NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
TABLE OF CONTENTS
I. Assessment: Physical Examination
II. Diagnostic Assessment
III. Alterations in Ventilation
I.
Assessment: Physical Examination
a. History
▪ Previous Health History
▪ Family History
▪ Lifestyle Patterns
▪ Current Health Status
b. Chronic Complaints
▪ Dyspnea
▪ Orthopnea
▪ Cough
▪ Sputum
▪ Wheezing
▪ Chest Pain
▪ Sleep Disturbances
Examination using IPPA
1. INSPECTION
• Involves
checking
for
the
presence/absence of several factors:
✓ Cyanosis – bluish discoloration
✓ Labored breathing
✓ Anterior-posterior diameter of
the chest
o Barrel Chest
▪ Occurs as a result of
overinflation of the lungs,
which
increases
the
anteroposterior diameter of
the thorax
▪ Occurs with aging and is a
hallmark
sign
of
emphysema and COPD
o Pigeon Chest
▪ Occurs when there is a
depression in the lower
portion of the sternum
▪ May compress the heart and
great vessels, resulting in
murmurs
•
o Funnel Chest
▪ Occurs as a result of the
anterior displacement of the
sternum,
which
also
increases
the
anteroposterior diameter.
o Thoracic Kyphosis
▪ The patient’s spine curves to
one side and the vertebrae
are rotated
▪ Because the rotation distorts
the lung tissue, it may be
more difficult to assess
respiratory status
✓ Chest deformities
✓ Patient’s posture
✓ Position of the trachea
✓ Respiratory rate
✓ Respiratory effort
✓ Duration of inspiration versus the
duration of expiration
✓ Thoracic expansion
✓ Patient’s extremities
Assess for:
 Apnea
• Absence of breathing
• The condition may be lifethreatening if periods of apnea
last long enough
• Should
be
addressed
immediately
 Hypernea
• Increased rate and depth
• Usually occurs with extreme
stress, fear or anxiety
 Kussmaul
• Rapid, deep, and labored
breathing
• Occurs in patients with
metabolic acidosis, especially
with
associated
diabetic
ketoacidosis
• Respiratory system tries to
lower the CO2 level in the blood
and restore it to normal pH
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
 Cheyne-Stokes
• Regular pattern characterized
alternating periods of deep,
rapid breathing followed by
periods of apnea
• May result from severe CHF,
drug overdose, increased ICP,
or renal failure
 Biot’s Respiration
• Irregular pattern characterized
by varying depth and rate of
respirations followed by periods
of apnea
• May be seen with meningitis or
severe brain damage
2. PALPATION
• Check for:
✓ Tactile Fremitus – palpable
vibrations
caused
by
the
transmission of air through the
bronchopulmonary system
✓ Fremitus – is increased normally
over the large bronchial tubes and
abnormally over areas in which
alveoli are filled with fluid or
exudates (pneumonia)
• Evaluate symmetry
 Chest wall should feel smooth,
warm, and dry
 Crepitus (feels like puffed rice puff
cereal cracking under the skin)
• Indicated that air is leaking from
the airways or lungs
 If the patient has chest tube, you
may find a small amount of
subcutaneous air around the
insertion site
 If the patient has no chest tube, or
the area of crepitus is getting larger,
ALERT THE PRACTITIONER RIGHT
AWAY
 Gentle palpation should not cause
the patients’ pain
 If patient complains of chest pain,
try to find a painful area on the
chest wall
3. PERCUSSION
• Find the boundaries of the lungs
• Determine whether the lungs are filled
with air, fluid, or solid material
• Evaluate the distance of the diaphragm
travels
between
the
patient’s
inhalation and exhalation
• Warning signs:
✓ Hyperresonance - it means you
have found an area of increased air
in the lung or pleural space.
- Expect to hear hyperresonance in
patients with:
o Pneumothorax
o Acute Asthma
o Bullous Emphysema
✓ Abnormal dullness – it means you
have found areas of decreased air
in
the
lungs
- Expect abnormal dullness in the
presence of:
o Pleural Fluid
o Consolidation atelectasis
o Tumor
4. AUSCULTATION
• As air moves through the bronchi, it
creates sound waves that travel to the
chest wall
• The sound produced by breathing
changes as air moves larger to smaller
airways
• Sounds also change if they pass
through fluid, mucus, or narrowed
airways
• Auscultation sites are the same as
percussion sites
• Listen to a full cycle of inspiration and
exhalation at each site, using the
diaphragm of the stethoscope
• Ask the patient to breathe through his
mouth if it does not cause discomfort,
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
nose breathing alters the pitch of
breath sounds
NORMAL BREATH SOUNDS
Tracheal
• Heard over the trachea
• Harsh and
discontinuous
• Occur when patient
inhales or exhales
Bronchial
• Usually heard next to
the trachea just above
or below the clavicle
• Loud, high-pitched, and
discontinuous
• Loudest when the
patient exhales
Bronchovesicular • Medium-pitched and
continuous
• Best heard over the
upper third of the
sternum and between
the scapulae when the
patient inhales or
exhales
Vesicular
• Heard over the rest of
the lungs
• Soft and low-pitched
• Prolonged during
inhalation and
shortened during
exhalation
• Check for:
✓ Vocal Fremitus - is the sound
produced by chest vibrations as the
patients
speaks
- abnormal transmission of voice
sounds
can
occur
over
consolidated areas because sound
travels well through fluid
ABNORMAL BREATH SOUNDS
Bronchophony • Ask patient to say “ninetynine” or “blue moon”
• Over normal tissue, the
words sound muffled
• Over consolidated areas,
the words sound
unusually loud
Egophony
• Ask the patient to say “e”
• Over normal lung tissue,
the sound is muffled
• Over the consolidated
areas, it sounds like letter
A
Whispered
• Ask the patient to whisper
Pectoriloquy
“1,2,3”
• Over normal lung tissue,
the most numbers are
almost indistinguishable
• Over consolidated tissue,
the numbers sound loud
and clear
✓ Adventitious
Sounds
–
abnormal no matter which part
of the lungs you can hear them
 Crackles
• Soft,
high-pitched,
discontinuous popping
sounds
that
occur
during inspiration (may
also be heard on
expiration
Types
▪ Course Crackles –
discontinuous popping
sounds
that
- Harsh, moist sound
originating in the large
bronchi
- obstructive pulmonary
disease
▪ Fine
Crackles
–
discontinuous popping
sounds heard in late
inspiration
- Sounds like hair
rubbing
together
- Originates in the alveoli
- Pneumonia, fibrosis,
bronchitis, pleural fluid
 Wheezes
• Usually
heard
on
expiration, but may be
heard on inspiration
• Associated
with
changes
in
airway
diameter
Types
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
Sonorous
Wheezes
(Ronchi) – Deep, lowpitched
rumbling
sounds heard primarily
during
expiration
- Caused by air moving
through
narrowed
tracheobronchial
passages
Associated
with
secretions or tumor
▪ Sibilant Wheezes –
Continuous musical,
high-pitched, whistlelike sounds heard during
inspiration and
expiration caused by air
passing through
narrowed or partially
obstructed airways
- Bronchospasm,
asthma, build-up of
secretions
 Friction Rubs
Types
▪ Pleural Friction Rub –
Harsh, crackling sound,
like two pieces of leather
being rubbed together
(sound imitated by
rubbing thumb and
finger together near the
ear)
Secondary
to
inflammation and loss of
lubricating pleural fluid
▪
II. Diagnostic Assessment
a. Non-Invasive
1. Oximetry
• Is a non-invasive technique that
measures the oxygen saturation of
arterial blood by using red and
infrared light that passes through
tissue and blood vessels.
•
Oxygen saturation – is determined
by the amount of each light
absorbed, with deoxygenated
hemoglobin absorbing more red
light and oxygenated hemoglobin
absorbing more infrared light.
b. Invasive
1. Arterial Blood Gas
• Assesses lung function in providing
oxygen and removing carbon
dioxide, as well as the kidney’s role
in maintaining normal pH through
bicarbonate regulation.
• These
measurements
guide
management
of
respiratory
conditions and oxygen therapy
adjustments.
2. Pulmonary Capillary Wedge
Pressure Pleural Fluid Analysis
• Is a measurement used to assess
left ventricular filling, left atrial
pressure, and mitral valve function.
• It is obtained by inserting a balloontipped catheter into a central vein,
advancing it to a pulmonary artery
branch, and inflating the balloon to
occlude the artery, which allows
the pressure in the left atrium to be
measured.
INDICATIONS
 Different between cardiogenic
pulmonary edema and noncardiogenic pulmonary edema
 Confirm
the
diagnosis
of
pulmonary arterial hypertension
 Assess the severity of mitral
stenosis
 Differentiate between different
forms of shock
 Measure
key
hemodynamic
parameters and assess response
to therapy
3. Pulmonary Angiography
• Is a diagnostic imaging procedure
that utilizes x-rays and a contrast
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
agent to visualize the blood vessels
supplying the lungs.
• This technique involves the
injection of a dye-like substance
through a small, slender catheter
inserted into the bloodstream,
enabling the assessment of the
internal structure and function of
the pulmonary arteries.
INDICATIONS
 Blood clot (pulmonary embolism)
 Bulging blood vessel (aneurysm)
 An artery abnormally connected to
a vein
 Heart and blood vessel problems
present at birth
 Foreign body in a blood vessel
 Narrowing of a blood vessel wall
4. Ventilation/Perfusion Scan
• Evaluates ventilation patterns and
pulmonary blood flow.
• They are less common for
mechanically ventilated patients,
as the ventilation assessment can
be challenging.
• This can assess ventilationperfusion mismatches, detect
emboli, and evaluate lung function,
especially in
patients
with
compromised reserves.
• Has 2 parts:
During ventilation – the patient
inhales the contrast medium gas;
ventilation patterns and adequacy
of ventilation are noted on the
scan
During perfusion – the contrast
medium is injected IV and the
pulmonary blood flow in the lungs I
visualized
USES
✓ Evaluate V mismatch
✓ Detect pulmonary embolism
✓ Evaluate pulmonary function,
especially in patients with
marginal lung reserves
✓ Less reliable then pulmonary
angiography, but poses fewer
risks
5. Capnography
• Provides a more comprehensive
and detailed measurement, which
is presented in both graphical and
numerical formats.
• Is currently the most widely
recommended
approach
for
monitoring
end-tidal
carbon
dioxide levels.
• Normal range for EtCO2: 35-45
mmHG
INDICATIONS
 Verification of artificial airway
placement
 Assessment
of
pulmonary
circulation and respiratory status
 Optimization
of
mechanical
ventilation
III. Alterations in Ventilation
1. Acute
and
Chronic
Obstructive
Pulmonary Disease
• Results from emphysema, chronic
bronchitis, asthma, or a combination
of these orders
• Is a chronic condition that can usually
be managed on an outpatient basis
even in advanced disease, when a
patient may require continuous oxygen
therapy
• Most common chronic lung disease
• Exacerbations
of
COPD
that
necessitate hospitalization are caused
by various factors that place additional
demand on the respiratory system,
such as infection, heart failure, and
exposure to allergens.
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
CAUSES
• Cigarette smoking or exposure to
cigarette smoke
• Recurrent or chronic respiratory
tract infections
• Air pollution
• Allergies
• Familial and hereditary factors
such as alpha 1 antitrypsin
deficiency paired with cigarette
smoking (also responsible for
emphysema)
SIGNS AND SYMPTOMS
According to the World Health
Organization (WHO), the following are the
most common signs and symptoms:
 Difficulty of breathing
 Chronic cough (sometimes with
phlegm)
 Feeling tired
RISK FACTORS
▪ Smoking
▪ Household air pollution
▪ Atmospheric pollution
▪ Asthma with airway remodelling
▪ Post-tuberculosis
▪ Genetic susceptibility
▪ Abnormal lung development
PATHOPHYSIOLOGY
o Patients with COPD have decreased
gas exchange ability due to alveolar
damage caused by exposure to smoke
or chemical irritants over a long period.
o Smoke inhalation impairs ciliary action
and macrophage function which
causes inflammation in the airways
and increased mucus production.
o In chronic bronchitis, mucus plugs
and narrowed airways cause air
trapping. Air trapping also occurs with
asthma and emphysema.
o In
emphysema,
permanent
enlargement of the
acini is
accompanied by destruction of the
alveolar walls. Obstruction and air
trapping result from tissue changes
rather than mucus production.
DIAGNOSIS
For Stable COPD Patients
✓ Pulmonary Function Test
• Increased
residual
volume,
decreased vital capacity and
amount of air exhaled in the first
second of expiration.
✓ Chest X-Ray
• Increased
broncho
vascular
markings and overaeration of the
lungs. In advanced disease, the
diaphragm is flattened and
broncho vascular markings may be
reduced.
✓ Arterial Blood Gas Analysis
• May show reduced PaO2 and
normal or increased PaCO2. In
advanced
COPD,
it
isn’t
uncommon for baseline PaCO2
levels to be 50mmHg or higher
✓ Electrocardiogram
• May show atrial arrhythmias and in
advanced disease, right ventricular
hypertrophy
✓ Complete Blood Count
• Reveals elevated hemoglobin
levels
For patients in Critical Situation
During exacerbation, diagnostic tests may
yield these additional results:
✓ Arterial Blood Gas Analysis
• Shows PaO2 below the patient’s
baseline or PaCO2 may be low,
normal, or high depending on the
patient's baseline data
✓ Chest X-Ray
• May show infiltrates if pneumonia
is present
✓ Electrocardiogram
• May show sinus tachycardia with
supraventricular and sometimes
ventricular arrhythmias
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
TREATMENT
Provide supportive treatments for your
patients with COPD
• Bronchodilators and membrane
stabilizing aerosols are useful in
maintaining open airways.
• Steroids may be given to reduce
inflammation if necessary. In some
cases,
continuous
oxygen
supplementation is needed.
• During exacerbations, management is
twofold. First, respiratory support is
given to avoid respiratory failure and
cardiac arrest. Equally important is
treatment addressing the underlying
cause of exacerbation.
• Your patient may receive oxygen
supplementation. Care must be taken
when the baseline PaCO2 level is high.
The patient’s respiratory center relies
on low oxygen levels to stimulate
breathing.
• Administer controlled oxygen by
monitoring ABG levels and patient
assessments.
• If respiratory failure is eminent, ET
intubation
and
mechanical
ventilation are needed.
• Aerosolized bronchodilators, such as
albuterol, are given to open airways.
Epinephrine, a potent bronchodilator
may be given.
• Corticosteroids are given (usually by
IV) to reduce inflammation.
• Diuretic agents may be given to
reduce edema and cardiac workload.
• Antiarrhythmic medications may be
given to control arrhythmias.
• The patient is usually put on
continuous ECG monitoring for
observation of the heart rate and
rhythm.
• Antibiotics are given to treat or prevent
infection.
•
If pneumothorax is present, a chest
tube may be inserted.
NURSING CONSIDERATIONS
▪ Assess respiratory status, auscultate
breath sounds, monitor oxygen
saturation, and ABG values, and
observe for a positive response to
oxygen therapy, such as improved
breathing, color, or oximetry, and ABG
values. Anticipate the need for
intubation and mechanical ventilation.
▪ Assess frequently and carefully.
Changes can be subtle and rapid. Be
sure to assess mental status because
it’s an early and sensitive indicator of
respiratory status. New onset of
confusion and agitation are ref flags, as
is lethargy.
▪ Monitor vital signs and heart rhythm
and observe for arrhythmias, which
indicate hypoxemia, right sided heart
failure, or an adverse effect of
bronchodilator use.
▪ Obtain laboratory tests as ordered,
and report results promptly.
▪ Offer support. Keep the environment
as calm as possible and the air
temperature warm. The patient may
not be able to speak easily because of
shortness of breath, so explain what’s
happening and try to anticipate his
needs.
2. Pulmonary Embolism
• It is an obstruction of the pulmonary
arterial bed
• It occurs when mass lodges in a
pulmonary artery branch, partially or
completely obstructing blood flow
distal to it (this causes a V mismatch,
resulting
in
hypoxemia
and
intrapulmonary shunting)
• It is one of the most common heart and
blood vessel diseases in the world
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
CAUSES
• Dislodged
thrombus
that
originated in the deep veins of the
legs (or less commonly, in the
pelvic, renal, or hepatic veins, or
right side of the heart)
• Other emboli arise from fat, air,
amniotic fluid, tumor cells, or
foreign object, such as a needle,
catheter part, or talc
• Another medical condition, like
cardiovascular disease (including
congestive heart failure, atrial
fibrillation, heart attack or stroke)
SIGNS AND SYMPTOMS
 Other symptoms depends on the
size of the embolus and if it is a fat
or air embolism
 A small embolism may not cause
any signs or symptoms
 An embolism that occludes less
than 50% of the artery bed may
cause a sense of impending doom,
dyspnea, tachycardia, confusion,
right-sided
heart
failure,
hypotension,
and
pulseless
electrical activity
 A fat embolism may produce no
symptoms for up to 24 hours or
symptoms
may
include
restlessness, confusion, shortness
of breath, petechiae on the chest,
wheezing and hypoxemia
 An air embolism may cause
palpitations,
weakness,
tachycardia, and hypoxia
RISK FACTORS
▪ Prolonged immobility
▪ Surgery
▪ Cancer and cancer treatment
▪ Hormonal medications
▪ Pregnancy
▪ Obesity
▪ Smoking
▪
▪
▪
▪
Heart disease
Genetic clotting disorders
Advance age
Chronic diseases
PATHOPHYSIOLOGY
o Trigger events – risk factor such as
prolonged
immobility,
surgery,
smoking, obesity, etc.
o Formation of thrombus – clot forms,
usually in the deep veins of the legs
(DVT)
o Clot dislodgement – part of the
thrombus breaks off (embolus) and
travels through the blood stream
o Embolus travels to the lungs –
embolus moves through the heart into
the pulmonary arteries. It lodges in the
pulmonary arteries and blocks blood
flow to the lung tissue
o Impaired gas exchange – obstruction
decreased blood flow to part of the
lungs. The affected area cannot
participate in gas exchange of oxygen
and carbon dioxide. This causes
increased ventilation-perfusion (V/Q)
mismatch
o Increased
pulmonary
artery
pressure – pulmonary hypertension
develops. Right heart strain as it works
harder to pump blood
o Clinical manifestations – signs and
symptoms such as shortness of
breath, chest pain and rapid heart rate
develops
o Possible complications – pulmonary
embolism can lead to complications
such as hypoxemia, right-sided heart
failure or even sudden death
DIAGNOSIS
✓ V Scan
✓ Pulmonary Angiography
✓ Angiography
✓ Electrocardiogram
✓ Chest X-Ray
✓ Arterial Blood Gas Analysis
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
✓ Pulmonary Artery Catheterization
✓ MRI
TREATMENT
The goal of treatment is to allow adequate
gas exchange until the obstruction can be
removed or resolves on its own.
• Oxygen Therapy – primary treatment
• In addition to oxygen therapy, these
treatment measures may be indicated:
o For patients with blood clots,
anticoagulation
with
low
molecular weight heparin, I.V.
unfractionated
heparin,
subcutaneous
unfractionated
heparin,
or
subcutaneous
fondaparinux (Arixtra) inhibits the
formation of more thrombi. It is
followed by warfarin (Coumadin)
for 3 to 6 months, depending on risk
factors.
o For
patients
with
massive
pulmonary embolism and shock
may need fibrinolytic therapy with
streptokinase (Streptase) or
alteplase (Acivase) to enhance
fibrinolysis of the pulmonary
emboli and remaining thrombi.
o Embolism from other sources may
necessitate other therapy to
dissolve the embolus, depending
on its nature. Septic embolism
calls for antibiotic therapy rather
than anticoagulation.
o If
hypotension
occurs,
vasopressors may be required to
maintain blood pressure.
• Surgery is indicated for patients who
cannot take anticoagulants because of
recent surgery or blood dyscrasia, or
who have recurrent emboli during
anticoagulant therapy.
o Surgery which should not be
performed without angiographic
evidence of pulmonary embolism,
consists
of
pulmonary
embolectomy,
pulmonary
endarterectomy, or insertion of
an inferior vena cava filter to filter
blood returning to the heart and
lungs
NURSING CONSIDERATIONS
▪ Monitor patient’s respiratory status,
oxygen saturation, and breath sounds
and administer oxygen therapy as
ordered. If breathing is severely
compromised, anticipate the need for
ET intubation and mechanical
ventilation.
▪ Monitor vital signs and heart rhythm to
detect arrhythmias secondary to
hypoxemia. Because many signs and
symptoms of pulmonary embolism
mimic those of MI. Obtain a 12-lead
ECG to rule out MI.
▪ Monitor PTT (partial prothrombin time)
regularly
for
patients
on
anticoagulation therapy. Effective
heparin therapy increases PTT to about
2 to 21/2 times normal.
▪ Keep antidotes for anticoagulants
readily available. These includes
protamine sulfate for heparin and
vitamin K for warfarin.
▪ During anticoagulant therapy, assess
your patient for epistaxis, petechiae,
and other signs of abnormal bleeding.
Apply pressure over venous puncture
sites for 5 to 10 minutes and 15 to 20
minutes for arterial sites, until bleeding
stops.
▪ Avoid giving aspirin and other
nonsteroidal anti-inflammatory drugs
(NSAIDs) if the patient is taking
anticoagulants.
▪ Encourage leg movement if the patient
is alert. Never massage the lower
extremities.
▪ Monitor nutritional intake to ensure
adequate calorie and fluid intake.
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
3. Acute Respiratory Distress Syndrome
• Is a life-threatening lung injury that
occurs when lung swelling causes fluid
to build up in the tiny elastic air sacs in
the lungs, and these air sacs is called
alveoli
• The fluid leaking into the air sacs keeps
the lungs from filling with enough air
CAUSES
• Sepsis
• Head, chest or other major injury
• Aspiration pneumonia
• Major trauma or burn
• Inhalation injury
• Drug overdose
• Other conditions and treatments
o
o
o
o
SIGNS AND SYMPTOMS
 Severe shortness of breath
 Rapid breathing (Tachypnea)
 Hypoxemia
 Cough
 Chest Pain or Discomfort
 Fatigue
RISK FACTORS
▪ Being older than 65
▪ Tobacco use
▪ Existing lung disease
▪ Infection
▪ Environment
▪ Lifestyle habits
▪ Family history and genetics
▪ Other medical conditions
injuries
-
o
or
PATHOPHYSIOLOGY
o Trigger events
- Risk factors such as infection,
tobacco use, existing lung disease,
etc.
o Inflammatory response
- The lung injury activates an intense
inflammatory response in the lungs
o Increased capillary permeability
Inflammation
causes
the
capillaries in the lungs to become
more permeable (leaky)
Alveolar edema
- The increased permeability allows
fluid to leak into the alveoli (air
sacs), causing pulmonary edema
Surfactant dysfunction
- The edema disrupts the function of
surfactant, a substance that helps
keep alveoli open.
Alveolar collapse
- Without
proper
surfactant
function, alveoli begin to collapse,
and the lungs become less
compliant (stiffer)
V/Q mismatch
- The collapsed alveoli lead to a
mismatch between ventilation (air
flow) and perfusion (blood flow) in
the lungs
Respiratory failure
- This
mismatch
results
in
hypoxemia (low blood oxygen) and
can progress to respiratory failure
DIAGNOSIS
✓ Chest X-Ray
• To know which parts of your lungs,
and how much of the lungs have
fluid in hem, and whether your
heart has gotten bigger.
✓ Blood Tests
• To measure oxygen levels in your
blood and determine the severity of
ARDS.
✓ ECG/EKG
• To measure your hearts electrical
activity
✓ CT Scan
• To give detailed information about
the lungs and heart.
• It combines X-ray images taken
from many directions and creates
cross-sectional views of internal
organs.
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
✓ Sputum Culture
• To find the cause of an infection.
STAGES
▪ Stage 1
- In this stage, fluid accumulates
interstitially within the pulmonary
spaces
- Involves dyspnea
- Respiratory and heart rate are
normal to high
- Diminished breath sounds
- Develops usually within the first
12hrs after the initial injury in
response to decreasing oxygen
levels in the blood
▪ Stage 2
- Called the late stage
- In this stage, interstitial fluid shifts
into the alveoli. This means that the
alveoli are now wet, and crackles
are apparent. Crackles in the lungs
are
one
of
the
primary
manifestations of late-stage ARDS.
- Marked by greater respiratory
distress
- Respiratory rate is high, may use
accessory muscles to breathe
- May appear restless, apprehensive,
and mentally sluggish or agitated
- Dry cough or frothy sputum
- Heart rate is elevated and the skin
is cool and clammy
- Symptoms at this stage are
sometimes incorrectly attributed
to trauma
▪ Stage 3
- Within this time, fluid has already
occupied the lungs, and pulmonary
fibrosis occurs
- Involves
obvious
respiratory
distress, with tachypnea, use of
accessory breathing muscles, and
decreased activity
- Patient exhibits tachycardia with
arrhythmias (usually premature
▪
ventricular contractions) and labile
blood pressure
- Skin is pale and cyanotic
- Auscultation
may
disclose
diminished breath sounds, basilar
crackles and ronchi
- This stage generally requires ET
intubation
and
mechanical
ventilation
Stage 4
- Oxygen is compromised at this
stage. The patient is hypoxic and is
acidic
- Decreasing respiratory and heart
rates
- Patient’s mental status nears loss
of consciousness.
- Skin is cool and cyanotic
- Breath sounds are severely
diminished to absent
TREATMENT
• The goal of therapy is to correct the
original cause and provide enough
oxygen
• Antibiotics and steroids may be
administered
• Diuretics may be needed to reduce
interstitial and pulmonary edema
o In later stages of ARDS, however,
vasopressors
are
usually
prescribed to maintain blood
pressure and blood supply to
critical tissues
• Respiratory
support
is
most
important
• Prone positioning may improve the
patient’s oxygenation
• Additional medications are generally
required
when intubation and
mechanical ventilation are instituted
• Sedatives, including opioids, and
sometimes, neuromuscular blocking
agents, minimize restlessness and
allow ventilation
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
NURSING CONSIDERATIONS
▪ Assess the patient’s respiratory status
at least every 2 hours or more often, if
indicated
▪ Administer oxygen as ordered. Monitor
FiO2 levels
▪ Auscultate
lugs
bilaterally
for
adventitious or diminished breath
sounds. Inspect the color and
character of sputum; clear, frothy
sputum indicates pulmonary edema.
To maintain PEEP, suction only as
needed.
▪ Check ventilator settings often. Assess
oxygen saturation continuously by
pulse oximetry or SvO2 by PA catheter.
Monitor serial ABG levels; document
ad report changes in oxygen saturation
as well as metabolic and respiratory
acidosis, and PaO2 changes.
▪ Monitor the patient’s level of
consciousness.
▪ Give sedatives as ordered to reduce
restlessness.
▪ Place the patient in a comfortable
position that maximizes air exchange
(semi-Fowlers or high Fowlers
position)
4. Acute Respiratory Failure
• Results when the lungs can’t
adequately oxygenate blood or
eliminate carbon dioxide
• In patients with normal lung tissue,
respiratory failure is indicated by a
PaCO2 above 50 mmHg and a PaO2
below 55 mmHg (these limits do not
apply to patients with chronic lung
disease such as COPD, who typically
have consistently high carbon dioxide
levels and low PaO2)
CAUSES
• Acute COPD exacerbation
• Aspiration pneumonia
• Obesiy
•
•
•
•
•
•
•
•
•
•
Pneumonia
Anesthesia
Pneumothorax
Atelectasis
Sleep apnea
Pulmonary edema
Pulmonary emboli
CNS disease
Head trauma
CNS depressants
SIGNS AND SYMPTOMS
 On inspection, note ashen skin
and cyanosis of the oral mucosa,
lips and nail beds. The patient may
use accessory muscles of
respiration to breathe and sit bolt
upright or slightly hunched over.
→ In later stages, as the patient’s
level of mentation decreases
due to hypoxemia, he may lie
down and appear confused
and disoriented.
→ If pneumothorax is present, you
may observe asymmetrical
chest movement. Tactile
fremitus may be present as
well.
 Look for these physical signs:
→ Tachypnea
→ Tachycardia
→ Cold, clammy skin and frank
diaphoresis are apparent,
especially around the forehead
and face
 Percussion
reveals
hyperresonance in patients with
COPD. In patients with atelectasis
or pneumonia, percussion sounds
are dull or flat.
 Lung auscultation usually reveals
diminished breath sounds
→ In patients with pneumothorax,
breath sounds are absent over
the affected lung tissue.
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
→ In other cases of respiratory
failure, adventitious breath
sounds such as wheezes and
rhonci, may be heard.
RISK FACTORS
▪ Age
▪ Lifestyle habits
▪ Environment
▪ Aspiration of gastric content
▪ Sepsis
▪ Upper or lower airway obstruction
▪ Other medical conditions
PATHOPHYSIOLOGY
o Underlying condition
- The process begins with underlying
condition
that
affects
the
respiratory system. This could be a
lung
disease,
chest
injury,
neurological disorder, or other
severe conditions
o Impaired Gas Exchange
- This condition leads to impaired
gas exchange in the lungs or
increases the work required to
breathe
o Hypoxemia/Hypercapnia
- As a result, the body experiences
hypoxemia (low level of oxygen)
and/or hypercapnia (high carbon
dioxide levels) in the blood
o Increased RR and depth
- The body responds by increasing
the rate and depth of breathing to
try to correct the gas imbalance
o Accessory Muscles Activations
- As breathing becomes more
difficult, accessory muscles of
respiration (like neck and chest
wall muscles) are recruited to help
o Increased O2 demand and CO2
production
- The increased work of breathing
raises the body’s oxygen demand
and carbon dioxide production
o Further Deterioration
- These further compromises gas
exchange, creating a vicious cycle
o Respiratory muscle fatigue and
failure
- Eventually, the respiratory muscles
become fatigued and can no longer
maintain adequate breathing,
leading to respiratory failure
DIAGNOSIS
✓ Arterial Blood Gas Analysis
✓ Chest X-Ray
✓ Electrocardiogram
✓ Pulse Oximetry
✓ White Blood Cells Count
✓ PA Catheterization
TREATMENT
• Restore adequate gas exchange –
primary goal of treatment
• Correct the underlying cause and
development of respiratory failure
• Oxygen therapy
o You may instruct the patient to try
pursed-lip breathing to prevent
alveolar collapse
• Reversal agents, such as a naloxone
(Narcan) are given if drug overdose is
suspected
• Bronchodilators are given
• Antibiotics are given
• Corticosteroids may be given
• Continuous IV solutions of positive
inotropic agents may be given to
increase
cardiac
output,
and
vasopressors may be given to induce
vasoconstriction to improve or
maintain blood pressure
• Diuretics may be given to reduce fluid
overload and edema
• Bypass the lungs. In recent studies
indicate
that
Extracorporeal
Membrane Oxygenation (ECMO) may
improve survival in patients with
severe acute respiratory failure.
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
NURSING CONSIDERATIONS
▪ Monitor patient’s respiratory status,
oxygen saturation, and breath sounds
and administer oxygen therapy as
ordered. If breathing is severely
compromised, anticipate the need for
ET intubation and mechanical
ventilation.
▪ Monitor vital signs and heart rhythm to
detect arrhythmias secondary to
hypoxemia. Because many signs and
symptoms of pulmonary embolism
mimic those of MI. Obtain a 12-lead
ECG to rule out MI.
▪ Monitor PTT (partial prothrombin time)
regularly
for
patients
on
anticoagulation therapy. Effective
heparin therapy increases PTT to about
2 to 21/2 times normal.
▪ Keep antidotes for anticoagulants
readily available. These includes
protamine sulfate for heparin and
vitamin K for warfarin.
▪ During anticoagulant therapy, assess
your patient for epistaxis, petechiae,
and other signs of abnormal bleeding.
Apply pressure over venous puncture
sites for 5 to 10 minutes and 15 to 20
minutes for arterial sites, until bleeding
stops.
▪ Avoid giving aspirin and other
nonsteroidal anti-inflammatory drugs
(NSAIDs) if the patient is taking
anticoagulants.
▪ Encourage leg movement if the patient
is alert. Never massage the lower
extremities.
▪ Monitor nutritional intake to ensure
adequate calorie and fluid intake.
5. Pneumonia
• Is a form of acute respiratory infection
that primarily affects the lung
parenchyma
• It occurs when the small air sacs in the
lungs responsible for gas exchange
•
•
(alveoli), become inflamed and filled
with fluid or pus
This accumulation of fluid disrupts
normal breathing and impair gas
exchange
Its severity can range from mild to lifethreatening, necessitating prompt
medical attention
CAUSES
Infectious agents may be bacterial, viral,
mycoplasmal,
rickettsial,
fungal,
protozoal, or mycobacterial
• Bacterial – the typical bacterial
which cause pneumonia are
Steptococcus
pneumoniae,
Staphylococcus aureus, Group A
Streptococcus,
Klebsiella
pneumoniae,
Haemophilus
influenzae, Moraxella catarhhalis,
anaerobes, and gram-negative
organisms
• Viral – the flu (influenza virus) and
the common cold (rhinovirus) are
the most common causes of viral
pneumonia in adults. Respiratory
syncytial virus (RSV) is the most
common cause of viral pneumonia
in young children. Many other
viruses can cause pneumonia,
including SARS-CoV-2, the virus
that causes COVID-19
• Mycoplasma
–
Mycoplasma
pneumoniae is the most common
and
well-known
cause
of
mycoplasma pneumonia. Other
mycoplasma species associated
with pneumonia are Mycoplasma
hominis, Ureaplasma urealyticum
and other atypical Mycoplasma
• Fungal – the most common fungal
pathogens
responsible
for
pneumonia include Aspergillus
species,
Candida
species,
Histoplasma
capsulatum,
Coccidioides
species,
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
•
•
Crytococcus
neoformans,
Pneumocystitis jirovecii
Protozoal – although less common,
some protozoal causes are
Pneumocystis
jirovecii,
Toxoplasma
gondii,
and
Leishmania species
Mycobacterium – lung infection
with M. tuberculosis usually
presents as a chronic consumptive
disease, but it can also cause acute
pnuemonia
TYPES OF PNEUMONIA BASED ON
LOCATION
1. Broncho Pneumonia – involving distal
airways and alveoli
2. Lobular Pneumonia – involving part of
a lobe
3. Lobar Pneumonia – involving an entire
lobe
CLASSIFICATION OF PNEUMONIA
1. Community-Acquired Pneumonia
- Acquired outside of a healthcare
facility
- The most commonly identified
pathogens are Streptococcus
pneumoniae,
Haemophilus
influenzae, Atypical bacteria (ie.
Chlamydia
pneumonia,
Mycoplasma
pneumonia,
Legionella species) and viruses
2. Hospital-Acquired Pneumonia
- This type of bacterial pneumonia
is acquired during a hospital stay.
It can be more serious than other
types as the bacteria involved may
be more resistant to antibiotics
- Also
called
nosocomial
pneumonia that occurs 48 hours
or more after hospital admission
and is not present at the
admission
time.
VentilatorAssociated Pneumonia (VAP)
represents a significant subset of
HAP occurring in intensive care
units (ICUs)
3. Aspiration Pneumonia
- Is an infection of the lungs caused
by inhaling saliva, food, liquid,
vomit, and even small foreign
objects
- It often results from impaired
swallowing or protective airway
reflexes
SIGNS AND SYMPTOMS
In Adults
 Cough (that may secrete greenish,
yellow, or even bloody mucus)
 Fever, sweating, and shaking chills
 Shortness of breath
 Rapid, shallow breathing
 Sharp or stabbing chest pain
 Loss of appetite
 Fatigue
 Nausea and vomiting
 Confusion or changes in mental
awareness (adults aged 65 and
older)
In Children
 Fever, chills
 Cough
 Fast breathing
 Breathing with grunting or wheezing
sounds
 Difficulty breathing
 Vomiting
 Chest pain
 Stomach pain
 Fatigue
 Loss of appetite (in older kids), or
poor feeding (infant)
RISK FACTORS
▪ Infants form birth to 2 years old
▪ People ages 65 years and older
▪ People with weakened immune
system
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
▪
▪
▪
▪
People who’ve been regularly
exposed to lung irritants
People with certain chronic
medical conditions such as:
o Asthma
o Liver disease
o Kidney disease
o Cystic fibrosis
o Diabetes
o COPD
o Sickle Cell Disease
People who’ve been recently or are
currently hospitalized, particularly
if they were or are on a ventilator
People who’ve had a brain disorder,
which can affect the ability to
swallow or cough
PATHOPHYSIOLOGY
o Causative Agent
- Infectious agents may be bacterial,
viral, mycoplasmal, rickettsial,
fungal, protozoal, or mycobacterial
o Entry of Pathogen
- Pathogen enters the lungs via
airways or aspirated material
o Infection of Alveoli
- Immune cells (white blood cells)
respond to fight infection. Alveoli
fill with fluid, pus, and cellular
debris, leading to the formation of
an abscess
o Abscess becomes encapsulated
- The body’s immune response
isolates
the
abscess
by
surrounding it with a thick, fibrous
wall, limiting its spread
o Impaired Gas Exchange
- Fluid-filled alveoli reduce oxygen
exchange. Oxygen levels in the
blood now decrease causing
hypoxemia.
Carbon
dioxide
removal is also affected
o Clinical Manifestations
- Signs and symptoms such as
cough, shortness of breath, and
rapid, shallow breathing develops
o Possible complications
- Pneumonia, if left untreated or
severe, can lead to complications
such as respiratory failure, sepsis,
lung abscess, or ARDS
DIAGNOSIS
✓ Chest X-Ray
• To confirm the infection and try to
identify the germ that is causing the
illness
✓ Sputum Specimen
• To identify the bacteria or fungi
causing the airways or lung
infection
✓ White Blood Cell Count
• To help diagnose and determine the
severity of pneumonia
✓ Arterial Blood Gas Analysis
• To evaluate pulmonary ventilation
and acid-base balance state by
determining the pressure value of
carbon dioxide and oxygen as well
as the pH value in blood
✓ Bronchoscopy/Transtracheal
Aspiration
• A technique for the collection of
bronchial secretions for laboratory
evaluation and culture
• This is useful when standard
sputum collection has not provided
adequate
material
or
determination of the infective
agent
✓ Pulse Oximetry
• Predict the severity of pneumonia
more accurately
• This can improve the correct
identification and treatment of
severe cases
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
TREATMENT
▪ Antibiotics treat bacterial pneumonia.
They can’t treat a virus but a provider
may prescribe them if you have a
bacterial infection at the same time as
a virus
▪ Antifungal
medications
treat
pneumonia caused by fungal infection
▪ Antiviral
medications.
Viral
pneumonia usually isn’t treated with
medication and can go away on its
own. A provider may prescribe
antivirals such as oseltamivir
(Tamiflu), zanamivir (Relenza) or
peramivir (Rapivab) to reduce how
long you’re sick and how sick you get
from a virus
▪ Oxygen therapy: If you’re not getting
enough oxygen, a provider may give
you extra oxygen through a tube in your
nose or a mask on your face
NURSING CONSIDERATIONS
▪ Adhere to standard precautions and
institute appropriate transmission
based precautions, depending on the
causative organism.
▪ Institute cardiac monitoring to detect
the development of arrhythmias
secondary to hypoxemia
▪ Reposition your client
▪ Obtain ordered diagnostic tests and
report results promptly
▪ Administer drug therapy as ordered
▪ Carefully monitor your patient’s intake
and output to allow early detection of
dehydration, fluid overload, and
accurate tracking of nutritional status
6. Pneumothorax
• Is an abnormal collection of air or gas
in the pleural space which may
interfere with normal breathing
causing the lungs to collapse
•
•
The amount of air trapped in the
intrapleural space determines the
degree of lung collapse
In some cases, venous return to the
heart is impeded, causing a lifethreatening condition called tension
pneumothorax
CLASSIFICATION OF PNEUMOTHORAX
1. Traumatic Pneumothorax
- Classified as open or closed (note
that an open [penetrating] wound
may cause closed pneumothorax)
2. Spontaneous Pneumothorax
- Also considered as closed, most
common in older patients with
COPD but can occur in young,
healthy patients as well
- Also classified as primary or
secondary pneumothorax
CAUSES
Traumatic
• Blunt trauma
• Penetrating trauma
• Iatrogenic causes
• Complications
from
surgical
procedures
Spontaneous
Primary
• Occurs without underlying lung
disease
Secondary
• Occurs with underlying lung
disease such as COPD, asthma,
cystic fibrosis, pneumonia, lung
cancer, and tuberculosis
SIGNS AND SYMPTOMS
 Sudden sharp pleuritic chest pain
 Chest movement
 Breathing and coughing exacerbate
pain
 Shortness of breath
 Hypotension and tachycardia
 Tracheal deviation to the opposite
side
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
 Distended jugular veins due to high
intrapleural pressure
 Fatigue
 Increased cardiovascular pressure
RISK FACTORS
▪ Lung disease
▪ Age
▪ Smoking
▪ Have
family
history
of
pneumothorax
▪ Have Marfan syndrome
▪ Have a tall, thin body type,
especially if you were assigned
male at birth
▪ Drug use, especially inhaled drugs
PATHOPHYSIOLOGY
o Trigger events
- The process begins with an injury to
the lung or chest wall. This could be
due to trauma, underlying lung
disease, or sometimes occur
spontaneously
o Air enters pleural space
- This injury creates a pathway to
enter the pleural space (the area
between the lung and chest wall).
Normally, this space has negative
pressure to keep the lungs
expanded
o Increased pressure
- As air continues to accumulate in
the pleural space, the pressure
within this area increases. This is
contrary to the normal negative
pressure that exists here
o Lung Collapse
- The increased pressure in the
pleural space overcomes the
elasticity of the lung tissue, causing
it to collapse inward away from the
chest wall. This is the defining
feature of a pneumothorax
o Decreased lung volume
- As the lung collapses, its volume
decreases significantly. The degree
of collapse can vary from partial to
complete, depending on the
severity of the pneumothorax
o Impaired gas exchange
- With less lung tissue actively
participating in respiration, gas
exchange becomes impaired.
Oxygen can’t efficiently enter the
bloodstream, and carbon dioxide
can’t be effectively removed
o Clinical manifestation
- The impaired gas exchange leads to
hypoxemia (low oxygen levels in the
blood) and potentially hypercapnia
(elevated carbon dioxide levels).
This imbalance can be detected on
blood gas analysis
o Possible complications
- In
severe
cases,
these
physiological
changes
can
progress to cause noticeable
respiratory distress. The increased
work of breathing and decreased
oxygenation can also put strain on
the heart, potentially leading to
cardiovascular complications.
DIAGNOSIS
✓ Arterial Blood Gas Analysis
✓ Chest X-Ray
✓ Electrocardiogram
TREATMENT
Open Traumatic Pneumothorax
▪ Surgical repair of affected tissues
▪ Chest
tube
placement
with
underwater seal
Spontaneous Pneumothorax
▪ Less than 30% lung collapse; bed rest,
monitoring oxygen and aspiration
▪ Greater than 30% lung collapse; chest
tube placement with underwater seal
or low-pressure suction
Tension Pneumothorax
▪ Immediate large-bore needle insertion
▪ Chest tube placement if necessary
▪ Analgesics for pain relief
NCM 118 – Critical Care
Concept: Responses to Altered Ventilatory Functions
Group Presenter: Group 1
NURSING CONSIDERATIONS
▪ Assess bilateral breath sounds every 12 hours and monitor oxygen saturation.
Perform ABG analysis as ordered
▪ Monitor hemodynamic parameters
and cardiac function due to risk of
arrhythmias from hypoxemia
▪ Watch for complications (pallor,
gasping, chest pain). Prepare for
intubation and mechanical ventilation
if needed
▪ Assist with chest tube insertion and
suction. Watch out for procedurerelated complications
▪ Check chest tube for proper drainage
and function
▪ Reposition patient to promote comfort
and drainage