Acute infective endocarditis with Acute infective endocarditis with vegetationsvegetations

Ventricular Aneurysm complicating Ventricular Aneurysm complicating MIMI

Acutemyocardial infarctionAcutemyocardial infarction

Left ventricular rupture complicating Left ventricular rupture complicating MIMI

Respiratory systemRespiratory system

Fatima Obeidat, MDFatima Obeidat, MD

1. Atelectasis1. Atelectasis

Also known as collapse, is loss of lung Also known as collapse, is loss of lung volume caused by volume caused by inadequate inadequate expansion of airspaces.expansion of airspaces.

It results in shunting of inadequately It results in shunting of inadequately oxygenated blood from pulmonary oxygenated blood from pulmonary arteries into veins, thus giving rise to arteries into veins, thus giving rise to hypoxia.hypoxia.

Compression atelectasis (sometimes called passive or relaxation atelectasis) is usually associated with accumulations of fluid, blood, or air within the pleural cavity, which mechanically collapse the adjacent lung. This is a frequent occurrence with pleural effusions, caused most commonly by congestive heart failure (CHF). Leakage of air into the pleural cavity (pneumothorax) also leads to compression atelectasis. Basal atelectasis resulting from the elevated position of the diaphragm commonly occurs in bedridden patients, in patients with ascites, and in patients during and after surgery.

On the basis of the On the basis of the underlying mechanism or underlying mechanism or the distribution of alveolar the distribution of alveolar collapse, atelectasis is collapse, atelectasis is classified into three forms:classified into three forms:

A. Resorption atelectasisA. Resorption atelectasis - Occurs when total obstruction Occurs when total obstruction

prevents air from reaching distal prevents air from reaching distal airways. airways.

- The air already present gradually The air already present gradually becomes absorbed, and alveolar becomes absorbed, and alveolar collapse follows. collapse follows.

- Causes Causes 1.The most common cause is total 1.The most common cause is total

obstruction of a bronchus by a obstruction of a bronchus by a mucous or mucopurulent plug, this mucous or mucopurulent plug, this frequently occurs postoperatively frequently occurs postoperatively

2. but may also complicate bronchial 2. but may also complicate bronchial asthma, chronic bronchitis, asthma, chronic bronchitis,

3. or the aspiration of foreign bodies, 3. or the aspiration of foreign bodies, particularly in children.particularly in children.

B. B. Compression AtelectasisCompression Atelectasis - sometimes called sometimes called passivepassive or or relaxation relaxation

atelectasisatelectasis is usually associated with is usually associated with accumulations of fluid, blood, or air within accumulations of fluid, blood, or air within the pleural cavity, which mechanically the pleural cavity, which mechanically collapse the adjacent lung.collapse the adjacent lung.

CausesCauses

1. This is a frequent occurrence with 1. This is a frequent occurrence with pleural effusions pleural effusions

2. Leakage of air into the pleural cavity 2. Leakage of air into the pleural cavity (pneumothorax). (pneumothorax).

3. Basal atelectasis resulting from the 3. Basal atelectasis resulting from the elevated position of the diaphragm elevated position of the diaphragm commonly occurs in bedridden commonly occurs in bedridden patients, in patients with ascites, and patients, in patients with ascites, and in patients during and after surgery. in patients during and after surgery.

C. C. Contraction (or cicatrization) Contraction (or cicatrization) atelectasisatelectasis::

- It occurs when either local or It occurs when either local or generalized fibrotic changes in the lung generalized fibrotic changes in the lung or pleura prevent expansion of the lungor pleura prevent expansion of the lung

NOTE:NOTE: Atelectasis (except that caused by Atelectasis (except that caused by contraction) is potentially reversible and contraction) is potentially reversible and should be treated promptly to prevent should be treated promptly to prevent hypoxemia and superimposed infection hypoxemia and superimposed infection of the collapsed lung. of the collapsed lung.

ACUTE LUNG INJURYACUTE LUNG INJURY

- The term The term acute lung injuryacute lung injury encompasses encompasses a spectrum of pulmonary lesions a spectrum of pulmonary lesions (endothelial and epithelial), which can be (endothelial and epithelial), which can be initiated by numerous conditions. initiated by numerous conditions.

- Clinically, acute lung injury manifests asClinically, acute lung injury manifests as

(1) the acute onset of dyspnea, (1) the acute onset of dyspnea, (2) decreased arterial oxygen pressure (2) decreased arterial oxygen pressure

(hypoxemia),(hypoxemia),(3) development of bilateral pulmonary (3) development of bilateral pulmonary

infiltrates on radiographs, infiltrates on radiographs,

(4) absence of clinical evidence of (4) absence of clinical evidence of primary left-sided heart failure. primary left-sided heart failure.

- Since the pulmonary infiltrates in Since the pulmonary infiltrates in acute lung injury are usually caused acute lung injury are usually caused by damage to the alveolar capillary by damage to the alveolar capillary membrane rather than left-sided heart membrane rather than left-sided heart failure , they represent an example of failure , they represent an example of noncardiogenic pulmonary edema.noncardiogenic pulmonary edema.

- Acute lung injury can progress to the Acute lung injury can progress to the more severe more severe acute respiratory distress acute respiratory distress syndrome,syndrome,

Acute Respiratory Distress Syndrome Acute Respiratory Distress Syndrome (ARDS) (ARDS)

- ARDS is a clinical syndrome caused by ARDS is a clinical syndrome caused by diffuse alveolar capillary and epithelial diffuse alveolar capillary and epithelial damage. damage.

- There is usually rapid onset of life-There is usually rapid onset of life-threatening respiratory insufficiency, threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy and that is refractory to oxygen therapy and that may progress to multisystem organ that may progress to multisystem organ failure. failure.

The histologic manifestation of ARDS The histologic manifestation of ARDS in the lungs is known as in the lungs is known as diffuse diffuse alveolar damage.alveolar damage.

ARDS can occur in a multitude of ARDS can occur in a multitude of clinical settings and is associated clinical settings and is associated with either direct injury to the lung or with either direct injury to the lung or indirect injury in the setting of a indirect injury in the setting of a systemic process .systemic process .

- - Direct causesDirect causes- PneumoniaPneumonia- Aspiration of gastric contentsAspiration of gastric contents

-Indirect cause-Indirect cause- PancreatitisPancreatitis- Septic ShockSeptic Shock

MorphologyMorphology In the In the acute phase of ARDSacute phase of ARDS- Microscopically, there is:Microscopically, there is:a.a. necrosis of alveolar epithelial cells,necrosis of alveolar epithelial cells,b.b. interstitial and intra-alveolar edema interstitial and intra-alveolar edema

and hemorrhage, and (particularly and hemorrhage, and (particularly with sepsis) collections of neutrophils with sepsis) collections of neutrophils in capillariesin capillaries. .

a.a. The most characteristic finding is The most characteristic finding is the presence of the presence of hyaline hyaline membranes,membranes, particularly lining the particularly lining the distended alveolar ducts . distended alveolar ducts .

- Such membranes consist of fibrin-- Such membranes consist of fibrin-rich edema fluid admixed with rich edema fluid admixed with remnants of necrotic epithelial cells. remnants of necrotic epithelial cells.

In the In the organizing stageorganizing stage there is there is

a.a. marked proliferation of type II marked proliferation of type II pneumocytes in an attempt to pneumocytes in an attempt to regenerate the alveolar lining. regenerate the alveolar lining.

b.b. Resolution is unusual; more commonly Resolution is unusual; more commonly there is organization of the fibrin there is organization of the fibrin exudates, with resultant intra-alveolar exudates, with resultant intra-alveolar fibrosis. fibrosis.

Clinical CourseClinical Course - Approximately 85% of patients develop Approximately 85% of patients develop

the clinical syndrome of acute lung the clinical syndrome of acute lung injury or ARDS within 72 hours of the injury or ARDS within 72 hours of the initiating insult. initiating insult.

- Despite improvements in supportive Despite improvements in supportive therapy the mortality rate among ARDS therapy the mortality rate among ARDS cases seen yearly is still about 60%. cases seen yearly is still about 60%.

- Predictors of poor prognosis in ARDS Predictors of poor prognosis in ARDS include :include :

a.a. advanced age, advanced age,

b.b. underlying bacteremia (sepsis), underlying bacteremia (sepsis),

c.c. and the development of multisystem and the development of multisystem (especially cardiac, renal, or hepatic) (especially cardiac, renal, or hepatic) failure. failure.

- If the patient survive the acute stage, If the patient survive the acute stage, diffuse interstitial fibrosis may occur diffuse interstitial fibrosis may occur and continue to compromise and continue to compromise respiratory function. respiratory function.

- However, in most patients who However, in most patients who survive the acute insult and are survive the acute insult and are spared the chronic sequela, normal spared the chronic sequela, normal respiratory function returns within 6 respiratory function returns within 6 to 12 monthsto 12 months