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Pathophysiology Chapter 13- Respiratory System Disorders

Terms in this set (86)

The upper respiratory tract is made up of-
The passageways that conduct air between the atmosphere and the lungs.
Includes the nasal passages, paranasal sinuses, nasopharynx, oropharynx, larynx, and pharyngeal tonsils (adenoids).
The lower respiratory tract consists of-
The trachea, bronchial tree, and the lungs, where gas exchange takes place.
Conduction Airways (Anatomic dead space) consist of-
Nasopharynx
Oropharynx
Larynx
Trachea
Bronchi
Bronchioles
Surfactant
Has a detergent action that reduces surface tension of the alveolar fluid, facilitating inspiration and preventing total collapse of the alveoli during expiration.
Airway resistance
Refers to the opposition to airflow.
Increases with-
- Asthma
- Bronchial constriction, especially in medium size airways.
- Low lung volume
Lung compliance
The ability of the lungs to expand/the extent to which they expand.
High compliance results in low elasticity.
- Emphysema causes overstretching of lungs -> inflate easily, but lose recoil.
Low compliance results in high elasticity.
- Pulmonary Fibrosis -> lungs filled with scar tissue, can't breathe in easily and deeply -> lungs recoil quickly.
Impaired expiration can cause an increase in ___________ volume, therefore-
Residual; increased carbon dioxide levels in body fluids.
The primary control centers for breathing are located in the ___________ and the __________.
Medulla; pons
Hypoxemia
The reduction of oxygen in the arterial blood.
Causes- inadequate amount of O2 in the air; disease within the respiratory, circulatory, or neurological system.
Symptoms- depends on severity
- Cyanosis, restlessness, agitation, impaired judgement.
- Metabolic acidosis
Hypercapnia
Increase of carbon dioxide content in the arterial blood.
Causes- disorders causing hypoventilation, mismatch in ventilation and perfusion.
Symptoms- depends on severity
- Can affect the kidney, nervous and cardiovascular systems.
- Respiratory acidosis
Movement of gas always occurs from a _______- pressure area to a ______- pressure area.
High; low
General manifestations of Respiratory Diseases include-
Sneezing
Coughing
Sputum (mucoid discharge)
Altered breathing patterns and characteristics
Abnormal or absent breath sounds
Dyspnea
Cyanosis
Pleural pain
Friction rub
Clubbed fingers
Changes to arterial blood gasses (ABGs)
Clubbing
A painless, firm, fibrotic enlargement at the end of the digit (finger or toe).
Sometimes results from chronic hypoxia associated with respiratory or cardiac diseases.
Paroxysmal nocturnal dyspnea
A sudden acute type of dyspnea common in patients with left-sided congestive heart failure. During sleep the body fluid is redistributed, leading to pulmonary edema, and the individual wakes up gasping for air and coughing.
Rales
Light bubbly or crackling sounds associated with serous secretions.
Rhonci
Deeper and harsher sounds resulting from thicker mucus.
Absence of breath sounds indicate-
Nonaeration or collapse of a lung (atelectasis)
Sputum
Normal- relatively thin, clear, and colorless or cream color.
Abnormal-
- Yellowish-green, cloudy, thick mucus is often an indication of a bacterial infection.
- Rusty or dark-colored sputum is usually a sign of pneumococcal pneumonia.
- Thick, tenacious (sticky) mucus may occur in patients with asthma or cystic fibrosis.
- Blood-tinged secretions may result from a chronic cough and irritation that causes rupture of superficial capillaries, but it may also be a sign of a tumor or TB.
- Hemoptysis is blood-tinged (bright red) frothy sputum that is usually associated with pulmonary edema.
Stridor
High-pitched crowing noise
Usually indicates upper airway obstruction
Rhinorrhea
"Runny nose"
Nasal cavity is filled with mucous fluid
Retractions
Inward movement of the muscle between the ribs as a result of reduced chest cavity.
Accessory muscle use
Muscles other than the diaphragm and intercostal muscles that may be used for labored breathing.
May include the sternocleidomastoid, scalene, pectoralis major, and serratus muscles.
The Common Cold (infectious rhinitis)
Caused by a viral infection of the upper respiratory tract. Spread by airborne or direct contact.
Most common cause is a rhinovirus.
There are over 200 possible causative organisms, so it's impossible to create a vaccine.
Prevention is key-
- Most common reservoir-> hands, children.
- Portal of entry-> nose, eyes
- Most contagious-> first 3 days
- Cold viruses can survive outside of the body for-> 5 hours
Pathophysiology, Concerns, and Treatment of The Common Cold
Patho-
After infection, inflammation of the mucus membranes within the nasal passages and pharynx occurs, causing them to become red + swollen.
Increased production of secretion also occurs.
Concerns
Secondary infections
- Strep throat (pharyngitis), sinusitis
Treatment- treat the symptoms
Symptoms of The Common Cold
Sore, scratchy throat
Sneezing
Dryness followed by copious nasal secretions/rhinorrhea/nasal obstruction
Coughing
Fever- common in children, not adults
Malaise, Fatigue, Headache, Myalgia
Hoarseness, Sinus congestion
Rhinosinusitis (sinusitis)
Inflammation of the nasal passages and para-nasal sinuses.
Patho- Obstruction from the exudate, swelling, and pressure causes the narrowing of the ostia that drains the sinuses.
Cause-
Viral, bacterial, or both.
Acute or chronic .
- Acute-> Rhinovirus
- Chronic-> Staphylococcus aureus
Manifestations of Rhinosinusitis (sinusitis)
Acute viral-
- Facial pain, headache, fever, purulent nasal discharge, decreased sense of smell, fever.
- Maxillary sinus involvement: pain in teeth and with bending over.
Acute bacterial-
- Symptoms similar to acute, but may be more pronounced (severe).
Chronic-
- More side effects-> Fullness in ears, postnasal drip, hoarseness, chronic cough, loss of taste and smell, dull/constant headache.
Influenza (flu)
An acute, highly contagious viral infection of both the upper and lower respiratory tracts.
Virus mutate constantly, preventing effective immune defense for prolonged periods of time.
- Sporadic or epidemic
- Three types: A, B, C
- Spread by droplets
Risk factors- age, other chronic medical conditions, pregnancy.
Manifestations-
- Sudden onset fever, fatigue, aches and pains.
- Secondary infection: viral or bacterial pneumonia
Most deaths during flu epidemics result from _________________.
Pneumonia
Treatment and prevention of Influenza (flu)
Treatment-
Symptomatic and supportive.
- unless secondary bacterial infection develops.
Antiviral drugs taken within the first 48 hours.
- may reduce symptoms and duration.
- reduces risk of infecting others
Prevention-
Respiratory hygiene
Vaccination is recommended for most individuals
Acute Bronchitis
Inflammation of the tracheobronchial tree.
Attributed to an infectious process.
- Manifests most often during respiratory infections.
- Commonly occurs during the winter season.
Many types of infectious organisms are involved.
Manifestations of Acute Bronchitis
Purulent, productive cough- yellow/green sputum
Fever, Malaise, Myalgia, Arthralgias
Rhinorrhea, nasal congestion
Sore throat
Wheezing, Dyspnea, Chest discomfort, Rhonchi
Pneumonia is classified based on-
1. Causative agent - viral, bacterial, fungal.
2. Anatomical location of infection - throughout both lung, or consolidated in one lobe.
3. Pathophysiological changes - changes in interstitial tissue, alveolar septae, alveoli.
4. Epidemiological data - nosocomial (hospital-acquired), community-acquired.
Lobar Pneumonia (pneumococcal pneumonia)
Infection is localized in one or more lobes.
Usually caused by streptococcus pneumoniae.
Community-based, often occurs in healthy young adults.
Pathophysiology of Lobar Pneumonia (pneumococcal pneumonia)
Inflammation and vascular congestion develop in the alveolar wall.
Exudate forms in the alveoli.
- contains fibrin and forms a consolidated mass.
- produces rusty sputum due to the presence of RBCs.
Adjacent pleurae are frequently involved, producing pleuritic pain at the site.
Infection may spread to the pleural cavity, causing empyema.
The filling of the alveoli with exudate reduces the diffusion of gases, particularly oxygen, and decreased blood flow to the affected lobe. Hypoxia and metabolic acidosis may occur.
Manifestations of Lobar Pneumonia (pneumococcal pneumonia)
Sudden onset
Systemic signs- high fever with chills, fatigue, leukocytosis.
Dyspnea, tachypnea, tachycardia.
Pleural pain
Rales
Productive cough- typical rusty colored sputum.
Confusion and disorientation
Bronchopneumonia
Diffuse pattern of infection in both lungs.
Cause can be due to several species of microorganisms.
Inflammatory exudate forms in the alveoli, interfering with oxygen diffusion.
Onset tends to be insidious.
S/S- moderate fever, cough, rales.
Productive cough with purulent sputum- usually yellow or green.
Treatment- antibacterial
Legionnaires' Disease
Caused by Legionella pneumophila
- thrives in warm, moist environments
- often a nosocomial infection
If untreated-
- causes severe congestion and consolidation, with necrosis in the lung, and possible fatal consequences.
Severe Acute Respiratory Syndrome (SARS)
An acute respiratory infection.
Causative microbe: SARS- associated coronavirus.
- transmitted by respiratory droplets-close contact.
Risk factors-
- travel to endemic or epidemic areas (China, Hong Kong, and Taiwan), or close contact with such a traveler.
Manifestations and Treatment of Severe Acute Respiratory Syndrome (SARS)
Manifestations-
First signs-
- Fever, headache, myalgia, chills, anorexia, possibly diarrhea.
Later signs-
- Dry cough, marked dyspnea, areas of interstitial congestion, hypoxia
Treatment-
- Antivirals, glucocorticoids
- High fatality rate (11%)
Tuberculosis (TB)
Bacterial lung infection usually caused by Mycobacterium tuberculosis.
- Spread by direct inhalation of infective droplet nuclei.
—
Tuberculosis (TB) Primary Infection
Occurs when the microorganisms (bacilli) first enter the lungs, are engulfed by macrophages, and cause a local inflammatory reaction.
Some bacilli migrate through the lymphatics, lodge in lymph nodes, activating the immune system (Type IV- cell mediated reaction).
Lymphocytes and macrophages cluster together to form a granuloma at the site of inflammation.
- Granuloma consists of dead macrophages and necrotic tissue.
- Granulomas are usually walled off by the body and calcified over time.
Can lead to active TB or latent TB
Tuberculosis (TB) Secondary Infection
Reactivation of TB
- Can occur years after primary infection.
- Usually due to a decrease in host resistance.
As organisms multiply, large areas of necrosis results.
Can spread to other areas of the body.
Manifestations are similar to active TB but more severe.
Manifestations of Active Tuberculosis (TB)
Often asymptomatic
- especially in the elderly and immunocompromised.
Early symptoms are vague-
- Anorexia, malaise, fatigue, low grade fever, night sweats
Other symptoms (may trigger them to seek help)-
- Pleuritic chest pain
- Cough (initially non-productive, but as the TB progresses it turns into a productive cough with purulent sputum).
- Hemoptysis (cough up blood), purulence.
- Weight loss
- Crackles and Wheezes
Mantoux skin test
Used to test for TB.
10mm = positive, or 5mm = positive for those with autoimmune disorders.
Positive = exposure, not necessarily that you have TB.
Tuberculosis (TB) - Chest X-Ray (CXR)
Required if positive skin test occurs.
CXR results-
1. Pleural effusion (often associated with active TB)
- accumulation of fluid in the pleural space. Appears white on x-ray.
- in middle, upper lobes with local lymph node inflammation.
2. Calcification r/t granulomas that formed (shows past or resolved TB).
- indicates healing and dormancy.
3. Simon's foci (nodules) (on the calcification ⬆️)
- usually indicates a reactivation of TB
- often seen in upper lobes
Cystic Fibrosis (CF)
An inherited (genetic) disorder. Gene is located on chromosome 7. Autosomal recessive.
Mean survival age is 37.
Produces tenacious (abnormally thick + sticky) mucus from exocrine glands.
Primarily affects the lungs and pancreas.
Pathophysiology of Cystic Fibrosis (CF)- Digestive and Reproductive tract
Digestive tract-
The first indication of abnormality may be meconium ileus in newborns (small intestine is blocked by mucus).
Blockage of pancreatic ducts.
- Decrease in pancreatic enzymes into the digestive tract -> malabsorption and malnutrition.
Obstruction of bile ducts.
Salivary glands often mildly affected.
Reproductive tract-
Obstruction of vas deferens in males, and obstruction of the cervix in females. Leading to sterility or infertility.
S/S of Cystic Fibrosis (CF)
Meconium ileus (at birth- small intestine is blocked by mucus)
Salty skin
Signs of malabsorption- steatorrhea (fatty stools), abdominal distention, failure to gain weight.
Chronic cough and frequent respiratory infections.
Failure to meet normal growth milestones.
Dehydration
Diagnosis of Cystic Fibrosis (CF)
Genetic testing
Sweat test
Pulmonary function tests- tested periodically throughout a patient's lifetime to monitor how they are doing.
Asthma
A disease that involves periodic episodes of severe but reversible bronchial obstruction in persons with hypersensitive or hyper-responsive airways.
- Presents as an acute attack.
- Genetically or environmentally induced
- Reaction rated as mild, intermittent, or severe.
Classifications-
-Acute- a single episode. Infection related. ex- bronchitis.
-Chronic- long term condition. Constant triggers.
Types of Asthma-
Extrinsic- involves acute episodes triggered by a type 1 hypersensitivity reaction to an inhaled allergen (trigger). Most common in children, can grow out of it.
Intrinsic- starts in adulthood. Other types of stimuli target hyper-responsive tissue in the airway, imitating the acute attack. Triggered by URI, colds, stress, smoke.
Pathophysiology of Cystic Fibrosis (CF)- Lungs and Sweat glands
Lungs-
Mucus obstructs airflow in the bronchioles and small bronchi. Causes permanent damage to bronchial walls. Lots of respiratory issues are seen in CF patients- infections, breathing.
Sweat glands
Sweat has high sodium chloride content.
Dehydration can increase viscosity of the mucus.
Pathophysiology of Asthma
Characterized by the sudden, spasmodic narrowing of bronchial airways due to-
1. Inflammation and increased mucus secretions.
2. Contraction of smooth muscle.
3. Increased secretion of thick mucus into the passages.
These changes created obstructed airways, partially or totally, and interfere with airflow and oxygen supply.
Manifestations of Asthma
Sudden dyspnea ,Wheezing, Chest tightness.
Rapid and labored breathing, with use of accessory muscles and possible chest retractions.
Thick and tenacious (sticky) mucus is coughed up.
Rapid pulse and respiration (trying to breath and get O2). Pulsus paradoxus may occur when the pulse differs on inspiration and expiration.
Severity depends on-
Cyanosis
Ability to lie flat
Ability to speak
Accessory muscle use
Status Asthmaticus
A life-threatening complication of asthma.
- Caused by prolonged bronchospasms and severe hypoxemia.
- Diagnosed when a severe asthma attack is resistant to bronchodilator therapy/medical interventions.
- Hypersensitivity to ASA (aspirin) may precipitate.
Additional symptoms-
- Bronchial edema
- Tenacious, thick secretions
- Mucus plugging (lump of mucus that lodged itself in a location. No air can pass)
- Atelectasis (partial collapse of lung tissue)
Chronic Obstructive Pulmonary Disease (COPD)
A group of common chronic respiratory disorders that are characterized by progressive tissue degeneration and obstruction in the tissue of the lungs.
Two types- 1) Chronic bronchitis 2) Emphysema.
Causes irreversible and progressive damage.
For diagnosis you need to have symptoms for 3 months in a row for 2 years.
Predisposing factors-
Smoking
Occupational
Airway infection (chronic)
Asthma
Airway hyper-responsiveness
Cor pulmonale
Right-sided congestive heart failure due to lung disease.
Emphysema
The destruction of the alveolar walls and septae, which leads to large, permanently inflated alveolar spaces.
- Recurrent inflammations releases enzymes that damage the lung cells causing the enlargement.
Causes-
Smoking
Alpha 1 antitrypsin deficiency (genetic)
Distinguishing characteristic- Airflow limitation caused by a lack of elastic recoil in the alveoli.
Pathophysiology of Emphysema
Destruction of the alveolar air spaces leads to-
- decreased elastic recoil
- impaired and decreased surface area for gas exchange.
Decreased recoil leads to-
- air trapping (residual air)
- increased intrathoracic pressure
Ventilation-Perfusion (V:Q) mismatch results-
-Ventilation without perfusion (air is getting to the alveoli but not perfusing)
- Hyperventilation
- Cardiac output decreases
- Results in limited blood flow through an oxygenated lung-
• Tissue hypoxia - suffering from low oxygen levels.
• Pulmonary cachexia - muscle wasting and weight loss (b/c aren't getting O2)
• Respiratory fatigue - eventually failure.
Manifestations of Emphysema
Emaciated (abnormally thin or weak)
Barrel chest (increased anterior-posterior diameter of the thorax)
Pursed lip breathing
Accessory muscle use
Tachypnea
Enlarged neck muscles
Tripod sitting position
Wheezing
Distant heart tones
Decreased breath sounds
Grunting
Pink puffers (because of the dyspnea, hyperventilation, and overinflation)
Chronic Bronchitis
Airway obstruction of the major and small airways.
Inflammation and obstruction, repeated infections, and chronic coughing characterize bronchitis.
Long term inflammation of the tracheobronchial tree accompanied by-
- chronic productive cough
- excessive mucus production
- airway obstruction
Inflammation caused by irritants or infection-
- most common irritant: smoke
Pathophysiology of Chronic Bronchitis
A chronic inflammatory response causes damage to the epithelial lining and smooth muscle.
- poorly ventilated lung with normal perfusion.
- the mucus and ciliary response is then impaired.
- obstruction occurs from inflammation + secretions.
• unable to clear bacteria and mucus normally.
Ventilation-perfusion (V:Q) mis-match results:
- cardiac output increases
- ventilation decreased
- results in rapid circulation of poorly ventilated lung. Causing- hypoxemia, polycemia (multiple production of RBCs), and CO2 retention
Manifestations of Chronic Bronchitis
Productive cough
Progression to intermittent dyspnea (SOB) over time
Accessory muscle use
Clubbing (r/t chronic hypoxia)
Reddish/grey/blue skin: "Blue bloater"
Over time- progressive heart failure (cor pulmonale) (r/t increased cardiac output) and respiratory failure.
- Weight gain
- Edema
Bronchiectasis
Localized, irreversible dilation of part of the bronchial tree.
Affected bronchi are dilated, inflamed, and collapse easily.
Usually caused by staphylococcus or klebsiella.
Can be a secondary infection in patients with cystic fibrosis.
Collapse -> causes airflow obstruction, impairs clearance of secretion.
S/S- Chronic cough and production of copious amounts of purulent sputum (1 to 2 cups per day).
Respiratory disorders- Infections
Common cold
Rhinosinusitis
Influenza
Acute Bronchitis
The Pneumonias
Severe acute respiratory syndrome (SARS)
Tuberculosis
Respiratory disorders- Obstructive diseases
Cystic fibrosis
Asthma
Status asthmaticus
Chronic obstructive pulmonary disease (COPD)
Emphysema
Chronic bronchitis
Bronchiectasis
Respiratory disorders- Vascular and Expansion disorders
Pulmonary embolism
Pulmonary edema
Atelectasis
Pleural effusion
Pneumothorax
Acute respiratory distress syndrome (ARDS)
Pulmonary edema
Refers to capillary fluid collecting in the alveoli.
This accumulation of fluid results in-
- lung stiffness
- difficult lung expansion
- impaired gas exchange
Life-threatening complication.
Most common cause- cardiac disease
Excessive amounts of fluid in the interstitial areas and alveoli interfere with the diffusion of oxygen, causing severe, hypoxemia, as well with the action of surfactant, leading to difficulty in expanding the lungs, which ultimately collapse.
Pulmonary edema- Risk factors
Cardiovascular causes-
- Coronary artery disease (CAD), Acute MI
- Left ventricle (LV) failure
- Hypertension
- Heart valve disease
Non-cardiogenic causes-
- Fluid overload
- Drug overdose
- Post-pneumonectomy
- ARDS
- Neurological dysfunction
- High altitude
- Inhalation of toxic gases
S/S of Pulmonary edema
Restlessness, edema
Orthopnea
Tachypnea, dyspnea
Cough with frothy (due to air mixed with secretions) pink (blood-tinged owing to ruptured capillaries in the lungs) sputum.
Cyanosis
N/V/D
Crackles, wheezes
Sense of suffocation
Confusion, stupor
Pulmonary Embolism (PE)
Occlusion of a portion of the pulmonary blood vessels by an embolus (mass) or thrombus (blood clots).
Most commonly originate from the deep leg veins (DVT- deep vein thrombosis).
If massive, can cause death within one or two hours.
Embolus vs. Thrombus
Embolus- matter that enter the systemic venous circulation. Examples- air, bone marrow, tumor cells, fat: from long bone, amniotic fluid, etc.
Thrombus- blood clot that causes an obstruction. Form due to- venous stasis, vessel wall injury, hypercoagulability.
Clinical risk factors for Pulmonary Embolus (PE)
Current deep vein thrombosis (DVT)- esp in legs
Prior history of DVT or PE
Recent surgery or pregnancy
Prolonged immobilization
Malignancy - esp lung or prostate
Obesity
Advancing age
Hypercoagulability
Smoking
Estrogen therapy
CHF
Major trauma
Typical Pathophysiology of Pulmonary Embolus (PE)
1. Emboli travels via the vena cava to the right side of the heart and then to the pulmonary artery.
2. Pulmonary vasoconstriction causes hypertension.
- Absent blood flow
• ventilation available
• perfusion limited
- Low surfactant -> atelectasis -> more hypoxemia.
3. Infarction or dissolution
- Infarct: rare, invasive
- Dissolution: reabsorption
Manifestations of Pulmonary Embolus (PE)
Dyspnea
Pleuritic chest pain
Apprehension, restlessness, feeling of impending doom.
Cough
Hemoptysis (coughing up blood)
Low SaO2 levels
Tachypnea
Crackles
Pleural friction rub
Tachycardia
Diaphoresis
Fever
Petechiae
Atelectasis
The nonaeration or collapse of lung tissue (alveoli collapse) leading to decreased gas exchange and hypoxia.
Results from-
Compression-
- outside of the airway. Ex- large heart or lymph nodes
Absorption (two types-
- Obstruction - something keeps air from entering airways
- Hypoinflation - incomplete expansion
Pleural effusion
The presence of excessive fluid in the pleural cavity.
Effusion causes- increases pressure in the pleural cavity, separation of the pleural membranes
Patho-
Increased amount of fluid enters the pleural space.
- Increased pressure in the pleural cavity causes separation of the pleural membranes.
This separation prevents expansion of the lung during inspiration.
A large amount of fluid can cause atelectasis.
Etiology of Pleural effusion
Exudative effusions-
A response to inflammation.
Increased capillary permeability allows fluid containing protein and WBCs to leak into the pleural cavity.
Transudate effusions-
Watery effusions (hydrothorax)
The result of increased hydrostatic pressure or decreased osmotic pressure in the blood vessels.
- fluid shift occurs
Commonly associated with liver and kidney disease.
Hemothorax
The fluid is blood resulting from trauma, cancer, or surgery.
S/S and Treatment of Pleural effusion
S/S- dyspnea, cyclic chest pain, increased respiratory + heart sounds.
Treatment- remove underlying cause, analyze fluid (to confirm cause), thoracocentesis, and chest drainage.
Pneumothorax
Air in the pleural cavity, causing lung collapse (atelectasis) on the affected side.
Two main types- open or closed
Closed Pneumothorax
Occurs when air can enter the pleural cavity through an opening directly from the internal airways. There is no opening in the chest wall.
Causes an increased pleural pressure which does not allow the lung to expand normally.
Types-
Spontaneous
- Primary: occurs in otherwise healthy individuals.
- Secondary: associated with an underlying condition.
Open Pneumothorax
Refers to atmospheric air entering the pleural cavity through an opening in the chest wall.
Types-
Traumatic
- blunt or penetrating trauma
- chest injuries, surgical complications
- fractured ribs.
Tension
- most serious form of Pneumothorax. Life-threatening, displaces structures (Mediastinal shift)
- associated with open chest injuries.
- air enters through pleural space but cannot leave.
S/S of Pneumothorax
Symptoms-
Sudden, sharp pleuritic pain
Asymmetrical chest wall movement
Shortness of breath
Cyanosis
Respiratory distress
Additional symptoms of a Tension Pneumothorax-
Mediastinal shift
Decreased cardiac output
Hypotension
Tachypnea and tachycardia
Adult or Acute Respiratory Distress Syndrome (ARDS)
Disruption to the pulmonary capillary membranes.
Causes of ARDS- shock, sepsis, trauma.
Characterized by-
Severe dyspnea, rapid onset.
Hypoxemia
Pulmonary infiltrates and edema
Restlessness, apprehension, retractions
Pathophysiology and Complications of Adult or Acute Respiratory Distress Syndrome (ARDS)
Patho-
Begins with injury to the alveolar wall and capillary membranes. This causes-
- release of chemical mediators.
- increased permeability of alveolar capillary membranes.
- increased fluids and protein levels in the interstitial area and alveoli.
- damage to the surfactant-producing cells.
Results in- decreased diffusion of oxygen, reduced blood flow to the lungs, difficulty in expanding the lungs, and diffuse atelectasis.
Complications- pneumonia, congestive heart failure (CHF)
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