Alterations in the Pulmonary System

Functions of the Respiratory System

• GAS EXCHANGE

• Lungs serve as a host defense by providing a barrier between the inside of the body and the external environment

• Lung is a metabolic organ that synthesizes and metabolizes certain compounds

Conducting Airways

• Section in which air moves as it passes between the atmosphere and the lungs (don’t participate in gas exchange)

• Warms, filters, moistens, and removes foreign materials via mucociliary blanket from air as it moves through structures

• Consists of:

- Nasal Passages

- Mouth & Pharynx

- Larynx

- Tracheobronchial Tree

Nasal Passages

• Preferred route of entrance for air

• Filters, warms, humidifies air; coarse hairs filter and trap large particles
  from the air

Mouth & Pharynx

• Mouth is alternate airway when nasal passages are plugged or large
  volumes of air are needed (Exercise)

• Oropharynx is the only opening between nose, mouth, and lungs-
  obstruction leads to immediate cessation of ventilation

Larynx

• Connects oropharynx with trachea between upper airways and lungs

• Two functions: speech & protecting the lungs from foreign substances

• Epiglottis is located above the larynx- opens during breathing and closes
  during swallowing to keep foreign substances out

• Substances other than air (liquid, food, etc.) that enter the airway are not
  easily removed. When they enter the lungs, aspiration pneumonia can
  occur

Tracheobronchial Tree

• Trachea- “windpipe;” connects larynx with major bronchi

• Bronchi- right and left mainstem bronchus; carina is a highly sensitive
  area between bronchi; each bronchus enters the lungs through a slit called
  the hilum; bronchi divide into segments and get smaller at the distal ends

• Bronchioles- Segmental bronchi continue to branch until they become the
  smaller, terminal bronchioles. Bronchospasm can narrow these conducting
  airways and impair airflow

Lungs & Respiratory Airways

• Area of gas exchange

• Other functions: inactivate vasoactive substances such as bradykinin, convert angiotensin
  I to angiotensin II, & serve as a reservoir for blood storage

• Consists of 

- Lobules

- Alveoli

- Pleura

- Pulmonary Vasculature

Lobules

• Smallest functional units of lungs

• A branch of a terminal bronchiole, an arteriole, the pulmonary capillaries, and a
  venule supply each lobule

• Blood enters lobules through a pulmonary artery and exits through a pulmonary
  vein.

Alveoli

• Specific site of gas exchange

• Alveolar sacs are thin-walled, cup shaped structures separated from each other by
  thin alveolar septa. A single network of capillaries occupies most of the septa.

• Approximately 300 million alveoli in an adult lung (large surface area)

• Type I and Type II alveolar cells (Type II synthesize pulmonary surfactant)

• Surfactant: Lipoprotein that reduces surface tension, allowing alveoli to stay
  “open”

• Alveolar macrophages: Responsible for destroying inhaled pathogens and
  removing inhaled particulate matter (dust or pollen). Expelled after activation by
  coughing or swallowing.

Pleura

• Thin, transparent, double-layered serous membrane lining the thoracic cavity and
  encasing the lungs

• Allows for no separation between the lungs and chest wall

• This cavity is an area where inflammation can occur and exudate can accumulate.

• Causes Pleural effusion

Pulmonary Circulation

• *Review circulation of blood through the heart to and from the lungs

• Pulmonary arteries (blood moves away from heart) vs Pulmonary veins (blood moves towards heart)

• Participates in gas exchange

Bronchial Circulation

• Distributes blood to the conducting airways and the supporting structures of the
  lungs

• Does not participate in gas exchange

Innervation of Lungs

• No pain receptors in the lung tissues = no perception of pain

• Pain receptors/fibers are ONLY located in the pleura

• Automonic NS → Sympathetic NS → Parasympathetic NS

• Parasympathetic NS: airway constriction and increased
  glandular secretions

• Sympathetic NS: airway relaxation, blood vessel constriction,
  and inhibition of glandular secretions

Exchange & Transport Gases

• Nitrogen is the most abundant gas in the air; Oxygen is about 21%

• Arterial Blood Gases: Inhale O2 → Exhale CO2

• Gas Exchange:

- Ventilation

- Perfusion

- Diffusion

• Should be balanced

• Deep breath enhance ventilation

Ventilation

• Exchange / movement of gases into and out of the lungs

• Influenced by:
  - Body position
  - Lung volumes
  - Blockages in the airway

• Degree to which the lungs inflate and deflate depends on the respiratory pressures
  inflating the lungs, compliance of the lungs, and resistance

• Pressures 

• Lung compliance 

• Airway resistance

What are the factors that affect Ventiltion?

Pressure

• Atmospheric pressure = 0 mmHg

• Intrathoracic pressure is negative (assists to stay inflated)

• Air moves between the lungs and atmosphere because of a pressure difference

Lung Compliance

• Ease with which the lungs can be inflated (how easy or difficult it is to fill lungs on air)

• Dependent upon elastin, collagen fibers, water, and surface tension within the
  lungs/thoracic cavity

• Decreased lung compliance: Stiff lungs or chest wall, lungs are difficult to
  inflate (pneumonia, pulmonary edema, fibrosis, ARDS

• Increased lung compliance: Lungs are very easy to inflate and have lost some
  elastic recoil (aging, emphysema)

• CO2  = a potential acid and normal by-product of metabolism; excess CO2 in the bloodstream combines with H2O to create carbonic acid (H2CO3); Acids are produced during metabolic processes

Airway Resistance

• Opposition to flow caused by the forces of friction.

• Impacted by bronchial smooth muscle, lung volume, and the bronchial tree

Lung Volume

• Amount of air exchanged during ventilation

Perfusion

• Primary functions of pulmonary circulation are to provide blood flow to gas
  exchange portion of lung and facilitate gas exchange (* Remeber blood flow thru heart)

• Consists of

- Pulmonary Circulation

- Hypoxia-induced Vasoconstriction

- Shunt

Pulmonary Circulation

• Pulmonary artery pressure (PAP) = about 25/10 mmHg

• Increased pressures may lead to pulmonary edema

Hypoxia-induced Vasoconstriction

• Pulmonary blood vessels are highly sensitive to hypoxia

• Severe pulmonary vasoconstriction when oxygen levels drop to 60 mmHg

• Prolonged hypoxia may lead to pulmonary hypertension, which will cause right-
  sided heart failure (COPD)

  
  

Shunt

• Blood moves from the right to the left side of circulation without being
  oxygenated

• Anatomic shunt: Blood moves from venous to arterial without moving through
  the lungs. May happen with some congenital heart defects.

• Physiologic shunt: “mismatching” of ventilation and perfusion within the lung;
  results in insufficient ventilation to be able to oxygenate the blood flowing
  through alveolar capillaries. Occurs with certain respiratory or heart diseases

• Atelectasis

• Obstruction

• Pneumonia

What are examples of Perfusion without ventilation?

Pulmonary Embolism

What is an example of Ventilation without perfusion?

Diffusion

• Transfer of gases between the alveoli and the pulmonary capillaries to the red blood
  cells.

• Increased when high concentration of oxygen is supplied

• Decreased with diseases that destroy lung tissue or increase the thickness of the alveolar-
  capillary membrane

O2 & CO2 Transport

• The movement of oxygen molecules to the cells and carbon dioxide
  molecules to the lungs by hemoglobin attached to red blood cells (RBCs).
  (Lungs → hemoglobin → Cells)

• Oxyhemoglobin- Hemoglobin bound with oxygen. 95%-98% saturated with O2 in
  arterial blood, and 75% saturated in venous blood.

• Carbaminohemoglobin- Hemoglobin bound with carbon dioxide

Affinity

• Hemoglobin’s ability to bind to oxygen.

• Hemoglobin molecule should bind to the oxygen molecule and should release to tisue/cells

• High affinity = Hemoglobin binds more readily to oxygen; tightly bound

• Decreased affinity = Hemoglobin releases the oxygen to the cells more
  easily

Dissociation

• the letting go of oxygen from the Hgb molecule

Oxygen Dissociation Curve

• How the affinity of Hgb to oxygen changes depending on the needs of the tissues

Control & Regulation of Breathing in brain

• Muscles that control respiration require continuous input from the nervous system.

• Movement of brain muscles responsible for ventilation is controlled by neurons in the pons and
  medulla.

• Brain injuries in this area affect breathing!

• Automatic components of breathing:

- chemoreceptiors

- lung receptors

- voluntary receptors 

Chemoreceptors

• Monitor O2, CO2, & pH; adjust ventilation to meet the body’s needs

• Central- Most important; sense changes in PCO2 levels. High PCO2 levels
  stimulate increase in ventilation for a short time.

• Peripheral- Monitor PO2 levels. Exert little control over ventilation until
  PO2 < 60 mmHg, then stimulate increased ventilation. Important for
  people with chronically elevated PCO2 levels.

Lung Receptors

• Monitor breathing pattern and function

Voluntary Components of Breathing

• Integrate breathing with voluntary acts such as speaking, blowing, singing, etc.

• Temporarily suspend automatic breathing

• Initiated by motor & premotor cortex

Cough Reflex

• One of the primary defense mechanisms in the respiratory system

• Sensitive receptors located in the tracheobronchial wall

• Conditions interfering with the this reflex:

- Weak abdominal or respiratory muscles
- Disease conditions affecting the closing of the glottis and laryngeal muscles
- Prolonged presence of nasogastric tube
- Depressed function of medullary centers in the brain
- Drugs that depress the cough center

Dyspnea

• Subjective sensation of difficulty breathing

• “Difficulty breathing” “Shortness of breath” “Breathlessness”

• Observed in at least three major cardiopulmonary disease states:
  - Primary lung diseases
  - Heart disease characterized by pulmonary congestion
  - Neuromuscular disorders

Changes in Breathing for Older Adults

• Decreased surface area and elasticity → less effective chess wall expansion; less effective gas exchange; decreased lung compliance

• Increased respiratory dead space → ventilation/perfusion inequality

Manifestations/Characteristics of Respiratory Disease

• Cyanosis (central: lips, peripheral: fingers/finger tips)

• Dysneas

• Hypercapnia (high CO2 levels, greater than 45)

• Hypoxiemia (decreased O2 in blood)

• Tachycardia (high HR than 100)

• Tachypnea (high respiratory rate high 28-30)

Manifestations of Hypoxemia

• Changes in level of consciousness (LOC)

- Stupor → Coma

- Restlessness, agitation, or combative behavior

• Cyanosis
  - Central
  - Peripheral

• Diaphoresis

• Hyperventilation

• Pallor

• SNS activation

• Severe Hypoxemia caues systemic hypoxic cell injury leading to accumulation of lactic acid and high sserum lactase levels

Chronic Hypoxemia

• Increased respiratory rate

• Pulmonary vasoconstriction

• Increased production of RBCs

Hypercapnia

• High levels of CO2 in the arterial blood:

• Causes:

- Confusion
- Respiratory acidosis

• If it is chronic, it may show no symptoms because they have adapted

Common Cold

• Viral infection of upper respiratory tract.

• Most common respiratory tract infection

• Most adults have 3-4 colds/year; school-age children may have 6-8 colds/year

• Common source of spread: FINGERS

• Common portals of entry: eyes and nasal mucosa

• Incubation period = 2 days; Duration of illness = 7 days

• Associated with number of viruses: Rhinoviruses, parainfluenza, respiratory syncytial virus (RSV), human metapneumovirus (hMPV), coronaviruses, adenoviruses, and bocaviruses(in children)

• Factors identifying type of virus: Season, Age, Immunologic State, Prior Exposure

Manifestations of Common Cold

• Dryness/stuffiness affecting mainly the nasopharynx

• Rhinitis

• Secretions are usually clear and watery

• Red, swollen mucous membranes of upper respiratory tract

• Postnasal dripping leading to sore throat and hoarseness

• Possible headache and generalized malaise

• Severe cases: chills, fever, and exhaustion

• Viral Shedding 

Rhinosinusitis

• Inflammation involving the nasal sinuses.

• Sinuses should remain sterile, but their lower oxygen content and warm/moist environment could
  facilitate the growth of organisms

• Most common causes are conditions that obstruct drainage from the sinuses
  - Swelling from viral upper respiratory tract infection or allergic rhinitis
  - Nasal polyps
  - Barotrauma from frequent changes in barometric pressure
  - Swimming, diving, and abuse of nasal decongestants

Acute Rhinosinusitis

• Caused by viruses, bacteria or mixed

• May last up to 4 weeks

• Common infecting organisms:
  - Haemophilus influenzae
  - Streptococcus pneumoniae

• Viral acute rhinosinusitis: 5-7 days

• Bacterial: worsening symptoms for 5-7 days or beyond 10 days

  
  

Manifestations of Acute Rhinosinusitis

• Facial pain

• Headache

• Purulent nasal discharge

• Decreased sense of smell

• Fever

Chronic Rhinosinusitis

• Usually bacterial or fungal in origin

• Duration = > 12 weeks

• Caused by anaerobic organisms alone or in combination with aerobic organisms:
  - Strep species
  - Staphylococuss aureus

• Possible presence of biofilms from Pseudomonas aeruginosa in ear, nose, throat

Manifestations of Chronic Rhinosinusitis

• Sinus pressure with nasal congestion

• Dull, constant headache

• Symptoms may persist for years with varying severity

• Episodes of acute sinusitis

• Mucosal changes often irreversible

Influenza

• Combined with pneumonia, “the flu” is the 8th leading cause of death in the US

• Infection rates – Highest among children and older adults

• Rates of serious illness/death – Highest among adults > 65

• Mode of transmission: Inhalation of droplet nuclei

• Incubation period: 1-4 days (average of 2 days)

• Persons may be contagious on day 1, even before showing symptoms, and remain infectious for
  - 1 week after illness onset.

• Viral shedding: May last up to 3 weeks

• Type A, B, and C cause epidemics in human

Influenza Type A

• Can infect multiple species (including avian and mammal species)

• Two subtypes based on two surface glycoproteins: Hemagglutinin (HA) and
  Neuraminidase (NA).

• Can develop new HA and NA subtypes in which the population is not protected.

• Antigenic shift: Major genetic rearrangement in either antigen HA or NA

• May lead to epidemic or pandemic

• Antigenic drift: Lesser change in the virus; may allow partial protection for some
  individuals due to cross-reacting antibodie

Pathogenesis of Influenza

• May cause three types of infections:

- Uncomplicated upper respiratory infection (rhinotracheitis)
- Viral pneumonia
- Viral infection followed by a bacterial infection

• Initially an upper airway infection

- Virus destroys mucous-secreting, ciliated, and epithelial cells
- Holes between cells allow extra-cellular fluid to escape (“runny nose”)

• If virus moves lower in the respiratory tract…
  - Severe shedding of bronchial and alveolar cells
  - Compromised natural defense mechanisms
  - Bacteria easily adhere to epithelial cells → Secondary bacterial infection
  

Manifestations of Influenza

• Fever & chills

• Malaise (feeling weak & tired)

• Muscle aching

• Headache

• Profuse, watery nasal discharge

• Nonproductive cough

• Sore throat

• Possible diarrhea

Pneumonias

• Inflammation of lower respiratory tract

• Inflammation of parenchymal structures in the lower respiratory tract (bronchioles & alveoli)

• Infections vs. Non-infectious agents/causes

- Infectious: bacteria, virus

- Non-infectious: inhaling food or liquid, aspiration, food going down to the lungs, vomiting inhaling/entering lungs, 

• Classification Pneumonia

- Source of infection

- Community acquired pneumonia

- Hospital acquired pneumonia

• An immunocompromised person with pneumonia is a high risk for lung infection

• Prevents Gas Exchange & Ventilation

• May also be classified as 

- Typical or atypical 

- Lobar pneumonia bronchopneumonia 

Pathophysiology of Pneumonia

• Defense mechanisms and anatomic structures assist in keeping the lower respiratory tract
  a sterile environment

• Organisms that make it past these barriers are eaten by macrophages in the alveoli

• Inflammatory process ensues

• Endotoxins are released by some microorganisms – damaging the mucus membranes of
  the bronchi & alveoli – resulting in inflammation and edema

• Exudate can then build up in the distal airways affecting Ventilation and Gas Exchange

Community-Acquired Pneumonia

• Infection that begins outside the hospital or is diagnosed within 48 hours after admission to the hospital in a person who has not resided in a long term care facility for 14 days or more before admission

• Either bacterial or viral

• Most common organism: Streptococcus Pneumonia  (S. Pneumonia)

• Other organisms

- H. influenza, S.aureus, gram-negative bacilli

- Mycoplasma pneumoniae, Legionella Chlamydia species, viruses (atypical agents)

Hospital Acquired Pneumonia

• Lower respiratory tract infection not present or incubation an admission to the hospital; usually >= 48 hours or more after admission

• Mostly bacterial 

• 30-50% mortality; More Serious

• Multiple causative agents

- P.aeroginosa, S.aureus, Enterbacter species, Klebsiella species, E. coli, Serratia

Acute Bacterial Pneumonia (Typical)

• S.Pneumonia is the most common cause of bacterial pneumonia

• Organisms in the upper airways may travel to the lower airways by aspiration

• Defense mechanisms prevent infection under normal conditions; pneumonia vaccine

Manifestations of Acute Bacterial Pneumonia (Typical)

• Chills

• Fever (no fever for Elderly, they Mainly have perfusion and confusion)

• Fine crackles (hear it in lungs)

• Malaise (tired)

• Pleuritic chest pain (pain worsens with inhalation and expiration)

• Productive cough with blood tinged/rusty colored/purulent sputum

Primary Atypical Pneumonia

• Often referred to as “walking pneumonia”

• Most common organisms: Mycoplasma pneumoniae

• Usually mild

Manifestations of Primary Atypical Pneumonia

• Dry hacking nonproductive cough

• Fever

• Headache

• Muscle aches

Tuberculosis (TB)

• Caused by Mycobacterium tuberculosis

• Droplets from coughs or sneezes by an infected person

• One of the leading cause of death for people with HIV or AIDS

• People with increased risk for TB: people for foreign countries, living in congested populations, people with HIV, the elderly, and other immunocompromised individual

• Waxy outer capsules are difficult to destroy. May be referred to as acid-fast bacilli (retain red dye on waxy capsule)

• May affect other organs besides the lungs

• Transmitted via very tiny droplet nuclei (1-5 microns [1 inch = 42,540 microns]) that remain in the air for several hours)

• Latents vs Active

- Latent may develop to active TB if the immune system fails; latent TB cannot be spread to another person

• TB skin test & BCG vaccine

Latent Tuberculosis (TB)

• Manifestation:

- TB may be alive but not growing in the body. There are NO symptoms of TB

• Skin Test Result

- Both can produce a positive skin test result. Remember the skin test is testing for cell-mediated immunity, so if the person has a decreased immune system they could even have a false negative

• NO ability to spread

• Chest X-ray:

- May or may not show small nodules on a chest xray

Active Tuberculosis (TB)

• Manifestations:

- Anorexia

- Blood-tinged sputum

- Cough - dry or productive

- Fatigue

- Fever

- Night sweats

- Weight loss

• Skin Test Results

- Both can produce a positive skin test result. Remember the skin test is testing for cell-mediated immunity, so if the person has a decreased immune system they could even have a false negative

• YES ability to spread

• Chest X-ray: 

- Cavitary lesions, opacities, infiltrates, or consolidations

Lung Cancer

• Risk Factors:

- Smoking, occupational/environmental hazards, genetics

• Most are carcinomas that originate in lung tissue

• Primary cancers from other tissues can metastasize to the lungs

• Four Major Types:

- Small-Cell Carcinoma (oat cell)

- Squamous cell carcinoma

- Adenocarcinoma

- Large cell carcinoma

Small Cell Carcinoma

• 20-25% 

• “Oat Cell”

• Cells grow in clusters

• Strong association with smoking

• High malignant

• Metastases usually evident at its of diagnosis (70%) 

• Brain metastases are common

• Poor prognosis

• Commonly associated with paraneoplastic syndromes

Squamous Cell Carcinoma

• 25-40% 

• Found most commonly in men

• Associated with smoking

• Usually originated in central bronchi

• Hypercalcemia (high calcium Ca levels)

Adenocarcinoma

• 20-40%

• Most common type in North America

• Weaker association with smoking

• Most common type for women and non-smokers

• Originate in bronchiolar or alveolar tissue

• Associated with areas of scarring in lungs

Large Cell Carcinoma

• 10-15% 

• Poor prognosis

• Spreads very early

• Invade subsegmental bronchi and larger airways

Manifestations of Lung Cancer

Depend on location, metasis, & stage

• anorexia

• chronic cough

• hemoptysis (Coughing up blood, because cancerous lesions erodes blood vessels)

• pain (may be difficult to pinpoint remember no pain receptors in lung tissue, only pleura)

• shortness of breath

• wheezing

• Metastasis is most common in brain, bone, and liver

Pleural Effusion

• Abnormal collection of fluid in pleural cavity. Fluid may be: exudates, purulent drainage (empyema - pus), chyle, blood, or serous transudate (hydrothorax). May be unilateral or bilateral

• Causes:

- Heart Failure (common)

- Renal Failure

- Liver Failure

- Malignancy 

- Infection

• Pathophysiology:

- Increased capillary permeability

- Decreased colloidal osmotic pressure

- Increased negative intrapleural pressure

- Impaired lymph drainage

Manifestations of Pleural Effusion

• Dyspnea

• Decreased lung expansion

• Diminished breath/lung sounds

• Hypoximea (low O2 in blood)

• Pleuritic pain (Large effusion - constant pain)

• Empyema: fever, increased WBC, other s/s inflammation

Hemothorax

• Specific type of pleural effusion: Blood in the pleural cavity

• Causes:
  - Chest injury
  - Complication of surgery
  - Malignancies
  - Vessel rupture

• Variations in severity based on size:
  - Minimal: < 250 mL
  - Moderate: 500 mL – 1000 mL (~ 1/3 of pleural space)
  - Large: > 1000 mL (1/2 or more of one side of the chest)

•  Manifestations: Dyspnea, Hypoxemia, & Hypovolemia → SHOCK

  
  

Pneumothorax

• Condition in which air enters the pleural space, causing atrial or complete collapse of the affected lung. It usually expressed expressed in percentages (5-95%)

• Types

- Spontaneous Pneumothorax (no injury)

- Primary pneumothorax

- Secondary pneumothorax

- Traumatic Pneumothorax (injury)

Spontaneous Pneumothorax

• No injury

• Rupture of air-filled bleb or blister on the surface of the lung

• Primary pneumothorax:

- Healthy individuals. Seen most often in tall boys and young men (10-30 years old). Smoking and family history may play a role.

• Secondary pneumothorax

- Underlying lung disease. Common cause- emphysema (Other conditions- asthma, TB, cystic fibrosis, lung cancer)

Traumatic Pneumothorax

• Injury

• Penetrating or non-penetrating chest injury

• Gun shots, stabbing, medical procedures, rib fractures

• Hemothorax commonly occurs with traumatic pneumothorax

Manifestations of Pneumothorax

• Asymmetrical chest expansion

• Chest Pain

• Decreased/absent breath sounds

• Dysnea

• Hypoxemia

• Tachycardia

• Tachypnea

Tension Pneumothorax

• LIFE THREATENING MEDICAL EMERGENCY

• Air enters pleural space but cannot escape

• Pressure increases with each breath

• As pressure increases, the affected lung collapses. The heart and great vessels are compressed. Mediastinal structures shift to the opposite side of the chest. The trachea is pushed from the normal, midline position. The unaffected lung becomes compressed

• Ventilation is severely impaired; More common with traumatic pneumothorax

Manifestations of Tension Pneumothorax

• Hypotension

• Distended neck veins

• Subcutaneous emphysema

• Tracheal deviation toward unaffected side

• May lead to shock

  
  

Atelectasis

• Incomplete expansion of a lung/portion of a lung

• Results in partial or complete lung collapse

• Decreased surface area for gas exchange

• Causes:

- Airway obstruction

- Lung compression

- Absence or loss of pulmonary surfactant (newborns)

- Increased risk after surgery secondary to pain, pain medications, and immobility

Manifestations of Atelectasis

• Cyanosis

• Decreased/absent breath sounds over the affected area

• Dyspnea

• Fever, s/s infection

• Hypoxemia

• Tachycardia

• Tachypnea

Asthma

• Chronic disorder of the airways that causes episodes of airway obstruction, bronchial
  hyperresponsiveness, airway inflammation, and airway remodeling (in some cases).

• Affects individuals of every age; many cases develop in childhood

• Risk Factors

- Genetic predisposition* for the development of an IgE response to common allergens

- Allergies

- Antenatal exposure to tobacco smoke and pollution

Pathophysiology of Asthma

• Exposure to stimulus (allergen) triggers the onset of an “asthma attack”

• Inflammatory response ensues

• Inflammatory mediators are released- stimulating the PNS, resulting in
  bronchoconstriction

• Mucosal edema and mucous production

• Airway narrows

• Air becomes trapped distal to the edematous airway- resulting in distended alveoli

• Blood flow to distended alveoli is reduced (decreased gas exchange)

Manifestation of Asthma

• Anxiety

• Chest tightness

• Cough

• SOB

• Tachycardia

• Tachypnea

• Accessory muscle use (diaphragm and neck muscles)

• Wheezing

Chronic Obstructive Pulmonary Disease (COPD)

• Group of chronic airway disease with chronic, recurrent obstruction of airflow

  progressive worsening of lung tissue

• Leading cause of morbidity and mortality worldwide

• Most common cause: smoking

• Less common: hereditary deficiency in a1 antitrysin

• Two types: Emphysema & Chronic Bronchitis (may have both) 

Emphysema

• Known as the “pink puffers” because:

- No cyanosis

- Accessory muscle use 

- Associated with smoking or inherited alpha1 - antitrysin

Pathophyiology of Emphysema

• Recurrent inflammation results in the release of proteolytic enzymes causing irreversible enlargement of the distal air spaces 

• Loss of lung elasticity

• Abnormal enlargement of airspace distal to terminal bronchioles 

• Destruction of alveolar walls and capillary beds

• Elastic recoil is lost

• Air trapping results → volume of air passively expired is reduced

• Hyperventilation and cardiac output

• Lung is oxygenated but limited blood flow prevents oxygenation of body tissue 

• Proportionate decrease in ventilation & perfusion

Manifestations of Emphysema

• Barrel chest there is an increased anterior-posterior diameter of the chest (related to
  hyperinflation)

• Diminished/Lost lung sounds air trapping

• Dyspnea begin as exertional, but worsen as the disease progresses

• Relatively normal ABG’s (until late stages)

• Muscle wasting

• Sitting upright/leaning forward

• Prolonged expiration

• Pursed lip breathing

• Accessory muscle use

Chronic Bronchitis

• Known as “Blue bloaters”

• Chronic inflammatory process with excessive bronchial mucous secretion

• Airflow is obstructed

  
  

Manifestations of Chronic Bronchitis

• Increased sputum production

• Coarse lung sounds so you may here fluid/secretions when you listen to their
  lungs

• Cyanosis

• Respiratory acidosis (Compensated?)

• Hypercapnia and Hypoxemia

• Frequent respiratory infections

• Polycythemia

• May develop pulmonary HTN and/or right-sided HF

• Accessory muscle use

Cyctic Fibrosis

• Genetic disorder: Autosomal Recessive

• Affects respiratory, gastrointestinal, and reproductive systems

• More common in Caucasians

• Excessive, thick mucus

• Pathophysiology:

- Genetic mutation increases absorption of sodium and water from the airways into the
blood, causing the mucociliary blanket of the respiratory epithelium to become more
viscid
- Result is the accumulation of thick respiratory secretions that predispose the individual to
recurrent pulmonary infections

Manifestations of Cystic Fibrosis

• Thick secretions → mucous plugs (water loss)

• Frequent lung infections

• Structural changes in the bronchial wall

• malnutrition

• High levels of NaCL in sweat 

• Abnormal pancreatic function

• SALTY: Skinny, Autosomal recessive, Lung infections, Thick mucous, Young age

Chronic Interstitial Lung Disease 

• Group of disease resulting from inflammatory condition that cause the lungs tissue to become stiff and difficult to expand (decreased compliance)

• Affects collagen and elastic connective tissues in the interstitium of alveolar walls

• Multiple Causes:

- Injury → inflammation → scarring

- Occupational: “Coal miner’s lung,” Asbestosis, Gases/fumes

- Drugs/Medications: Cancer drugs and others

- Immunologic: Sarcoidosis (inflammation, increased collagen, & connective tissue), Collagen vascular disease (Lupus) 

Manifestations of Chronic Interstitial Lung Disease 

• Increased work of breathing

• Exercise intolerance

• Small, frequent breaths

• Hypoxemia

Pulmonary Embolism

• Occlusion of pulmonary vessel with an embolus

• Embolism may be a blood clot, air, fat, amniotic fluid, fat from bone marrow

• Common cause: Deep Vein Thrombosis

• Massive PE: Occlusion of major artery → Infarction of large
  portion of lung tissue

• Smaller PE: Embolism lodged in a more distal site → May not cause infarction of lung tissue

Risk Factors of Pulmonary Embolism

• Virchhow’s Triad

• Ventilation-Perfusion mismatch (ventilation without perfusion)

• Immobility

• Post-surgica

• Pregnancy

• Oral contraceptives/hormone replacement

Manifestations of Pulmonary Embolism

• Sudden onset of chest pain & dyspnea

• Tachypnea

• Anxiety

• Cough (blood tinged)

• Hypoxemia

• Tachycardia

Respiratory Failure

• Result of another problem

- Gas exchange failure / Ventilation failure

• Failure to oxygenate the blood and/or eliminate CO2

• Manifestations:
  - Change in level of consciousness
  - Cyanosis
  - Hypoxemia
  - Hypercapnia
  - Tachycardia
  - Tachypnea

•  Acute Lung Injury

• Acute Respiratory Distress Syndrome