LO

1.

1. Nasal Cannula
What percentage of oxygen does a nasal cannula provide?
Most cannulae can only provide oxygen at low flow rates—up to (hingga) 5
litres per minute (L/min)—delivering an oxygen concentration of 28–44%.
Rates above 5 L/min can result in discomfort to the patient, drying of
the nasal passages, and possibly nose bleeds (epistaxis).
The nasal cannula is often used in elderly patients or patients who can benefit
from oxygen therapy but do not require it to self respirate. These patients do
not need oxygen to the degree of wearing a non-rebreather mask. It is
especially useful in those patients where vasoconstriction could negatively
impact their condition, such as those suffering from strokes.
A nasal cannula may also be used by pilots and passengers in small,
unpressurized aircraft that do not exceed certain altitudes. The cannula
provides extra oxygen to compensate for the lower oxygen content available
for breathing at the low ambient air pressures of high altitude, preventing
hypoxia.
2. The simple face mask (SFM) is a basic disposable mask (masker sekali
pakai) , made of clear plastic, to provide oxygen therapy for patients who are
experiencing conditions such as chest pain (possible heart attacks), dizziness,
and minor hemorrhages. This mask is only meant for patients who are able to
breathe on their own, but who may require a higher oxygen concentration
than the 21% concentration found in ambient air (di udara sekitar). Patients
 who are unable to breathe on their own are placed on a medical
ventilator instead. The simple face mask can deliver higher flow rates than
nasal cannula (6–10 liters per minute) for an FiO2 of 40–60% oxygen.
3. The venturi mask, also known as an air-entrainment mask, is a medical device to deliver a
oxygen concentration to patients on controlled oxygen therapy. Venturi masks are
considered high-flow oxygen therapy devices. This is because venturi masks are able to
provide total inspiratory flow at a specified FiO2 to patients therapy. The kits usually
include multiple jets, which are usually color-coded, in order to set the
desired FiO2.
Use[edit] =Delivering supplemental oxygen at a precise concentration
Since the jets in venturi masks generally limit oxygen flow at 12 to 15 liters
per minute the total flow decreases as the ratio decreases. At an oxygen flow
rate of 12 liters per minute and a 30% FiO2 setting, the total flow would be 108
L/min. At a 40% FiO2 setting, the total flow would decrease to 48 L/min.
4. What percentage of oxygen does a partial rebreather mask deliver?
90 percent
A non-rebreather mask can deliver an oxygen concentration of 90 percent
or more. A BVM can deliver up to 100 percent oxygen to a breathing or non-
breathing victim when attached to emergency oxygen. Squeezing the bag as
the victim inhales helps deliver more oxygen. BVM flow rates should be set
at 15 LPM or more. The non-rebreather mask is utilized for patients with physical
trauma, chronic airway limitation, cluster headache, smoke inhalation, and carbon
monoxide poisoning, or any other patients who require high-concentration oxygen, but do
not require breathing assistance.

2. When a person speaks, the vocal cords create vibrations (vocal fremitus)
in the tracheobronchial tree and through the lungs and chest wall, where they
can be felt (tactile fremitus). ... An increase in tactile fremitus indicates
denser or inflamed lung tissue, which can be caused by diseases such
as pneumonia.
Tactile fremitus is pathologically decreased or absent over areas of pleural
effusion or pneumothorax (when there is air outside the lung in the chest cavity,
preventing lung expansion).
The reason for increased fremitus in a consolidated lung is the fact that the sound waves
are transmitted with less delay in a solid or fluid medium (the consolidation) than in a
gaseous medium (aerated lung). Conversely, the reason for decreased fremitus in a
pleural effusion or pneumothorax (or any pathology separating the lung tissue itself from
the body wall) is that this increased space diminishes or prevents entirely sound
transmission.

3. Pneumothorax
A pneumothorax is an abnormal collection of air in the pleural space between the lung and
the chest wall.[3] Symptoms typically include sudden onset of sharp, one-sided chest
pain and shortness of breath. In a minority of cases the amount of air in the chest increases
when a one-way valve is formed by an area of damaged tissue, leading to a tension
pneumothorax.[3] This condition can cause a steadily worsening oxygen shortage and low
blood pressure.[3] Unless reversed by effective treatment this can be fatal.[3] Very rarely both
lungs may be affected by a pneumothorax.[6] It is often called a collapsed lung, although that
term may also refer to atelectasis.[1] Atelectasis is the collapse or closure of a lung resulting
in reduced or absent gas exchange. A primary spontaneous pneumothorax is one that
occurs without an apparent cause and in the absence of significant lung disease.[3] A
secondary spontaneous pneumothorax occurs in the presence of existing lung
 disease.[3][7] Smoking increases the risk of primary spontaneous pneumothorax, while the
main underlying causes for secondary pneumothorax are COPD, asthma,
and tuberculosis.[3][4] A pneumothorax can also be caused by physical trauma to
the chest (including a blast injury) or as a complication of a healthcare intervention, in which
case it is called a traumatic pneumothorax.[8][9]

Signs and symptoms

A primary spontaneous pneumothorax (PSP) tends to occur in a young adult without
underlying lung problems, and usually causes limited symptoms. Chest pain and sometimes mild
breathlessness are the usual predominant presenting features.[12][13] People who are affected by a
PSP are often unaware of the potential danger and may wait several days before seeking
medical attention.[14] PSPs more commonly occur during changes in atmospheric pressure,
explaining to some extent why episodes of pneumothorax may happen in clusters.[13] It is rare for
a PSP to cause a tension pneumothorax.[12]

Secondary spontaneous pneumothoraces (SSPs), by definition, occur in individuals with

significant underlying lung disease. Symptoms in SSPs tend to be more severe than in PSPs, as
the unaffected lungs are generally unable to replace the loss of function in the affected
lungs. Hypoxemia (decreased blood-oxygen levels) is usually present and may be observed
as cyanosis (blue discoloration of the lips and skin). Hypercapnia (accumulation of carbon
dioxide in the blood) is sometimes encountered; this may cause confusion and – if very severe –
may result in comas. The sudden onset of breathlessness in someone with chronic obstructive
pulmonary disease (COPD), cystic fibrosis, or other serious lung diseases should therefore
prompt investigations to identify the possibility of a pneumothorax.[12][14]

Traumatic pneumothorax most commonly occurs when the chest wall is pierced (ditusuk) ,
such as when a stab wound or gunshot wound (luka tusuk/luka tembak ) allows air to enter
the pleural space, or because some other mechanical injury to the lung compromises the
integrity of the involved structures. Traumatic pneumothoraces have been found to occur in up to
half of all cases of chest trauma, with only rib fractures being more common in this group. The
pneumothorax can be occult (not readily apparent) in half of these cases, but may enlarge –
particularly if mechanical ventilation is required.[13] They are also encountered in people already
receiving mechanical ventilation for some other reason.[13]

Upon physical examination, breath sounds (heard with a stethoscope) may be diminished on the
affected side, partly because air in the pleural space dampens (menghambat) the transmission of
sound. Measures of the conduction of vocal vibrations to the surface of the chest may be
altered. Percussion of the chest may be perceived as hyperresonant (like a booming drum),
and vocal resonance and tactile fremitus can both be noticeably decreased. Importantly, the
volume of the pneumothorax may not be well correlated with the intensity of the symptoms
experienced by the victim,[14] and physical signs may not be apparent if the pneumothorax is
relatively small.[13][14]

Tension pneumothorax
Although multiple definitions exist, a tension pneumothorax is generally considered to be present
when a pneumothorax (primary spontaneous, secondary spontaneous, or traumatic) leads to
significant impairment of respiration and/or blood circulation.[15] Tension pneumothorax tends to
occur in clinical situations such as ventilation, resuscitation, trauma, or in people with lung
disease.[14]
The most common findings in people with tension pneumothorax are chest pain and respiratory
distress, often with an increased heart rate (tachycardia) and rapid breathing (tachypnea) in the
initial stages. Other findings may include quieter breath sounds on one side of the chest,
low oxygen levels and blood pressure, and displacement of the trachea away from the affected
side. Rarely, there may be cyanosis (bluish discoloration of the skin due to low oxygen
levels), altered level of consciousness, a hyperresonant percussion note on examination of the
affected side with reduced expansion and decreased movement, pain in the epigastrium (upper
abdomen), displacement of the apex beat (heart impulse), and resonant sound when tapping
the sternum.[15] This is a medical emergency and may require immediate treatment without further
investigations (see below).[14][15]
Tension pneumothorax may also occur in someone who is receiving mechanical ventilation, in
which case it may be difficult to spot as the person is typically receiving sedation; it is often noted
because of a sudden deterioration in condition.[15] Recent studies have shown that the
development of tension features may not always be as rapid as previously thought. Deviation of
the trachea to one side and the presence of raised jugular venous pressure (distended neck
veins) are not reliable as clinical signs

Cause[edit]
Spontaneous pneumothoraces are divided into two types: primary, which occurs in the absence
of known lung disease, and secondary, which occurs in someone with underlying lung
disease.[16] The cause of primary spontaneous pneumothorax is unknown, but established risk
factors include male sex, smoking, and a family history of pneumothorax.[17] Smoking
either cannabis or tobacco increases the risk.[3] The various suspected underlying mechanisms
are discussed below.[12][13]

Secondary spontaneous[edit]
Secondary spontaneous pneumothorax occurs in the setting of a variety of lung diseases. The
most common is chronic obstructive pulmonary disease (COPD), which accounts for
approximately 70% of cases.[17]

Traumatic[edit]
A traumatic pneumothorax may result from either blunt trauma or penetrating injury to the chest
wall.[13] The most common mechanism is due to the penetration of sharp bony points at a new rib
fracture, which damages lung tissue.[17] Traumatic pneumothorax may also be observed in
those exposed to blasts, even though there is no apparent injury to the chest.[9]
They may be classified as "open" or "closed". In an open pneumothorax there is a passage from
the external environment into the pleural space through the chest wall. When air is drawn into the
pleural space through this passageway it is known as a sucking chest wound. A closed
pneumothorax is when the chest wall remains intact.[22]
Intrapleural pressure is normally negative (less than atmospheric pressure) because of inward
lung and outward chest wall recoil. In pneumothorax, air enters the pleural space from outside
the chest or from the lung itself via mediastinal tissue planes or direct pleural perforation.
Intrapleural pressure increases, and lung volume decreases.

The V/Q ratio is the amount of air that reaches your alveoli divided by the amount of blood
flow in the capillaries in your lungs
Tension pneumothorax is a pneumothorax causing a progressive rise in intrapleural pressure
to levels that become positive throughout the respiratory cycle and collapses the lung, shifts
the mediastinum, and impairs venous return to the heart. Air continues to get into the pleural
space but cannot exit. Without appropriate treatment, the impaired venous return can cause
systemic hypotension and respiratory and cardiac arrest (pulseless electrical activity) within
minutes. Tension pneumothorax most commonly occurs in patients receiving positive-pressure
ventilation (with mechanical ventilation or particularly during resuscitation). Rarely, it is a
complication of traumatic pneumothorax, when a chest wound acts as a one-way valve that
traps increasing volumes of air in the pleural space during inspiration.
Diagnosis
A pneumothorax is generally diagnosed using a chest X-ray. In some cases, a computerized
tomography (CT) scan may be needed to provide more-detailed images. Ultrasound imaging
also may be used to identify a pneumothorax.
Treatment

Treatment options may include observation, needle aspiration, chest tube insertion,
nonsurgical repair or surgery.
Observation

If only a small portion of your lung is collapsed, your doctor may simply monitor your
condition with a series of chest X-rays until the excess air is completely absorbed and
your lung has re-expanded. This may take several weeks.
Needle aspiration or chest tube insertion

If a larger area of your lung has collapsed, it's likely that a needle or chest tube will be
used to remove the excess air.

 Needle aspiration. A hollow needle with small flexible tube (catheter) is inserted
between the ribs into the air-filled space that is pressing on the collapsed lung. The
needle is removed and a syringe is attached to the catheter so that the doctor can
pull out the excess air. The catheter may be left in for a few hours to ensure the
lung is re-expanded and the pneumothorax does not recur.

 Chest tube insertion. A flexible chest tube is inserted into the air-filled space and
may be attached to a one-way valve device that continuously removes air from the
chest cavity until your lung is re-expanded and healed.
Nonsurgical repair

If a chest tube doesn't re-expand your lung, nonsurgical options to close the air leak may
include:

 Using a substance to irritate the tissues around the lung so that they'll stick
together and seal any leaks. This can be done through the chest tube, but may be
done during surgery.

 Drawing blood from your arm and placing it into the chest tube. The blood creates
a fibrinous patch on the lung (autologous blood patch), sealing the air leak.

 Passing a thin tube (bronchoscope) down your throat and into your lungs to look at
your lungs and air passages and place a one-way valve. The valve allows the lung
to re-expand and the air leak to heal.

Pleurodesis

Pleurodesis is a more invasive form of treatment for a pneumothorax. This

procedure is commonly recommended for individuals who’ve had repeated
episodes of pneumothorax.During pleurodesis, your doctor irritates the
pleural space so that air and fluid can no longer accumulate. The term
“pleura” refers to the membrane surrounding each lung. Pleurodesis is
performed to make your lungs’ membranes stick to the chest cavity. Once
the pleura adheres to the chest wall, the pleural space no longer expands,
and this prevents formation of a future pneumothorax.Mechanical
pleurodesis is performed manually. During surgery, your surgeon brushes
the pleura to cause inflammation. Chemical pleurodesis is another form of
treatment. Your doctor will deliver chemical irritants to the pleura through a
chest tube. The irritation and inflammation cause the lung pleura and chest
wall lining to stick together.

Surgery

There are several types of surgery for pneumothorax. One option is

a thoracotomy. During this surgery, your surgeon will create an incision
(irisan) in the pleural space. Another option is thoracoscopy, also known as
video-assisted thoracoscopic surgery (VATS). Your surgeon inserts a tiny
camera through your chest wall to help them see inside your chest. A
thoracoscopy can help your surgeon decide on the treatment for your
pneumothorax. The possibilities include sewing blisters closed, closing air
leaks, or removing the collapsed portion of your lung, which is called
a lobectomy.

Pharmacotherapy
The following medications may be used to aid in the management of patients with
pneumothorax:
 Local anesthetics (eg, lidocaine hydrochloride)
 Opioid anesthetics (eg, fentanyl citrate, morphine)
 Benzodiazepines (eg, midazolam, lorazepam)
 Antibiotics (eg, doxycycline, cefazolin)

DIAGNOSIS
Chest pain, Tachypnea, Hyper resonance of the chest wall on the affected side, Dyspnea,
Anxiety, Diminished breath sounds on the affected side
Whereas late findings includes
Decreased level of consciousness, Tracheal deviation toward the contralateral side
Hypotension, Distension of neck veins (may not be present if hypotension is severe),
Cyanosis

IMAGING STUDIES
Chest radiography

Chest radiographic findings may include

increased thoracic volume, increased rib
separation, ipsilateral flattening of heart
border, contralateral mediastinal
deviation, and the midiaphragmatic
depression.

Chest CT scanning
A CT scan is more sensitive than a chest
radiograph in the evaluation of small
pneumothoraces and
pneumomediastinum, although the
clinical significance of these occult
pneumothoraces is unclear, particularly in
the stable nonintubated patient. The occult
pneumothorax is being diagnosed more
frequently as methods of evaluating and
diagnosing trauma patients become more
sensitive. At present, CT scan is the gold
standard for detecting occult traumatic
pneumothorax not apparent on supine
chest X-ray radiograph
Ultrasonography
Use of bedside ultrasonography in the diagnosis of pneumothorax is a relatively recent
development. In some trauma centers, pneumothorax detection is included as part of their
focused abdominal sonography for trauma (FAST) examination.[25]Ultrasonographic
features used in the diagnosis of pneumothorax include absence of lung sliding (high
sensitivity and specificity), absence of comet-tail artifact (high sensitivity, lower specificity),
and presence of lung point (high specificity, lower sensitivity). In a study, ultrasonography
performed on patients with blunt thoracic trauma had 94% sensitivity and 100% specificity
for pneumothorax detection compared with spiral CT scanning

Arterial blood gas analysis

Arterial blood gas (ABG) does not replace physical diagnosis nor should treatment be
delayed while awaiting results if symptomatic pneumothorax is suspected. However, ABG
analysis may be useful in evaluating hypoxia, hypercarbia, and respiratory acidosis.

Electrocardiography
In left-sided pneumothorax electrocardiogram (ECG) shows: rightward shift of the frontal
QRS axis, diminution (pengecilan) of the precordial R voltage, decrease in QRS amplitude,
and precordial T-wave inversion. With right pneumothorax ECG may show diminution of the
precordial QRS voltage, right axis deviation, and a prominent R wave in V2 with associated
loss of S wave voltage, mimicking posterior myocardial infarction.
Chest X-ray
Diagnostic tests
 Arterial blood gas analysis (ABG) to detect respiratory acidosis
 Chest x-ray (confirmatory test)
 Ideally in two projections (PA and lateral), in supine and upright position

 Ipsilateral pleural line with reduced/absent lung markings
 Sudden change in radiolucency
 Deep sulcus sign: dark and deep costophrenic angle on the affected side
 If pulmonary disease is present: airway or parenchymal lesions
 Additional features in tension pneumothorax:
 Ipsilateral diaphragmatic flattening/inversion and widened intercostal spaces
 Tracheal deviation towards the contralateral side

An arterial blood gas test may be performed to measure the amount of carbon
dioxide and oxygen in the blood. Higher than normal levels of carbon dioxide and
low levels of oxygen are indicators of a collapsed lung.
The main physiological change in pneumothorax is a reduction of arterial oxygen tension
in addition to the reduced vital capacity. Patients experiencing primary pneumothorax
endure (menanggung) the vital capacity reduction .Vital capacity atau kapasitas vital paru
merupakan jumlah udara yang dapat dikeluarkan pada saat ekspirasi setelah inspirasi
maksimal.relatively well, but in patients suffering from secondary pneumothorax and
underlying pulmonary disease, the vital capacity reduction can led to alveolar
hypoventilation and
respiratory failure. In a
study evaluating 12 patients
diagnosed with spontaneous
pneumothorax, 9 patients
(75%) had a PO2≤80 mm
Hg, and 2 patients, who
were both diagnosed with
secondary pneumothorax,
had a PO2≤55 mm Hg1.
Hypoventilation (also
known as respiratory
depression) occurs when
ventilation is inadequate
(hypo meaning "below")
to perform needed gas exchange. By definition it causes an increased
concentration of carbon dioxide (hypercapnia) and respiratory acidosis.
Reduced oxygen tension may be caused by an anatomic shunt and, in some cases,
alveolar hypoventilation in the pneumothorax area created from the reduced ventilation-
perfusion ratio in the pulmonary alveoli. as it is sometimes called, is a condition
arising from too much carbon dioxide in the blood. It is often caused by
hypoventilation or disordered breathing where not enough oxygen enters
the lungs and not enough carbon dioxide is emitted. (It is a waste product made by
 your body. Your blood carries carbon dioxide to your lungs. You breathe out carbon
dioxide and breathe in oxygen)

Answer and Explanation: A collapsed lung will not allow your lung to function to its
full capacity. A collapsed lung doesn't move air in and out and bring it in contact with the
blood to get oxygen from the air to the red blood cells and to remove carbon dioxide from the
blood and carry it out of the body with the expired air. Those are the functions of the lung, so a
collapsed lung is not functional. The condition ranges in severity. If there's only a small
amount of air trapped in the pleural space, as can be the case in a spontaneous
pneumothorax, it can often heal on its own if there have been no further
complications. More serious cases that involve larger volumes of air can
become fatal if left untreated

A collapsed lung occurs when air escapes from the lung. The air then fills the
space outside of the lung, between the lung and chest wall. This buildup of air puts
pressure on the lung, so it cannot expand as much as it normally does when you
take a breath.

Atelectasis is the collapse or closure of a lung resulting in reduced or absent gas exchange.
Atelectasis is defined as incomplete air filling and underexpansion of pulmonary tissue. It
should be distinguished from consolidation, which also represents incomplete air filling of
the lung. It is usually unilateral, affecting part or all of one lung.[2] It is a condition where
the alveoli are deflated down to little or no volume, as distinct from pulmonary consolidation, in
which they are filled with liquid. It is often called a collapsed lung, although that term may also
refer to pneumothorax.
A pulmonary consolidation is a region of normally compressible lung tissue that has filled with
liquid instead of air.[1] The condition is marked by induration[2] (swelling or hardening of normally
soft tissue) of a normally aerated lung. It is considered a radiologic sign. Consolidation occurs
through accumulation of inflammatory cellular exudate in the alveoli and adjoining ducts. The
liquid can be pulmonary edema, inflammatory exudate, pus, inhaled water, or blood (from
bronchial tree or hemorrhage from a pulmonary artery). Consolidation must be present to
diagnose pneumonia: the signs of lobar pneumonia are characteristic and clinically referred to as
consolidation.[3]

Lung edema
Cardiogenic pulmonary edema (CPE) is defined as pulmonary edema due to increased
capillary hydrostatic pressure secondary to elevated pulmonary venous pressure. CPE reflects
the accumulation of fluid with a low-protein content in the lung interstitium and alveoli as a
result of cardiac dysfunction.
Pulmonary edema can be caused by the following major pathophysiologic mechanisms:
 Imbalance of Starling forces - Ie, increased pulmonary capillary pressure,
decreased plasma oncotic pressure, increased negative interstitial pressure
 Damage to the alveolar-capillary barrier
 Lymphatic obstruction
 Idiopathic (unknown) mechanism
 Signs & symptoms:
 Dyspnea
 Orthopnea (inability to lie down flat due to breathlessness)
 Paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night)
 Coughing up blood (pink frothy sputum)
 Excessive sweating
 Anxiety
 Pale skin
 Peripheral pitting edema (due to left ventricular failure)
 Raised JVP
 Hepatomegaly
 End-respiratory crackles and 3rd heart sound on auscultation

Etiology
CPE is caused by elevated pulmonary capillary hydrostatic pressure leading to transudation
of fluid into the pulmonary interstitium and alveoli. Increased LA pressure increases
pulmonary venous pressure and pressure in the lung microvasculature, resulting in pulmonary
edema.
The progression of fluid accumulation in CPE can be identified as 3 distinct physiologic
stages.
 Stage 1
In stage 1, elevated LA pressure causes distention and opening of small pulmonary
vessels. At this stage, blood gas exchange does not deteriorate, (memburuk) or it may
even be slightly improved.
 Stage 2
In stage 2, fluid and colloid shift into the lung interstitium from the pulmonary
capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid.
The continuing filtration of liquid and solutes may overpower the drainage capacity of
the lymphatics. In this case, the fluid initially collects in the relatively compliant
interstitial compartment, which is generally the perivascular tissue of the large
vessels, especially in the dependent zones.
The accumulation of liquid in the interstitium may compromise (membahayakan) the
small airways, leading to mild hypoxemia. Hypoxemia at this stage is rarely of
sufficient magnitude to stimulate tachypnea. Tachypnea at this stage is mainly the
 result of the stimulation of juxtapulmonary capillary (J-type) receptors, which are
nonmyelinated nerve endings located near the alveoli. J-type receptors are involved in
reflexes modulating respiration and heart rates.
 Stage 3
In stage 3, as fluid filtration continues to increase and the filling of loose interstitial
space occurs, fluid accumulates in the relatively noncompliant interstitial space. The
interstitial space can contain up to 500mL of fluid. With further accumulations, the
fluid crosses the alveolar epithelium in to the alveoli, leading to alveolar flooding. At
this stage, abnormalities in gas exchange are noticeable, vital capacity and other
respiratory volumes are substantially reduced, and hypoxemia becomes more severe.

The initial management of pulmonary edema, irrespective of the type or cause, is

supporting vital functions. Therefore, if the level of consciousness is decreased it may be
required to proceed to proceed to tracheal intubation and mechanical ventilation to prevent
airway compromise. Hypoxia (low O2 level) may require supplementary O2.
Acute cardiogenic pulmonary edema often responds rapidly to medical
treatment. Positioning upright may relieve symptoms. Loop diuretics such
as furosemide or bumetanide are administered, often together with morphine or diamorphine
to reduce respiratory distress. Both diuretics and morphine may have vasodilator effects, but
specific vasodilators may be used (particularly intravenous glyceryl trinitrate or ISDN)
provided the blood pressure is adequate.