NUR 445 Exam 3// Brady Questions and Answers| New Update with 100% Correct Answers
acute lung failure also known as acute respiratory failure
-clinical condition in which pulmonary system fails to maintain adequate gas exchange
-results from a deficiency in the performance of the pulmonary system and usually occurs
secondary to another disorder that has altered the normal function of the pulmonary system in
such a way to decrease the ventilatory drive, decrease muscle strength, decrease chest wall
elasticity, decrease the lung's capacity for gas exchange increase airway resistance, or increase
metabolic oxygen requirements
acute lung failure can be classified as type 1: hypoxemic normocapnic respiratory failure or
type 2: hypoxemic hypercapnic respiratory failure, depending on analysis of ABG's
type one respiratory failure: hypoxemic normocapnic respiratory failure pt presents with a
**low arterial oxygen pressure (PaO2) and a ***normal arterial carbon dioxide (PaCO2)
-usually results from V/W mismatching and intrapulmonary shunting
type 2 respiratory failure: hypoxemic hypercapnic respiratory failure pt presents with
***low PaO2 and **high PaCO2
-usually results from alveolar hypoventilation which may or may not be accompanied by V/Q
mismatching and intrapulmonary shunting
causes of Acute Lung Failure (ALF) can be classified as extrapulmonary or intrapulmonary
depending on the origin of the patient's primary disorder
extrapulmonary causes of ALF disorders that affect the brain, the spinal cord, the
neuromuscular system, the thorax, the pleura, and the upper airways
intrapulmonary causes of ALF disorders that affect the lower airways and alveoli, the
pulmonary circulation, and the alveolar-capillary membrane
,Patho of ALF ***hypoxemia is hallmark: main causes of hypoxemia are alveolar
hypoventilation, ventilation-perfusion (V/Q) mismatching, and intrapulmonary shunting
-hypercapnia may be present, depending on the underlying cause of the prob
alveolar hypoventilation occurs when the amount of oxygen being brought into the alveoli is
insufficient to meet the metabolic needs of the body.
-can be the result of increasing metabolic oxygen needs or decreasing ventilation
(-hypoxemia caused by this is associated with hypercapnia and commonly results from
extrapulmonary disorders)
ventilation-perfusion mismatching occurs when ventilation and blood flow are mismatched
in various regions of the lung in excess of what is normal
-blood passes through alveoli that are underventilated for the given amount of perfusion,
leaving those areas with a lower than normal amount of oxygen
(-this is the most common cause of hypoxemia and is usually the result of alveoli that are
partially collapsed or partially filled with fluid)
intrapulmonary shunting -a.k.a. an extreme form of V/Q mismatching
-occurs when blood reaches the arterial system without participating in gas exchange
-the mixing of unoxygenated (shunted) blood and oxygenated blood lowers the average level of
oxygen present in the blood.
-occurs when blood passes through a portion of a lung that is not ventilated; this may be a
result of (1) alveolar collapse secondary to atelectasis, or (2) alveolar flooding with pus, blood,
or fluid
(-if allowed to progress, hypoxemia can result in a deficit of oxygen at the cellular level. as the
tissue demands for oxygen continues and the supply diminishes an oxygen supply-demand
imbalance occurs and tissue hypoxia develops. decreased oxygen to the cells contributes to the
impaired tissue perfusion and the development of lactic acidosis and MODS
clinical manifestations of ALF -depends on the underlying cause and the extent of tissue
hypoxia
,-sx usually due to development of hypoxemia, hypercapnia, and acidosis. bc sx are so varied,
they are not considered reliable in predicting the degree of hypoxemia or hypercapnia or
severity of ALF
dx of ALF -dx best accomplished by ABG analysis, which confirms the level of PaCO2, PaO2,
and blood pH
-generally PaO2 is less than 60 mm Hg
-if the pt is also experiencing hypercapnia, the PaCO2 will be greater than 45 mm Hg. In pts with
chronically elevated PaCO2 levels, this criteria must be broadened to include a pH less than
7.35
-bronchoscopy is also performed, chest radiography, thoracic ultrasound, thoracic CT, and lung
fxn studies
medical management of ALF tx the underlying cause, promote adequate gas exchange,
correcting acidosis, initiating nutrition support and preventing complications
positioning for ALF -**gravity
-goal is to place least affected area (healthy lung) of the patient's lung in the most dependent
position (healthy/good lung down)**
-elevate bed 30-45 degrees
-repositioning every 2 hours
acute respiratory distress syndrome (ARDS) systemic process that is considered to be the
pulmonary manifestation of MODS
-characterized by noncardiac pulmonary edema and disruption of the alveolar-capillary
membrane as a result of injury to either the pulmonary vasculature or the airways
patho of ARDS occurs in 3 phases: exudative, fibroproliferative, and resolution
-initiated with stimulation of inflammatory-immune system as a result of an indirect or direct
injury (direct injury=lung is DIRECTLY injured, indirect= something else in the body is injured
and it ends up affecting the lungs)
, exudative phase of ARDS occurs within 72 hours after initial insult
-(the definition of exudate is fluid leaking out of blood vessels and into nearby tissues// this is
what is occurring in the pulmonary capillaries and alveoli which decreases surfactant and
causes alveolar collapse***)
-mediators cause injury to the pulmonary capillaries, resulting in increased capillary membrane
permeability leading to leakage of fluid filled with protein, blood, cells, fibrin, and activated
cellular and humoral mediators into the pulmonary interstitium. Damage to these capillaries
also causes development of microthrombi and elevation of pulmonary artery pressure. as fluid
enters the interstitium, the lymphatics are overwhelmed and unable to drain all the
accumulating fluid, resulting in interstitial edema. fluid is then forced from the interstitial space
into the alveoli, resulting in alveoli edema. All this damage leads to impaired surfactant
production, which leads to alveolar collapse
sx of exudative phase of ARDS -hypoxemia// occurs bc of intrapulmonary shunting and V/Q
mismatch secondary to compression, collapse and flooding of the alveoli and small airways.
-increased work of breathing// result of increased airway resistance , decreased fxnl residual
capacity and decreased lung compliance secondary to atelectasis and compression of small
airways
-these both lead to pt fatigue, and the development of alveolar hypoventilation
-pulmonary HTN// result of damage to pulmonary capillaries, microthrombi, and hypoxic
vasoconstriction leading to the development of increased alveolar dead space and right
ventricular overload
-right ventricular afterload increases// leads to right ventricular dysfxn, and decrease in CO
***tachypnea, restlessness, apprehension, and moderate increase in accessory muscle use
fibroproliferative phase of ARDS begins as distorted healing and starts in the lungs
-cellular granulation and collagen deposits occur within the alveolar-capillary membrane
-alveoli become enlarged and irregularly shaped (fibrotic) and the pulmonary capillaries
become scarred and obliterated
-this leads to further stiffening of the lungs, increasing pulmonary HTN and continued hypoxia
acute lung failure also known as acute respiratory failure
-clinical condition in which pulmonary system fails to maintain adequate gas exchange
-results from a deficiency in the performance of the pulmonary system and usually occurs
secondary to another disorder that has altered the normal function of the pulmonary system in
such a way to decrease the ventilatory drive, decrease muscle strength, decrease chest wall
elasticity, decrease the lung's capacity for gas exchange increase airway resistance, or increase
metabolic oxygen requirements
acute lung failure can be classified as type 1: hypoxemic normocapnic respiratory failure or
type 2: hypoxemic hypercapnic respiratory failure, depending on analysis of ABG's
type one respiratory failure: hypoxemic normocapnic respiratory failure pt presents with a
**low arterial oxygen pressure (PaO2) and a ***normal arterial carbon dioxide (PaCO2)
-usually results from V/W mismatching and intrapulmonary shunting
type 2 respiratory failure: hypoxemic hypercapnic respiratory failure pt presents with
***low PaO2 and **high PaCO2
-usually results from alveolar hypoventilation which may or may not be accompanied by V/Q
mismatching and intrapulmonary shunting
causes of Acute Lung Failure (ALF) can be classified as extrapulmonary or intrapulmonary
depending on the origin of the patient's primary disorder
extrapulmonary causes of ALF disorders that affect the brain, the spinal cord, the
neuromuscular system, the thorax, the pleura, and the upper airways
intrapulmonary causes of ALF disorders that affect the lower airways and alveoli, the
pulmonary circulation, and the alveolar-capillary membrane
,Patho of ALF ***hypoxemia is hallmark: main causes of hypoxemia are alveolar
hypoventilation, ventilation-perfusion (V/Q) mismatching, and intrapulmonary shunting
-hypercapnia may be present, depending on the underlying cause of the prob
alveolar hypoventilation occurs when the amount of oxygen being brought into the alveoli is
insufficient to meet the metabolic needs of the body.
-can be the result of increasing metabolic oxygen needs or decreasing ventilation
(-hypoxemia caused by this is associated with hypercapnia and commonly results from
extrapulmonary disorders)
ventilation-perfusion mismatching occurs when ventilation and blood flow are mismatched
in various regions of the lung in excess of what is normal
-blood passes through alveoli that are underventilated for the given amount of perfusion,
leaving those areas with a lower than normal amount of oxygen
(-this is the most common cause of hypoxemia and is usually the result of alveoli that are
partially collapsed or partially filled with fluid)
intrapulmonary shunting -a.k.a. an extreme form of V/Q mismatching
-occurs when blood reaches the arterial system without participating in gas exchange
-the mixing of unoxygenated (shunted) blood and oxygenated blood lowers the average level of
oxygen present in the blood.
-occurs when blood passes through a portion of a lung that is not ventilated; this may be a
result of (1) alveolar collapse secondary to atelectasis, or (2) alveolar flooding with pus, blood,
or fluid
(-if allowed to progress, hypoxemia can result in a deficit of oxygen at the cellular level. as the
tissue demands for oxygen continues and the supply diminishes an oxygen supply-demand
imbalance occurs and tissue hypoxia develops. decreased oxygen to the cells contributes to the
impaired tissue perfusion and the development of lactic acidosis and MODS
clinical manifestations of ALF -depends on the underlying cause and the extent of tissue
hypoxia
,-sx usually due to development of hypoxemia, hypercapnia, and acidosis. bc sx are so varied,
they are not considered reliable in predicting the degree of hypoxemia or hypercapnia or
severity of ALF
dx of ALF -dx best accomplished by ABG analysis, which confirms the level of PaCO2, PaO2,
and blood pH
-generally PaO2 is less than 60 mm Hg
-if the pt is also experiencing hypercapnia, the PaCO2 will be greater than 45 mm Hg. In pts with
chronically elevated PaCO2 levels, this criteria must be broadened to include a pH less than
7.35
-bronchoscopy is also performed, chest radiography, thoracic ultrasound, thoracic CT, and lung
fxn studies
medical management of ALF tx the underlying cause, promote adequate gas exchange,
correcting acidosis, initiating nutrition support and preventing complications
positioning for ALF -**gravity
-goal is to place least affected area (healthy lung) of the patient's lung in the most dependent
position (healthy/good lung down)**
-elevate bed 30-45 degrees
-repositioning every 2 hours
acute respiratory distress syndrome (ARDS) systemic process that is considered to be the
pulmonary manifestation of MODS
-characterized by noncardiac pulmonary edema and disruption of the alveolar-capillary
membrane as a result of injury to either the pulmonary vasculature or the airways
patho of ARDS occurs in 3 phases: exudative, fibroproliferative, and resolution
-initiated with stimulation of inflammatory-immune system as a result of an indirect or direct
injury (direct injury=lung is DIRECTLY injured, indirect= something else in the body is injured
and it ends up affecting the lungs)
, exudative phase of ARDS occurs within 72 hours after initial insult
-(the definition of exudate is fluid leaking out of blood vessels and into nearby tissues// this is
what is occurring in the pulmonary capillaries and alveoli which decreases surfactant and
causes alveolar collapse***)
-mediators cause injury to the pulmonary capillaries, resulting in increased capillary membrane
permeability leading to leakage of fluid filled with protein, blood, cells, fibrin, and activated
cellular and humoral mediators into the pulmonary interstitium. Damage to these capillaries
also causes development of microthrombi and elevation of pulmonary artery pressure. as fluid
enters the interstitium, the lymphatics are overwhelmed and unable to drain all the
accumulating fluid, resulting in interstitial edema. fluid is then forced from the interstitial space
into the alveoli, resulting in alveoli edema. All this damage leads to impaired surfactant
production, which leads to alveolar collapse
sx of exudative phase of ARDS -hypoxemia// occurs bc of intrapulmonary shunting and V/Q
mismatch secondary to compression, collapse and flooding of the alveoli and small airways.
-increased work of breathing// result of increased airway resistance , decreased fxnl residual
capacity and decreased lung compliance secondary to atelectasis and compression of small
airways
-these both lead to pt fatigue, and the development of alveolar hypoventilation
-pulmonary HTN// result of damage to pulmonary capillaries, microthrombi, and hypoxic
vasoconstriction leading to the development of increased alveolar dead space and right
ventricular overload
-right ventricular afterload increases// leads to right ventricular dysfxn, and decrease in CO
***tachypnea, restlessness, apprehension, and moderate increase in accessory muscle use
fibroproliferative phase of ARDS begins as distorted healing and starts in the lungs
-cellular granulation and collagen deposits occur within the alveolar-capillary membrane
-alveoli become enlarged and irregularly shaped (fibrotic) and the pulmonary capillaries
become scarred and obliterated
-this leads to further stiffening of the lungs, increasing pulmonary HTN and continued hypoxia
