Respiratory Pathophysiology 

S&S of Pulmonary Disease

  • Dyspnea: subjective sensation of uncomfortable breathing (SOB & difficulty breathing)
  • Orthopnea: dyspnea while laying down
  • Paroxysmal nocturnal dsypnea (PND): violent attacks of severe SOB and coughing; only occurs at night and awakes person from sleep
      * The emotional is more severe than the physical for patients
  • Finger clubbing → hypoxic epithelial tissue compensates and grows new blood vessels
      * 160º → normal finger and nail bed
      * 180º → early clubbing
      * \
        > 180º → moderate & advanced clubbing
  • Coughing
      * Acute cough → less than 14 days
      * Chronic cough → more than 14 days
  • Sputum: should generally be odorless (if putrid = tissue death)
      * ==Productive cough:== coughing up sputum
      * ==Non-productive cough:== no sputum
      * Bloody: hemoptysis
        * @@Blood-streaked sputum:@@ inflammation, lung cancer in lower airway
        * @@Pink sputum:@@ sputum evenly mixed with blood from alveoli and or small peripheral bronchi → CHF (pulmonary edema)
        * @@Massive blood:@@ TB, tumor, abscess, pulmonary embolism
      * Yellow(ish):Yellow(ish): purulent/pus = bacterial pneumonia
      * %%Green/greenish:%% longstanding lung infection = chronic bronchitis
      * ==Rust colored:== TB, pneumococcal pneumonia

Breathing Patterns

  • Tachy=fast/rapid
  • Brady=slow
  • Hypoventilation → Hypercapnia (deep breath)
  • Hyperventilation → Hypocapnia (shallow depth)
  • Eupnea: normal breathing rate and pattern
  • Tachypnea: increased respiratory rate, caused by: fever, anxiety, shock
  • Bradypnea: Decreased respiratory rate, caused by: sleep, drugs, metabolic disorders, head injury, stroke
  • Apnea: absence of breathing, caused by: death, head injury, stroke
  • Hyperpnea: normal rate, but deep respirations, caused by: emotional stress, diabetic ketoacidosis
  • ==Cheyne-Stokes:== gradual increases and decreases in respirations with periods of apnea, caused by: NEURONEURO, increasing intracranial pressure, brain stem injury
  • Biot’s: rapid deep respirations (gasps) with short pauses between sets, caused by: spinal meningitis, CNS causes, head injury
  • ==Kussmaul’s:== tachypnea and hypernea, caused by: renal failure, metabolic acidosis, diabetic ketoacidosis
  • Apneustic: prolong inspiratory phase with shortened expiratory phase, caused by: lesion in brain stem

Adventitious Breath Sounds

  • Crackles (rales): bronchioectasis, bronchitis, pneumonia, fibrosis, CHF; course vs. fine
      * Discontinuous
  • Wheezes: asthma, COPD and airway obstruction
      * Continuous
  • Rhonchi: suggests secretions in the large airway
      * Continuous

Pleural Abnormalities

  • Pneumothorax → air ends up in thoracic cavity → causes lung collapse
      * %%Spontaneous (PRIMARY) pneumothorax:%% just happens, occurs in thin, tall, white, male, smokers at risk
      * Secondarypneumothorax:Secondary pneumothorax: caused by obvious lung diseases; people with cancer, cysts, infection, inflammation (always pathogenic causes)
      * @@Traumatic pneumothorax: @@
        * Iatrogenic → hospital caused (bronchoscopy most common cause)
        * Blunt vs. penetrating → stab wounds, GSWs, car crash
      * ==Tension pneumothorax:== complication from primary OR secondary pneumothorax; causes the pressure to shift to non-affected side (can cause tracheal deviation, heart compression), ⬆️ in mortality

Lung Diseases

Restrictive Pulmonary Disorder

  • Lungs are restricted from fully expanding; troublesinhalingtroubles inhaling
      * Air has a problem going into the lungs
  • Condition: stiffness in the lungs, chest wall, weak muscles, or damaged nerves may cause restriction

Obstructive Pulmonary Disorder

  • HardtoexhalealltheairinthelungsHard to exhale all the air in the lungs
      * Air had a problem leaving the lungs, trapped in alveoli
  • Damage to the lungs or narrowing of the airways → high amounts of air may still linger in the lungs, ⬆️ in CO2 levels

Types of Restrictive Lung Disorders

  • Parenchymal:
      * Atelectasis
      * Fluid (edema, pus, blood)
      * ARDS
      * Trauma
      * Autoimmune
      * Chronic infections
      * Occupational
      * Environmental
  • Extra-pulmonary
      * Obesity
      * Scoliosis
  • Neuromuscular
      * Myasthenia gravis
      * ALS

Types of Obstructive Lung Disorders

  • Airway narrowing and obstruction that is worse with expiration
      * Accessory muscles of expiration required
      * Increased work of breathing
  • Dyspnea and wheezing most seen with this disorder
  • Asthma, COPD (emphysema & chronic bronchitis)

Atelectasis

  • RESTRICTIVE
  • Loss of lung volume due to the collapse of alveoli
Pathogenesis:
  • ^^Absorptions (obstructive)^^ → can develop pneumonia → the reason why patients have to get up and walk after surgery → spirometer also reduces risk
  • %%Non-obstructive →%% loss of contact between visceral and parietal pleura; surfectant impairment (adhesive)
      * Compression (fluid, air, mass, bed-ridden)
      * Contraction (smokers, fibrosis, infection, pneumoconiosis)

ARDS

  • RESTRICTIVE
  • Acute respiratory distress syndrome
  • ==Most severe form of acute lung injury==; ==highest mortality rate== (impacts both alveoli & blood vessels/ alveolocapillary membrane)
Development

Acute lung injury (to blood vessels) → endothelial cell damage → activation of neutrophils/macrophages/platelets → release of inflammatory cytokines → increase aveolocapillary permeability w/edema → V/Q mismatch (shunt) & hypoxemia → ==acute respiratory failure ==

Acute lung injury (to alveoli)→ epithelial cell damage → type II pneumocyte damage → decreased surfectant → alveoli collapse → atelectasis and decreased lung compliance → decreased tidal volume & hypercapnia (muscles tire out) → ==acute respiratory failure ==

Manifestations
  • Dyspnea & hypoxemia (O2 sats drop)
  • Pulmonary edema
  • Increased work of breathing → hyperventilation and respir. alkalosis
  • Bilateral infiltrates on chest x-ray
  • Respiratory failure, decreased cardiac output, hypotension, death
Diagnosis & Care
  • Have to treat accordingly = supportive care
  • Hx of lung injury
  • Physical exam (won’t really show)
  • Analysis of ABGs
  • Radiologic exam

  • No exact Tx… only support
      * COVID → give antibiotics
      * Smoke inhalation → O2 treatment
      * Chemical inhalation → no Tx, have the let the chemicals absorb into the body before Tx can even be considered to treat

Asthma

  • OBSTRUCTIVE
  • Reversible airflow obstruction
  • LOCATION: Small bronchi, bronchioles
  • Typer I hypersensitivity reaction
  • Most common chronic disease in children
  • NO KNOWN CAUSE (genetic vs. environmental)
Pathogenesis
  1. Allergen or irritant exposure
  2. Mast cell degranulation and release of mediators → bind to receptors
  3. Mediator effects:

   
   1. Mucus production → mucus plug
   2. Vascular leak → cell edema
   3. Airway smooth muscle constriction → bronchoconstriction
   4. Neutrophil activiation → release of serotonin, histamine, and heparin

  • Trifecta of Asthma: a,b,c only
  • All have one thing shared: air is trapped in the alveoli and can’t get out (can get air in but not out)
Manifestations
  • Cough
  • Wheezing
      * Expiratory only = mild & moderate
      * Expiratory & inspiratory = SEVERE
  • SOB, tachypnea
  • Nasal flaring
  • Use of accessory muscles
  • Exercise intolerance → seen in adult population (cool weather can cause bronchospasms)
Diagnosis
  • Clinical, doesn’t require $ testing
  • ABGs
  • Pulse Ox.
  • Chest radiography
      * ABGs and Pulse Ox. determine severity
Management
  • Corticosteroids → decreases inflammatory response (edemas, mucus plugs, etc.)
  • Beta agonist: albuterol → inhaled, smooth muscle relaxation
  • Anti-cholinergic: ipratropium → relaxes muscle
  • Phosphodiesterase enzyme inhibitor: theophylline (xanthine) → vasodilation
  • Mast cell stabilizer: cromolyn sodium → for those who go outside and exercise
  • Leukotrine receptor antagonist: Zafirulkast → blocks inflammatory response
  • Monoclonal antibodies: omalizumab
  • Combination drugs → steroids, agonists/cholinergic drugs mixed together

How many attacks = how many drugs the patient will take

Classification of Asthmas
ClassDays w/symptomsNights w/symptoms
Severe persistentContinualFrequent
Moderate persistentDaily>5/mo
Mild persistent>2/wk3-4/mo
Mild intermittent<2/wk<2/mo

COPD

  • OBSTRUCTIVE
  • Chronic obstructive pulmonary disease
  • Umbrella term for other disease (chronic bronchitis & emphysema)
  • Not fully reversible, but can be managed
  • %%MOST COMMON CHRONIC LUNG DISEASE IN THE WORLD%%
  • Risk Factors:
      * Tobacco smoke → vaping popular in US, smoking still popular in Europe/Asia
      * Air pollution → highly populated cities with smog/pollution
      * Genetics
^^Chronic Bronchitis^^
  • ^^BLUE BLOATERS ^^
  • Hypersecretion of mucus and chronic productive cough that lasts for at least %%3 consecutive months of the year%% and for at least %%2 consecutive years%%
  • LOCATION: Bronchi
  • Hx of smoking
  • Living in urban areas, “dirty air”
  • ==3rd leading cause of death in the US==
  • Greater than 40 years old
  • ^^Overweight, cyanotic, elevated Hgb’s, peripheral edemas, rhonchi and wheezing ^^
      * Frequent infections, common CHF, large amounts of purulent pus coughed up
==Emphysema==
  • ==PINK PUFFERS==
  • Abnormal, permanent dilation of gas-exchange airways accompanied by the destruction of alveolar walls (elastic septum) without obvious fibrosis
  • LOCATION: Alveoli
  • Disease of the air spaces
  • Loss of elastic recoil
  • @@Barrel chested, pursed lips, older and thin, severe dyspnea, quiet chest @@
      * Little sputum, late CHF
  • Caused by smoking or inherited deficit of alpha 1-antitrypsin
      * Trypsin digests elastic fibers, antitrypsin prevents it from digesting the elastic fibers, appears like a history of smoking; ==this deficit is seen in younger patients only== ==; loses the ability to protect elastic fibers==
Diagnosis
  • Spirometry
  • ERB measured for COPD
      * IRB & ERB = functional vital capacity
  • Pulmonary function test = baseline
  • ABGs → checks for pH of blood, PO2, PCO2, HCO3-
  • Serum chemistries
  • Alpha-1-antitrypsin levels → ALWAYS DO THIS (young vs. old patients)
  • Sputum evaluation → bacteria → inflammation/infection → antibiotics to treat
Treatment & Management
  • ==In truth, some patients just won’t make the changes and won’t care about their health ==
  • Improvement of functional status, symptoms, and quality of life
  • Preventing recurrences
  • NO Tx available to improve lung function, other than lung transplants
  • O2 therapy when appropriate
  • Smoking cessation may reduce mortality

Pneumonia

  • Any infection of the lung tissue (parenchyma); alveoli filled with fluid & pus
  • %%Typical pneumonia:%% fever (high, 101.5), cough (productive), rigor (chills); lobar pneumonia & bronchopneumonia
  • ==Atypical pneumonia==: fever (low, <100), cough (non-productive); “walking pneumonia (PAP)”
Community Acquired Pneumonia
  • Clinical setting = community (walking into hospital/doctor’s office)
  • Non-hospitalized or previous ambulatory patient
  • Bronchial breath sounds and crackles on auscultation; fever, cough, sputum production, rigors, pleuritic chest pain, dyspnea, tachycardia
  • %%TYPICAL%%%%:%%
      * ==S. pneumonia==, H. influenza, Legionella
        * S. pneumonia is most common and most fatal
  • ==ATYPICAL: ==
      * Mycoplasma, Chlamydia
        * Virus
          * Respiratory syncytial virus → children
          * Para-influenza → children
          * Influenza A & B → older population
          * Adenovirus → military barracks
Nosocomial Pneumonia
  • Gram - rods
  • MRSA
  • Alcoholics, bed-ridden, stroke, unconscious
  • ==Ventilators = highest chance to develop nosocomial infections (pseudomonas aerugionsa) ==
  • Asplenic patients
  • Chronic
  • Necrotizing
  • Immunocompromised (HIV, cancer therapy)

Pulmonary Tuberculosis

  • Caused by an acid-fast bacillus, mycobacterium tuberculosis (AIRBORNE)
      * Living in crowded conditions
      * Immunodeficiency
      * Malnutrition & alcoholism → seen in the homeless
      * War
      * Chronic disease
  • Pathogenesis → tubercule/granuloma formation → caseous necrosis
Clinical Presentation (for chronic infectious disease)
  • Cough w/blood
  • Weight loss/anorexia
  • Fever (low grade, 100-100.5)
  • ==NIGHT SWEATS = distinctive sign of active infection ==
  • Hemoptysis
  • Chest pain
  • Fatigue
Active Infections
  • Acid-fast sputum smear test (when + = active TB)
      * Early morning, 3 consecutive days of collecting
  • Chest radiography → shows active TB
  • Drug susceptibility testing
  • Tx depends
Diagnostics
  • Blood test: IGRAs
      * $
      * Single patient visit
      * CDC recommended
  • Tuberculin skin test: TST
      * Recorded 2-3 days after 1st administration
5 mm==HIGH RISK ==HIV infected patients, people exposed to a person w/active TB, asplenic patients
10 mmModerate riskRecent immigrants, drug users (injections), children <4yrs, infants/children/adolescents exposed to adults at high risk for developing TB
15 mmLow riskAny person including persons with NO known risk factors for TB
  • HIV serology test → HIV & TB go hand in hand, so always good to check if HIV is +