Respiratory Pathophysiology

Meet the lungs

Upper respiratory
The oronasopharynx, the pharynx, the larynx, and the upper part of the trachea is called the upper respiratory tract.

Lower respiratory
Conversely, the lower respiratory tract includes the lower trachea, the mainstem bronchi, the segmental bronchi, the bronchioles and the alveoli.

*Respiratory infections often spread among these structures due to the continuous nature of the mucosal lining.

*Respiratory illnesses can be caused by viruses or bacteria.

Viruses commonly causing respiratory illness
Respiratory syncytial virus
Non-polio enteroviruses (coxsackie A&B)
Parainfluenza viruses

Bacterial agents causing respiratory illness include
Group A beta-hemolytic streptococci
Haemophilus influenza
Chlamydia trachomatis
Mycoplasma and pneumococci.

*Be aware that vaccines have been developed to protect children from Haemophilus influenza (ACT-Hib, Pedvax) and against 13 different strains of the pneumococci (Prevnar 13).

Control located in the Pons and the Medulla
Medulla controls inspiratory phase q 2 seconds by stimulating phrenic nerves of diaphragm
Medulla controls expiratory phase, forced expiration because normal quiet expiration is a cessation of activity following inspiration.
Rate and depth of respirations affected by CNS
Drugs slow, shallow rate
Hypothalamus response to emotions or stretch receptors, voluntary singing
CO2 controls when CO2 rises breathing resumes automatically
Chemoreceptors in Medulla and peripheral chemoreceptors (located in carotid bodies and aorta) respond to changes in CO2, O2 and ph

* Individuals with chronic lung disease are dependent on low oxygen levels rather than elevations in CO2 to drive inspiration…what implications does this have for nurses?

Gas exchange:
Flow between gases in the aveoli air and the blood in the pulmonary circulation
Diffusion of O2 and CO2 depends on the concentrations or partial pressures of gases
Movement always occurs from an area of high pressure to an area of low pressure
Each gas diffuses independent of other gases concentrations (Dalton’s Law)

Factors affecting gas exchange include:
*Fluid accumulation in the alveoli
*Surface area and and thickness of alveolar membranes, grape clusters, destruction of alveoli as w/ emphysema or scarring results in less surface area

Tests for pulmonary function:
Spirometry-pulmonary function testing
Arterial blood gases
Exercise tolerance
Culture and sensitivity – sputum cultures

*General manifestations of respiratory disease
Breathing patterns
Breath sounds
Pleural pain
Friction rub
Clubbed fingers
Changes in arterial blood gases
Acid-base imbalance

Common cold (infectious rhinitis)

The respiratory system


Types A, B and C
Viral infection
Affects upper and lower respiratory tracts
Mutate constantly, preventing an effective immune response
Elderly and very young most at risk
Can be mild, moderate or severe

Clinical Manifestations:
Sudden acute onset fever, fatigue, aches (myalgia)
Dry cough, sore throat, photophobia, chills, exhaustion
Can be complicated by secondary infection usually pneumonia
Incubation 1-4 days but can pass the virus a day before – 5 days after
Symptomatic care Tylenol, Motrin, fluids, rest
Amantadine hydrochloride – Symmetrel within 24-48 hours –for A
Zanamivir, Rimantadine, Tamiflu for A or B
Flu vaccines injectable or nasal (live)
No nasal for asthma, immune compromised, allergy eggs, hx Guillain-Barre
Greatest danger secondary infection

Can develop as a primary infection or secondary
Causative agent may be virus, bacterial, or fungus
Most cases organism enters lungs by inhalation
Risk after fluid aspiration or when fluids pool
Distributuion of lesions can be diffuse and patchy or lobar (see below)
Nosocomial hospital acquired

Lobar pneumonia
Usually bacterial, strep
Consolidated in one lobe
Emphyema when infection spreads into the pleural cavity, can cause adhesions
Chest xray confirms and sputum culture
Filling of alveoli with exudate decreases diffusion of gases
Dehydration from fever, hyperventilation and decreased fluid intake

Pneumococcal pneumonia:
Sudden, fever, chills, fatigue, leukocytosis
Dyspnea, tachypnea, tackycardia
Pleuritic pain
Rales, productive cough

Diffuse pattern primarily in the lower lobes
Often infected by organisms draining from upper passages
Onset insidious, fever, cough, rales
Sputum culture and sensitivity

Caused by gram negative Legionella pneumophilia
Microbes thrive in warm moist environments, air conditioning, spas
Difficult to identify because inside macrophages
Requires special medium

Primary atypical pneumonia
Small bacterium, lacks cell wall, found upper respiratory tract
Transmitted by aerosol
Tetracycline or erythromycin

Viral pneumonia
Caused by RSV, adenoviruses, influenza A or B
Diffuse inflammation with little exudate
Cough unproductive

Severe acute respiratory syndrome (SARS)
First noted China 2002
Genetic sequence found 2003, previously unknown
Coronavirus, RNA virus transmitted during close contact
8,000 cases, 800 deaths in 29 countries
Incubation period 2-7 days
Flu-like symptoms, fever, headache, myalgia, chills, anorexia, diarrhea
Later dry cough, dyspnea
Chest xrays patchy diffuse
Lymphopenia, thrombocytopenia
Elevated c reactive protein
Mechanical ventilation necessary
Treatment ribavirin and glucocoticoid
Fatality rate 10% to 50% in patients older than 60
Takes 3 weeks to build up antibodies

Once declining now increasing1-2% are drug resistant
Poverty, crowding
HIV, homelessness increases incidence
Number of latent cases large
10% will go on to become active infections
Caused by Mycobacterium tuberculosis
Acid fast aerobic slow growing bacillus
Can survive in dried sputum for weeks

TB infection
Microbes enter system engulfed by macrophages
Local reaction,
Bacilli to local lymph nodes, activating type IV cell mediated hypersensitivity
Lymphocytes, macrophages form granuloma contains bacilli
Forms a tubercule, caseation necrosis inside
Walled off, calcifies
Hypersensitivity is the basis for the tuberculin skin test, Mantoux

Secondary infection, reinfection, TB disease

Signs and symptoms:
Anorexia, malaise, fatigue, weight loss, low grade fever, night sweats

Acid fast sputum staining, sputum culture, xray, CT scan

Rifampin, isoniazid (INH), ethambutol, streptomycin lasting 6 months -1 year
Sputum negative after 1-2 months
Compliance important
Contacts should have TB testing and prophylactic isoniazid for 1 year

Involves the passage of food, fluid, vomitus, drugs or other foreign material into the lungs
Right lower lobe often destination
Normally a cough removes material from the upper tract
Vocal cords and epiglottis prevent entry of material into the lower tract
Aspiration pneumonia >inflammation, increased mucous, restricted airways
Aspiration is easier to prevent than fix
Seen in children
Adults talking eating – café coronary, food w/ alcohol depressed reflexes
Heimlich maneuver for adults, back blows infants


Episodes of severe but reversible bronchial obstruction
Hypersensitive or hyperresponsive airways
Characterized by edematous airways clogged with mucous
Smooth muscles of bronchi and bronchioles constrict
Air trapping occurs
Signs and Symptoms:
Cough, dyspnea, tight feeling in chest
Breathing rapid, labored
Hypoxia >resp. alkalosis > resp. acidosis
Severe respiratory distress > respiratory failure

Nursing Actions:
Skin tests for allergens
Avoidance of triggers
Good ventilation
Regular walking or swimming lessons – improve cardiovascular fitness, V stress
Prophylactic meds
Monitor for respiratory distress
Controlled breathing techniques
Stress reduction techniques
Administer bronchodilators and steroids as ordered
Maintain hydration
O2 and nebulizer therapy
Monitor blood gases and O2 sats, should be greater than 95%
Teach! Allergens, use of metered dose inhaler (MDI), management

Chronic obstructive pulmonary disease (COPD)
Common chronic respiratory disorders characterized by irreversible progressive damage and obstruction of the airways in the lungs
Chronic asthma, chronic bronchitis and emphysema, may overlap

Destruction of alveolar walls leading to permanently inflated alveolar spaces
Genetic component – lack protein which inhibits destructive neutrophil enzymes
Cigarette smoking increases neutrophils in lungs

*Breakdown of aveoli > loss of surface area for gas exchange, loss of capillaries, loss of elastic fibers, altered ventilation ration, fibrosis, difficult expiration > air trapping, over inflation > damaged aveoli may coalesce creating large air filled spaces, blebs, which can rupture and cause pneumothorax

Signs and symptoms:
Anorexia, fatigue, weight loss
Clubbed fingers
Diagnosed with chest xrays and pulmonary function tests

Avoidance of respiratory irritants
Smoking cessation
Pulmonary rehabilitation – exercise
Breathing techniques – pursed lip breathing maximizes expiration
Bronchodilators, antibiotics, O2
Lung reduction surgery


Gould, B. E., & Dyer, R. M. (2011). Pathophysiology for the health professions (4 ed.). St. Louis, Missouri: Saunders Elsevier.

Story, L. (2012). Pathophysiology: A practical approach. Sudbury, MA: Jones & Bartlett Learning .


Meet the lungs

Respiratory system