cont. copd versus astha

Management of exacerbation

An exacerbation of COPD may present with signs and symptoms like increased dyspnea, increased sputum production, and purulence, respiratory failure, changes in mental status or worsening blood gas abnormalities.

Primary causes for an acute exacerbation

Tracheobronchial infection and air-pollution.

Oxygen therapy

Can be administered as long-term continuous therapy, during exercise or to prevent acute dyspnea to improve the patient’s quality of life and survival.

Pulmonary rehabilitation

A management approach for COPD patients to improve functional capacity and quality of life.

Surgical management

1. Bullectomy; 2. Lung volume reduction surgery; 3. Lung transplantation.

Bullectomy

Bullae are enlarged airspace’s that do not contribute to ventilation but occupy space in the thorax, these areas may be surgically excised.

Lung volume reduction surgery

It involves the removal of a portion of the diseased lung parenchyma. This allows functional tissue to expand.

Lung transplantation

Required when the damage is too much.

Complications of COPD

1. Respiratory insufficiency and respiratory failure are major life-threatening complications of COPD; 2. Pneumonia and respiratory infection; 3. Right-sided heart failure; 4. Pulmonary hypertension; 5. Pneumothorax; 6. Skeleton muscle dysfunction; 7. Depression and anxiety disorders.

Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome (ARDS) is a clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure.

ARDS

It is a form of acute respiratory failure that occurs as a complication of some other condition, is caused by a diffuse lung injury and leads to extravascular lung fluid.

Pathophysiology of ARDS

1. Insult (direct and indirect); 2. Activation of inflammatory cells and mediators (serotonin, histamine, bradykinin); 3. Damage to alveolar capillary membrane; 4. Increased permeability of alveolar capillary membrane; 5. Influx of protein rich edema fluid and inflammatory cells into air filled spaces; 6. Dysfunction of surfactant; 7. Loss of lung tissue.

Effects of ARDS

1. Outward migration of blood cells and fluids from capillaries; 2. Atelectasis; 3. Pulmonary edema; 4. Hyaline membrane formation; 5. Lung compliance; 6. Impairment in gas exchange; 7. ARDS; 8. Pulmonary hypertension.

Phases of ARDS

Three distinct stages (or phases) of the syndrome including: 1. Exudative stage; 2. Proliferative (or fibroproliferative) stage; 3. Fibrotic stage.

Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome (ARDS) is a clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure. It is a form of acute respiratory failure that occurs as a complication of some other condition, is caused by a diffuse lung injury and leads to extravascular lung fluid.

Pathophysiology of ARDS

1. Insult (direct and indirect); 2. Activation of inflammatory cells and mediators (serotonin, histamine, bradykinin); 3. Damage to alveolar capillary membrane; 4. Increased permeability of alveolar capillary membrane; 5. Influx of protein rich edema fluid and inflammatory cells into air filled spaces; 6. Dysfunction of surfactant; 7. Loss of lung tissue.

Effects of ARDS

1. Outward migration of blood cells and fluids from capillaries; 2. Atelectasis; 3. Pulmonary Edema; 4. Hyaline membrane formation; 5. Lung compliance; 6. Impairment in gas exchange; 7. ARDS; 8. Pulmonary hypertension.

Phases of ARDS

Three distinct stages (or phases) of the syndrome including: 1. Exudative stage; 2. Proliferative (or fibroproliferative) stage; 3. Fibrotic stage.

Exudative Stage (0-6 Days)

Characterized by: Accumulation of excessive fluid in the lungs due to exudation (leaking of fluids) and acute injury. Hypoxemia is usually most severe during this phase of acute injury, as is injury to the endothelium (lining membrane) and epithelium (surface layer).

Proliferative (or fibroproliferative) stage

This stage occurs after the acute exudative phase. There is organization of the intra-alveolar exudate, proliferation of type II pneumocytes, and fibroblast activity.

Fibrotic stage

This stage is characterized by progressive fibrosis of the lung, resulting in decreased lung compliance and persistent impairment in gas exchange.

Exudative Stage (0-6 Days)

Characterized by accumulation of excessive fluid in the lungs due to exudation (leaking of fluids) and acute injury. Hypoxemia is usually most severe during this phase of acute injury, as is injury to the endothelium (lining membrane) and epithelium (surface layer).

Proliferative stage

Characterized by organization of the alveolar exudate, regeneration of epithelial cells, and beginning of fibrosis.

Fibrotic stage

Characterized by extensive fibrosis, collagen deposition, and irreversible changes in the lung architecture.

COPD and Asthma

COPD and asthma are both obstructive airway diseases but differ in their causes, progression, and reversibility of airflow limitation.

COPD

Usually caused by long-term exposure to irritants such as cigarette smoke or environmental pollutants. Airflow limitation is persistent and progressive.

Asthma

Usually associated with airway inflammation and bronchial hyperresponsiveness. Airflow limitation is usually reversible.

COPD versus Asthma

1. COPD: persistent airflow limitation; 2. Asthma: reversible airflow limitation; 3. COPD: progressive disease; 4. Asthma: variable symptoms; 5. COPD: commonly associated with smoking; 6. Asthma: commonly associated with allergens and triggers.