot or Moses basket
in the same room as you for the first 6 months
● use a mattress that's firm, flat, waterproof
and in good condition
● breastfeed your baby, if you can – see
benefits of breastfeeding for more information
Do not:
● smoke during pregnancy or let anyone
smoke in the same room as your baby – both
before and after birth
● sleep on a bed, sofa or armchair with your
baby
● share a bed with your baby if you or your
partner smoke or take drugs, or if you've been
drinking alcohol
● let your baby get too hot or too cold – a room
temperature of 16C to 20C, with light bedding or
a lightweight baby sleeping bag, will provide a
comfortable sleeping environment for your baby
Read more about reducing the risk of SIDS.
Seeking medical advice if your baby is unwell
Babies often have minor illnesses that you do not
need to worry about. Give your baby plenty of
fluids to drink and do not let them get too hot.
If you're worried about your baby at any point,
see your GP or call NHS 111 for advice.
Dial 999 for an ambulance if your baby:
● stops breathing or turns blue
● is struggling for breath
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● is unconscious or seems unaware of what's
going on
● will not wake up
● has a fit for the first time, even if they seem
to recover
Read more about spotting signs of serious
illness in children.
Support services
If a baby dies suddenly and unexpectedly, there
will need to be an investigation into how and why
they died. A post-mortem examination will
usually be necessary, which can be very
distressing for the family.
The police and healthcare professionals work
closely to investigate unexpected infant deaths
and ensure the family is supported. They should
be able to put you in touch with local sources of
help and support.
Many people find talking to others who have had
similar experiences helps them to cope with their
bereavement.
→ The Acute Respiratory Distress Syndrome:
Pathogenesis and Treatment
Lung function tests can be used to:
■ Compare your lung function with known
standards that show how well your lungs should
be working.
■ Measure the effect of chronic diseases like
asthma, chronic obstructive lung disease
(COPD), or cystic fibrosis on lung function.
■ Identify early changes in lung function that
might show a need for a change in treatment.
■ Detect narrowing in the airways.
■ Decide if a medicine (such as a bronchodilator)
could be helpful to use.
■ Show whether exposure to substances in your
home or workplace may have harmed your
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lungs. ■ Determine your ability to tolerate
surgery and medical procedures.
To get the most accurate results from your
breathing tests:
■ Do not smoke for at least 1 hour before the
test.
■ Do not drink alcohol for at least 4 hours before
the test.
■ Do not exercise heavily for at least 30 minutes
before the test.
■ Do not wear tight clothing that makes it difficult
for you to take a deep breath.
■ Do not eat a large meal within 2 hours before
the test.
■ Ask your health care provider if there are any
medicines that you should not take on the day of
your test.
What is spirometry?
Spirometry is one of the most commonly ordered
tests of your lung function. The spirometer
measures how much air you can breathe into
your lungs and how much air you can quickly
blow out of your lungs. This test is done by
having you take in a deep breath and then, as
fast as you can, blow out all of the air. You will
be blowing into a tube connected to a machine
(spirometer). To get the “best” test result, the test
is repeated three times.
You will be given a rest between tests. The test
is often repeated after giving you a breathing
medicine (bronchodilator) to find out how much
better you might breathe with this type of
medicine. It can take practice to be able to do a
spirometry test well. The staff person will work
with you to learn how to do the test correctly.
It usually takes 30 minutes to complete this test.
What should I know before doing a spirometry
test?
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■ You may be asked not to take your breathing
medicines before this test.
■ Instructions will be given on how to do this test.
If you do not understand the instructions, ask the
staff to repeat them.
■ It takes effort to do this test and you may
become tired. This is expected.
■ If you become light-headed or dizzy during this
test, immediately stop blowing and let the staff
know.
What are diffusion studies?
Diffusion tests find out how well the oxygen in the
air you breathe in moves from your lungs into
your blood.
Pulmonary Function Tests
Pulmonary function tests (PFT’s) are breathing
tests to find out how well you move air in and out
of your lungs and how well oxygen enters your
blood stream. The most common PFT’s are
spirometry (spy-RAH-me-tree), diffusion studies,
and body plethysmography (ple-thiz-MA-gra-
fee). Sometimes only one test is done, other
times all tests will be scheduled on the same
day.
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2014
Online Version Updated October 2019
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Thoracic Society
American Thoracic Society
PATIENT EDUCATION | INFORMATION
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Like spirometry, this test is done by having you
breathe into a mouthpiece connected to a
machine. You will be asked to empty your lungs
by gently breathing out as much air as you can.
Then you will breathe in a quick (but deep
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 NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
Bambam2017
breath), hold your breath for 10 seconds, and
then breathe out as instructed.
You will do the test several times. It usually takes
about 30 minutes to complete this test.
What should I know before doing a diffusion
test? ■ Do not smoke and stay away from others
who are smoking on the day of the test.
■ If you are on oxygen, you will usually be asked
to be
off oxygen for a few minutes before taking this
test.
What is body plethysmography?
Body plethysmography is a test to find out how
much air is in your lungs after you take in a deep
breath, and how much air is left in your lungs
after breathing out as much as you can. No
matter how hard you try, you can never get all of
the air out of your lungs. Measuring the total
amount of air your lungs can hold and the
amount of air left in your lungs after you breathe
out gives your healthcare provider information
about how well your lungs are working and helps
guide your treatment. This test requires that you
sit in box with large windows (like a telephone
booth) that you can see through. You will be
asked to wear a nose clip and you will be given
instructions on how to breathe through the
mouthpiece. You will be asked to take short,
shallow breaths through the mouthpiece when it
is blocked for a few seconds, which may be
uncomfortable. If you have difficulty with being in
closed spaces (claustrophobia), mention this to
your provider ordering the test. This will avoid
any misunderstanding and discomfort to you. It
usually takes about 15 minutes to complete.
Some PFT labs will use other tests instead of
plethysmography to measure the total volume of
air in your lungs.
What should I know before doing a
plethysmography test?
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■ If you are on oxygen, you will usually be asked
to be off oxygen during this test.
■ Let the staff know if you have difficulty in closed
spaces.
What are normal results for lung function tests?
Because everyone’s body and lungs are different
sizes, normal results differ from person to
person. For instance, taller people and males
tend to have larger lungs whereas shorter people
and females have smaller lungs. It is normal for
your lung function to fall slightly as you age.
These standards that your healthcare provider
uses, are based on your height, age, and sex at
birth. These numbers are called the “predicted
values”. Your measured values will be compared
to these predicted values.
R Action Steps
✔ Ask questions if you do not understand the
instructions for the lung function test.
✔ If you have a cold or flu, let the test center
know because you may need to reschedule your
test.
✔ If you have difficulty with closed
spaces(claustrophobia), let the test center know
in case one of the tests involves being enclosed.
✔ Ask if there are any medicines you should
stop taking before being tested and for how long
you should stop it.
✔ After your pulmonary function testing is over,
you can return to your normal activities.
Healthcare Provider’s Con
REMINDERS FOR 6M MIDTERMS READ ABOUT
CARE OF PATIENTS WITH CHEST TUBE AND
ITS NURSING INTERVENTIONS
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NCM 112: Oxygen Exchange and Utilization Cebu Doctors’ University Fated Nurses
Ms. Kerstine Iza Benolerao, RN
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