Question | Answer |
What is Alectasis? | The loss of lung volume caused by inadequate expansion of air spaces |
What is the general consequence of atelactasis? | Shunting of inadequately oxygenated blood from pulmonary arteries into veins, thus giving rise to hypoxia |
What are the three forms of atelactasis? | 1) Resorption
2) Compression
3) Contraction |
When does resorption atelactasis occur? | In the case of obstruction. preventing air from reaching distal airways |
Why is it called resorption atelactasis? | Because the air present gradually become absorbed and alveolar collapse follows |
What part of the lung is affected by resorption atelactasis? | Either an entire lung, a complete lobe, or one or more segments. |
What is the most common cause of resorption collapse? | Obstruction of a bronchus by a mucus or mucopurelent plug |
In what cases can the bronchus be obstructed by a mucus or mucopurulent plug? | 1) Postoperatively
2) Complicated bronchial asthma, bronchiectasis, or bronchitis |
How else may the bronchus be obstructed? | 1) Tumor
2) Foreign body aspiration (mainly in children) |
What are some other names for compression atelactasis? | Passive/ Relaxation atelactasis |
How does compression atelactasis occur? | Accumulation of fluid, blood, or air within the pleural cavity which mechanically collapses the adjacent lung |
What is the most common cause of compression atelactasis? | Pleural effusion, caused by congestive heart failure |
What are some other causes of compression atelactasis? | 1) Leakage of air into the pleural cavity (pneumothorax)
2) Hemothorax
3) Basal atelactasis resulting from the elevated position of the diaphragm |
Basal atelactasis commonly occurs in: | 1) Bedridden patients
2) Ascites |
What is another name for contraction atelactasis? | Cicatrization atelactasis |
When does contraction atelactasis occur? | When either local or generalized fibrotic changes in the lung or pleura or prevents expansion of air spaces |
Which type(s) of atelactasis is/are reversible? | Compression and Resorption |
Which type(s) of atelactasis is/are irreversible? | Contraction |
Treating atelactasis early on prevents: | Hypoxemia and superimposed infection of the collapsed lung |
Acute lung injury includes: | A spectrum of bilateral pulmonary damage (endothelial and epithelial) which can be initiated by numerous conditions |
What are the clinical manifestations of Acute lung injury? | 1) Acute onset of dyspnea
2) Decreased arterial oxygen pressure (hypoxemia)
3) Bilateral pulmonary infiltrates on the chest radiograph
4) Absence of clinical evidence of left sided heart failure |
Accumulations in this type of injury are considered noncardiogenic pulmonary edema because: | The pulmonary infiltrates in acute lung injury are caused by damage to the alveolar capillary membrane rather than by left sided heart failure |
Acute lung injury can progress to: | ARDS (Acute respiratory distress syndrome) |
What is ARDS? | A clinical syndrome caused by diffuse alveolar capillary and epithelial damagage |
ARDS is usually characterized by: | 1) Rapid onset of respiratory insufficiency (possibly fatal)
2) Severe arterial hypoxemia which is refractory to oxygen therapy and may progress to organ failure (multisystemic) |
The histologic manifestation of ARDS is known as: | DAD (Diffuse alveolar damage) |
ARDS is associated with two types of lung injury. What are they? | 1) Direct injury to the lung
2) Indirect injury in the setting of a systemic process |
What are the common causes of direct lung injury? | Pneumonia
Aspiration of gastric contents |
What are the uncommon causes of direct lung injury? | Pulmonary contusion |
What are the common causes of indirect lung injury? | Sepsis
Severe trauma with shock |
What are the uncommon causes of indirect lung injury? | Acute pancreatitis |
What is the cause of ARDS in newborns? | Primary deficiency of surfactant |
What are the two barriers of the alveolar capillary membrane? | 1) The microvascular endothelium
2) Alveolar epithelium |
IN ARDS, what occurs to these barriers? | The integrity of these barriers is compromised by either endothelial or epithelial injury, or both (the most common) |
The acute consequences of damage to the alveolar capillary membrane include: | 1) Increased vascular permeability and alveolar flooding
2) Loss of diffusion capacity
3) Widespread surfactant abnormalities (damage to type 2 pneumocytes) |
In, ARDS, lung injury is caused by an imbalance of? | Pro-inflammatory and anti-inflammatory mediators |
As early as 30 minutes after an acute insult: | 1) IL-8 synthesis increases (a neutrophil chemotactic and activating agent) by pulmonary macrophages
2) IL-1, TNF, and manily neutrophils released --> endothelial activation and damage
3) Neutrophils release oxidants, proteases, leukotrienes |
Assault on the endothelium and epithelium increases: | Vascular leakiness and loss of sufactant
The alveaolar unit is unable to expand |
The destructive neutrophilic forces can be counteracted by: | Endogenous anti-Proteases, antioxidants, and inflammatory cytokines (IL-10) |
The balance between the _____ and ______ factors determines the degree of tissue injury and clinical severity of ARDS | Destructive/ Protective |
Which type of cells are thought to have an important role in the pathenogenesis of ARDS? | Neutrophils |
Describe the general morphology of the lungs in acute ARDS | Red, Firm, Airless, and heavy |
Microscopic findings of ARDS affected lung: | 1) Capillary congestion
2) Necrosis of alveolar epithelial cells
3) Interstitial and intra alveolar edema and hemorrhage
4) Increased neutrophils in vascular space, interstitium, and the alveoli |
What is the most characteristic finding in ARDS? | Hyaline membranes in the alveolar ducts |
What do these hyaline membranes consist of? | 1) Fibrin-rich edema fluid
2) Remnants of necrotic epithelial cells |
In the organizing stage of ARDS, type 2 pneumocytes: | Vigorously proliferate and attempt to regenerate the alveolar lining |
Resolution of the lungs after ARDS is: | Unusual |
What happens instead of resolution? | 1) Organization of fibrin exudates, with resultant intra alveolar fibrosis
2) Marked thickening of the alveolar septa, caused by proliferation of interstitial cells and deposition of collagen |
How long does it take most patients to develop the clinical syndrome of acute lung injury or ARDS? | (85%) Within 72 hours of the initiating insult |
The mortality rate from ARDS has decreased from? | 60-40% |
Predictors of poor prognosis include: | 1) Advanced age
2) Underlying bacteremia (sepsis)
3) Multi-system organ failure (especially cardiac, renal, or hepatic) |
After the patient survives the acute stage: | Diffuse interstitial fibrosis may occur with continued compromise of respiratory function |
In patients who survive the acute insult and are spared the chronic stage: | Normal respiratory function returns within 6-12 months |