Respiratory Review Two

​Pulmonary Edema

•Signs and symptoms

• Cough, orthopnea, rales—in mild cases

• Hemoptysis

•Frothy, blood-tinged sputum

•Treatment

• Treat causative factors.

• Supportive care

•Possibility of positive-pressure mechanical ventilation

Multiple Choice

A patient with hypoproteinemia could develop pulmonary edema because of

• pulmonary hypertension

• decreased osmotic pressure

• increased capillary permeability

• increased osmotic pressure

•Inflammation in lungs is present.

•Increases permeability of capillaries

•Plasma protein levels are low.

•Decreases osmotic pressure of plasma

•Pulmonary hypertension develops.

Atelectasis

• Leads to decreased gas exchange and hypoxia

•Alveoli become airless.

• Collapse and inflammation or atrophy occur.

•Process interferes with blood flow through the lung.

•Both ventilation and perfusion are altered.

•Affects oxygen diffusion

Multiple Choice

All of the following are causes of atelectasis EXCEPT:

• Tumor

• Increased surfactant

• Mucus plug

• Post- op

Mechanisms that can result in atelectasis

•Obstructive or resorption atelectasis

• Caused by total obstruction of airway

•Compression atelectasis

• Mass or tumor exerts pressure on part of the lung.

•Increased surface tension in alveoli

• Prevents expansion of lung

•Fibrotic tissue in lungs or pleura

• May restrict expansion and lead to collapse

•Postoperative atelectasis

Can occur after surgery

Multiple Choice

The signs and symptoms of a small atelectatic area is/are

• Dyspnea

• Chest pain

• Both

• Neither

Pulmonary Embolus

•Blood clot or mass that obstructs pulmonary artery or any of its branches

•Effect of embolus depends on material, size, and location

•Small pulmonary emboli might be “silent” unless they involve a large area of lung.

•Large emboli may cause sudden death.

•90% of pulmonary emboli originate from deep vein thromboses in legs; are preventable

Pulmonary Embolus

•Signs and symptoms

• Transient chest pain, cough, dyspnea—small emboli

• Larger emboli—increased chest pain with coughing or deep breathing; tachypnea and dyspnea develop suddenly.

• Later—hemoptysis and fever

• Hypoxia—causes anxiety, restlessness, pallor, tachycardia

• Massive emboli

• Severe crushing chest pain, low blood pressure, rapid weak pulse, loss of consciousness

Pulmonary Embolus Tx

Treatment

Assessment of risk factors

Prolonged bed rest and compression stockings

Surgically Inserted filter into vena cava (some cases)

Heparin or streptokinase

Mechanical ventilation

Embolectomy

​Atelectasis

•Signs and symptoms

•Small areas are asymptomatic.

•Large areas

• Dyspnea

• Increased heat and respiratory rates

• Chest pain

Pleural Effusion

•Exudative effusions

• Response to inflammation

•Transudate effusions

• Watery effusions (hydrothorax)

• Result of increased hydrostatic pressure or decreased osmotic pressure in blood vessels

Pleural Effusion

•Signs and symptoms

• Dyspnea

• Cyclic chest pain

• Increased respiratory and heart rates

•Treatment

• Remove underlying cause to treat respiratory impairment.

• Analyze fluid to confirm cause.

• Chest drainage, thoracocentesis to remove fluid and relieve pressure

Pneumothorax

•Closed pneumothorax

• Air can enter pleural cavity from internal airways—no opening in chest wall

•Simple or spontaneous pneumothorax

• Tear on the surface of the lung

•Secondary pneumothorax

• Associated with underlying respiratory disease

• Rupture of an emphysematous bleb on lung surface or erosion by a tumor or tubercular cavitation

Multiple Choice

A tension pneumothorax is life-threatening because

• decreased venous return

• decreased pressure in the thorax

• increased ventilation

• increased stroke volume

Pnthx

•Open pneumothorax

• Amospheric air enters the pleural cavity though an opening in the chest wall.

• “Sucking” wound

• Large opening in chest wall

•Tension pneumothorax

• Most serious form

• Result of an opening through chest wall and parietal pleura or from a tear in the lung tissue and visceral pleura

• Air entry into pleural cavity on inspiration but hole closes on expiration

• Trapping air leads to increased pleural pressure and atelectasis

IRDS

•Usually related to premature birth

•Lack of surfactant in alveoli

•Poorly developed alveoli are difficult to inflate.

• Diffuse atelectasis results.  

• Decreased pulmonary blood flow—pulmonary vasoconstriction—severe hypoxia

•Poor lung perfusion and lack of surfactant

•Increased alveolar capillary permeability

•Fluid and protein are leaking into the interstitial area and alveoli, hyaline membrane formation

Multiple Choice

Adult Respiratory Distress Syndrome is caused by

• Increased permeability of pulmonary capillaries

• Release of chemical mediators

• Damage to surfactant producing cells

• Increased fluid and protein in the interstitium and alveoli

ARDS

•Results from injury to the alveolar wall and capillary membrane

•Causes the release of chemical mediators

• Increases permeability of alveolar capillary membranes

• Increased fluid and protein in interstitial area and alveoli

• Damage to surfactant-producing cells

• Diffuse necrosis and fibrosis if patient survives

•Multitude of predisposing conditions

•Often associated with multiple organ dysfunction or failure