Respiratory Pathophysiology
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): purulent/pus = bacterial pneumonia
Green/greenish: longstanding lung infection = chronic bronchitis
Rust colored: TB, pneumococcal pneumonia
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: NEURO, 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
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
Pneumothorax → air ends up in thoracic cavity → causes lung collapse
Spontaneous (PRIMARY) pneumothorax: just happens, occurs in thin, tall, white, male, smokers at risk
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
Lungs are restricted from fully expanding; troubles inhaling
Air has a problem going into the lungs
Condition: stiffness in the lungs, chest wall, weak muscles, or damaged nerves may cause restriction
Hard 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
Parenchymal:
Atelectasis
Fluid (edema, pus, blood)
ARDS
Trauma
Autoimmune
Chronic infections
Occupational
Environmental
Extra-pulmonary
Obesity
Scoliosis
Neuromuscular
Myasthenia gravis
ALS
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)
RESTRICTIVE
Loss of lung volume due to the collapse of alveoli
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)
RESTRICTIVE
Acute respiratory distress syndrome
Most severe form of acute lung injury; highest mortality rate (impacts both alveoli & blood vessels/ alveolocapillary membrane)
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 ==
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
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
OBSTRUCTIVE
Reversible airflow obstruction
LOCATION: Small bronchi, bronchioles
Typer I hypersensitivity reaction
Most common chronic disease in children
NO KNOWN CAUSE (genetic vs. environmental)
Allergen or irritant exposure
Mast cell degranulation and release of mediators → bind to receptors
Mediator effects:
Mucus production → mucus plug
Vascular leak → cell edema
Airway smooth muscle constriction → bronchoconstriction
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)
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)
Clinical, doesn’t require $ testing
ABGs
Pulse Ox.
Chest radiography
ABGs and Pulse Ox. determine severity
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
Class | Days w/symptoms | Nights w/symptoms |
---|---|---|
Severe persistent | Continual | Frequent |
Moderate persistent | Daily | >5/mo |
Mild persistent | >2/wk | 3-4/mo |
Mild intermittent | <2/wk | <2/mo |
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
^^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
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
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
==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
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)”
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
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)
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
Cough w/blood
Weight loss/anorexia
Fever (low grade, 100-100.5)
==NIGHT SWEATS = distinctive sign of active infection ==
Hemoptysis
Chest pain
Fatigue
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
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 mm | Moderate risk | Recent immigrants, drug users (injections), children <4yrs, infants/children/adolescents exposed to adults at high risk for developing TB |
15 mm | Low risk | Any 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 +
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): purulent/pus = bacterial pneumonia
Green/greenish: longstanding lung infection = chronic bronchitis
Rust colored: TB, pneumococcal pneumonia
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: NEURO, 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
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
Pneumothorax → air ends up in thoracic cavity → causes lung collapse
Spontaneous (PRIMARY) pneumothorax: just happens, occurs in thin, tall, white, male, smokers at risk
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
Lungs are restricted from fully expanding; troubles inhaling
Air has a problem going into the lungs
Condition: stiffness in the lungs, chest wall, weak muscles, or damaged nerves may cause restriction
Hard 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
Parenchymal:
Atelectasis
Fluid (edema, pus, blood)
ARDS
Trauma
Autoimmune
Chronic infections
Occupational
Environmental
Extra-pulmonary
Obesity
Scoliosis
Neuromuscular
Myasthenia gravis
ALS
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)
RESTRICTIVE
Loss of lung volume due to the collapse of alveoli
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)
RESTRICTIVE
Acute respiratory distress syndrome
Most severe form of acute lung injury; highest mortality rate (impacts both alveoli & blood vessels/ alveolocapillary membrane)
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 ==
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
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
OBSTRUCTIVE
Reversible airflow obstruction
LOCATION: Small bronchi, bronchioles
Typer I hypersensitivity reaction
Most common chronic disease in children
NO KNOWN CAUSE (genetic vs. environmental)
Allergen or irritant exposure
Mast cell degranulation and release of mediators → bind to receptors
Mediator effects:
Mucus production → mucus plug
Vascular leak → cell edema
Airway smooth muscle constriction → bronchoconstriction
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)
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)
Clinical, doesn’t require $ testing
ABGs
Pulse Ox.
Chest radiography
ABGs and Pulse Ox. determine severity
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
Class | Days w/symptoms | Nights w/symptoms |
---|---|---|
Severe persistent | Continual | Frequent |
Moderate persistent | Daily | >5/mo |
Mild persistent | >2/wk | 3-4/mo |
Mild intermittent | <2/wk | <2/mo |
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
^^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
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
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
==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
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)”
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
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)
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
Cough w/blood
Weight loss/anorexia
Fever (low grade, 100-100.5)
==NIGHT SWEATS = distinctive sign of active infection ==
Hemoptysis
Chest pain
Fatigue
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
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 mm | Moderate risk | Recent immigrants, drug users (injections), children <4yrs, infants/children/adolescents exposed to adults at high risk for developing TB |
15 mm | Low risk | Any 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 +