Lung Compliance

• Ability of lungs to stretch and expand
  
  

Low = More work needed to inflate
High = Hard to expel air out

Factors Influencing Ventilation (SNS & PNS)
Low O2 demands

• PNS when demand is low
• Vagus nerve secretes Ach --> stimulates bronchial smooth muscle --> decreases airway radies (bronchconstriction)
  
  

High O2 demands

• SNS when demand is increased
• Norepinephrine & epinephrine from adrenal medulla --> stimulates beta 2 receptors on bronchial smooth muscles --> increase airway radii (bronchodilation)

Geriatric Considerations

• Reduced elastin and increased collagen
• Decreased elastic recoil d/t rib & cartilage calcification
• Less strength of diaphragm, intercostal muscles, and accessory muscles
• Cilia loss with reduced cough power
• Reduced pulmonary blood flow
• All increase work of breathing

Hypercapnia

• Aka hypercarbia
• Increased blood CO2
• Inversely related to ventilation
• Severe hypoventilation has hypoxemia and hypercapnia
  
  

Causes

• Hypoventilation
• Lung disease
• Decrease LOC
• Rebreathing CO2
  
  

Clinical Manifestations

• Increased PO2 --> Increased H+ --> Decreased pH blood = Respiratory Acidosis
• Kidneys compensate by increasing H+ excretion and HCO3- retention
• Chronic hypercapnia doesn't show S&S until PCO2 is greatly elevated or PO2 is greatly reduced

Hypocapnia

• Low PCO2
• From hyperventilation
  
  

Causes:

• Pain, fever, anxiety, sepsis
• High altitude
• Brainstem injury

Clinical Manifestations

• SNS compensation of shunting
• CNS effects:
  
  • Slight impairment of mental performance/euphoria
  • Agitation, confusion, impaired judgment
• Pulmonary vasoconstriction
  
  • Increased pulmonary arterial pressure to increase perfusion
  • Increased production of erythrocytes
• Cyanosis

Under-perfusion V/Q

• Under-perfused
• Adequate ventilation but inadequate perfusion
• Abnormal pulmonary blood flow
  
  • Pulmonary embolus, heart failure, hypotension
    
    

High V/Q Ratio
4ml/ <5ml = >0.8

Physiological Dead Space

Under-ventilated V/Q

• Under-ventilated
• Adequate perfusion but inadequate ventilation
• Alveolar collapse/consolidation, obstruction
  
  

Low V/Q Ratio
4ml/ >5ml = <0.8

Shunt

Deep Vein Thrombosis (DVT)
3 Factors (Virchow's Triad)

• Venous stasis/slow blood
  
  • From immobility, trauma, pregnancy, obstetric surgery, cancer, and estrogen use
  • 50% idiopathic
• Hypercoagulability
• Damage to the venous wall
  
  

Clinical Manifestations

• Warm, painful, swollen, edematous, red
  
  

Pulmonary Embolus

• Traveled DVT blood clot that obstructs pulmonary blood flow
  
  

Causes:

• 90% from deep veins in pelvis or legs
• Air from IV infusion
• Fat from broken bone marrow

• Amniotic fluid entering maternal circulation at delivery

  
  

• Mortality rate = >30% with big PE

• Under-perfusion V/Q mismatch
  
  

Clinical Manifestations

• Obstruction --> reflexive bronchoconstriction --> Poor ventilation & diffusion --> Loss of surfactant
• Depends on size of thrombus
• Restlessness, anxiety
• Increased HR & RR, dyspnea
• Chest pain
• Hemoptysis
• Hypoxemia
  

• Usually undetected unless it's a massive PE
  
  

Treatment & Prevention

• Mobilize patients and teach lower leg movements (q1h, per hour)
• Anti-coagulants, active ROM, compression hose w/pneumatic compression
• If confirmed DVT/PE, anticoagulants, thrombolytics, oxygen, bed rest
  
  

DON'T RUB IT

Pathophysiology (Atopic Asthma)

Acute Phase (10-20 min after contact with allergen)

• Antigens bind to presensitized mast cells on mucosal surface of airways
• Chemical mediators released resulting in mucous production and bronchospasm from stimulation from PNS receptors on airway surface
  
  

Late Phase (4-8 hours)

• Release of inflammatory mediators from mast cells, macrophages, and epithelial cells, leading to migration of other inflammatory cells
• Changes in mucociliary function and epithelial edema and injury
• Respiratory tract clearance of secretions decreases
• Airway responsiveness increases to hypersensitivity
• Chronic inflammation --> Airway remodeling & airflow limitations

Pathopyshiology (Exercise-Induced)

• Common in children and adolescents
• Bronchospasm occurs within minutes of exercise
  
  • Resolves in an hour
• Heat & water loss activates inflammatory mechanisms
  
  • Mediator release from basophils & tissue mast cells
  • Leads to bronchoconstrction

Clinical Manifestations of Asthma

Acute episode

• Dyspnea, orthopnea (flat dyspnea) with dry/productive cough
• Hypoxemia
• Decreased ventilation with wheezing, chest tightness, accessory muscle use
  
  • Increased O2 demands = Increased WOB (work of breathing)

• Under-ventilation V/Q

  
  

• May be symptom free between attacks

• Nocturnal asthma
• Status asthmaticus

Treatment & Prevention

• Avoid triggers
• Annual influenza vaccine
• Fast-acting medications to alleviate acute attacks
• Early treatment for respiratory infections
• Longer-acting inhaled corticosteroids inhaled daily
  

1, Chronic Bronchitis
Diagnosed by:

• Hypersecretion of bronchiol mucous
• Hypertrophy of submucosal glands in trachea and bronchi
• Chronic or recurrent productive cough >3 months duration for >2 successive years
  
  
  

• Persistent, irreversible
• Male:Female = 1:2
  
  

Etiology

• Smoking (90%)
• Repeated airway infections & genetics
• Physical/chemical irritants
  
  

Pathophysiology

• Irritants activate neutrophils
  
  • Chronic airway inflammation and obstruction of major & small airways
  • Leads to swelling of bronchial mucosa & alveoli, resulting in scarring, fibrosis, increased wall thickness, mucous, and mucous plugs
• Airway narrowed & proper oxygenation prevented
  
  • Chronic hypoxia & hypercapnia, leading to pulmonary vessel vasoconstriction
  • Under-ventilation V/Q mismatch
• Impaired or absent cilia
• Colonized with H.influenza (bacterial, not flu) and S.pneumoniae
  
  

Clinical Manifestations

• Peripheral edema
• Digital clubbing
• Polycythemia (increased RBC abnormally)
• Recurrent cough/sputum
• Cyanosis

2. Emphysema

• Damaged distal alveoli
• Progressive over long time
  
  

Etiology

• Smoking
• Air pollution
• Certain occupations
• Alpha1-Antitrypsin deficiency (if patients <50 years old)
  
  

Pathophysiology

• Irritants stimulate inflammatory cells into the lungs
  
  • Increase in proteases release, which destroy elastin
• DIstal alveoli enlarged & damaged
  
  • Loss of elastic tissue in lung
  • Loss of radial traction (normally holds airway open)
  • Alveolar collapse with air trapping
• Loss of elastic alveolar wall and air trapping leads to bullae (large thin-walled cysts in the lung) forming
  
  

Clinical Manifestations

• Thin, pink
• Airways collapse during exhalation
  
  • Forced exhalation
  • Pursed-lips and accessory muscles
• Minimal or absent cough
• Barrel chest with CO2 retention

Clinical Manifestations for COPD

• History of smoking
• Laboured breathing (air hunger)
• Accessory muscle use
• Hypoxemia/hypercapnia
• Right sided heart failure (cor pulmonale)
  
  • Increased thoracic pressures --> RV afterload increases --> R heart failure
• Frequent pulmonary infections
• Gradual, progressive, with frequent exacerbations
• Ultimately develop respiratory failure

Clinical Manifestations & Prevention (Secondary)

• Decreased or no breath sounds
• Increased RR, dyspnea, cyanosis, hypoxemia, intercostal retractions
• Pneumonia risk
• Reduce airway obstruction and re-inflate akveoli
  
  

Prevention

• Ambulation
• Deep breathing and coughing
• Positiioning
• Incentive spirometer q1h

COPD Treatment & Prevention
Prevention

• Adequate rest & hydration
• Physical reconditioning
• Influenza and pneumococcal vaccines
• Smoking cessation
  
  

Treatment

• Low dose O2 therapy
  
  • SaO2 86-90%
    -Medications
  • Inhaled Beta2 agonists & anticholinergic agents
  • Cough suppressants
  • Antimicrobial agents (infections)

Etiology

• Aspiration of oro-pharyngeal secretions with normal flora/gastric contents (25-35%)
• Inhalation of contaminants
• Contamination from circulatory system

Pathophysiology

• Organisms enter lung, grow, trigger inflammation
• Invades alveolar septa
• Alveolar spaces fill with exudative fluid
• Consolidates and difficult to expectorate
• No exudative fluids with viral pneumonia

Community Acquired

• Bacterial/Viral
• Commonly S.pneumoniae
• Could be admitted to hospital
  
  

Hospital Acquired

• Mostly bacterial (P.aeruginosa, S,aureus, E.coli)
• 2nd most common hospital acquired infection
• 60% mortality rate

Clinical Manifestations

• Productive cough with pus and phlegm (sputum)
• Fever and chills
• General discomfort, unease, ill feelings (malaise)
• Loss of appetite with N&A
• Sharp chest pains that get worse with breathing/coughing
• SOB
• Hypotension & tachycardia

Prevention

• Infection control
• HOB 30-45 degrees
• Feed upright
• Oral care
• Promote adequate nutrition
• Limit visitors

1. Spontaneous

• Rupture of bleb or lesion on lung surface
• Primary: Occurs in healthy, tall, thin men w/o risk factors
• Secondary: In people with COPD and other lung diseases
• Alveolar pressure > pleural pressure = aur flows from alveoli to pleural space --> collapse of lung

2. Traumatic

• From penetrating or blunt chest injuries
• Commonly dislocated ribs or central line insertion
  

3. Tension

• Trauma where intrapleural pressure > atmospheric pressure
• Air enters pleural space during inspiration but can't leave (trapdoor)
• Air builds up in pleural space --> lung on ipsilateral (same) side collapses
• Forces mediastinum toward contralateral (opposite) side
• Compresses vena cava
  
  • Decrease venous return and cardiac output

Hemothorax

• Collection of blood
• Rupture of big vessel, like an aortic aneurysm
• Chest surgery

Clinical Manifestations

• Chest pain & tachypnea
• Dyspnea with cough
• Hypotension with tachycardia
• Hypoxemia with O2 desaturation
  On examination:
• Midline shift (mediastinal shift)
• Absent breath sounds on side of collapse
  
  

Treatment

• Chest tube drainage with suction to let air escape without re-entry
• Supplemental O2

Empyema

• Contains pus, glucose, proteins, leukocytes

• Infections/abscess in pleural cavity that ruptures

  
  

• Transudative effusion (CHF, hypoproteinemia)

• Exudative effusion
  
  • Protein rich with inflammation
  • In TB, malignancies, immune disorders, infections
    
    

Needs thoracentesis