ACUTE RESPIRATORY DISTRESS - Usually events that lead to major
SYNDROME (ARDS) systemic inflammation in the
body, which can be indirectly
This occurs when the capillary damage the capillary membrane
membrane that surrounds the alveoli or directly damage the capillary
sac becomes damaged, which causes membrane.
fluid to leak into the alveoli sac.
Indirect (source isn’t the lungs): the
This will result to: Impaired gas capillary membrane is indirectly
exchange. damaged. There is a systemic
Gas exchange doesn’t occur properly inflammatory response system (SIRS)
due to many reasons, such as fluid in by the immune system.
the alveoli sac, collapsed alveoli sacs,
and a decrease in lung compliance Common cause:
(hence the lungs are becoming less Sepsis ( most common and there
elastic “stiff”). is a very poor prognosis if the
patient has a gram negative
This will lead to oxygen not being able to bacteria)
cross the alveolar capillary membrane to Burns
go back in the blood to oxygenate it, Blood transfusion (multiple)
which will result in hypoxemia. In turn, Pancreatitis
the organs of the body will suffer due to Drug overdose
this and death can occur if treatment
does not happen. In majority cases of Direct (source is the lungs): capillary
ARDS, the patient will need respiratory membrane is directly damaged.
assistance via a ventilator with PEEP. Pneumonia
Aspiration
ARDS can be: Inhaling a toxic substance
A fast onset Significant drowning event
It tends to occur in people who Embolism
are already sick (hospitalized)
and develops as a complication. How it happens?
Ex. A patient who has - Pathophysiology: Phases (varies
experienced severe burns is at on severity, this is worst case
risk for ARDS due to systemic scenario)
inflammation present in the body.
It has a high mortality rate. Exudative Phase: occurs about 24
hours after injury to the lung (directly or
Etiology: indirectly)
What can cause the capillary
membrane to become more What happens during this phase?
permeable and leak fluid? Damage to the capillary membrane that
leads to pulmonary edema. This causes
, the leaking of fluid, proteins, and other AND a hallmark sign and symptom:
substances into the interstitium and then REFRACTORY HYPOXEMIA
into the alveoli sac. It is very important - Refractory hypoxemia is where
to note this fluid contains a LOT of the patient will maintain a low
protein. Significance? Remember blood oxygen level even though
proteins regulate water pressure, they are receiving high amounts
oncotic pressure! So, if the fluid is high of oxygen.
in protein it’s going to draw even MORE
fluid into the interstitium and then the Early: Due to all this the patient will
alveoli sac. experience an increase in breathing (still
have hypoxemia).
Cells that produce surfactant become
overwhelmed and damaged. WHY? The body is trying to increase the
Role of surfactant: decreases surface oxygen level, but it won’t be able to! This
tension in the lungs. In other words, the will cause the patient to blow off too
alveoli sacs stay stable. Therefore, much carbon dioxide (CO2 can still
when a person exhales the sac does cross the membrane but O2 can’t)
NOT collapse. ….respiratory ALKALOSIS will develop
BUT in the late phase (as the patient
A decrease in surfactant creates an progresses to the 2nd and 3rd phases
unpredictable alveoli sac that can easily (late), carbon dioxide levels start to rise.
collapse. This is because the hyaline membrane
continues to develop leading to carbon
This leads to: ATELETASIS will occur dioxide not being able to cross over to
(collapse of the lung tissue). be exhaled, and the patient will no
longer be able to maintain breathing due
To make matters worse: a membrane to weak respiratory muscles.
that is made up of dead cells and other Respiratory acidosis will start to develop
substances start to collect on the alveoli. later on.
This is called a hyaline membrane.
This membrane will continue to develop Proliferative Phase: occurs about 14
in the next phase and will cause the days after the injury (grow or reproduce
lungs to become LESS elastic and can new cells quickly)
further impair gas exchange! repair structures, fluid in the sac
is reabsorbed, but lung tissue
End Result? With all the fluid in the becomes very dense and
alveoli sac (pulmonary edema), fibrous….lung compliance and
development of a hyaline membrane, hypoxemia becomes even worse
collapsing of the sacs, and decreased
surfactant = inadequate ventilation Fibrotic Phase: occurs about 3 weeks
where alveoli sacs are NOT getting after injury….major fibrosis of the lung
enough air (leading to V/Q mismatch) tissue, decreases lung compliance and
SYNDROME (ARDS) systemic inflammation in the
body, which can be indirectly
This occurs when the capillary damage the capillary membrane
membrane that surrounds the alveoli or directly damage the capillary
sac becomes damaged, which causes membrane.
fluid to leak into the alveoli sac.
Indirect (source isn’t the lungs): the
This will result to: Impaired gas capillary membrane is indirectly
exchange. damaged. There is a systemic
Gas exchange doesn’t occur properly inflammatory response system (SIRS)
due to many reasons, such as fluid in by the immune system.
the alveoli sac, collapsed alveoli sacs,
and a decrease in lung compliance Common cause:
(hence the lungs are becoming less Sepsis ( most common and there
elastic “stiff”). is a very poor prognosis if the
patient has a gram negative
This will lead to oxygen not being able to bacteria)
cross the alveolar capillary membrane to Burns
go back in the blood to oxygenate it, Blood transfusion (multiple)
which will result in hypoxemia. In turn, Pancreatitis
the organs of the body will suffer due to Drug overdose
this and death can occur if treatment
does not happen. In majority cases of Direct (source is the lungs): capillary
ARDS, the patient will need respiratory membrane is directly damaged.
assistance via a ventilator with PEEP. Pneumonia
Aspiration
ARDS can be: Inhaling a toxic substance
A fast onset Significant drowning event
It tends to occur in people who Embolism
are already sick (hospitalized)
and develops as a complication. How it happens?
Ex. A patient who has - Pathophysiology: Phases (varies
experienced severe burns is at on severity, this is worst case
risk for ARDS due to systemic scenario)
inflammation present in the body.
It has a high mortality rate. Exudative Phase: occurs about 24
hours after injury to the lung (directly or
Etiology: indirectly)
What can cause the capillary
membrane to become more What happens during this phase?
permeable and leak fluid? Damage to the capillary membrane that
leads to pulmonary edema. This causes
, the leaking of fluid, proteins, and other AND a hallmark sign and symptom:
substances into the interstitium and then REFRACTORY HYPOXEMIA
into the alveoli sac. It is very important - Refractory hypoxemia is where
to note this fluid contains a LOT of the patient will maintain a low
protein. Significance? Remember blood oxygen level even though
proteins regulate water pressure, they are receiving high amounts
oncotic pressure! So, if the fluid is high of oxygen.
in protein it’s going to draw even MORE
fluid into the interstitium and then the Early: Due to all this the patient will
alveoli sac. experience an increase in breathing (still
have hypoxemia).
Cells that produce surfactant become
overwhelmed and damaged. WHY? The body is trying to increase the
Role of surfactant: decreases surface oxygen level, but it won’t be able to! This
tension in the lungs. In other words, the will cause the patient to blow off too
alveoli sacs stay stable. Therefore, much carbon dioxide (CO2 can still
when a person exhales the sac does cross the membrane but O2 can’t)
NOT collapse. ….respiratory ALKALOSIS will develop
BUT in the late phase (as the patient
A decrease in surfactant creates an progresses to the 2nd and 3rd phases
unpredictable alveoli sac that can easily (late), carbon dioxide levels start to rise.
collapse. This is because the hyaline membrane
continues to develop leading to carbon
This leads to: ATELETASIS will occur dioxide not being able to cross over to
(collapse of the lung tissue). be exhaled, and the patient will no
longer be able to maintain breathing due
To make matters worse: a membrane to weak respiratory muscles.
that is made up of dead cells and other Respiratory acidosis will start to develop
substances start to collect on the alveoli. later on.
This is called a hyaline membrane.
This membrane will continue to develop Proliferative Phase: occurs about 14
in the next phase and will cause the days after the injury (grow or reproduce
lungs to become LESS elastic and can new cells quickly)
further impair gas exchange! repair structures, fluid in the sac
is reabsorbed, but lung tissue
End Result? With all the fluid in the becomes very dense and
alveoli sac (pulmonary edema), fibrous….lung compliance and
development of a hyaline membrane, hypoxemia becomes even worse
collapsing of the sacs, and decreased
surfactant = inadequate ventilation Fibrotic Phase: occurs about 3 weeks
where alveoli sacs are NOT getting after injury….major fibrosis of the lung
enough air (leading to V/Q mismatch) tissue, decreases lung compliance and
