RESPONSES TO ALTERED VENTILATORY FUNCTION
Anatomy and Physiology
Larynx
•
•
•
Located at the top of the trachea, houses the
vocal cords
Transition point between the upper and lower
airways
The larynx is composed of nine cartilage
segments.
o Largest segment: thyroid cartilage
Epiglottis
•
•
•
A flap of tissue that closes over the top of the
larynx when the patient swallows.
Protects the patient from aspiring food/fluid into
the lower airways
During defecation, especially if associated with
straining or constipation, inhaled air is
temporarily held in the lungs due to the closure
of the epiglottis (closure of epiglottis results to
abrupt increase in intrathoracic pressure)
*contraction of intrabdominal muscle = increased
intraabdominal and intrathoracic pressure (Valsalva
Maneuver)
Lower Airway- Trachea, Bronchi, Lungs
•
•
Begins with the trachea, divides at the carina
into the left and right mainstem bronchi (right
mainstem is shorter, wider, and more vertical
than the left mainstem)
Mainstem bronchi:
o Lobar bronchi
o Tertiary bronchi
o Terminal bronchioles: smallest airways
without an alveoli
 Respiratory bronchioles
 Alveolar ducts
 Alveoli: end point of the
respiratory tract where gas
exchange takes place
• Contains macrophages
that perform phagocytic
role
•
Circulation
Oxygen depleted blood enters the lungs from the
pulmonary artery of the right ventricle  Flows
through the main pulmonary arteries into the smaller
vessels of the pleural cavities  Main bronchi,
through the arterioles  Capillary networks in the
alveoli
Gas Exchange: oxygen and carbon dioxide effusion
Takes place in the alveoli  pulmonary capillaries 
Oxygenated blood flow through progressively larger
vessels  enters the main pulmonary veins  left
atrium
Pulmonary Circulation
Right and left pulmonary arteries carry deoxygenated
blood  these arteries divide to form distal branches
called arterioles  terminate as a concentrated
capillary network in the alveoli and alveolar sac,
where gas exchange occurs  venules (end
branches of the pulmonary veins) collect oxygenated
blood from the capillaries  transport it to larger
vessels, which carry it to the pulmonary veins
pulmonary veins enter the left side of the heart,
where oxygenated blood is distributed throughout the
body.
Right ventricle  pulmonary artery arterioles 
capillary in the alveoli and alveolar sac  gas
exchange  venules  larger vessels  pulmonary
veins  left atrium
Pleura
•
•
•
•
Lungs and Lobes
•
The right lung is larger and has three lobes
(upper, middle, and lower)
The left lung is smaller and has only two lobes
(upper and lower)
Each lung is wrapped in a lining called the
visceral pleura
All areas of the thoracic cavity that come in
contact with the lungs are lined with the Parietal
Pleura
A small amount of pleura fluid fills the are
between the two layers of the pleura to allows
the layers to slide smoothly over each other as
the chest expands and contracts.
The parietal pleura also contain nerve ending
that transmit pain signals when inflammation
occurs.
Alveoli
•
Gas exchange units of the lungs
•
•
Adult: 300 million alveoli
It consists of Type I and Type II epithelial cells:
o Type 1 cells form the alveolar walls,
through which gas exchange occurs.
o Type II cells produce surfactant,
(lipoprotein/ lipid type substance) that
coats the alveoli.
 decreases surface tension and
protects the alveoli
 during inspiration, surfactant
allows alveoli to expand
 during expiration, surfactant
prevents alveolar collapse.
Bony Thorax
•
•
•
•
•
Clavicles
Sternum
Scapula
12 set of ribs
12 thoracic vertebrae
Ribs
•
•
•
•
Made of bone and cartilage and allow the chest
to expand and contract during each breath.
All ribs are attached to vertebrae.
The first seven ribs also are attached directly to
the sternum
The eighth, ninth, and tenth ribs are attached to
the ribs above them
•
The eleventh and twelfth ribs are called floating
ribs
Accessory Inspiratory Muscles
*Primary muscle used in breathing: diaphragm
•
•
•
•
Inspiratory muscle relaxes, causing the lungs to
recoil to their resting size and position.
The diaphragm ascends
Positive alveolar pressure is maintained
Air moves out of the lungs.
Respiration:
•
effective respiration requires gas exchange in
the lungs (external respiration) and in the tissues
(internal respiration)
Oxygen to Lungs
3 External Respiration Processes:
1. Ventilation: gas distribution into and out of the
pulmonary airways
2. Pulmonary perfusion: blood flow from right
side of the heart through pulmonary circulation
and into left side of heart
3. Diffusion: gas movement from an area of
greater to lesser concentration through
semipermeable membrane
Various pressures in respiration:
•
•
•
•
Airway pressure: pressure in the conduction
airways
Intrapleural pressure: pressure in the narrow
space bet. Visceral and parietal pleura
Intra alveolar pressure: pressure inside alveoli
Intrathoracic pressure: pressure within entire
thoracic cavity
Oxygen to Tissue
•
Internal respiration occurs only through diffusion
when the RBC’s release O2 and absorb CO2.
VENTILATION AND PERFUSION
Ineffective gas exchange causes 3 outcomes:
At Rest
•
•
•
Inspiratory muscles relax
Atmospheric pressure is maintained in the
tracheobronchial tree
No air movement occurs
Inhalation
•
•
•
•
Inspiratory muscle contract
The diaphragm descends
Negative alveolar pressure is maintained
Air moves into the lungs
Exhalation
1. Shunting
• reduced causes oxygenated blood to
move from right side of heart to systemic
circulation
• may result from physical defect that
allows unoxygenated blood to bypass
functioning alveoli
• may also result when airway obstruction
prevents O2 from reaching adequately
perfused area in lungs.
• Common causes
 ARDS (acute respiratory
distress syndrome)
 Atelectasis
 Pneumonia
 Pulmonary edema.
be measures as partial pressure of arterial oxygen
(PaO2) in blood  After oxyhemoglobin is created,
RBC’s carry it via circulatory system to tissues
throughout the body  internal respiration occurs by
cellular diffusion when RBC’s release oxygen and
absorb CO2 produced by cellular metabolism.  RBC’s
then transport CO2 back to lungs for removal during
expiration.
ACID-BASE BALANCE
2. Dead Space Ventilation
• This is the air not included in gas
exchange.
• Reduced perfusion to lung unit
• Occurs when alveoli do not have
adequate blood supply for gas exchange
to occur
o Pulmonary Emboli and
Pulmonary Infarction
• Part of the tidal volume that does not
participate in the alveolar gas exchange
•
•
•
*CO2 is 20x more soluble than O2*
o it dissolves in the blood, where most of
its forms into bicarbonate (a base) and
smaller amounts form into carbonic acid
The lungs control bicarbonate levels by
converting bicarbonate to carbon dioxide and
water for excretion.
In response, the medulla sends signals to lungs
to adjust rate and depth of ventilation  controls
acid base balance by adjusting the amount of
carbon dioxide that’s lost.
Metabolic Alkalosis
•
•
•
•
•
Results from excess bicarbonate retention
Increased exhalation of CO2
Rate and depth of ventilation decrease to retain
CO2
Increased carbonic acid levels
Hyperventilation
o Causes respiratory alkalosis
Metabolic Acidosis
•
3. Silent Unit
• Combination of Shunting and DeadSpace Ventilation.
• Occurs when little to no
perfusion/ventilation
• Pneumothorax and severe ARDS
•
•
Lungs increase rate and depth of ventilation to
exhale excess CO2
Hypoventilation
CO2 retention
o Causes respiratory acidosis
Physical Assessment
History
•
•
•
Ask short open-ended question
Conduct interview is short several sessions
Ask family to provide information
Respiratory disorders may be caused or exacerbated by
obesity, smoking, and workplace conditions
Previous Health Status
OXYGEN TRANSPORT
Most oxygen collected in lungs binds with hemoglobin to
form oxyhemoglobin  small portion of it dissolves in
plasma  portion of oxygen that dissolves in plasma can
•
•
•
•
•
•
Smoking habit
Exposure to 2nd hand smoking
Allergies
Previous surgeries
Respiratory diseases: Pneumonia and TB
Current immunizations: flu shot or
pneumococcal vaccine.
•
Family History
•
•
Family history of cancer, sickle cell anemia,
heart disease, chronic illness; asthma or
emphysema
Determine if patient lives with anyone who has
infectious disease: TB or influenza
Lifestyle Patterns
•
•
•
•
o
Respiratory equipment, O2, nebulizers and et
Sputum production
•
•
•
Workplaces can be causes for lung diseases
such as coal mining, construction work and etc.
Ask about patient’s home community and other
environmental factors
Interpersonal relationships, stress management
Sex habits, use of drugs w/c may be connected
with immunodeficiency syndrome-related
pulmonary disorders.
A pulmonary illness which often results in the
production of sputum
If a patient produces sputum, ask them to
estimate the amount produces in teaspoons or
any common measurement.
Questions:
o What is the color and consistency of
your sputum?
o Has it changed recently? If so, how?
o Do you often cough up blood? If so, how
much and how often?
Yellow, green,
brown
Yellow
Current Health Status
•
•
Rust colored
(yellow mixed
with blood)
Mucoid, viscid,
blood streaked
Persistent slightly
blood streaked
Ask why patient is seeking care because many
respiratory diseases are chronic
Ask how patient’s latest acute episodes occurred
and what relief measures were used.
Chronic complaints:
Large amount of
clotted blood
Cough
•
•
•
A frequent respiratory symptom with varying
significance
External agents, inflammation of the respiratory
mucosa or pressure may stimulate cough
specifically:
o Smoke
o Allergies
o Heartburn
o Asthma
o Certain medication (ACE inhibitors, Beta
blockers)
Questions to be asked:
o At what time of the day do you cough
the most?
o IS the cough productive? Has it changed
recently? If so, how?
o What relieves the cough? What makes it
worse?
Sleep disturbance
•
•
May be related to obstructive sleep apnea or any
other sleeping disorder requiring additional
evaluation
If the patient complains of being drowsy or
irritable in daytime, ask these questions:
o How many hours of continuous sleep do
you get each night?
o DO you wake up often during the night?
Does your family complain about you
snoring or restlessness?
bacterial infection
many eosinophils,
signifies allergy
May signify TB
Sign of viral infection
Present in patient
with carcinoma
present in patient
with pulmonary
infarct
Wheezing
•
Questions to ask:
o When does wheezing occur?
o What makes you wheeze?
o Do you wheeze loudly enough for others
to hear it?
o What helps stop your wheezing?
Dyspnea
•
•
•
•
Commonly seen in patients with pulmonary or
cardiac compromise
Information about onset of symptoms gives
clues about source and duration of problem
Assess patient’s SOB to rate usual level of
dyspnea
Then ask CURRENT level of dyspnea
GRADING: Ask patient to describe how various
activities affect breathing objectively and briefly.
Grade 0 not tr public by breathlessness except with
strenuous exercise
Grade 1 trouble by shortness of breath when
hurrying on a level path or walking up a
slight hill
Grade 2 walks more slowly on level path because
of breathlessness than people of the same
age or has to stop to breathe when
walking on a level path at his own pace
Grade 3
stops to breathe after walking about 100
yards on a level path
Grade 4 too breathless to leave the house or
breathless when dressing or undressing
• The nurse asks these questions:
o Does the dyspnea occur when the
patient is lying flat?
o Does the dyspnea awaken the patient at
night? paroxysmal nocturnal dyspnea
o Does the dyspnea occur only with
exertion?
*paroxysmal nocturnal dyspnea and orthopnea often
signify heart failure, but may occur in variety of
pulmonary disorders
Physical Assessment:
•
•
•
•
•
•
Orthopnea
•
•
•
•
Refers to SOB when lying down
Patient sleeps with upper body elevated
Ask patient how many pillows are usually used
A patient who uses three pillows is indicated to
have “3 pillow orthopnea
Chest pain
•
•
•
•
Chest pain due to respiratory problem is usually
result of pleural inflammation, inflammation of
the costochondral junctions, or soreness of
chest muscles because of coughing
May be result of indigestion
Less common causes:
o Rib or vertebral fractures
Questions:
o Where is the pain?
o What does it feel like?
o Is it sharp, stabbing, burning or aching?
o Does it move to another area?
o How long does it last?
o What causes it?
o What makes it better?
Begin after taking the patient’s history
If the patient is in respiratory distress, establish
the priorities of nursing assessment (progress
from most critical to less critical factors, e.g.
ABCs)
Examine the back first using IPPA (Inspection,
Palpation, Percussion, Auscultation)
Always compare one side with the other; then
examine the front of the chest using the same
sequence
The patient can lie back when you examine the
front of their chest if that is more comfortable for
them
Before you begin the PE, make sure the room is
well-lit and warm; introduce yourself to the
patient and explain why you are there
Inspection
•
This involves checking for presence or absence
of several factors:
o Cyanosis: bluish discoloration
o Labored breathing
o Anterior-posterior diameter of the chest
o Chest deformities
o Patient posture
o Position of Trachea
o RR
o Respiratory effort
o Duration of inspiration vs expiration
o Thoracic expansion
o Patient’s extremities
Common Abnormalities
- Occurs as result of
Barrel chest
overinflation w/c
increases anteroposterior
diameter
- Occurs with aging and is
a hallmark sign of
emphysema and COPD
Funnel chest (Pectus
Excavatum)
Pigeon chest (Pectus
Carinatum)
- Occur as a result of the
anterior displacement of
the sternum, which also
increases the
anteroposterior diameter.
- May occur with rickets,
Marfan syndrome, or
sever kyphoscoliosis
- Occurs when there is
depression in the lower
portion of the sternum
- May compress heart
and great vessels,
resulting in murmurs.
- Rickets or Marfan
Syndrome
Thoracic Kyphoscoliosis
APNEA
HYPERPNEA
KUSSMAUL
CHEYNE- STOKES
BIOT’S RESPIRATION
- The patient’s spine
curves to one side and
the vertebrae are rotated.
- Because the rotation
distorts lung tissue, it may
be more difficult to
assess respiratory status
- Absence of breathing
- Periods of apnea may
be short and occur
sporadically, such as
Cheyne Stokes
respirations or other
abnormal respiratory
patterns.
- May be life-threatening
if periods of apnea last
long enough and should
be addressed
immediately.
- Increased rate and
depth
- Usually occurs with
extreme exercise, fear
or anxiety
- Causes
hyperventilation orders
of CNS, overdose of
drug salicylate or sever
anxiety
- Rapid, deep and
labored
- Occurs with metabolic
acidosis, especially
when associated with
diabetic ketoacidosis
- Respiratory system
tries to lower the CO2
level in the blood and
restore it to normal pH
- Regular pattern
characterized by
alternating periods of
deep, rapid breathing
followed by periods of
apnea
- May result from sever
CHF, drug overdose
increases ICP or renal
failure.
- May be noted in
elderly persons, during
sleep not related to any
disease process.
- Irregular pattern
characterized by
varying depth and rate
of respirations followed
by periods of apnea.
- May be seen with
meningitis or severe
brain damage.
Palpation
Anterior
Thorax
Sequence of Palpation
Posterior
Thorax
Normal
Findings
Chest wall should be smooth, warm,
and dry.
- Feels like a puffed rice cereal
crackling under the skin.
Crepitus
- Indicates air is leaking from
airways or lungs.
*If a patient has a chest tube, you may find a small
amount of subcutaneous air around the insertion site.
*If the patient has no chest tube, or area of crepitus is
getting larger, ALERT PRACTICIONER RIGHT AWAY.
Guide in assessing some types of chest pain:
• Painful costochondral joints are typically
located at the midclavicular line or next to the
sternum.
• A rib or vertebral fracture is quite painful over
the fracture.
• Sore muscles may result from protracted
coughing.
• A collapsed lung can cause pain in addition to
dyspnea.
Decreased at level of
diaphragm
- Pneumothorax
- Emphysema
- Respiratory depression
- Diaphragm paralysis
- Atelectasis
- Obesity
- Ascites
Percussion
Percuss the chest to:
•
•
Tactile Fremitus
•
•
•
•
Palpate for tactile fremitus (palpable vibrations
caused by the transmission of air through the
bronchopulmonary system.
Fremitus is decreased:
o Over areas where pleural fluid collects
o When patient speaks softly
o With pneumothorax, atelectasis, and
emphysema.
Fremitus increased normally over the large
bronchial tubes and abnormally over areas in
which alveoli are filled with fluid or exudates
(PNEUMONIA)
Find boundaries of the lungs
Determine whether the lungs are filled with air,
fluid, or solid material
Evaluate the distance the diaphragm travels
between the patient’s inhalation and exhalation.
Evaluate chest wall symmetry and expansion:
•
•
•
Place your hands on the front of the chest wall
with your thumbs touching each other at the
second intercostal space.
As the patient inhales deeply, watch your
thumbs. (They should separate simultaneously
and equally to a distance several centimeters
away from the sternum)
Repeat the measurement at the fifth intercostal
space. You may take the same measurement on
the back of the chest near the 10th rib.
Chest Expansion Warning Signs
- Pleural effusion
Expand Asymmetrically
- Atelectasis
- Pneumonia
Auscultation
•
•
•
As air moves through the bronchi, it creates
sound waves that travel to the chest wall.
The sound produces by breathing changes as
air moves from larger to smaller airways.
Sounds also change if they pass through fluid,
mucus, or narrowed airways.
•
Auscultation sites are the same as percussion
sites.
o Listen to a full cycle of inspiration and
expiration at each site, using the
diaphragm of the stethoscope.
o Ask the patient to breathe through his
mouth if it doesn’t cause discomfort;
nose breathing alters the pitch of breath
sounds.
Normal Breath Sounds
- Heard over trachea
- Sounds harsh and
discontinuous.
Tracheal breath sounds
- Occurs when patient
inhales or exhales
- Usually heard next to
the trachea just above or
below clavicle
- Sounds loud, highBronchial breath sounds
pitched, and
discontinuous.
- Loudest when patient
exhales
- Are medium-pitched and
continuous
- Best heard over the
Bronchovesicular sounds upper third of the sternum
and between the
scapulae when the
patient inhales or exhales
- Heard over the rest of
the lungs, are soft and
low-pitched
Vesicular sounds
- Prolonged during
inhalation and shortened
during exhalation.
Vocal Fremitus
•
•
Is the sound produces by chest vibrations as the
patient speaks
Abnormal transmission of voice sounds can
occur over consolidated areas because sound
travels well through fluid.
3 Common Abnormal Voice Sounds
Bronchopho Egopho Whispered
ny
ny
Pectoriloquy
Instruction Ask the
Ask the
Ask the
s
patient to
patient
patient to
say “99” or
to say
whisper,
“blue
“E”
“1,2,3”
moon”.
Over
normal
tissue
the words
sound
muffled
sound is
muffled.
Over
consolidat
ed areas:
words
sound
unusually
loud.
it
sounds
like
letter A.
Numbers
sound loud
and clear.
Adventitious sounds
•
are abnormal no matter where you hear them
from lungs
Crackles
soft, high-pitched,
discontinuous popping
sounds that occur during
inspiration (May also be
heard on expiration)
Wheezes
- Usually heard on
expiration but may be
heard on inspiration
- Associated with
changes in the airway
diameter
Friction Rubs
Numbers are
indistinguisha
ble.
Diagnostic Assessment
Course crackles
- Discontinuous popping
sounds heard in early
inspiration; 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,
and bronchitis pleural
fluid
Sonorous wheezes
(Ronchi)
- Deep, low-pitched
rumbling sounds heard
primarily during
expiration; caused by air
moving through narrows
tracheobronchial
passages
- Associated with
secretions or tumor
Sibilant Wheezes
- Continuous, musical,
high-pitched, whistle-like
sounds heard during
inspiration and expiration
caused by air passing
through narrows or
partially obstructed
airways
- Bronchospasm, asthma,
build-up of secretions
Pleural friction rub
- Harsh, cracking 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 fluid.
Non-invasive
OXIMETRY
A noninvasive technique that measures the
arterial oxyhemoglobin saturation (SpO2) of
arterial blood.
A sensor, or probe, uses a beam of red and
infrared light that travels through tissue and
blood vessels
Oxygen saturation is determined by the
amount of each light absorbed; nonoxygenated
hemoglobin absorbs more red light, and
oxygenated hemoglobin absorbs more
infrared light
Sensors are available for use on a finger, a toe,
a foot (on infants), an earlobe, forehead, and the
bridge of the nose
A range of 95% to 100% is considered normal
For patients with chronic lung disease, a level of
88% to 92% may be considered within normal
limits
o Chronic and severe COVID
Unreliable when vasoconstriction medications
or IV dyes are used and when in shock, cardiac
arrest, or severe anemia.
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Invasive
ABG
•
•
•
•
•
•
Nursing Considerations
Assess for the presence of health problems
that may impact oxygenation.
Assess the patient’s respiratory rate and
depth and mental status, skin temperature
and color, and CRT.
Assess the quality of the pulse proximal to the
sensor application site.
Assess for edema of the sensor site.
If absent or weak signal: check vital signs and
patient condition; check connections and
circulation to site.
If extremity is cold, cover with a warm blanket
and/or use another site.
If a bright light (sunlight or fluorescent light) is
suspected of causing equipment malfunction,
turn off light or cover the probe with a dry
washcloth (bright light can interfere with
operation of light sensors and cause an
unreliable report).
Excessive motion of the sensor probe site,
such as with extremity tremors or shivering,
can also interfere with obtaining an accurate
reading.
•
Assess the ability of the lungs to provide
adequate oxygen and remove carbon dioxide
and the ability of the kidneys to reabsorb or
excrete bicarbonate ions to maintain normal
body pH.
Measurements of blood pH and of arterial
oxygen and carbon dioxide tensions are
obtained when managing patients with
respiratory problems and adjusting oxygen
therapy as needed
Obtained through an arterial puncture at the
radial, brachial, or femoral artery, or through an
indwelling arterial catheter
•
•
•
Nursing Considerations
In most critical care units, a doctor, respiratory
therapist, or specially trained critical care
nurse draws ABG samples, usually from an
arterial line if the patient has one.
The most common site is the radial artery, but
the brachial or femoral arteries can be used.
When a radial artery is used, an Allen’s test is
done before drawing the sample to determine
whether the ulnar artery can provide adequate
circulation to the hand, in case the radial
artery is damaged.
After obtaining the sample, apply pressure to
the puncture site for 5 minutes and tape a
gauze pad firmly in place. Regularly monitor
the site for bleeding and check the arm for
signs of complications, such as swelling,
discoloration, pain, numbness, and tingling.
Note whether the patient is breathing room air
or oxygen. If the patient is on oxygen via
nasal cannula document the number of
liters. If the patient is receiving oxygen by
mask or mechanical ventilation, document
the fraction of inspired oxygen (Fio2).
Examples of conditions that can interfere with
test results are failure to properly heparinize
the syringe before drawing a blood sample or
exposing the sample to air.
o Venous blood in the sample may
lower Pao2 levels and elevate Paco2
levels.
o Make sure you remove all air
bubbles in the sample syringe
because air bubbles also alter results.
Make sure the sample of arterial blood is kept
cold and delivered as soon as possible to the
laboratory for analysis. Some chemical
reactions that alter findings continue to take
place after the blood is drawn; rapid cooling
and analysis of the sample minimizes this.
PULMONARY CAPILLARY WEDGE PRESSUREPLEURAL FLUID ANALYSIS
•
•
Used to assess left ventricular filling, represent
left atrial pressure, and assess mitral valve
function
Measured by inserting a balloon-tipped, multilumen catheter (Swan-Ganz catheter) into a
•
central vein and advancing the catheter into a
branch of the pulmonary artery
The balloon is then inflated, which occludes the
branch of the pulmonary artery and then
provides a pressure reading that is equivalent to
the pressure of the left atrium
Indications:
•
•
•
•
•
Differentiate 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
Nursing Considerations
Site Care and Catheter Safety
• A sterile dressing is placed over the insertion
site and the catheter is taped in place. The
insertion site should be assessed for infection
and the dressing changed every 72 hours and
PRN.
• The placement of the catheter, stated in
centimeters, should be documented, and
assessed every shift.
• The integrity of the sterile sleeve must be
maintained so the catheter can be advanced
or pulled back without contamination.
• The catheter tubing should be labeled and all
the connections secure. The balloon should
always be deflated, and the syringe closed
and locked unless you are taking a PCWP
measurement.
Patient Activity and Positioning
• Many physicians allow stable patients who
have PA catheters, such as post CABG
patients, to get out of bed and sit. The nurse
must position the patient in a manner that
avoids dislodging the catheter.
• Proper positioning during hemodynamic
readings will ensure accuracy.
Dysrhythmia Prevention
• Continuous EKG monitoring is essential while
the PA catheter is in place.
• Do not advance the catheter unless the
balloon is inflated.
• Antiarrhythmic medications should be readily
available to treat lethal dysrhythmias.
Monitoring Hemodynamic Values for Response to
Treatments
• The purpose of the PA catheter is to assist
healthcare team members in assessing the
patient’s condition and response to treatment.
Therefore, accurate documentation of values
before and after treatment changes is
necessary.
PULMONARY ANGIOGRAPHY
•
An X-ray of the blood vessels that supply the
LUNGS
Indications:
•
•
•
•
•
•
Blood clot (pulmonary embolism)
Bulging blood vessel (aneurysm)
An artery abnormally connected to a vein
(arteriovenous malformation)
Heart and blood vessel problems present at birth
Foreign body in a blood vessel
Narrowing of a blood vessel wall (stenosis)
Nursing Considerations
Before
• Stop taking certain medicines before the
procedure, if instructed by HCP.
• NPO.
• Have someone drive you home from the
hospital.
• Empty the bladder before the procedure.
During
• Remove jewelry or other objects.
• Supine on the X-ray table.
• An intravenous (IV) line will be put in your arm
or hand.
• Small sticky pads (electrodes) will be put on
the chest. (They will connect with wires to a
machine (ECG) that records the electrical
activity of your heart. Your heart rate, blood
pressure, and breathing will be watched
during the procedure).
• Hair at the site of the catheter insertion in the
groin or arm may be trimmed. The skin will be
cleaned. A numbing medicine (local
anesthetic) will be injected into the area.
• A thin, flexible tube (catheter) will be put in the
groin or arm. The catheter will be gently
guided through the vein to the right side of the
heart. Fluoroscopy may be used during this
process to help get the catheter to the right
place.
• Contrast dye will be injected into your IV line.
You may feel some effects when this is done.
These effects may include a flushing
sensation, a salty or metallic taste in the
mouth, a brief headache, nausea, or vomiting.
These effects usually last for a few moments.
Tell the radiologist if you feel any trouble
breathing, sweating, numbness, or heart
palpitations.
• After the contrast dye is injected, a series of
X-ray images will be taken.
• The groin or arm catheter will be removed.
Pressure will be applied over the area to stop
bleeding.
• A dressing will be applied to the site. A small,
soft weight may be placed over the site for a
After
•
•
•
period of time. This is to prevent more
bleeding or a hematoma at the site.
•
lie flat in a recovery room for 1-2 hours.
Monitor the V/S.
Monitor the groin or arm puncture site for
bleeding. You will need to keep your leg or
arm straight.
• Give pain medication as needed.
At home
• Patients can go back to their normal diet and
activities if instructed by the HCP
• Increase oral fluids to flush out the contrast
dye from the body
• Refrain from doing strenuous activity for a few
days.
• No hot bath or shower for a day or two.
•
•
*Check the puncture site in your groin or arm several
times a day. Check for bleeding, pain, swelling,
change in color, or change in temperature. A small
bruise is normal. A small amount of blood is also
normal.
•
When to call HCP?
•
•
•
•
Fever of 100.4°F (38°C) or higher
Redness or swelling of the groin or arm site
A lot of blood at the groin or arm site
Pain, coolness, numbness, tingling, or loss of
function in your arm or leg
VENTILATION- PERFUSION (V/Q) SCAN
•
•
•
•
•
Indications:
o Evaluate V mismatch
o Detect pulmonary emboli
o Evaluate pulmonary function, especially
in patients with marginal lung reserves.
Although less reliable than pulmonary
angiography, V scanning carries fewer risks.
Two parts:
o During ventilation portion of the test,
the patient inhales the contrast medium
gas; ventilation patterns and adequacy
of ventilation are noted on the scan.
o During the perfusion scan, the contrast
medium is injected I.V. and the
pulmonary blood flow to the lungs is
visualized.
V scans aren’t commonly used for patients on
mechanical ventilators because the ventilation
portion of the test is difficult to perform.
(Pulmonary angiography is the preferred test for
critically ill patient with a suspected pulmonary embolus)
Nursing Considerations
Explain the test to the patient and his family,
telling them who perform the test and where
it’s done.
Like pulmonary angiography, a V scan
requires the injection of a contrast medium.
Confirm that the patient doesn’t have an
allergy to the contrast material.
Explain to the patient that the test has two
parts.
o During the ventilation portion, a
mask is placed over his mouth and
nose and the patient breathes in the
contrast medium gas mixed with air
while the scanner takes pictures of
the lungs.
o For the perfusion portion, the patient
is placed in a supine position on a
movable table as the contrast medium
is injected into the IV line while the
scanner again takes pictures of the
lungs.
After the procedure, maintain bed rest as
ordered and monitor the patient’s vital signs,
oxygen saturation levels, and heart rhythm.
Monitor for adverse reactions to the contrast
medium, which may include restlessness,
tachypnea and respiratory distress,
tachycardia, urticaria, and nausea and
vomiting. Keep emergency equipment nearby
in case of a reaction.
CAPNOGRAPHY
•
•
Delivers a more comprehensive measurement
that is displayed in both graphical (waveform)
and numerical form
For this reason, capnography is currently the
most widely recommended method for
monitoring EtCO2
EtCO2 (35-45 mmHg)
- Level of carbon dioxide that is released at the end of
an exhaled breath
- Its level reflects the adequacy with which carbon
dioxide (CO2) is carried in the blood back to the lungs
and exhaled
- Abnormal Values:
*EtCO2 <35 mmHg = Hyperventilation/ Hypocapnia
*EtCO2 >45 mmHg = Hypoventilation/Hypercapnia
Indications:
•
•
•
Verification of artificial airway placement
Assessment of pulmonary circulation and
respiratory status
Optimization of mechanical ventilation
Nursing Consideration
If EtCO2 is 45 to 50 mmHg (Hypoventilation)
• Attempt to stimulate and arouse the patient. If
patient is immediately aroused and breathing
normally, monitor every 15 minutes for 1 hour.
• Assess vital signs for decompensation (02
sat, BP, HR, RR, and LOC).
• Check patient for normal signs of ventilation
and assess for hypoventilation via
assessment of RR, quality, and depth.
• Assess pain, level of sedation, and consider
decreasing narcotic dose and/or frequency.
• Reposition the device if necessary.
If EtCO2 remains >45 mmHg despite interventions
• Contact physician.
If EtCO2 is >50 mmHg or greater
• If it does not return to normal within 5
minutes, call Rapid Response Team and
notify MD immediately to report patient
condition.
• Consider obtaining ABG (RT or RRT can also
be consulted during this process).
• If the patient does not immediately arouse,
evaluate the appropriateness of administering
Narcan to partially OR completely reverse
sedation.
• Patients may be referred to an intensive care
unit when nursing staff has concerns about
possible respiratory compromise.
If RR falls below 7 per minute, whether EtCO2 is
normal or not
• Evaluate patient for sleep apnea. Sleep
apnea patients are encouraged to remain
non-supine.
• Patients can potentially have a normal EtCO2
and low respiratory rate. In these instances, it
is appropriate to monitor, contact respiratory
therapy or RRT if there is any question
regarding accuracy of EtCO2 measurement.
Documentation
•
•
•
During acute pain management, monitor and
document EtCO2 every 1 hour until satisfactory
pain control is achieved.
Once patient comfort is achieved, monitor and
document EtCO2 (and displayed respiratory
rate) every four (4) hours, and more frequently
as patient condition warrants.
Some conditions may suggest a need for
increased monitoring and documentation.
Examples of conditions that require increased
monitoring are:
o Additional boluses
o Continuous IV
o Risk factors for complications
associated with narcotic administration
such as advanced age or obesity
Pre-existing conditions including
allergies or sleep apnea
o Current medication use
Document all interventions performed as a result
of changes in ETC02 and respiratory rate.
EtCO2 values should be trended, monitored,
and documented more frequently if values fall
outside the normal range of 35 to 45mmHg.
All reports to physicians, respiratory therapy or
RRT must be documented.
o
•
•
•
Discontinuation
•
EtCO2 monitoring may be discontinued when:
o PCA pump is discontinued
o 6 hours after continuous epidural
infusion is discontinued
o IV narcotics discontinued.
Nursing Diagnosis
•
•
•
•
•
Ineffective Airway Clearance related to
excessive and tenacious secretions.
Impaired Gas Exchange related to Activity
Intolerance
Anxiety related to Breathlessness
Powerlessness related to feelings of loss of
control.
High Risk for Ineffective Therapeutic Regimen
Management related to Lack of Knowledge
ALTERATIONS IN VENTILATION
•
ACUTE AND CHRONIC OBSTRUCTIVE PULMONARY
DISEASE
•
•
•
•
results from emphysema, chronic bronchitis,
asthma, or a combination of these disorders
Most common chronic lung disease
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.
Exacerbations of COPD that necessitate
hospitalization are caused by various factors that
place additional demand on the respiratory
system, such infection, heart failure, and
exposure to allergens.
•
•
Causes
o
o
o
o
o
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)
How it Happens
•
•
•
•
•
Patients with COPD have decreased gas
exchange ability due to alveolar damage caused
by exposure to smoke or chemical irritants over
a long period.
Smoke inhalation impairs ciliary action and
macrophage function and causes inflammation
in the airways and increased mucus production.
Early inflammatory changes may be reversed if
the patient stops smoking before lung disease
becomes extensive.
In chronic bronchitis, mucus plugs and
narrowed airways cause air trapping. Air
trapping also occurs with asthma and
emphysema.
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.
Here’s what happens in air trapping:
o Hyperinflation of the alveoli occurs on
expiration.
o On inspiration, airways enlarge, allowing
air to pass beyond the obstruction
o On expiration, airways narrow and
prevent gas flow.
As the alveolar walls are destroyed, they’re no
longer separate, but coalesce into large air
pockets that put additional pressure on
surrounding tissues. This affects the lung’s blood
supply as well because it increases the pressure
needed to push blood through the lungs.
o This form of high blood pressure is
known as pulmonary hypertension.
Eventually, the high workload overwhelms the
right side of the heart and hypertrophy and rightsided failure (cor pulmonale) result. Patients
commonly have supraventricular arrhythmias
such as atrial fibrillation, which increase the
danger of thrombus formation.
Because gas exchange is impaired, (PaCO2
above 40 mmHg) - Increased rate and increased
depth (hypercapnia) becomes the norm for these
patients.
o The respiratory center of the brain,
which stimulates breathing when Paco2
rises, becomes dependent instead on
low Pao2.
o This is an important consideration when
oxygen is given for hypoxemia.
What to Look for
The patient most likely has a history of COPD and may
be able to identify the precipitating cause (exposure to
allergen, for example)
•
•
•
•
•
•
The patient is also likely to have tachycardia
and an irregular heart rhythm as well as
tachypnea and dyspnea on exertion.
Fever may be present in the case of infection.
When you inspect the chest, you may notice that
the anterolateral diameter is increased (barrel
chest), and the patient may appear generally
cachectic.
He may be coughing, with copious sputum
production, if he has chronic bronchitis, or he
may be wheezing.
When you listen to breath sounds, listen for a
prolonged expiratory phase, perhaps crackles
or rhonchi, and generally some decreased air
movement.
Patients with COPD have abnormal breath
sounds to begin with, and it may be hard to tell
at first what’s baseline and what’s newly
abnormal. As you listen over several hours or
days abnormal breath sounds eventually
become apparent.
Diagnosis
Stable COPD patients exhibit these abnormal diagnostic
test results, which may be considered their baseline
values:
Pulmonary function test: increased residual
volume, decreased vital capacity and amount of
air exhaled in the first second of expiration.
Chest X-ray: increased bronchovascular
markings and overaeration of the lungs.
o In advanced disease, the diaphragm is
flattened and bronchovascular markings
may be reduced.
ABG analysis may show reduced Pao2 and
normal or increased Paco2.
o In advanced COPD, it isn’t uncommon
for baseline Paco2 levels to be 50 mm
Hg or higher.
ECG may show atrial arrhythmias and, in
advanced disease, right ventricular hypertrophy.
Blood count reveals elevated hemoglobin
levels.
•
•
•
•
•
If respiratory failure is imminent, 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 I.V.) 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.
•
•
•
•
•
•
•
•
Diagnosis (Critical Situation)
During an exacerbation, diagnostic tests may yield these
additional results:
ABG analysis shows PaO2 below the patient’s
baseline
o PaCO2 may be low, normal, or high,
depending on the patient’s baseline
Chest X-ray may show infiltrates if pneumonia is
present
ECG may show sinus tachycardia with
supraventricular, ventricular arrythmias and,
sometimes, ventricular arrhythmias
•
•
•
•
•
•
•
•
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.
o First, respiratory support is given to
avoid respiratory failure and cardiac
arrest.
o Equally important is treatment
addressing the underlying cause of
the exacerbation.
Your patient may receive oxygen
supplementation. Care must be taken when
the baseline PaCO2 level is high.
o The patient’s respiratory center relies
on low oxygen levels to stimulate
breathing.
Administer controlled oxygen therapy by
monitoring ABG levels and patient
assessments.
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 red flags, as is
lethargy.
Monitor vital signs and heart rhythm and
observe for arrhythmias, which may indicate
hypoxemia, right-sided heart failure, or an
adverse effect of bronchodilator use.
Obtain laboratory tests as ordered and report
results promptly.
Offer emotional 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.
•
•
•
•
•
PULMONARY EMBOLISM
•
•
is an obstruction of the pulmonary arterial bed
Occurs when a 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)
Causes:
•
Most common source of pulmonary embolism is
a dislodged thrombus that originated in the deep
•
veins of the leg 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 a foreign object, such as a
needle, catheter part, or talc (from drugs
intended for oral administration that are injected
I.V. by addicts)
•
•
Risk Factors:
•
•
•
•
•
•
Predisposing disorders, including lung
disorders, cardiac disorders (valvular disease
and arrhythmias, such as atrial fibrillation),
infection, diabetes, history of thromboembolism,
sickle cell disease, and polycythemia
Venous stasis in those who are on prolonged
bed rest, immobile, obese, burn victims, older
than age 40, or in orthopedic casts
Venous injury caused by surgery (especially of
the legs, pelvis, abdomen, and thorax), longbone or pelvic fractures, I.V. drug abuse, I.V.
therapy, or manipulation or disconnection of
central lines
Increased blood coagulability resulting from
cancer, high estrogen hormonal contraceptive
use, or pregnancy.
Fat embolism risk factors include
osteomyelitis, long-bone fractures, burns, and
adipose tissue or liver trauma
Risk factors for air embolism include
cardiopulmonary bypass, hemodialysis, deep
vein catheter insertion, and endoscopy
Pathophysiology:
A thrombus forms as a result of trauma to the vascular
wall, venous statis, or hypercoagulability of the blood 
further trauma, clot dissolution, sudden muscle spasm,
pressure change, or a change in peripheral blood flow
can cause the thrombus to loosen or fragment  after it
is dislodge, the thrombus becomes an embolus and
floats through the venous system to the right side of the
heart and on the pulmonary vasculature, where it lodges
in a small vessel and occludes blood flow beyond the
occlusion  a V mismatch results in hypoxemia that is
commonly irreversible
What to look for
The patient’s history may reveal a predisposing condition
or another risk factor for pulmonary embolism
Signs and Symptoms
Other symptoms depend 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
pulmonary artery bed may cause shortness of
breath, anxiety, chest pain, S3 or S4 heart
sound, and crackles on auscultation.
An embolism that occludes more than 50% of
the artery bed may cause a sense of impending
doom, dyspnea, tachycardia, confusion, rightsided heart failure, hypotension, and pulseless
electrical activity
A fat embolism may produce no symptoms for
up to 24 hours
o 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
Diagnosis
•
•
•
•
•
•
•
•
V scan: demonstrates a mismatch, indicating
abnormal perfusion
Pulmonary angiography: may reveal a
pulmonary vessel filling defect or an abrupt
vessel ending, indicating pulmonary embolism.
Angiography: is the definitive test for
pulmonary embolus.
ECG: results distinguish pulmonary embolism
from myocardial infarction (MI) and show right
axis deviation; right bundle-branch block; tall,
peaked P waves; depressed ST segments; Twave inversions; and supraventricular
arrhythmias
Chest X-ray is used to rule out other pulmonary
diseases, but it is inconclusive within 1 to 2
hours of the embolic event; it may also indicate
areas of atelectasis, an elevated diaphragm,
pleural effusion, a prominent pulmonary artery
and, occasionally, the characteristic wedgeshaped infiltrate that suggests pulmonary
infarction
ABG analysis reveals hypoxemia and possibly
hypocapnia due to tachypnea
PA catheterization may reveal an elevated
central venous pressure and PAP and a normal
PAWP
MRI is used to identify the embolus or blood flow
changes indicating an embolus
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 Patients with massive pulmonary
embolism and shock may need
fibrinolytic therapy with
streptokinase (Streptase) or alteplase
(Activase) 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, for example, calls
for antibiotic therapy rather than
anticoagulation.
o If hypotension occurs, vasopressors
may be required to maintain BP.
Surgery is indicated for patients who cannot
take anticoagulants because of recent surgery
or blood dyscrasia, or who have recurrent
emboli during anticoagulant therapy.
Surgery, which should not be performed
without angiographic evidence of pulmonary
embolism
o pulmonary embolectomy
o pulmonary endarterectomy, or
o insertion of an inferior vena cava filter
to filter blood returning to the heart
and lungs.
Nursing Consideration
Monitor the 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.
Obtain laboratory tests as ordered and report
results promptly.
Monitor PTT 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.
o These include protamine sulfate for
heparin and vitamin K for warfarin.
Blood products may be needed in
case of life-threatening bleeding.
During anticoagulant therapy, assess your
patient for epistaxis, petechiae, and other
signs of abnormal bleeding.
o 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.
Promote your patient’s comfort by
repositioning him often and administering
analgesics for pain.
Encourage leg movement if the patient is
alert. Never massage the lower extremities.
Monitor nutritional intake to ensure adequate
calorie and fluid intake.
Explain all procedures to the patient.
•
•
•
•
•
•
ACUTE RESPIRATORY DISTRESS SYNDROME
(ARDS)
•
•
•
•
A type of pulmonary edema not related to heart
failure
May follow direct or indirect lung injury and can
quickly lead to acute respiratory failure
3 hallmark features:
1. Bilateral patchy infiltrates on chest Xray
2. No signs or symptoms of heart failure
3. No improvement in PaO2 despite increasing
oxygen delivery
Prognosis for patients with ARDS varies
depending on the cause and the patient’s age
and health status before developing ARDS
Causes:
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Sepsis
Lung injury from trauma such as chest contusion
Pulmonary embolism (air, fat, amniotic fluid, or
thrombus)
Shock (any type)
Disseminated intravascular coagulation
Pancreatitis
Massive blood transfusions
Burns
Cardiopulmonary bypass
Drug overdose
Aspiration of stomach contents
Pneumonitis
Near drowning
Pneumonia
Inhalation of noxious gases (ammonia, chlorine)
Pathophysiology:
In ARDS, the tissues lining the alveoli and the pulmonary
capillaries are injured, either directly by aspiration of
gastric contents or inhalation of noxious gases, or
indirectly, by chemical mediators released into the
bloodstream in response to systemic disease.
Inflammation follows injury
The injured tissues release cytokines and other
molecules that cause inflammation as white blood cells
(WBCs) collect at the site and swelling occurs. The
tissues become more permeable to fluid and proteins,
and the hydrostatic pressure gradient between the
alveoli and the capillaries is reversed 
Impaired exchange
Proteins and fluid begin to move from the capillaries into
the alveoli. When this happens, gas exchange is
impaired in the affected alveoli. As the process
continues, the alveoli collapse (atelectasis), and gas
exchange becomes impossible.
•
Auscultation may disclose diminished breath
sounds, basilar crackles, and rhonchi
This stage generally requires ET intubation and
mechanical ventilation
4. Stage IV
• 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
What to Look for
ARDS occurs in 4 stages, each with these typical signs
and symptoms:
1. Stage I: develops usually within 12 hours after
the initial injury in response to decreasing
oxygen level in the blood.
• Involves dyspnea
• Respiratory and heart rates are normal to
high
• diminished breath sounds, particularly when
the patient is tachypneic
• Develops usually within the first _____ hours
after the initial injury in response to
decreasing oxygen levels in the blood
2. Stage II
• Marked by greater respiratory distress
• RR is high, may use accessory muscles to
breathe
• may appear restless, apprehensive, and
mentally sluggish or agitated
•
dry cough or frothy sputum
• HR is elevated and the skin is cool and
clammy
• Lung auscultation may reveal basilar
crackles
Diagnosis
•
•
Symptoms at this stage are sometimes incorrectly
attributed to trauma
3. Stage III
• Involves obvious respiratory distress, with
tachypnea, use of accessory breathing
muscles, and decreased acuity
• Patient exhibits tachycardia with arrhythmias
(usually premature ventricular contractions)
and labile blood pressure
• Skin is pale and cyanotic
•
ABG analysis initially shows decreased PaO2
despite oxygen supplementation. Because of
tachypnea, PaCO2 is also decreased, causing
an increase in blood pH (respiratory alkalosis).
o As ARDS worsens, PaCO2 increases
and pH decreases as the patient
becomes acidotic.
o This is worsened by metabolic acidosis
caused by a lack of oxygen that forces
the body to switch to anaerobic
metabolism.
Chest Xray may be normal.
o Basilar infiltrates begin to appear in
about 24 hours.
o In later stages, lung fields have a ground
glass appearance and, eventually, as
fluid fills the alveoli, white patches
appear.
o These may eventually cover both lung
fields entirely in later stages of ARDS.
PA Catheterization may be used to identify the
cause of pulmonary edema through pulmonary
artery wedge pressure (PAWP) measurement.
PAWP is 19 mm Hg or lower in patients with
ARDS.
A differential diagnosis must be done to rule
out cardiogenic pulmonary edema, pulmonary
vasculitis, and diffuse pulmonary hemorrhage.
o Tests used to determine the causative
agent may include sputum analysis,
blood cultures, toxicology tests, and
serum amylase levels (to rule out
pancreatitis).
•
•
•
•
Treatment
The goal of therapy: correct the original cause,
provide enough oxygen
• Antibiotics and steroids may be
administered
• Diuretics may be needed to reduce interstitial
and pulmonary edema. 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
•
•
•
•
•
•
•
•
•
Pharmacology
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
Nursing Considerations
ARDS requires careful monitoring and supportive
care.
• Assess the patient’s respiratory status at least
every 2 hours or more often, if indicated.
• Administer oxygen as ordered. Monitor FiO2
levels.
• Auscultate lungs 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 and report
changes in oxygen saturation as well as
metabolic and respiratory acidosis and PaO2
changes.
Monitor vital signs. Institute cardiac
monitoring and observe for arrhythmias that
may result from hypoxemia, acid–base
disturbances, or electrolyte imbalance.
Monitor the patient’s LOC.
Be alert for signs of treatment-induced
complications (arrhythmias, disseminated
intravascular coagulation, GI bleeding,
infection, malnutrition, paralytic ileus,
pneumothorax, pulmonary fibrosis, renal
failure, thrombocytopenia, and tracheal
stenosis).
Be alert for the development of multiple organ
dysfunction syndrome. Monitor renal, GI, and
neurologic system function.
Give sedatives as ordered to reduce
restlessness. Administer sedatives and
analgesics at regular intervals if the patient on
mechanical ventilator is receiving
neuromuscular blocking agents.
Provide routine eye care and instill artificial
tears to prevent corneal drying and abrasion
from the loss of the blink reflex in
mechanically ventilated patients.
Administer anti-infective agents as ordered
Place the patient in a comfortable position
that maximizes air exchange (semi-Fowler’s
or high Fowler’s position).
Allow for periods of rest.
If your patient has a PA catheter in place,
know the desired PAWP level and check
readings as indicated. Watch for decreased
SvO2. Because PEEP may reduce cardiac
output, check for hypotension, tachycardia,
and decreased urine output.
Evaluate the patient’s serum electrolyte levels
frequently as ordered. Measure urine output
hourly to ensure adequate renal function.
Monitor intake and output. Weigh the patient
daily.
Record caloric intake. Administer tube
feedings and parenteral nutrition as ordered.
Perform passive ROM exercises _________
Provide meticulous skin care to prevent
breakdown like ulcerations.
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 mm
Hg and a PaO2 below 55 mmHg
o (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:
Conditions that cause alveolar hypoventilation, V
mismatch, or right-to-left shunting can lead to respiratory
failure. These include:
•
•
•
•
•
•
•
•
•
•
•
•
Acute COPD exacerbation
Aspiration pneumonia
pneumonia
obesity
Anesthesia
Pneumothorax
Atelectasis
Sleep apnea
Pulmonary edema
Pulmonary emboli
CNS disease (such as myasthenia gravis,
Guillain Barre syndrome, and amyotrophic
lateral sclerosis)
Head trauma
CNS depressants
Pathophysiology:
As tissue hypoxemia develops, tissues resort to
anaerobic metabolism, which results in a buildup of lactic
acid, a by-product of anaerobic metabolism, and thus
metabolic acidosis. This takes longer to develop than
respiratory acidosis, but the result is increasing acidity of
the blood, which interferes with normal metabolism of all
body systems.
Signs and Symptoms
•
•
•
•
Respiratory failure results from impaired gas exchange.
Any condition associated with V mismatch caused by
alveolar hypoventilation or intrapulmonary shunting can
lead to acute respiratory failure if left untreated.
Poor ventilation
Alveolar hypoventilation occurs when respiratory effort is
diminished or when airway obstruction leads to
decreased airflow in the alveoli. This can occur with
neuromuscular diseases or conditions that interfere with
respiration.
Poor oxygenation
Blood that passes through the lungs but is not
oxygenated due to alveolar hypoventilation is known as
shunted blood. Blood flow in the lung can be impaired by
obstruction or hypovolemia. Obstruction is the most
acute form and is most commonly caused by pulmonary
emboli.) 
The rise and fall of partial pressures
When PaCO2 levels rise above normal, and pH drops
below normal, respiratory acidosis develops. PaO2
levels also drop below normal in acute respiratory
failure. Other organ systems respond with compensatory
responses. For example, the sympathetic nervous
system triggers vasoconstriction, increases peripheral
resistance, and increases the heart rate. 
Lots of lactic acid
•
The patient’s history may reveal an underlying
respiratory condition or an acute process leading
to respiratory failure (such as asphyxia, drug
overdose, or trauma)
There is usually little time to collect a thorough
history and the patient typically cannot give the
history himself (family members or medical
records may be the main sources of such
information)
Physical assessment findings vary, depending
on the duration of the condition. Initially, the
body responds with secretion of epinephrine.
Eventually, as the patient’s condition worsens,
epinephrine secretion has less effect.
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. He may be agitated or highly anxious. 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 of respiratory
failure:
o Tachypnea: >20 cpm
o Tachycardia: may not be seen in
patients with heart disease who are
taking medications that prevent
tachycardia. Pulse may be strong and
rapid initially, but thready and irregular in
later stages.
o Cold, clammy skin and frank diaphoresis
are apparent, especially around the
forehead and face.
o Percussion reveals hyperresonance in
patients with COPD. In patients with
atelectasis or pneumonia, percussion
sounds are dull or flat.
o Lung auscultation usually reveals
diminished breath sounds.
o In patients with pneumothorax, breath
sounds are absent over the affected
lung tissue. In other cases of respiratory
failure, adventitious breath sounds, such
as wheezes in asthma and rhonchi in
bronchitis, may be heard.
•
•
Diagnosis
ABG: indicates early respiratory failure - PaO2
is low (usually less than 60 mmHg) and PaCO2
is high (greater than 45 mmHg) and the HCO3
level is normal. The pH is also low.
Chest X-ray is used to identify pulmonary
diseases, such as emphysema, atelectasis,
pneumothorax, infiltrates, and effusions.
Electrocardiogram (ECG) can demonstrate
arrhythmias, commonly found with cor
pulmonale and myocardial hypoxia
Pulse Oximetry reveals a decreasing Spo2
level
WBC count aids detection of an underlying
infection.
o Blood cultures, sputum cultures, and
Gram stain may also be used to identify
pathogens.
Abnormally low hemoglobin and hematocrit
levels signal blood loss indicating decrease
oxygen carrying capacity.
PA catheterization is used to distinguish
pulmonary causes from cardiovascular causes
of acute respiratory failure, and to monitor the
effects of treatment. SvO2 levels less than 50%
indicate impaired tissue oxygenation.
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Treatment
Primary goal - restore adequate gas
exchange.
Secondary goal - correct the underlying
cause and development of respiratory failure.
Oxygen therapy. Initiated immediately to
optimize oxygenation of pulmonary blood.
You may instruct the patient to try pursed lip
breathing to prevent alveolar collapse.
If the patent can’t breathe adequately on his
own, ET intubation and mechanical
ventilation are instituted.
High frequency or pressure ventilation is
sometimes used to force airways open.
o NIV
Pharmacology
Reversal agents, such a naloxone (Narcan),
are given if drug overdose is suspected
Bronchodilators to open airways
Antibiotics for infection
Corticosteroids to reduce inflammation
Continuous I.V. solutions of positive
inotropic agents may be given to increase
cardiac output
Vasopressors may be given to induce
vasoconstriction to improve or maintain blood
pressure.
Fluids are generally restricted to reduce
cardiac workload and edema.
Diuretics may be given to reduce fluid
overload and edema
Bypass the lungs
Recent studies indicate that Extracorporeal
Membrane Oxygenation (ECMO) may improve
survival in patients with severe acute respiratory
failure.
•
•
•
•
•
•
•
Nursing Consideration
Assess the patient’s respiratory status at least
every 2 hours or more often, as indicated.
Observe for a positive response to oxygen
therapy.
Position the patient for optimal breathing effort
when he isn’t intubated. Put the call bell within
easy reach to reassure the patient and
prevent unnecessary exertion when he needs
to call the nurse.
Maintain a normothermic environment to
reduce the patient’s oxygen demand.
Monitor vital signs, heart rhythm, and fluid
intake and output, including daily weights, to
identify fluid overload (from I.V. fluids and
medications) or impending dehydration (from
aggressive diuretic therapy).
After intubation, auscultate the lungs
(accidental intubation of the esophagus or the
mainstem bronchus).
o Risk for aspiration (broken teeth,
nosebleeds, and vagal reflexes
causing bradycardia, arrhythmias,
and hypotension)
Do not suction too often without identifying the
underlying cause of an equipment alarm.
Use strict sterile technique during
suctioning.
o Watch oximetry and capnography
values because these are important
indicators of changes in the patient’s
condition.
Note the amount and quality of lung
secretions and look for changes in the
patient’s status. Use sterile technique.
Check cuff pressure on the ET tube to prevent
erosion from an overinflated cuff. Normal cuff
pressure is about 20 mm Hg.
Provide a means of communication for
patients who are intubated and alert.
Explain all procedures to the patient and his
family.
•
•
•
•
•
PNEUMONIA
•
•
•
•
•
An acute infection of the lung parenchyma
that commonly impairs gas exchange
More than 3 million cases of pneumonia are
diagnosed yearly in the United States
The prognosis is good for patients with
pneumonia who are otherwise healthy
Debilitated patients are at much greater risk;
bacterial pneumonia is a leading cause of
death among such individuals
Pneumonia occurs in both sexes and in all
ages, but older adults are at greater risk for
developing it
Causes
•
•
•
Causes:
•
•
Infectious agents may be
o Bacterial
o Viral
o Mycoplasmal
o Rickettsial
o Fungal
o Protozoal
o Mycobacterial
Types of pneumonia based on location of the
infection include:
Broncho pneumonia – involving distal
airways and alveoli
o Lobular pneumonia – involving part of
a lobe
o Lobar pneumonia – involving an entire
lobe
Pneumonia may be classified as communityacquired, hospital-acquired (nosocomial), or
aspiration pneumonia
o Community acquired – occurs in the
community setting or within the first 48
hours of admission to a health care
facility because of community exposure
o Nosocomial Pneumonia – hospitalacquired pneumonia refers to the
development of pneumonia 48 hours
after admission to a health care facility.
 Example: development of
pneumonia after ET intubation
and placement on a ventilator
o Aspiration pneumonia – occur in the
community or health care facility setting
o
o
Primary Pneumonia results from inhalation of
pathogen, such as bacteria or virus.
o Examples are pneumococcal and viral
pneumonia.
Secondary Pneumonia may follow initial lung
damage from a noxious chemical or other insult
(superinfection) or may result from
hematogenous spread of bacteria from a distant
area.
Aspiration Pneumonia results from inhalation
of foreign matter, such as vomitus or food
particles, into the bronchi.
o It is more common in elderly and
debilitated patients; those receive NG
tube feedings, and those with an
impaired gag reflex, poor oral hygiene,
or decreased LOC.
•
•
•
more commonly attacks bronchiolar epithelial
cells, causing interstitial inflammation and
desquamation.
It then spreads to the alveoli.
In advanced infection, a hyaline membrane may
form, further compromising gas exchange.
Aspiration Pneumonia
•
triggers similar inflammatory changes in the
affected area, and also inactivates surfactant
over a large area, leading to alveolar collapse.
Acidic gastric contents may directly damage the
airways and alveoli, and small particles may
cause obstruction. The resulting inflammation
makes the lungs susceptible to secondary
bacterial pneumonia.
Signs and Symptoms:
•
•
•
Pleuritic chest pain, cough, shortness of breath,
and fever
The patient’s cough may be dry or very
productive; the sputum may be creamy yellow,
green, or rust-colored
In advanced cases of all types of pneumonia,
o Percussion: dullness over the affected
area of the lung
o Auscultation: crackles, wheezes, or
rhonchi over the affected areas as well
as decreased breath sounds and
decreased tactile fremitus.
Diagnosis
•
•
•
Pathophysiology:
•
Bacterial Pneumonia
•
•
•
an infection initially triggers alveolar
inflammation and edema.
Capillaries become engorged with blood,
causing stasis.
As the alveolocapillary membrane breaks down,
the alveoli fill with blood and inflammatory
exudates, resulting in atelectasis.
Viral Pneumonia
•
•
Chest Xray disclose infiltrates, confirming the
diagnosis
Sputum specimen for Gram stain and culture
and sensitivity testing may reveal
inflammatory cells as well as bacterial cells
WBC count and differential may indicate the
presence and type of infection.
o Elevated polymorphonucleocytes may
indicate bacterial infection; in viral or
mycoplasmal pneumonia, though, WBC
count may not be elevated at all.
ABG analysis may be done to determine the
extent of respiratory compromise due to alveolar
inflammation
Bronchoscopy or transtracheal aspiration
allows the collection of material for cultures to
identify the specific infectious organism.
o Pleural fluid may also be sampled for
culture and Gram stain.
Pulse oximetry may show a reduced oxygen
saturation level.
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Treatment
Antimicrobial therapy is started
immediately. The type of antibiotic used
depends on the infectious agent.
The patient may receive oxygen
supplementation, including ET intubation
and mechanical ventilation in severe cases
when respiratory arrest is imminent.
In severe cases, PEEP may be needed to
prevent alveolar collapse.
Other treatment measures include:
o Bronchodilator therapy
o Antitussives for cough
o High-calorie diet and adequate fluid
intake
o Bed rest
o Analgesics for pleuritic chest pain
Nursing Considerations
Maintain a patent airway and oxygenation.
Place the patient in fowler’s position and give
supplemental oxygen as ordered.
Monitor oxygen saturation and ABG levels as
ordered.
Assess respiratory status at least every 2
hours. Monitor for crackles, wheezes, or
rhonchi.
Encourage coughing and deep breathing.
In severe cases, anticipate the need for ET
intubation and mechanical ventilation.
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 patient to maximize chest
expansion, allow rest, and reduce discomfort
and anxiety.
Obtain ordered diagnostic tests and report
results promptly.
Administer drug therapy as ordered.
Carefully monitor your patient’s intake and
output to allow early identification of
dehydration, fluid overload, and accurate
tracking of nutritional status.
Determine if the patient is a candidate for the
pneumococcal and influenza vaccines.
PNEUMOTHORAX
•
•
An accumulation of air in the pleural cavity
that leads to partial or complete lung 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 life-threatening condition
called tension pneumothorax
•
Can be classified as either traumatic or
spontaneous
o Traumatic Pneumothorax – classified
as open or closed (note than an open
[penetrating] wound may cause closed
pneumothorax)
o Spontaneous Pneumothorax – also
considered as closed, most common in
older patients with COPD but can occur
in young, healthy patients as well
Causes:
Traumatic Pneumothorax
•
•
Open Pneumothorax:
o Penetrating chest injury (stab or gunshot
wound)
o Insertion of a central venous catheter
o Chest surgery
o Transbronchial biopsy
o Thoracentesis or closed pleural biopsy
Closed Pneumothorax:
o Blunt chest trauma
o Air leakage from ruptured blebs
o Rupture resulting from barotrauma
caused high intrathoracic pressures
during mechanical ventilation
o Tubercular or cancerous lesions that
erode into the pleural space
o Interstitial lung disease such as
eosinophilic granuloma
Spontaneous Pneumothorax
o
Rupture of a subpleural bleb (a small
thin-walled air-containing spaces) at the
surface of a lung
Tension Pneumothorax
o
o
o
o
o
Penetrating chest wound treated with an
airtight dressing
Fractured ribs
Mechanical ventilation
High-level of PEEP that causes alveolar
blebs to rupture
Chest tube occlusion or malfunction
Pathophysiology:
Traumatic Pneumothorax
Open pneumothorax- atmospheric air flows directly into
the pleural cavity under negative pressure  air
pressure in the pleural cavity becomes positive, the lung
on the affected side collapses, causing decreased total
lung capacity  develops a V imbalance that leads to
hypoxia.
Closed pneumothorax occurs when an opening is
created between the intrapleural space and the
parenchyma of the lung  air enters the pleural space
from within the lung, causing increased pleural pressure
and preventing lung expansion during inspiration.
•
•
Spontaneous Pneumothorax
Rupture of a subpleural bleb  air leakage into the
pleural spaces, which causes the lung to collapse 
hypoxia results from decreased total lung capacity, vital
capacity, and lung compliance
Tension Pneumothorax
Results when air in the pleural space is under higher
pressure than air in the adjacent lung  air enters the
pleural space from the site of pleural rupture, which acts
as a one-way valve (thus, air enters the pleural space
on inspiration but cannot escape as the rupture site
closes on expiration)  more air enters with each
inspiration and air pressure begins to exceed barometric
pressure  the air pushes against the recoiled lung,
causing atelectasis, and pushes against the
mediastinum, compressing and displacing the heart and
great vessels  the mediastinum eventually shifts away
from the affected side, affecting venous return, and
putting ever greater pressure on the heart, great vessels,
trachea, and contralateral lung.
Without immediate treatment, this emergency can
rapidly become fatal.
Signs and Symptoms
Assessment depends on the severity of the
pneumothorax.
Spontaneous pneumothorax
that releases a small amount of air into the pleural space
may cause no signs and symptoms.
Tension pneumothorax
causes the most severe respiratory.
•
•
•
sudden, sharp, pleuritic chest pain, chest
movement, breathing, and coughing exacerbate
the pain, shortness of breath.
Inspection: asymmetric chest wall movement
with over expansion and rigidity on the affected
side,
o skin may be cool and clammy and
cyanotic,
Palpation: crackling beneath the skin
(subcutaneous emphysema) and decreased
vocal fremitus, hyperresonance on the affected
side,
Auscultation: decreased or absent breath
sounds on the affected side, and vital signs may
follow the pattern of respiratory distress seen
with respiratory failure.
Also causes:
o Hypotension and tachycardia
o Tracheal deviation to the opposite side
o Distended jugular veins due to high
intrapleural pressure, mediastinal shift,
and increased cardiovascular pressure
Diagnosis
•
•
•
Chest X-rays reveal air in the pleural space and
a mediastinal shift that confirm pneumothorax
ABG reveals hypoxemia, usually with elevated
PaCO2 and normal bicarbonate ion levels in the
early stages
ECG may reveal decreased QRS amplitude,
precordial T-wave inversion, rightward shift of
frontal QRS axis, and small precordial R voltage
Treatment
depends on the cause and severity
Open or traumatic pneumothorax
• surgical repair of affected tissues, followed by
chest tube placement with an underwater
seal.
Spontaneous pneumothorax
• with less than 30% lung collapse, no signs of
increased pleural pressure, and no dyspnea
or indications of physiologic compromise, may
be corrected with:
o Bed rest to preserve energy
o Monitoring of vital signs to detect
physiologic compromise
o Oxygen administration to improve
hypoxia
o Aspiration of air from the intrapleural
space with a large bore needle
attached to a syringe to restore
negative pressure within the pleural
space
• Greater than 30% lung collapse may
necessitate other measures, such as:
o Placing a chest tube in the second or
third intercostal space in the
midclavicular line to re-expand the
lung by restoring negative intrapleural
pressure
o Connecting the chest tube to an
underwater seal or low-pressure
suction to re-expand the lung
Tension pneumothorax
• Immediate large-bore needle insertion into the
pleural space through the second intercostal
space to re-expand the lung, followed by
insertion of a chest tube if large amounts of
air escape through the needle after insertion
• Analgesics to promote comfort and encourage
deep breathing and coughing
or fluid has drained out, usually within a few days.
Occasionally special medicines are given through a
chest tube when the fluid or air does not resolve within a
few days.
PEEP
PEEP is a mode of therapy used in conjunction with
mechanical ventilation. At the end of mechanical or
spontaneous exhalation, PEEP maintains the patient's
airway pressure above the atmospheric level by exerting
pressure that opposes passive emptying of the lung.
This pressure is typically achieved by maintaining a
positive pressure flow at the end of exhalation.
Applying PEEP increases alveolar pressure and alveolar
volume. The increased lung volume increases the
surface area by reopening and stabilizing collapsed or
unstable alveoli. This splinting, or propping open, of the
alveoli with positive pressure improves the ventilationperfusion match, reducing the shunt effect.
ET Tube
•
•
•
•
•
•
•
Nursing Considerations:
Assess bilateral breath sounds, at least every
1 to 2 hours. Monitor oxygen saturation levels
closely for changes; ABG analysis as ordered.
Monitor hemodynamic parameters frequently
as appropriate and indicated; anticipate the
need for cardiac monitoring because
hypoxemia can predispose the patient to
arrhythmias.
Watch for complications, (pallor, gasping
respirations, and sudden chest pain).
Carefully monitor vital signs. If your patient’s
respiratory status deteriorates, anticipate the
need for ET intubation and mechanical
ventilation and assist as necessary.
Assist with the chest tube insertion and
connect to suction, as ordered. Monitor your
patient for possible complications associated
with chest tube insertion.
Check chest tube devices frequently for
drainage and proper functioning.
Reposition your patient to promote comfort
and drainage.
Additional Notes:
Chest Tube Thoracostomy
Chest tube thoracostomy involves placing a hollow
plastic tube between the ribs and into the chest to drain
fluid or air from around the lungs. The tube is often
hooked up to a suction machine to help with drainage.
The tube remains in the chest until all or most of the air
"Endotracheal" means "through the trachea". It is a term
that describes a breathing tube that is inserted through
the windpipe or trachea. It is commonly called an ETT or
ET tube. An endotracheal tube is an example of an
artificial airway. A tracheostomy is another type of
artificial airway.
An endotracheal tube is needed to mechanically
ventilate a patient (or breathe for them by a machine).
Each breath is pushed into the endotracheal tube and
into the lung.